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In a case study published online on March 2 in JAMA Dermatology, Geller et al examined the relationship between total nevi, atypical nevi, and melanoma thickness. The study included 566 patients with melanoma. They were administered written surveys and underwent skin examinations at academic centers in Michigan and California within 3 months of diagnosis, measuring current total nevus count and atypical nevus count in addition to cataloguing melanoma thickness, histologic subtype, patient age, sex, marital status, skin self-examination and physician skin examination tendency, other health care visits, and mode of melanoma discovery.

Many epidemiologic trends were noted, but in summary, most melanoma patients had 0 to 20 total nevi (66.4%) and no atypical nevi (73.3%), a trend most pronounced in older patients (≥60 years). In patients younger than 60 years, higher nevus count (>50) was associated with thinner melanomas (≤2.0 mm), and the presence of more than 5 atypical nevi was associated with thicker melanomas (>2.0 mm).

What’s the issue?Studies clarifying the overall clinical characteristics of patients with aggressive melanomas appear every month in reputable journals, touting that concurrent total nevus count is important; or nevus size is important; or atypia is important; or clinical stigmata, medical history, and family history are important. Who is correct? Is everyone correct? On the pathology arm of the argument, Rosendahl et al (J Am Acad Dermatol. 2015;73:507-512) highlighted the same dilemma in which clinicians do not agree on the histopathologic features of nevi that consistently put patients at risk for individual lesion or de novo melanoma.

For me, each clinic day involves performing many total-body skin examinations, and many of these patients have innumerable nevi and various scars from lesions removed over the years with “atypical mole,” “premelanoma,” “precancer,” and various other self-reported labels. Some lesions may have documented pathology reports, but many do not. Some reports refer to dysplasia as a gradient, some do not. Some reports include molecular testing or clinical markers to grade lesions, and each can vary between institutions and pathologists. On the macroscopic level, clinically atypical nevi do not have a widely agreed upon set of criteria or threshold for biopsy; some clinicians use dermoscopic markers, and others utilize some version of the ABCDE (a=asymmetry; b=border; c=color; d=diameter; e=evolving) features.

The Geller et al study supports that these melanoma patients did not necessarily have more total nevi, and younger patients with aggressive melanoma may have a tendency toward more clinically atypical nevi. Although the study establishes what those institutions and clinicians determined to be atypical, I’m not sure that this is something that most clinicians widely agree upon. Additionally, these features were not paired with histopathologic dysplasia because the lesions were not biopsied.

What I find in conversation with colleagues is that some agree with what Geller et al defined as atypical, but some clinicians do not even refer to nevi as clinically atypical in a medical record unless they have pathology evidence of atypia (or the term their pathologist may use), which may be to avoid controversy regarding legal implications of atypia or “open-note” misunderstanding that the patient may have about this term, likening it to Papanicolaou test premalignancy verbiage.

I am not aware of one dermatologist or dermatopathologist who does not find this quandary to be frustrating. How do any of us really know which patients to follow more often for melanoma surveillance? How does your practice or institution report atypia in the clinical and histopathologic setting, and what do you find are the most important markers for development of melanoma?

We want to know your views! Tell us what you think.

In a case study published online on March 2 in JAMA Dermatology, Geller et al examined the relationship between total nevi, atypical nevi, and melanoma thickness. The study included 566 patients with melanoma. They were administered written surveys and underwent skin examinations at academic centers in Michigan and California within 3 months of diagnosis, measuring current total nevus count and atypical nevus count in addition to cataloguing melanoma thickness, histologic subtype, patient age, sex, marital status, skin self-examination and physician skin examination tendency, other health care visits, and mode of melanoma discovery.

Many epidemiologic trends were noted, but in summary, most melanoma patients had 0 to 20 total nevi (66.4%) and no atypical nevi (73.3%), a trend most pronounced in older patients (≥60 years). In patients younger than 60 years, higher nevus count (>50) was associated with thinner melanomas (≤2.0 mm), and the presence of more than 5 atypical nevi was associated with thicker melanomas (>2.0 mm).

What’s the issue?Studies clarifying the overall clinical characteristics of patients with aggressive melanomas appear every month in reputable journals, touting that concurrent total nevus count is important; or nevus size is important; or atypia is important; or clinical stigmata, medical history, and family history are important. Who is correct? Is everyone correct? On the pathology arm of the argument, Rosendahl et al (J Am Acad Dermatol. 2015;73:507-512) highlighted the same dilemma in which clinicians do not agree on the histopathologic features of nevi that consistently put patients at risk for individual lesion or de novo melanoma.

For me, each clinic day involves performing many total-body skin examinations, and many of these patients have innumerable nevi and various scars from lesions removed over the years with “atypical mole,” “premelanoma,” “precancer,” and various other self-reported labels. Some lesions may have documented pathology reports, but many do not. Some reports refer to dysplasia as a gradient, some do not. Some reports include molecular testing or clinical markers to grade lesions, and each can vary between institutions and pathologists. On the macroscopic level, clinically atypical nevi do not have a widely agreed upon set of criteria or threshold for biopsy; some clinicians use dermoscopic markers, and others utilize some version of the ABCDE (a=asymmetry; b=border; c=color; d=diameter; e=evolving) features.

The Geller et al study supports that these melanoma patients did not necessarily have more total nevi, and younger patients with aggressive melanoma may have a tendency toward more clinically atypical nevi. Although the study establishes what those institutions and clinicians determined to be atypical, I’m not sure that this is something that most clinicians widely agree upon. Additionally, these features were not paired with histopathologic dysplasia because the lesions were not biopsied.

What I find in conversation with colleagues is that some agree with what Geller et al defined as atypical, but some clinicians do not even refer to nevi as clinically atypical in a medical record unless they have pathology evidence of atypia (or the term their pathologist may use), which may be to avoid controversy regarding legal implications of atypia or “open-note” misunderstanding that the patient may have about this term, likening it to Papanicolaou test premalignancy verbiage.

I am not aware of one dermatologist or dermatopathologist who does not find this quandary to be frustrating. How do any of us really know which patients to follow more often for melanoma surveillance? How does your practice or institution report atypia in the clinical and histopathologic setting, and what do you find are the most important markers for development of melanoma?

We want to know your views! Tell us what you think.

In a case study published online on March 2 in JAMA Dermatology, Geller et al examined the relationship between total nevi, atypical nevi, and melanoma thickness. The study included 566 patients with melanoma. They were administered written surveys and underwent skin examinations at academic centers in Michigan and California within 3 months of diagnosis, measuring current total nevus count and atypical nevus count in addition to cataloguing melanoma thickness, histologic subtype, patient age, sex, marital status, skin self-examination and physician skin examination tendency, other health care visits, and mode of melanoma discovery.

Many epidemiologic trends were noted, but in summary, most melanoma patients had 0 to 20 total nevi (66.4%) and no atypical nevi (73.3%), a trend most pronounced in older patients (≥60 years). In patients younger than 60 years, higher nevus count (>50) was associated with thinner melanomas (≤2.0 mm), and the presence of more than 5 atypical nevi was associated with thicker melanomas (>2.0 mm).

What’s the issue?Studies clarifying the overall clinical characteristics of patients with aggressive melanomas appear every month in reputable journals, touting that concurrent total nevus count is important; or nevus size is important; or atypia is important; or clinical stigmata, medical history, and family history are important. Who is correct? Is everyone correct? On the pathology arm of the argument, Rosendahl et al (J Am Acad Dermatol. 2015;73:507-512) highlighted the same dilemma in which clinicians do not agree on the histopathologic features of nevi that consistently put patients at risk for individual lesion or de novo melanoma.

For me, each clinic day involves performing many total-body skin examinations, and many of these patients have innumerable nevi and various scars from lesions removed over the years with “atypical mole,” “premelanoma,” “precancer,” and various other self-reported labels. Some lesions may have documented pathology reports, but many do not. Some reports refer to dysplasia as a gradient, some do not. Some reports include molecular testing or clinical markers to grade lesions, and each can vary between institutions and pathologists. On the macroscopic level, clinically atypical nevi do not have a widely agreed upon set of criteria or threshold for biopsy; some clinicians use dermoscopic markers, and others utilize some version of the ABCDE (a=asymmetry; b=border; c=color; d=diameter; e=evolving) features.

The Geller et al study supports that these melanoma patients did not necessarily have more total nevi, and younger patients with aggressive melanoma may have a tendency toward more clinically atypical nevi. Although the study establishes what those institutions and clinicians determined to be atypical, I’m not sure that this is something that most clinicians widely agree upon. Additionally, these features were not paired with histopathologic dysplasia because the lesions were not biopsied.

What I find in conversation with colleagues is that some agree with what Geller et al defined as atypical, but some clinicians do not even refer to nevi as clinically atypical in a medical record unless they have pathology evidence of atypia (or the term their pathologist may use), which may be to avoid controversy regarding legal implications of atypia or “open-note” misunderstanding that the patient may have about this term, likening it to Papanicolaou test premalignancy verbiage.

I am not aware of one dermatologist or dermatopathologist who does not find this quandary to be frustrating. How do any of us really know which patients to follow more often for melanoma surveillance? How does your practice or institution report atypia in the clinical and histopathologic setting, and what do you find are the most important markers for development of melanoma?

We want to know your views! Tell us what you think.

Biologic agents for the treatment of psoriasis are approved for patients 18 years and older. Although some biologics are approved for juvenile idiopathic arthritis, the lack of approved biologic therapies for children with psoriasis has been a major gap in our treatment of the disease. The incidence of moderate to severe psoriasis in the pediatric population is much lower than in adults, but there are still many patients younger than 18 years who would benefit from systemic therapies.

A recent press release indicates that the US Food and Drug Administration has accepted for review a supplemental biologics license application for the expanded use of etanercept to treat pediatric patients with chronic severe plaque psoriasis.

In February 2016 Paller et al (J Am Acad Dermatol. 2016;74:280.e3-287.e3) published data evaluating long-term safety and efficacy of etanercept in children and adolescents with moderate to severe plaque psoriasis. This 5-year, open-label extension study enrolled those patients aged 4 to 17 years who had participated in an initial 48-week parent study. End points included occurrence of adverse events (AEs) and serious AEs including infections as well as rates of 75% and 90% improvement in psoriasis area and severity index (PASI) score and clear or almost clear status on the static physician global assessment.

Of 182 patients enrolled, 181 received etanercept and 69 completed 264 weeks of treatment. Through week 264, 161 (89.0%) patients reported an AE, most commonly upper respiratory tract infection (37.6%), nasopharyngitis (26.0%), and headache (21.5%). Seven patients reported 8 Serious AEs (n=8) were reported in 7 patients, and only 1 case of cellulitis was considered treatment related. No cases of opportunistic infections or malignancy were reported. Rates of 75% improvement (∼60%–70%) and 90% improvement (∼30%–40%) in PASI score were maintained through week 264 as well as static physician global assessment status of clear or almost clear (∼40%–50%).

What’s the issue?

If approved, etanercept would be the first US Food and Drug Administration–approved systemic drug for pediatric psoriasis patients, which would open up options for many patients in need. Would you be willing to treat your pediatric psoriasis patients with a biologic?

We want to know your views! Tell us what you think.

Biologic agents for the treatment of psoriasis are approved for patients 18 years and older. Although some biologics are approved for juvenile idiopathic arthritis, the lack of approved biologic therapies for children with psoriasis has been a major gap in our treatment of the disease. The incidence of moderate to severe psoriasis in the pediatric population is much lower than in adults, but there are still many patients younger than 18 years who would benefit from systemic therapies.

A recent press release indicates that the US Food and Drug Administration has accepted for review a supplemental biologics license application for the expanded use of etanercept to treat pediatric patients with chronic severe plaque psoriasis.

