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Dana Turner

Apr 26
0

Director of Equity, Diversity and Inclusion (DEDI) Call for Applications

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Director of Equity, Diversity and Inclusion (DEDI) Call for Applications
ODAC Dermatology, Aesthetic & Surgical Conference has announced a call for applications for the role of Director of Equity, Diversity and Inclusion (DEDI). This newly defined position will work closely with the ODAC Advisory Board and the @SanovaWorks_ Events Division, to promote the development and implementation of educational offerings aimed at improving cultural competence, diversity, and equity within the field of dermatology. Additionally, this role will assist in creating a conference experience conducive to a collaborative learning environment that enhances professional development and advancement for all.
To qualify for consideration, applicants should possess the following experience and skills:
·    Board-certified dermatologist, 3-5 years out of residency preferred
·    Demonstrated knowledge of inclusive dermatological education that is representative of diverse patient populations
·    Training or teaching facilitation in the field of dermatology
·    Demonstrated leadership role experience with the ability to work independently
·    Commitment to promoting diversity in dermatology as evidenced by current work in healthcare community engagement
·    Strong collaborative skills with the ability to facilitate dialogue and engage in difficult conversations to sustain a culturally responsive environment
·    Excellent written and oral communication skills with knowledge of language sensitive to inclusivity of all backgrounds and communities
·    The Director of Equity, Diversity and Inclusion may not concurrently serve in the same role/capacity at other dermatology conferences
Apr 20
1

SKIN OF COLOR UPDATE PRE-CONFERENCE VIRTUAL SYMPOSIUM

By | Medical Dermatology, Sessions, Skin of Color Update Agenda | No Comments
SKIN OF COLOR UPDATE PRE-CONFERENCE VIRTUAL SYMPOSIUM
Register Now
A Case-Based Conversation with The Experts: Treating Pigmentary Disorders in Skin of Color Patients
SKIN OF COLOR UPDATE PRE-CONFERNECE VIRTUAL SYMPOSIUM
TUESDAY, AUGUST 3RD | 6:00PM ET – 9:00PM ET
The Skin of Color Update invites you to join its pre-conference symposium where co-chairs Drs. Andrew Alexis and Eliot Battle will host an interactive, case-based conversation with pigmentary disorders experts. Faculty will review treatment options for common as well as challenging and less frequently discussed pigmentary conditions in skin of color patients. Through a detailed review of each case, panelists will provide guidance and evidence-based treatment protocols as well as practical pearls drawn from their clinical experience. You will walk away from this session armed with clinical pearls immediately useful in your practice. In addition, all panelists will participate in live Q&A sessions to answer your most pressing questions about treating pigmentary disorders in SOC.
AGENDA
6:00-6:05 PM – Welcome & Introductions from Symposium Moderators – Andrew F. Alexis, MD, MPH & Elliot F. Battle, MD
6:05-6:20 PM – A Challenging Case of Melasma – Heather Woolery-Lloyd, MD
6:20-6:35 PM – A Case of Vitiligo Treated with Pulsed Corticosteroids/JAK-Inhibitor – Seemal Desai, MD
6:35-6:50 PM – Post-Inflammatory Hyperpigmentation(PIH) Topical & Procedural Treatment – Neelam Vashi, MD
6:50-7:00 PM – Live Audience Q&A
7:00-8:00PM – For Patients with Plaque Psoriasis: An Oral, Non-Biologic Therapy With Data on Clearer Skin and Symptoms – Paul Wallace, MD, MPA (Non-CE Workshop)
8:00-8:05 PM – Welcome & Introductions from Symposium Moderators – Andrew F. Alexis, MD, MPH & Elliot F. Battle, MD
8:05-8:20 PM – A Challenging Case of Erythema Dyschromicum Perstans – Nada Elbuluk, MD, MSc
8:20-8:35 PM – A Case of Hypopigmented Mycosis Fungoides – Eva Kerby, MD
8:35-8:50 PM – Lichen Planus Pigmentosus – Mukta Sackdev, MD
8:50-9:00 PM – Live Audience Q&A
SYMPOSIUM CO-CHARIS
Andrew F. Alexis, MD, MPH
Eliot F. Battle, MD
EXPERT FACULTY
Seemal R. Desai, MD, FAAD
Nada Elbuluk MD, MSc
Eva Kerby, MD
Heather Woolery-Lloyd, MD
Mukta Sachdev, MD
Neelam Vashi, MD
Register Now
Mar 12
0

Treating Alopecia in Skin of Color Patients: How to Arrest Loss and Promote Regrowth

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Treating Alopecia in Skin of Color Patients

Source: Next Steps in Derm

Can you improve your culturally-competent hair loss consultation? Would you like to grow your toolbox for comprehensive alopecia treatment? If so, you are in the right place!

Hair loss is a frequent concern for patients visiting the dermatologist, especially in patients with pigmented skin types. Kinky or coiled hair has an innate fragility that makes African Americans especially prone to hair loss concerns. At the  2020 Skin of Color Virtual Update, Dr. Susan Taylor discussed Conventional Treatment Approaches for Hair & Scalp Disorders in Skin of Color Patients. Dr. Taylor advised how to have a culturally competent hair loss consultation, reviewed common patterns of hair loss, and highlighted comprehensive treatment of multifactorial causes of alopecia.

Before we get into therapeutic strategies for alopecia, let’s highlight important considerations to institute an effective treatment plan:

  • Understand common ethnic hairstyles and practices
  • Recognize the impact of hair and scalp disorders
  • Clearly identify the problem and obtain a thorough history, including details regarding hair care practices, products used, and symptoms
  • Complete physical examination and consider scalp biopsy
  • Accurately diagnose the disease (see Table 1 for common causes of alopecia)
  • Effectively and competently partner with the patient to treat the disorder with appropriate therapy
Common Cause of Scarring Non-Scarring Alopecia

Dr. Taylor stressed the importance of culturally competent questioning during the visit. For example, asking an African American woman if she shampoos daily can reduce the patient’s confidence in the physician’s understanding of her hair type, especially during a race discordant visit. To build confidence, it is critical to understand routine hair practices and to be familiar with common products.

During the hair loss consultation, it is important to understand the problem experienced by the patient. Frequent symptoms noted by the patient that can clue in the underlying alopecia include:

    • Hair length is not increasing.
    • There is hair breakage.
    • Hair is falling out at the root.
    • There is decreased hair density.
    • There is focal or localized hair loss.

Other considerations include the duration of hair loss, any associated symptoms, and presence of family history of hair loss. Further, it is important to ask about their hair care history. The types of hairstyles used by the patient and the hair care routine should be discussed.

The physical exam should be thorough to evaluate the scalp and hair density, a hair pull test, and examination of the eyebrows and eyelashes. The presence of weaves, braids, or wig caps may impede evaluation. If the patient has any of these hairpieces on the scalp that cannot be easily removed during the visit, the patient should return for evaluation after these are removed. History can still be discussed during the visit, however, the co-pay should be refunded, and the patient should be offered an earlier appointment for evaluation of the hair and scalp.

Now that we have discussed how to approach the consultation, let’s get into the alopecias! Dr. Taylor highlighted central centrifugal cicatricial alopecia, traction alopecia, and frontal fibrosing alopecia, as well as tips to minimize breakage, reduce hair tension, and scalp care to treat seborrheic dermatitis.

