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November 1971

Mechanism of Aspergillus-Induced Microangiopathic Hemolytic Anemia

Author Affiliations


From the departments of pathology and medicine, Harvard Medical School, and the James Homer Wright Pathology Laboratories and the Departments of Medicine, Massachusetts General Hospital, Boston. Dr. Robboy is now with US Ireland Army Hospital, Fort Knox, Kentucky.

Arch Intern Med. 1971;128(5):790-793. doi:10.1001/archinte.1971.00310230120013

Florid microangiopathic hemolytic anemia (MHA) is encountered in few disease states. The most common are thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome of infancy, and disseminated intravascular coagulation (DIC). Red blood cell (RBC) fragmentation may occur clinically in the latter secondary to carcinoma1 or septicemia and in the laboratory following intravenous injections of thrombin or endotoxin into animals.2 Less frequently, fragmentation is seen with malignant hypertension, severe preeclampsia or eclampsia, or acute necrotizing glomerulonephritis.2

Recently, we encountered a patient who developed MHA and DIC while he was receiving steroids and antibiotics. Subsequently we encountered a second patient who developed leukoerythroblastosis and DIC, suggestive of MHA, while she too was receiving steroids.3 Two additional cases4,5 (Table) suggested that this peculiar combination of findings was not coincidental. These microangiopathic changes appear to be in vivo manifestations of the in vitro models of Bull et al6 in which RBC moving at high speeds

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