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Case series reveals recurrent pancytopenia, coagulopathy, and renal failure in patients with unsuspected quinine exposure, indicating immune destruction across multiple blood cell lineages.
Brief Reports1 August 1993Recurrent Pancytopenia, Coagulopathy, and Renal Failure Associated with Multiple Quinine-dependent AntibodiesRobert B. Maguire, MD, David F. Stroncek, MD, and Allan C. Campbell, MDRobert B. Maguire, MDFrom the University of Illinois College of Medicine at Peoria, St. Francis Medical Center, and Proctor Hospital, Peoria, Illinois; the University of Minnesota Medical School, Minneapolis, Minnesota; the American Red Cross, St. Paul, Minnesota., David F. Stroncek, MDFrom the University of Illinois College of Medicine at Peoria, St. Francis Medical Center, and Proctor Hospital, Peoria, Illinois; the University of Minnesota Medical School, Minneapolis, Minnesota; the American Red Cross, St. Paul, Minnesota., and Allan C. Campbell, MDFrom the University of Illinois College of Medicine at Peoria, St. Francis Medical Center, and Proctor Hospital, Peoria, Illinois; the University of Minnesota Medical School, Minneapolis, Minnesota; the American Red Cross, St. Paul, Minnesota.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-119-3-199308010-00006 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Immune thrombocytopenia mediated by drug-dependent antibodies to platelets is a well-known adverse reaction to quinine [1, 2]. Recent reports of disseminated intravascular coagulation [3] and the hemolytic uremic syndrome [4, 5] in association with multiple quinine-dependent antibodies suggest the existence of immune-mediated effects on cell lines other than platelets. We describe two patients who were not known to be taking quinine and who had a recurrent febrile illness associated with pancytopenia and renal failure along with serologic evidence of drug-dependent platelet, neutrophil, and erythrocyte antibodies.Case ReportsPatient 1A 41-year-old white woman came to the emergency department in August ...References1. Belkin GA. Cocktail purpura. An unusual case of quinine sensitivity. Ann Intern Med. 1967; 66:583-6. Google Scholar2. Berndt MC, Chong BH, Andrews RK. Biochemistry of drug-dependent platelet autoantigens. In: Kunicki TJ, George JN; eds. Platelet Immunobiology: Molecular and Clinical Aspects. Philadelphia: J.B. Lippincott; 1989:132. Google Scholar3. Spearing RL, Hickton CM, Sizeland P, Hannah A, Bailey RR. Quinine-induced disseminated intravascular coagulation. Lancet. 1990; 336:1535-7. Google Scholar4. Gottschall JL, Elliot W, Lianos E, McFarland JG, Wolfmeyer K, Aster RH. Quinine-induced immune thrombocytopenia associated with hemolytic uremic syndrome: a new clinical entity. Blood. 1991; 77:306-10. Google Scholar5. Stroncek DF, Vercellotti GM, Hammerschmidt DE, Christie DJ, Shankar RA, Jacob HS. Characterization of multiple quinine-dependent antibodies in a patient with episodic hemolytic uremic syndrome and immune agranulocytosis. Blood. 1992; 80:241-8. Google Scholar6. Hyler SE, Sussman N. Chronic factitious disorder with physical symptoms (the Munchausen syndrome). Psychiatr Clin North Am. 1981; 4:365-77. Google Scholar7. Reid DM, Shulman NR. Drug purpura due to surreptitious quinidine intake. Ann Intern Med. 1988; 108:206-8. Google Scholar8. Chong BH, Berndt MC, Koutts J, Castaldi PA. Quinidine-induced thrombocytopenia and leukopenia: demonstration and characterization of distinct antiplatelet and antileukocyte antibodies. Blood. 1983; 62:1218-23. Google Scholar9. Salama A, Mueller-Ekhardt C. Immune-mediated blood cell dyscrasias related to drugs. Semin Hematol. 1992; 29:54-63. Google Scholar Author, Article, and Disclosure InformationAffiliations: From the University of Illinois College of Medicine at Peoria, St. Francis Medical Center, and Proctor Hospital, Peoria, Illinois; the University of Minnesota Medical School, Minneapolis, Minnesota; the American Red Cross, St. Paul, Minnesota.Corresponding Author: David Stroncek, MD, University of Minnesota Hospital and Clinic, Department of Laboratory Medicine and Pathology, Blood Bank Laboratory, Box 198 UMHC/D211 Mayo, 420 Delaware Street SE, Minneapolis, MN 55455.Acknowledgments: The authors thank Mary Egging, Gail Eiber, Greg Herr, Jane Swanson, and Shelley Pulkrabek for their technical assistance and Bobbie Gibson for help in manuscript preparation.Grant Support: In part by funds from the Residents' Research Fund, St. Francis Medical Center, and The American Red Cross St. Paul Regional Blood Services. 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