Abstract

Gout, an inflammatory arthritis, is caused by an accumulation of monosodium urate crystals in the joints and soft tissues when serum uric acid concentrations rise above the physiological saturation limit (≥ 6.4 mg/dL). Here, we report the case of a 19 year-old male who presented with gradually progressive, nontender swelling of multiple joints of the upper and lower limbs of eight months’ duration. He had been receiving frusemide 40 mg, spirinolactone 50 mg, metoprolol 50 mg, and erythromycin 250 mg twice daily for the previous 12 months on account of rheumatic mitral stenosis (moderate). Though a histological diagnosis of gout is the gold standard, in our case we diagnosed frusemide-induced secondary gout with malignant course. This was based on a combination of an imaging tool (radiology showing well defined, ‘punched-out’ erosions with overhanging edges), and clinical presentation (soft tissue nodules, i.e. tophi , calcification of tophi, and asymmetric involvement). Frusemide was stopped, allopurinol and other urate lowering agent were started which led to regression of his swelling.

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