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Bone marrow failure in children with acute liver failure
Insights
Bone marrow failure affects over 10% of children with acute liver failure, sometimes linked to specific viral infections. Treatment with antithymocyte globulin (ATG) or antilymphocyte globulin (ALG) shows success in managing this complication.
Area of Science:
- Pediatric Hematology
- Hepatology
- Infectious Diseases
Background:
- Aplastic anemia is a rare, fatal complication of acute liver failure (ALF) in children.
- Etiology remains unknown, with treatment options including immunosuppression or transplantation.
- This study investigates the incidence, causes, treatment, and outcomes of bone marrow failure in pediatric ALF.
Purpose of the Study:
- To determine the incidence of bone marrow failure in children with ALF.
- To identify potential causes and associated infections.
- To evaluate treatment strategies and patient outcomes.
Main Methods:
- Retrospective chart review of 75 pediatric patients diagnosed with ALF.
- Analysis of patient demographics, clinical presentation, laboratory data, and treatment received.
- Assessment of bone marrow recovery and patient survival.
Main Results:
- Bone marrow failure (aplastic anemia or transient suppression) occurred in 8/75 (10.7%) pediatric ALF patients.
- Associated causes included parvovirus B19 and non-A, non-B, non-C hepatitis.
- Treatment with antithymocyte globulin (ATG) or antilymphocyte globulin (ALG) led to recovery in most cases, though outcomes varied with liver transplantation.
Conclusions:
- Bone marrow failure is a significant complication in pediatric ALF, occurring in over 10% of cases.
- Viral infections are implicated, highlighting the need for targeted diagnostics.
- Immunosuppressive therapy (ATG/ALG) is effective and well-tolerated for managing bone marrow failure in this population.
Background:
Aplastic anemia is a rare but well-recognized complication of acute hepatitis and acute liver failure. The cause is unknown, and the condition is fatal without bone marrow recovery. Treatment includes immunosuppression regimens or bone marrow transplantation. The purpose of this study was to investigate the incidence, cause, treatment, and outcomes of this disorder in children.
Methods:
Retrospective chart review of 75 patients with acute liver failure in a major pediatric liver center.
Results:
Eight patients had evidence of bone marrow failure. Of those, six had aplastic anemia, and two had transient bone marrow suppression. There were five boys, median age 57 months (range, 36-132 months). Two had parvovirus B19, six had non-A, non-B, non-C hepatitis. Five underwent liver transplantation: auxiliary in one, orthotopic in four. The interval between initial symptoms and development of aplastic anemia and/or bone marrow suppression was 21 to 99 days (median, 39 days). Four patients with aplastic anemia received intravenous antithymocyte globulin (ATG) or antilymphocyte globulin (ALG). Median recovery period of granulopoiesis was 62 days (range, 27-115 days). Two made a full recovery, one had myelodysplasia, and one with unresponsive disease died of septic complications. Four did not receive ATG/ALG, two had aplastic anemia, and two had bone marrow suppression. Three underwent liver transplantation, and all four resumed granulopoiesis. One child who underwent liver transplantation died of sepsis with chronic rejection. Median recovery of granulopoiesis was 99 days (range, 20-153 days).
Conclusions:
Bone marrow failure occurs in 10.7% of children with acute liver failure. It sometimes occurs in association with non-A, non-B, non-C hepatitis and parvovirus B19 infection. Treatment with ATG/ALG is successful and is well tolerated in most cases.