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Alpha-Interferon for Severe Cold Agglutinin Disease

Brian M. O'Connor, MD; Jacqueline S. Clifford, BS; William D. Lawrence, MD; and Gerald L. Logue, MD
[+] Article and Author Information

Requests for Reprints: William D. Lawrence, MD, Century Medical Associates, 1616 Kensington Avenue, Buffalo, NY 14215.

Current Author Addresses: Drs. O'Connor and Logue: Department of Medicine, Buffalo Veterans Administration Medical Center, 3495 Bailey Avenue, Buffalo, NY 14215.

Ms. Clifford: Department of Pathology, Buffalo Veterans Administration Medical Center, 3495 Bailey Avenue, Buffalo, NY 14215.

Dr. Lawrence: Century Medical Associates, 1616 Kensington Avenue, Buffalo, NY 14215.


Ann Intern Med. 1989;111(3):255-256. doi:10.7326/0003-4819-111-3-255
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This excerpt has been provided in the absence of an abstract.

Cold agglutinin disease may be classified as primary or secondary. Monoclonal IgM (occasionally IgG or IgA) proteins with the ability to bind to erythrocytes below body core temperature are found in the sera of patients with the primary (idiopathic) and secondary forms associated with lymphoproliferative disorders (1). In these disorders mild to moderate hemolytic anemia results from the deposition of complement as the cold agglutinin binds to the erythrocyte in the acral circulation. On exposure to cold, episodes of hemoglobinuria related to marked intravascular hemolysis may occur. Exposure to cold may also produce painful acrocyanosis caused by sludging and deoxygenation

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