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Melanoma

THE COMPARISON

A Acral lentiginous melanoma on the sole of the foot of a 30-year-old Black woman. The depth of the lesion was 2 mm with a positive sentinel lymph node biopsy.

B Nodular melanoma on the shoulder of a 63-year-old Hispanic woman. The depth of the lesion was 5.5 mm with a positive sentinel lymph node biopsy.

Melanoma occurs less frequently in individuals with darker skin types than in those with lighter skin types but is associated with higher rates of morbidity and mortality in this patient population.1-7 In the cases shown here (A and B), both patients had advanced melanomas with large primary lesions and lymph node metastases.

Melanoma

Epidemiology

A systematic review by Higgins et al6 reported the following on the epidemiology of melanomas in patients with skin of color:

  • African Americans have deeper tumors at the time of diagnosis, in addition to increased rates of regionally advanced and distant disease. Lesions generally are located on the lower extremities and have an increased propensity for ulceration. Acral lentiginous melanoma is the most common melanoma subtype found in African American patients.6
  • In Hispanic individuals, superficial spreading melanoma is the most common melanoma subtype. Lower extremity lesions are more common relative to White individuals. Hispanic individuals have the highest rate of oral cavity melanomas across all ethnic groups.6
  • In Asian individuals, acral and subungual sites are most common. Specifically, Pacific Islanders have the highest proportion of mucosal melanomas across all ethnic groups.6

Key clinical features in people with darker skin tones

Melanomas are found more often on the palms, soles, nail units, oral cavity, and mucosae.6 The melanomas have the same clinical and dermoscopic features found in individuals with lighter skin tones.

Worth noting

Factors that may contribute to the diagnosis of more advanced melanomas in racial/ethnic minorities in the United States include:

  • decreased access to health care based on lack of health insurance and low socioeconomic status,
  • less awareness of the risk of melanoma among patients and health care providers because melanoma is less common in persons of color, and
  • lesions found in areas less likely to be seen in screening examinations, such as the soles of the feet and the oral and genital mucosae.

Health disparity highlight

  • In a large US study of 96,953 patients with a diagnosis of cutaneous melanoma from 1992 to 2009, the proportion of later-stage melanoma—stages II to IV—was greater in Black patients compared to White patients.7
  • Based on this same data set, White patients had the longest survival time (P <. 05), followed by Hispanic (P < .05), Asian American/Native American/Pacific Islander (P < .05), and Black (P < .05) patients, respectively.7
  • In Miami-Dade County, one study of 1690 melanoma cases found that 48% of Black patients had regional or distant disease at presentation compared to 22% of White patients (P = .015).5 Analysis of multiple factors found that only race was a significant predictor for late-stage melanoma (P < .001). Black patients in this study were 3 times more likely than others to be diagnosed with melanoma at a late stage (P = .07).5
  • Black patients in the United States are more likely to have a delayed time from diagnosis to definitive surgery even when researchers controlled for type of health insurance and stage of diagnosis.8

Final thoughts

Efforts are needed to overcome these disparities by:

  • educating patients with skin of color and their health care providers about the risks of advanced melanoma with the goal of prevention and earlier diagnosis;
  • breaking down barriers to care caused by poverty, lack of health insurance, and systemic racism; and
  • eliminating factors that lead to delays from diagnosis to definitive surgery.
References

1. Wu XC, Eide MJ, King J, et al. Racial and ethnic variations in incidence and survival of cutaneous melanoma in the United States, 1999-2006. J Am Acad Dermatol. 2011;65(5 suppl 1):S26-S37. doi: 10.1016/j.jaad.2001.05.034

2. Cormier JN, Xing Y, Ding M, et al. Ethnic differences among patients with cutaneous melanoma. Arch Intern Med. 2006;166:1907-1914. doi: 10.1001/archinte.166.17.1907

3. Cress RD, Holly EA. Incidence of cutaneous melanoma among non-Hispanic whites, Hispanics, Asians, and blacks: an analysis of California cancer registry data, 1988-93. Cancer Causes Control. 1997;8:246-252. doi: 10.1023/a:1018432632528

4. Hu S, Parker DF, Thomas AG, et al. Advanced presentation of melanoma in African Americans: the Miami-Dade County experience. J Am Acad Dermatol. 2004;51:1031-1032. doi: 10.1016/ j.jaad.2004.05.005

5. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142: 704-708. doi: 10.1001/archderm.142.6.704

6. Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801. doi: 10.1097/DSS.0000000000001759

7. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival [published online July 28, 2016]. J Am Acad Dermatol. 2016;75:983-991. doi: 10.1016/j.jaad.2016.06.006

8. Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016) [published online August 27, 2020]. J Am Acad Dermatol. 2021;84:1585-1593. doi: 10.1016/ j.jaad.2020.08.097

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

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

The authors reported no potential conflict of interest relevant to this article.

Simultaneously published in Cutis and The Journal of Family Practice.

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Author and Disclosure Information

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

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

The authors reported no potential conflict of interest relevant to this article.

Simultaneously published in Cutis and The Journal of Family Practice.

Author and Disclosure Information

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

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

The authors reported no potential conflict of interest relevant to this article.

Simultaneously published in Cutis and The Journal of Family Practice.

Article PDF
Article PDF

THE COMPARISON

A Acral lentiginous melanoma on the sole of the foot of a 30-year-old Black woman. The depth of the lesion was 2 mm with a positive sentinel lymph node biopsy.

B Nodular melanoma on the shoulder of a 63-year-old Hispanic woman. The depth of the lesion was 5.5 mm with a positive sentinel lymph node biopsy.

Melanoma occurs less frequently in individuals with darker skin types than in those with lighter skin types but is associated with higher rates of morbidity and mortality in this patient population.1-7 In the cases shown here (A and B), both patients had advanced melanomas with large primary lesions and lymph node metastases.

Melanoma

Epidemiology

A systematic review by Higgins et al6 reported the following on the epidemiology of melanomas in patients with skin of color:

  • African Americans have deeper tumors at the time of diagnosis, in addition to increased rates of regionally advanced and distant disease. Lesions generally are located on the lower extremities and have an increased propensity for ulceration. Acral lentiginous melanoma is the most common melanoma subtype found in African American patients.6
  • In Hispanic individuals, superficial spreading melanoma is the most common melanoma subtype. Lower extremity lesions are more common relative to White individuals. Hispanic individuals have the highest rate of oral cavity melanomas across all ethnic groups.6
  • In Asian individuals, acral and subungual sites are most common. Specifically, Pacific Islanders have the highest proportion of mucosal melanomas across all ethnic groups.6

Key clinical features in people with darker skin tones

Melanomas are found more often on the palms, soles, nail units, oral cavity, and mucosae.6 The melanomas have the same clinical and dermoscopic features found in individuals with lighter skin tones.

Worth noting

Factors that may contribute to the diagnosis of more advanced melanomas in racial/ethnic minorities in the United States include:

  • decreased access to health care based on lack of health insurance and low socioeconomic status,
  • less awareness of the risk of melanoma among patients and health care providers because melanoma is less common in persons of color, and
  • lesions found in areas less likely to be seen in screening examinations, such as the soles of the feet and the oral and genital mucosae.

Health disparity highlight

  • In a large US study of 96,953 patients with a diagnosis of cutaneous melanoma from 1992 to 2009, the proportion of later-stage melanoma—stages II to IV—was greater in Black patients compared to White patients.7
  • Based on this same data set, White patients had the longest survival time (P <. 05), followed by Hispanic (P < .05), Asian American/Native American/Pacific Islander (P < .05), and Black (P < .05) patients, respectively.7
  • In Miami-Dade County, one study of 1690 melanoma cases found that 48% of Black patients had regional or distant disease at presentation compared to 22% of White patients (P = .015).5 Analysis of multiple factors found that only race was a significant predictor for late-stage melanoma (P < .001). Black patients in this study were 3 times more likely than others to be diagnosed with melanoma at a late stage (P = .07).5
  • Black patients in the United States are more likely to have a delayed time from diagnosis to definitive surgery even when researchers controlled for type of health insurance and stage of diagnosis.8

Final thoughts

Efforts are needed to overcome these disparities by:

  • educating patients with skin of color and their health care providers about the risks of advanced melanoma with the goal of prevention and earlier diagnosis;
  • breaking down barriers to care caused by poverty, lack of health insurance, and systemic racism; and
  • eliminating factors that lead to delays from diagnosis to definitive surgery.

THE COMPARISON

A Acral lentiginous melanoma on the sole of the foot of a 30-year-old Black woman. The depth of the lesion was 2 mm with a positive sentinel lymph node biopsy.

B Nodular melanoma on the shoulder of a 63-year-old Hispanic woman. The depth of the lesion was 5.5 mm with a positive sentinel lymph node biopsy.

Melanoma occurs less frequently in individuals with darker skin types than in those with lighter skin types but is associated with higher rates of morbidity and mortality in this patient population.1-7 In the cases shown here (A and B), both patients had advanced melanomas with large primary lesions and lymph node metastases.

Melanoma

Epidemiology

A systematic review by Higgins et al6 reported the following on the epidemiology of melanomas in patients with skin of color:

  • African Americans have deeper tumors at the time of diagnosis, in addition to increased rates of regionally advanced and distant disease. Lesions generally are located on the lower extremities and have an increased propensity for ulceration. Acral lentiginous melanoma is the most common melanoma subtype found in African American patients.6
  • In Hispanic individuals, superficial spreading melanoma is the most common melanoma subtype. Lower extremity lesions are more common relative to White individuals. Hispanic individuals have the highest rate of oral cavity melanomas across all ethnic groups.6
  • In Asian individuals, acral and subungual sites are most common. Specifically, Pacific Islanders have the highest proportion of mucosal melanomas across all ethnic groups.6

Key clinical features in people with darker skin tones

Melanomas are found more often on the palms, soles, nail units, oral cavity, and mucosae.6 The melanomas have the same clinical and dermoscopic features found in individuals with lighter skin tones.

Worth noting

Factors that may contribute to the diagnosis of more advanced melanomas in racial/ethnic minorities in the United States include:

  • decreased access to health care based on lack of health insurance and low socioeconomic status,
  • less awareness of the risk of melanoma among patients and health care providers because melanoma is less common in persons of color, and
  • lesions found in areas less likely to be seen in screening examinations, such as the soles of the feet and the oral and genital mucosae.