Central centrifugal cicatricial alopecia (CCCA) is a scarring alopecia seen in about 5.6% of African American women. It frequently starts with increased hair breakage at the vertex, and patients often have associated symptoms of itching, burning, tenderness, and soreness of the scalp. The goals of treatment are to aggressively treat the CCCA in the early stages to prevent progression, relieve symptoms, and possibly have some regrowth in the affected areas. There are no randomized controlled trials for CCCA treatment, thus evidence for treatment comes from case reports and series. The mainstay of treatment is corticosteroids (topical and intralesional), anti-inflammatory antibiotics, antimalarials, and minoxidil (topical and oral formulations). Anti-seborrheic shampoos, hair transplantation, and platelet-rich plasma injections serve as adjuncts to treatment. See Table 2 for detailed treatment options. Frequently multiple agents are used in combination to control the disease.

Two important areas of focus when treating CCCA that Dr. Taylor highlighted are practices to minimize hair breakage and treatment of frequently concurrent seborrheic dermatitis.

Read More…..

Mar 05
0
Cutaneous Sarcoidosis

Hypopigmented Cutaneous Sarcoidosis Responsive to Minocycline

By | Case Reports, SOC Manuscripts | No Comments

Hypopigmented patches and plaques are a rare presentation of cutaneous sarcoidosis. JDD authors describe a case of generalized hypopigmented cutaneous sarcoidosis that showed good response to minocycline therapy.

Introduction

A 58-year-old African-American male with a past medical history of hypertension, diabetes mellitus, tobacco use, glucose-6-phosphate dehydrogenase (G6PD) deficiency, and hyperlipidemia presented with a two-year history of asymptomatic light spots on his trunk and upper extremities. He reported a history of cutaneous sarcoidosis a decade prior, characterized by erythematous papules and plaques that had regressed with hydroxychloroquine therapy. The newer light patches were not responsive to mid-potency topical steroids or tacrolimus 0.1% ointment. Review of systems was negative. The patient denied any new medications or history of travel outside of the metropolitan area.

 

Physical examination of the skin was significant for multiple hypopigmented patches on the face, neck, and extremities; hypopigmented plaques on the back (Figure 1); and annular plaques of hypopigmented papules on the chest and abdomen (Figure 2). The lesions were not hypoesthetic. There was no lymphadenopathy and physical exam was otherwise unremarkable.

 

A biopsy from the left arm showed a superficial and deep multinodular granulomatous infiltrate sparing the epidermis (Figure 3). The granulomas were predominantly composed of epithelioid histiocytes with a few scattered lymphocytes (Figure 4). Special stains for microorganisms were negative. There was no appreciable epidermal change or pigment incontinence. The histopathological picture was consistent with recurrent cutaneous sarcoidosis.
Computed tomography of the chest with and without contrast showed no evidence of active pulmonary sarcoidosis or lymphadenopathy. An ophthalmologic exam, abdominal ultrasound, and spirometry were within normal limits, as were serum cal cium and angiotensin-converting enzyme (ACE) levels.

 

Because the patient’s skin manifestations had resolved with hydroxychloroquine in the past, this treatment was restarted at 200 mg twice-daily. Unfortunately, laboratory monitoring revealed hepatic transaminitis and mild anemia 2 months into the treatment course, corresponding with only minimal improvement of the hypopigmented plaques, necessitating discontinuation of hydroxychloroquine. Minocycline at a dose of 100 mg twice daily was then initiated 4 months after normalization of liver function tests. After 5 months of treatment, all hypopigmented patches, papules, and plaques had completely or partially repigmented and were appreciably smoother and flatter (Figures 5 and 6). The patient tolerated the medication well with no adverse effects.

 

Cutaneous Sarcoidosis

FIGURE 1. Hypopigmented plaques over the back.

Cutaneous Sarcoidosis

FIGURE 2. Hypopigmented annular plaques of papules on the abdomen.

Cutaneous Sarcoidosis

FIGURE 3. Hematoxylin and eosin stain of a left arm skin biopsy show-ing dermal granulomatous inflammation.

Cutaneous Sarcoidosis

FIGURE 4. Hematoxylin and eosin stain of a left arm skin biopsy at higher magnification demonstrating well-formed naked granulomas.

Cutaneous Sarcoidosis

FIGURE 5. Flattening and repigmentation of plaques on the back after treatment with minocycline.

Cutaneous Sarcoidosis

FIGURE 6. Repigmentation of annuli on the anterior trunk after treat-ment with minocycline.

 

Discussion

The skin is one of myriad organs potentially affected by sarcoidosis, a multisystem idiopathic disorder characterized histologically by infiltration of noncaseating granulomas. Cutaneous manifestations of sarcoidosis are protean, including papules and plaques of various morphology and distribution, subcutaneous nodules, pruritus, ichthyosis, erythroderma, ulceration, verrucosis, nail disease, and infiltrative scars.1 In the United States, sarcoidosis is more common in African-Americans than in other ethnic groups, and cutaneous manifestations in individuals of African descent are more likely to be atypical.2

In 1973, Cornelius et al reported 4 patients who presented with hypopigmented and depigmented patches and plaques that showed the naked tuberculoid granulomas characteristic of sarcoidosis on skin biopsy.3 The distribution in these cases was variable, with generalization in one patient and localization to the face, legs only, or legs and arms in the other three. Histologically, no difference in epidermal melanocyte count was noted between affected and unaffected skin, but relative hypomelanosis of the malphigian and corneal layers was appreciated. All patients had multisystem disease. Four years later, Hubler described a “hypomelanotic canopy” in a woman with lupus pernio and lymphadenopathy whose hypopigmented patches overlay deep subcutaneous nodules on the arms.4Biopsy of an enlarged lymph node revealed epithelioid granulomas that were reduplicated on skin biopsy. Interestingly, cutaneous hypopigmentation lacking any histological evidence of granulomatous dermatitis has also been observed in the setting of systemic sarcoidosis;5,6 this highlights the need for vigilant continued surveillance when the clinical index of suspicion for sarcoidosis is high and biopsy is noncorroborative.

 

The etiopathogenesis of hypopigmentation in sarcoidosis, like the disease itself, is unknown. Theories regarding the likely mul tifactorial cause of sarcoidosis center around T-cell—mediated autoimmunity, genetic predisposition, and aberrant response to bacterial or other antigens; the evidence for each has been extensively reviewed elsewhere.1,7 The rare cutaneous hypopigmentation seen in dark-skinned individuals with sarcoidosis appears to represent a melanopenic hypomelanosis, as opposed to postinflammatory hypopigmentation or melanocytopenia.3,4,8 In our patient, there were no epidermal changes, interface in flammation, or melanin-containing dermal macrophages to suggest postinflammatory dyspigmentation.

