Hepatitis Associated with Aplastic Anemia: Do CD8(+) Kupffer Cells Have a Role in the Pathogenesis?

Excerpt

Hepatitis-associated aplastic anemia (HAAA), first described by Lorenz and Quaiser in 1955 [1], is a rare phenomenon which usually affects adolescents and young men [2] and is more common in the East than in the West [3‐5]. It represents a minor proportion of all aplastic anemia cases [6] and may occur in 28% of young adults after liver transplantation for non-A, non-B hepatitis [7]. Although a limited number of aplastic anemia cases have been reported in association with hepatitis A, B, and G, parvovirus B19, Epstein-Barr virus (EBV), transfusion transmitted virus (TTV), and echovirus [8‐20], the causative agent in most of the cases still remains unknown [21, 23]. Patients typically develop severe aplastic anemia 2 to 3 months after an episode of acute hepatitis. Aplastic anemia is always fatal if untreated [2, 11] and the hepatitis associated with this may be mild and transient [2, 22], fulminant [7, 23], or chronic [2]. There is no known relation to blood transfusion, drugs, or toxins. Though not clearly defined thus far, immunologic mechanisms seem to be responsible for HAAA, particularly because immunosuppressive therapy has shown some promising results. Nonetheless, most successful outcomes have been achieved by HLA-matched bone marrow transplantation (BMT) [21]. …