The Use of Tranexamic Acid and Microneedling in the Treatment of Melasma: A Systematic Review

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The Use of Tranexamic Acid and Microneedling in the Treatment of Melasma: A Systematic Review

Melasma (also known as chloasma faciei) is a common chronic skin disorder that results in well-demarcated, hyperpigmented, tan to dark patches that mostly appear in sun-exposed areas such as the face and neck and sometimes the arms. The exact prevalence or incidence is not known but is estimated to be 1% to 50% overall depending on the ethnic population and geographic location.1,2 Melasma predominantly affects women, but research has shown that approximately 10% to 20% of men are affected by this condition.3,4 Although melasma can affect patients of all skin types, it primarily affects those with darker skin tones.5 The groups most often affected are women of Black, Hispanic, Middle Eastern, and Southeast Asian ethnicity. Although the pathogenesis is complex and not fully understood, multiple pathways and etiologies have been theorized to cause melasma. Potential causes include exposure to UV radiation, oral contraceptives, hormonal changes, medications, thyroid dysfunction, genetics, and pregnancy.6,7 Cytokines and growth factors, including adipokine and angiopoietin, synthesized by sebaceous glands play a role in the pathogenic mechanism of melasma. Cytokines and growth factors are hypothesized to modulate the function of melanocytes.8 Both melanocytes and sebocytes are controlled by α–melanocyte-stimulating hormone. Therefore, overexpression of α–melanocyte-stimulating hormone will result in overproduction of these 2 cell types, resulting in melasma. Melasma can be classified into 4 subtypes using Wood lamp examination: epidermal, dermal, mixed, or indeterminate.3 Furthermore, melasma is divided into subgroups based on the location: malar region, mandibular region, and centrofacial patch pattern.9,10 The involvement of sebaceous glands in the pathogenesis of melasma may explain the predilection for the centrofacial region, which is the most common pattern.

The severity of melasma can be assessed using the melasma area and severity index (MASI), which is calculated by subjective assessment of 3 main factors: (1) facial area of involvement; (2) darkness of affected region; and (3) homogeneity, with the extent of melasma indicated by a score ranging from 0 to 48.11 The modified MASI (mMASI) subsequently was introduced to assist with assessing the severity of melasma and creating distinct ranges for mild, moderate, and severe cases, ranging from 0 (mild) to 24 (severe).12 Both indices are used in research to assess the improvement of melasma with treatment.

Patients with melasma report a decrease in quality of life, increased emotional stress, and lower self-esteem due to cosmesis.13 Treatment of melasma can be highly challenging and often is complicated by relapsing. Historically, the treatment of melasma has included the use of chemical lightening agents. Additional treatment options include the use of lasers and complex chemical peels,9,10 but these interventions may result in adverse outcomes for individuals with darker skin tones. The current gold-standard treatment is topical hydroquinone and broad-spectrum sunscreen. Although hydroquinone is effective in the treatment of melasma, relapse is common. The goal of melasma management is not only to treat acute hyperpigmentation but also to prevent relapse. Other therapies that currently are being explored for the clinically sustained treatment of melasma include tranexamic acid (TXA)(trans-4-[aminomethyl]cyclohexanecarboxylic acid),9,10 an antifibrinolytic agent routinely used to prevent blood loss during surgery and in the management of menorrhagia. It is a synthetic derivative of lysine and serves as a potent plasmin inhibitor by blocking the lysine-binding sites of plasminogen molecules, thus preventing the conversion of plasminogen to plasmin. It also prevents fibrinolysis and blood loss.

In addition to its hemostatic properties, TXA has been found to have hypopigmentation properties.14,15 Plasminogen also can be found in human epidermal basal cells and human keratinocytes, and it is postulated that TXA’s interaction with these cells explains its hypopigmentation properties. Both UV radiation and hormones activate plasminogen into plasmin, resulting in the activation of tyrosinase and melanogenesis.14,15 Tranexamic acid is postulated to inhibit the keratinocyte-plasminogen pathway, thus leading to the inhibition of UV-induced and hormone-induced pigmentation. Also, TXA serves as a competitive inhibitor for tyrosinase due to its structural similarity to tyrosine.15 The combination of these 2 mechanisms contributes to the skin-lightening effects of TXA, making it a potential treatment for melasma.

Furthermore, the use of microneedling is being explored as a treatment option for melasma. Microneedling creates microscopic punctures in the skin using tiny needles, resulting in a wound-healing response and skin resurfacing. The microneedling technique is utilized to create small holes in the skin, with needle depths that can be adjusted from 0.5 to 3.5 mm to target different layers of the dermis and allow for discreet application of TXA.16 We sought to look at the current literature on the use and effectiveness of microneedling in combination with TXA to treat melasma and prevent relapse.

 

 

Methods

A systematic review was performed of PubMed articles indexed for MEDLINE and Embase in November 2021 to compile available articles that studied TXA and microneedling as a treatment for melasma. The PubMed search terms were (melasma) AND (microneedling* OR ‘tranexamic acid’ OR TXA or TA). The Embase search terms were (cholasma OR melasma) AND (tranexamic acid OR TXA) AND (microneedling)(Figure). The search was then limited to ”randomized controlled trial” and ”clinical trial” in English-language journals. Duplicates were excluded. After thorough evaluation, articles that discussed the use of TXA in combination with treatment options other than microneedling also were excluded.

Flow diagram of study selection. Asterisk indicates platelet-rich plasma, vitamin C, kojic acid, niacinamide, Kligman’s therapy (fluocinolone + hydroquinone + tretinoin), retinoic acid, and cysteamine.

Results

The literature search yielded a total of 12 articles that assessed the effectiveness of TXA and microneedling for the treatment of melasma (Table).17-28 Several articles concluded that TXA was equally effective at reducing melasma lesions when compared with the standard treatment of hydroquinone. Some of the reviewed articles also demonstrated the effectiveness of microneedling in improving melasma lesions as a stand-alone treatment. These studies highlighted the enhanced efficacy of the combined treatment of TXA and microneedling compared with their individual uses.17-28

Comment

Melasma is a common chronic hyperpigmentation disorder, making its treatment clinically challenging. Many patients experience symptom relapses, and limited effective treatment options make achieving complete clearance difficult, underscoring the need for improved therapeutic approaches. Recently, researchers have explored alternative treatments to address the challenges of melasma management. Tranexamic acid is an antifibrinolytic used to prevent blood loss and has emerged as a potential treatment for melasma. Similarly, microneedling—a technique in which multiple punctures are made in the skin to activate and stimulate wound healing and skin rejuvenation—shows promise for melasma.

Oral TXA for Melasma—Oral TXA has been shown to reduce melasma lesions. Del Rosario et al17 recruited 44 women (39 of whom completed the study) with moderate to severe melasma and randomized them into 2 groups: oral TXA and placebo. This study demonstrated a 49% reduction in the mMASI score in all participants taking oral TXA (250 mg twice daily [BID]) compared with an 18% reduction in the control group (placebo capsule BID) after 3 months of treatment. In patients with moderate and severe melasma, 45% and 51% mMASI score reductions were reported in the treatment group, respectively, vs 16% and 19% score reductions in placebo group, respectively. These researchers concluded that oral TXA may be effective at treating moderate to severe melasma. Although patients with severe melasma had a better response to treatment, their improvement was not sustained compared with patients with moderate melasma after a 3-month posttreatment follow-up.17

Microneedling Plus TXA for Melasma—Microneedling alone has been shown to be effective for melasma. El Attar et al18 conducted a split-face study of microneedling (1.5-mm depth) plus topical TXA (0.5 mL)(right side of the face[treatment arm]) compared with microneedling (1.5-mm depth) plus topical vitamin C (0.5 mL)(left side of the face [control group]) in 20 women with melasma. The sessions were repeated every 2 weeks for a total of 6 sessions. Although researchers found no statistically significant differences between the 2 treatment sides, microneedling plus TXA showed a slight advantage over microneedling plus vitamin C in dermoscopic examination. Both sides showed improvement in pigmented lesions, but vitamin C–treated lesions did not show an improvement in vascularity vs TXA.18

Saleh et al19 further showed that combination treatment with microneedling and TXA may improve clinical outcomes better than microneedling alone. Their study demonstrated a reduction in MASI score that was significantly higher in the combination treatment group compared with the microneedling alone group (P=.001). There was a significant reduction in melanoma antigen recognized by T cells 1 (MART-1)–positive cells in the combination treatment group compared with the microneedling alone group (P=.001). Lastly, combined therapy improved melasma patches better than microneedling alone.19

 

Xu et al20 conducted a split-face study (N=28) exploring the effectiveness of transdermal application of topical TXA using a microarray pen with microneedles (vibration at 3000×/min) plus topical TXA on one side of the face, while the other side received only topical TXA as a control. After 12 weeks of treatment, combination therapy with microneedling and TXA decreased brown spot scores, lowered melanin index (MI) values, improved blinded physician assessment, and improved patient satisfaction vs TXA therapy alone.20

Kaur et al21 conducted a split-face, randomized, controlled trial of microneedling (1-mm depth) with TXA solution 10% vs microneedling (1-mm depth) with distilled water alone for 8 weeks (N=40). They graded participant responses to treatment using reductions in mMASI scores12 at every 2 weeks of follow-up (no response, minimal or poor response=0%–25%; partial or fair response=26%–50%; good response=51%–75%; and excellent response=>75%). They reported an overall reduction in mMASI scores for both the treatment side and the control side in all participants, showing a 65.92% improvement in mean mMASI scores on the treatment side vs 20.75% improvement on the control side at week 8. Both sides showed statistically significant reductions in mean mMASI scores (P<.05). Clinically, 40% (16/40) of participants showed an excellent response to combined treatment compared with 0% (0/40) to microneedling alone. Overall, patient satisfaction was similar across both groups. This study demonstrated that microneedling alone improves melasma, but a combination of microneedling plus TXA showed a better clinical reduction in melasma. However, the researchers did not follow up with participants posttreatment, so it remains unclear if the improved clinical outcomes were sustained long-term.21

Ebrahim et al22 reported that the combination of 0.5 mL TXA (4 mg/mL) and microneedling (0.25- to 1-mm depth) was effective for melasma. Although there was improvement within microneedling and TXA, the study also showed that intradermal injection of TXA was significant in reducing mean mMASI scores and improving melasma (P<.001). The reduction in mMASI scores for the group receiving intradermal injections of TXA (left side; 74.8% reduction in mean mMASI score) vs the group receiving microneedling application of TXA (right side; 73.6% reduction in mean mMASI score) was not statistically significant. These findings suggest that the mode of TXA application may not be critical in determining clinical responses to TXA treatment. Although there was no reported statistically significant difference in clinical outcomes between the 2 treatments, patient satisfaction was higher on the microneedling side. Only 8 of 50 participants (16%) experienced recurrence 3 months posttreatment.22

Saki et al23 compared the efficacy of topical hydroquinone (2%) to intradermal TXA injections in treating melasma. They found intradermal TXA injections to be a clinically effective mode of treatment.23

Sharma et al24 explored the efficacy and safety of oral TXA by randomly assigning 100 Indian patients (20 of whom withdrew before study completion) with melasma into 2 groups: group A received TXA 250 mg twice daily, and group B received intradermal microinjections of TXA (4 mg/mL) every 4 weeks. The MASI scores were assessed at 4-week intervals for a total of 12 weeks. There was a decrease in MASI scores in both groups, and there was no statistically significant difference in mean percentage reduction in MASI scores between the 2 routes of drug administration, further suggesting the effectiveness of TXA independent of administration route. Two patients in group A relapsed at 24 weeks, and there were no relapses in group B, which may suggest a minimal superiority of TXA plus microneedling at providing more sustainable results compared with oral TXA alone. A notable limitation of this study was a high dropout rate as well as lack of long-term follow-up with participants, limiting the generalizability of the conclusions.24

Cassiano et al25 assigned 64 women with melasma to 1 of 3 treatment groups or a control group to compare the effectiveness of microneedling (M group: 1.5 mm; 2 sessions), oral TXA (T group: 250 mg/d twice daily for 60 days), and a combination of microneedling (2 sessions) and oral TXA (MT group: 250 mg/d twice daily for 60 days)with placebo for clinically reducing melasma lesions. The intervention period was 60 days followed by a 60-day maintenance phase for a total study period of 120 days. The researchers evaluated mMASI scores, quality of life, and difference in colorimetric luminosity. All treatment groups showed a reduction in mMASI scores at both 30 days and 60 days, indicating improved melasma severity. The MT and T groups had more significant improvement at 30 days compared with the control group (P<.03), suggesting that microneedling plus TXA and TXA alone promote faster improvement in melasma lesions. By 60 days, the M, T, and MT groups outperformed the control group, with no significant differences between the M, T, and MT groups. However, at the 120-day maintenance follow-up, the T group did not maintain its improvement compared with the control group. The M and MT groups showed no significance difference in effectiveness at 120 days, suggesting that microneedling may promote less frequent relapse and sustained remission compared to TXA alone.25

Hydroquinone for Melasma—Additional studies on the use of TXA treatments show that TXA may be an equally effective alternative to the standard use of hydroquinone treatment. Shamsi Meymandi et al26 did not find a statistically significant difference in treatment with TXA plus microneedling vs the standard regimen of hydroquinone. More importantly, patient and physician satisfaction assessments were similar between the 2 groups. Compared to hydroquinone, nightly treatment is not necessary with microneedling and TXA.26

Xing et al27 supported these conclusions with their study. They compared 3 study arms for a duration of 12 weeks: group A received topical 1.8% liposomal TXA BID, group B received stamp-mode electric microneedling with 5% TXA weekly, and group C applied 2% ­hydroquinone cream nightly. The study concluded that all 3 groups showed a significant reduction in mean MI by the end of the study, but a better MI improvement was observed in groups B and C (both P<.001) compared with group A (P<.01).27

Zaky et al28 showed that both hydroquinone and combination treatment of TXA plus microneedling are effective at improving melasma lesions. Further studies are needed to definitively conclude if combination treatment is more efficacious than hydroquinone; if the combination is more effective, it provides a treatment option for patients with melasma who may not be good candidates for hydroquinone treatment.

Study Limitations—One limitation in all the studies evaluated is the sample size. Because they all had small sample sizes, it is difficult to definitively conclude that the combination TXA and microneedling is an effective and appropriate treatment for patients with melasma. Furthermore, the quality of these studies was mostly dependent on subjectivity of the mMASI scores. Future large randomized controlled trials with a diverse participant population are needed to assess the effectiveness of TXA and microneedling in melasma treatment.

Another limitation is that many of the studies did not follow the patients longitudinally, which did not allow for an evaluation of whether patients had a relapse of melasma. Due to the chronic nature of melasma and frequent disease recurrence, future longitudinal studies are needed to monitor for disease recurrence.

Conclusion

Tranexamic acid and microneedling are potential treatment options for patients with melasma, and combination therapy appears more effective than either TXA or microneedling alone at providing sustained improvement of melasma lesions. Combination therapy appears safe and well tolerated, but its effect on reducing long-term disease recurrence is yet to be established.

