Arthritis deferiprone

Oxidation of deferiprone with hypochlorous acid, the major oxidant of neutrophil leukocytes, results in the formation of a chemically reactive species, consistent with the quinone metabolite of deferiprone. Deferiprone-related agranulocytosis presumably results from a T cell-mediated immunological reaction, induced by a reactive metabolite of deferiprone (18). In one case agranulocytosis and systemic vasculitis (with arthritis, palpable purpura of the legs, erythema of the palms and soles, and desquamation of the skin over the distal phalanges) occurred in association with deferiprone (22). 

Castriota-Scanderbeg A, Sacco M. Agranulocytosis, arthritis and systemic vasculitis in a patient receiving the oral iron chelator LI (deferiprone). Br J Haematol 1997 96(2) 254-5. 

Cardiovascular A severe cardiomyopathy with congestive heart failure has been reported after withdrawal of deferiprone for severe arthritis [29 ]. 

Most patients with joint symptoms due to deferiprone are able to continue taking it, with or without NSAIDs. In 60 patients taking deferiprone, arthropathy occurred in only two, one of whom was described in detail, illustrating that deferiprone-induced arthritis can be severe and disabling [37 ]. 

Another patient, with suspected deferiprone-related heart failure, had acute severe bilateral arthritis of the knees 6 weeks after starting deferiprone, necessitating drug withdrawal [29 ]. 

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