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Rheumatoid Arthritis and Pure Red Cell Aplasia

EMMANUEL N. DESSYPRIS, M.D.; MARIA R. BAER, M.D.; JOHN S. SERGENT, M.D.; and SANFORD B. KRANTZ, M.D.
[+] Article and Author Information

Grant support: in part by the Veterans Administration, grant RR-95 from the General Clinical Research Centers Program of the Division of Research Resources, and grants AM-15555 and T32 AM-07186 from the National Institutes of Health.

▸Requests for reprints should be addressed to Emmanuel N. Dessypris, M.D.; Veterans Administration Medical Center, 1310 24th Avenue South; Nashville, TN 37203.


Nashville, Tennessee


Ann Intern Med. 1984;100(2):202-206. doi:10.7326/0003-4819-100-2-202
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Three patients with severe, deforming, and long-standing rheumatoid arthritis developed pure red cell aplasia that did not remit after withdrawal of medications, ran a chronic course, and in two patients remitted only after cytotoxic immunosuppressive treatment. An IgG inhibitor of autologous erythroid colony-forming and burst-forming unit growth in vitro was found in the serum of one patient. This specific erythropoietic inhibitor persisted in lower titer in the patient's serum even after an azathioprine-induced remission of pure red cell aplasia, indicating the possible need for maintenance immunosuppressive therapy. Chronic pure red cell aplasia may be another extra-articular manifestation of rheumatoid arthritis and should be considered when severe anemia develops in the absence of blood loss or hemolysis.

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