Abstract
Gout is a metabolic disorder of purine metabolism that results in crystallization of uric acid in the form of monosodium urate crystals, affects 8.3 million Americans and is the most common cause of inflammatory arthritis in adults. Urate lowering therapy is the mainstay of treatment for chronic gout. Initial treatments of choice in gout include allopurinol, a purine analog which inhibits xanthine oxidase and decreases the production of uric acid as well as probenecid which increases the urinary excretion of uric acid. However, 3% of patients will fail these treatments. In 2010, pegloticase, a recombinant urate oxidase conjugated to polyethylene glycol, was approved for these patients. Pegloticase has been shown to rapidly normalize plasma uric acid values, resolve tophi and improve quality of life in these patients. Hereby we present a case of a 50-year-old African male admitted to the hospital with symptomatic anemia 1 week after pegloticase infusion. He was found to have glucose-6-phosphate dehydrogenase deficiency, predisposing him to hemolytic anemia. Hereby we discuss his clinical course, and suggest glucose-6-phosphate dehydrogenase deficiency screening prior to pegloticase infusion.