|LETTER TO EDITOR
|Year : 2004 | Volume
| Issue : 4 | Page : 242-243
Colocalisation of alopecia areata and lichen planus
Bikash Ranjan Kar , Gigi Ebenezer , CK Job
Departments of Dermatology, Schieffelin Leprosy Research & Training Centre, Karigiri, Vellore, India
Dept of Dermatology, SLR & TC, Karigiri, India
|How to cite this article:|
Kar BR, Ebenezer G, Job C K. Colocalisation of alopecia areata and lichen planus. Indian J Dermatol Venereol Leprol 2004;70:242-3
|How to cite this URL:|
Kar BR, Ebenezer G, Job C K. Colocalisation of alopecia areata and lichen planus. Indian J Dermatol Venereol Leprol [serial online] 2004 [cited 2020 Oct 25];70:242-3. Available from: https://www.ijdvl.com/text.asp?2004/70/4/242/12365
Frequent associations between alopecia areata and immune-mediated cutaneous disorders have been reported. Being common skin disorders, lichen planus and alopecia areata may rarely coexist. We report a case of co-localization of lichen planus and alopecia areata.
A 42-year-old man presented with a single patch of non-scarring hair loss of 4 months' duration over the right parieto-occipital region. Alopecia areata was diagnosed and he was treated with topical betamethasone dipropionate. With that the lesion became static. He had no other lesion on any hair-bearing area.
Three months after the appearance of the initial lesion he developed a solitary violaceous papule in the center of the patch [Figure - 1]. The lesion was pruritic and mildly scaly. No mucosal lesion was present. A biopsy from the patch of alopecia revealed a typical perifollicular “swarm of bees” type lymphocytic infiltrate consistent with a diagnosis of alopecia areata (AA) [Figure - 2]. A biopsy from the central papular lesion showed hyperkeratosis, wedge-shaped hypergranulosis, irregular acanthosis, basal cell liquefaction and a band-like lymphocytic infiltrate and pigment incontinence in the superficial dermis suggestive of a diagnosis of lichen planus (LP) [Figure - 3].
Kanwar et al reported 20-nail dystrophy in a patient of AA due to LP. Brenner et al reported a case of coincidence of five dermatological disorders: vitiligo, AA, onychodystrophy, morphea and LP. Similarly, ulcerative colitis, myasthenia gravis, LP, AA and vitiligo were present in a single patient reported. Patients with AA were found to be at a higher risk for developing LP (RR=2.7; 95% confidence interval, 1.1 to 6.5). However, co-localization is very rare. Dhar et al had reported one child with co-localization of lesions both conditions. The incidence of AA in the Indian population is 0.7%7 whereas it is 0.8% for LP.8 The coexistence of these disorders may be purely coincidental. Gilhar et al found that induction of AA was possible with injection of CD8+ cells cultured with follicular homogenate but not with cultured CD4+ cells. The T lymphocyte is also pivotal in regulating epidermal cell recognition and epithelial destruction in lichen planus. T cells become activated via antigen-presenting cells such as Langerhans cells in conjunction with epidermal keratinocytes and co-stimulatory molecules. Though both CD4+ and CD8+ T cells are found in the lesional skin of LP, progression of disease leads to the preferen-tial accumulation of CD8+ cells. The majority of the lymphocytes in the infiltrate of LP are CD8+ and CD45RO (memory)-positive cells and express the g/d T-cell-receptor. The ensuing immune reaction by CD8+ T lymphocytes against activated keratinocytes results in epidermal cell damage and development of the lichenoid reaction that is the hallmark of lichen planus.
Further studies might clarify whether co-localization of lichen planus and alopecia areata is a mere coincidence or represents a common pathogenic mechanism in these two predominantly CD8+ T lymphocyte-mediated disorders.
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