Health disparity highlight

  • In a large US study of 96,953 patients with a diagnosis of cutaneous melanoma from 1992 to 2009, the proportion of later-stage melanoma—stages II to IV—was greater in Black patients compared to White patients.7
  • Based on this same data set, White patients had the longest survival time (P <. 05), followed by Hispanic (P < .05), Asian American/Native American/Pacific Islander (P < .05), and Black (P < .05) patients, respectively.7
  • In Miami-Dade County, one study of 1690 melanoma cases found that 48% of Black patients had regional or distant disease at presentation compared to 22% of White patients (P = .015).5 Analysis of multiple factors found that only race was a significant predictor for late-stage melanoma (P < .001). Black patients in this study were 3 times more likely than others to be diagnosed with melanoma at a late stage (P = .07).5
  • Black patients in the United States are more likely to have a delayed time from diagnosis to definitive surgery even when researchers controlled for type of health insurance and stage of diagnosis.8

Final thoughts

Efforts are needed to overcome these disparities by:

  • educating patients with skin of color and their health care providers about the risks of advanced melanoma with the goal of prevention and earlier diagnosis;
  • breaking down barriers to care caused by poverty, lack of health insurance, and systemic racism; and
  • eliminating factors that lead to delays from diagnosis to definitive surgery.
References

1. Wu XC, Eide MJ, King J, et al. Racial and ethnic variations in incidence and survival of cutaneous melanoma in the United States, 1999-2006. J Am Acad Dermatol. 2011;65(5 suppl 1):S26-S37. doi: 10.1016/j.jaad.2001.05.034

2. Cormier JN, Xing Y, Ding M, et al. Ethnic differences among patients with cutaneous melanoma. Arch Intern Med. 2006;166:1907-1914. doi: 10.1001/archinte.166.17.1907

3. Cress RD, Holly EA. Incidence of cutaneous melanoma among non-Hispanic whites, Hispanics, Asians, and blacks: an analysis of California cancer registry data, 1988-93. Cancer Causes Control. 1997;8:246-252. doi: 10.1023/a:1018432632528

4. Hu S, Parker DF, Thomas AG, et al. Advanced presentation of melanoma in African Americans: the Miami-Dade County experience. J Am Acad Dermatol. 2004;51:1031-1032. doi: 10.1016/ j.jaad.2004.05.005

5. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142: 704-708. doi: 10.1001/archderm.142.6.704

6. Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801. doi: 10.1097/DSS.0000000000001759

7. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival [published online July 28, 2016]. J Am Acad Dermatol. 2016;75:983-991. doi: 10.1016/j.jaad.2016.06.006

8. Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016) [published online August 27, 2020]. J Am Acad Dermatol. 2021;84:1585-1593. doi: 10.1016/ j.jaad.2020.08.097

References

1. Wu XC, Eide MJ, King J, et al. Racial and ethnic variations in incidence and survival of cutaneous melanoma in the United States, 1999-2006. J Am Acad Dermatol. 2011;65(5 suppl 1):S26-S37. doi: 10.1016/j.jaad.2001.05.034

2. Cormier JN, Xing Y, Ding M, et al. Ethnic differences among patients with cutaneous melanoma. Arch Intern Med. 2006;166:1907-1914. doi: 10.1001/archinte.166.17.1907

3. Cress RD, Holly EA. Incidence of cutaneous melanoma among non-Hispanic whites, Hispanics, Asians, and blacks: an analysis of California cancer registry data, 1988-93. Cancer Causes Control. 1997;8:246-252. doi: 10.1023/a:1018432632528

4. Hu S, Parker DF, Thomas AG, et al. Advanced presentation of melanoma in African Americans: the Miami-Dade County experience. J Am Acad Dermatol. 2004;51:1031-1032. doi: 10.1016/ j.jaad.2004.05.005

5. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142: 704-708. doi: 10.1001/archderm.142.6.704

6. Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801. doi: 10.1097/DSS.0000000000001759

7. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival [published online July 28, 2016]. J Am Acad Dermatol. 2016;75:983-991. doi: 10.1016/j.jaad.2016.06.006

8. Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016) [published online August 27, 2020]. J Am Acad Dermatol. 2021;84:1585-1593. doi: 10.1016/ j.jaad.2020.08.097

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Melanoma

Article Type
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Melanoma
Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Acral lentiginous melanoma on the sole of the foot in a 30-year-old Black woman. The depth of the lesion was 2 mm with a positive sentinel lymph node biopsy.

B Nodular melanoma on the shoulder of a 63-year-old Hispanic woman. The depth of the lesion was 5.5 mm with a positive sentinel lymph node biopsy.

 

Melanoma occurs less frequently in individuals with darker skin types than in lighter skin types but is associated with higher rates of morbidity and mortality in this patient population.1-7 In the cases shown here (A and B), both patients had advanced melanomas with large primary lesions and lymph node metastases.

Epidemiology

A systematic review by Higgins et al6 reported the following on the epidemiology of melanomas in patients with skin of color:

  • African Americans have deeper tumors at the time of diagnosis, in addition to increased rates of regionally advanced and distant disease. Lesions generally are located on the lower extremities and have an increased propensity for ulceration. Acral lentiginous melanoma is the most common melanoma subtype found in African American patients.6
  • In Hispanic individuals, superficial spreading melanoma is the most common melanoma subtype. Lower extremity lesions are more common relative to White individuals. Hispanic individuals have the highest rate of oral cavity melanomas across all ethnic groups.6
  • In Asian individuals, acral and subungual sites are most common. Specifically, Pacific Islanders have the highest proportion of mucosal melanomas across all ethnic groups.6
 

Key clinical features in people with darker skin tones

Melanomas are found more often on the palms, soles, nail units, oral cavity, and mucosae.6 The melanomas have the same clinical and dermoscopic features found in individuals with lighter skin tones.

Worth noting

Factors that may contribute to the diagnosis of more advanced melanomas in racial/ethnic minorities in the United States include:

  • decreased access to health care based on lack of health insurance and low socioeconomic status,
  • less awareness of the risk of melanoma among patients and health care providers because melanoma is less common in persons of color, and
  • lesions found in areas less likely to be seen in screening examinations, such as the soles of the feet and the oral and genital mucosae.

Health disparity highlight

  • In a large US study of 96,953 patients with a diagnosis of cutaneous melanoma from 1992 to 2009, the proportion of later-stage melanoma—stages II to IV—was greater in Black patients compared to White patients.7
  • Based on this same data set, White patients had the longest survival time (P<.05), followed by Hispanic (P<.05), Asian American/Native American/Pacific Islander (P<.05), and Black (P<.05) patients, respectively.7
  • In Miami-Dade County, one study of 1690 melanoma cases found that 48% of Black patients had regional or distant disease at presentation compared to 22% of White patients (P=.015).5 Analysis of multiple factors found that only race was a significant predictor for late-stage melanoma (P<.001). Black patients in this study were 3 times more likely than others to be diagnosed with melanoma at a late stage (P=.07).5
  • Black patients in the United States are more likely to have a delayed time from diagnosis to definitive surgery even when controlled for type of health insurance and stage of diagnosis.8

Final thoughts

Efforts are needed to overcome these disparities by:

  • educating patients with skin of color and their health care providers about the risks of advanced melanoma with the goal of prevention and earlier diagnosis;
  • breaking down barriers to care caused by poverty, lack of health insurance, and systemic racism; and
  • eliminating factors that lead to delays from diagnosis to definitive surgery.
References
  1. Wu XC, Eide MJ, King J, et al. Racial and ethnic variations in incidence and survival of cutaneous melanoma in the United States, 1999-2006. J Am Acad Dermatol. 2011;65(5 suppl 1):S26-S37. doi:10.1016/j.jaad.2001.05.034
  2. Cormier JN, Xing Y, Ding M, et al. Ethnic differences among patients with cutaneous melanoma. Arch Intern Med. 2006;166:1907-1914. doi:10.1001/archinte.166.17.1907
  3. Cress RD, Holly EA. Incidence of cutaneous melanoma among non-Hispanic whites, Hispanics, Asians, and blacks: an analysis of California cancer registry data, 1988-93. Cancer Causes Control. 1997;8:246-252. doi:10.1023/a:1018432632528
  4. Hu S, Parker DF, Thomas AG, et al. Advanced presentation of melanoma in African Americans: the Miami-Dade County experience. J Am Acad Dermatol. 2004;51:1031-1032. doi:10.1016/j. jaad.2004.05.005
  5. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142:704-708. doi:10.1001/archderm.142.6.704
  6. Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801. doi:10.1097/DSS.0000000000001759
  7. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival [published online July 28, 2016]. J Am Acad Dermatol. 2016;75:983-991. doi:10.1016/j.jaad.2016.06.006
  8. Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016)[published online August 27, 2020]. J Am Acad Dermatol. 2021;84:1585-1593. doi:10.1016/j. jaad.2020.08.097
Article PDF
Author and Disclosure Information

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

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

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

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

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

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

Author and Disclosure Information

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

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

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

Article PDF
Article PDF

Melanoma
Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Acral lentiginous melanoma on the sole of the foot in a 30-year-old Black woman. The depth of the lesion was 2 mm with a positive sentinel lymph node biopsy.

B Nodular melanoma on the shoulder of a 63-year-old Hispanic woman. The depth of the lesion was 5.5 mm with a positive sentinel lymph node biopsy.

 

Melanoma occurs less frequently in individuals with darker skin types than in lighter skin types but is associated with higher rates of morbidity and mortality in this patient population.1-7 In the cases shown here (A and B), both patients had advanced melanomas with large primary lesions and lymph node metastases.

Epidemiology

A systematic review by Higgins et al6 reported the following on the epidemiology of melanomas in patients with skin of color:

  • African Americans have deeper tumors at the time of diagnosis, in addition to increased rates of regionally advanced and distant disease. Lesions generally are located on the lower extremities and have an increased propensity for ulceration. Acral lentiginous melanoma is the most common melanoma subtype found in African American patients.6
  • In Hispanic individuals, superficial spreading melanoma is the most common melanoma subtype. Lower extremity lesions are more common relative to White individuals. Hispanic individuals have the highest rate of oral cavity melanomas across all ethnic groups.6
  • In Asian individuals, acral and subungual sites are most common. Specifically, Pacific Islanders have the highest proportion of mucosal melanomas across all ethnic groups.6
 

Key clinical features in people with darker skin tones

Melanomas are found more often on the palms, soles, nail units, oral cavity, and mucosae.6 The melanomas have the same clinical and dermoscopic features found in individuals with lighter skin tones.