References
  1. Neagu N, Conforti C, Agozzino M, et al. Melasma treatment: a systematic review. J Dermatolog Treat. 2022;33:1816-1837. doi:10.1080/09546634.2021.1914313
  2. Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther (Heidelb). 2017;7:305-318. doi:10.1007/s13555-017-0194-1
  3. Mahajan VK, Patil A, Blicharz L, et al. Medical therapies for melasma. J Cosmet Dermatol. 2022;21:3707-3728. doi:10.1111/jocd.15242
  4. Rigopoulos D, Gregoriou S, Katsambas A. Hyperpigmentation and melasma. J Cosmet Dermatol. 2007;6:195-202. doi:10.1111/j.1473-2165.2007.00321.x
  5. Kagha K, Fabi S, Goldman M. Melasma’s impact on quality of life. J Drugs Dermatol. 2020;19:184-187. doi:10.36849/JDD.2020.4663
  6. Lutfi RJ, Fridmanis M, Misiunas AL, et al. Association of melasma with thyroid autoimmunity and other thyroidal abnormalities and their relationship to the origin of the melasma. J Clin Endocrinol Metab. 1985;61:28-31. doi:10.1210/jcem-61-1-28
  7. Handel AC, Lima PB, Tonolli VM, et al. Risk factors for facial melasma in women: a case-control study. Br J Dermatol. 2014;171:588-594. doi:10.1111/bjd.13059
  8. Filoni A, Mariano M, Cameli N. Melasma: how hormones can modulate skin pigmentation. J Cosmet Dermatol. 2019;18:458-463. doi:10.1111/jocd.12877
  9. Rodrigues M, Pandya AG. Melasma: clinical diagnosis and management options. Australasian J Dermatol. 2015;56:151-163.
  10. Huerth KA, Hassan S, Callender VD. Therapeutic insights in melasma and hyperpigmentation management. J Drugs Dermatol. 2019;18:718-727.
  11. Pandya AG, Hynan LS, Bhore R, et al. Reliability assessment and validation of the Melasma Area and Severity Index (MASI) and a new modified MASI scoring method. J Am Acad Dermatol. 2011;64:78-­83.e832. doi:10.1016/j.jaad.2009.10.051
  12. Rodrigues M, Ayala-Cortés AS, Rodríguez-Arámbula A, et al. Interpretability of the modified Melasma Area and Severity Index (mMASI). JAMA Dermatol. 2016;152:1051-1052. doi:10.1001/jamadermatol.2016.1006
  13. Ikino JK, Nunes DH, da Silva VPM, et al. Melasma and assessment of the quality of life in Brazilian women. An Bras Dermatol. 2015;90:196-200. doi:10.1590/abd1806-4841.20152771
  14. Taraz M, Niknam S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies. Dermatolog Ther. 2017;30:E12465. doi:10.1111/dth.12465
  15. Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825. doi:10.1097/DSS.0000000000001518
  16. Singh A, Yadav S. Microneedling: advances and widening horizons. Indian Dermatol Online J. 2016;7:244-254. doi:10.4103/2229-5178.185468
  17. Del Rosario E, Florez-Pollack S, Zapata L, et al. Randomized, placebo-controlled, double-blind study of oral tranexamic acid in the treatment of moderate-to-severe melasma. J Am Acad Dermatol. 2018;78:363-369. doi:10.1016/j.jaad.2017.09.053
  18. El Attar Y, Doghaim N, El Far N, et al. Efficacy and safety of tranexamic acid versus vitamin C after microneedling in treatment of melasma: clinical and dermoscopic study. J Cosmet Dermatol. 2022;21:2817-2825. doi:10.1111/jocd.14538
  19. Saleh FY, Abdel-Azim ES, Ragaie MH, et al. Topical tranexamic acid with microneedling versus microneedling alone in treatment of melasma: clinical, histopathologic, and immunohistochemical study. J Egyptian Womens Dermatolog Soc. 2019;16:89-96. doi:10.4103/jewd.jewd_25_19
  20. Xu Y, Ma R, Juliandri J, et al. Efficacy of functional microarray of microneedles combined with topical tranexamic acid for melasma: a randomized, self-controlled, split-face study. Medicine (Baltimore). 2017;96:e6897. doi:10.1097/MD.0000000000006897
  21. Kaur A, Bhalla M, Pal Thami G, et al. Clinical efficacy of topical tranexamic acid with microneedling in melasma. Dermatol Surg. 2020;46:E96-E101. doi:10.1097/DSS.0000000000002520
  22. Ebrahim HM, Said Abdelshafy A, Khattab F, et al. Tranexamic acid for melasma treatment: a split-face study. Dermatol Surg. 2020;46:E102-E107. doi:10.1097/DSS.0000000000002449
  23. Saki N, Darayesh M, Heiran A. Comparing the efficacy of topical hydroquinone 2% versus intradermal tranexamic acid microinjections in treating melasma: a split-face controlled trial. J Dermatolog Treat. 2018;29:405-410. doi:10.1080/09546634.2017.1392476
  24. Sharma R, Mahajan VK, Mehta KS, et al. Therapeutic efficacy and safety of oral tranexamic acid and that of tranexamic acid local infiltration with microinjections in patients with melasma: a comparative study. Clin Exp Dermatol. 2017;42:728-734. doi:10.1111/ced.13164
  25. Cassiano D, Esposito ACC, Hassun K, et al. Efficacy and safety of microneedling and oral tranexamic acid in the treatment of facial melasma in women: an open, evaluator-blinded, randomized clinical trial. J Am Acad Dermatol. 2020;83:1176-1178. doi:10.1016/j.jaad.2020.02.002
  26. Shamsi Meymandi S, Mozayyeni A, Shamsi Meymandi M, et al. Efficacy of microneedling plus topical 4% tranexamic acid solution vs 4% hydroquinone in the treatment of melasma: a single-blind randomized clinical trial. J Cosmet Dermatol. 2020;19:2906-2911. doi:10.1111/jocd.13392
  27. Xing X, Chen L, Xu Z, et al. The efficacy and safety of topical tranexamic acid (liposomal or lotion with microneedling) versus conventional hydroquinone in the treatment of melasma. J Cosmet Dermatol. 2020;19:3238-3244. doi:10.1111/jocd.13810
  28. Zaky MS, Obaid ZM, Khalil EA, et al. Microneedling-assisted topical tranexamic acid solution versus 4% hydroquinone for treating melasma: a split-face randomized study. J Cosmet Dermatol. 2021;20:4011-4016. doi:10.1111/jocd.14440
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Idowu D. Olugbade is from the Warren Alpert Medical School of Brown University, Providence, Rhode Island. Dr. Negbenebor is from the Department of Dermatology, University of Iowa, Iowa City.

The authors report no conflict of interest.

Correspondence: Nicole A. Negbenebor, MD (nicole-negbenebor@uiowa.edu).

Cutis. 2024 August;114(2):E15-E23. doi:10.12788/cutis.1080

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Idowu D. Olugbade is from the Warren Alpert Medical School of Brown University, Providence, Rhode Island. Dr. Negbenebor is from the Department of Dermatology, University of Iowa, Iowa City.

The authors report no conflict of interest.

Correspondence: Nicole A. Negbenebor, MD (nicole-negbenebor@uiowa.edu).

Cutis. 2024 August;114(2):E15-E23. doi:10.12788/cutis.1080

Author and Disclosure Information

Idowu D. Olugbade is from the Warren Alpert Medical School of Brown University, Providence, Rhode Island. Dr. Negbenebor is from the Department of Dermatology, University of Iowa, Iowa City.

The authors report no conflict of interest.

Correspondence: Nicole A. Negbenebor, MD (nicole-negbenebor@uiowa.edu).

Cutis. 2024 August;114(2):E15-E23. doi:10.12788/cutis.1080

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Melasma (also known as chloasma faciei) is a common chronic skin disorder that results in well-demarcated, hyperpigmented, tan to dark patches that mostly appear in sun-exposed areas such as the face and neck and sometimes the arms. The exact prevalence or incidence is not known but is estimated to be 1% to 50% overall depending on the ethnic population and geographic location.1,2 Melasma predominantly affects women, but research has shown that approximately 10% to 20% of men are affected by this condition.3,4 Although melasma can affect patients of all skin types, it primarily affects those with darker skin tones.5 The groups most often affected are women of Black, Hispanic, Middle Eastern, and Southeast Asian ethnicity. Although the pathogenesis is complex and not fully understood, multiple pathways and etiologies have been theorized to cause melasma. Potential causes include exposure to UV radiation, oral contraceptives, hormonal changes, medications, thyroid dysfunction, genetics, and pregnancy.6,7 Cytokines and growth factors, including adipokine and angiopoietin, synthesized by sebaceous glands play a role in the pathogenic mechanism of melasma. Cytokines and growth factors are hypothesized to modulate the function of melanocytes.8 Both melanocytes and sebocytes are controlled by α–melanocyte-stimulating hormone. Therefore, overexpression of α–melanocyte-stimulating hormone will result in overproduction of these 2 cell types, resulting in melasma. Melasma can be classified into 4 subtypes using Wood lamp examination: epidermal, dermal, mixed, or indeterminate.3 Furthermore, melasma is divided into subgroups based on the location: malar region, mandibular region, and centrofacial patch pattern.9,10 The involvement of sebaceous glands in the pathogenesis of melasma may explain the predilection for the centrofacial region, which is the most common pattern.

The severity of melasma can be assessed using the melasma area and severity index (MASI), which is calculated by subjective assessment of 3 main factors: (1) facial area of involvement; (2) darkness of affected region; and (3) homogeneity, with the extent of melasma indicated by a score ranging from 0 to 48.11 The modified MASI (mMASI) subsequently was introduced to assist with assessing the severity of melasma and creating distinct ranges for mild, moderate, and severe cases, ranging from 0 (mild) to 24 (severe).12 Both indices are used in research to assess the improvement of melasma with treatment.

Patients with melasma report a decrease in quality of life, increased emotional stress, and lower self-esteem due to cosmesis.13 Treatment of melasma can be highly challenging and often is complicated by relapsing. Historically, the treatment of melasma has included the use of chemical lightening agents. Additional treatment options include the use of lasers and complex chemical peels,9,10 but these interventions may result in adverse outcomes for individuals with darker skin tones. The current gold-standard treatment is topical hydroquinone and broad-spectrum sunscreen. Although hydroquinone is effective in the treatment of melasma, relapse is common. The goal of melasma management is not only to treat acute hyperpigmentation but also to prevent relapse. Other therapies that currently are being explored for the clinically sustained treatment of melasma include tranexamic acid (TXA)(trans-4-[aminomethyl]cyclohexanecarboxylic acid),9,10 an antifibrinolytic agent routinely used to prevent blood loss during surgery and in the management of menorrhagia. It is a synthetic derivative of lysine and serves as a potent plasmin inhibitor by blocking the lysine-binding sites of plasminogen molecules, thus preventing the conversion of plasminogen to plasmin. It also prevents fibrinolysis and blood loss.

In addition to its hemostatic properties, TXA has been found to have hypopigmentation properties.14,15 Plasminogen also can be found in human epidermal basal cells and human keratinocytes, and it is postulated that TXA’s interaction with these cells explains its hypopigmentation properties. Both UV radiation and hormones activate plasminogen into plasmin, resulting in the activation of tyrosinase and melanogenesis.14,15 Tranexamic acid is postulated to inhibit the keratinocyte-plasminogen pathway, thus leading to the inhibition of UV-induced and hormone-induced pigmentation. Also, TXA serves as a competitive inhibitor for tyrosinase due to its structural similarity to tyrosine.15 The combination of these 2 mechanisms contributes to the skin-lightening effects of TXA, making it a potential treatment for melasma.

Furthermore, the use of microneedling is being explored as a treatment option for melasma. Microneedling creates microscopic punctures in the skin using tiny needles, resulting in a wound-healing response and skin resurfacing. The microneedling technique is utilized to create small holes in the skin, with needle depths that can be adjusted from 0.5 to 3.5 mm to target different layers of the dermis and allow for discreet application of TXA.16 We sought to look at the current literature on the use and effectiveness of microneedling in combination with TXA to treat melasma and prevent relapse.

 

 

Methods

A systematic review was performed of PubMed articles indexed for MEDLINE and Embase in November 2021 to compile available articles that studied TXA and microneedling as a treatment for melasma. The PubMed search terms were (melasma) AND (microneedling* OR ‘tranexamic acid’ OR TXA or TA). The Embase search terms were (cholasma OR melasma) AND (tranexamic acid OR TXA) AND (microneedling)(Figure). The search was then limited to ”randomized controlled trial” and ”clinical trial” in English-language journals. Duplicates were excluded. After thorough evaluation, articles that discussed the use of TXA in combination with treatment options other than microneedling also were excluded.

Flow diagram of study selection. Asterisk indicates platelet-rich plasma, vitamin C, kojic acid, niacinamide, Kligman’s therapy (fluocinolone + hydroquinone + tretinoin), retinoic acid, and cysteamine.

Results

The literature search yielded a total of 12 articles that assessed the effectiveness of TXA and microneedling for the treatment of melasma (Table).17-28 Several articles concluded that TXA was equally effective at reducing melasma lesions when compared with the standard treatment of hydroquinone. Some of the reviewed articles also demonstrated the effectiveness of microneedling in improving melasma lesions as a stand-alone treatment. These studies highlighted the enhanced efficacy of the combined treatment of TXA and microneedling compared with their individual uses.17-28

Comment

Melasma is a common chronic hyperpigmentation disorder, making its treatment clinically challenging. Many patients experience symptom relapses, and limited effective treatment options make achieving complete clearance difficult, underscoring the need for improved therapeutic approaches. Recently, researchers have explored alternative treatments to address the challenges of melasma management. Tranexamic acid is an antifibrinolytic used to prevent blood loss and has emerged as a potential treatment for melasma. Similarly, microneedling—a technique in which multiple punctures are made in the skin to activate and stimulate wound healing and skin rejuvenation—shows promise for melasma.

