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Acquired aplastic anaemia in seven children with severe hepatitis with or without liver failure
Author(s) -
Honkaniemi Emma,
Gustafsson Britt,
Fischler Björn,
Nemeth Antal,
Frost BrittMarie,
Papadogiannakis Nikos,
Winiarski Jacek
Publication year - 2007
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.2007.00491.x
Subject(s) - medicine , aplastic anemia , hepatitis , viral hepatitis , liver biopsy , bone marrow failure , etiology , hepatitis c , immunology , bone marrow , autoimmune hepatitis , gastroenterology , pediatrics , biopsy , haematopoiesis , stem cell , biology , genetics
Aim: Aplastic anaemia following hepatitis may develop in as many as 1 of 3 patients with non‐A, non‐B and non‐C hepatitis. Several causative factors have been discussed, such as viral infections and autoimmunity. Here we describe the natural history of this condition in 7 children and investigate possible hepatitis‐causing agents. Methods: We reviewed the medical records, bone marrow and liver biopsies of 7 children with severe hepatitis, with or without liver failure, who subsequently had developed aplastic anaemia. Results: The median time from onset of hepatic symptoms until diagnosed onset of aplasia was 54 days. No associated viral infections could be identified. On liver biopsy, a majority had lobular inflammation but lacked signs of autoimmune hepatitis, findings compatible with a viral aetiology. Three of 6 children had low reticulocyte counts already at onset of hepatitis. All, but one patient is alive at median follow‐up of 8 years. Conclusion: The unknown pathogenetic mechanism appears to target liver and bone marrow simultaneously, because half of the children concomitantly had low reticulocyte counts and severe liver failure.