Contact immunotherapy-induced Renbök phenomenon in a patient with alopecia areata and psoriasis vulgaris

ARTICLE

Auteur(s) : Taisuke Ito, Hideo Hashizume, Masahiro Takigawa

Department of Dermatology, Hamamatsu University School of Medicine, Hamamatsu, Japan, 1-20-1 Handayama, Higashi-ku, Hamamatsu 431-3192 Japan

Happle et al. first introduced the term “Renbök phenomenon”, derived from the reversal of “Köbner”, to describe the observation of normal hair growth in psoriatic lesions in patients with co-existing psoriasis and alopecia areata (AA) [1]. Although the exact mechanism of this unique phenomenon is unknown, it has been proposed that biological events inherent in psoriasis may act on hair follicles to restore hair growth in AA. We herein describe the Renbök phenomenon related to contact immunotherapy in a patient suffering from AA and psoriasis vulgaris.

A 15-year-old girl presented with a 3-year history of patchy hair loss on the vertex of the scalp with a gradual increase in the number of lesions. In addition, scaly and erythematous eruptions appeared on her scalp and upper extremities one year after the onset of scalp hair loss. Initial examination at our outpatient clinic revealed multiple hair loss patches on her scalp and scaly lesions on her scalp and upper extremities. Interestingly, the presence of terminal hair coincided with the scaly lesions (figure 1A). There was no associated systemic disease nor was there any family history of AA or psoriasis vulgaris.

Hematoxylin and eosin (H-E)-stained sections of a biopsy specimen from a hair loss patch revealed lymphocyte infiltration around atrophic hair follicles, compatible with the diagnosis of AA. The biopsy specimen from a scaly lesion of the right antebrachium showed parakeratosis, psoriasiform acanthosis, thin but club-shaped rete ridges, Munro’s microabscesses and perivascular infiltration of lymphocytes. Results of laboratory studies including a hemogram and blood chemistry tests and thyroid autoantibodies were normal or negative. She had HLA-DQB1* 0301 (a gene susceptibility to AA) but was negative for HLA-Cw6 and HLA-DR7, which are genetic loci relating to psoriasis [2].

Contact immunotherapy with squaric acid dibutylester (SADBE), and topical maxacalcitol and betamethasone butyrate propionate were instituted for AA and psoriasis, respectively. Three months following contact immunotherapy, terminal hairs re-grew but psoriatic lesions developed at the sites of SADBE application (figure 1B), which were then successfully treated with maxacalcitol lotion. Other pre-existing psoriatic lesions responded well with the 4 weeks of the topical treatment. One year later, the hair loss and psoriasis were markedly improved, although a few hair loss patches occasionally recurred.

In our case, contact immunotherapy was effective for AA but also induced psoriatic lesions at the site of treatment. Orecchia et al. report a case of alopecia universalis in which there was a concomitant appearance of hair regrowth and psoriatic plaques in the same area following contact immunotherapy with SADBE [3]. Contact immunotherapy appears to modulate cytokine production in the skin with a decrease in the mRNA expression of interferon (IFN)-γ while mRNA for IL-2, IL-8, IL-10 and tumor necrosis factor (TNF)-α is increased [4]. AA is regarded as a tissue-specific autoimmune disease against melanin-associated proteins in the hair follicle [5]. IFN-γ may contribute to initiating the disease process by collapsing the hair follicle immune privilege and resulting in the exposure of autoantigens [5]. On the other hand, TNF-α is a crucial cytokine in psoriatic lesions [6]. Therefore, we propose that a change in the cytokine milieu due to contact immunotherapy may play an important role in both the improvement of alopecia and the induction of psoriasis.

Acknowledgements

References

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