Oral TXA for Melasma—Oral TXA has been shown to reduce melasma lesions. Del Rosario et al17 recruited 44 women (39 of whom completed the study) with moderate to severe melasma and randomized them into 2 groups: oral TXA and placebo. This study demonstrated a 49% reduction in the mMASI score in all participants taking oral TXA (250 mg twice daily [BID]) compared with an 18% reduction in the control group (placebo capsule BID) after 3 months of treatment. In patients with moderate and severe melasma, 45% and 51% mMASI score reductions were reported in the treatment group, respectively, vs 16% and 19% score reductions in placebo group, respectively. These researchers concluded that oral TXA may be effective at treating moderate to severe melasma. Although patients with severe melasma had a better response to treatment, their improvement was not sustained compared with patients with moderate melasma after a 3-month posttreatment follow-up.17

Microneedling Plus TXA for Melasma—Microneedling alone has been shown to be effective for melasma. El Attar et al18 conducted a split-face study of microneedling (1.5-mm depth) plus topical TXA (0.5 mL)(right side of the face[treatment arm]) compared with microneedling (1.5-mm depth) plus topical vitamin C (0.5 mL)(left side of the face [control group]) in 20 women with melasma. The sessions were repeated every 2 weeks for a total of 6 sessions. Although researchers found no statistically significant differences between the 2 treatment sides, microneedling plus TXA showed a slight advantage over microneedling plus vitamin C in dermoscopic examination. Both sides showed improvement in pigmented lesions, but vitamin C–treated lesions did not show an improvement in vascularity vs TXA.18

Saleh et al19 further showed that combination treatment with microneedling and TXA may improve clinical outcomes better than microneedling alone. Their study demonstrated a reduction in MASI score that was significantly higher in the combination treatment group compared with the microneedling alone group (P=.001). There was a significant reduction in melanoma antigen recognized by T cells 1 (MART-1)–positive cells in the combination treatment group compared with the microneedling alone group (P=.001). Lastly, combined therapy improved melasma patches better than microneedling alone.19

 

Xu et al20 conducted a split-face study (N=28) exploring the effectiveness of transdermal application of topical TXA using a microarray pen with microneedles (vibration at 3000×/min) plus topical TXA on one side of the face, while the other side received only topical TXA as a control. After 12 weeks of treatment, combination therapy with microneedling and TXA decreased brown spot scores, lowered melanin index (MI) values, improved blinded physician assessment, and improved patient satisfaction vs TXA therapy alone.20

Kaur et al21 conducted a split-face, randomized, controlled trial of microneedling (1-mm depth) with TXA solution 10% vs microneedling (1-mm depth) with distilled water alone for 8 weeks (N=40). They graded participant responses to treatment using reductions in mMASI scores12 at every 2 weeks of follow-up (no response, minimal or poor response=0%–25%; partial or fair response=26%–50%; good response=51%–75%; and excellent response=>75%). They reported an overall reduction in mMASI scores for both the treatment side and the control side in all participants, showing a 65.92% improvement in mean mMASI scores on the treatment side vs 20.75% improvement on the control side at week 8. Both sides showed statistically significant reductions in mean mMASI scores (P<.05). Clinically, 40% (16/40) of participants showed an excellent response to combined treatment compared with 0% (0/40) to microneedling alone. Overall, patient satisfaction was similar across both groups. This study demonstrated that microneedling alone improves melasma, but a combination of microneedling plus TXA showed a better clinical reduction in melasma. However, the researchers did not follow up with participants posttreatment, so it remains unclear if the improved clinical outcomes were sustained long-term.21

Ebrahim et al22 reported that the combination of 0.5 mL TXA (4 mg/mL) and microneedling (0.25- to 1-mm depth) was effective for melasma. Although there was improvement within microneedling and TXA, the study also showed that intradermal injection of TXA was significant in reducing mean mMASI scores and improving melasma (P<.001). The reduction in mMASI scores for the group receiving intradermal injections of TXA (left side; 74.8% reduction in mean mMASI score) vs the group receiving microneedling application of TXA (right side; 73.6% reduction in mean mMASI score) was not statistically significant. These findings suggest that the mode of TXA application may not be critical in determining clinical responses to TXA treatment. Although there was no reported statistically significant difference in clinical outcomes between the 2 treatments, patient satisfaction was higher on the microneedling side. Only 8 of 50 participants (16%) experienced recurrence 3 months posttreatment.22

Saki et al23 compared the efficacy of topical hydroquinone (2%) to intradermal TXA injections in treating melasma. They found intradermal TXA injections to be a clinically effective mode of treatment.23

Sharma et al24 explored the efficacy and safety of oral TXA by randomly assigning 100 Indian patients (20 of whom withdrew before study completion) with melasma into 2 groups: group A received TXA 250 mg twice daily, and group B received intradermal microinjections of TXA (4 mg/mL) every 4 weeks. The MASI scores were assessed at 4-week intervals for a total of 12 weeks. There was a decrease in MASI scores in both groups, and there was no statistically significant difference in mean percentage reduction in MASI scores between the 2 routes of drug administration, further suggesting the effectiveness of TXA independent of administration route. Two patients in group A relapsed at 24 weeks, and there were no relapses in group B, which may suggest a minimal superiority of TXA plus microneedling at providing more sustainable results compared with oral TXA alone. A notable limitation of this study was a high dropout rate as well as lack of long-term follow-up with participants, limiting the generalizability of the conclusions.24

Cassiano et al25 assigned 64 women with melasma to 1 of 3 treatment groups or a control group to compare the effectiveness of microneedling (M group: 1.5 mm; 2 sessions), oral TXA (T group: 250 mg/d twice daily for 60 days), and a combination of microneedling (2 sessions) and oral TXA (MT group: 250 mg/d twice daily for 60 days)with placebo for clinically reducing melasma lesions. The intervention period was 60 days followed by a 60-day maintenance phase for a total study period of 120 days. The researchers evaluated mMASI scores, quality of life, and difference in colorimetric luminosity. All treatment groups showed a reduction in mMASI scores at both 30 days and 60 days, indicating improved melasma severity. The MT and T groups had more significant improvement at 30 days compared with the control group (P<.03), suggesting that microneedling plus TXA and TXA alone promote faster improvement in melasma lesions. By 60 days, the M, T, and MT groups outperformed the control group, with no significant differences between the M, T, and MT groups. However, at the 120-day maintenance follow-up, the T group did not maintain its improvement compared with the control group. The M and MT groups showed no significance difference in effectiveness at 120 days, suggesting that microneedling may promote less frequent relapse and sustained remission compared to TXA alone.25

Hydroquinone for Melasma—Additional studies on the use of TXA treatments show that TXA may be an equally effective alternative to the standard use of hydroquinone treatment. Shamsi Meymandi et al26 did not find a statistically significant difference in treatment with TXA plus microneedling vs the standard regimen of hydroquinone. More importantly, patient and physician satisfaction assessments were similar between the 2 groups. Compared to hydroquinone, nightly treatment is not necessary with microneedling and TXA.26

Xing et al27 supported these conclusions with their study. They compared 3 study arms for a duration of 12 weeks: group A received topical 1.8% liposomal TXA BID, group B received stamp-mode electric microneedling with 5% TXA weekly, and group C applied 2% ­hydroquinone cream nightly. The study concluded that all 3 groups showed a significant reduction in mean MI by the end of the study, but a better MI improvement was observed in groups B and C (both P<.001) compared with group A (P<.01).27

Zaky et al28 showed that both hydroquinone and combination treatment of TXA plus microneedling are effective at improving melasma lesions. Further studies are needed to definitively conclude if combination treatment is more efficacious than hydroquinone; if the combination is more effective, it provides a treatment option for patients with melasma who may not be good candidates for hydroquinone treatment.

Study Limitations—One limitation in all the studies evaluated is the sample size. Because they all had small sample sizes, it is difficult to definitively conclude that the combination TXA and microneedling is an effective and appropriate treatment for patients with melasma. Furthermore, the quality of these studies was mostly dependent on subjectivity of the mMASI scores. Future large randomized controlled trials with a diverse participant population are needed to assess the effectiveness of TXA and microneedling in melasma treatment.

Another limitation is that many of the studies did not follow the patients longitudinally, which did not allow for an evaluation of whether patients had a relapse of melasma. Due to the chronic nature of melasma and frequent disease recurrence, future longitudinal studies are needed to monitor for disease recurrence.

Conclusion

Tranexamic acid and microneedling are potential treatment options for patients with melasma, and combination therapy appears more effective than either TXA or microneedling alone at providing sustained improvement of melasma lesions. Combination therapy appears safe and well tolerated, but its effect on reducing long-term disease recurrence is yet to be established.

Melasma (also known as chloasma faciei) is a common chronic skin disorder that results in well-demarcated, hyperpigmented, tan to dark patches that mostly appear in sun-exposed areas such as the face and neck and sometimes the arms. The exact prevalence or incidence is not known but is estimated to be 1% to 50% overall depending on the ethnic population and geographic location.1,2 Melasma predominantly affects women, but research has shown that approximately 10% to 20% of men are affected by this condition.3,4 Although melasma can affect patients of all skin types, it primarily affects those with darker skin tones.5 The groups most often affected are women of Black, Hispanic, Middle Eastern, and Southeast Asian ethnicity. Although the pathogenesis is complex and not fully understood, multiple pathways and etiologies have been theorized to cause melasma. Potential causes include exposure to UV radiation, oral contraceptives, hormonal changes, medications, thyroid dysfunction, genetics, and pregnancy.6,7 Cytokines and growth factors, including adipokine and angiopoietin, synthesized by sebaceous glands play a role in the pathogenic mechanism of melasma. Cytokines and growth factors are hypothesized to modulate the function of melanocytes.8 Both melanocytes and sebocytes are controlled by α–melanocyte-stimulating hormone. Therefore, overexpression of α–melanocyte-stimulating hormone will result in overproduction of these 2 cell types, resulting in melasma. Melasma can be classified into 4 subtypes using Wood lamp examination: epidermal, dermal, mixed, or indeterminate.3 Furthermore, melasma is divided into subgroups based on the location: malar region, mandibular region, and centrofacial patch pattern.9,10 The involvement of sebaceous glands in the pathogenesis of melasma may explain the predilection for the centrofacial region, which is the most common pattern.

The severity of melasma can be assessed using the melasma area and severity index (MASI), which is calculated by subjective assessment of 3 main factors: (1) facial area of involvement; (2) darkness of affected region; and (3) homogeneity, with the extent of melasma indicated by a score ranging from 0 to 48.11 The modified MASI (mMASI) subsequently was introduced to assist with assessing the severity of melasma and creating distinct ranges for mild, moderate, and severe cases, ranging from 0 (mild) to 24 (severe).12 Both indices are used in research to assess the improvement of melasma with treatment.

Patients with melasma report a decrease in quality of life, increased emotional stress, and lower self-esteem due to cosmesis.13 Treatment of melasma can be highly challenging and often is complicated by relapsing. Historically, the treatment of melasma has included the use of chemical lightening agents. Additional treatment options include the use of lasers and complex chemical peels,9,10 but these interventions may result in adverse outcomes for individuals with darker skin tones. The current gold-standard treatment is topical hydroquinone and broad-spectrum sunscreen. Although hydroquinone is effective in the treatment of melasma, relapse is common. The goal of melasma management is not only to treat acute hyperpigmentation but also to prevent relapse. Other therapies that currently are being explored for the clinically sustained treatment of melasma include tranexamic acid (TXA)(trans-4-[aminomethyl]cyclohexanecarboxylic acid),9,10 an antifibrinolytic agent routinely used to prevent blood loss during surgery and in the management of menorrhagia. It is a synthetic derivative of lysine and serves as a potent plasmin inhibitor by blocking the lysine-binding sites of plasminogen molecules, thus preventing the conversion of plasminogen to plasmin. It also prevents fibrinolysis and blood loss.

In addition to its hemostatic properties, TXA has been found to have hypopigmentation properties.14,15 Plasminogen also can be found in human epidermal basal cells and human keratinocytes, and it is postulated that TXA’s interaction with these cells explains its hypopigmentation properties. Both UV radiation and hormones activate plasminogen into plasmin, resulting in the activation of tyrosinase and melanogenesis.14,15 Tranexamic acid is postulated to inhibit the keratinocyte-plasminogen pathway, thus leading to the inhibition of UV-induced and hormone-induced pigmentation. Also, TXA serves as a competitive inhibitor for tyrosinase due to its structural similarity to tyrosine.15 The combination of these 2 mechanisms contributes to the skin-lightening effects of TXA, making it a potential treatment for melasma.

Furthermore, the use of microneedling is being explored as a treatment option for melasma. Microneedling creates microscopic punctures in the skin using tiny needles, resulting in a wound-healing response and skin resurfacing. The microneedling technique is utilized to create small holes in the skin, with needle depths that can be adjusted from 0.5 to 3.5 mm to target different layers of the dermis and allow for discreet application of TXA.16 We sought to look at the current literature on the use and effectiveness of microneedling in combination with TXA to treat melasma and prevent relapse.

 

 

Methods

A systematic review was performed of PubMed articles indexed for MEDLINE and Embase in November 2021 to compile available articles that studied TXA and microneedling as a treatment for melasma. The PubMed search terms were (melasma) AND (microneedling* OR ‘tranexamic acid’ OR TXA or TA). The Embase search terms were (cholasma OR melasma) AND (tranexamic acid OR TXA) AND (microneedling)(Figure). The search was then limited to ”randomized controlled trial” and ”clinical trial” in English-language journals. Duplicates were excluded. After thorough evaluation, articles that discussed the use of TXA in combination with treatment options other than microneedling also were excluded.

Flow diagram of study selection. Asterisk indicates platelet-rich plasma, vitamin C, kojic acid, niacinamide, Kligman’s therapy (fluocinolone + hydroquinone + tretinoin), retinoic acid, and cysteamine.

Results

The literature search yielded a total of 12 articles that assessed the effectiveness of TXA and microneedling for the treatment of melasma (Table).17-28 Several articles concluded that TXA was equally effective at reducing melasma lesions when compared with the standard treatment of hydroquinone. Some of the reviewed articles also demonstrated the effectiveness of microneedling in improving melasma lesions as a stand-alone treatment. These studies highlighted the enhanced efficacy of the combined treatment of TXA and microneedling compared with their individual uses.17-28

Comment

Melasma is a common chronic hyperpigmentation disorder, making its treatment clinically challenging. Many patients experience symptom relapses, and limited effective treatment options make achieving complete clearance difficult, underscoring the need for improved therapeutic approaches. Recently, researchers have explored alternative treatments to address the challenges of melasma management. Tranexamic acid is an antifibrinolytic used to prevent blood loss and has emerged as a potential treatment for melasma. Similarly, microneedling—a technique in which multiple punctures are made in the skin to activate and stimulate wound healing and skin rejuvenation—shows promise for melasma.

Oral TXA for Melasma—Oral TXA has been shown to reduce melasma lesions. Del Rosario et al17 recruited 44 women (39 of whom completed the study) with moderate to severe melasma and randomized them into 2 groups: oral TXA and placebo. This study demonstrated a 49% reduction in the mMASI score in all participants taking oral TXA (250 mg twice daily [BID]) compared with an 18% reduction in the control group (placebo capsule BID) after 3 months of treatment. In patients with moderate and severe melasma, 45% and 51% mMASI score reductions were reported in the treatment group, respectively, vs 16% and 19% score reductions in placebo group, respectively. These researchers concluded that oral TXA may be effective at treating moderate to severe melasma. Although patients with severe melasma had a better response to treatment, their improvement was not sustained compared with patients with moderate melasma after a 3-month posttreatment follow-up.17

Microneedling Plus TXA for Melasma—Microneedling alone has been shown to be effective for melasma. El Attar et al18 conducted a split-face study of microneedling (1.5-mm depth) plus topical TXA (0.5 mL)(right side of the face[treatment arm]) compared with microneedling (1.5-mm depth) plus topical vitamin C (0.5 mL)(left side of the face [control group]) in 20 women with melasma. The sessions were repeated every 2 weeks for a total of 6 sessions. Although researchers found no statistically significant differences between the 2 treatment sides, microneedling plus TXA showed a slight advantage over microneedling plus vitamin C in dermoscopic examination. Both sides showed improvement in pigmented lesions, but vitamin C–treated lesions did not show an improvement in vascularity vs TXA.18

Saleh et al19 further showed that combination treatment with microneedling and TXA may improve clinical outcomes better than microneedling alone. Their study demonstrated a reduction in MASI score that was significantly higher in the combination treatment group compared with the microneedling alone group (P=.001). There was a significant reduction in melanoma antigen recognized by T cells 1 (MART-1)–positive cells in the combination treatment group compared with the microneedling alone group (P=.001). Lastly, combined therapy improved melasma patches better than microneedling alone.19

 

Xu et al20 conducted a split-face study (N=28) exploring the effectiveness of transdermal application of topical TXA using a microarray pen with microneedles (vibration at 3000×/min) plus topical TXA on one side of the face, while the other side received only topical TXA as a control. After 12 weeks of treatment, combination therapy with microneedling and TXA decreased brown spot scores, lowered melanin index (MI) values, improved blinded physician assessment, and improved patient satisfaction vs TXA therapy alone.20

