Dr. Warren Heymann on Psoriatic Alopecia and Sebaceous Glands: An Unfinished Symphony | PracticeUpdate
Dr. Warren Heymann on Psoriatic Alopecia and Sebaceous Glands: An Unfinished Symphony
Every so often, patients with psoriasis would ask me about their hair loss, and I assumed that it was mechanical in nature, probably due to breakage of hair getting tangled in scales, and traumatized by pruritus. George et al., in their review of psoriatic alopecia, state, "Alopecia and other hair abnormalities occurring in patients with psoriasis were first recognized over four decades ago, yet psoriatic alopecia is not a well-known concept among clinicians."1 I am embarrassed to admit that I am one of those clinicians. It's time to appreciate the presentations of psoriatic alopecia – although much remains to be learned of its pathogenesis.
In a retrospective review of 33 scalp biopsies on 31 patients having histopathologic diagnosis of psoriasis, alopecia was a presenting feature in 48% of cases. The most common follicular-related changes were infundibular dilatation (87%) followed by perifollicular fibrosis (77%), perifollicular lymphocytic inflammation (68%), thinning of the follicular infundibulum (55%), and fibrous tracts (28%). Of interest, sebaceous glands were absent in 60% and atrophic in 25% of cases.2
Alopecia may occur within the plaque itself; it is usually non-scarring and improves with therapy. Scarring may occur in the context of secondary infection. Psoriatic alopecia may also appear as a generalized telogen effluvium, be associated with alopecia areata, or be due to medication, notably methotrexate or retinoids. Increasingly, there have been reports of psoriatic alopecia secondary to TNF-alpha inhibitors.1
TNF-alpha inhibitors may yield psoriatic alopecia in the context of their paradoxical reaction of causing (or exacerbating) psoriasis, regardless of whether prescribed for psoriasis, rheumatoid arthritis or Crohn's disease. In most cases, alopecia in psoriatic patients improves with standard therapy (such as topical steroids) or upon discontinuation of the inducing medication.
One of the major intrigues is trying to decipher what role the sebaceous gland has in this process. Liakou et al., performing histological and stereological analyses of involved and healthy skin of 14 psoriatic patients, were able to demonstrate a significant reduction of the number of sebaceous glands and the volume of the individual glands themselves. The authors speculated that the sebocytes may not differentiate properly in psoriasis, and may play a role in the pathogenesis of psoriasis and psoriatic alopecia.3 In a transcriptome study of lesional psoriatic skin vs normal skin, Rittié et al. found that a co-expressed gene module (N5) enriched 11.5-fold for lipid biosynthetic genes. They also observed fewer visible hairs in psoriatic skin, compared with uninvolved nonlesional psoriatic skin or normal skin (P < .0001). Sebaceous glands were markedly atrophic in psoriatic versus non-lesional psoriatic skin with a 91% average reduction in volume. These results suggested that loss of visible hair in psoriasis may result from abnormal sebaceous gland function.4
As stated earlier, there have been an increasing number of reports of TNF-associated psoriatic alopecia. Afanasiev et al. reported 3 cases in middle-aged women, with histories of either Crohn's disease or inflammatory arthritis, but without a prior history of psoriasis. Two patients received adalimumab and one infliximab. All 3 developed psoriatic plaques in the scalp with alopecia, after a variable length of time of being on TNF-inhibitors, ranging from 4 months to 3 years. Each patient improved after discontinuing the TNF inhibitor. Histologically, marked atrophy of the sebaceous glands was observed. A re-biopsy of the scalp in one of the patients showed regrowth of the sebaceous lobules upon stopping the TNF inhibitor therapy. The authors concluded that atrophy of sebaceous lobules is a potentially reversible, characteristic, and conspicuous feature of tumor necrosis factor inhibitor-associated psoriatic alopecia; this may be distinguished from idiopathic psoriatic alopecia by the clinical history of drug exposure and sometimes by the histologic presence of a mixed inflammatory response including plasma cells and eosinophils.5
The role of the sebaceous gland in psoriatic alopecia is speculative. Perhaps there is a mechanical component, in that drier hair may be more brittle and subject to trauma. The sebaceous gland is located just superior to the bulge area that harbors hair follicle stem cells; could it be that diminution of the sebaceous gland has some bearing on the regenerative capability of the hair follicle? Much remains to be learned about the relationship of the sebaceous gland with psoriatic alopecia. Until such time, patients may be reassured that their alopecia will likely improve with topical treatments, and/or removal of the offending agent.
Disclaimer: First published on Dr. Warren Heymann's Dermatology Insights and Inquiries website on June 25, 2017. Republished with permission.
Benjamin Hidalgo-Matlock
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