 

Minocycline represents an attractive alternative treatment for chronic sarcoidosis in patients who might otherwise be treated with long-term corticosteroids, antimalarials, methotrexate, or other immunosuppressants. The tetracycline class of antibiotics has previously demonstrated utility in a variety of dermatoses and autoimmune-connective tissue diseases, and may be particularly efficacious for granulomatous skin conditions.9,10 Tetracyclines have specifically shown efficacy in the treatment of granulomatous periorificial dermatitis, cheilitis granulomatosa, granulomatous rosacea, and silicone granulomas.11-14 More recently, tetracyclines proved beneficial in treating granuloma annulare (GA), an entity often with significant clinicopathological overlap with cutaneous sarcoidosis.15,16 Marcus et al showed that, in combination with rifampin and ofloxacin, 3 to 5 courses of monthly minocycline therapy led to complete clearance of GA in 6 patients, half of whom had generalized disease.15 In this series, the rationale for selection of the same triple combination antimicrobial therapy as that used for paucibacillary leprosy (PBL) was that the clinical and histological similarities between PBL and GA might impart an equally similar response to treatment. The same logic could be extrapolated further to include patients with cutaneous sarcoidosis as candidates for a treatment regimen, including minocycline, with or without rifampin and ofloxacin.

 

Minocycline as monotherapy was efficacious for the treatment of chronic cutaneous sarcoidosis in an open observational study of 12 patients by Bachelez et al.17 The cutaneous manifestations of patients in the Bachelez group included classic plaques, papulonodules, subcutaneous nodules, and lupus pernio. Ten of 12 patients completely or partially responded to treatment, which was generally well tolerated except for drug hypersensitivity syndrome in one patient with a history of other autoimmune diseases. Park et al later reported a patient with cutaneous, lacrimal gland, pulmonary, and ocular (choroidal) sarcoidosis that responded to minocycline.18

Miyazaki et al described a patient with a unique presentation of muscular sarcoidosis of the limbs, as well as uveitis and pulmonary disease, in whom clinical response to minocycline was paralleled by normalization of an elevated ACE level.19 The patient relapsed off of minocycline, but rapidly responded to reintroduction of the medication. Immunohistochemical staining of muscle biopsy specimens for Propionibacterium acnes showed multiple small particles within granuloma macrophages and giant cells, substantiating the theory that sarcoidosis is an infectious disease or an aberrant immunologic response to bacteria. Evidence for the role of other infectious agents in sarcoidosis, especially Mycobacterium tuberculosis, has been mixed and inconclusive.20 That sarcoidosis is purely an infectious disease is certainly within the realm of possibility,21 but the recurrence of disease once antibiotics are discontinued argues against this theory.19 An alternative explanation is that the benefits of tetracyclines in sarcoidosis and other autoimmune diseases are derived more from their nonantibiotic immunomodulating properties. The anti-inflammatory properties ascribed to minocycline include inhibition of T cell activation, proliferation, and transmigration as well as expression of nitric oxide synthetase and matrix metallopeptidase 9 (MMP-9).9Furthermore, tetracyclines have been shown to inhibit granuloma formation in vitro.22

 

Conclusion

The role of tetracyclines in the therapeutic armamentarium of sarcoidosis, especially in those who cannot tolerate antimalarials or other immunomodulating medications, is likely to expand. Whether minocycline is particularly effective for the hypopigmented variety of cutaneous sarcoidosis remains to be seen.

 

Disclosures

The authors have no relevant conflicts of interest to disclose.

References

  1. English JC 3rd, Callen JP. Sarcoidosis. In: Callen JP, Jorizzo JL, Bolognia JL, et al, eds. Dermatological Signs of Internal Disease. 4th ed. China: Elsevier; 2009:287-295.
  2. Jayck WK. Cutaneous sarcoidosis in black South Africans.Int J Dermatol. 1999;38(11):841-845.
  3. Cornelius CE 3rd, Stein KM, Hanshaw WJ, Spott DA. Hypopigmentation and sarcoidosis. Arch Dermatol.1973;108(2):249-251.
  4. Hubler WR Jr. Hypomelanotic canopy of sarcoidosis. Cutis.1977;19(1):86-88.
  5. Alexis JB. Sarcoidosis presenting as cutaneous hypopigmentation with repeatedly negative skin biopsies.Int J Dermatol. 1994;33(1):44-45.
  6. Hall RS, Floro JF, and King LE Jr. Hypopigmented lesions in sarcoidosis. J Am Acad Dermatol. 1984;11(6):1163-1164.
  7. English JC 3rd, Patel PJ, Greer KE. Sarcoidosis. J Am Acad Dermatol. 2001;44(5):725-743.
  8. Clayton R, Breathnach A, Martin B, et al. Hypopigmented sarcoidosis in the Negro. Report of eight cases with ultrastructural observations. Br J Dermatol.1977;96(2):119-125.
  9. Sapadin AN, Fleischmajer R. Tetracyclines: nonantibiotic properties and their clinical implications. J Am Acad Dermatol. 2006;54(2):258-265.
  10. Stone M, Fortin PR, Pacheco-Tena C, Inman, RD. Should tetracycline treatment be used more extensively for rheumatoid arthritis? Metaanalysis demonstrates clinical benefit with reduction in disease activity J Rheumatol.2003;30(10):2112-2122.
  11. Falk ES. Sarcoid-like granulomatous periocular dermatitis treated with tetracycline. Acta Derm Venereol.1985;65(3):270-272.
  12. Camacho F, García-Bravo B, and Carrizosa A. Treatment of Miescher’s cheilitis granulomatosa in Melkersson-Rosenthal syndrome. J Eur Acad Dermatol Venereol.2001;15(6):546-549.
  13. Mullanax MG, Kierland RR. Granulomatous rosacea. Arch Dermatol. 1970;101(2):206-211.
  14. Senet P, Bachelez H, Ollivaud L, Vignon-Pennamen D, Dubertret L. Mi- nocycline for the treatment of cutaneous silicone granulomas. Br J Dermatol. 1999;140(5):985-987.
  15. Marcus DV, Mahmoud BH, Hamzavi IH. Granuloma annulare treat- ed with rifampin, ofloxacin, and minocycline combination therapy Arch Dermatol. 2009;145(7):787-789.
  16. Duarte AF, Mota A, Pereira MA, Baudrier T, Azevedo F. Generalized granuloma annulare—response to doxycycline.J Eur Acad Derma- tol Venereol. 2009;23(1):84-85.
  17. Bachelez H, Senet P, Cadranel J, Kaoukhov A, Dubertret L. The use of tetracyclines for the treatment of sarcoidosis.Arch Dermatol. 2001;137(1):69-73.
  18. Park DJ, Woog JJ, Pulido JS, Cameron JD. Minocycline for the treatment of ocular and ocular adnexal sarcoidosis.Arch Ophthal- mol. 2007;125(5):705-709.
  19. Miyazaki E, Ando M, Fukami T, Nureki S, Eishi Y, Kumamoto T. Mi- nocycline for the treatment of sarcoidosis: Is the mechanism of action immunomodulating or antimicrobial effect? Clin Rheumatol. 2008;27(9):1195-1197.
  20. Tchernev G. Cutaneous sarcoidosis: the “great imitator”: etiopathogenesis, morphology, differential diagnosis, and clinical management. Am J Clin Dermatol. 2006;7(6):375-382.
  21. Marshall TG, Marshall FE. Sarcoidosis succumbs to antibiotics—implications for autoimmune disease.Autoimmun Rev.
  22. Webster GF, Toso SM, and Hegemann L. Inhibition of a model of in vitro granuloma formation by tetracyclines and ciprofloxacin. Involvement of protein kinase C. Arch Dermatol. 1994;130(6):748-752.

Originally published in the Journal of Drugs in Dermatology in April 2012. 