Worth noting

Factors that may contribute to the diagnosis of more advanced melanomas in racial/ethnic minorities in the United States include:

  • decreased access to health care based on lack of health insurance and low socioeconomic status,
  • less awareness of the risk of melanoma among patients and health care providers because melanoma is less common in persons of color, and
  • lesions found in areas less likely to be seen in screening examinations, such as the soles of the feet and the oral and genital mucosae.

Health disparity highlight

  • In a large US study of 96,953 patients with a diagnosis of cutaneous melanoma from 1992 to 2009, the proportion of later-stage melanoma—stages II to IV—was greater in Black patients compared to White patients.7
  • Based on this same data set, White patients had the longest survival time (P<.05), followed by Hispanic (P<.05), Asian American/Native American/Pacific Islander (P<.05), and Black (P<.05) patients, respectively.7
  • In Miami-Dade County, one study of 1690 melanoma cases found that 48% of Black patients had regional or distant disease at presentation compared to 22% of White patients (P=.015).5 Analysis of multiple factors found that only race was a significant predictor for late-stage melanoma (P<.001). Black patients in this study were 3 times more likely than others to be diagnosed with melanoma at a late stage (P=.07).5
  • Black patients in the United States are more likely to have a delayed time from diagnosis to definitive surgery even when controlled for type of health insurance and stage of diagnosis.8

Final thoughts

Efforts are needed to overcome these disparities by:

  • educating patients with skin of color and their health care providers about the risks of advanced melanoma with the goal of prevention and earlier diagnosis;
  • breaking down barriers to care caused by poverty, lack of health insurance, and systemic racism; and
  • eliminating factors that lead to delays from diagnosis to definitive surgery.

Melanoma
Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Acral lentiginous melanoma on the sole of the foot in a 30-year-old Black woman. The depth of the lesion was 2 mm with a positive sentinel lymph node biopsy.

B Nodular melanoma on the shoulder of a 63-year-old Hispanic woman. The depth of the lesion was 5.5 mm with a positive sentinel lymph node biopsy.

 

Melanoma occurs less frequently in individuals with darker skin types than in lighter skin types but is associated with higher rates of morbidity and mortality in this patient population.1-7 In the cases shown here (A and B), both patients had advanced melanomas with large primary lesions and lymph node metastases.

Epidemiology

A systematic review by Higgins et al6 reported the following on the epidemiology of melanomas in patients with skin of color:

  • African Americans have deeper tumors at the time of diagnosis, in addition to increased rates of regionally advanced and distant disease. Lesions generally are located on the lower extremities and have an increased propensity for ulceration. Acral lentiginous melanoma is the most common melanoma subtype found in African American patients.6
  • In Hispanic individuals, superficial spreading melanoma is the most common melanoma subtype. Lower extremity lesions are more common relative to White individuals. Hispanic individuals have the highest rate of oral cavity melanomas across all ethnic groups.6
  • In Asian individuals, acral and subungual sites are most common. Specifically, Pacific Islanders have the highest proportion of mucosal melanomas across all ethnic groups.6
 

Key clinical features in people with darker skin tones

Melanomas are found more often on the palms, soles, nail units, oral cavity, and mucosae.6 The melanomas have the same clinical and dermoscopic features found in individuals with lighter skin tones.

Worth noting

Factors that may contribute to the diagnosis of more advanced melanomas in racial/ethnic minorities in the United States include:

  • decreased access to health care based on lack of health insurance and low socioeconomic status,
  • less awareness of the risk of melanoma among patients and health care providers because melanoma is less common in persons of color, and
  • lesions found in areas less likely to be seen in screening examinations, such as the soles of the feet and the oral and genital mucosae.

Health disparity highlight

  • In a large US study of 96,953 patients with a diagnosis of cutaneous melanoma from 1992 to 2009, the proportion of later-stage melanoma—stages II to IV—was greater in Black patients compared to White patients.7
  • Based on this same data set, White patients had the longest survival time (P<.05), followed by Hispanic (P<.05), Asian American/Native American/Pacific Islander (P<.05), and Black (P<.05) patients, respectively.7
  • In Miami-Dade County, one study of 1690 melanoma cases found that 48% of Black patients had regional or distant disease at presentation compared to 22% of White patients (P=.015).5 Analysis of multiple factors found that only race was a significant predictor for late-stage melanoma (P<.001). Black patients in this study were 3 times more likely than others to be diagnosed with melanoma at a late stage (P=.07).5
  • Black patients in the United States are more likely to have a delayed time from diagnosis to definitive surgery even when controlled for type of health insurance and stage of diagnosis.8

Final thoughts

Efforts are needed to overcome these disparities by:

  • educating patients with skin of color and their health care providers about the risks of advanced melanoma with the goal of prevention and earlier diagnosis;
  • breaking down barriers to care caused by poverty, lack of health insurance, and systemic racism; and
  • eliminating factors that lead to delays from diagnosis to definitive surgery.
References
  1. Wu XC, Eide MJ, King J, et al. Racial and ethnic variations in incidence and survival of cutaneous melanoma in the United States, 1999-2006. J Am Acad Dermatol. 2011;65(5 suppl 1):S26-S37. doi:10.1016/j.jaad.2001.05.034
  2. Cormier JN, Xing Y, Ding M, et al. Ethnic differences among patients with cutaneous melanoma. Arch Intern Med. 2006;166:1907-1914. doi:10.1001/archinte.166.17.1907
  3. Cress RD, Holly EA. Incidence of cutaneous melanoma among non-Hispanic whites, Hispanics, Asians, and blacks: an analysis of California cancer registry data, 1988-93. Cancer Causes Control. 1997;8:246-252. doi:10.1023/a:1018432632528
  4. Hu S, Parker DF, Thomas AG, et al. Advanced presentation of melanoma in African Americans: the Miami-Dade County experience. J Am Acad Dermatol. 2004;51:1031-1032. doi:10.1016/j. jaad.2004.05.005
  5. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142:704-708. doi:10.1001/archderm.142.6.704
  6. Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801. doi:10.1097/DSS.0000000000001759
  7. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival [published online July 28, 2016]. J Am Acad Dermatol. 2016;75:983-991. doi:10.1016/j.jaad.2016.06.006
  8. Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016)[published online August 27, 2020]. J Am Acad Dermatol. 2021;84:1585-1593. doi:10.1016/j. jaad.2020.08.097
References
  1. Wu XC, Eide MJ, King J, et al. Racial and ethnic variations in incidence and survival of cutaneous melanoma in the United States, 1999-2006. J Am Acad Dermatol. 2011;65(5 suppl 1):S26-S37. doi:10.1016/j.jaad.2001.05.034
  2. Cormier JN, Xing Y, Ding M, et al. Ethnic differences among patients with cutaneous melanoma. Arch Intern Med. 2006;166:1907-1914. doi:10.1001/archinte.166.17.1907
  3. Cress RD, Holly EA. Incidence of cutaneous melanoma among non-Hispanic whites, Hispanics, Asians, and blacks: an analysis of California cancer registry data, 1988-93. Cancer Causes Control. 1997;8:246-252. doi:10.1023/a:1018432632528
  4. Hu S, Parker DF, Thomas AG, et al. Advanced presentation of melanoma in African Americans: the Miami-Dade County experience. J Am Acad Dermatol. 2004;51:1031-1032. doi:10.1016/j. jaad.2004.05.005
  5. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142:704-708. doi:10.1001/archderm.142.6.704
  6. Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801. doi:10.1097/DSS.0000000000001759
  7. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival [published online July 28, 2016]. J Am Acad Dermatol. 2016;75:983-991. doi:10.1016/j.jaad.2016.06.006
  8. Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016)[published online August 27, 2020]. J Am Acad Dermatol. 2021;84:1585-1593. doi:10.1016/j. jaad.2020.08.097
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Central centrifugal cicatricial alopecia

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Central centrifugal cicatricial alopecia

THE PRESENTATION

A Early central centrifugal cicatricial alopecia with a small central patch of hair loss in a 45-year-old Black woman.

B Late central centrifugal cicatricial alopecia with a large central patch of hair loss in a 43-year-old Black woman.

Central centrifugal cicatricial alopecia

Scarring alopecia is a collection of hair loss disorders including chronic cutaneous lupus erythematosus (discoid lupus), lichen planopilaris, dissecting cellulitis, acne keloidalis, and central centrifugal cicatricial alopecia.1 CCCA (formerly hot comb alopecia or follicular degeneration syndrome) is a progressive, scarring, inflammatory alopecia and represents the most common form of scarring alopecia in women of African descent. It results in permanent destruction of hair follicles.

 

Epidemiology

CCCA predominantly affects women of African descent but also may affect men. The prevalence of CCCA in those of African descent has varied in the literature. Khumalo2 reported a prevalence of 1.2% for women younger than 50 years and 6.7% in women older than 50 years. CCCA has been reported in other ethnic groups, such as those of Asian descent.3

Historically, hair care practices that are more common in those of African descent, such as high-tension hairstyles as well as heat and chemical hair relaxers, were implicated in the development of CCCA. However, the causes of CCCA are most likely multifactorial, including family history, genetic mutations, and hair care practices.4-7PADI3 mutations likely predispose some women to CCCA. Mutations in PADI3, which encodes peptidyl arginine deiminase 3 (an enzyme that modifies proteins crucial for the formation of hair shafts), were found in some patients with CCCA.8 Moreover, other genetic defects also likely play a role.7

Key clinical features

Early recognition is key for patients with CCCA.

  • CCCA begins in the central scalp (crown area, vertex) and spreads centrifugally.
  • Scalp symptoms such as tenderness, pain, a tingling or crawling sensation, and itching may occur.9 Some patients may not have any symptoms at all, and hair loss may progress painlessly.
  • Central hair breakage—forme fruste CCCA—may be a presenting sign of CCCA.9
  • Loss of follicular ostia and mottled hypopigmented and hyperpigmented macules are common findings.6
  • CCCA can be diagnosed clinically and by histopathology.

Worth noting

Patients may experience hair loss and scalp symptoms for years before seeking medical evaluation. In some cultures, hair breakage or itching on the top of the scalp may be viewed as a normal occurrence in life.

It is important to set patient expectations that CCCA is a scarring alopecia, and the initial goal often is to maintain the patient's existing hair. However, hair and areas responding to treatment should still be treated. Without any intervention, the resulting scarring from CCCA may permanently scar follicles on the entire scalp.

Continue to: Due to the inflammatory...