In February 2016 Paller et al (J Am Acad Dermatol. 2016;74:280.e3-287.e3) published data evaluating long-term safety and efficacy of etanercept in children and adolescents with moderate to severe plaque psoriasis. This 5-year, open-label extension study enrolled those patients aged 4 to 17 years who had participated in an initial 48-week parent study. End points included occurrence of adverse events (AEs) and serious AEs including infections as well as rates of 75% and 90% improvement in psoriasis area and severity index (PASI) score and clear or almost clear status on the static physician global assessment.

Of 182 patients enrolled, 181 received etanercept and 69 completed 264 weeks of treatment. Through week 264, 161 (89.0%) patients reported an AE, most commonly upper respiratory tract infection (37.6%), nasopharyngitis (26.0%), and headache (21.5%). Seven patients reported 8 Serious AEs (n=8) were reported in 7 patients, and only 1 case of cellulitis was considered treatment related. No cases of opportunistic infections or malignancy were reported. Rates of 75% improvement (∼60%–70%) and 90% improvement (∼30%–40%) in PASI score were maintained through week 264 as well as static physician global assessment status of clear or almost clear (∼40%–50%).

What’s the issue?

If approved, etanercept would be the first US Food and Drug Administration–approved systemic drug for pediatric psoriasis patients, which would open up options for many patients in need. Would you be willing to treat your pediatric psoriasis patients with a biologic?

We want to know your views! Tell us what you think.

Biologic agents for the treatment of psoriasis are approved for patients 18 years and older. Although some biologics are approved for juvenile idiopathic arthritis, the lack of approved biologic therapies for children with psoriasis has been a major gap in our treatment of the disease. The incidence of moderate to severe psoriasis in the pediatric population is much lower than in adults, but there are still many patients younger than 18 years who would benefit from systemic therapies.

A recent press release indicates that the US Food and Drug Administration has accepted for review a supplemental biologics license application for the expanded use of etanercept to treat pediatric patients with chronic severe plaque psoriasis.

In February 2016 Paller et al (J Am Acad Dermatol. 2016;74:280.e3-287.e3) published data evaluating long-term safety and efficacy of etanercept in children and adolescents with moderate to severe plaque psoriasis. This 5-year, open-label extension study enrolled those patients aged 4 to 17 years who had participated in an initial 48-week parent study. End points included occurrence of adverse events (AEs) and serious AEs including infections as well as rates of 75% and 90% improvement in psoriasis area and severity index (PASI) score and clear or almost clear status on the static physician global assessment.

Of 182 patients enrolled, 181 received etanercept and 69 completed 264 weeks of treatment. Through week 264, 161 (89.0%) patients reported an AE, most commonly upper respiratory tract infection (37.6%), nasopharyngitis (26.0%), and headache (21.5%). Seven patients reported 8 Serious AEs (n=8) were reported in 7 patients, and only 1 case of cellulitis was considered treatment related. No cases of opportunistic infections or malignancy were reported. Rates of 75% improvement (∼60%–70%) and 90% improvement (∼30%–40%) in PASI score were maintained through week 264 as well as static physician global assessment status of clear or almost clear (∼40%–50%).

What’s the issue?

If approved, etanercept would be the first US Food and Drug Administration–approved systemic drug for pediatric psoriasis patients, which would open up options for many patients in need. Would you be willing to treat your pediatric psoriasis patients with a biologic?

We want to know your views! Tell us what you think.

Chen et al (N Engl J Med. 2015;373:1618-1626) performed a multicenter, phase 3, double-blind, randomized, placebo-controlled trial. Results demonstrated that nicotinamide effectively decreased the rates of new nonmelanoma skin cancers (NMSCs) and actinic keratoses (AKs) in high-risk patients who had at least 2 histologically confirmed NMSCs in the last 5 years. In comparison to participants who received placebo, individuals who received nicotinamide 500 mg twice daily during the 12-month study (branded with a predictive acronym ONTRAC [oral nicotinamide to reduce actinic cancer]) had reduced rates of AKs of up to 20%, basal cell carcinomas of 20%, squamous cell carcinomas of 30%, and NMSCs of 23%. However, the effect of nicotinamide on NMSCs was not maintained at evaluation 6 months after discontinuation; the number of basal cell carcinomas was similar, and the number of squamous cell carcinomas was greater in participants who received nicotinamide in comparison to individuals who received placebo.

What’s the issue?

The risk for skin cancer is increased by UV radiation that damages DNA, suppresses cutaneous immunity, and inhibits DNA repair by depleting cellular adenosine triphosphate. Nicotinamide, an amide form of vitamin B₃, has been demonstrated to not only reduce UV radiation–induced immunosuppression but also to prevent UV radiation–induced adenosine triphosphate depletion and glycolic blockade. Nicotinamide, which is classified as a food additive, also has neuroprotective and antioxidant functions and reduces pigmentation, wrinkles, and sebum production. Although oral nicotinamide has been demonstrated to reduce NMSCs and AKs, topical application has been shown to improve many skin conditions such as acne, atopic dermatitis, isoniazid-induced pellagra, and rosacea.

In contrast to nicotinic acid (niacin), nicotinamide is not associated with headaches, hypotension, flushing, itching, or vasodilatation. At high oral doses, side effects of nicotinamide that have been hypothesized or observed in animals, humans, or both have included the development of Parkinson disease, insulin sensitivity and diabetes mellitus, and liver toxicity. Although there are no reports in humans of growth retardation, teratogenicity, or oncogenicity, Rolfe (J Cosmet Dermatol. 2014;13:324-328) discussed that fetal blood levels of nicotinamide are greater than corresponding maternal blood levels because it is able to cross the placenta. However, according to Chen et al, no clinically significant between-group differences were found with respect to the number or types of adverse events that occurred in the placebo participants and the individuals who received 1000 mg daily of nicotinamide. Chen et al implied that there were additional benefits in the recipients of nicotinamide with regards to cognitive function and transepidermal water loss.

Perhaps all patients with a history of AKs, basal cell carcinomas, or squamous cell carcinomas should receive lifelong nicotinamide. Also, it might be reasonable to consider that all individuals older than 18 years who are not pregnant or breastfeeding with increased sun exposure but no history of AKs or NMSC add nicotinamide to their daily diets as a proactive measure for chemoprevention. Would you suggest nicotinamide to your patients?

We want to know your views! Tell us what you think.

Chen et al (N Engl J Med. 2015;373:1618-1626) performed a multicenter, phase 3, double-blind, randomized, placebo-controlled trial. Results demonstrated that nicotinamide effectively decreased the rates of new nonmelanoma skin cancers (NMSCs) and actinic keratoses (AKs) in high-risk patients who had at least 2 histologically confirmed NMSCs in the last 5 years. In comparison to participants who received placebo, individuals who received nicotinamide 500 mg twice daily during the 12-month study (branded with a predictive acronym ONTRAC [oral nicotinamide to reduce actinic cancer]) had reduced rates of AKs of up to 20%, basal cell carcinomas of 20%, squamous cell carcinomas of 30%, and NMSCs of 23%. However, the effect of nicotinamide on NMSCs was not maintained at evaluation 6 months after discontinuation; the number of basal cell carcinomas was similar, and the number of squamous cell carcinomas was greater in participants who received nicotinamide in comparison to individuals who received placebo.

What’s the issue?

The risk for skin cancer is increased by UV radiation that damages DNA, suppresses cutaneous immunity, and inhibits DNA repair by depleting cellular adenosine triphosphate. Nicotinamide, an amide form of vitamin B₃, has been demonstrated to not only reduce UV radiation–induced immunosuppression but also to prevent UV radiation–induced adenosine triphosphate depletion and glycolic blockade. Nicotinamide, which is classified as a food additive, also has neuroprotective and antioxidant functions and reduces pigmentation, wrinkles, and sebum production. Although oral nicotinamide has been demonstrated to reduce NMSCs and AKs, topical application has been shown to improve many skin conditions such as acne, atopic dermatitis, isoniazid-induced pellagra, and rosacea.

In contrast to nicotinic acid (niacin), nicotinamide is not associated with headaches, hypotension, flushing, itching, or vasodilatation. At high oral doses, side effects of nicotinamide that have been hypothesized or observed in animals, humans, or both have included the development of Parkinson disease, insulin sensitivity and diabetes mellitus, and liver toxicity. Although there are no reports in humans of growth retardation, teratogenicity, or oncogenicity, Rolfe (J Cosmet Dermatol. 2014;13:324-328) discussed that fetal blood levels of nicotinamide are greater than corresponding maternal blood levels because it is able to cross the placenta. However, according to Chen et al, no clinically significant between-group differences were found with respect to the number or types of adverse events that occurred in the placebo participants and the individuals who received 1000 mg daily of nicotinamide. Chen et al implied that there were additional benefits in the recipients of nicotinamide with regards to cognitive function and transepidermal water loss.

Perhaps all patients with a history of AKs, basal cell carcinomas, or squamous cell carcinomas should receive lifelong nicotinamide. Also, it might be reasonable to consider that all individuals older than 18 years who are not pregnant or breastfeeding with increased sun exposure but no history of AKs or NMSC add nicotinamide to their daily diets as a proactive measure for chemoprevention. Would you suggest nicotinamide to your patients?

We want to know your views! Tell us what you think.

Chen et al (N Engl J Med. 2015;373:1618-1626) performed a multicenter, phase 3, double-blind, randomized, placebo-controlled trial. Results demonstrated that nicotinamide effectively decreased the rates of new nonmelanoma skin cancers (NMSCs) and actinic keratoses (AKs) in high-risk patients who had at least 2 histologically confirmed NMSCs in the last 5 years. In comparison to participants who received placebo, individuals who received nicotinamide 500 mg twice daily during the 12-month study (branded with a predictive acronym ONTRAC [oral nicotinamide to reduce actinic cancer]) had reduced rates of AKs of up to 20%, basal cell carcinomas of 20%, squamous cell carcinomas of 30%, and NMSCs of 23%. However, the effect of nicotinamide on NMSCs was not maintained at evaluation 6 months after discontinuation; the number of basal cell carcinomas was similar, and the number of squamous cell carcinomas was greater in participants who received nicotinamide in comparison to individuals who received placebo.

What’s the issue?

The risk for skin cancer is increased by UV radiation that damages DNA, suppresses cutaneous immunity, and inhibits DNA repair by depleting cellular adenosine triphosphate. Nicotinamide, an amide form of vitamin B₃, has been demonstrated to not only reduce UV radiation–induced immunosuppression but also to prevent UV radiation–induced adenosine triphosphate depletion and glycolic blockade. Nicotinamide, which is classified as a food additive, also has neuroprotective and antioxidant functions and reduces pigmentation, wrinkles, and sebum production. Although oral nicotinamide has been demonstrated to reduce NMSCs and AKs, topical application has been shown to improve many skin conditions such as acne, atopic dermatitis, isoniazid-induced pellagra, and rosacea.

In contrast to nicotinic acid (niacin), nicotinamide is not associated with headaches, hypotension, flushing, itching, or vasodilatation. At high oral doses, side effects of nicotinamide that have been hypothesized or observed in animals, humans, or both have included the development of Parkinson disease, insulin sensitivity and diabetes mellitus, and liver toxicity. Although there are no reports in humans of growth retardation, teratogenicity, or oncogenicity, Rolfe (J Cosmet Dermatol. 2014;13:324-328) discussed that fetal blood levels of nicotinamide are greater than corresponding maternal blood levels because it is able to cross the placenta. However, according to Chen et al, no clinically significant between-group differences were found with respect to the number or types of adverse events that occurred in the placebo participants and the individuals who received 1000 mg daily of nicotinamide. Chen et al implied that there were additional benefits in the recipients of nicotinamide with regards to cognitive function and transepidermal water loss.