Schmitt, C. E., Fabi, S. G., Kukreja, T., & Feinberg, J. S. (2012). Hypopigmented cutaneous sarcoidosis responsive to minocycline. Journal of drugs in dermatology: JDD, 11(3), 385-389. https://jddonline.com/articles/dermatology/S1545961612P0385X  

Content and images republished with permission from the Journal of Drugs in Dermatology.

Adapted from original article for length and style.

The Journal of Drugs in Dermatology is available complimentary to US dermatologists, US dermatology residents, and US dermatology NP/PA. Create an account on JDDonline.com and access over 15 years of PubMed/MEDLINE archived content.

Did you enjoy this case report? You can find more here.

Feb 12
3
Pemphigus Foliaceus

Psoriasiform Pemphigus Foliaceus in an African American Female: An Important Clinical Manifestation

By | Case Reports, SOC Manuscripts | No Comments

JDD authors document and highlight this atypical psoriasiform presentation of Pemphigus Foliaceus in a patient with skin of color to raise awareness and improve diagnosis and outcomes.

Case Report

A 50-year-old African-American woman presented to the dermatology clinic with a pruritic eruption of 3 years’ duration that began as discrete plaques on the inframammary folds and subsequently spread towards the mid-chest, ears, back, elbows, knees, and scalp. Past treatments by other clinicians included clotrimazole cream and a topical corticosteroid of unknown potency without significant improvement. She denied any new medications and was taking aspirin, divalproex, mirtazapine, cetirizine, venlafaxine, atorvastatin, and omeprazole.

On clinical examination, the patient had well-demarcated, pink, atrophic plaques and superficial erosions over the inframammary folds and mid-chest (Figures 1). She also had well-demarcated, hyperpigmented, hyperkeratotic scaly plaques over the abdomen, suprapubic region, elbows, knees, and back with sporadic small superficial blisters (Figure 2). Complete blood count, complete metabolic panel, rheumatoid factor, and antinuclear antibody were within normal limits. Rapid plasma reagin test was negative. Erythrocyte sedimentation rate was elevated at 54 millimeter/hour (reference range 0-22 millimeter/hour). A punch biopsy of the right abdomen was performed and revealed psoriasiform epidermal hyperplasia, focal parakeratosis, and acantholysis throughout the superficial spinous and granular layers (Figure 3). Only a sparse inflammatory infiltrate was present in the underlying dermis. These clinical and histological findings supported the diagnosis of pemphigus foliaceus (PF). Patient was started on 50 mg oral dapsone daily.

Pemphigus Foliaceus

FIGURE 1. Well-demarcated, scaly plaques over the mid-chest and inframammary folds, with a single superficial erosion on the right medial chest.

Pemphigus Foliaceus

FIGURE 2. A plaque from the abdomen demonstrates “corn flake-like” scale.

Pemphigus Foliaceus

FIGURE 3. Composite photomicrograph, hematoxylin, and eosin, original magnification x200.

 

Discussion

Herein, we present a case of Pemphigus Foliaceus with a psoriasiform clinical presentation in an African-American patient. PF is an autoimmune skin disease caused by antibodies against the desmosomal glycoprotein, desmoglein 1.¹ Desmogleins, members of the cadherin family, serve to anchor epidermal desmosomes between adjacent keratinocytes and assist in epithelial differentiation.² Antibodies targeting desmoglein 1 result in acantholysis in the upper epidermis with limited separation in the basal layers and minimal mucosal involvement as desmoglein 1 is primarily expressed in the granular layer of the non-mucosal epidermis.¹ Patients present with scaly plaques on an erythematous base and fragile shallow blisters which are infrequently found intact; rarely, the condition can progress to exfoliative erythroderma.1,3 Initially, PF usually presents on the trunk, face, or scalp, but may subsequently involve other regions of the skin.1 Diagnosis may be confirmed with biopsy and direct immunofluorescence with intercellular IgG and C3 limited to the upper epidermis. Treatment includes oral and topical steroids, azathioprine, dapsone, and rituximab. The differential diagnosis for PF may include systemic lupus erythematosus, bullous impetigo, psoriasis, and seborrheic keratosis depending on the presentation.1

Physical exam findings in this patient were suggestive of PF due to the presence of superficial secondary erosions and “corn flake-like” scales, but psoriasis was included in the differential diagnosis due to the presence of discrete plaques with an erythematous border. PF is a relatively rare condition with a prevalence of less than 1 case per 100,000 and is about 5 to 10 times less common than pemphigus vulgaris.4 In contrast, psoriasis impacts approximately 2-4% of people in the United States.5 An endemic form of PF, fogo selvagem, has been reported in Brazil, Colombia, Peru, and Tunisia, while pemphigus vulgaris is more common in Mediterranean and Ashkenazi Jewish populations.4

We hypothesize that patients with psoriasiform presentations of PF may be misdiagnosed with plaque psoriasis. One author (JJ) has previous significant clinical experience with patients with skin of color and has seen other skin of color patients present with a psoriasiform manifestation of PF. PF and psoriasis share similar treatments including topical corticosteroids and immunosuppressants, and this may lead to underreporting of PF with psoriasiform manifestations. It is important to distinguish between these findings as there is evidence that ultraviolet light, a common treatment for psoriasis, may exacerbate PF.6,7 We performed a search of the published literature and identified one article that describes three patients with pemphigus erythematosus, a variant of PF, which was misdiagnosed as psoriasis.8 No identified articles described cases of PF with a psoriasiform presentation in patients with skin of color. We document and highlight this atypical psoriasiform presentation of PF in a patient with skin of color to raise awareness and improve diagnosis and patient outcomes.

Disclosures

The authors have no relevant disclosures. The contents do not represent the views of the U.S. Department of Veterans Affairs or the United States Government. This material is the result of work supported with resources and the use of facilities at the Sacramento VA Medical Center.

 

References

  1. James KA, Culton DA, Diaz LA. Diagnosis and clinical features of pemphigus foliaceus. Dermatol Clin. 2011;29(3):405-412, viii.
  2. Simpson CL, Patel DM, Green KJ. Deconstructing the skin: cytoarchitectural determinants of epidermal morphogenesis. Nat Rev Mol Cell Biol. 2011;12(9):565-580.
  3. Kershenovich R, Hodak E, Mimouni D. Diagnosis and classification of pemphigus and bullous pemphigoid. Autoimmun Rev. 2014;13(4):477-481.
  4. Meyer N, Misery L. Geoepidemiologic considerations of auto-immune pemphigus. Autoimmun Rev. 2010;9(5):A379-A382.
  5. Rachakonda TD, Schupp CW, Armstrong AW. Psoriasis prevalence among adults in the United States. J Am Acad Dermatol. 2014;70(3):512-516.
  6. Ruocco V, Ruocco E, Schiavo AL, Brunetti G, Guerrera LP, Wolf R. Pemphigus: Etiology, pathogenesis, and inducing or triggering factors: Facts and controversies. Clin Dermatol. 2013;31(4):374-381.
  7. Aghassi D, Dover JS. Pemphigus foliaceus induced by psoralen-UV-A. Arch Dermatol. 1998;134(10):1300-1301.
  8. Oktarina DA, Poot AM, Kramer D, Diercks GF, Jonkman MF, Pas HH. The IgG “lupus-band” deposition pattern of pemphigus erythematosus: association with the desmoglein 1 ectodomain as revealed by 3 cases. Arch Dermatol. 2012;148(10):1173-1178.

Originally published in the Journal of Drugs in Dermatology in April 2018. 