 

 

Due to the inflammatory nature of CCCA, potent topical corticosteroids (eg, clobetasol propionate), intralesional corticosteroids (eg, triamcinolone acetonide), and oral antiinflammatory agents (eg, doxycycline) are utilized in the treatment of CCCA. Minoxidil is another treatment option. Adjuvant therapies such as topical metformin also have been tried.10 Importantly, treatment of CCCA may halt further permanent destruction of hair follicles, but scalp symptoms may reappear periodically and require re-treatment with anti-inflammatory agents.

Health care highlight

Thorough scalp examination and awareness of clinical features of CCCA may prompt earlier diagnosis and prevent future severe permanent alopecia. Clinicians should encourage patients with suggestive signs or symptoms of CCCA to seek care from a dermatologist.

References

1. Sperling LC. Scarring alopecia and the dermatopathologist. J Cutan Pathol. 2001;28:333-342. doi:10.1034/ j.1600-0560.2001.280701.x

2. Khumalo NP. Prevalence of central centrifugal cicatricial alopecia. Arch Dermatol. 2011;147:1453-1454. doi:10.1001/ archderm.147.12.1453

3. Su HJ, Cheng AY, Liu CH, et al. Primary scarring alopecia: a retrospective study of 89 patients in Taiwan [published online January 16, 2018]. J Dermatol. 2018;45:450-455. doi:10.1111/ 1346-8138.14217

4. Sperling LC, Cowper SE. The histopathology of primary cicatricial alopecia. Semin Cutan Med Surg. 2006;25:41-50

5. Dlova NC, Forder M. Central centrifugal cicatricial alopecia: possible familial aetiology in two African families from South Africa. Int J Dermatol. 2012;51(supp 1):17-20, 20-23.

6. Ogunleye TA, Quinn CR, McMichael A. Alopecia. In: Taylor SC, Kelly AP, Lim HW, et al, eds. Dermatology for Skin of Color. McGraw Hill; 2016:253-264.

7. Uitto J. Genetic susceptibility to alopecia [published online February 13, 2019]. N Engl J Med. 2019;380:873-876. doi:10.1056/ NEJMe1900042

8. Malki L, Sarig O, Romano MT, et al. Variant PADI3 in central centrifugal cicatricial alopecia. N Engl J Med. 2019;380:833-841.

9. Callender VD, Wright DR, Davis EC, et al. Hair breakage as a presenting sign of early or occult central centrifugal cicatricial alopecia: clinicopathologic findings in 9 patients. Arch Dermatol. 2012;148:1047-1052.

10. Araoye EF, Thomas JAL, Aguh CU. Hair regrowth in 2 patients with recalcitrant central centrifugal cicatricial alopecia after use of topical metformin. JAAD Case Rep. 2020;6:106-108. doi:10.1016/ j.jdcr.2019.12.008.

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

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

The authors reported no potential conflict of interest relevant to this article.

Simultaneously published in Cutis and The Journal of Family Practice.

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

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

The authors reported no potential conflict of interest relevant to this article.

Simultaneously published in Cutis and The Journal of Family Practice.

Author and Disclosure Information

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

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

The authors reported no potential conflict of interest relevant to this article.

Simultaneously published in Cutis and The Journal of Family Practice.

Article PDF
Article PDF

THE PRESENTATION

A Early central centrifugal cicatricial alopecia with a small central patch of hair loss in a 45-year-old Black woman.

B Late central centrifugal cicatricial alopecia with a large central patch of hair loss in a 43-year-old Black woman.

Central centrifugal cicatricial alopecia

Scarring alopecia is a collection of hair loss disorders including chronic cutaneous lupus erythematosus (discoid lupus), lichen planopilaris, dissecting cellulitis, acne keloidalis, and central centrifugal cicatricial alopecia.1 CCCA (formerly hot comb alopecia or follicular degeneration syndrome) is a progressive, scarring, inflammatory alopecia and represents the most common form of scarring alopecia in women of African descent. It results in permanent destruction of hair follicles.

 

Epidemiology

CCCA predominantly affects women of African descent but also may affect men. The prevalence of CCCA in those of African descent has varied in the literature. Khumalo2 reported a prevalence of 1.2% for women younger than 50 years and 6.7% in women older than 50 years. CCCA has been reported in other ethnic groups, such as those of Asian descent.3

Historically, hair care practices that are more common in those of African descent, such as high-tension hairstyles as well as heat and chemical hair relaxers, were implicated in the development of CCCA. However, the causes of CCCA are most likely multifactorial, including family history, genetic mutations, and hair care practices.4-7PADI3 mutations likely predispose some women to CCCA. Mutations in PADI3, which encodes peptidyl arginine deiminase 3 (an enzyme that modifies proteins crucial for the formation of hair shafts), were found in some patients with CCCA.8 Moreover, other genetic defects also likely play a role.7

Key clinical features

Early recognition is key for patients with CCCA.

  • CCCA begins in the central scalp (crown area, vertex) and spreads centrifugally.
  • Scalp symptoms such as tenderness, pain, a tingling or crawling sensation, and itching may occur.9 Some patients may not have any symptoms at all, and hair loss may progress painlessly.
  • Central hair breakage—forme fruste CCCA—may be a presenting sign of CCCA.9
  • Loss of follicular ostia and mottled hypopigmented and hyperpigmented macules are common findings.6
  • CCCA can be diagnosed clinically and by histopathology.

Worth noting

Patients may experience hair loss and scalp symptoms for years before seeking medical evaluation. In some cultures, hair breakage or itching on the top of the scalp may be viewed as a normal occurrence in life.

It is important to set patient expectations that CCCA is a scarring alopecia, and the initial goal often is to maintain the patient's existing hair. However, hair and areas responding to treatment should still be treated. Without any intervention, the resulting scarring from CCCA may permanently scar follicles on the entire scalp.

Continue to: Due to the inflammatory...

 

 

Due to the inflammatory nature of CCCA, potent topical corticosteroids (eg, clobetasol propionate), intralesional corticosteroids (eg, triamcinolone acetonide), and oral antiinflammatory agents (eg, doxycycline) are utilized in the treatment of CCCA. Minoxidil is another treatment option. Adjuvant therapies such as topical metformin also have been tried.10 Importantly, treatment of CCCA may halt further permanent destruction of hair follicles, but scalp symptoms may reappear periodically and require re-treatment with anti-inflammatory agents.

Health care highlight

Thorough scalp examination and awareness of clinical features of CCCA may prompt earlier diagnosis and prevent future severe permanent alopecia. Clinicians should encourage patients with suggestive signs or symptoms of CCCA to seek care from a dermatologist.

THE PRESENTATION

A Early central centrifugal cicatricial alopecia with a small central patch of hair loss in a 45-year-old Black woman.

B Late central centrifugal cicatricial alopecia with a large central patch of hair loss in a 43-year-old Black woman.

Central centrifugal cicatricial alopecia

Scarring alopecia is a collection of hair loss disorders including chronic cutaneous lupus erythematosus (discoid lupus), lichen planopilaris, dissecting cellulitis, acne keloidalis, and central centrifugal cicatricial alopecia.1 CCCA (formerly hot comb alopecia or follicular degeneration syndrome) is a progressive, scarring, inflammatory alopecia and represents the most common form of scarring alopecia in women of African descent. It results in permanent destruction of hair follicles.

 

Epidemiology

CCCA predominantly affects women of African descent but also may affect men. The prevalence of CCCA in those of African descent has varied in the literature. Khumalo2 reported a prevalence of 1.2% for women younger than 50 years and 6.7% in women older than 50 years. CCCA has been reported in other ethnic groups, such as those of Asian descent.3

Historically, hair care practices that are more common in those of African descent, such as high-tension hairstyles as well as heat and chemical hair relaxers, were implicated in the development of CCCA. However, the causes of CCCA are most likely multifactorial, including family history, genetic mutations, and hair care practices.4-7PADI3 mutations likely predispose some women to CCCA. Mutations in PADI3, which encodes peptidyl arginine deiminase 3 (an enzyme that modifies proteins crucial for the formation of hair shafts), were found in some patients with CCCA.8 Moreover, other genetic defects also likely play a role.7

Key clinical features

Early recognition is key for patients with CCCA.

  • CCCA begins in the central scalp (crown area, vertex) and spreads centrifugally.
  • Scalp symptoms such as tenderness, pain, a tingling or crawling sensation, and itching may occur.9 Some patients may not have any symptoms at all, and hair loss may progress painlessly.
  • Central hair breakage—forme fruste CCCA—may be a presenting sign of CCCA.9
  • Loss of follicular ostia and mottled hypopigmented and hyperpigmented macules are common findings.6
  • CCCA can be diagnosed clinically and by histopathology.

Worth noting

Patients may experience hair loss and scalp symptoms for years before seeking medical evaluation. In some cultures, hair breakage or itching on the top of the scalp may be viewed as a normal occurrence in life.

It is important to set patient expectations that CCCA is a scarring alopecia, and the initial goal often is to maintain the patient's existing hair. However, hair and areas responding to treatment should still be treated. Without any intervention, the resulting scarring from CCCA may permanently scar follicles on the entire scalp.

Continue to: Due to the inflammatory...

 

 

Due to the inflammatory nature of CCCA, potent topical corticosteroids (eg, clobetasol propionate), intralesional corticosteroids (eg, triamcinolone acetonide), and oral antiinflammatory agents (eg, doxycycline) are utilized in the treatment of CCCA. Minoxidil is another treatment option. Adjuvant therapies such as topical metformin also have been tried.10 Importantly, treatment of CCCA may halt further permanent destruction of hair follicles, but scalp symptoms may reappear periodically and require re-treatment with anti-inflammatory agents.

Health care highlight

Thorough scalp examination and awareness of clinical features of CCCA may prompt earlier diagnosis and prevent future severe permanent alopecia. Clinicians should encourage patients with suggestive signs or symptoms of CCCA to seek care from a dermatologist.

References

1. Sperling LC. Scarring alopecia and the dermatopathologist. J Cutan Pathol. 2001;28:333-342. doi:10.1034/ j.1600-0560.2001.280701.x

2. Khumalo NP. Prevalence of central centrifugal cicatricial alopecia. Arch Dermatol. 2011;147:1453-1454. doi:10.1001/ archderm.147.12.1453

3. Su HJ, Cheng AY, Liu CH, et al. Primary scarring alopecia: a retrospective study of 89 patients in Taiwan [published online January 16, 2018]. J Dermatol. 2018;45:450-455. doi:10.1111/ 1346-8138.14217

4. Sperling LC, Cowper SE. The histopathology of primary cicatricial alopecia. Semin Cutan Med Surg. 2006;25:41-50

5. Dlova NC, Forder M. Central centrifugal cicatricial alopecia: possible familial aetiology in two African families from South Africa. Int J Dermatol. 2012;51(supp 1):17-20, 20-23.