Kaur et al21 conducted a split-face, randomized, controlled trial of microneedling (1-mm depth) with TXA solution 10% vs microneedling (1-mm depth) with distilled water alone for 8 weeks (N=40). They graded participant responses to treatment using reductions in mMASI scores12 at every 2 weeks of follow-up (no response, minimal or poor response=0%–25%; partial or fair response=26%–50%; good response=51%–75%; and excellent response=>75%). They reported an overall reduction in mMASI scores for both the treatment side and the control side in all participants, showing a 65.92% improvement in mean mMASI scores on the treatment side vs 20.75% improvement on the control side at week 8. Both sides showed statistically significant reductions in mean mMASI scores (P<.05). Clinically, 40% (16/40) of participants showed an excellent response to combined treatment compared with 0% (0/40) to microneedling alone. Overall, patient satisfaction was similar across both groups. This study demonstrated that microneedling alone improves melasma, but a combination of microneedling plus TXA showed a better clinical reduction in melasma. However, the researchers did not follow up with participants posttreatment, so it remains unclear if the improved clinical outcomes were sustained long-term.21

Ebrahim et al22 reported that the combination of 0.5 mL TXA (4 mg/mL) and microneedling (0.25- to 1-mm depth) was effective for melasma. Although there was improvement within microneedling and TXA, the study also showed that intradermal injection of TXA was significant in reducing mean mMASI scores and improving melasma (P<.001). The reduction in mMASI scores for the group receiving intradermal injections of TXA (left side; 74.8% reduction in mean mMASI score) vs the group receiving microneedling application of TXA (right side; 73.6% reduction in mean mMASI score) was not statistically significant. These findings suggest that the mode of TXA application may not be critical in determining clinical responses to TXA treatment. Although there was no reported statistically significant difference in clinical outcomes between the 2 treatments, patient satisfaction was higher on the microneedling side. Only 8 of 50 participants (16%) experienced recurrence 3 months posttreatment.22

Saki et al23 compared the efficacy of topical hydroquinone (2%) to intradermal TXA injections in treating melasma. They found intradermal TXA injections to be a clinically effective mode of treatment.23

Sharma et al24 explored the efficacy and safety of oral TXA by randomly assigning 100 Indian patients (20 of whom withdrew before study completion) with melasma into 2 groups: group A received TXA 250 mg twice daily, and group B received intradermal microinjections of TXA (4 mg/mL) every 4 weeks. The MASI scores were assessed at 4-week intervals for a total of 12 weeks. There was a decrease in MASI scores in both groups, and there was no statistically significant difference in mean percentage reduction in MASI scores between the 2 routes of drug administration, further suggesting the effectiveness of TXA independent of administration route. Two patients in group A relapsed at 24 weeks, and there were no relapses in group B, which may suggest a minimal superiority of TXA plus microneedling at providing more sustainable results compared with oral TXA alone. A notable limitation of this study was a high dropout rate as well as lack of long-term follow-up with participants, limiting the generalizability of the conclusions.24

Cassiano et al25 assigned 64 women with melasma to 1 of 3 treatment groups or a control group to compare the effectiveness of microneedling (M group: 1.5 mm; 2 sessions), oral TXA (T group: 250 mg/d twice daily for 60 days), and a combination of microneedling (2 sessions) and oral TXA (MT group: 250 mg/d twice daily for 60 days)with placebo for clinically reducing melasma lesions. The intervention period was 60 days followed by a 60-day maintenance phase for a total study period of 120 days. The researchers evaluated mMASI scores, quality of life, and difference in colorimetric luminosity. All treatment groups showed a reduction in mMASI scores at both 30 days and 60 days, indicating improved melasma severity. The MT and T groups had more significant improvement at 30 days compared with the control group (P<.03), suggesting that microneedling plus TXA and TXA alone promote faster improvement in melasma lesions. By 60 days, the M, T, and MT groups outperformed the control group, with no significant differences between the M, T, and MT groups. However, at the 120-day maintenance follow-up, the T group did not maintain its improvement compared with the control group. The M and MT groups showed no significance difference in effectiveness at 120 days, suggesting that microneedling may promote less frequent relapse and sustained remission compared to TXA alone.25

Hydroquinone for Melasma—Additional studies on the use of TXA treatments show that TXA may be an equally effective alternative to the standard use of hydroquinone treatment. Shamsi Meymandi et al26 did not find a statistically significant difference in treatment with TXA plus microneedling vs the standard regimen of hydroquinone. More importantly, patient and physician satisfaction assessments were similar between the 2 groups. Compared to hydroquinone, nightly treatment is not necessary with microneedling and TXA.26

Xing et al27 supported these conclusions with their study. They compared 3 study arms for a duration of 12 weeks: group A received topical 1.8% liposomal TXA BID, group B received stamp-mode electric microneedling with 5% TXA weekly, and group C applied 2% ­hydroquinone cream nightly. The study concluded that all 3 groups showed a significant reduction in mean MI by the end of the study, but a better MI improvement was observed in groups B and C (both P<.001) compared with group A (P<.01).27

Zaky et al28 showed that both hydroquinone and combination treatment of TXA plus microneedling are effective at improving melasma lesions. Further studies are needed to definitively conclude if combination treatment is more efficacious than hydroquinone; if the combination is more effective, it provides a treatment option for patients with melasma who may not be good candidates for hydroquinone treatment.

Study Limitations—One limitation in all the studies evaluated is the sample size. Because they all had small sample sizes, it is difficult to definitively conclude that the combination TXA and microneedling is an effective and appropriate treatment for patients with melasma. Furthermore, the quality of these studies was mostly dependent on subjectivity of the mMASI scores. Future large randomized controlled trials with a diverse participant population are needed to assess the effectiveness of TXA and microneedling in melasma treatment.

Another limitation is that many of the studies did not follow the patients longitudinally, which did not allow for an evaluation of whether patients had a relapse of melasma. Due to the chronic nature of melasma and frequent disease recurrence, future longitudinal studies are needed to monitor for disease recurrence.

Conclusion

Tranexamic acid and microneedling are potential treatment options for patients with melasma, and combination therapy appears more effective than either TXA or microneedling alone at providing sustained improvement of melasma lesions. Combination therapy appears safe and well tolerated, but its effect on reducing long-term disease recurrence is yet to be established.

References
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  19. Saleh FY, Abdel-Azim ES, Ragaie MH, et al. Topical tranexamic acid with microneedling versus microneedling alone in treatment of melasma: clinical, histopathologic, and immunohistochemical study. J Egyptian Womens Dermatolog Soc. 2019;16:89-96. doi:10.4103/jewd.jewd_25_19
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  25. Cassiano D, Esposito ACC, Hassun K, et al. Efficacy and safety of microneedling and oral tranexamic acid in the treatment of facial melasma in women: an open, evaluator-blinded, randomized clinical trial. J Am Acad Dermatol. 2020;83:1176-1178. doi:10.1016/j.jaad.2020.02.002
  26. Shamsi Meymandi S, Mozayyeni A, Shamsi Meymandi M, et al. Efficacy of microneedling plus topical 4% tranexamic acid solution vs 4% hydroquinone in the treatment of melasma: a single-blind randomized clinical trial. J Cosmet Dermatol. 2020;19:2906-2911. doi:10.1111/jocd.13392
  27. Xing X, Chen L, Xu Z, et al. The efficacy and safety of topical tranexamic acid (liposomal or lotion with microneedling) versus conventional hydroquinone in the treatment of melasma. J Cosmet Dermatol. 2020;19:3238-3244. doi:10.1111/jocd.13810
  28. Zaky MS, Obaid ZM, Khalil EA, et al. Microneedling-assisted topical tranexamic acid solution versus 4% hydroquinone for treating melasma: a split-face randomized study. J Cosmet Dermatol. 2021;20:4011-4016. doi:10.1111/jocd.14440
References
  1. Neagu N, Conforti C, Agozzino M, et al. Melasma treatment: a systematic review. J Dermatolog Treat. 2022;33:1816-1837. doi:10.1080/09546634.2021.1914313
  2. Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther (Heidelb). 2017;7:305-318. doi:10.1007/s13555-017-0194-1
  3. Mahajan VK, Patil A, Blicharz L, et al. Medical therapies for melasma. J Cosmet Dermatol. 2022;21:3707-3728. doi:10.1111/jocd.15242
  4. Rigopoulos D, Gregoriou S, Katsambas A. Hyperpigmentation and melasma. J Cosmet Dermatol. 2007;6:195-202. doi:10.1111/j.1473-2165.2007.00321.x
  5. Kagha K, Fabi S, Goldman M. Melasma’s impact on quality of life. J Drugs Dermatol. 2020;19:184-187. doi:10.36849/JDD.2020.4663
  6. Lutfi RJ, Fridmanis M, Misiunas AL, et al. Association of melasma with thyroid autoimmunity and other thyroidal abnormalities and their relationship to the origin of the melasma. J Clin Endocrinol Metab. 1985;61:28-31. doi:10.1210/jcem-61-1-28
  7. Handel AC, Lima PB, Tonolli VM, et al. Risk factors for facial melasma in women: a case-control study. Br J Dermatol. 2014;171:588-594. doi:10.1111/bjd.13059
  8. Filoni A, Mariano M, Cameli N. Melasma: how hormones can modulate skin pigmentation. J Cosmet Dermatol. 2019;18:458-463. doi:10.1111/jocd.12877
  9. Rodrigues M, Pandya AG. Melasma: clinical diagnosis and management options. Australasian J Dermatol. 2015;56:151-163.
  10. Huerth KA, Hassan S, Callender VD. Therapeutic insights in melasma and hyperpigmentation management. J Drugs Dermatol. 2019;18:718-727.
  11. Pandya AG, Hynan LS, Bhore R, et al. Reliability assessment and validation of the Melasma Area and Severity Index (MASI) and a new modified MASI scoring method. J Am Acad Dermatol. 2011;64:78-­83.e832. doi:10.1016/j.jaad.2009.10.051
  12. Rodrigues M, Ayala-Cortés AS, Rodríguez-Arámbula A, et al. Interpretability of the modified Melasma Area and Severity Index (mMASI). JAMA Dermatol. 2016;152:1051-1052. doi:10.1001/jamadermatol.2016.1006
  13. Ikino JK, Nunes DH, da Silva VPM, et al. Melasma and assessment of the quality of life in Brazilian women. An Bras Dermatol. 2015;90:196-200. doi:10.1590/abd1806-4841.20152771
  14. Taraz M, Niknam S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies. Dermatolog Ther. 2017;30:E12465. doi:10.1111/dth.12465
  15. Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825. doi:10.1097/DSS.0000000000001518
  16. Singh A, Yadav S. Microneedling: advances and widening horizons. Indian Dermatol Online J. 2016;7:244-254. doi:10.4103/2229-5178.185468
  17. Del Rosario E, Florez-Pollack S, Zapata L, et al. Randomized, placebo-controlled, double-blind study of oral tranexamic acid in the treatment of moderate-to-severe melasma. J Am Acad Dermatol. 2018;78:363-369. doi:10.1016/j.jaad.2017.09.053
  18. El Attar Y, Doghaim N, El Far N, et al. Efficacy and safety of tranexamic acid versus vitamin C after microneedling in treatment of melasma: clinical and dermoscopic study. J Cosmet Dermatol. 2022;21:2817-2825. doi:10.1111/jocd.14538
  19. Saleh FY, Abdel-Azim ES, Ragaie MH, et al. Topical tranexamic acid with microneedling versus microneedling alone in treatment of melasma: clinical, histopathologic, and immunohistochemical study. J Egyptian Womens Dermatolog Soc. 2019;16:89-96. doi:10.4103/jewd.jewd_25_19
  20. Xu Y, Ma R, Juliandri J, et al. Efficacy of functional microarray of microneedles combined with topical tranexamic acid for melasma: a randomized, self-controlled, split-face study. Medicine (Baltimore). 2017;96:e6897. doi:10.1097/MD.0000000000006897
  21. Kaur A, Bhalla M, Pal Thami G, et al. Clinical efficacy of topical tranexamic acid with microneedling in melasma. Dermatol Surg. 2020;46:E96-E101. doi:10.1097/DSS.0000000000002520
  22. Ebrahim HM, Said Abdelshafy A, Khattab F, et al. Tranexamic acid for melasma treatment: a split-face study. Dermatol Surg. 2020;46:E102-E107. doi:10.1097/DSS.0000000000002449
  23. Saki N, Darayesh M, Heiran A. Comparing the efficacy of topical hydroquinone 2% versus intradermal tranexamic acid microinjections in treating melasma: a split-face controlled trial. J Dermatolog Treat. 2018;29:405-410. doi:10.1080/09546634.2017.1392476
  24. Sharma R, Mahajan VK, Mehta KS, et al. Therapeutic efficacy and safety of oral tranexamic acid and that of tranexamic acid local infiltration with microinjections in patients with melasma: a comparative study. Clin Exp Dermatol. 2017;42:728-734. doi:10.1111/ced.13164
  25. Cassiano D, Esposito ACC, Hassun K, et al. Efficacy and safety of microneedling and oral tranexamic acid in the treatment of facial melasma in women: an open, evaluator-blinded, randomized clinical trial. J Am Acad Dermatol. 2020;83:1176-1178. doi:10.1016/j.jaad.2020.02.002
  26. Shamsi Meymandi S, Mozayyeni A, Shamsi Meymandi M, et al. Efficacy of microneedling plus topical 4% tranexamic acid solution vs 4% hydroquinone in the treatment of melasma: a single-blind randomized clinical trial. J Cosmet Dermatol. 2020;19:2906-2911. doi:10.1111/jocd.13392
  27. Xing X, Chen L, Xu Z, et al. The efficacy and safety of topical tranexamic acid (liposomal or lotion with microneedling) versus conventional hydroquinone in the treatment of melasma. J Cosmet Dermatol. 2020;19:3238-3244. doi:10.1111/jocd.13810
  28. Zaky MS, Obaid ZM, Khalil EA, et al. Microneedling-assisted topical tranexamic acid solution versus 4% hydroquinone for treating melasma: a split-face randomized study. J Cosmet Dermatol. 2021;20:4011-4016. doi:10.1111/jocd.14440
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  • Combination therapy with tranexamic acid (TXA) and microneedling is a safe and effective treatment for melasma.
  • Combining TXA with microneedling may result in decreased melasma relapse rates.
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Suture Selection to Minimize Postoperative Postinflammatory Hyperpigmentation in Patients With Skin of Color During Mohs Micrographic Surgery

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Suture Selection to Minimize Postoperative Postinflammatory Hyperpigmentation in Patients With Skin of Color During Mohs Micrographic Surgery

Practice Gap

Proper suture selection is imperative for appropriate wound healing to minimize the risk for infection and inflammation and to reduce scarring. In Mohs micrographic surgery (MMS), suture selection should be given high consideration in patients with skin of color.1 Using the right type of suture and wound closure technique can lead to favorable aesthetic outcomes by preventing postoperative postinflammatory hyperpigmentation (PIH) and keloids. Data on the choice of suture material in patients with skin of color are limited.

Suture selection depends on a variety of factors including but not limited to the location of the wound on the body, risk for infection, cost, availability, and the personal preference and experience of the MMS surgeon. During the COVID-19 pandemic, suturepreference among dermatologic surgeons shifted to fast-absorbing gut sutures,2 offering alternatives to synthetic monofilament polypropylene and nylon sutures. Absorbable sutures reduced the need for in-person follow-up visits without increasing the incidence of postoperative complications.