Evan Austin BS, Jillian W. Millsop MD, Haines Ely MD, Jared Jagdeo MD MS, and Joshua M. Schulman MD (2018). Psoriasiform Pemphigus Foliaceus in an African American Female: An Important Clinical Manifestation. Journal of Drugs in Dermatology, 17(14), 471-473. https://jddonline.com/articles/dermatology/S1545961618P0471X 

Content and images republished with permission from the Journal of Drugs in Dermatology.

Adapted from original article for length and style.

The Journal of Drugs in Dermatology is available complimentary to US dermatologists, US dermatology residents, and US dermatology NP/PA. Create an account on JDDonline.com and access over 15 years of PubMed/MEDLINE archived content.

Did you enjoy this case report? You can find more here.

Feb 10
0

SOCU Pearls Galore: AD, HS, Hair Care in SOC, and Medication Compliance Among Teens

By | Uncategorized | No Comments
Skin of Color Update Q&A Session Pearls

Source: Next Steps in Derm

The following is a summary of one of the many Q&A sessions held during the 2020 Skin of Color Virtual Update. During this particular session, questions were moderated by SOCU Co-Chair Dr. Andrew Alexis and answered by Drs. Ginette Okoye and Candrice Heath. The audience posed important questions and the faculty offered insightful answers regarding atopic dermatitis, hidradenitis suppurativa, hairstyle recommendations for patients with traction alopecia and follicular disorders,  and medication compliance among teens.

Q1. Dr. Alexis: “Dr. Okoye, when do you use spironolactone for Hidradenitis Suppurativa and when do you consider it for patients? What has been your experience?”

A1. Dr. Okoye: “Thank you for your question. Spironolactone like metformin is a good adjunct for other treatments with HS. I really never use it alone. It’s not a slam dunk by any means. I combine it with other modalities like metformin or a biologic or even antibiotics. I prefer to use spironolactone in patients who report flair with their menses. I specifically target these patients. I usually start at 50 mg/day or 100 mg/day, depending on their weight, intending to go as high as 200 mg/day.  If they can tolerate it, I will leave them on that. It is one of the many layers as I mentioned.”

Q2. Dr. Alexis: “Excellent. Staying on the same theme of HS, a real burning question a lot of us have is what if you’ve tried adalimumab for HS and it’s not working? What do you do next?”

A2. Dr. Okoye: “There are 3 types of people who receive adalimumab. There are patients with a nice response who get about 50 percent or maybe a little bit more. There are patients that are the same and nothing happens, according to the patient, and then there are people who seem to get worse. For the latter two groups, I try to stick with a biologic and attack a different pole of the immune system. My next option is usually Utsekinumab. First, because it is not a TNF alpha inhibitor and second, it has weight-based dosing, I can use a higher dose and use it every 4 weeks if I can get it covered. I’ve also had better luck getting it covered by insurance than the other biologics. I would say maybe a year or two ago, my next option may have been infliximab but if I find a patient does not respond to adalimumab that TNF alpha pole of the disease may not be as active in that person so I tend not to use infliximab in those patients anymore.”

Q3. Dr. Alexis: “Thank you. That’s very helpful. I’m going to give you one last HS question for the time being before we shift gears. This is a practical one in terms of diagnostic criteria for HS. The audience member says he or she has a lot of patients who have recurrent folliculitis of the thighs with one or more comedones in the area and would this be considered an HS variant?”

A3. Dr. Okoye: “Well, it depends. In order to diagnose someone with HS, we need to have typical HS lesions in typical HS locations (intertriginous areas) and they need to have recurrences. Some of these lesions include abscesses and sinus tracts.  Follicular papules and follicular pustules can be one of those typical lesions of HS, in my opinion. There are different subtypes of HS. One of them is called follicular subtype with more of a folliculitis type picture and they can have epidermal inclusion cysts and comedones. So yes, I suspect that your patient does have HS, just this particular subtype.”

Q4. Dr. Alexis: “Terrific, thank you. Now over to Dr. Heath. A general but very practical question. What pearls do you have for addressing medication compliance among teens since we know that is a unique group with unique challenges?”

A4. Dr. Heath: “Absolutely. I love the teenage population. One of my biggest tips is definitely to let them off the hook. So, what I mean by that is let them know they don’t have to do the regimen every single day. Say this in front of the parents so that skin disease does not become a battle at home. If the parents are not bugging them about it all the time, and the kid actually does commit to using it a few times and see some improvement, then I definitely let them know “great, you made and effort, let’s try to step it up if you can”. This strategy helps decrease the battle between parents and teens. Also, get them engaged in the visit. It is their skin so I speak directly to the teenager, especially if the parent is answering a lot about the patient’s health history questions, in which case I politely stop them and tell them that I really want to hear from the patient (and say the patient’s name). This makes them feel that it is their body and a really important time in their life where they can start to feel independence and positivity around seeking health care in general. One other tip is, once I give them step by step instructions to follow, I ask them to snap a picture with their cell phone or give them the idea of hanging the directions on the mirror in the bathroom, which can serve as a reminder. Those are just a few tips!”

Q5.  Dr. Alexis: “Another question for you Dr. Heath, about hair. What hairstyles do you typically recommend to patients and their families in the context of traction alopecia and follicular disorders that you see commonly in SOC and do you partner with any salons in the area?”

A5. Dr. Heath: “This is a very important question.  Not everyone is well versed in what is the cool hairstyle of the day. I simply start with whatever hairstyle you choose if it hurts, I would like for you to stop or loosen it. Also, if braids or cornrows are being used, I ask them “what about making the hairstyle already look like it’s one or two weeks old?”. This gives them a visual of how loose the braids should be to the scalp. I have not given a specific hairstyle, but I have given them some guidance. If it hurts, then you should stop or modify, and if it requires braids close to the scalp make it look older. Another example is doing crochet braids. This hairstyle involves hair being braided back and then just like you are knitting, very lightweight hair is attached to the braids going back. Often this is done with synthetic hair and the style doesn’t last as long as with regular human hair. So this does two things: 1) I have instructed them to use a hair that is now lighter, and a hairstyle that will self-destruct way sooner than something they would have spent 300 dollars on, so they would feel more comfortable replacing it because they didn’t spend that much. With regards to partnering with salons, if you’re new to a specific area or you’re just venturing out with skin of color and you want to give them more resources, one great place to start is online. I’m active on social media and a lot of salons and hairstylists will put their work online. I examine their work and look at the content they produce to see if we have the same hair values. See if they’re talking about healthy hair or if they have hairstyles that look too tight. Sometimes it can take time. Don’t rush it. Ask your patients who have very well-maintained hair that does not look tight: “Oh who does your hair? They’re doing a great job on their side while we are treating you medically.” You can make a list and go online and look these people up. You can talk to them or stop by. It helps them to know that you are invested in this person getting better and you’d love for them to have the client for a long time. But if the client doesn’t have any hair, they won’t be able to go there for a long time., so we (both parties) have a common goal”.

A5. Dr. Alexis: “Similar approaches have worked for me. Sometimes I will get patients who have very early CCCA/traction alopecia sent by the stylist and I want to know who that stylist is! I have a handful of excellent ones who can diagnose it early I have a very good relationship with them!”