6. Ogunleye TA, Quinn CR, McMichael A. Alopecia. In: Taylor SC, Kelly AP, Lim HW, et al, eds. Dermatology for Skin of Color. McGraw Hill; 2016:253-264.

7. Uitto J. Genetic susceptibility to alopecia [published online February 13, 2019]. N Engl J Med. 2019;380:873-876. doi:10.1056/ NEJMe1900042

8. Malki L, Sarig O, Romano MT, et al. Variant PADI3 in central centrifugal cicatricial alopecia. N Engl J Med. 2019;380:833-841.

9. Callender VD, Wright DR, Davis EC, et al. Hair breakage as a presenting sign of early or occult central centrifugal cicatricial alopecia: clinicopathologic findings in 9 patients. Arch Dermatol. 2012;148:1047-1052.

10. Araoye EF, Thomas JAL, Aguh CU. Hair regrowth in 2 patients with recalcitrant central centrifugal cicatricial alopecia after use of topical metformin. JAAD Case Rep. 2020;6:106-108. doi:10.1016/ j.jdcr.2019.12.008.

References

1. Sperling LC. Scarring alopecia and the dermatopathologist. J Cutan Pathol. 2001;28:333-342. doi:10.1034/ j.1600-0560.2001.280701.x

2. Khumalo NP. Prevalence of central centrifugal cicatricial alopecia. Arch Dermatol. 2011;147:1453-1454. doi:10.1001/ archderm.147.12.1453

3. Su HJ, Cheng AY, Liu CH, et al. Primary scarring alopecia: a retrospective study of 89 patients in Taiwan [published online January 16, 2018]. J Dermatol. 2018;45:450-455. doi:10.1111/ 1346-8138.14217

4. Sperling LC, Cowper SE. The histopathology of primary cicatricial alopecia. Semin Cutan Med Surg. 2006;25:41-50

5. Dlova NC, Forder M. Central centrifugal cicatricial alopecia: possible familial aetiology in two African families from South Africa. Int J Dermatol. 2012;51(supp 1):17-20, 20-23.

6. Ogunleye TA, Quinn CR, McMichael A. Alopecia. In: Taylor SC, Kelly AP, Lim HW, et al, eds. Dermatology for Skin of Color. McGraw Hill; 2016:253-264.

7. Uitto J. Genetic susceptibility to alopecia [published online February 13, 2019]. N Engl J Med. 2019;380:873-876. doi:10.1056/ NEJMe1900042

8. Malki L, Sarig O, Romano MT, et al. Variant PADI3 in central centrifugal cicatricial alopecia. N Engl J Med. 2019;380:833-841.

9. Callender VD, Wright DR, Davis EC, et al. Hair breakage as a presenting sign of early or occult central centrifugal cicatricial alopecia: clinicopathologic findings in 9 patients. Arch Dermatol. 2012;148:1047-1052.

10. Araoye EF, Thomas JAL, Aguh CU. Hair regrowth in 2 patients with recalcitrant central centrifugal cicatricial alopecia after use of topical metformin. JAAD Case Rep. 2020;6:106-108. doi:10.1016/ j.jdcr.2019.12.008.

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Central Centrifugal Cicatricial Alopecia

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Central Centrifugal Cicatricial Alopecia

Central centrifugal cicatricial alopecia
Photographs courtesy of Richard P. Usatine, MD.

THE PRESENTATION

A Early central centrifugal cicatricial alopecia with a small central patch of hair loss in a 45-year-old Black woman.

B Late central centrifugal cicatricial alopecia with a large central patch of hair loss in a 43-year-old Black woman.

Scarring alopecia is a collection of hair loss disorders including chronic cutaneous lupus erythematosus (discoid lupus), lichen planopilaris, dissecting cellulitis, acne keloidalis, and central centrifugal cicatricial alopecia (CCCA).1 Central centrifugal cicatricial alopecia (formerly hot comb alopecia or follicular degeneration syndrome) is a progressive, scarring, inflammatory alopecia and represents the most common form of scarring alopecia in women of African descent. It results in permanent destruction of hair follicles.

Epidemiology

Central centrifugal cicatricial alopecia predominantly affects women of African descent but also may affect men. The prevalence of CCCA in those of African descent has varied in the literature. Khumalo2 reported a prevalence of 1.2% for women younger than 50 years and 6.7% in women older than 50 years. Central centrifugal cicatricial alopecia has been reported in other ethnic groups, such as those of Asian descent.3

Historically, hair care practices that are more common in those of African descent, such as high-tension hairstyles as well as heat and chemical hair relaxers, were implicated in the development of CCCA. However, the causes of CCCA are most likely multifactorial, including family history, genetic mutations, and hair care practices.4-7PADI3 mutations likely predispose some women to CCCA. Mutations in PADI3, which encodes peptidyl arginine deiminase 3 (an enzyme that modifies proteins crucial for the formation of hair shafts), were found in some patients with CCCA.8 Moreover, other genetic defects also likely play a role.7

Key clinical features

Early recognition is key for patients with CCCA.

• Central centrifugal cicatricial alopecia begins in the central scalp (crown area, vertex) and spreads centrifugally.

• Scalp symptoms such as tenderness, pain, a tingling or crawling sensation, and itching may occur.9 Some patients may not have any symptoms at all, and hair loss may progress painlessly.

• Central hair breakage—forme fruste CCCA—may be a presenting sign of CCCA.9

• Loss of follicular ostia and mottled hypopigmented and hyperpigmented macules are common findings.6

• Central centrifugal cicatricial alopecia can be diagnosed clinically and by histopathology.

Worth noting

Patients may experience hair loss and scalp symptoms for years before seeking medical evaluation. In some cultures, hair breakage or itching on the top of the scalp may be viewed as a normal occurrence in life.

It is important to set patient expectations that CCCA is a scarring alopecia, and the initial goal often is to maintain the patient's existing hair. However, hair and areas responding to treatment should still be treated. Without any intervention, the resulting scarring from CCCA may permanently scar follicles on the entire scalp.

Due to the inflammatory nature of CCCA, potent topical corticosteroids (eg, clobetasol propionate), intralesional corticosteroids (eg, triamcinolone acetonide), and oral anti-inflammatory agents (eg, doxycycline) are utilized in the treatment of CCCA. Minoxidil is another treatment option. Adjuvant therapies such as topical metformin also have been tried.10 Importantly, treatment of CCCA may halt further permanent destruction of hair follicles, but scalp symptoms may reappear periodically and require re-treatment with anti-inflammatory agents.

Health care highlight

Thorough scalp examination and awareness of clinical features of CCCA may prompt earlier diagnosis and prevent future severe permanent alopecia. Clinicians should encourage patients with suggestive signs or symptoms of CCCA to seek care from a dermatologist.

References
  1. Sperling LC. Scarring alopecia and the dermatopathologist. J Cutan Pathol. 2001;28:333-342. doi:10.1034/j.1600-0560.2001 .280701.x
  2. Khumalo NP. Prevalence of central centrifugal cicatricial alopecia. Arch Dermatol. 2011;147:1453-1454. doi:10.1001/archderm.147.12.1453
  3. Su HJ, Cheng AY, Liu CH, et al. Primary scarring alopecia: a retrospective study of 89 patients in Taiwan [published online January 16, 2018]. J Dermatol. 2018;45:450-455. doi:10.1111 /1346-8138.14217
  4. Sperling LC, Cowper SE. The histopathology of primary cicatricial alopecia. Semin Cutan Med Surg. 2006;25:41-50
  5. Dlova NC, Forder M. Central centrifugal cicatricial alopecia: possible familial aetiology in two African families from South Africa. Int J Dermatol. 2012;51(supp 1):17-20, 20-23.
  6. Ogunleye TA, Quinn CR, McMichael A. Alopecia. In: Taylor SC, Kelly AP, Lim HW, et al, eds. Dermatology for Skin of Color. McGraw Hill; 2016:253-264.
  7. Uitto J. Genetic susceptibility to alopecia [published online February 13, 2019]. N Engl J Med. 2019;380:873-876. doi:10.1056 /NEJMe1900042
  8. Malki L, Sarig O, Romano MT, et al. Variant PADI3 in central centrifugal cicatricial alopecia. N Engl J Med. 2019;380:833-841.
  9. Callender VD, Wright DR, Davis EC, et al. Hair breakage as a presenting sign of early or occult central centrifugal cicatricial alopecia: clinicopathologic findings in 9 patients. Arch Dermatol. 2012;148:1047-1052.
  10. Araoye EF, Thomas JAL, Aguh CU. Hair regrowth in 2 patients with recalcitrant central centrifugal cicatricial alopecia after use of topical metformin. JAAD Case Rep. 2020;6:106-108. doi:10.1016/j .jdcr.2019.12.008
Article PDF
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Candrice R. Heath, MD
Assistant Professor, Department of Dermatology
Lewis Katz School of Medicine
Temple University
Philadelphia, Pennsylvania

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

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

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

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

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

Author and Disclosure Information

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

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

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

Article PDF
Article PDF

Central centrifugal cicatricial alopecia
Photographs courtesy of Richard P. Usatine, MD.

THE PRESENTATION

A Early central centrifugal cicatricial alopecia with a small central patch of hair loss in a 45-year-old Black woman.

B Late central centrifugal cicatricial alopecia with a large central patch of hair loss in a 43-year-old Black woman.

Scarring alopecia is a collection of hair loss disorders including chronic cutaneous lupus erythematosus (discoid lupus), lichen planopilaris, dissecting cellulitis, acne keloidalis, and central centrifugal cicatricial alopecia (CCCA).1 Central centrifugal cicatricial alopecia (formerly hot comb alopecia or follicular degeneration syndrome) is a progressive, scarring, inflammatory alopecia and represents the most common form of scarring alopecia in women of African descent. It results in permanent destruction of hair follicles.

