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Acquired aplastic anaemia in seven children with severe hepatitis with or without liver failure
Emma Honkaniemi1, Britt Gustafsson, Björn Fischler
1Department of Paediatrics, Karolinska University Hospital, Huddinge, Clintec, Karolinska Institutet, S-141 86 Stockholm, Sweden. emma.honkaniemi@karolinska.se
Insights
Hepatitis can lead to aplastic anemia in children, affecting both the liver and bone marrow. This study investigated the condition
Area of Science:
- Pediatric Hematology
- Hepatology
- Virology
Background:
- Aplastic anemia can follow hepatitis, particularly non-A, non-B, non-C types.
- Potential causes include viral infections and autoimmunity.
- The condition affects liver and bone marrow function.
Purpose of the Study:
- To describe the natural history of aplastic anemia following hepatitis in children.
- To investigate potential hepatitis-causing agents in this context.
Main Methods:
- Retrospective review of medical records.
- Analysis of bone marrow and liver biopsies.
- Evaluation of 7 children with severe hepatitis and subsequent aplastic anemia.
Main Results:
- Median time from hepatitis onset to aplastic anemia diagnosis was 54 days.
- No specific viral infections were identified.
- Liver biopsies showed lobular inflammation, suggesting viral etiology, not autoimmune hepatitis.
- Some children presented with low reticulocyte counts during hepatitis onset.
Conclusions:
- The pathogenesis likely involves simultaneous targeting of liver and bone marrow.
- Low reticulocyte counts and severe liver failure can occur concurrently.
- The exact causative agent remains unknown.
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.
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