Q6. Dr. Alexis: “I have some questions for myself that I’m going to take about atopic dermatitis.  One question that I have is about hyperpigmentation and lichenification left behind from an atopic dermatitis flare. How do you manage the pigmentary sequelae?”

A6. Dr. Alexis: “This is really an area where we want to educate the patient on the importance of treating the underlying cause of the pigmentary sequelae. There is no use in chasing after hyperpigmentation without actually controlling the chronic, underlying inflammatory disease that is atopic dermatitis. So really emphasize the core aspects of treating the active disease. As far as treating the pigmentation itself, you are left with an area of persistent post-inflammatory hyperpigmentation. My treatment of that is delayed action. Why? Because many of the skin lightening agents that we would consider can be irritating to the skin especially in the context of someone who has a compromised barrier as an atopic dermatitis patient would. The endpoint for knowing when is the time to consider a bleaching agent is when I or the patient palpate the area and it’s completely smooth and there is no elevation, scaling,  any sign of erythema whatsoever, no pruritus and it is just a persistent hyperpigmented macule or a patch, that persisted there for at least four weeks after the last activity. That’s when you want to consider a bleaching agent, not before. Really leveraging the non-corticosteroid topical agents such as TCIs, PDE4 inhibitors, and also if it’s a more moderate to severe patient, systemic agents like Dupilumab really can improve the sequalae too, anecdotally, because if you control the underlying inflammatory pathways there is less development of new areas of dyspigmentation and you have a better opportunity to clear the pigmentation that does occur.”

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Jan 28
0

Alopecia in Skin of Color: Alternative Therapies

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Alopecia in Skin of Color Dermatology Conference

Source: Next Steps in Derm

Management of alopecia in skin of color is challenging due to a paucity of research into its pathophysiology coupled with a poor understanding of the basic hair care practices in this patient population. For the patient, it is often associated with severe emotional distress. Unfortunately, many forms of hair loss are refractory to standard therapies.

At the 2020 Skin of Color Virtual Update, Dr. Crystal Aguh highlighted emerging therapies for various forms of alopecia in skin of color as our understanding of these conditions continue to unfold.

Central Centrifugal Cicatricial Alopecia (CCCA) is the prototypical form of hair loss in black women. It is a progressive form of scarring alopecia where fibrosis, not inflammation, is the predominant finding. The literature supports preferential expression of fibroproliferative genes in patients with CCCA. In fact, Dr. Aguh’s group demonstrated that PRKAA2, a gene that encodes for adenosine monophosphate kinase (AMPK), was under-expressed by a 1/3 in CCCA scalp samples.

So why metformin?

Reduced activity of AMPK is also implicated in the pathogenesis of hepatic fibrosis and idiopathic pulmonary fibrosis. In mouse model of IPF, metformin was found to reverse and accelerate resolution of the fibrotic processes via deactivation and apoptosis of myofibroblasts through AMPK activation.

    • Dosage: 10-20% Topical Metformin compounded in lipoderm once daily.
    • At that concentration, there is limited systemic absorption.
    • Main side effects are scalp dryness and irritation. Dr. Aguh recommends applying light oil (olive or Jojoba) coat to scalp to help with irritation and dryness.
    • It works 10-15 % of the time.

Another form of alopecia that disproportionately affects women is Lichen planopilaris (LPP). LPP is an inflammatory form of primary scarring alopecia. Signs of clinical activity include follicular hyperkeratosis, perifollicular erythema, and loss of follicular ostia. Patients also report loss of body hair. Meanwhile frontal fibrosing alopecia (FFA) is a subtype of lichen planopilaris characterized by slow recession of the frontal and bitemporal hairline. Dr. Aguh highlighted two adjunctive options for the treatment of LPP and FFA for patients who have failed standard therapies.

1. Naltrexone

    • mu-opioid receptor antagonist currently FDA approved for the treatment of opioid and alcohol dependence. In dermatology, it has been used off-label for the treatment of pruritus and as an anti-inflammatory agent.
    • It is hypothesized that lower than standard doses of naltrexone inhibits cellular proliferation of T and B cells and block Toll-like receptor 4, resulting in an analgesic and anti-inflammatory effect.
    • In one case series of four patients with LPP, use of naltrexone led to reduction in symptoms of pruritus, clinical evidence of inflammation of the scalp, and disease progression.
    • Dose: 3 mg daily
    • Drawback: 3 mg pills have to be compounded as the standard pill comes in 50 mg

2. 3% Tacrolimus cleanser (in Cetaphil cleanser)

    • Tacrolimus is a commonly anti-inflammatory agent for inflammatory skin conditions including lichen planopilaris.
    • Higher strengths of tacrolimus can be compounded to improve efficacy.
    • One retrospective study demonstrated that patients treated with 0.3% tacrolimus were significantly more likely to stabilize in 3 months compared with patients treated with clobetasol/betamethasone.
    • Drawback: very expensive. It costs about $120 for 30 ml of cleanser.

Acquired Trichorrhexis Nodosa (ATN) is a recurrent hair breakage that occurs as a result of damaging hair practices. Common culprits include chemical relaxers, thermal styling, and hair coloring. Patients will often complain of lack of hair growth. It can involve all parts of the scalp but nape of the neck is often affected. Dr. Aguh’s stressed that proper hair care is key for successful treatment. She proposed the following regimen for curly damaged hair:

    • Apply protein treatment to dry or damp hair. Cover with shower cap or heating source for 30 minutes.
    • Wash hair once weekly with gentle shampoo (sulfate-free or containing a gentle sulfate)
    • Deep condition with every shampoo. Follow deep conditioning with moisturizing rinse-out conditioner.
    • Add leave in conditioner after washing, at least 3x/week. Glycerin based leave in conditioners can be especially helpful for very dry hair
    • End washing session with light oil.

Traction Alopecia is another very common form of hair loss, especially in black women. It is likely due to the curly hair type, intrinsic low density of the hair at baseline as well as hairstyle practices. Dr. Aguh found that oral minoxidil, in lieu of topical minoxidil, is very effective for this type of hair loss.

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Oct 01
0

Top Black Hair Loss Videos and Black Hair Loss Treatment Videos on YouTube

By | Aesthetic Dermatology, Media Coverage, Medical Dermatology, Sessions, Skin of Color Update Agenda | No Comments
Thin on Top Abstract Image

Next Steps in Derm recently published a highlight from the Skin of Color Update Virtual 2020 poster session.

