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Immunologic Defects in Young Male Patients with Hepatitis-Associated Aplastic Anemia

KENNETH A. FOON, M.D.; RONALD T. MITSUYASU, M.D.; ROBERT W. SCHROFF, Ph.D.; ROSEMARY E. McINTYRE, M.D.; RICHARD CHAMPLIN, M.D.; and ROBERT PETER GALE, M.D.
[+] Article and Author Information

Grant support: in part by grants CA-23175, CA-15688, and CA-12800 from the National Cancer Institute, and contract NO1-CO-75380 with the National Cancer Institute. Robert Peter Gale is a Scholar of the Leukemia Society of America.

▸Requests for reprints should be addressed to Kenneth Foon, M.D.; Biological Response Modifiers Program, National Cancer Institute—Frederick Cancer Research Facility, Building 560; Frederick, MD 21701.


Frederick, Maryland; and Los Angeles, California


Ann Intern Med. 1984;100(5):657-662. doi:10.7326/0003-4819-100-5-657
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Extensive immunologic studies were done in 97 patients with severe aplastic anemia between 1973 and 1979. Sixteen young male patients with hepatitis-associated aplastic anemia appeared to constitute a unique subset. Compared with most patients with aplastic anemia from other causes, these 16 patients had significant reductions in the mean values of circulating T lymphocytes, serum IgG and IgM, mitogen reactivity, and decreased cutaneous hypersensitivity. The ratio of peripheral blood helper to suppressor T lymphocytes identified by monoclonal antibodies was within normal limits in 3 patients studied with hepatitis-associated aplastic anemia. Interestingly, the ratio was low (< 1) in 3 of 7 patients studied with aplastic anemia from other causes, although the mean for these 7 patients was normal. These data suggest that patients in this subset with hepatitis-associated severe aplastic anemia have a severe immunodeficiency. Whether this immunodeficiency is the cause or result of the hepatitis or aplastic anemia, or both, is unknown.

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