Epidemiology

Central centrifugal cicatricial alopecia predominantly affects women of African descent but also may affect men. The prevalence of CCCA in those of African descent has varied in the literature. Khumalo2 reported a prevalence of 1.2% for women younger than 50 years and 6.7% in women older than 50 years. Central centrifugal cicatricial alopecia has been reported in other ethnic groups, such as those of Asian descent.3

Historically, hair care practices that are more common in those of African descent, such as high-tension hairstyles as well as heat and chemical hair relaxers, were implicated in the development of CCCA. However, the causes of CCCA are most likely multifactorial, including family history, genetic mutations, and hair care practices.4-7PADI3 mutations likely predispose some women to CCCA. Mutations in PADI3, which encodes peptidyl arginine deiminase 3 (an enzyme that modifies proteins crucial for the formation of hair shafts), were found in some patients with CCCA.8 Moreover, other genetic defects also likely play a role.7

Key clinical features

Early recognition is key for patients with CCCA.

• Central centrifugal cicatricial alopecia begins in the central scalp (crown area, vertex) and spreads centrifugally.

• Scalp symptoms such as tenderness, pain, a tingling or crawling sensation, and itching may occur.9 Some patients may not have any symptoms at all, and hair loss may progress painlessly.

• Central hair breakage—forme fruste CCCA—may be a presenting sign of CCCA.9

• Loss of follicular ostia and mottled hypopigmented and hyperpigmented macules are common findings.6

• Central centrifugal cicatricial alopecia can be diagnosed clinically and by histopathology.

Worth noting

Patients may experience hair loss and scalp symptoms for years before seeking medical evaluation. In some cultures, hair breakage or itching on the top of the scalp may be viewed as a normal occurrence in life.

It is important to set patient expectations that CCCA is a scarring alopecia, and the initial goal often is to maintain the patient's existing hair. However, hair and areas responding to treatment should still be treated. Without any intervention, the resulting scarring from CCCA may permanently scar follicles on the entire scalp.

Due to the inflammatory nature of CCCA, potent topical corticosteroids (eg, clobetasol propionate), intralesional corticosteroids (eg, triamcinolone acetonide), and oral anti-inflammatory agents (eg, doxycycline) are utilized in the treatment of CCCA. Minoxidil is another treatment option. Adjuvant therapies such as topical metformin also have been tried.10 Importantly, treatment of CCCA may halt further permanent destruction of hair follicles, but scalp symptoms may reappear periodically and require re-treatment with anti-inflammatory agents.

Health care highlight

Thorough scalp examination and awareness of clinical features of CCCA may prompt earlier diagnosis and prevent future severe permanent alopecia. Clinicians should encourage patients with suggestive signs or symptoms of CCCA to seek care from a dermatologist.

Central centrifugal cicatricial alopecia
Photographs courtesy of Richard P. Usatine, MD.

THE PRESENTATION

A Early central centrifugal cicatricial alopecia with a small central patch of hair loss in a 45-year-old Black woman.

B Late central centrifugal cicatricial alopecia with a large central patch of hair loss in a 43-year-old Black woman.

Scarring alopecia is a collection of hair loss disorders including chronic cutaneous lupus erythematosus (discoid lupus), lichen planopilaris, dissecting cellulitis, acne keloidalis, and central centrifugal cicatricial alopecia (CCCA).1 Central centrifugal cicatricial alopecia (formerly hot comb alopecia or follicular degeneration syndrome) is a progressive, scarring, inflammatory alopecia and represents the most common form of scarring alopecia in women of African descent. It results in permanent destruction of hair follicles.

Epidemiology

Central centrifugal cicatricial alopecia predominantly affects women of African descent but also may affect men. The prevalence of CCCA in those of African descent has varied in the literature. Khumalo2 reported a prevalence of 1.2% for women younger than 50 years and 6.7% in women older than 50 years. Central centrifugal cicatricial alopecia has been reported in other ethnic groups, such as those of Asian descent.3

Historically, hair care practices that are more common in those of African descent, such as high-tension hairstyles as well as heat and chemical hair relaxers, were implicated in the development of CCCA. However, the causes of CCCA are most likely multifactorial, including family history, genetic mutations, and hair care practices.4-7PADI3 mutations likely predispose some women to CCCA. Mutations in PADI3, which encodes peptidyl arginine deiminase 3 (an enzyme that modifies proteins crucial for the formation of hair shafts), were found in some patients with CCCA.8 Moreover, other genetic defects also likely play a role.7

Key clinical features

Early recognition is key for patients with CCCA.

• Central centrifugal cicatricial alopecia begins in the central scalp (crown area, vertex) and spreads centrifugally.

• Scalp symptoms such as tenderness, pain, a tingling or crawling sensation, and itching may occur.9 Some patients may not have any symptoms at all, and hair loss may progress painlessly.

• Central hair breakage—forme fruste CCCA—may be a presenting sign of CCCA.9

• Loss of follicular ostia and mottled hypopigmented and hyperpigmented macules are common findings.6

• Central centrifugal cicatricial alopecia can be diagnosed clinically and by histopathology.

Worth noting

Patients may experience hair loss and scalp symptoms for years before seeking medical evaluation. In some cultures, hair breakage or itching on the top of the scalp may be viewed as a normal occurrence in life.

It is important to set patient expectations that CCCA is a scarring alopecia, and the initial goal often is to maintain the patient's existing hair. However, hair and areas responding to treatment should still be treated. Without any intervention, the resulting scarring from CCCA may permanently scar follicles on the entire scalp.

Due to the inflammatory nature of CCCA, potent topical corticosteroids (eg, clobetasol propionate), intralesional corticosteroids (eg, triamcinolone acetonide), and oral anti-inflammatory agents (eg, doxycycline) are utilized in the treatment of CCCA. Minoxidil is another treatment option. Adjuvant therapies such as topical metformin also have been tried.10 Importantly, treatment of CCCA may halt further permanent destruction of hair follicles, but scalp symptoms may reappear periodically and require re-treatment with anti-inflammatory agents.

Health care highlight

Thorough scalp examination and awareness of clinical features of CCCA may prompt earlier diagnosis and prevent future severe permanent alopecia. Clinicians should encourage patients with suggestive signs or symptoms of CCCA to seek care from a dermatologist.

References
  1. Sperling LC. Scarring alopecia and the dermatopathologist. J Cutan Pathol. 2001;28:333-342. doi:10.1034/j.1600-0560.2001 .280701.x
  2. Khumalo NP. Prevalence of central centrifugal cicatricial alopecia. Arch Dermatol. 2011;147:1453-1454. doi:10.1001/archderm.147.12.1453
  3. Su HJ, Cheng AY, Liu CH, et al. Primary scarring alopecia: a retrospective study of 89 patients in Taiwan [published online January 16, 2018]. J Dermatol. 2018;45:450-455. doi:10.1111 /1346-8138.14217
  4. Sperling LC, Cowper SE. The histopathology of primary cicatricial alopecia. Semin Cutan Med Surg. 2006;25:41-50
  5. Dlova NC, Forder M. Central centrifugal cicatricial alopecia: possible familial aetiology in two African families from South Africa. Int J Dermatol. 2012;51(supp 1):17-20, 20-23.
  6. Ogunleye TA, Quinn CR, McMichael A. Alopecia. In: Taylor SC, Kelly AP, Lim HW, et al, eds. Dermatology for Skin of Color. McGraw Hill; 2016:253-264.
  7. Uitto J. Genetic susceptibility to alopecia [published online February 13, 2019]. N Engl J Med. 2019;380:873-876. doi:10.1056 /NEJMe1900042
  8. Malki L, Sarig O, Romano MT, et al. Variant PADI3 in central centrifugal cicatricial alopecia. N Engl J Med. 2019;380:833-841.
  9. Callender VD, Wright DR, Davis EC, et al. Hair breakage as a presenting sign of early or occult central centrifugal cicatricial alopecia: clinicopathologic findings in 9 patients. Arch Dermatol. 2012;148:1047-1052.
  10. Araoye EF, Thomas JAL, Aguh CU. Hair regrowth in 2 patients with recalcitrant central centrifugal cicatricial alopecia after use of topical metformin. JAAD Case Rep. 2020;6:106-108. doi:10.1016/j .jdcr.2019.12.008
References
  1. Sperling LC. Scarring alopecia and the dermatopathologist. J Cutan Pathol. 2001;28:333-342. doi:10.1034/j.1600-0560.2001 .280701.x
  2. Khumalo NP. Prevalence of central centrifugal cicatricial alopecia. Arch Dermatol. 2011;147:1453-1454. doi:10.1001/archderm.147.12.1453
  3. Su HJ, Cheng AY, Liu CH, et al. Primary scarring alopecia: a retrospective study of 89 patients in Taiwan [published online January 16, 2018]. J Dermatol. 2018;45:450-455. doi:10.1111 /1346-8138.14217
  4. Sperling LC, Cowper SE. The histopathology of primary cicatricial alopecia. Semin Cutan Med Surg. 2006;25:41-50
  5. Dlova NC, Forder M. Central centrifugal cicatricial alopecia: possible familial aetiology in two African families from South Africa. Int J Dermatol. 2012;51(supp 1):17-20, 20-23.
  6. Ogunleye TA, Quinn CR, McMichael A. Alopecia. In: Taylor SC, Kelly AP, Lim HW, et al, eds. Dermatology for Skin of Color. McGraw Hill; 2016:253-264.
  7. Uitto J. Genetic susceptibility to alopecia [published online February 13, 2019]. N Engl J Med. 2019;380:873-876. doi:10.1056 /NEJMe1900042
  8. Malki L, Sarig O, Romano MT, et al. Variant PADI3 in central centrifugal cicatricial alopecia. N Engl J Med. 2019;380:833-841.
  9. Callender VD, Wright DR, Davis EC, et al. Hair breakage as a presenting sign of early or occult central centrifugal cicatricial alopecia: clinicopathologic findings in 9 patients. Arch Dermatol. 2012;148:1047-1052.
  10. Araoye EF, Thomas JAL, Aguh CU. Hair regrowth in 2 patients with recalcitrant central centrifugal cicatricial alopecia after use of topical metformin. JAAD Case Rep. 2020;6:106-108. doi:10.1016/j .jdcr.2019.12.008
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Discoid lupus

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Discoid lupus

THE COMPARISON

A Multicolored (pink, brown, and white) indurated plaques in a butterfly distribution on the face of a 30-year-old woman with a darker skin tone.

B Pink, elevated, indurated plaques with hypopigmentation in a butterfly distribution on the face of a 19-year-old woman with a lighter skin tone.

