Acute hepatitis as a prequel to very severe aplastic anemia

Abstract

Severe aplastic anemia is a rare and potentially life-threatening disease of the bone marrow often requiring allogeneic hematopoietic stem cell transplantation. Pathogenesis of the disease can vary and often remains enigmatic. Occasionally, severe aplastic anemia is associated with prior severe acute hepatitis. Differential diagnosis of acute non-viral hepatitis challenges the physician as pathogenesis remains unclear.We here present a case of a young patient presenting with acute hepatitis followed by severe aplastic anemia successfully treated with allogeneic hematopoietic stem cell transplantation. Due to immunosuppressive treatment with azathioprine for acute hepatitis of putative autoimmune pathogenesis and coincident infection with parvovirus B19, diagnosis of the sequential disease of acute hepatitis followed by severe aplastic anemia was complicated. We discuss the caveats and present a review of the literature.

Cynomolgus monkeys (Macaca fascicularis) experimentally and naturally infected with hepatitis E virus: The bone marrow as a possible new viral target

“…Experimentally infected animals, with chronic and acute hepatitis E, presented incipient histological signs, suggesting BM hyperactivation and dysfunction, characterized by vacuolization in endosteal cells, with some fields suggesting displasic focal disease. Medical research studies described severe aplastic anemia in association with parvovirus B19 (B19V), hepatitis A virus (HAV) and hepatitis C virus (HCV) infections [ 32 – 34 ]. Besides, recent studies described association between endosteal niche and loss of hematopoiesis homeostasis [ 35 , 36 ].…”

Diagnostic work‐up for severe aplastic anemia in children: Consensus of the North American Pediatric Aplastic Anemia Consortium

“…In a study of 213 children, Führer et al reported that the underlying etiology of aplastic anemia was 80% idiopathic, 9% post‐hepatitis, 7% other post‐viral, and 4% related to drugs and toxins 39 . Hepatitis‐associated aplastic anemia (HAAA) has been reported to constitute anywhere from 2% to 21% of SAA cases, depending upon the geographic region and study 37,38,40–44 . On rare occasions, hepatitis viruses including A, B, C, D, E and G, as well as parvovirus, cytomegalovirus (CMV), and Epstein–Barr virus (EBV), have been associated with the development of SAA 37,42,45–49 .…”

“…39 Hepatitis-associated aplastic anemia (HAAA) has been reported to constitute anywhere from 2% to 21% of SAA cases, depending upon the geographic region and study. 37,38,[40][41][42][43][44] On rare occasions, hepatitis viruses including A, B, C, D, E and G, as well as parvovirus, cytomegalovirus (CMV), and Epstein-Barr virus (EBV), have been associated with the development of SAA. 37,42,[45][46][47][48][49] However, in most cases of HAAA a cause cannot be identified, and the time interval between onset of hepatitis and a diagnosis of SAA can vary from 6 months to a concurrent presentation.…”

Niedokrwistość aplastyczna związana z zapaleniem wątroby

“…W większości opisywanych przypadków nie zaobserwowano obecności wirusów hepatotropowych [7][8][9][10][11][12][13][14][15][16]. Wśród [15].…”