Perhaps all patients with a history of AKs, basal cell carcinomas, or squamous cell carcinomas should receive lifelong nicotinamide. Also, it might be reasonable to consider that all individuals older than 18 years who are not pregnant or breastfeeding with increased sun exposure but no history of AKs or NMSC add nicotinamide to their daily diets as a proactive measure for chemoprevention. Would you suggest nicotinamide to your patients?

We want to know your views! Tell us what you think.

Injectable soft-tissue fillers continue to be popular in the cosmetic arena. In the United States there are many fillers currently on the market and many more coming through the pipeline. A multitude of products are available outside the United States. As with any procedure, the more fillers we inject, the more complications we are bound to see.

Conrad et al (Modern Plastic Surgery. 2015;5:14-18) performed a retrospective analysis of patients treated over a 10-year period with soft-tissue injections (1559 patients) looking for cases complicated by abscess formation. Four patients were identified (0.3% of total patients). The authors discussed the 4 cases, the patients’ medical history and experience with other injectable agents, and the management of each complication.

Case 1 was a 52-year-old woman with systemic lupus erythematosus on a low-dose steroid who presented with an inflammatory response in the lower lip 7 days following injection with a hyaluronic acid (HA)–based gel filler in 2011. Her history was notable for prior HA filler in 2008 and polyacrylamide filler in 2009 and 2010. She was treated with 4 sessions of incision and drainage (I&D) and systemic clindamycin. Most of the cultures were negative, but one showed streptococci.

Case 2 was a 56-year-old woman treated in the nasolabial fold with HA in 2009. She developed inflammation shortly after and an abscess at the site a month later. She was treated with clindamycin both times, though cultures were negative. Furthermore, the abscess was treated with I&D and an intralesional steroid. She was a smoker and had been treated with a polymethyl methacrylate filler in 2002 and subsequently in 2013 with no issues.

Case 3 was a 39-year-old woman injected with an HA filler in the upper and lower lips in 2011. One month later she developed abscesses in both areas that were treated twice with I&D. Cultures were negative. She had a history of polyacrylamide injections of the nasolabial fold in 2009. The patient’s medical history was notable for scleroderma.

Case 4 was a 58-year-old woman injected with an HA filler in 2009 in the prejowl sulcus and nasolabial fold. She developed recurrent sterile abscesses in the areas 8 months after treatment that were managed by drainage of the areas and intralesional steroid injections over the ensuing 6 months. The scars were then excised, lasered 6 weeks later, and then filled in with expanded polytetrafluoroethylene implants, followed by 1 more session of laser resurfacing. She had a history of polymethyl methacrylate filler in 2002.

All patients eventually recovered. The authors stressed 3 important factors in managing dermal filler complications: (1) identifying the causative pathogen, (2) choosing the appropriate treatment of delayed-onset abscess formation, and (3) identifying the risk factors for patients at risk for abscess formation.

The issue of biofilms complicates the ability to identify the bacterial agent, yet biofilms are becoming recognized as the causative factors in what were previously thought of as sterile abscesses. The authors suggested using a peptide nucleic acid fluorescent in situ hybridization test to identify the biofilm bacteria. Conrad et el also discussed the development of slippery liquid-infused porous surfaces technology to coat the inside of syringes to help prevent biofilm formation.

The management of these patients is tricky because it is difficult to differentiate between a biofilm abscess and a hypersensitivity reaction. For this reason, the authors advocated using hyaluronidase versus intralesional steroids in the initial management to make the area more susceptible to antibiotics and to avoid promoting the growth of bacteria with the use of steroids. For patient risk factors, the authors focused on the fact that 2 of 4 patients had concomitant autoimmune disorders—scleroderma and systemic lupus erythematosus—that may have predisposed them to infection. Lastly, 2 patients had prior polyacrylamide injections and the authors also speculated if the positive charge of this filler attracted bacteria.

What’s the issue?

The use of fillers will continue to increase as there are more fillers with novel properties entering the market. As with new technology, only time will tell if we will see any particular type of reaction or risk for infection with them. The issue of biofilm bacterial contamination is real. It is recognized as one of the causes of capsular contraction following breast implant surgery. The etiology may not be from contamination during production but from contamination of the filler after injection due to any transient bacteremia that the patient may experience. A concern is that dental manipulation (eg, dental cleaning, filling of dental caries, periodontal surgery) during the 2- to 4-week postfiller period may “seed” bacteria into the area and cause the bacteria to settle and grow on the foreign substance. For patients who have semipermanent or permanent fillers such as polyacrylamide, polymethyl methacrylate beads, or poly-L-lactic acid, biofilm risk is greater and can occur months to years after the procedure. I have personally seen 2 cases of poly-L-lactic acid filler develop red, tender, sterile abscesses 1 year after placement in the tissue. Both cases responded to prolonged clarithromycin use (2 months). However, these cases highlight the fact that the fillers persist long after we place them, and any bacteremia, even mild, can cause an unsightly reaction.

Have you seen delayed soft-tissue filler reactions in your practice? Given this information, will you change the way you advise patients on dental procedures in the 2- to 4-week postfiller period?

We want to know your views! Tell us what you think.

Injectable soft-tissue fillers continue to be popular in the cosmetic arena. In the United States there are many fillers currently on the market and many more coming through the pipeline. A multitude of products are available outside the United States. As with any procedure, the more fillers we inject, the more complications we are bound to see.

Conrad et al (Modern Plastic Surgery. 2015;5:14-18) performed a retrospective analysis of patients treated over a 10-year period with soft-tissue injections (1559 patients) looking for cases complicated by abscess formation. Four patients were identified (0.3% of total patients). The authors discussed the 4 cases, the patients’ medical history and experience with other injectable agents, and the management of each complication.

Case 1 was a 52-year-old woman with systemic lupus erythematosus on a low-dose steroid who presented with an inflammatory response in the lower lip 7 days following injection with a hyaluronic acid (HA)–based gel filler in 2011. Her history was notable for prior HA filler in 2008 and polyacrylamide filler in 2009 and 2010. She was treated with 4 sessions of incision and drainage (I&D) and systemic clindamycin. Most of the cultures were negative, but one showed streptococci.

Case 2 was a 56-year-old woman treated in the nasolabial fold with HA in 2009. She developed inflammation shortly after and an abscess at the site a month later. She was treated with clindamycin both times, though cultures were negative. Furthermore, the abscess was treated with I&D and an intralesional steroid. She was a smoker and had been treated with a polymethyl methacrylate filler in 2002 and subsequently in 2013 with no issues.

Case 3 was a 39-year-old woman injected with an HA filler in the upper and lower lips in 2011. One month later she developed abscesses in both areas that were treated twice with I&D. Cultures were negative. She had a history of polyacrylamide injections of the nasolabial fold in 2009. The patient’s medical history was notable for scleroderma.

Case 4 was a 58-year-old woman injected with an HA filler in 2009 in the prejowl sulcus and nasolabial fold. She developed recurrent sterile abscesses in the areas 8 months after treatment that were managed by drainage of the areas and intralesional steroid injections over the ensuing 6 months. The scars were then excised, lasered 6 weeks later, and then filled in with expanded polytetrafluoroethylene implants, followed by 1 more session of laser resurfacing. She had a history of polymethyl methacrylate filler in 2002.

All patients eventually recovered. The authors stressed 3 important factors in managing dermal filler complications: (1) identifying the causative pathogen, (2) choosing the appropriate treatment of delayed-onset abscess formation, and (3) identifying the risk factors for patients at risk for abscess formation.

The issue of biofilms complicates the ability to identify the bacterial agent, yet biofilms are becoming recognized as the causative factors in what were previously thought of as sterile abscesses. The authors suggested using a peptide nucleic acid fluorescent in situ hybridization test to identify the biofilm bacteria. Conrad et el also discussed the development of slippery liquid-infused porous surfaces technology to coat the inside of syringes to help prevent biofilm formation.

The management of these patients is tricky because it is difficult to differentiate between a biofilm abscess and a hypersensitivity reaction. For this reason, the authors advocated using hyaluronidase versus intralesional steroids in the initial management to make the area more susceptible to antibiotics and to avoid promoting the growth of bacteria with the use of steroids. For patient risk factors, the authors focused on the fact that 2 of 4 patients had concomitant autoimmune disorders—scleroderma and systemic lupus erythematosus—that may have predisposed them to infection. Lastly, 2 patients had prior polyacrylamide injections and the authors also speculated if the positive charge of this filler attracted bacteria.

What’s the issue?

The use of fillers will continue to increase as there are more fillers with novel properties entering the market. As with new technology, only time will tell if we will see any particular type of reaction or risk for infection with them. The issue of biofilm bacterial contamination is real. It is recognized as one of the causes of capsular contraction following breast implant surgery. The etiology may not be from contamination during production but from contamination of the filler after injection due to any transient bacteremia that the patient may experience. A concern is that dental manipulation (eg, dental cleaning, filling of dental caries, periodontal surgery) during the 2- to 4-week postfiller period may “seed” bacteria into the area and cause the bacteria to settle and grow on the foreign substance. For patients who have semipermanent or permanent fillers such as polyacrylamide, polymethyl methacrylate beads, or poly-L-lactic acid, biofilm risk is greater and can occur months to years after the procedure. I have personally seen 2 cases of poly-L-lactic acid filler develop red, tender, sterile abscesses 1 year after placement in the tissue. Both cases responded to prolonged clarithromycin use (2 months). However, these cases highlight the fact that the fillers persist long after we place them, and any bacteremia, even mild, can cause an unsightly reaction.

Have you seen delayed soft-tissue filler reactions in your practice? Given this information, will you change the way you advise patients on dental procedures in the 2- to 4-week postfiller period?

We want to know your views! Tell us what you think.

Injectable soft-tissue fillers continue to be popular in the cosmetic arena. In the United States there are many fillers currently on the market and many more coming through the pipeline. A multitude of products are available outside the United States. As with any procedure, the more fillers we inject, the more complications we are bound to see.

Conrad et al (Modern Plastic Surgery. 2015;5:14-18) performed a retrospective analysis of patients treated over a 10-year period with soft-tissue injections (1559 patients) looking for cases complicated by abscess formation. Four patients were identified (0.3% of total patients). The authors discussed the 4 cases, the patients’ medical history and experience with other injectable agents, and the management of each complication.

Case 1 was a 52-year-old woman with systemic lupus erythematosus on a low-dose steroid who presented with an inflammatory response in the lower lip 7 days following injection with a hyaluronic acid (HA)–based gel filler in 2011. Her history was notable for prior HA filler in 2008 and polyacrylamide filler in 2009 and 2010. She was treated with 4 sessions of incision and drainage (I&D) and systemic clindamycin. Most of the cultures were negative, but one showed streptococci.

Case 2 was a 56-year-old woman treated in the nasolabial fold with HA in 2009. She developed inflammation shortly after and an abscess at the site a month later. She was treated with clindamycin both times, though cultures were negative. Furthermore, the abscess was treated with I&D and an intralesional steroid. She was a smoker and had been treated with a polymethyl methacrylate filler in 2002 and subsequently in 2013 with no issues.

Case 3 was a 39-year-old woman injected with an HA filler in the upper and lower lips in 2011. One month later she developed abscesses in both areas that were treated twice with I&D. Cultures were negative. She had a history of polyacrylamide injections of the nasolabial fold in 2009. The patient’s medical history was notable for scleroderma.

