engleski

Spiny follicular hyperkeratosis in a psoriasis patient treated with ustekinumab

We present a psoriasis patient developing asymptomatic white spiny follicular hyperkeratoses (SFH) after being treated with ustekinumab for 3 months. This type of eruption has been described under several names including spiny follicular keratoderma, hyperkeratotic spicules, filiform hyperkeratoses, parakeratotic horns, and follicular hyperkeratoses (1). Facial hyperkeratotic spicule eruption was reported in association with monoclonal gammopathy. Drug-induced filiform hyperkeratosis has been reported with cyclosporine, with BRAF inhibitors (vemurafenib), with acitretin and with vismodegib and sorafenib. Our patient started ustekinumab treatment in June 2015. At the same time he was treated with metothrexate, folic acid, metformin and lisinopril/hydrochlorothiazide. Three months after ustekinumab introduction patient noticed growth of tiny skin projections located on the face, scalp, upper trunk and upper arms. Each spiny lesion was approximately 0, 5 to 1 mm in diameter and up to 5 mm high. A biopsy of a white spiny keratotic projection showed orthokeratosis, achantosis and mild spongiosis in epidermis, inflammatory infiltrate in chorium and dilatated acrotrichiums. Condition resolved in several weeks without any treatment and without ustekinumab cessation. RESULTS: A similar condition viral-associated trichodysplasia (TS) was originally described in 1999 as a folliculocentric viral infection in a patient who was receiving cyclosporine after kidney and pancreas transplantation. Trichodysplasia spinulosa associated polyomavirus (TSPyV) was identified in TS lesions and shown to be the probable cause of this disease (2). Pathogenesis both of viral-associated TS and BRAF inhibitor-induced SFH is based on the paradoxical activation of MAPK (mitogen- activated protein kinase) pathway, which regulates a variety of cellular processes including cell division, differentiation and apoptosis . Our patient developed SFH possibly due to use of ustekinumab, IL-12 and IL-23 inhibitor. The latter has a role in differentiation process of the skin (12), suggesting that inhibition of IL-23 might explain the imperfect keratinization process observed in SFH. Considering that in our patient drug was not stopped and the condition resolved in several weeks without any treatment, possible cause could be ustekinumab-induced imunosupression and consequent viral infection.

ustekinumab, psoriasis, spiny follicular hyperkeratosis

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