Despite these benefits, research suggests that natural absorbable gut sutures induce cutaneous inflammation and should be avoided in patients with skin of color.1,3,4 Nonabsorbable sutures are less reactive, reducing PIH after MMS in patients with skin of color.

Tools and Technique

Use of nonabsorbable stitches is a practical solution to reduce the risk for inflammation in patients with skin of color. Increased inflammation can lead to PIH and increase the risk for keloids in this patient population. Some patients will experience PIH after a surgical procedure regardless of the sutures used to repair the closure; however, one of our goals with patients with skin of color undergoing MMS is to reduce the inflammatory risk that could lead to PIH to ensure optimal aesthetic outcomes.

A middle-aged African woman with darker skin and a history of developing PIH after trauma to the skin presented to our clinic for MMS of a dermatofibrosarcoma protuberans on the upper abdomen. We used a simple running suture with 4-0 nylon to close the surgical wound. We avoided fast-absorbing gut sutures because they have high tissue reactivity1,4; use of sutures with low tissue reactivity, such as nylon and polypropylene, decreases the risk for inflammation without compromising alignment of wound edges and overall cosmesis of the repair. Prolene also is cost-effective and presents a decreased risk for wound dehiscence.5 After cauterizing the wound, we placed multiple synthetic absorbable sutures first to close the wound. We then did a double-running suture of nonabsorbable monofilament suture to reapproximate the epidermal edges with minimal tension. We placed 2 sets of running stitches to minimize the risk for dehiscence along the scar.

The patient was required to return for removal of the nonabsorbable sutures; this postoperative visit was covered by health insurance at no additional cost to the patient. In comparison, long-term repeat visits to treat PIH with a laser or chemical peel would have been more costly. Given that treatment of PIH is considered cosmetic, laser treatment would have been priced at several hundred dollars per session at our institution, and the patient would likely have had a copay for a pretreatment lightening cream such as hydroquinone. Our patient had a favorable cosmetic outcome and reported no or minimal evidence of PIH months after the procedure.

Patients should be instructed to apply petrolatum twice daily, use sun-protective clothing, and cover sutures to minimize exposure to the sun and prevent crusting of the wound. Postinflammatory hyperpigmentation can be proactively treated postoperatively with topical hydroquinone, which was not needed in our patient.

 

 

Practice Implications

Although some studies suggest that there are no cosmetic differences between absorbable and nonabsorbable sutures, the effect of suture type in patients with skin of color undergoing MMS often is unreported or is not studied.6,7 The high reactivity and cutaneous inflammation associated with absorbable gut sutures are important considerations in this patient population.

In patients with skin of color undergoing MMS, we use nonabsorbable epidermal sutures such as nylon and Prolene because of their low reactivity and association with favorable aesthetic outcomes. Nonabsorbable sutures can be safely used in patients of all ages who are undergoing MMS under local anesthesia.

An exception would be the use of the absorbable suture Monocryl (J&J MedTech) in patients with skin of color who need a running subcuticular wound closure because it has low tissue reactivity and maintains high tensile strength. Monocryl has been shown to create less-reactive scars, which decreases the risk for keloids.8,9

More clinical studies are needed to assess the increased susceptibility to PIH in patients with skin of color when using absorbable gut sutures.

References
  1. Williams R, Ciocon D. Mohs micrographic surgery in skin of color. J Drugs Dermatol. 2022;21:536-541. doi:10.36849/JDD.6469
  2. Gallop J, Andrasik W, Lucas J. Successful use of percutaneous dissolvable sutures during COVID-19 pandemic: a retrospective review. J Cutan Med Surg. 2023;27:34-38. doi:10.1177/12034754221143083
  3. Byrne M, Aly A. The surgical suture. Aesthet Surg J. 2019;39(suppl 2):S67-S72. doi:10.1093/asj/sjz036
  4. Koppa M, House R, Tobin V, et al. Suture material choice can increase risk of hypersensitivity in hand trauma patients. Eur J Plast Surg. 2023;46:239-243. doi:10.1007/s00238-022-01986-7
  5. Pandey S, Singh M, Singh K, et al. A prospective randomized study comparing non-absorbable polypropylene (Prolene®) and delayed absorbable polyglactin 910 (Vicryl®) suture material in mass closure of vertical laparotomy wounds. Indian J Surg. 2013;75:306-310. doi:10.1007/s12262-012-0492-x
  6. Parell GJ, Becker GD. Comparison of absorbable with nonabsorbable sutures in closure of facial skin wounds. Arch Facial Plast Surg. 2003;5:488-490. doi:10.1001/archfaci.5.6.488
  7. Kim J, Singh Maan H, Cool AJ, et al. Fast absorbing gut suture versus cyanoacrylate tissue adhesive in the epidermal closure of linear repairs following Mohs micrographic surgery. J Clin Aesthet Dermatol. 2015;8:24-29.
  8. Niessen FB, Spauwen PH, Kon M. The role of suture material in hypertrophic scar formation: Monocryl vs. Vicryl-Rapide. Ann Plast Surg. 1997;39:254-260. doi:10.1097/00000637-199709000-00006
  9. Fosko SW, Heap D. Surgical pearl: an economical means of skin closure with absorbable suture. J Am Acad Dermatol. 1998;39(2 pt 1):248-250. doi:10.1016/s0190-9622(98)70084-2
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Carolina Gonzalez Bravo is from the Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City. Dr. Negbenebor is from the Department of Dermatology, University of Iowa Hospitals & Clinics, Iowa City.

Carolina Gonzalez Bravo reports no conflict of interest. Dr. Negbenebor has served as a speaker for Nema Beauty Cosmetics.

Correspondence: Nicole A. Negbenebor, MD, 200 Hawkins Dr, Iowa City, IA 52242 (nicole-negbenebor@uiowa.edu).

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Carolina Gonzalez Bravo is from the Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City. Dr. Negbenebor is from the Department of Dermatology, University of Iowa Hospitals & Clinics, Iowa City.

Carolina Gonzalez Bravo reports no conflict of interest. Dr. Negbenebor has served as a speaker for Nema Beauty Cosmetics.

Correspondence: Nicole A. Negbenebor, MD, 200 Hawkins Dr, Iowa City, IA 52242 (nicole-negbenebor@uiowa.edu).

Author and Disclosure Information

Carolina Gonzalez Bravo is from the Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City. Dr. Negbenebor is from the Department of Dermatology, University of Iowa Hospitals & Clinics, Iowa City.

Carolina Gonzalez Bravo reports no conflict of interest. Dr. Negbenebor has served as a speaker for Nema Beauty Cosmetics.

Correspondence: Nicole A. Negbenebor, MD, 200 Hawkins Dr, Iowa City, IA 52242 (nicole-negbenebor@uiowa.edu).

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Practice Gap

Proper suture selection is imperative for appropriate wound healing to minimize the risk for infection and inflammation and to reduce scarring. In Mohs micrographic surgery (MMS), suture selection should be given high consideration in patients with skin of color.1 Using the right type of suture and wound closure technique can lead to favorable aesthetic outcomes by preventing postoperative postinflammatory hyperpigmentation (PIH) and keloids. Data on the choice of suture material in patients with skin of color are limited.

Suture selection depends on a variety of factors including but not limited to the location of the wound on the body, risk for infection, cost, availability, and the personal preference and experience of the MMS surgeon. During the COVID-19 pandemic, suturepreference among dermatologic surgeons shifted to fast-absorbing gut sutures,2 offering alternatives to synthetic monofilament polypropylene and nylon sutures. Absorbable sutures reduced the need for in-person follow-up visits without increasing the incidence of postoperative complications.

Despite these benefits, research suggests that natural absorbable gut sutures induce cutaneous inflammation and should be avoided in patients with skin of color.1,3,4 Nonabsorbable sutures are less reactive, reducing PIH after MMS in patients with skin of color.

Tools and Technique

Use of nonabsorbable stitches is a practical solution to reduce the risk for inflammation in patients with skin of color. Increased inflammation can lead to PIH and increase the risk for keloids in this patient population. Some patients will experience PIH after a surgical procedure regardless of the sutures used to repair the closure; however, one of our goals with patients with skin of color undergoing MMS is to reduce the inflammatory risk that could lead to PIH to ensure optimal aesthetic outcomes.

A middle-aged African woman with darker skin and a history of developing PIH after trauma to the skin presented to our clinic for MMS of a dermatofibrosarcoma protuberans on the upper abdomen. We used a simple running suture with 4-0 nylon to close the surgical wound. We avoided fast-absorbing gut sutures because they have high tissue reactivity1,4; use of sutures with low tissue reactivity, such as nylon and polypropylene, decreases the risk for inflammation without compromising alignment of wound edges and overall cosmesis of the repair. Prolene also is cost-effective and presents a decreased risk for wound dehiscence.5 After cauterizing the wound, we placed multiple synthetic absorbable sutures first to close the wound. We then did a double-running suture of nonabsorbable monofilament suture to reapproximate the epidermal edges with minimal tension. We placed 2 sets of running stitches to minimize the risk for dehiscence along the scar.

The patient was required to return for removal of the nonabsorbable sutures; this postoperative visit was covered by health insurance at no additional cost to the patient. In comparison, long-term repeat visits to treat PIH with a laser or chemical peel would have been more costly. Given that treatment of PIH is considered cosmetic, laser treatment would have been priced at several hundred dollars per session at our institution, and the patient would likely have had a copay for a pretreatment lightening cream such as hydroquinone. Our patient had a favorable cosmetic outcome and reported no or minimal evidence of PIH months after the procedure.

Patients should be instructed to apply petrolatum twice daily, use sun-protective clothing, and cover sutures to minimize exposure to the sun and prevent crusting of the wound. Postinflammatory hyperpigmentation can be proactively treated postoperatively with topical hydroquinone, which was not needed in our patient.

 

 

Practice Implications

Although some studies suggest that there are no cosmetic differences between absorbable and nonabsorbable sutures, the effect of suture type in patients with skin of color undergoing MMS often is unreported or is not studied.6,7 The high reactivity and cutaneous inflammation associated with absorbable gut sutures are important considerations in this patient population.

In patients with skin of color undergoing MMS, we use nonabsorbable epidermal sutures such as nylon and Prolene because of their low reactivity and association with favorable aesthetic outcomes. Nonabsorbable sutures can be safely used in patients of all ages who are undergoing MMS under local anesthesia.

An exception would be the use of the absorbable suture Monocryl (J&J MedTech) in patients with skin of color who need a running subcuticular wound closure because it has low tissue reactivity and maintains high tensile strength. Monocryl has been shown to create less-reactive scars, which decreases the risk for keloids.8,9

More clinical studies are needed to assess the increased susceptibility to PIH in patients with skin of color when using absorbable gut sutures.

Practice Gap

Proper suture selection is imperative for appropriate wound healing to minimize the risk for infection and inflammation and to reduce scarring. In Mohs micrographic surgery (MMS), suture selection should be given high consideration in patients with skin of color.1 Using the right type of suture and wound closure technique can lead to favorable aesthetic outcomes by preventing postoperative postinflammatory hyperpigmentation (PIH) and keloids. Data on the choice of suture material in patients with skin of color are limited.

Suture selection depends on a variety of factors including but not limited to the location of the wound on the body, risk for infection, cost, availability, and the personal preference and experience of the MMS surgeon. During the COVID-19 pandemic, suturepreference among dermatologic surgeons shifted to fast-absorbing gut sutures,2 offering alternatives to synthetic monofilament polypropylene and nylon sutures. Absorbable sutures reduced the need for in-person follow-up visits without increasing the incidence of postoperative complications.

Despite these benefits, research suggests that natural absorbable gut sutures induce cutaneous inflammation and should be avoided in patients with skin of color.1,3,4 Nonabsorbable sutures are less reactive, reducing PIH after MMS in patients with skin of color.

Tools and Technique

Use of nonabsorbable stitches is a practical solution to reduce the risk for inflammation in patients with skin of color. Increased inflammation can lead to PIH and increase the risk for keloids in this patient population. Some patients will experience PIH after a surgical procedure regardless of the sutures used to repair the closure; however, one of our goals with patients with skin of color undergoing MMS is to reduce the inflammatory risk that could lead to PIH to ensure optimal aesthetic outcomes.

A middle-aged African woman with darker skin and a history of developing PIH after trauma to the skin presented to our clinic for MMS of a dermatofibrosarcoma protuberans on the upper abdomen. We used a simple running suture with 4-0 nylon to close the surgical wound. We avoided fast-absorbing gut sutures because they have high tissue reactivity1,4; use of sutures with low tissue reactivity, such as nylon and polypropylene, decreases the risk for inflammation without compromising alignment of wound edges and overall cosmesis of the repair. Prolene also is cost-effective and presents a decreased risk for wound dehiscence.5 After cauterizing the wound, we placed multiple synthetic absorbable sutures first to close the wound. We then did a double-running suture of nonabsorbable monofilament suture to reapproximate the epidermal edges with minimal tension. We placed 2 sets of running stitches to minimize the risk for dehiscence along the scar.

The patient was required to return for removal of the nonabsorbable sutures; this postoperative visit was covered by health insurance at no additional cost to the patient. In comparison, long-term repeat visits to treat PIH with a laser or chemical peel would have been more costly. Given that treatment of PIH is considered cosmetic, laser treatment would have been priced at several hundred dollars per session at our institution, and the patient would likely have had a copay for a pretreatment lightening cream such as hydroquinone. Our patient had a favorable cosmetic outcome and reported no or minimal evidence of PIH months after the procedure.

Patients should be instructed to apply petrolatum twice daily, use sun-protective clothing, and cover sutures to minimize exposure to the sun and prevent crusting of the wound. Postinflammatory hyperpigmentation can be proactively treated postoperatively with topical hydroquinone, which was not needed in our patient.

 

 

Practice Implications

Although some studies suggest that there are no cosmetic differences between absorbable and nonabsorbable sutures, the effect of suture type in patients with skin of color undergoing MMS often is unreported or is not studied.6,7 The high reactivity and cutaneous inflammation associated with absorbable gut sutures are important considerations in this patient population.

In patients with skin of color undergoing MMS, we use nonabsorbable epidermal sutures such as nylon and Prolene because of their low reactivity and association with favorable aesthetic outcomes. Nonabsorbable sutures can be safely used in patients of all ages who are undergoing MMS under local anesthesia.

An exception would be the use of the absorbable suture Monocryl (J&J MedTech) in patients with skin of color who need a running subcuticular wound closure because it has low tissue reactivity and maintains high tensile strength. Monocryl has been shown to create less-reactive scars, which decreases the risk for keloids.8,9

More clinical studies are needed to assess the increased susceptibility to PIH in patients with skin of color when using absorbable gut sutures.