Case 4 was a 58-year-old woman injected with an HA filler in 2009 in the prejowl sulcus and nasolabial fold. She developed recurrent sterile abscesses in the areas 8 months after treatment that were managed by drainage of the areas and intralesional steroid injections over the ensuing 6 months. The scars were then excised, lasered 6 weeks later, and then filled in with expanded polytetrafluoroethylene implants, followed by 1 more session of laser resurfacing. She had a history of polymethyl methacrylate filler in 2002.

All patients eventually recovered. The authors stressed 3 important factors in managing dermal filler complications: (1) identifying the causative pathogen, (2) choosing the appropriate treatment of delayed-onset abscess formation, and (3) identifying the risk factors for patients at risk for abscess formation.

The issue of biofilms complicates the ability to identify the bacterial agent, yet biofilms are becoming recognized as the causative factors in what were previously thought of as sterile abscesses. The authors suggested using a peptide nucleic acid fluorescent in situ hybridization test to identify the biofilm bacteria. Conrad et el also discussed the development of slippery liquid-infused porous surfaces technology to coat the inside of syringes to help prevent biofilm formation.

The management of these patients is tricky because it is difficult to differentiate between a biofilm abscess and a hypersensitivity reaction. For this reason, the authors advocated using hyaluronidase versus intralesional steroids in the initial management to make the area more susceptible to antibiotics and to avoid promoting the growth of bacteria with the use of steroids. For patient risk factors, the authors focused on the fact that 2 of 4 patients had concomitant autoimmune disorders—scleroderma and systemic lupus erythematosus—that may have predisposed them to infection. Lastly, 2 patients had prior polyacrylamide injections and the authors also speculated if the positive charge of this filler attracted bacteria.

What’s the issue?

The use of fillers will continue to increase as there are more fillers with novel properties entering the market. As with new technology, only time will tell if we will see any particular type of reaction or risk for infection with them. The issue of biofilm bacterial contamination is real. It is recognized as one of the causes of capsular contraction following breast implant surgery. The etiology may not be from contamination during production but from contamination of the filler after injection due to any transient bacteremia that the patient may experience. A concern is that dental manipulation (eg, dental cleaning, filling of dental caries, periodontal surgery) during the 2- to 4-week postfiller period may “seed” bacteria into the area and cause the bacteria to settle and grow on the foreign substance. For patients who have semipermanent or permanent fillers such as polyacrylamide, polymethyl methacrylate beads, or poly-L-lactic acid, biofilm risk is greater and can occur months to years after the procedure. I have personally seen 2 cases of poly-L-lactic acid filler develop red, tender, sterile abscesses 1 year after placement in the tissue. Both cases responded to prolonged clarithromycin use (2 months). However, these cases highlight the fact that the fillers persist long after we place them, and any bacteremia, even mild, can cause an unsightly reaction.

Have you seen delayed soft-tissue filler reactions in your practice? Given this information, will you change the way you advise patients on dental procedures in the 2- to 4-week postfiller period?

We want to know your views! Tell us what you think.

The primary comorbidity of psoriasis is psoriatic arthritis (PsA). The true incidence of PsA has long been an issue of debate. To estimate the incidence of PsA in patients with psoriasis and to identify risk factors for its development, Eder at al conducted a prospective cohort study involving psoriasis patients without arthritis at study entry that was published online in Arthritis & Rheumatology.

The investigators collected information from patients concerning lifestyle habits, comorbidities, psoriasis activity, and medications. The patients were evaluated at enrollment and annually. A general physical examination, assessment of psoriasis severity, and assessment for the development of musculoskeletal symptoms were conducted at each visit. A diagnosis of PsA was determined by a rheumatologist on the basis of clinical, laboratory, and imaging data; patients also had to fulfill the CASPAR (Classification Criteria for Psoriatic Arthritis) criteria (confirmed cases). The annual incidence of PsA was estimated using an event per person-years analysis.

The results from 464 patients who were followed for 8 years were analyzed. The annual incidence of confirmed PsA was 2.7 per 100 patients with psoriasis (95% CI, 2.1-3.6). Overall, 51 patients developed PsA over the course of the study and an additional 9 were considered suspect cases.

The following baseline variables were associated with the development of PsA in multivariate analysis: severe psoriasis (relative risk [RR], 5.4; P=.006), low level of education (college/university vs high school incomplete: RR, 4.5; P=.005; high school education vs high school incomplete: RR, 3.3; P=.049), and use of retinoid medications (RR, 3.4; P=.02). In addition, psoriatic nail pitting (RR, 2.5; P=.002) and uveitis (RR, 31.5; P<.001) were time-dependent predictors for PsA development.

The authors concluded that the incidence of PsA in patients with psoriasis was higher than previously reported. Possible factors for this finding might include differences in patient recruitment as well as self-reported PsA diagnoses.

What’s the issue?

This prospective analysis is interesting. The incidence of PsA was higher than reported. It reinforces the need for continual evaluation of joint symptoms in patients with psoriasis, even if they have had psoriasis for many years. How will this analysis impact your evaluation of psoriatic patients?

We want to know your views! Tell us what you think.

The primary comorbidity of psoriasis is psoriatic arthritis (PsA). The true incidence of PsA has long been an issue of debate. To estimate the incidence of PsA in patients with psoriasis and to identify risk factors for its development, Eder at al conducted a prospective cohort study involving psoriasis patients without arthritis at study entry that was published online in Arthritis & Rheumatology.

The investigators collected information from patients concerning lifestyle habits, comorbidities, psoriasis activity, and medications. The patients were evaluated at enrollment and annually. A general physical examination, assessment of psoriasis severity, and assessment for the development of musculoskeletal symptoms were conducted at each visit. A diagnosis of PsA was determined by a rheumatologist on the basis of clinical, laboratory, and imaging data; patients also had to fulfill the CASPAR (Classification Criteria for Psoriatic Arthritis) criteria (confirmed cases). The annual incidence of PsA was estimated using an event per person-years analysis.

The results from 464 patients who were followed for 8 years were analyzed. The annual incidence of confirmed PsA was 2.7 per 100 patients with psoriasis (95% CI, 2.1-3.6). Overall, 51 patients developed PsA over the course of the study and an additional 9 were considered suspect cases.

The following baseline variables were associated with the development of PsA in multivariate analysis: severe psoriasis (relative risk [RR], 5.4; P=.006), low level of education (college/university vs high school incomplete: RR, 4.5; P=.005; high school education vs high school incomplete: RR, 3.3; P=.049), and use of retinoid medications (RR, 3.4; P=.02). In addition, psoriatic nail pitting (RR, 2.5; P=.002) and uveitis (RR, 31.5; P<.001) were time-dependent predictors for PsA development.

The authors concluded that the incidence of PsA in patients with psoriasis was higher than previously reported. Possible factors for this finding might include differences in patient recruitment as well as self-reported PsA diagnoses.

What’s the issue?

This prospective analysis is interesting. The incidence of PsA was higher than reported. It reinforces the need for continual evaluation of joint symptoms in patients with psoriasis, even if they have had psoriasis for many years. How will this analysis impact your evaluation of psoriatic patients?

We want to know your views! Tell us what you think.

The primary comorbidity of psoriasis is psoriatic arthritis (PsA). The true incidence of PsA has long been an issue of debate. To estimate the incidence of PsA in patients with psoriasis and to identify risk factors for its development, Eder at al conducted a prospective cohort study involving psoriasis patients without arthritis at study entry that was published online in Arthritis & Rheumatology.

The investigators collected information from patients concerning lifestyle habits, comorbidities, psoriasis activity, and medications. The patients were evaluated at enrollment and annually. A general physical examination, assessment of psoriasis severity, and assessment for the development of musculoskeletal symptoms were conducted at each visit. A diagnosis of PsA was determined by a rheumatologist on the basis of clinical, laboratory, and imaging data; patients also had to fulfill the CASPAR (Classification Criteria for Psoriatic Arthritis) criteria (confirmed cases). The annual incidence of PsA was estimated using an event per person-years analysis.

The results from 464 patients who were followed for 8 years were analyzed. The annual incidence of confirmed PsA was 2.7 per 100 patients with psoriasis (95% CI, 2.1-3.6). Overall, 51 patients developed PsA over the course of the study and an additional 9 were considered suspect cases.

The following baseline variables were associated with the development of PsA in multivariate analysis: severe psoriasis (relative risk [RR], 5.4; P=.006), low level of education (college/university vs high school incomplete: RR, 4.5; P=.005; high school education vs high school incomplete: RR, 3.3; P=.049), and use of retinoid medications (RR, 3.4; P=.02). In addition, psoriatic nail pitting (RR, 2.5; P=.002) and uveitis (RR, 31.5; P<.001) were time-dependent predictors for PsA development.

The authors concluded that the incidence of PsA in patients with psoriasis was higher than previously reported. Possible factors for this finding might include differences in patient recruitment as well as self-reported PsA diagnoses.

What’s the issue?

This prospective analysis is interesting. The incidence of PsA was higher than reported. It reinforces the need for continual evaluation of joint symptoms in patients with psoriasis, even if they have had psoriasis for many years. How will this analysis impact your evaluation of psoriatic patients?

We want to know your views! Tell us what you think.

In recent years, resistance to antimicrobial drugs has become increasingly widespread, resulting in a health threat of epidemic proportions. The long list of drug-resistant bacteria continues to expand at an accelerated pace. What does this mean in the dermatology world? We are not the only problem but are certainly part of the problem, representing 5% of all antibiotic prescriptions annually even though we represent only 1% of all physicians in the United States. These prescriptions certainly do not just include skin and soft tissue functions, as a survey-based study by Chouake et al (J Drugs Dermatol. 2014;13:119-124.) showed that dermatologists are overusing antibiotics in the treatment of simple skin abscesses such as acne vulgaris, one of the most common inflammatory skin diseases.

Although the inappropriate utilization of antibiotics for acne has been a subject of great discourse for years, it recently reentered the limelight in a study by Nagler et al published online in October 2015 in the Journal of the American Academy of Dermatology. They showed that patients who ultimately were treated with isotretinoin had been receiving antibiotics for months without any sign of therapeutic life or course end in sight. This retrospective chart review evaluated the duration of systemic antibiotic use prior to starting isotretinoin in 137 patients with inflammatory/nodulocystic acne. Antibiotic use continued for a mean of 331.3 days (median, 238 days). Duration of antibiotic use was divided into categories: 3 months or less (15.3%), 6 months or more (64.2%), or 1 year or more (33.6%).

Let’s take a broad look at antimicrobial resistance. Bacterial drug resistance has numerous negative effects on medicine and society. Drug-resistant bacterial infections result in higher doses of drugs, the addition of treatments with higher toxicity, longer hospital stays, and increased mortality. In the United States, infections due to antibiotic-resistant bacteria add $20 billion to total health care costs plus $35 billion in costs to society.

Unfortunately, it is relatively easy for bacterium to develop drug resistance through 3 simple steps: acquisition by microbes of resistance genes, expression of those resistance genes, and selection for pathogens expressing those resistance genes. The selective pressure in favor of resistance occurs whenever microbes are exposed to a drug but not eradicated, either by the killing effects of the drug itself or by inhibitory effects of the drug followed by killing by the host’s immune system. In any setting that creates this selective pressure in favor of drug resistance, such as poor patient compliance (ie, infrequent dosing, taking an antibiotic for too long as we see with the use of antibiotics for the treatment of inflammatory skin diseases such as acne), the likelihood of that resistance actually developing is increased. In addition, drugs that inhibit but do not kill microbes are more likely to allow some microbial cells to live and therefore develop resistance when exposed to a drug, which accounts for the majority of antibiotics in our armament. Lastly, abuse of broad-spectrum antibiotics has further spurred the emergence of many antibiotic-resistant strains. For instance, Pseudomonas aeruginosa is one of many evolving multidrug-resistant microorganisms that have been collectively coined the “ESKAPE” pathogens (Enterococcus faecalis, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, P aeruginosa, Enterobacter species) to emphasize the fact that they “escape” the effects of many antibacterial agents.