Thin on Top: A Cross-Sectional Analysis of the Top Black Hair Loss Videos and Black Hair Loss Treatment Videos on YouTube

Esther B. Henebeng BS¹, Uzoamaka Okoro MD, MSc², Ogechi Ezemma BA¹, Kristina Monteiro PhD¹, Afiya M. Mbilishaka PhD³, Chesahna Kindred MD, MBA4
¹The Warren Alpert Medical School, Brown University, Providence, RI, ²Dwight D. Eisenhower Army Medical Center, Fort Gordon, GA, ³University of the District of Columbia, Washington, DC,4Howard University College of Medicine, Washington, DC

Introduction

Alopecia, or hair loss, is a prevalent concern for both men and women, that has substantial impact on quality of life.¹ Many forms of alopecia in Black women are associated with or worsened by traumatic styling practices such as braiding, weaving, thermal or chemical hair straightening. Therapy is tailored to the specific diagnosis and can include altering haircare practices, topical or oral medications (ex. minoxidil), and in-office treatments (ex. intralesional injections, hair transplant).² However, studies have shown a considerable amount of Black women are concerned physicians may not understand their hair and fail to engage in discussions about hair issues for this reason.³ More than 50% of Black women experience hair loss, with a majority of women searching for treatment options from online resources instead of seeking care from a primary care physician or dermatologist.4 YouTube is one of the most frequently used websites, with 77% of Black adults using the social media platform.5 Although dermatologists have established an online presence, approximately 75% of the top dermatology-related videos on YouTube are from non-dermatologist sources.6 This is particularly concerning because videos from third parties have been found to suffer from incomplete information, overall poor quality, and can contribute to potential harm or delay in appropriate diagnosis.6,7

Behbahani et al showed that YouTube is a highly utilized resource for hair loss treatment information, but found no significant difference between the overall quality of board certified dermatologist and non-physician videos.7 However, videos from lay media or individuals have been shown to have lower accuracy in comparison to videos from health care sources.8 Examination of top YouTube videos regarding “hair” and “hair loss” demonstrated very few videos displaying more textured or tightly coiled hair types associated with Black hair. Consequently, our project will evaluate the accuracy, quality, viewer engagement, and viewer experience of “Black hair loss” and “Black hair loss treatment” videos on YouTube.

Objectives

    • Evaluate the accuracy of Black hair loss and Black hair loss treatment videos on YouTube in comparison to published, peer-reviewed articles found via PubMed literature review
    • Compare the quality, viewer engagement, and viewer experience of non-health care and health care sources

Methods

YouTube was searched for the following: “Black hair loss” and “Black hair loss treatment” on June 18, 2020. The first 60 videos per search term were examined and categorized into health care or non-health care sources. Two independent raters evaluated each video with four validated instruments: 1) Accuracy in Digital Health, 2) Accuracy Scale, 3) Armstrong Viewer Assessment, and 4) Global Quality Scale.8 Viewer engagement ratio was defined as (number of likes + dislikes + comments) / total views. Discrepancies between coders were resolved through discussion. Duplicate and non-English videos were excluded. Significant differences between health care and non-health care sources were determined using Mann- Whitney U test.

Results

Our search yielded a total of seventy-eight unique YouTube videos. Three videos made no claims to assess accuracy and were excluded from analysis (*).

Twenty-two (28.2%) of the videos were from health care sources and fifty-six (71.8%) from non-health care sources. Health care sources were made up of dermatologists, nondermatologist medical doctors, and university/professional organizations. Non-health care sources included individuals, hairstylists, companies, and lay media. Speakers in 45 of the YouTube videos (57.7%) self-identified as Black based on video content or a publicly accessible social media post. Of the 45, there were only 2 videos categorized as health-care sources that had a self-identified Black speaker.

Discussion

There are over 20 million total views for the top 78 videos on Black hair loss and Black hair loss treatment. These videos typically range from 1 minute to 10 minutes long, with varying levels of engagement. Videos by Black speakers were found to have higher levels of engagement (0.02 ± 0.02, P = <0.001). Many of the videos by non-health care sources were inaccurate or made claims with no evidence supported by PubMed literature review. A few speakers encouraged viewers to try potentially harmful practices to stimulate hair growth (ex. Vicks VapoRub to scalp, prolonged protective styles, intermittent fasting or detoxing). When compared to non-health care sources, health care sources had lower mean numbers of views (81,965 vs 330,113, P = 0.008). Furthermore, health care sources were less engaging than non-health care sources (0.01±0.01 vs 0.02 ±0.02, P = 0.012), but more accurate (Accuracy in Digital Health: 3.77 ±0.43 vs 2.00 ±1.57, P = <0.001; Accuracy Scale: 3.91 ±0.30 vs 2.15 ±1.25, P = <0.001). Most inaccuracies from health care sources were primarily associated with the promotion of a product or treatment that does not have proven efficacy. Fewer inaccuracies were related to incorrect comments regarding hair physiology and causes of hair loss. Nevertheless, health care sources provided a superior viewer experience (Armstrong Viewer Assessment: 3.09 ±0.53 vs 2.55 ±1.01, P = 0.023) and were of higher quality (Global Quality Scale: 3.64 ±0.85 vs 2.47 ±1.09, P = <0.001) in comparison to non-health care sources.

Conclusion

    • Social media platforms can improve a patient’s access to care and serve as an inclusive environment to share educational content.
    • Our findings suggest that many of the top YouTube videos on “Black hair loss” and “Black hair loss treatment” are inaccurate.
    • Health care sources should be cautious when suggesting products or treatments that are not evidence-based.
    • Even though health care sources were more accurate, they had less viewer engagement when compared to non-health care sources.
    • The data supports the need for further diversity in dermatology as Black speakers were found to have greater levels of engagement and participation.
    • Lastly, our results also underscore the need for dermatologists to work in tandem with non-health care sources (ex. hairstylists) who may have a larger following on social media in order to dispel misinformation online.

Click here to view the full summary and images

Jul 14
5

The Relevance of Vitamin D Supplementation for People of Color in the Era of COVID-19

By | COVID-19 Resources, Skin of Color Update Agenda | No Comments
Vitamin D

Source: JDD Online

The Journal of Drugs in Dermatology recently featured the article, The Relevance of Vitamin D Supplementation for People of Color in the Era of COVID-19, authored by Skin of Color Virtual Update faculty, Pearl E. Grimes MD, and Andrew F. Alexis MD MPH along with Nada Elbuluk MD MSU.

Introduction

African Americans (AA) and other people of color are dying at highly disproportionate rates from COVID-19. The statistics are staggering: in New York City alone, per 100,000 population, death rates in AA were 92.3, and in Hispanics 74.3, compared to 45.2 in Whites and 34.5 in Asians.1 Similar numbers have been reported in other cities and are presumed underestimations, given limited racial/ethnic reporting. In the states currently releasing the number of COVID-19 deaths by race and ethnicity, Blacks make up roughly 13 percent of the population, but 27 percent of the deaths. According to the American Public Media Research Lab, the rate of COVID-19 deaths nationally for Blacks has been reported as twice the rate of deaths of Asians and Latinos in the US and more than 2.5 times the rate for White residents.

Socio-economic reasons, pre-existing comorbidities, work circumstances, inconsistent healthcare access, stress, and decreased immunity, amongst other factors, have been posited as reasons for this shocking disparity. People of color, in particular AA and Hispanics, are more likely to be uninsured and to be frontline workers during the COVID-19 pandemic. This is compounded by the fact that comorbidities such as hypertension, diabetes, asthma, obesity, and cardiovascular disease are more common in AA and are also associated with higher COVID-19 mortality rates. Emerging evidence suggests that Vitamin D deficiency may represent another risk factor for poor outcomes from COVID-19.

Relevance of Vitamin D
Vitamin D is a secosteroid hormone synthesized in the skin following exposure to UVB ultraviolet radiation where it mediates the conversion of 7-dehydrocholesterol to pre-Vitamin D3. Following transport to the liver, it is hydroxylated to 25(OH)D, the primary circulating form typically used to measure serum Vitamin D levels. 25(OH)D is subsequently converted to the biologically active form 1,25, dihydroxy vitamin D in the kidneys by 1-alpha hydrolase. This active form binds to its nuclear Vitamin D receptor to induce the transcription of over 200 genes, affecting a wide range of physiologic functions.

