nce immune responses, secondary infection and prolonged scratching can modify the clinical appearance of Hansen disease, this remains an important consideration for the diagnosis of chronic dermatoses. A 42-year-old man presented with intensely pruritic lesions of the neck, shoulders, upper chest and trunk since five years associated with chronic diarrhoea, progressive memory impairment and loss of weight. On examination, hyperpigmented, scaly and excoriated plaques were seen over the neck and upper trunk, multiple crusted or eroded papules and plaques were seen over the chest and there were additional scaly plaques seen over the posterior trunk and one lower limb. Photosensitive eruption was seen along with neurocognitive changes and diarrhoea, which led to a working diagnosis of pellagra; other diagnoses included psoriasis and pemphigus foliaceus. A bacterial culture obtained from an eroded lesion was positive for methicillin-sensitive Staphylococcus aureus. No clinical response was seen with nutritional supplementation, nicotinamide, systemic and topical corticosteroids, emollients and directed antibiotic therapy. Biopsy of skin from the chest showed that the dermis had well formed tuberculoid granulomas, while the epidermis showed parakeratosis, acanthosis and spongiosis. Near destruction of nerves and adnexal structures, epithelioid histiocytes, Langhans-type and foreign-body-type giant cells, a dense lymphocytic rim and prominent superficial dermal oedema were conspicuous features of granulomas, which were perivascular, perineural and periappendageal. This was consistent with finding a borderline tuberculoid Hansen disease and Type 1 lepra reaction. The case describes how a compelling clinical picture of pellagra may mimic leprosy and how careful histopathologic evaluation of a chronic dermatosis, when it fails to improve as expected, can help avoid the diagnosis of leprosy.