All of the above does not take into account the environmental factors that play a role in this resistance. The close quarters, mass/public transportation, and stressful pace of life of urban living not only bring these organisms together to share resistance genes but also increase our susceptibility.

What’s the issue?

We can all do our part in the fight against microbial resistance and join the antimicrobial stewardship. Here are a couple tips for dermatologists:

1. Stop using over-the-counter antibiotic ointment for every biopsy or minor procedure, which is one of the recommendations of the American Academy of Dermatology based on the ABIM Foundation’s Choosing Wisely campaign.
2. Oral and topical antibiotics for inflammatory skin diseases such as acne, rosacea, and hidradenitis suppurativa should only be used temporarily or at subantimicrobial dosing. Always combine a benzoyl peroxide–containing wash with a topical or oral antibiotic to hit the bacteria with multiple mechanisms of antibacterial activity to limit resistance. Don’t use benzoyl peroxide stronger than 2.5% for the face; make sure to wash it off completely to avoid staining your towels, sheets, and clothing.

We can all play our part in the fight against antimicrobial resistance. How do you fight the resistance?

We want to know your views! Tell us what you think.

In recent years, resistance to antimicrobial drugs has become increasingly widespread, resulting in a health threat of epidemic proportions. The long list of drug-resistant bacteria continues to expand at an accelerated pace. What does this mean in the dermatology world? We are not the only problem but are certainly part of the problem, representing 5% of all antibiotic prescriptions annually even though we represent only 1% of all physicians in the United States. These prescriptions certainly do not just include skin and soft tissue functions, as a survey-based study by Chouake et al (J Drugs Dermatol. 2014;13:119-124.) showed that dermatologists are overusing antibiotics in the treatment of simple skin abscesses such as acne vulgaris, one of the most common inflammatory skin diseases.

Although the inappropriate utilization of antibiotics for acne has been a subject of great discourse for years, it recently reentered the limelight in a study by Nagler et al published online in October 2015 in the Journal of the American Academy of Dermatology. They showed that patients who ultimately were treated with isotretinoin had been receiving antibiotics for months without any sign of therapeutic life or course end in sight. This retrospective chart review evaluated the duration of systemic antibiotic use prior to starting isotretinoin in 137 patients with inflammatory/nodulocystic acne. Antibiotic use continued for a mean of 331.3 days (median, 238 days). Duration of antibiotic use was divided into categories: 3 months or less (15.3%), 6 months or more (64.2%), or 1 year or more (33.6%).

Let’s take a broad look at antimicrobial resistance. Bacterial drug resistance has numerous negative effects on medicine and society. Drug-resistant bacterial infections result in higher doses of drugs, the addition of treatments with higher toxicity, longer hospital stays, and increased mortality. In the United States, infections due to antibiotic-resistant bacteria add $20 billion to total health care costs plus $35 billion in costs to society.

Unfortunately, it is relatively easy for bacterium to develop drug resistance through 3 simple steps: acquisition by microbes of resistance genes, expression of those resistance genes, and selection for pathogens expressing those resistance genes. The selective pressure in favor of resistance occurs whenever microbes are exposed to a drug but not eradicated, either by the killing effects of the drug itself or by inhibitory effects of the drug followed by killing by the host’s immune system. In any setting that creates this selective pressure in favor of drug resistance, such as poor patient compliance (ie, infrequent dosing, taking an antibiotic for too long as we see with the use of antibiotics for the treatment of inflammatory skin diseases such as acne), the likelihood of that resistance actually developing is increased. In addition, drugs that inhibit but do not kill microbes are more likely to allow some microbial cells to live and therefore develop resistance when exposed to a drug, which accounts for the majority of antibiotics in our armament. Lastly, abuse of broad-spectrum antibiotics has further spurred the emergence of many antibiotic-resistant strains. For instance, Pseudomonas aeruginosa is one of many evolving multidrug-resistant microorganisms that have been collectively coined the “ESKAPE” pathogens (Enterococcus faecalis, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, P aeruginosa, Enterobacter species) to emphasize the fact that they “escape” the effects of many antibacterial agents.

All of the above does not take into account the environmental factors that play a role in this resistance. The close quarters, mass/public transportation, and stressful pace of life of urban living not only bring these organisms together to share resistance genes but also increase our susceptibility.

What’s the issue?

We can all do our part in the fight against microbial resistance and join the antimicrobial stewardship. Here are a couple tips for dermatologists:

1. Stop using over-the-counter antibiotic ointment for every biopsy or minor procedure, which is one of the recommendations of the American Academy of Dermatology based on the ABIM Foundation’s Choosing Wisely campaign.
2. Oral and topical antibiotics for inflammatory skin diseases such as acne, rosacea, and hidradenitis suppurativa should only be used temporarily or at subantimicrobial dosing. Always combine a benzoyl peroxide–containing wash with a topical or oral antibiotic to hit the bacteria with multiple mechanisms of antibacterial activity to limit resistance. Don’t use benzoyl peroxide stronger than 2.5% for the face; make sure to wash it off completely to avoid staining your towels, sheets, and clothing.

We can all play our part in the fight against antimicrobial resistance. How do you fight the resistance?

We want to know your views! Tell us what you think.

In recent years, resistance to antimicrobial drugs has become increasingly widespread, resulting in a health threat of epidemic proportions. The long list of drug-resistant bacteria continues to expand at an accelerated pace. What does this mean in the dermatology world? We are not the only problem but are certainly part of the problem, representing 5% of all antibiotic prescriptions annually even though we represent only 1% of all physicians in the United States. These prescriptions certainly do not just include skin and soft tissue functions, as a survey-based study by Chouake et al (J Drugs Dermatol. 2014;13:119-124.) showed that dermatologists are overusing antibiotics in the treatment of simple skin abscesses such as acne vulgaris, one of the most common inflammatory skin diseases.

Although the inappropriate utilization of antibiotics for acne has been a subject of great discourse for years, it recently reentered the limelight in a study by Nagler et al published online in October 2015 in the Journal of the American Academy of Dermatology. They showed that patients who ultimately were treated with isotretinoin had been receiving antibiotics for months without any sign of therapeutic life or course end in sight. This retrospective chart review evaluated the duration of systemic antibiotic use prior to starting isotretinoin in 137 patients with inflammatory/nodulocystic acne. Antibiotic use continued for a mean of 331.3 days (median, 238 days). Duration of antibiotic use was divided into categories: 3 months or less (15.3%), 6 months or more (64.2%), or 1 year or more (33.6%).

Let’s take a broad look at antimicrobial resistance. Bacterial drug resistance has numerous negative effects on medicine and society. Drug-resistant bacterial infections result in higher doses of drugs, the addition of treatments with higher toxicity, longer hospital stays, and increased mortality. In the United States, infections due to antibiotic-resistant bacteria add $20 billion to total health care costs plus $35 billion in costs to society.

Unfortunately, it is relatively easy for bacterium to develop drug resistance through 3 simple steps: acquisition by microbes of resistance genes, expression of those resistance genes, and selection for pathogens expressing those resistance genes. The selective pressure in favor of resistance occurs whenever microbes are exposed to a drug but not eradicated, either by the killing effects of the drug itself or by inhibitory effects of the drug followed by killing by the host’s immune system. In any setting that creates this selective pressure in favor of drug resistance, such as poor patient compliance (ie, infrequent dosing, taking an antibiotic for too long as we see with the use of antibiotics for the treatment of inflammatory skin diseases such as acne), the likelihood of that resistance actually developing is increased. In addition, drugs that inhibit but do not kill microbes are more likely to allow some microbial cells to live and therefore develop resistance when exposed to a drug, which accounts for the majority of antibiotics in our armament. Lastly, abuse of broad-spectrum antibiotics has further spurred the emergence of many antibiotic-resistant strains. For instance, Pseudomonas aeruginosa is one of many evolving multidrug-resistant microorganisms that have been collectively coined the “ESKAPE” pathogens (Enterococcus faecalis, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, P aeruginosa, Enterobacter species) to emphasize the fact that they “escape” the effects of many antibacterial agents.

All of the above does not take into account the environmental factors that play a role in this resistance. The close quarters, mass/public transportation, and stressful pace of life of urban living not only bring these organisms together to share resistance genes but also increase our susceptibility.

What’s the issue?

We can all do our part in the fight against microbial resistance and join the antimicrobial stewardship. Here are a couple tips for dermatologists:

1. Stop using over-the-counter antibiotic ointment for every biopsy or minor procedure, which is one of the recommendations of the American Academy of Dermatology based on the ABIM Foundation’s Choosing Wisely campaign.
2. Oral and topical antibiotics for inflammatory skin diseases such as acne, rosacea, and hidradenitis suppurativa should only be used temporarily or at subantimicrobial dosing. Always combine a benzoyl peroxide–containing wash with a topical or oral antibiotic to hit the bacteria with multiple mechanisms of antibacterial activity to limit resistance. Don’t use benzoyl peroxide stronger than 2.5% for the face; make sure to wash it off completely to avoid staining your towels, sheets, and clothing.

We can all play our part in the fight against antimicrobial resistance. How do you fight the resistance?

We want to know your views! Tell us what you think.

It is now common for patients to arrive in a physician office and never see the physician. Instead, patients are seen by so-called physician extenders. As our population ages, the need for medical care continues to grow beyond the capacity of the 900,000 US physicians that provide required services, particularly in the first level (primary care). The response to the physician shortage has entailed a variety of strategies. There has been a major immigration of foreign physicians, particularly from India; US medical schools have been encouraged to increase enrollment; and new medical schools have been inaugurated. Physicians have been pushed to adopt electronic medical records to permit increased throughput of patients in office practices. These multiple approaches have had an effect, though sometimes the results are undesirable. For example, complicated computer programs often detract from the physician-patient relationship.

One of the early solutions offered to deal with the doctor shortage in primary care was the concept of physician extenders (PEs), also called mid-level practitioners, who are professionals trained to take on a number of the simpler tasks performed by physicians. There are 2 basic classes of PEs: nurse practitioners and physician assistants. Nurse practitioners are originally trained to perform nursing but then undertake a course of study including scientific courses and clinical exposure to various parts of medicine. Physician assistants receive similar training. The duration of training for PEs usually is 18 to 24 months, whereas physicians attend medical school for 4 years. Unlike physicians, mid-level practitioners do not enter physician postgraduate residency training programs, which last many years.

The original concept was that PEs would work side by side with physicians who would supervise the care provided by the PEs. This team concept was designed to free physicians from the more mundane aspects of medical care and allow them to focus on the more challenging diagnostic and therapeutic issues presented by individual patients. In an era in which the burden of documentation has become increasingly onerous, the assistance of paraprofessionals can spare physicians the entry of redundant details in electronic databases that do not contribute to patient welfare.

However, research suggests that the concept of mid-level providers undertaking first-level care side by side with physicians has diverged from the original goal. An article by Coldiron and Ratnarathorn (JAMA Dermatol. 2014;150:1153-1159) studied Medicare billing data. The authors discovered that a variety of activities, many with higher reimbursement than primary care, were billed directly by PEs without apparent physician involvement, including a large number of complex invasive procedures, more than half in dermatology. Their article focused on dermatologic procedures, such as the destruction of skin cancers and advanced surgical repairs, but they listed many other procedures that are typically in the domain of highly trained physicians, including radiologic interpretations such as mammography and joint injections such as spinal injections. The data they presented were substantiated by publications in the medical literature suggesting that mid-level providers at certain hospitals even perform heart catheterizations and gastrointestinal endoscopies.

