A study of the mechanism of bone marrow failure in hepatitis-associated aplastic anemia.

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Hepatitis-associated aplastic anemia (H-AA) is a varient of acquired AA, in which hepatitis precedes AA by a period of weeks to months. Both etiology of hepatitis and a mechanism of bone marrow failure are unknown. Although hepatitis E virus (HEV) was studied by HEVIgG and HEVIgM in 16 patients with H-AA, it was not detected in all of them. Based on our result, it is concluded that HEV is not a candidate virus for H-AA. We studied HLA antigen in 30pts. with H-AA, 60pts. with idiopathic AA and 250 normal controls. The frequencies of DR9 antigen was significantly increased in the pts. with H-AA, compared to pts, with idiopathic AA or normal controls (relative risk : 4.1). In pts with HAA, absolute numbers of total lymphocytes, especially CD4 lymphocytes are markedly decreased. We analyzed the expression of Fas antigen on peripheral lymphocytes and BM CD34+cells of pts. with AA. Higher expression of Fas antigen on peripheral lymphocytes and BM CD34+cells was found in pts. with H-AA than in pts. with idiopathic AA or normal controls. Expression of Fas-ligand was also increased on peripheral and BM CD+3 lymphocytes. These results suggest that increased programmed cell death though Fas/Fas ligand system in HLA restricted individuals is a possible mechanism of bone marrow failure in pts. with H-AA.