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Two Distinct Quinidine-Induced Rheumatic Syndromes

MICHAEL G. COHEN, M.B.B.S.; SUMANT KEVAT, M.B.B.S.; MICHAEL V. PROWSE, M.B.B.S.; and MICHAEL J. AHERN, M.B.B.S.
[+] Article and Author Information

Grant support: in part by the Sutton Rheumatism Research Funds. Michael G. Cohen, M.B.B.S., is the recipient of the Frank G. Spurway Scholarship from the Arthritis Foundation of Australia.

▸Requests for reprints should be addressed to Michael G. Cohen, M.B.B.S.; Sydney University Department of Rheumatology, Royal North Shore Hospital, St. Leonards, 2065, New South Wales, Australia.


St. Leonards, Concord, and Daw Park, New South Wales, Australia


© 1988 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1988;108(3):369-371. doi:10.7326/0003-4819-108-3-369
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Of seven patients with quinidine-induced polyarthropathy, four had positive antinuclear antibodies and could be considered to have had quinidine-induced lupus erythematosus. The remaining three patients had milder symptoms, which occurred soon after the start of quinidine therapy, and did not have antinuclear antibodies. To confirm the association, the latter three patients were rechallenged with quinidine therapy, which caused recurrence of symptoms within 1 week. Antihistone antibodies, which are characteristic of drug-induced lupus erythematosus associated with procainamide and hydralazine therapy, were detected in all patients with quinidine-induced lupus erythematosus. An unusual characteristic of antihistone antibodies seen in two patients was the presence of high levels of IgG antibodies to histone H1 as well as H2A-H2B and H3-H4 complexes, without antibodies to the individual core histones.

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