There have been no apologies for the unsupervised conduct of physician activities by nonphysicians. On the contrary, many PEs claim to be as well trained and proficient as medical doctors. Coldiron and Ratnarathorn argued otherwise. They pointed out that physicians receive an average of 10,000 hours of training compared to 2000 hours for mid-level practitioners, and they raised concerns about misdiagnoses, complications, and unnecessary procedures performed by PEs without supervision. In an editorial, Jalian and Avram (JAMA Dermatol. 2014;150:1149-1151) pointed out that a disproportionate number of cases of lawsuits for laser-induced injuries are related to performance by nonphysicians.

The pressures to allow nonphysicians to practice medicine independently are increasing. There is a shortage of physicians, especially in states such as Massachusetts that have substantial governmental limitation of physician reimbursement. In Massachusetts, regulations encourage mid-level practitioners to practice without physician supervision and even call themselves “doctors.” Furthermore, hospitals have faced residency funding cuts by Medicare and have had regulatory limitation of work hours by medical doctors in residency training. As a result, many institutions have turned to PEs to perform procedures that are typically performed by medical doctors.

Perhaps the greatest pressure favoring use of nonphysicians is financial. Mid-level practitioners receive lower salaries, typically 45% less, than medical doctors. In an era in which lowering costs has supplanted the goal of offering the best medical care possible, the attraction of replacement of a physician by a professional with less training becomes irresistible. It also is of concern that many physicians ignore the requirement to supervise the work of mid-level practitioners to maximize profit. Physicians often hire a mid-level provider rather than finding another physician to partner in their practice. Patients referred to a dermatologist often are seen by a PE and never even see the physician.

The concept of PEs working in a team with physicians remains an excellent approach to remedying the shortage of medical doctors, but we need to return to the original plan. Physician extenders should perform primary care rather than complex and lucrative subspecialties. There must be adequate supervision and definitely participation by physicians in rendering care.

All of the authors in the articles cited argue for greater regulation of unsupervised PEs to prevent performance of procedures where they lack expertise. Although the regulatory approach is sensible, it is more important to ensure that patients choose who gives them their medical care. They should not be obligated to see mid-level practitioners if they want to see a medical doctor. Above all, patients must be informed of the qualifications of those who provide their medical care. They should not be blindsided when they arrive for an appointment with their physician and find themselves shunted to a PE. We must not allow financial considerations to override the integrity of the medical care process.

What do you think is the optimal and safest role for PEs in a dermatology practice?

We want to know your views! Tell us what you think.

It is now common for patients to arrive in a physician office and never see the physician. Instead, patients are seen by so-called physician extenders. As our population ages, the need for medical care continues to grow beyond the capacity of the 900,000 US physicians that provide required services, particularly in the first level (primary care). The response to the physician shortage has entailed a variety of strategies. There has been a major immigration of foreign physicians, particularly from India; US medical schools have been encouraged to increase enrollment; and new medical schools have been inaugurated. Physicians have been pushed to adopt electronic medical records to permit increased throughput of patients in office practices. These multiple approaches have had an effect, though sometimes the results are undesirable. For example, complicated computer programs often detract from the physician-patient relationship.

One of the early solutions offered to deal with the doctor shortage in primary care was the concept of physician extenders (PEs), also called mid-level practitioners, who are professionals trained to take on a number of the simpler tasks performed by physicians. There are 2 basic classes of PEs: nurse practitioners and physician assistants. Nurse practitioners are originally trained to perform nursing but then undertake a course of study including scientific courses and clinical exposure to various parts of medicine. Physician assistants receive similar training. The duration of training for PEs usually is 18 to 24 months, whereas physicians attend medical school for 4 years. Unlike physicians, mid-level practitioners do not enter physician postgraduate residency training programs, which last many years.

The original concept was that PEs would work side by side with physicians who would supervise the care provided by the PEs. This team concept was designed to free physicians from the more mundane aspects of medical care and allow them to focus on the more challenging diagnostic and therapeutic issues presented by individual patients. In an era in which the burden of documentation has become increasingly onerous, the assistance of paraprofessionals can spare physicians the entry of redundant details in electronic databases that do not contribute to patient welfare.

However, research suggests that the concept of mid-level providers undertaking first-level care side by side with physicians has diverged from the original goal. An article by Coldiron and Ratnarathorn (JAMA Dermatol. 2014;150:1153-1159) studied Medicare billing data. The authors discovered that a variety of activities, many with higher reimbursement than primary care, were billed directly by PEs without apparent physician involvement, including a large number of complex invasive procedures, more than half in dermatology. Their article focused on dermatologic procedures, such as the destruction of skin cancers and advanced surgical repairs, but they listed many other procedures that are typically in the domain of highly trained physicians, including radiologic interpretations such as mammography and joint injections such as spinal injections. The data they presented were substantiated by publications in the medical literature suggesting that mid-level providers at certain hospitals even perform heart catheterizations and gastrointestinal endoscopies.

There have been no apologies for the unsupervised conduct of physician activities by nonphysicians. On the contrary, many PEs claim to be as well trained and proficient as medical doctors. Coldiron and Ratnarathorn argued otherwise. They pointed out that physicians receive an average of 10,000 hours of training compared to 2000 hours for mid-level practitioners, and they raised concerns about misdiagnoses, complications, and unnecessary procedures performed by PEs without supervision. In an editorial, Jalian and Avram (JAMA Dermatol. 2014;150:1149-1151) pointed out that a disproportionate number of cases of lawsuits for laser-induced injuries are related to performance by nonphysicians.

The pressures to allow nonphysicians to practice medicine independently are increasing. There is a shortage of physicians, especially in states such as Massachusetts that have substantial governmental limitation of physician reimbursement. In Massachusetts, regulations encourage mid-level practitioners to practice without physician supervision and even call themselves “doctors.” Furthermore, hospitals have faced residency funding cuts by Medicare and have had regulatory limitation of work hours by medical doctors in residency training. As a result, many institutions have turned to PEs to perform procedures that are typically performed by medical doctors.

Perhaps the greatest pressure favoring use of nonphysicians is financial. Mid-level practitioners receive lower salaries, typically 45% less, than medical doctors. In an era in which lowering costs has supplanted the goal of offering the best medical care possible, the attraction of replacement of a physician by a professional with less training becomes irresistible. It also is of concern that many physicians ignore the requirement to supervise the work of mid-level practitioners to maximize profit. Physicians often hire a mid-level provider rather than finding another physician to partner in their practice. Patients referred to a dermatologist often are seen by a PE and never even see the physician.

The concept of PEs working in a team with physicians remains an excellent approach to remedying the shortage of medical doctors, but we need to return to the original plan. Physician extenders should perform primary care rather than complex and lucrative subspecialties. There must be adequate supervision and definitely participation by physicians in rendering care.

All of the authors in the articles cited argue for greater regulation of unsupervised PEs to prevent performance of procedures where they lack expertise. Although the regulatory approach is sensible, it is more important to ensure that patients choose who gives them their medical care. They should not be obligated to see mid-level practitioners if they want to see a medical doctor. Above all, patients must be informed of the qualifications of those who provide their medical care. They should not be blindsided when they arrive for an appointment with their physician and find themselves shunted to a PE. We must not allow financial considerations to override the integrity of the medical care process.

What do you think is the optimal and safest role for PEs in a dermatology practice?

We want to know your views! Tell us what you think.

It is now common for patients to arrive in a physician office and never see the physician. Instead, patients are seen by so-called physician extenders. As our population ages, the need for medical care continues to grow beyond the capacity of the 900,000 US physicians that provide required services, particularly in the first level (primary care). The response to the physician shortage has entailed a variety of strategies. There has been a major immigration of foreign physicians, particularly from India; US medical schools have been encouraged to increase enrollment; and new medical schools have been inaugurated. Physicians have been pushed to adopt electronic medical records to permit increased throughput of patients in office practices. These multiple approaches have had an effect, though sometimes the results are undesirable. For example, complicated computer programs often detract from the physician-patient relationship.

One of the early solutions offered to deal with the doctor shortage in primary care was the concept of physician extenders (PEs), also called mid-level practitioners, who are professionals trained to take on a number of the simpler tasks performed by physicians. There are 2 basic classes of PEs: nurse practitioners and physician assistants. Nurse practitioners are originally trained to perform nursing but then undertake a course of study including scientific courses and clinical exposure to various parts of medicine. Physician assistants receive similar training. The duration of training for PEs usually is 18 to 24 months, whereas physicians attend medical school for 4 years. Unlike physicians, mid-level practitioners do not enter physician postgraduate residency training programs, which last many years.

The original concept was that PEs would work side by side with physicians who would supervise the care provided by the PEs. This team concept was designed to free physicians from the more mundane aspects of medical care and allow them to focus on the more challenging diagnostic and therapeutic issues presented by individual patients. In an era in which the burden of documentation has become increasingly onerous, the assistance of paraprofessionals can spare physicians the entry of redundant details in electronic databases that do not contribute to patient welfare.

However, research suggests that the concept of mid-level providers undertaking first-level care side by side with physicians has diverged from the original goal. An article by Coldiron and Ratnarathorn (JAMA Dermatol. 2014;150:1153-1159) studied Medicare billing data. The authors discovered that a variety of activities, many with higher reimbursement than primary care, were billed directly by PEs without apparent physician involvement, including a large number of complex invasive procedures, more than half in dermatology. Their article focused on dermatologic procedures, such as the destruction of skin cancers and advanced surgical repairs, but they listed many other procedures that are typically in the domain of highly trained physicians, including radiologic interpretations such as mammography and joint injections such as spinal injections. The data they presented were substantiated by publications in the medical literature suggesting that mid-level providers at certain hospitals even perform heart catheterizations and gastrointestinal endoscopies.

There have been no apologies for the unsupervised conduct of physician activities by nonphysicians. On the contrary, many PEs claim to be as well trained and proficient as medical doctors. Coldiron and Ratnarathorn argued otherwise. They pointed out that physicians receive an average of 10,000 hours of training compared to 2000 hours for mid-level practitioners, and they raised concerns about misdiagnoses, complications, and unnecessary procedures performed by PEs without supervision. In an editorial, Jalian and Avram (JAMA Dermatol. 2014;150:1149-1151) pointed out that a disproportionate number of cases of lawsuits for laser-induced injuries are related to performance by nonphysicians.

The pressures to allow nonphysicians to practice medicine independently are increasing. There is a shortage of physicians, especially in states such as Massachusetts that have substantial governmental limitation of physician reimbursement. In Massachusetts, regulations encourage mid-level practitioners to practice without physician supervision and even call themselves “doctors.” Furthermore, hospitals have faced residency funding cuts by Medicare and have had regulatory limitation of work hours by medical doctors in residency training. As a result, many institutions have turned to PEs to perform procedures that are typically performed by medical doctors.

Perhaps the greatest pressure favoring use of nonphysicians is financial. Mid-level practitioners receive lower salaries, typically 45% less, than medical doctors. In an era in which lowering costs has supplanted the goal of offering the best medical care possible, the attraction of replacement of a physician by a professional with less training becomes irresistible. It also is of concern that many physicians ignore the requirement to supervise the work of mid-level practitioners to maximize profit. Physicians often hire a mid-level provider rather than finding another physician to partner in their practice. Patients referred to a dermatologist often are seen by a PE and never even see the physician.

The concept of PEs working in a team with physicians remains an excellent approach to remedying the shortage of medical doctors, but we need to return to the original plan. Physician extenders should perform primary care rather than complex and lucrative subspecialties. There must be adequate supervision and definitely participation by physicians in rendering care.