References
  1. Williams R, Ciocon D. Mohs micrographic surgery in skin of color. J Drugs Dermatol. 2022;21:536-541. doi:10.36849/JDD.6469
  2. Gallop J, Andrasik W, Lucas J. Successful use of percutaneous dissolvable sutures during COVID-19 pandemic: a retrospective review. J Cutan Med Surg. 2023;27:34-38. doi:10.1177/12034754221143083
  3. Byrne M, Aly A. The surgical suture. Aesthet Surg J. 2019;39(suppl 2):S67-S72. doi:10.1093/asj/sjz036
  4. Koppa M, House R, Tobin V, et al. Suture material choice can increase risk of hypersensitivity in hand trauma patients. Eur J Plast Surg. 2023;46:239-243. doi:10.1007/s00238-022-01986-7
  5. Pandey S, Singh M, Singh K, et al. A prospective randomized study comparing non-absorbable polypropylene (Prolene®) and delayed absorbable polyglactin 910 (Vicryl®) suture material in mass closure of vertical laparotomy wounds. Indian J Surg. 2013;75:306-310. doi:10.1007/s12262-012-0492-x
  6. Parell GJ, Becker GD. Comparison of absorbable with nonabsorbable sutures in closure of facial skin wounds. Arch Facial Plast Surg. 2003;5:488-490. doi:10.1001/archfaci.5.6.488
  7. Kim J, Singh Maan H, Cool AJ, et al. Fast absorbing gut suture versus cyanoacrylate tissue adhesive in the epidermal closure of linear repairs following Mohs micrographic surgery. J Clin Aesthet Dermatol. 2015;8:24-29.
  8. Niessen FB, Spauwen PH, Kon M. The role of suture material in hypertrophic scar formation: Monocryl vs. Vicryl-Rapide. Ann Plast Surg. 1997;39:254-260. doi:10.1097/00000637-199709000-00006
  9. Fosko SW, Heap D. Surgical pearl: an economical means of skin closure with absorbable suture. J Am Acad Dermatol. 1998;39(2 pt 1):248-250. doi:10.1016/s0190-9622(98)70084-2
References
  1. Williams R, Ciocon D. Mohs micrographic surgery in skin of color. J Drugs Dermatol. 2022;21:536-541. doi:10.36849/JDD.6469
  2. Gallop J, Andrasik W, Lucas J. Successful use of percutaneous dissolvable sutures during COVID-19 pandemic: a retrospective review. J Cutan Med Surg. 2023;27:34-38. doi:10.1177/12034754221143083
  3. Byrne M, Aly A. The surgical suture. Aesthet Surg J. 2019;39(suppl 2):S67-S72. doi:10.1093/asj/sjz036
  4. Koppa M, House R, Tobin V, et al. Suture material choice can increase risk of hypersensitivity in hand trauma patients. Eur J Plast Surg. 2023;46:239-243. doi:10.1007/s00238-022-01986-7
  5. Pandey S, Singh M, Singh K, et al. A prospective randomized study comparing non-absorbable polypropylene (Prolene®) and delayed absorbable polyglactin 910 (Vicryl®) suture material in mass closure of vertical laparotomy wounds. Indian J Surg. 2013;75:306-310. doi:10.1007/s12262-012-0492-x
  6. Parell GJ, Becker GD. Comparison of absorbable with nonabsorbable sutures in closure of facial skin wounds. Arch Facial Plast Surg. 2003;5:488-490. doi:10.1001/archfaci.5.6.488
  7. Kim J, Singh Maan H, Cool AJ, et al. Fast absorbing gut suture versus cyanoacrylate tissue adhesive in the epidermal closure of linear repairs following Mohs micrographic surgery. J Clin Aesthet Dermatol. 2015;8:24-29.
  8. Niessen FB, Spauwen PH, Kon M. The role of suture material in hypertrophic scar formation: Monocryl vs. Vicryl-Rapide. Ann Plast Surg. 1997;39:254-260. doi:10.1097/00000637-199709000-00006
  9. Fosko SW, Heap D. Surgical pearl: an economical means of skin closure with absorbable suture. J Am Acad Dermatol. 1998;39(2 pt 1):248-250. doi:10.1016/s0190-9622(98)70084-2
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Suture Selection to Minimize Postoperative Postinflammatory Hyperpigmentation in Patients With Skin of Color During Mohs Micrographic Surgery
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Melasma

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Melasma

THE COMPARISON

A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.

B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.

C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.

Melasma

Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.

Epidemiology

Melasma commonly affects women ages 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2

Key clinical features in people with darker skin tones

Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5

Worth noting

Prevention

  • Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.
  • Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.
  • Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.

Treatment

  • First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).
  • Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or a-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1
  • Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or secondline topical therapy.
  • Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots, and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8
  • Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10
  • Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.

Health disparity highlight

Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and self-esteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out of pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.

References

1. Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106

2. Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.

3. Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.

4. Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.

5. Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.

6. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.

7. Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies. Dermatol Ther. 2017;30(3). doi:10.1111/dth.12465

8. Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.

9. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.

10. Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.

11. Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.

12. Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.

13. Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone/tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.

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Nicole A. Negbenebor, MD
Mohs Micrographic Surgery and Dermatologic Oncology Fellow, University of Iowa, Iowa City

Candrice R. Heath, MD
Department of Dermatology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA

Richard P. Usatine, MD
Family and Community Medicine, Dermatology and Cutaneous Surgery, University of Texas Health, San Antonio

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Nicole A. Negbenebor, MD
Mohs Micrographic Surgery and Dermatologic Oncology Fellow, University of Iowa, Iowa City

Candrice R. Heath, MD
Department of Dermatology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA

Richard P. Usatine, MD
Family and Community Medicine, Dermatology and Cutaneous Surgery, University of Texas Health, San Antonio

Author and Disclosure Information

Nicole A. Negbenebor, MD
Mohs Micrographic Surgery and Dermatologic Oncology Fellow, University of Iowa, Iowa City

Candrice R. Heath, MD
Department of Dermatology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA

Richard P. Usatine, MD
Family and Community Medicine, Dermatology and Cutaneous Surgery, University of Texas Health, San Antonio

Article PDF
Article PDF

THE COMPARISON

A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.

B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.

C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.

Melasma

Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.

Epidemiology

Melasma commonly affects women ages 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2

Key clinical features in people with darker skin tones

Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5

Worth noting

Prevention

  • Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.
  • Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.
  • Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.

Treatment

  • First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).
  • Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or a-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1
  • Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or secondline topical therapy.
  • Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots, and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8
  • Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10
  • Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.

Health disparity highlight

Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and self-esteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out of pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.

THE COMPARISON

A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.

B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.

C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.

Melasma

Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.

Epidemiology

Melasma commonly affects women ages 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2

Key clinical features in people with darker skin tones

Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5

Worth noting

Prevention

  • Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.
  • Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.
  • Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.

Treatment

  • First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).
  • Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or a-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1
  • Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or secondline topical therapy.
  • Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots, and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8
  • Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10
  • Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.

Health disparity highlight

Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and self-esteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out of pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.

References

1. Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106

2. Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.

3. Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.

4. Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.

5. Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.

6. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.

7. Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies. Dermatol Ther. 2017;30(3). doi:10.1111/dth.12465

8. Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.

9. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.

10. Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.

11. Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.

12. Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.

13. Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone/tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.

References

1. Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106

2. Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.

3. Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.

4. Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.

5. Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.

6. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.

7. Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies. Dermatol Ther. 2017;30(3). doi:10.1111/dth.12465

8. Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.

9. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.

10. Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.

11. Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.

12. Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.

13. Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone/tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.

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Melasma

Article Type
Changed
Wed, 04/05/2023 - 11:29
Display Headline
Melasma

THE COMPARISON

A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.

B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.

C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.

Melasma
Photographs courtesy of Richard P. Usatine, MD.

Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.

Epidemiology

Melasma commonly affects women aged 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2

Key clinical features in people with darker skin tones

Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5

Worth noting

Prevention

• Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.

• Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.

• Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.

Treatment

• First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).

• Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or α-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1

• Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or second-line topical therapy.

• Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8

• Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10

• Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.

Health disparity highlight

Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and selfesteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out-of-pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.

References
  1. Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106
  2. Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.
  3. Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.
  4. Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.
  5. Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.
  6. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.
  7. Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies [published online January 30, 2017]. Dermatol Ther. doi:10.1111/dth.12465
  8. Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.
  9. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.
  10. Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.
  11. Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.
  12. Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.
  13. Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone /tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.
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Nicole A. Negbenebor, MD
Mohs Micrographic Surgery and Dermatologic Oncology Fellow
University of Iowa
Iowa City

Richard P. Usatine, MD
Professor, Family and Community Medicine
Professor, Dermatology and Cutaneous Surgery
University of Texas Health
San Antonio

Candrice R. Heath, MD
Assistant Professor, Department of Dermatology
Lewis Katz School of Medicine
Temple University
Philadelphia, Pennsylvania

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

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Nicole A. Negbenebor, MD
Mohs Micrographic Surgery and Dermatologic Oncology Fellow
University of Iowa
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Richard P. Usatine, MD
Professor, Family and Community Medicine
Professor, Dermatology and Cutaneous Surgery
University of Texas Health
San Antonio

Candrice R. Heath, MD
Assistant Professor, Department of Dermatology
Lewis Katz School of Medicine
Temple University
Philadelphia, Pennsylvania

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

Author and Disclosure Information

Nicole A. Negbenebor, MD
Mohs Micrographic Surgery and Dermatologic Oncology Fellow
University of Iowa
Iowa City

Richard P. Usatine, MD
Professor, Family and Community Medicine
Professor, Dermatology and Cutaneous Surgery
University of Texas Health
San Antonio

Candrice R. Heath, MD
Assistant Professor, Department of Dermatology
Lewis Katz School of Medicine
Temple University
Philadelphia, Pennsylvania

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

Article PDF
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THE COMPARISON

A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.

B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.

C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.

Melasma
Photographs courtesy of Richard P. Usatine, MD.

Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.

Epidemiology

Melasma commonly affects women aged 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2

Key clinical features in people with darker skin tones

Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5

Worth noting

Prevention

• Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.

• Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.

• Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.

Treatment

• First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).

• Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or α-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1

• Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or second-line topical therapy.

• Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8

• Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10

• Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.

Health disparity highlight

Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and selfesteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out-of-pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.

THE COMPARISON

A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.

B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.

C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.

Melasma
Photographs courtesy of Richard P. Usatine, MD.

Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.

Epidemiology

Melasma commonly affects women aged 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2

Key clinical features in people with darker skin tones

Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5

Worth noting

Prevention

• Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.

• Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.

• Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.

Treatment

• First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).

• Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or α-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1

• Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or second-line topical therapy.

• Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8

• Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10

• Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.

Health disparity highlight

Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and selfesteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out-of-pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.

References
  1. Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106
  2. Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.
  3. Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.
  4. Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.
  5. Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.
  6. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.
  7. Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies [published online January 30, 2017]. Dermatol Ther. doi:10.1111/dth.12465
  8. Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.
  9. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.
  10. Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.
  11. Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.
  12. Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.
  13. Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone /tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.
References
  1. Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106
  2. Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.
  3. Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.
  4. Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.
  5. Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.
  6. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.
  7. Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies [published online January 30, 2017]. Dermatol Ther. doi:10.1111/dth.12465
  8. Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.
  9. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.
  10. Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.
  11. Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.
  12. Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.
  13. Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone /tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.
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The Power of a Multidisciplinary Tumor Board: Managing Unresectable and/or High-Risk Skin Cancers

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Multidisciplinary tumor boards are composed of providers from many fields who deliver coordinated care for patients with unresectable and high-risk skin cancers. Providers who comprise the tumor board often are radiation oncologists, hematologists/oncologists, general surgeons, dermatologists, dermatologic surgeons, and pathologists. The benefit of having a tumor board is that each patient is evaluated simultaneously by a group of physicians from various specialties who bring diverse perspectives that will contribute to the overall treatment plan. The cases often encompass high-risk tumors including unresectable basal cell carcinomas or invasive melanomas. By combining knowledge from each specialty in a team approach, the tumor board can effectively and holistically develop a care plan for each patient.

For the tumor board at the Warren Alpert Medical School of Brown University (Providence, Rhode Island), we often prepare a presentation with comprehensive details about the patient and tumor. During the presentation, we also propose a treatment plan prior to describing each patient at the weekly conference and amend the plans during the discussion. Tumor boards also provide a consulting role to the community and hospital providers in which patients are being referred by their primary provider and are seeking a second opinion or guidance.

In many ways, the tumor board is a multidisciplinary approach for patient advocacy in the form of treatment. These physicians meet on a regular basis to check on the patient’s progress and continually reevaluate how to have discussions about the patient’s care. There are many reasons why it is important to refer patients to a multidisciplinary tumor board.

Improved Workup and Diagnosis

One of the values of a tumor board is that it allows for patient data to be collected and assembled in a way that tells a story. The specialist from each field can then discuss and weigh the benefits and risks for each diagnostic test that should be performed for the workup in each patient. Physicians who refer their patients to the tumor board use their recommendations to both confirm the diagnosis and shift their treatment plans, depending on the information presented during the meeting.1 There may be a change in the tumor type, decision to refer for surgery, cancer staging, and list of viable options, especially after reviewing pathology and imaging.2 The discussion of the treatment plan may consider not only surgical considerations but also the patient’s quality of life. At times, noninvasive interventions are more appropriate and align with the patient’s goals of care. In addition, during the tumor board clinic there may be new tumors that are identified and biopsied, providing increased diagnosis and surveillance for patients who may have a higher risk for developing skin cancer.

Education for Residents and Providers

The multidisciplinary tumor board not only helps patients but also educates both residents and providers on the evidence-based therapeutic management of high-risk tumors.2 Research literature on cutaneous oncology is dynamic, and the weekly tumor board meetings help providers stay informed about the best and most effective treatments for their patients.3 In addition to the attending specialists, participants of the tumor board also may include residents, medical students, medical assistance staff, nurses, physician assistants, and fellows. Furthermore, the recommendations given by the tumor board serve to educate both the patient and the provider who referred them to the tumor board. Although we have access to excellent dermatology textbooks as residents, the most impactful educational experience is seeing the patients in tumor board clinic and participating in the immensely educational discussions at the weekly conferences. Through this experience, I have learned that treatment plans should be personalized to the patient. There are many factors to take into consideration when deciphering what the best course of treatment will be for a patient. Sometimes the best option is Mohs micrographic surgery, while other times it may be scheduling several sessions of palliative radiation oncology. Treatment depends on the individual patient and their condition.

Coordination of Care

During a week that I was on call, I was consulted to biopsy a patient with a giant hemorrhagic basal cell carcinoma that caused substantial cheek and nose distortion as well as anemia secondary to acute blood loss. The patient not only did not have a dermatologist but also did not have a primary care physician given he had not had contact with the health care system in more than 30 years. The reason for him not seeking care was multifactorial, but the approach to his care became multidisciplinary. We sought to connect him with the right providers to help him in any way that we could. We presented him at our multidisciplinary tumor board and started him on sonedigib, a medication that binds to and inhibits the smoothened protein.4 Through the tumor board, we were able to establish sustained contact with the patient. The tumor board created effective communication between providers to get him the referrals that he needed for dermatology, pathology, radiation oncology, hematology/oncology, and otolaryngology. The discussions centered around being cognizant of the patient’s apprehension with the health care system as well as providing medical and surgical treatment that would help his quality of life. We built a consensus on what the best plan was for the patient and his family. This consensus would have been more difficult had it not been for the combined specialties of the tumor board. In general, studies have shown that weekly tumor boards have resulted in decreased mortality rates for patients with advanced cancers.5

Final Thoughts

The multidisciplinary tumor board is a powerful resource for hospitals and the greater medical community. At these weekly conferences you realize there may still be hope that begins at the line where your expertise ends. It represents a team of providers who compassionately refuse to give up on patients when they are the last refuge.

References
  1. Foster TJ, Bouchard-Fortier A, Olivotto IA, et al. Effect of multidisciplinary case conferences on physician decision making: breast diagnostic rounds. Cureus. 2016;8:E895.
  2. El Saghir NS, Charara RN, Kreidieh FY, et al. Global practice and efficiency of multidisciplinary tumor boards: results of an American Society of Clinical Oncology international survey. J Glob Oncol. 2015;1:57-64.
  3. Mori S, Navarrete-Dechent C, Petukhova TA, et al. Tumor board conferences for multidisciplinary skin cancer management: a survey of US cancer centers. J Natl Compr Canc Netw. 2018;16:1209-1215.
  4. Dummer R, Ascierto PA, Basset-Seguin N, et al. Sonidegib and vismodegib in the treatment of patients with locally advanced basal cell carcinoma: a joint expert opinion. J Eur Acad Dermatol Venereol. 2020;34:1944-1956.
  5. Kehl KL, Landrum MB, Kahn KL, et al. Tumor board participation among physicians caring for patients with lung or colorectal cancer. J Oncol Pract. 2015;11:E267-E278.
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The author reports no conflict of interest.

