Leprosy is a chronic, infectious, and debilitating disorder that primarily affects the skin and peripheral nerves. The disease course may be complicated by immune-mediated reactions during or after therapy, which may further worsen nerve damage. Type II lepra reaction (T2LR) is a painful inflammatory condition with systemic features, such as fever, tender erythematous nodules, arthritis, neuritis, orchitis, lymphadenitis, and iritis. Erythema nodosum leprosum (ENL), the hallmark of type II lepra reactions, results in hospitalization and consequent impairment in quality of life. The treatment options include long-term high-dose systemic corticosteroids, thalidomide, and/or clofazimine. However, the prognosis is often complicated by the adverse effects of the drugs; therefore, there is a need for alternative and safer therapies.
Herein, we present the case of a 31-year-old male with recurrent lepra reactions who did not respond adequately to steroids. Therefore, we initiated therapy with tofacitinib, a non-selective inhibitor of the Janus kinase/signal transduction and transcription activation (JAK/STAT) pathway. The results included complete resolution of abnormalities on blood laboratory investigations and symptomatic resolution of symptoms. In this article, we delve into the possible role of tofacitinib in T2LR and other inflammatory conditions.
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