Cutaneous lupus erythematosus may occur with or without systemic lupus erythematosus. Discoid lupus erythematosus (DLE), a form of chronic cutaneous lupus, is most commonly found on the scalp, face, and ears.1

Discoid lupus

Epidemiology

DLE is most common in adult women (age range, 20–40 years).2 It occurs more frequently in women of African descent.3,4

Key clinical features in people with darker skin tones

Clinical features of DLE lesions include erythema, induration, follicular plugging, dyspigmentation, and scarring alopecia.1 In patients of African descent, lesions may be annular and hypopigmented to depigmented centrally with a border of hyperpigmentation. Active lesions may be painful and/or pruritic.2

DLE lesions occur in photodistributed areas, although not exclusively. Photoprotective clothing and sunscreen are an important part of the treatment plan.1 Although sunscreen is recommended for patients with DLE, those with darker skin tones may find some sunscreens cosmetically unappealing due to a mismatch with their normal skin color.5 Tinted sunscreens may be beneficial additions.

Worth noting

Approximately 5% to 25% of patients with cutaneous lupus go on to develop systemic lupus erythematosus.6

Health disparity highlight

Discoid lesions may cause cutaneous scars that are quite disfiguring and may negatively impact quality of life. Some patients may have a few scattered lesions, whereas others have extensive disease covering most of the scalp. DLE lesions of the scalp have classic clinical features including hair loss, erythema, hypopigmentation, and hyperpigmentation. The clinician’s comfort with performing a scalp examination with cultural humility is an important acquired skill and is especially important when the examination is performed on patients with more tightly coiled hair.7 For example, physicians may adopt the “compliment, discuss, and suggest” method when counseling patients.8

References

1. Bolognia JL, Jorizzo JJ, Schaffer JV, et al. Dermatology. 3rd ed. Elsevier; 2012.

2. Otberg N, Wu W-Y, McElwee KJ, et al. Diagnosis and management of primary cicatricial alopecia: part I. Skinmed. 2008;7:19-26. doi:10.1111/j.1540-9740.2007.07163.x

3. Callen JP. Chronic cutaneous lupus erythematosus. clinical, laboratory, therapeutic, and prognostic examination of 62 patients. Arch Dermatol. 1982;118:412-416. doi:10.1001/archderm.118.6.412

4. McCarty DJ, Manzi S, Medsger TA Jr, et al. Incidence of systemic lupus erythematosus. race and gender differences. Arthritis Rheum. 1995;38:1260-1270. doi:10.1002/art.1780380914

5. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. In press.

6. Zhou W, Wu H, Zhao M, et al. New insights into the progression from cutaneous lupus to systemic lupus erythematosus. Expert Rev Clin Immunol. 2020;16:829-837. doi:10.1080/17446 66X.2020.1805316

7. Grayson C, Heath C. An approach to examining tightly coiled hair among patients with hair loss in race-discordant patient-physician interactions. JAMA Dermatol. 2021;157:505-506. doi:10.1001/jamadermatol.2021.0338

8. Grayson C, Heath CR. Counseling about traction alopecia: a “compliment, discuss, and suggest” method. Cutis. 2021;108:20-22.

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

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

The authors reported no potential conflict of interest relevant to this article.

Simultaneously published in Cutis and The Journal of Family Practice.

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

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

The authors reported no potential conflict of interest relevant to this article.

Simultaneously published in Cutis and The Journal of Family Practice.

Author and Disclosure Information

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

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

The authors reported no potential conflict of interest relevant to this article.

Simultaneously published in Cutis and The Journal of Family Practice.

Article PDF
Article PDF

THE COMPARISON

A Multicolored (pink, brown, and white) indurated plaques in a butterfly distribution on the face of a 30-year-old woman with a darker skin tone.

B Pink, elevated, indurated plaques with hypopigmentation in a butterfly distribution on the face of a 19-year-old woman with a lighter skin tone.

Cutaneous lupus erythematosus may occur with or without systemic lupus erythematosus. Discoid lupus erythematosus (DLE), a form of chronic cutaneous lupus, is most commonly found on the scalp, face, and ears.1

Discoid lupus

Epidemiology

DLE is most common in adult women (age range, 20–40 years).2 It occurs more frequently in women of African descent.3,4

Key clinical features in people with darker skin tones

Clinical features of DLE lesions include erythema, induration, follicular plugging, dyspigmentation, and scarring alopecia.1 In patients of African descent, lesions may be annular and hypopigmented to depigmented centrally with a border of hyperpigmentation. Active lesions may be painful and/or pruritic.2

DLE lesions occur in photodistributed areas, although not exclusively. Photoprotective clothing and sunscreen are an important part of the treatment plan.1 Although sunscreen is recommended for patients with DLE, those with darker skin tones may find some sunscreens cosmetically unappealing due to a mismatch with their normal skin color.5 Tinted sunscreens may be beneficial additions.

Worth noting

Approximately 5% to 25% of patients with cutaneous lupus go on to develop systemic lupus erythematosus.6

Health disparity highlight

Discoid lesions may cause cutaneous scars that are quite disfiguring and may negatively impact quality of life. Some patients may have a few scattered lesions, whereas others have extensive disease covering most of the scalp. DLE lesions of the scalp have classic clinical features including hair loss, erythema, hypopigmentation, and hyperpigmentation. The clinician’s comfort with performing a scalp examination with cultural humility is an important acquired skill and is especially important when the examination is performed on patients with more tightly coiled hair.7 For example, physicians may adopt the “compliment, discuss, and suggest” method when counseling patients.8

THE COMPARISON

A Multicolored (pink, brown, and white) indurated plaques in a butterfly distribution on the face of a 30-year-old woman with a darker skin tone.

B Pink, elevated, indurated plaques with hypopigmentation in a butterfly distribution on the face of a 19-year-old woman with a lighter skin tone.

Cutaneous lupus erythematosus may occur with or without systemic lupus erythematosus. Discoid lupus erythematosus (DLE), a form of chronic cutaneous lupus, is most commonly found on the scalp, face, and ears.1

Discoid lupus

Epidemiology

DLE is most common in adult women (age range, 20–40 years).2 It occurs more frequently in women of African descent.3,4

Key clinical features in people with darker skin tones

Clinical features of DLE lesions include erythema, induration, follicular plugging, dyspigmentation, and scarring alopecia.1 In patients of African descent, lesions may be annular and hypopigmented to depigmented centrally with a border of hyperpigmentation. Active lesions may be painful and/or pruritic.2

DLE lesions occur in photodistributed areas, although not exclusively. Photoprotective clothing and sunscreen are an important part of the treatment plan.1 Although sunscreen is recommended for patients with DLE, those with darker skin tones may find some sunscreens cosmetically unappealing due to a mismatch with their normal skin color.5 Tinted sunscreens may be beneficial additions.

Worth noting

Approximately 5% to 25% of patients with cutaneous lupus go on to develop systemic lupus erythematosus.6

Health disparity highlight

Discoid lesions may cause cutaneous scars that are quite disfiguring and may negatively impact quality of life. Some patients may have a few scattered lesions, whereas others have extensive disease covering most of the scalp. DLE lesions of the scalp have classic clinical features including hair loss, erythema, hypopigmentation, and hyperpigmentation. The clinician’s comfort with performing a scalp examination with cultural humility is an important acquired skill and is especially important when the examination is performed on patients with more tightly coiled hair.7 For example, physicians may adopt the “compliment, discuss, and suggest” method when counseling patients.8

References

1. Bolognia JL, Jorizzo JJ, Schaffer JV, et al. Dermatology. 3rd ed. Elsevier; 2012.

2. Otberg N, Wu W-Y, McElwee KJ, et al. Diagnosis and management of primary cicatricial alopecia: part I. Skinmed. 2008;7:19-26. doi:10.1111/j.1540-9740.2007.07163.x

3. Callen JP. Chronic cutaneous lupus erythematosus. clinical, laboratory, therapeutic, and prognostic examination of 62 patients. Arch Dermatol. 1982;118:412-416. doi:10.1001/archderm.118.6.412

4. McCarty DJ, Manzi S, Medsger TA Jr, et al. Incidence of systemic lupus erythematosus. race and gender differences. Arthritis Rheum. 1995;38:1260-1270. doi:10.1002/art.1780380914

5. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. In press.

6. Zhou W, Wu H, Zhao M, et al. New insights into the progression from cutaneous lupus to systemic lupus erythematosus. Expert Rev Clin Immunol. 2020;16:829-837. doi:10.1080/17446 66X.2020.1805316

7. Grayson C, Heath C. An approach to examining tightly coiled hair among patients with hair loss in race-discordant patient-physician interactions. JAMA Dermatol. 2021;157:505-506. doi:10.1001/jamadermatol.2021.0338

8. Grayson C, Heath CR. Counseling about traction alopecia: a “compliment, discuss, and suggest” method. Cutis. 2021;108:20-22.

References

1. Bolognia JL, Jorizzo JJ, Schaffer JV, et al. Dermatology. 3rd ed. Elsevier; 2012.

2. Otberg N, Wu W-Y, McElwee KJ, et al. Diagnosis and management of primary cicatricial alopecia: part I. Skinmed. 2008;7:19-26. doi:10.1111/j.1540-9740.2007.07163.x

3. Callen JP. Chronic cutaneous lupus erythematosus. clinical, laboratory, therapeutic, and prognostic examination of 62 patients. Arch Dermatol. 1982;118:412-416. doi:10.1001/archderm.118.6.412

4. McCarty DJ, Manzi S, Medsger TA Jr, et al. Incidence of systemic lupus erythematosus. race and gender differences. Arthritis Rheum. 1995;38:1260-1270. doi:10.1002/art.1780380914

5. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. In press.

6. Zhou W, Wu H, Zhao M, et al. New insights into the progression from cutaneous lupus to systemic lupus erythematosus. Expert Rev Clin Immunol. 2020;16:829-837. doi:10.1080/17446 66X.2020.1805316

7. Grayson C, Heath C. An approach to examining tightly coiled hair among patients with hair loss in race-discordant patient-physician interactions. JAMA Dermatol. 2021;157:505-506. doi:10.1001/jamadermatol.2021.0338

8. Grayson C, Heath CR. Counseling about traction alopecia: a “compliment, discuss, and suggest” method. Cutis. 2021;108:20-22.

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Discoid Lupus

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Discoid Lupus

Discoid lupus
Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Multicolored (pink, brown, and white) indurated plaques in a butterfly distribution on the face of a 30-year-old woman with a darker skin tone.

B Pink, elevated, indurated plaques with hypopigmentation in a butterfly distribution on the face of a 19-year-old woman with a lighter skin tone.