Multiple studies have documented significant Vitamin D deficiency in people of color, especially in AA. Heavily melanized skin retards the synthesis of Vitamin D and necessitates longer periods of sun exposure for adequate synthesis of Vitamin D. Ginde et al. assessed demographic differences and trends of Vitamin D insufficiency in a US population.2Serum 25(OH)D levels were compared over two time periods (1988–1994 and 2001–2004) from the Third National Health and Nutrition Examination Survey (NHANES III) data base including two large populations (n=18,883 and n=13,369, respectively). Non-Hispanic Blacks had a significantly higher prevalence of Vitamin D deficiency, increasing in severity in the later data base. Recent NHANES data from 2011–2014 further documented the high risk of deficiency in non-Hispanic Blacks. In a recent prospective cohort study of 14,319 subjects, an estimated 65.4% of non-Hispanic Blacks were deficient in Vitamin D, compared to 29% of Hispanics and 14% of non-Hispanic Whites.3

Vitamin D deficiency has been shown to be a risk factor for many of the comorbidities that disproportionately plague AA including diabetes, hypertension, cardiovascular disease, autoimmune diseases such as lupus erythematosus, as well as aggressive forms of breast and prostate cancer.4 While the classic role of Vitamin D involves calcium and phosphorus homeostasis for healthy bone metabolism, it exerts a spectrum of pleotropic effects impacting cell growth, differentiation, inflammation, and immune regulation. Healthy levels of Vitamin D have been linked to significantly reduced mortality and improved health outcomes. Numerous investigations document the prolific role of Vitamin D in antimicrobial defense and modulation of the innate and adaptive immune responses. It mediates the induction of key antimicrobial peptides in the respiratory epithelium including cathelicidin (LL37) and beta defensins, which destroy invading organisms. In addition, Vitamin D inhibits the production of pro-inflammatory cytokines including IL-2, IFN-γ, TNF-α, and IL-6, while promoting Th2 responses by increasing IL-4, IL-5, and IL-10 production, hence skewing T cell responses to a down regulated, anti-inflammatory state.4

For the general population, the US Institutes of Medicine (IOM) recommends Vitamin D supplementation at doses that vary according to age and are based primarily on bone health. Current IOM supplementation recommendations are 400 IU (10ug) for infants, 600 IU/d (15ug) for children, adolescents, and adults, and 800 IU/d (20ug) for adults aged over 70 years to maintain a 25(OH)D concentration of 20ng/mL or higher. However, in individuals who are deficient in Vitamin D (25(OH)D level <20 ng/ mL), of which patients with skin of color are at a higher risk, supplementation is considerably higher. These recommendations are summarized summarized in Table 1.5

Conclusions

Vitamin D deficiency has been well documented in people of color, in particular AA. The aforementioned data suggest a relationship between low Vitamin D status and COVID-19 mortality rates. While myriad socioeconomic and health care disparities may be contributing factors, we must indeed consider key biological variables, including Vitamin D status, that may impact these observations. Future prospective studies are necessary to confirm these findings. As there is currently no readily available treatment or vaccine for COVID-19, treating physicians should be cognizant of the higher prevalence of Vitamin D deficiency in skin of color populations and its emerging potential role in COVID-19 outcomes. Given the devastating statistics of COVID-19 among minority communities and the multifaceted role of Vitamin D in skin and systemic health, dermatologists are essential partners in decreasing health care disparities by initiating the vitamin D dialogue. As such, we can play an invaluable role in improving the health outcomes of our patients, particularly people of color, during and beyond the COVID-19 pandemic.

Read Full Article….

Jul 01
0

Frontal Fibrosing Alopecia Presenting as Androgenetic Alopecia in an African American Woman

By | Aesthetic Dermatology, Medical Dermatology, Sessions, Skin of Color Update Agenda | No Comments
Alopecia patient picture

Source: Next Steps in Derm

Frontal fibrosing alopecia (FFA) is a primary lymphocytic cicatricial alopecia that is currently regarded as a variant of lichen planopilaris. FFA has historically been considered rare in black patients, in whom traction alopecia, central centrifugal cicatricial alopecia, and androgenetic alopecia are frequently assumed to be more common. JDD author Kimberly Huerth, MD, ME describes a case of FFA in a black woman that both clinically resembled androgenetic alopecia and lacked many of the physical exam and dermoscopic findings associated with FFA. In doing so, she highlights the need for physicians to have a high index of suspicion for FFA in any black patient who presents with frontotemporal alopecia.

REPORT OF A CASE

A 53-year-old African American woman presented with a 6-month history of asymptomatic, moderately severe hair loss along the frontal hairline, which had not stabilized or improved with minoxidil 2% solution BID. Physical exam revealed decreased hair density affecting the frontal scalp, suggestive of androgenetic alopecia (Figure1). Dermoscopic examination showed decreased follicular ostia without perifollicular scaling or erythema. Eyebrow alopecia, facial papules, and glabellar red dots were absent, and there was no associated loss of body hair. A 4-mm punch biopsy sent for histopathologic examination revealed dense, chronic, perifollicular inflammation affecting the mid and upper portions of the follicles, with loss of associated sebaceous glands. Involved hairs demonstrated vacuolar interface disruption of the basilar and epibasilar layers at the level of the isthmus and infundibulum, with prominent exocytosis of lymphocytes into the outer root sheath. There was no miniaturization, dermal mucin, or inflammation affecting the epidermis, arrector pili muscles, and eccrine glands (Figure 2).

A diagnosis of FFA was confirmed by these findings. Our patient was managed with intralesional triamcinolone acetonide (10mg/cc) injections, clobetasol 0.05% ointment BID, hydroxychloroquine 200 mg PO BID, and minoxidil 5 mg PO daily. Unfortunately, her alopecia did not stabilize with these measures.

DISCUSSION

FFA is a primary lymphocytic cicatricial alopecia that is currently regarded as a variant of lichen planopilaris. It is characterized by band-like frontotemporal hairline recession, often with associated eyebrow alopecia, perifollicular erythema, and scaling. Clinical findings are frequently accompanied by pruritus and burning of the affected scalp. Since it was first described in 1994,1 FFA has largely been viewed as an alopecia of post-menopausal Caucasian women. This archetype has been maintained by patient demographics of subsequent published case series.2,3 FFA may thus be underdiagnosed in black women, in whom traction alopecia, central centrifugal cicatricial alopecia, and androgenetic alopecia are assumed to be more common. Furthermore, FFA can manifest uniquely in black women, who may be premenopausal4,5 and asymptomatic4 at the time of presentation. Classic signs of FFA may be subtle or absent among black patients, as increased pigmentation may render erythema difficult to appreciate, while oils and hair care products may diminish the appearance of scale.

It is important for dermatologists to both recognize that FFA is not uncommon in the black population,4,5 and to acknowledge how it initially came to be regarded as a disease of post-menopausal white women. Several of the larger published series come from geographic areas that lack a substantial skin of color population.2,3 There are also socioeconomic factors to consider. One series comprised exclusively of Caucasian women found their patients to be more affluent, which was speculated to be a surrogate marker for an unknown risk factor associated with the development of FFA.3 What these authors did not discuss, however, is that affluence enables access to specialty medical care. Affluence affects insurance status, which has been shown to vary widely among racial groups.6 Insurance status in turn bears upon who has access to dermatologic care, and who is ultimately included in a case series.

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