Correspondence: Nicole A. Negbenebor, MD (nicole_negbenebor@brown.edu).

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Multidisciplinary tumor boards are composed of providers from many fields who deliver coordinated care for patients with unresectable and high-risk skin cancers. Providers who comprise the tumor board often are radiation oncologists, hematologists/oncologists, general surgeons, dermatologists, dermatologic surgeons, and pathologists. The benefit of having a tumor board is that each patient is evaluated simultaneously by a group of physicians from various specialties who bring diverse perspectives that will contribute to the overall treatment plan. The cases often encompass high-risk tumors including unresectable basal cell carcinomas or invasive melanomas. By combining knowledge from each specialty in a team approach, the tumor board can effectively and holistically develop a care plan for each patient.

For the tumor board at the Warren Alpert Medical School of Brown University (Providence, Rhode Island), we often prepare a presentation with comprehensive details about the patient and tumor. During the presentation, we also propose a treatment plan prior to describing each patient at the weekly conference and amend the plans during the discussion. Tumor boards also provide a consulting role to the community and hospital providers in which patients are being referred by their primary provider and are seeking a second opinion or guidance.

In many ways, the tumor board is a multidisciplinary approach for patient advocacy in the form of treatment. These physicians meet on a regular basis to check on the patient’s progress and continually reevaluate how to have discussions about the patient’s care. There are many reasons why it is important to refer patients to a multidisciplinary tumor board.

Improved Workup and Diagnosis

One of the values of a tumor board is that it allows for patient data to be collected and assembled in a way that tells a story. The specialist from each field can then discuss and weigh the benefits and risks for each diagnostic test that should be performed for the workup in each patient. Physicians who refer their patients to the tumor board use their recommendations to both confirm the diagnosis and shift their treatment plans, depending on the information presented during the meeting.1 There may be a change in the tumor type, decision to refer for surgery, cancer staging, and list of viable options, especially after reviewing pathology and imaging.2 The discussion of the treatment plan may consider not only surgical considerations but also the patient’s quality of life. At times, noninvasive interventions are more appropriate and align with the patient’s goals of care. In addition, during the tumor board clinic there may be new tumors that are identified and biopsied, providing increased diagnosis and surveillance for patients who may have a higher risk for developing skin cancer.

Education for Residents and Providers

The multidisciplinary tumor board not only helps patients but also educates both residents and providers on the evidence-based therapeutic management of high-risk tumors.2 Research literature on cutaneous oncology is dynamic, and the weekly tumor board meetings help providers stay informed about the best and most effective treatments for their patients.3 In addition to the attending specialists, participants of the tumor board also may include residents, medical students, medical assistance staff, nurses, physician assistants, and fellows. Furthermore, the recommendations given by the tumor board serve to educate both the patient and the provider who referred them to the tumor board. Although we have access to excellent dermatology textbooks as residents, the most impactful educational experience is seeing the patients in tumor board clinic and participating in the immensely educational discussions at the weekly conferences. Through this experience, I have learned that treatment plans should be personalized to the patient. There are many factors to take into consideration when deciphering what the best course of treatment will be for a patient. Sometimes the best option is Mohs micrographic surgery, while other times it may be scheduling several sessions of palliative radiation oncology. Treatment depends on the individual patient and their condition.

Coordination of Care

During a week that I was on call, I was consulted to biopsy a patient with a giant hemorrhagic basal cell carcinoma that caused substantial cheek and nose distortion as well as anemia secondary to acute blood loss. The patient not only did not have a dermatologist but also did not have a primary care physician given he had not had contact with the health care system in more than 30 years. The reason for him not seeking care was multifactorial, but the approach to his care became multidisciplinary. We sought to connect him with the right providers to help him in any way that we could. We presented him at our multidisciplinary tumor board and started him on sonedigib, a medication that binds to and inhibits the smoothened protein.4 Through the tumor board, we were able to establish sustained contact with the patient. The tumor board created effective communication between providers to get him the referrals that he needed for dermatology, pathology, radiation oncology, hematology/oncology, and otolaryngology. The discussions centered around being cognizant of the patient’s apprehension with the health care system as well as providing medical and surgical treatment that would help his quality of life. We built a consensus on what the best plan was for the patient and his family. This consensus would have been more difficult had it not been for the combined specialties of the tumor board. In general, studies have shown that weekly tumor boards have resulted in decreased mortality rates for patients with advanced cancers.5

Final Thoughts

The multidisciplinary tumor board is a powerful resource for hospitals and the greater medical community. At these weekly conferences you realize there may still be hope that begins at the line where your expertise ends. It represents a team of providers who compassionately refuse to give up on patients when they are the last refuge.

Multidisciplinary tumor boards are composed of providers from many fields who deliver coordinated care for patients with unresectable and high-risk skin cancers. Providers who comprise the tumor board often are radiation oncologists, hematologists/oncologists, general surgeons, dermatologists, dermatologic surgeons, and pathologists. The benefit of having a tumor board is that each patient is evaluated simultaneously by a group of physicians from various specialties who bring diverse perspectives that will contribute to the overall treatment plan. The cases often encompass high-risk tumors including unresectable basal cell carcinomas or invasive melanomas. By combining knowledge from each specialty in a team approach, the tumor board can effectively and holistically develop a care plan for each patient.

For the tumor board at the Warren Alpert Medical School of Brown University (Providence, Rhode Island), we often prepare a presentation with comprehensive details about the patient and tumor. During the presentation, we also propose a treatment plan prior to describing each patient at the weekly conference and amend the plans during the discussion. Tumor boards also provide a consulting role to the community and hospital providers in which patients are being referred by their primary provider and are seeking a second opinion or guidance.

In many ways, the tumor board is a multidisciplinary approach for patient advocacy in the form of treatment. These physicians meet on a regular basis to check on the patient’s progress and continually reevaluate how to have discussions about the patient’s care. There are many reasons why it is important to refer patients to a multidisciplinary tumor board.

Improved Workup and Diagnosis

One of the values of a tumor board is that it allows for patient data to be collected and assembled in a way that tells a story. The specialist from each field can then discuss and weigh the benefits and risks for each diagnostic test that should be performed for the workup in each patient. Physicians who refer their patients to the tumor board use their recommendations to both confirm the diagnosis and shift their treatment plans, depending on the information presented during the meeting.1 There may be a change in the tumor type, decision to refer for surgery, cancer staging, and list of viable options, especially after reviewing pathology and imaging.2 The discussion of the treatment plan may consider not only surgical considerations but also the patient’s quality of life. At times, noninvasive interventions are more appropriate and align with the patient’s goals of care. In addition, during the tumor board clinic there may be new tumors that are identified and biopsied, providing increased diagnosis and surveillance for patients who may have a higher risk for developing skin cancer.

Education for Residents and Providers

The multidisciplinary tumor board not only helps patients but also educates both residents and providers on the evidence-based therapeutic management of high-risk tumors.2 Research literature on cutaneous oncology is dynamic, and the weekly tumor board meetings help providers stay informed about the best and most effective treatments for their patients.3 In addition to the attending specialists, participants of the tumor board also may include residents, medical students, medical assistance staff, nurses, physician assistants, and fellows. Furthermore, the recommendations given by the tumor board serve to educate both the patient and the provider who referred them to the tumor board. Although we have access to excellent dermatology textbooks as residents, the most impactful educational experience is seeing the patients in tumor board clinic and participating in the immensely educational discussions at the weekly conferences. Through this experience, I have learned that treatment plans should be personalized to the patient. There are many factors to take into consideration when deciphering what the best course of treatment will be for a patient. Sometimes the best option is Mohs micrographic surgery, while other times it may be scheduling several sessions of palliative radiation oncology. Treatment depends on the individual patient and their condition.

Coordination of Care

During a week that I was on call, I was consulted to biopsy a patient with a giant hemorrhagic basal cell carcinoma that caused substantial cheek and nose distortion as well as anemia secondary to acute blood loss. The patient not only did not have a dermatologist but also did not have a primary care physician given he had not had contact with the health care system in more than 30 years. The reason for him not seeking care was multifactorial, but the approach to his care became multidisciplinary. We sought to connect him with the right providers to help him in any way that we could. We presented him at our multidisciplinary tumor board and started him on sonedigib, a medication that binds to and inhibits the smoothened protein.4 Through the tumor board, we were able to establish sustained contact with the patient. The tumor board created effective communication between providers to get him the referrals that he needed for dermatology, pathology, radiation oncology, hematology/oncology, and otolaryngology. The discussions centered around being cognizant of the patient’s apprehension with the health care system as well as providing medical and surgical treatment that would help his quality of life. We built a consensus on what the best plan was for the patient and his family. This consensus would have been more difficult had it not been for the combined specialties of the tumor board. In general, studies have shown that weekly tumor boards have resulted in decreased mortality rates for patients with advanced cancers.5

Final Thoughts

The multidisciplinary tumor board is a powerful resource for hospitals and the greater medical community. At these weekly conferences you realize there may still be hope that begins at the line where your expertise ends. It represents a team of providers who compassionately refuse to give up on patients when they are the last refuge.

References
  1. Foster TJ, Bouchard-Fortier A, Olivotto IA, et al. Effect of multidisciplinary case conferences on physician decision making: breast diagnostic rounds. Cureus. 2016;8:E895.
  2. El Saghir NS, Charara RN, Kreidieh FY, et al. Global practice and efficiency of multidisciplinary tumor boards: results of an American Society of Clinical Oncology international survey. J Glob Oncol. 2015;1:57-64.
  3. Mori S, Navarrete-Dechent C, Petukhova TA, et al. Tumor board conferences for multidisciplinary skin cancer management: a survey of US cancer centers. J Natl Compr Canc Netw. 2018;16:1209-1215.
  4. Dummer R, Ascierto PA, Basset-Seguin N, et al. Sonidegib and vismodegib in the treatment of patients with locally advanced basal cell carcinoma: a joint expert opinion. J Eur Acad Dermatol Venereol. 2020;34:1944-1956.
  5. Kehl KL, Landrum MB, Kahn KL, et al. Tumor board participation among physicians caring for patients with lung or colorectal cancer. J Oncol Pract. 2015;11:E267-E278.
References
  1. Foster TJ, Bouchard-Fortier A, Olivotto IA, et al. Effect of multidisciplinary case conferences on physician decision making: breast diagnostic rounds. Cureus. 2016;8:E895.
  2. El Saghir NS, Charara RN, Kreidieh FY, et al. Global practice and efficiency of multidisciplinary tumor boards: results of an American Society of Clinical Oncology international survey. J Glob Oncol. 2015;1:57-64.
  3. Mori S, Navarrete-Dechent C, Petukhova TA, et al. Tumor board conferences for multidisciplinary skin cancer management: a survey of US cancer centers. J Natl Compr Canc Netw. 2018;16:1209-1215.
  4. Dummer R, Ascierto PA, Basset-Seguin N, et al. Sonidegib and vismodegib in the treatment of patients with locally advanced basal cell carcinoma: a joint expert opinion. J Eur Acad Dermatol Venereol. 2020;34:1944-1956.
  5. Kehl KL, Landrum MB, Kahn KL, et al. Tumor board participation among physicians caring for patients with lung or colorectal cancer. J Oncol Pract. 2015;11:E267-E278.
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  • Participating in a multidisciplinary tumor board allows residents to learn more about how to manage and treat high-risk skin cancers. The multidisciplinary team approach provides high-quality care for challenging patients.
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Advice for Applying to Dermatology as an Applicant of Color: Keep Going

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As the dermatology admissions cycle restarts, I reflect back on my journey as a Black woman applying to dermatology. Before deciding, I internally questioned, “Is dermatology right for me?” There were not many faces that looked like mine within the field. After committing to dermatology, I asked dermatologists—almost any who would spare a few minutes to talk to me—how to get into this specialty and be successful when applying. I spoke to advisors and friends at my home department, emailed dermatologists far and wide, approached conference lecturers after their presentations, sought out advice from current residents, and asked prior applicants what they thought was important to match into dermatology. There had been too many unmatched students before me who had achieved good grades and aced US Medical Licensing Examination Step 1. The equation for success was missing a variable.

Mentorship

One weekend, I attended a conference for patients with skin of color. I talked to a student who had taken a year off (retroactively after not matching in prior years). She told me that the biggest key to matching was mentorship; forming a strong relationship with a clinician or investigator who had seen how well you perform in clinic or during research was paramount. Having a collaborator or instructor write you a letter of recommendation and make calls on your behalf could be the difference between matching or taking another year off. More often than any other aspect of the application, it is a lack of mentorship that many students of color do not have access to when pursuing a highly competitive specialty such as dermatology.1,2 In such a small field, applicants need someone to vouch for them—to speak on their behalf compassionately, invite them to collaborate on research projects, and inform them of conference opportunities to present their work.

Representation in Dermatology

We are told that you can accomplish anything with hard work and grit; however, without the platform to show how effectively you have worked, your efforts may never be seen. The diversity statistics for dermatology are clear and disheartening. Although 13% of Americans are Black, only 3% of all dermatologists are Black.2,3 Just over 4% of dermatologists are Hispanic compared with 16% of the general population. The Association of American Medical Colleges reported that the overall 2015 medical school acceptance rate was 41%.4 White (44%), Asian (42%), and Hispanic or Latino (42%) applicants all had similar acceptance rates; however, only one-third of Black applicants were accepted. At graduation in 2015, White individuals were 51% of matriculants. Medical graduates were only 6% Black.4 What percentage of these 6% Black graduates thought about applying into dermatology? How many had someone to encourage them to pursue the specialty or a mentor who they could ask about the nuances and strategy to be a competitive applicant?

In addition to discrimination, social psychologists have described stereotype threat, a risk for minorities that occurs when negative stereotypes associated with an individual’s group status become relevant after perceived cues.5 Therefore, some students of color might avoid competitive specialties such as dermatology because of this internalized lack of confidence in their own abilities and performance thinking, “I’ll never be good enough to match into dermatology.” I have seen this discouraging perception when classmates doubt their own talent and achievements, which is a variation of imposter syndrome—when an individual doubts their abilities and may have an internal fear of eventually being exposed as a fraud.



After several publications received press coverage on the lack of diversity in dermatology applicant selection,3,6,7 I looked around at my interview group composed of 25 to 40 interviewees and on average saw 2 to 3 Black applicants around the room. We always found a way during the packed interview day to find time to introduce ourselves. I almost always left with a new friend who shared feelings of anxiety, uncertainty, hope, and gratefulness from being the few Black people in the room. Bootstrapping might have helped us to make it into medical school, pass shelf examinations, and even get a great Step 1 score. However, the addition of mentorship—or better yet, sponsorship—helped to get us an interview in this competitive field. The impact of mentorship has been especially true for research, which has shown that students often gravitate toward mentors who look like them.8 However, the reality is that many Black and Hispanic students may be at a disadvantage for finding mentors in this way given that there are less than 10% of dermatologists who identify as individuals with skin of color. During the process of applying to dermatology, my greatest advocates were ethnically and racially diverse. The proverb is that it takes a village to raise a child; this reality extends to the medical student’s ability to thrive, not only in residency but also in the residency application process. My sponsors have been as different as their advice and perspectives, which helped me to think about the varied ways I viewed myself as an applicant and shaped what I looked for in residency.

