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

doi:10.1059/0003-4819-100-5-657

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

Frederick, Maryland; and Los Angeles, California

Abstract

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.

Article and Author Information

▸From the Biologic Therapeutics Branch, Biologic Response Modifiers Program, Division of Cancer Treatment, National Cancer Institute, Frederick Cancer Research Facility, Frederick, Maryland; and the Division of Hematology-Oncology and the Medical Immunology Laboratory, the Departments of Medicine, Microbiology, and Immunology, Transplantation Biology Unit, University of California School of Medicine and the Wadsworth Medical Center, Los Angeles, California.
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.