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Summary Erythema nodosum leprosum (ENL) is a severe immune reaction commonly encountered as a complication in patients with multibacillary leprosy. Management of chronic ENL in leprosy is challenging and necessitates the use of systemic immunosuppressants, including corticosteroids and thalidomide. No single drug is universally effective and most current therapeutic agents carry a significant risk of systemic toxicity. Apremilast is an orally effective phosphodiesterase‐4 inhibitor with a potent immunomodulatory action and is clinically effective in inflammatory conditions like chronic plaque psoriasis. We report two patients with poorly controlled chronic ENL, despite the use of multiple therapeutic agents. Both patients demonstrated significant clinical improvement with apremilast, without any adverse effects, thereby suggesting its potential as a novel therapeutic option in chronic ENL. What's already known about this topic? Erythema nodosum leprosum (ENL) is an immune‐mediated reaction in patients with multibacillary leprosy, with chronicity and recurrences frequently reported. Management of chronic ENL requires systemic immunosuppressants like corticosteroids, which may not be universally effective and carry a risk of serious toxicity. Apremilast is an oral immunomodulator with good efficacy in inflammatory conditions like chronic plaque psoriasis. What does this study? Apremilast may be an effective therapeutic agent in patients with chronic ENL.

We report two cases of synovial chondromatosis presenting with peripheral nerve compression syndromes involving respectively the median nerve at the wrist and the posterior interosseous nerve at the elbow. Only one previous instance of nerve compression due to this condition has been described, involving the ulnar nerve at the elbow. In one of our cases the disease process was at an early stage in its natural history and in the other at an advanced stage. The occurrence of nerve compression was related to the site rather than the stage of the disease. Full recovery followed local excision with decompression of the peripheral nerve involved.

Dear Editor, Coronavirus disease (COVID-19) is a global pandemic caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which has caused unforeseen mortality, morbidity, and severe economic disruptions in recent times. Of late, there has been a growing interest regarding the dermatological manifestations in COVID-19. In an early retrospective study among 140 patients, Zhang et al 1 reported 11.4% patients to have drug hypersensitivity and 1.4% to have urticaria. In a report from Italy, 18/88 (20.5%) patients had dermatological manifestations, with 3 patients reporting widespread urticaria. 2 As per one review, 88/256 (34.3%) patients across 16 studies demonstrated skin manifestations, mostly as erythematous maculopapular rash, urticaria, or vesicular rash. 3 On closer look, we find urticaria to be a commonly reported finding among COVID-19 patients. In one of the large prospective studies involving 375 COVID-19 cases, urticaria was present in 19% cases, with mean duration of urticaria being 6.8 days. 4 Although there was a report of one COVID-19 patient presenting with urticaria and dry cough without any fever, 5 the timing of appearance of urticaria was variable, with lesions appearing before, with, as well as >48 hours after onset of fever. 6-9 In most cases, diagnosis of urticaria was made clinically and oral second-generation antihistamines were prescribed with satisfactory results. 6-9 Although skin manifestations did not correlate with disease severity in most case reports, 2,6 the prospective study from Spain suggested that the presence of urticaria and maculopapular lesions was associated with more severe COVID-19 illness and a higher (2%) mortality. 4 Pathophysiology of urticaria in COVID-19 infection is hypothesized to be multifactorial. Although drug-induced urticaria may be an obvious explanation, urticaria preceded drug therapy or showed spontaneous remission despite continuation of therapy for COVID-19, 6 suggesting that drugs alone may not account for many cases. A direct role of virus-induced mast cell degranulation may be one possibility. SARS-CoV-2 enters cells using angiotensin-converting enzyme-2 protein, which is also present in vascular tissues. Deposition of antigenantibody complexes leading to complement activation and mast cell degranulation, as well as bradykinin involvement, has been suggested as mechanisms of virus-induced urticaria or urticarial vasculitis.