All of the authors in the articles cited argue for greater regulation of unsupervised PEs to prevent performance of procedures where they lack expertise. Although the regulatory approach is sensible, it is more important to ensure that patients choose who gives them their medical care. They should not be obligated to see mid-level practitioners if they want to see a medical doctor. Above all, patients must be informed of the qualifications of those who provide their medical care. They should not be blindsided when they arrive for an appointment with their physician and find themselves shunted to a PE. We must not allow financial considerations to override the integrity of the medical care process.

What do you think is the optimal and safest role for PEs in a dermatology practice?

We want to know your views! Tell us what you think.

Cryolipolysis is a popular noninvasive treatment for areas of excess adipose deposition, such as in the abdomen and flanks. During the 60-minute procedure, a uniquely shaped treatment applicator is applied to the area with suction, causing cold exposure–induced crystallization of adipocytes through apoptosis. Overall, cryolipolysis treatment has a good safety profile and is well tolerated by patients without the need for anesthesia. A rare side effect of cryolipolysis is paradoxical adipose hyperplasia, which has been reported to be more common in men. Another rare adverse effect is the development of substantial posttreatment pain. Most patients usually experience minimal posttreatment discomfort and the phenomenon of delayed posttreatment pain rarely has been reported in the literature.

An online article published in Dermatologic Surgery in November evaluated posttreatment pain. Keaney et al performed a retrospective review that looked at the incidence of posttreatment pain after cryolipolysis as well as any correlating factors among patients that experience this pain.

In this retrospective chart review, 125 patients who received 554 consecutive cryolipolysis procedures over 1 year were evaluated for at least 2 of the following symptoms: (1) neuropathic symptoms (ie, stabbing, burning, shooting pain within treatment area), (2) increased pain at night that disturbed sleep, and (3) discomfort not alleviated by analgesic medication (ie, nonsteroidal anti-inflammatory drugs, narcotics). In these patients, 114 treatments were performed on 27 men and 440 treatments on 98 women; 36.6% of treatments were performed on the lower abdomen, 34.7% on the flanks, 11.9% on the upper abdomen, 9.4% on the back, 6.0% on the thighs, and 1.4% on the chest. A small cryolipolysis applicator was used for 95% of the treatments and a large applicator for 5% of the treatments.

Of 125 patients, 19 (15.2%) developed delayed postcryolipolysis pain and all were female patients. These patients received a total of 75 treatments (3.9 treatments per patient). All but 1 patient developed pain on the abdomen. One patient had pain on the flanks only. Three patients had pain at multiple sites (eg, abdomen and flanks, abdomen and thighs). Younger women (average age, 39 years) were more likely to have posttreatment pain. The number of treatments did not correlate with the development of pain. The average onset of pain was 3 days, with an average resolution time of 11 days (range, 2–60 days). Three patients underwent a second cryolipolysis treatment in the same area, which induced delayed pain again. Six patients underwent treatments on other body regions and did not develop pain.

Although postcryolipolysis pain is self-limiting and self-resolving, it can still be debilitating in some cases. Keaney et al managed the posttreatment discomfort with compression garments, lidocaine 5% transdermal patches, low-dose gabapentin, and/or acetaminophen with codeine. Low-dose oral gabapentin appears to have a good effect in pain treatment for these patients, which had a complete response in 14 patients as the sole treatment. Interestingly, 2 other large patient series were reported, with 518 patients in one study (Dermatol Surg. 2013;39:1209-1216) and 528 treatments in another study (Aesthetic Surg J. 2013;33:835-846); there were only 3 reports of mild to moderate pain.

What’s the issue?

Delayed posttreatment pain seems to be a common phenomenon, affecting primarily younger women who have had cryolipolysis of the abdominal region. It is reassuring that this pain is self-limiting and that it is responsive to oral gabapentin treatment. However, it is important to discuss this possible not-so-rare side effect with patients considering this treatment. Do you discuss delayed posttreatment pain with your cryolipolysis patients?

We want to know your views! Tell us what you think.

Cryolipolysis is a popular noninvasive treatment for areas of excess adipose deposition, such as in the abdomen and flanks. During the 60-minute procedure, a uniquely shaped treatment applicator is applied to the area with suction, causing cold exposure–induced crystallization of adipocytes through apoptosis. Overall, cryolipolysis treatment has a good safety profile and is well tolerated by patients without the need for anesthesia. A rare side effect of cryolipolysis is paradoxical adipose hyperplasia, which has been reported to be more common in men. Another rare adverse effect is the development of substantial posttreatment pain. Most patients usually experience minimal posttreatment discomfort and the phenomenon of delayed posttreatment pain rarely has been reported in the literature.

An online article published in Dermatologic Surgery in November evaluated posttreatment pain. Keaney et al performed a retrospective review that looked at the incidence of posttreatment pain after cryolipolysis as well as any correlating factors among patients that experience this pain.

In this retrospective chart review, 125 patients who received 554 consecutive cryolipolysis procedures over 1 year were evaluated for at least 2 of the following symptoms: (1) neuropathic symptoms (ie, stabbing, burning, shooting pain within treatment area), (2) increased pain at night that disturbed sleep, and (3) discomfort not alleviated by analgesic medication (ie, nonsteroidal anti-inflammatory drugs, narcotics). In these patients, 114 treatments were performed on 27 men and 440 treatments on 98 women; 36.6% of treatments were performed on the lower abdomen, 34.7% on the flanks, 11.9% on the upper abdomen, 9.4% on the back, 6.0% on the thighs, and 1.4% on the chest. A small cryolipolysis applicator was used for 95% of the treatments and a large applicator for 5% of the treatments.

Of 125 patients, 19 (15.2%) developed delayed postcryolipolysis pain and all were female patients. These patients received a total of 75 treatments (3.9 treatments per patient). All but 1 patient developed pain on the abdomen. One patient had pain on the flanks only. Three patients had pain at multiple sites (eg, abdomen and flanks, abdomen and thighs). Younger women (average age, 39 years) were more likely to have posttreatment pain. The number of treatments did not correlate with the development of pain. The average onset of pain was 3 days, with an average resolution time of 11 days (range, 2–60 days). Three patients underwent a second cryolipolysis treatment in the same area, which induced delayed pain again. Six patients underwent treatments on other body regions and did not develop pain.

Although postcryolipolysis pain is self-limiting and self-resolving, it can still be debilitating in some cases. Keaney et al managed the posttreatment discomfort with compression garments, lidocaine 5% transdermal patches, low-dose gabapentin, and/or acetaminophen with codeine. Low-dose oral gabapentin appears to have a good effect in pain treatment for these patients, which had a complete response in 14 patients as the sole treatment. Interestingly, 2 other large patient series were reported, with 518 patients in one study (Dermatol Surg. 2013;39:1209-1216) and 528 treatments in another study (Aesthetic Surg J. 2013;33:835-846); there were only 3 reports of mild to moderate pain.

What’s the issue?

Delayed posttreatment pain seems to be a common phenomenon, affecting primarily younger women who have had cryolipolysis of the abdominal region. It is reassuring that this pain is self-limiting and that it is responsive to oral gabapentin treatment. However, it is important to discuss this possible not-so-rare side effect with patients considering this treatment. Do you discuss delayed posttreatment pain with your cryolipolysis patients?

We want to know your views! Tell us what you think.

Cryolipolysis is a popular noninvasive treatment for areas of excess adipose deposition, such as in the abdomen and flanks. During the 60-minute procedure, a uniquely shaped treatment applicator is applied to the area with suction, causing cold exposure–induced crystallization of adipocytes through apoptosis. Overall, cryolipolysis treatment has a good safety profile and is well tolerated by patients without the need for anesthesia. A rare side effect of cryolipolysis is paradoxical adipose hyperplasia, which has been reported to be more common in men. Another rare adverse effect is the development of substantial posttreatment pain. Most patients usually experience minimal posttreatment discomfort and the phenomenon of delayed posttreatment pain rarely has been reported in the literature.

An online article published in Dermatologic Surgery in November evaluated posttreatment pain. Keaney et al performed a retrospective review that looked at the incidence of posttreatment pain after cryolipolysis as well as any correlating factors among patients that experience this pain.

In this retrospective chart review, 125 patients who received 554 consecutive cryolipolysis procedures over 1 year were evaluated for at least 2 of the following symptoms: (1) neuropathic symptoms (ie, stabbing, burning, shooting pain within treatment area), (2) increased pain at night that disturbed sleep, and (3) discomfort not alleviated by analgesic medication (ie, nonsteroidal anti-inflammatory drugs, narcotics). In these patients, 114 treatments were performed on 27 men and 440 treatments on 98 women; 36.6% of treatments were performed on the lower abdomen, 34.7% on the flanks, 11.9% on the upper abdomen, 9.4% on the back, 6.0% on the thighs, and 1.4% on the chest. A small cryolipolysis applicator was used for 95% of the treatments and a large applicator for 5% of the treatments.

Of 125 patients, 19 (15.2%) developed delayed postcryolipolysis pain and all were female patients. These patients received a total of 75 treatments (3.9 treatments per patient). All but 1 patient developed pain on the abdomen. One patient had pain on the flanks only. Three patients had pain at multiple sites (eg, abdomen and flanks, abdomen and thighs). Younger women (average age, 39 years) were more likely to have posttreatment pain. The number of treatments did not correlate with the development of pain. The average onset of pain was 3 days, with an average resolution time of 11 days (range, 2–60 days). Three patients underwent a second cryolipolysis treatment in the same area, which induced delayed pain again. Six patients underwent treatments on other body regions and did not develop pain.

Although postcryolipolysis pain is self-limiting and self-resolving, it can still be debilitating in some cases. Keaney et al managed the posttreatment discomfort with compression garments, lidocaine 5% transdermal patches, low-dose gabapentin, and/or acetaminophen with codeine. Low-dose oral gabapentin appears to have a good effect in pain treatment for these patients, which had a complete response in 14 patients as the sole treatment. Interestingly, 2 other large patient series were reported, with 518 patients in one study (Dermatol Surg. 2013;39:1209-1216) and 528 treatments in another study (Aesthetic Surg J. 2013;33:835-846); there were only 3 reports of mild to moderate pain.

What’s the issue?

Delayed posttreatment pain seems to be a common phenomenon, affecting primarily younger women who have had cryolipolysis of the abdominal region. It is reassuring that this pain is self-limiting and that it is responsive to oral gabapentin treatment. However, it is important to discuss this possible not-so-rare side effect with patients considering this treatment. Do you discuss delayed posttreatment pain with your cryolipolysis patients?

We want to know your views! Tell us what you think.

One of the biggest burdens of modern clinical dermatology practice is the ability to obtain appropriate drug therapy for patients. In the current health care environment, insurance formularies have become increasingly restrictive and more individuals have to deal with high-deductible insurance plans.

In a JAMA Dermatology study published online on November 25, Rosenberg and Rosenberg sought to determine changes in the prices of commonly prescribed dermatologic medications since 2009 and identify trends in price increases for different classes of drugs. To perform this analysis, they sent surveys to 4 national chain pharmacies requesting price information for commonly prescribed dermatologic therapies in 2009, 2011, 2014, and 2015. The initial survey requested information on 72 brand-name drugs.

The findings of the analysis were staggering. Of the 19 brand-name drugs analyzed, the retail prices of 7 drugs more than quadrupled over the study period. The mean price increase for this group of drugs was 401% during the entire survey period.

Rosenberg and Rosenberg grouped the price increase by therapeutic class. Prices of topical antineoplastic therapies had the largest mean absolute and percentage increase ($10,926.58 [1240%]). Prices of drugs in the anti-infective class had the smallest mean absolute increase ($333.99); prices of psoriasis medications had the smallest mean percentage increase (180%). Prices of acne and rosacea medications had a mean increase of 195%, and prices of topical corticosteroids experienced a mean increase of 290%. Selected generic drugs examined in 2011 and 2014 also increased a mean of 279% during the 3-year period.