Cutaneous lupus erythematosus may occur with or without systemic lupus erythematosus. Discoid lupus erythematosus (DLE), a form of chronic cutaneous lupus, is most commonly found on the scalp, face, and ears.1

Epidemiology

Discoid lupus erythematosus is most common in adult women (age range, 20–40 years).2 It occurs more frequently in women of African descent.3,4

Key clinical features in people with darker skin tones:

Clinical features of DLE lesions include erythema, induration, follicular plugging, dyspigmentation, and scarring alopecia.1 In patients of African descent, lesions may be annular and hypopigmented to depigmented centrally with a border of hyperpigmentation. Active lesions may be painful and/or pruritic.2

Discoid lupus erythematosus lesions occur in photodistributed areas, although not exclusively. Photoprotective clothing and sunscreen are an important part of the treatment plan.1 Although sunscreen is recommended for patients with DLE, those with darker skin tones may find some sunscreens cosmetically unappealing due to a mismatch with their normal skin color.5 Tinted sunscreens may be beneficial additions.

Worth noting

Approximately 5% to 25% of patients with cutaneous lupus go on to develop systemic lupus erythematosus.6

Health disparity highlight

Discoid lesions may cause cutaneous scars that are quite disfiguring and may negatively impact quality of life. Some patients may have a few scattered lesions, whereas others have extensive disease covering most of the scalp. Discoid lupus erythematosus lesions of the scalp have classic clinical features including hair loss, erythema, hypopigmentation, and hyperpigmentation. The clinician’s comfort with performing a scalp examination with cultural humility is an important acquired skill and is especially important when the examination is performed on patients with more tightly coiled hair.7 For example, physicians may adopt the “compliment, discuss, and suggest” method when counseling patients.8

References
  1. Bolognia JL, Jorizzo JJ, Schaffer JV, et al. Dermatology. 3rd ed. Elsevier; 2012.
  2. Otberg N, Wu W-Y, McElwee KJ, et al. Diagnosis and management of primary cicatricial alopecia: part I. Skinmed. 2008;7:19-26. doi:10.1111/j.1540-9740.2007.07163.x
  3. Callen JP. Chronic cutaneous lupus erythematosus. clinical, laboratory, therapeutic, and prognostic examination of 62 patients. Arch Dermatol. 1982;118:412-416. doi:10.1001/archderm.118.6.412
  4. McCarty DJ, Manzi S, Medsger TA Jr, et al. Incidence of systemic lupus erythematosus. race and gender differences. Arthritis Rheum. 1995;38:1260-1270. doi:10.1002/art.1780380914
  5. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. In press.
  6. Zhou W, Wu H, Zhao M, et al. New insights into the progression from cutaneous lupus to systemic lupus erythematosus. Expert Rev Clin Immunol. 2020;16:829-837. doi:10.1080/17446 66X.2020.1805316
  7. Grayson C, Heath C. An approach to examining tightly coiled hair among patients with hair loss in race-discordant patientphysician interactions. JAMA Dermatol. 2021;157:505-506. doi:10.1001/jamadermatol.2021.0338
  8. Grayson C, Heath CR. Counseling about traction alopecia: a “compliment, discuss, and suggest” method. Cutis. 2021;108:20-22.
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Candrice R. Heath, MD
Assistant Professor, Department of Dermatology
Lewis Katz School of Medicine
Temple University
Philadelphia, Pennsylvania

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

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

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

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

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

Author and Disclosure Information

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

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

The authors report no conflict of interest.

Simultaneously published in Cutis and The Journal of Family Practice.

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Discoid lupus
Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Multicolored (pink, brown, and white) indurated plaques in a butterfly distribution on the face of a 30-year-old woman with a darker skin tone.

B Pink, elevated, indurated plaques with hypopigmentation in a butterfly distribution on the face of a 19-year-old woman with a lighter skin tone.

Cutaneous lupus erythematosus may occur with or without systemic lupus erythematosus. Discoid lupus erythematosus (DLE), a form of chronic cutaneous lupus, is most commonly found on the scalp, face, and ears.1

Epidemiology

Discoid lupus erythematosus is most common in adult women (age range, 20–40 years).2 It occurs more frequently in women of African descent.3,4

Key clinical features in people with darker skin tones:

Clinical features of DLE lesions include erythema, induration, follicular plugging, dyspigmentation, and scarring alopecia.1 In patients of African descent, lesions may be annular and hypopigmented to depigmented centrally with a border of hyperpigmentation. Active lesions may be painful and/or pruritic.2

Discoid lupus erythematosus lesions occur in photodistributed areas, although not exclusively. Photoprotective clothing and sunscreen are an important part of the treatment plan.1 Although sunscreen is recommended for patients with DLE, those with darker skin tones may find some sunscreens cosmetically unappealing due to a mismatch with their normal skin color.5 Tinted sunscreens may be beneficial additions.

Worth noting

Approximately 5% to 25% of patients with cutaneous lupus go on to develop systemic lupus erythematosus.6

Health disparity highlight

Discoid lesions may cause cutaneous scars that are quite disfiguring and may negatively impact quality of life. Some patients may have a few scattered lesions, whereas others have extensive disease covering most of the scalp. Discoid lupus erythematosus lesions of the scalp have classic clinical features including hair loss, erythema, hypopigmentation, and hyperpigmentation. The clinician’s comfort with performing a scalp examination with cultural humility is an important acquired skill and is especially important when the examination is performed on patients with more tightly coiled hair.7 For example, physicians may adopt the “compliment, discuss, and suggest” method when counseling patients.8

Discoid lupus
Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Multicolored (pink, brown, and white) indurated plaques in a butterfly distribution on the face of a 30-year-old woman with a darker skin tone.

B Pink, elevated, indurated plaques with hypopigmentation in a butterfly distribution on the face of a 19-year-old woman with a lighter skin tone.

Cutaneous lupus erythematosus may occur with or without systemic lupus erythematosus. Discoid lupus erythematosus (DLE), a form of chronic cutaneous lupus, is most commonly found on the scalp, face, and ears.1

Epidemiology

Discoid lupus erythematosus is most common in adult women (age range, 20–40 years).2 It occurs more frequently in women of African descent.3,4

Key clinical features in people with darker skin tones:

Clinical features of DLE lesions include erythema, induration, follicular plugging, dyspigmentation, and scarring alopecia.1 In patients of African descent, lesions may be annular and hypopigmented to depigmented centrally with a border of hyperpigmentation. Active lesions may be painful and/or pruritic.2

Discoid lupus erythematosus lesions occur in photodistributed areas, although not exclusively. Photoprotective clothing and sunscreen are an important part of the treatment plan.1 Although sunscreen is recommended for patients with DLE, those with darker skin tones may find some sunscreens cosmetically unappealing due to a mismatch with their normal skin color.5 Tinted sunscreens may be beneficial additions.

Worth noting

Approximately 5% to 25% of patients with cutaneous lupus go on to develop systemic lupus erythematosus.6

Health disparity highlight

Discoid lesions may cause cutaneous scars that are quite disfiguring and may negatively impact quality of life. Some patients may have a few scattered lesions, whereas others have extensive disease covering most of the scalp. Discoid lupus erythematosus lesions of the scalp have classic clinical features including hair loss, erythema, hypopigmentation, and hyperpigmentation. The clinician’s comfort with performing a scalp examination with cultural humility is an important acquired skill and is especially important when the examination is performed on patients with more tightly coiled hair.7 For example, physicians may adopt the “compliment, discuss, and suggest” method when counseling patients.8

References
  1. Bolognia JL, Jorizzo JJ, Schaffer JV, et al. Dermatology. 3rd ed. Elsevier; 2012.
  2. Otberg N, Wu W-Y, McElwee KJ, et al. Diagnosis and management of primary cicatricial alopecia: part I. Skinmed. 2008;7:19-26. doi:10.1111/j.1540-9740.2007.07163.x
  3. Callen JP. Chronic cutaneous lupus erythematosus. clinical, laboratory, therapeutic, and prognostic examination of 62 patients. Arch Dermatol. 1982;118:412-416. doi:10.1001/archderm.118.6.412
  4. McCarty DJ, Manzi S, Medsger TA Jr, et al. Incidence of systemic lupus erythematosus. race and gender differences. Arthritis Rheum. 1995;38:1260-1270. doi:10.1002/art.1780380914
  5. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. In press.
  6. Zhou W, Wu H, Zhao M, et al. New insights into the progression from cutaneous lupus to systemic lupus erythematosus. Expert Rev Clin Immunol. 2020;16:829-837. doi:10.1080/17446 66X.2020.1805316
  7. Grayson C, Heath C. An approach to examining tightly coiled hair among patients with hair loss in race-discordant patientphysician interactions. JAMA Dermatol. 2021;157:505-506. doi:10.1001/jamadermatol.2021.0338
  8. Grayson C, Heath CR. Counseling about traction alopecia: a “compliment, discuss, and suggest” method. Cutis. 2021;108:20-22.
References
  1. Bolognia JL, Jorizzo JJ, Schaffer JV, et al. Dermatology. 3rd ed. Elsevier; 2012.
  2. Otberg N, Wu W-Y, McElwee KJ, et al. Diagnosis and management of primary cicatricial alopecia: part I. Skinmed. 2008;7:19-26. doi:10.1111/j.1540-9740.2007.07163.x
  3. Callen JP. Chronic cutaneous lupus erythematosus. clinical, laboratory, therapeutic, and prognostic examination of 62 patients. Arch Dermatol. 1982;118:412-416. doi:10.1001/archderm.118.6.412
  4. McCarty DJ, Manzi S, Medsger TA Jr, et al. Incidence of systemic lupus erythematosus. race and gender differences. Arthritis Rheum. 1995;38:1260-1270. doi:10.1002/art.1780380914
  5. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. In press.
  6. Zhou W, Wu H, Zhao M, et al. New insights into the progression from cutaneous lupus to systemic lupus erythematosus. Expert Rev Clin Immunol. 2020;16:829-837. doi:10.1080/17446 66X.2020.1805316
  7. Grayson C, Heath C. An approach to examining tightly coiled hair among patients with hair loss in race-discordant patientphysician interactions. JAMA Dermatol. 2021;157:505-506. doi:10.1001/jamadermatol.2021.0338
  8. Grayson C, Heath CR. Counseling about traction alopecia: a “compliment, discuss, and suggest” method. Cutis. 2021;108:20-22.
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