Final Thoughts

Now that I have been a resident in the Department of Dermatology at the Warren Alpert Medical School of Brown University, I excitedly look for opportunities to mentor medical students and help create equity in the application process. Dermatology needs to increase the representation of minority applicants. Efforts to encourage minority medical students include joining the National Medical Association dermatology section through the Student National Medical Association, membership in the Skin of Color Society, getting involved with the Dermatology Interest Group at more medical schools, and awareness of medical student–friendly dermatology conferences. In addition, I was able to establish lifelong mentorship through the American Academy of Dermatology’s Minority Diversity Mentorship Program. One important component is an enhanced effort to increase the number of financial scholarships for away rotations (post–coronavirus disease 2019 pandemic) or application expenses geared to help underrepresented minorities. To truly increase diversity in dermatology, perhaps we need more physicians and residents willing to encourage students of color that dermatology is achievable.

References
  1. Brunsma DL, Embrick DG, Shin JH. Graduate students of color: race, racism, and mentoring in the white waters of academia. Sociology of Race and Ethnicity. 2017;3:1-13.
  2. Oyesanya T, Grossberg AL, Okoye GA. Increasing minority representation in the dermatology department: the Johns Hopkins experience. JAMA Dermatol. 2018;154:1133-1134.
  3. Pandya AG, Alexis AF, Berger TG, et al. Increasing racial and ethnic diversity in dermatology: a call to action. J Am Acad Dermatol. 2016;74:584-587.
  4. Current trends in medical education. American Association of Medical Colleges. Accessed January 20, 2021. http://www.aamcdiversityfactsandfigures2016.org/report-section/section-3/
  5. Spencer SJ, Logel C, Davies PG. Stereotype threat [published online September 10, 2015]. Annu Rev Psychol. 2016;67:415-437.
  6. Granstein RD, Cornelius L, Shinkai K. Diversity in dermatology—a call for action. JAMA Dermatol. 2017;153:499-500.
  7. Pritchett EN, Pandya AG, Ferguson NN, et al. Diversity in dermatology: roadmap for improvement. J Am Acad Dermatol. 2018;79:337-341.
  8. Blake-Beard S, Bayne ML, Crosby FJ, et al. Matching by race and gender in mentoring relationships: keeping our eyes on the prize. J Social Issues. 2011;67:622-643.
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Author and Disclosure Information

From the Department of Dermatology, Warren Alpert Medical School of Brown University, Providence, Rhode Island.

The author reports no conflict of interest.

Correspondence: Nicole A. Negbenebor, MD (nicole_negbenebor@brown.edu). 

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From the Department of Dermatology, Warren Alpert Medical School of Brown University, Providence, Rhode Island.

The author reports no conflict of interest.

Correspondence: Nicole A. Negbenebor, MD (nicole_negbenebor@brown.edu). 

Author and Disclosure Information

From the Department of Dermatology, Warren Alpert Medical School of Brown University, Providence, Rhode Island.

The author reports no conflict of interest.

Correspondence: Nicole A. Negbenebor, MD (nicole_negbenebor@brown.edu). 

Article PDF
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As the dermatology admissions cycle restarts, I reflect back on my journey as a Black woman applying to dermatology. Before deciding, I internally questioned, “Is dermatology right for me?” There were not many faces that looked like mine within the field. After committing to dermatology, I asked dermatologists—almost any who would spare a few minutes to talk to me—how to get into this specialty and be successful when applying. I spoke to advisors and friends at my home department, emailed dermatologists far and wide, approached conference lecturers after their presentations, sought out advice from current residents, and asked prior applicants what they thought was important to match into dermatology. There had been too many unmatched students before me who had achieved good grades and aced US Medical Licensing Examination Step 1. The equation for success was missing a variable.

Mentorship

One weekend, I attended a conference for patients with skin of color. I talked to a student who had taken a year off (retroactively after not matching in prior years). She told me that the biggest key to matching was mentorship; forming a strong relationship with a clinician or investigator who had seen how well you perform in clinic or during research was paramount. Having a collaborator or instructor write you a letter of recommendation and make calls on your behalf could be the difference between matching or taking another year off. More often than any other aspect of the application, it is a lack of mentorship that many students of color do not have access to when pursuing a highly competitive specialty such as dermatology.1,2 In such a small field, applicants need someone to vouch for them—to speak on their behalf compassionately, invite them to collaborate on research projects, and inform them of conference opportunities to present their work.

Representation in Dermatology

We are told that you can accomplish anything with hard work and grit; however, without the platform to show how effectively you have worked, your efforts may never be seen. The diversity statistics for dermatology are clear and disheartening. Although 13% of Americans are Black, only 3% of all dermatologists are Black.2,3 Just over 4% of dermatologists are Hispanic compared with 16% of the general population. The Association of American Medical Colleges reported that the overall 2015 medical school acceptance rate was 41%.4 White (44%), Asian (42%), and Hispanic or Latino (42%) applicants all had similar acceptance rates; however, only one-third of Black applicants were accepted. At graduation in 2015, White individuals were 51% of matriculants. Medical graduates were only 6% Black.4 What percentage of these 6% Black graduates thought about applying into dermatology? How many had someone to encourage them to pursue the specialty or a mentor who they could ask about the nuances and strategy to be a competitive applicant?

In addition to discrimination, social psychologists have described stereotype threat, a risk for minorities that occurs when negative stereotypes associated with an individual’s group status become relevant after perceived cues.5 Therefore, some students of color might avoid competitive specialties such as dermatology because of this internalized lack of confidence in their own abilities and performance thinking, “I’ll never be good enough to match into dermatology.” I have seen this discouraging perception when classmates doubt their own talent and achievements, which is a variation of imposter syndrome—when an individual doubts their abilities and may have an internal fear of eventually being exposed as a fraud.



After several publications received press coverage on the lack of diversity in dermatology applicant selection,3,6,7 I looked around at my interview group composed of 25 to 40 interviewees and on average saw 2 to 3 Black applicants around the room. We always found a way during the packed interview day to find time to introduce ourselves. I almost always left with a new friend who shared feelings of anxiety, uncertainty, hope, and gratefulness from being the few Black people in the room. Bootstrapping might have helped us to make it into medical school, pass shelf examinations, and even get a great Step 1 score. However, the addition of mentorship—or better yet, sponsorship—helped to get us an interview in this competitive field. The impact of mentorship has been especially true for research, which has shown that students often gravitate toward mentors who look like them.8 However, the reality is that many Black and Hispanic students may be at a disadvantage for finding mentors in this way given that there are less than 10% of dermatologists who identify as individuals with skin of color. During the process of applying to dermatology, my greatest advocates were ethnically and racially diverse. The proverb is that it takes a village to raise a child; this reality extends to the medical student’s ability to thrive, not only in residency but also in the residency application process. My sponsors have been as different as their advice and perspectives, which helped me to think about the varied ways I viewed myself as an applicant and shaped what I looked for in residency.

Final Thoughts

Now that I have been a resident in the Department of Dermatology at the Warren Alpert Medical School of Brown University, I excitedly look for opportunities to mentor medical students and help create equity in the application process. Dermatology needs to increase the representation of minority applicants. Efforts to encourage minority medical students include joining the National Medical Association dermatology section through the Student National Medical Association, membership in the Skin of Color Society, getting involved with the Dermatology Interest Group at more medical schools, and awareness of medical student–friendly dermatology conferences. In addition, I was able to establish lifelong mentorship through the American Academy of Dermatology’s Minority Diversity Mentorship Program. One important component is an enhanced effort to increase the number of financial scholarships for away rotations (post–coronavirus disease 2019 pandemic) or application expenses geared to help underrepresented minorities. To truly increase diversity in dermatology, perhaps we need more physicians and residents willing to encourage students of color that dermatology is achievable.

As the dermatology admissions cycle restarts, I reflect back on my journey as a Black woman applying to dermatology. Before deciding, I internally questioned, “Is dermatology right for me?” There were not many faces that looked like mine within the field. After committing to dermatology, I asked dermatologists—almost any who would spare a few minutes to talk to me—how to get into this specialty and be successful when applying. I spoke to advisors and friends at my home department, emailed dermatologists far and wide, approached conference lecturers after their presentations, sought out advice from current residents, and asked prior applicants what they thought was important to match into dermatology. There had been too many unmatched students before me who had achieved good grades and aced US Medical Licensing Examination Step 1. The equation for success was missing a variable.

Mentorship

One weekend, I attended a conference for patients with skin of color. I talked to a student who had taken a year off (retroactively after not matching in prior years). She told me that the biggest key to matching was mentorship; forming a strong relationship with a clinician or investigator who had seen how well you perform in clinic or during research was paramount. Having a collaborator or instructor write you a letter of recommendation and make calls on your behalf could be the difference between matching or taking another year off. More often than any other aspect of the application, it is a lack of mentorship that many students of color do not have access to when pursuing a highly competitive specialty such as dermatology.1,2 In such a small field, applicants need someone to vouch for them—to speak on their behalf compassionately, invite them to collaborate on research projects, and inform them of conference opportunities to present their work.

Representation in Dermatology

We are told that you can accomplish anything with hard work and grit; however, without the platform to show how effectively you have worked, your efforts may never be seen. The diversity statistics for dermatology are clear and disheartening. Although 13% of Americans are Black, only 3% of all dermatologists are Black.2,3 Just over 4% of dermatologists are Hispanic compared with 16% of the general population. The Association of American Medical Colleges reported that the overall 2015 medical school acceptance rate was 41%.4 White (44%), Asian (42%), and Hispanic or Latino (42%) applicants all had similar acceptance rates; however, only one-third of Black applicants were accepted. At graduation in 2015, White individuals were 51% of matriculants. Medical graduates were only 6% Black.4 What percentage of these 6% Black graduates thought about applying into dermatology? How many had someone to encourage them to pursue the specialty or a mentor who they could ask about the nuances and strategy to be a competitive applicant?

In addition to discrimination, social psychologists have described stereotype threat, a risk for minorities that occurs when negative stereotypes associated with an individual’s group status become relevant after perceived cues.5 Therefore, some students of color might avoid competitive specialties such as dermatology because of this internalized lack of confidence in their own abilities and performance thinking, “I’ll never be good enough to match into dermatology.” I have seen this discouraging perception when classmates doubt their own talent and achievements, which is a variation of imposter syndrome—when an individual doubts their abilities and may have an internal fear of eventually being exposed as a fraud.



After several publications received press coverage on the lack of diversity in dermatology applicant selection,3,6,7 I looked around at my interview group composed of 25 to 40 interviewees and on average saw 2 to 3 Black applicants around the room. We always found a way during the packed interview day to find time to introduce ourselves. I almost always left with a new friend who shared feelings of anxiety, uncertainty, hope, and gratefulness from being the few Black people in the room. Bootstrapping might have helped us to make it into medical school, pass shelf examinations, and even get a great Step 1 score. However, the addition of mentorship—or better yet, sponsorship—helped to get us an interview in this competitive field. The impact of mentorship has been especially true for research, which has shown that students often gravitate toward mentors who look like them.8 However, the reality is that many Black and Hispanic students may be at a disadvantage for finding mentors in this way given that there are less than 10% of dermatologists who identify as individuals with skin of color. During the process of applying to dermatology, my greatest advocates were ethnically and racially diverse. The proverb is that it takes a village to raise a child; this reality extends to the medical student’s ability to thrive, not only in residency but also in the residency application process. My sponsors have been as different as their advice and perspectives, which helped me to think about the varied ways I viewed myself as an applicant and shaped what I looked for in residency.

Final Thoughts

Now that I have been a resident in the Department of Dermatology at the Warren Alpert Medical School of Brown University, I excitedly look for opportunities to mentor medical students and help create equity in the application process. Dermatology needs to increase the representation of minority applicants. Efforts to encourage minority medical students include joining the National Medical Association dermatology section through the Student National Medical Association, membership in the Skin of Color Society, getting involved with the Dermatology Interest Group at more medical schools, and awareness of medical student–friendly dermatology conferences. In addition, I was able to establish lifelong mentorship through the American Academy of Dermatology’s Minority Diversity Mentorship Program. One important component is an enhanced effort to increase the number of financial scholarships for away rotations (post–coronavirus disease 2019 pandemic) or application expenses geared to help underrepresented minorities. To truly increase diversity in dermatology, perhaps we need more physicians and residents willing to encourage students of color that dermatology is achievable.

References
  1. Brunsma DL, Embrick DG, Shin JH. Graduate students of color: race, racism, and mentoring in the white waters of academia. Sociology of Race and Ethnicity. 2017;3:1-13.
  2. Oyesanya T, Grossberg AL, Okoye GA. Increasing minority representation in the dermatology department: the Johns Hopkins experience. JAMA Dermatol. 2018;154:1133-1134.
  3. Pandya AG, Alexis AF, Berger TG, et al. Increasing racial and ethnic diversity in dermatology: a call to action. J Am Acad Dermatol. 2016;74:584-587.
  4. Current trends in medical education. American Association of Medical Colleges. Accessed January 20, 2021. http://www.aamcdiversityfactsandfigures2016.org/report-section/section-3/
  5. Spencer SJ, Logel C, Davies PG. Stereotype threat [published online September 10, 2015]. Annu Rev Psychol. 2016;67:415-437.
  6. Granstein RD, Cornelius L, Shinkai K. Diversity in dermatology—a call for action. JAMA Dermatol. 2017;153:499-500.
  7. Pritchett EN, Pandya AG, Ferguson NN, et al. Diversity in dermatology: roadmap for improvement. J Am Acad Dermatol. 2018;79:337-341.
  8. Blake-Beard S, Bayne ML, Crosby FJ, et al. Matching by race and gender in mentoring relationships: keeping our eyes on the prize. J Social Issues. 2011;67:622-643.
References
  1. Brunsma DL, Embrick DG, Shin JH. Graduate students of color: race, racism, and mentoring in the white waters of academia. Sociology of Race and Ethnicity. 2017;3:1-13.
  2. Oyesanya T, Grossberg AL, Okoye GA. Increasing minority representation in the dermatology department: the Johns Hopkins experience. JAMA Dermatol. 2018;154:1133-1134.
  3. Pandya AG, Alexis AF, Berger TG, et al. Increasing racial and ethnic diversity in dermatology: a call to action. J Am Acad Dermatol. 2016;74:584-587.
  4. Current trends in medical education. American Association of Medical Colleges. Accessed January 20, 2021. http://www.aamcdiversityfactsandfigures2016.org/report-section/section-3/
  5. Spencer SJ, Logel C, Davies PG. Stereotype threat [published online September 10, 2015]. Annu Rev Psychol. 2016;67:415-437.
  6. Granstein RD, Cornelius L, Shinkai K. Diversity in dermatology—a call for action. JAMA Dermatol. 2017;153:499-500.
  7. Pritchett EN, Pandya AG, Ferguson NN, et al. Diversity in dermatology: roadmap for improvement. J Am Acad Dermatol. 2018;79:337-341.
  8. Blake-Beard S, Bayne ML, Crosby FJ, et al. Matching by race and gender in mentoring relationships: keeping our eyes on the prize. J Social Issues. 2011;67:622-643.
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Cutis - 107(1)
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  • Finding a strong mentor who can both advocate for and help guide a student of color through the admissions process is integral to matching into dermatology
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