Rosenberg and Rosenberg noted that the increases for commonly prescribed medications greatly outpaced inflation, national health expenditure growth, and increases in reimbursements for physician services. They did not detect any specific trend to explain the substantial increase in the costs of dermatologic prescription drugs and they did not investigate reasons for the price increases.

What’s the issue?

Price increases for psoriatic and other therapies are creating barriers to both our appropriate treatment of patients and our ability to effectively practice medicine. How are you coping with this challenge in your practice?

We want to know your views! Tell us what you think.

One of the biggest burdens of modern clinical dermatology practice is the ability to obtain appropriate drug therapy for patients. In the current health care environment, insurance formularies have become increasingly restrictive and more individuals have to deal with high-deductible insurance plans.

In a JAMA Dermatology study published online on November 25, Rosenberg and Rosenberg sought to determine changes in the prices of commonly prescribed dermatologic medications since 2009 and identify trends in price increases for different classes of drugs. To perform this analysis, they sent surveys to 4 national chain pharmacies requesting price information for commonly prescribed dermatologic therapies in 2009, 2011, 2014, and 2015. The initial survey requested information on 72 brand-name drugs.

The findings of the analysis were staggering. Of the 19 brand-name drugs analyzed, the retail prices of 7 drugs more than quadrupled over the study period. The mean price increase for this group of drugs was 401% during the entire survey period.

Rosenberg and Rosenberg grouped the price increase by therapeutic class. Prices of topical antineoplastic therapies had the largest mean absolute and percentage increase ($10,926.58 [1240%]). Prices of drugs in the anti-infective class had the smallest mean absolute increase ($333.99); prices of psoriasis medications had the smallest mean percentage increase (180%). Prices of acne and rosacea medications had a mean increase of 195%, and prices of topical corticosteroids experienced a mean increase of 290%. Selected generic drugs examined in 2011 and 2014 also increased a mean of 279% during the 3-year period.

Rosenberg and Rosenberg noted that the increases for commonly prescribed medications greatly outpaced inflation, national health expenditure growth, and increases in reimbursements for physician services. They did not detect any specific trend to explain the substantial increase in the costs of dermatologic prescription drugs and they did not investigate reasons for the price increases.

What’s the issue?

Price increases for psoriatic and other therapies are creating barriers to both our appropriate treatment of patients and our ability to effectively practice medicine. How are you coping with this challenge in your practice?

We want to know your views! Tell us what you think.

One of the biggest burdens of modern clinical dermatology practice is the ability to obtain appropriate drug therapy for patients. In the current health care environment, insurance formularies have become increasingly restrictive and more individuals have to deal with high-deductible insurance plans.

In a JAMA Dermatology study published online on November 25, Rosenberg and Rosenberg sought to determine changes in the prices of commonly prescribed dermatologic medications since 2009 and identify trends in price increases for different classes of drugs. To perform this analysis, they sent surveys to 4 national chain pharmacies requesting price information for commonly prescribed dermatologic therapies in 2009, 2011, 2014, and 2015. The initial survey requested information on 72 brand-name drugs.

The findings of the analysis were staggering. Of the 19 brand-name drugs analyzed, the retail prices of 7 drugs more than quadrupled over the study period. The mean price increase for this group of drugs was 401% during the entire survey period.

Rosenberg and Rosenberg grouped the price increase by therapeutic class. Prices of topical antineoplastic therapies had the largest mean absolute and percentage increase ($10,926.58 [1240%]). Prices of drugs in the anti-infective class had the smallest mean absolute increase ($333.99); prices of psoriasis medications had the smallest mean percentage increase (180%). Prices of acne and rosacea medications had a mean increase of 195%, and prices of topical corticosteroids experienced a mean increase of 290%. Selected generic drugs examined in 2011 and 2014 also increased a mean of 279% during the 3-year period.

Rosenberg and Rosenberg noted that the increases for commonly prescribed medications greatly outpaced inflation, national health expenditure growth, and increases in reimbursements for physician services. They did not detect any specific trend to explain the substantial increase in the costs of dermatologic prescription drugs and they did not investigate reasons for the price increases.

What’s the issue?

Price increases for psoriatic and other therapies are creating barriers to both our appropriate treatment of patients and our ability to effectively practice medicine. How are you coping with this challenge in your practice?

We want to know your views! Tell us what you think.

In a JAMA Dermatology article published online on December 2, Lee et al challenged the commonly held belief that laboratory studies should be monitored frequently for patients on isotretinoin. In this systematic review and meta-analysis, abnormalities in liver function tests (LFTs), complete blood cell count (CBC), and lipid panel were compared in a set of 22 randomized clinical trials and 4 retrospective studies (1574 patients). Results revealed changes in the mean laboratory values from baseline (99% CI) of the following: aspartate aminotransferase, 22.67 U/L (19.94–25.41 U/L); alanine aminotransferase, 21.77 U/L (18.96–24.59 U/L); alkaline phosphatase, 88.35 U/L (58.94–117.76 U/L); white blood cell count portion of CBC, 6890/µL (5700–8030/µL); lipid panel (triglycerides, 119.98 mg/dL [98.58–141.39 mg/dL]; total cholesterol, 184.74 mg/dL [178.17–191.31 mg/dL]; low-density lipoprotein cholesterol, 109.23 mg/dL [103.68–114.79 mg/dL]; high-density lipoprotein cholesterol, 42.80 mg/dL [39.84–45.76 mg/dL]).

Although these laboratory values were altered as noted above, only 0.5% of patients exhibited test results statistically above or below the mean laboratory values. Additionally, of these laboratory abnormalities, mean changes were not considered to be high risk based on National Institutes of Health clinical center reference ranges.

What’s the issue?

Last year the residents in-training in our department noted variations in what each faculty member was recommending for isotretinoin laboratory monitoring. Practices ranged from initial then monthly full CBC, LFTs, and lipid panel, to those who only checked these laboratory results initially and at 1 month, to those who only performed review of systems-germane parameters. After reviewing the literature, individual preferences, and cost comparisons, a consensus was reached: tests for aspartate aminotransferase, alanine aminotransferase (in lieu of LFT panel), total cholesterol, triglycerides (in lieu of lipid panel), and relevant pregnancy screens would be performed initially, at month 1, and at month 2.

Lee et al also determined that monthly laboratory testing may not be necessary, especially for this low-risk category of patients, but further study is required to determine if there is a standardized way to approach laboratory testing from a safety and economic standpoint, as each dermatologist who prescribes isotretinoin can identify individual cases in which laboratory monitoring was helpful or uncovered individual comorbidities or toxicities in addition to instances where blood work was prohibitively redundant and expensive.

What is your approach to blood work in isotretinoin patients, and can you identify individual patient populations that require more or less stringent laboratory monitoring?

We want to know your views! Tell us what you think.

In a JAMA Dermatology article published online on December 2, Lee et al challenged the commonly held belief that laboratory studies should be monitored frequently for patients on isotretinoin. In this systematic review and meta-analysis, abnormalities in liver function tests (LFTs), complete blood cell count (CBC), and lipid panel were compared in a set of 22 randomized clinical trials and 4 retrospective studies (1574 patients). Results revealed changes in the mean laboratory values from baseline (99% CI) of the following: aspartate aminotransferase, 22.67 U/L (19.94–25.41 U/L); alanine aminotransferase, 21.77 U/L (18.96–24.59 U/L); alkaline phosphatase, 88.35 U/L (58.94–117.76 U/L); white blood cell count portion of CBC, 6890/µL (5700–8030/µL); lipid panel (triglycerides, 119.98 mg/dL [98.58–141.39 mg/dL]; total cholesterol, 184.74 mg/dL [178.17–191.31 mg/dL]; low-density lipoprotein cholesterol, 109.23 mg/dL [103.68–114.79 mg/dL]; high-density lipoprotein cholesterol, 42.80 mg/dL [39.84–45.76 mg/dL]).

Although these laboratory values were altered as noted above, only 0.5% of patients exhibited test results statistically above or below the mean laboratory values. Additionally, of these laboratory abnormalities, mean changes were not considered to be high risk based on National Institutes of Health clinical center reference ranges.

What’s the issue?

Last year the residents in-training in our department noted variations in what each faculty member was recommending for isotretinoin laboratory monitoring. Practices ranged from initial then monthly full CBC, LFTs, and lipid panel, to those who only checked these laboratory results initially and at 1 month, to those who only performed review of systems-germane parameters. After reviewing the literature, individual preferences, and cost comparisons, a consensus was reached: tests for aspartate aminotransferase, alanine aminotransferase (in lieu of LFT panel), total cholesterol, triglycerides (in lieu of lipid panel), and relevant pregnancy screens would be performed initially, at month 1, and at month 2.

Lee et al also determined that monthly laboratory testing may not be necessary, especially for this low-risk category of patients, but further study is required to determine if there is a standardized way to approach laboratory testing from a safety and economic standpoint, as each dermatologist who prescribes isotretinoin can identify individual cases in which laboratory monitoring was helpful or uncovered individual comorbidities or toxicities in addition to instances where blood work was prohibitively redundant and expensive.

What is your approach to blood work in isotretinoin patients, and can you identify individual patient populations that require more or less stringent laboratory monitoring?

We want to know your views! Tell us what you think.

In a JAMA Dermatology article published online on December 2, Lee et al challenged the commonly held belief that laboratory studies should be monitored frequently for patients on isotretinoin. In this systematic review and meta-analysis, abnormalities in liver function tests (LFTs), complete blood cell count (CBC), and lipid panel were compared in a set of 22 randomized clinical trials and 4 retrospective studies (1574 patients). Results revealed changes in the mean laboratory values from baseline (99% CI) of the following: aspartate aminotransferase, 22.67 U/L (19.94–25.41 U/L); alanine aminotransferase, 21.77 U/L (18.96–24.59 U/L); alkaline phosphatase, 88.35 U/L (58.94–117.76 U/L); white blood cell count portion of CBC, 6890/µL (5700–8030/µL); lipid panel (triglycerides, 119.98 mg/dL [98.58–141.39 mg/dL]; total cholesterol, 184.74 mg/dL [178.17–191.31 mg/dL]; low-density lipoprotein cholesterol, 109.23 mg/dL [103.68–114.79 mg/dL]; high-density lipoprotein cholesterol, 42.80 mg/dL [39.84–45.76 mg/dL]).

Although these laboratory values were altered as noted above, only 0.5% of patients exhibited test results statistically above or below the mean laboratory values. Additionally, of these laboratory abnormalities, mean changes were not considered to be high risk based on National Institutes of Health clinical center reference ranges.

What’s the issue?

Last year the residents in-training in our department noted variations in what each faculty member was recommending for isotretinoin laboratory monitoring. Practices ranged from initial then monthly full CBC, LFTs, and lipid panel, to those who only checked these laboratory results initially and at 1 month, to those who only performed review of systems-germane parameters. After reviewing the literature, individual preferences, and cost comparisons, a consensus was reached: tests for aspartate aminotransferase, alanine aminotransferase (in lieu of LFT panel), total cholesterol, triglycerides (in lieu of lipid panel), and relevant pregnancy screens would be performed initially, at month 1, and at month 2.

Lee et al also determined that monthly laboratory testing may not be necessary, especially for this low-risk category of patients, but further study is required to determine if there is a standardized way to approach laboratory testing from a safety and economic standpoint, as each dermatologist who prescribes isotretinoin can identify individual cases in which laboratory monitoring was helpful or uncovered individual comorbidities or toxicities in addition to instances where blood work was prohibitively redundant and expensive.

What is your approach to blood work in isotretinoin patients, and can you identify individual patient populations that require more or less stringent laboratory monitoring?

We want to know your views! Tell us what you think.