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[Chronic idiopathic hypertransaminasemia]
Insights
Pediatric idiopathic hypertransaminasemia often shows mild aminotransferase elevations. Liver biopsy is recommended for diagnosis, revealing metabolic issues in most children, guiding further investigation.
Area of Science:
- Pediatric Gastroenterology and Hepatology
- Clinical Biochemistry
- Diagnostic Pathology
Background:
- Elevated aminotransferase serum levels are common in children.
- Idiopathic hypertransaminasemia lacks a clear cause in many pediatric cases.
- Understanding the underlying etiology is crucial for appropriate management.
Purpose of the Study:
- To retrospectively evaluate clinical patterns of chronic idiopathic hypertransaminasemia in children.
- To assess the diagnostic utility of various investigations, including liver biopsy.
- To identify underlying causes and guide diagnostic approaches.
Main Methods:
- Retrospective analysis of 108 pediatric patients with chronic idiopathic hypertransaminasemia.
- Data collected via questionnaires sent to 11 Italian Pediatric Centers.
- Review of clinical data, liver function tests, ultrasound, and liver histology where available.
Main Results:
- Most patients were asymptomatic with mild aminotransferase elevations (rarely >5x normal).
- Only 25.9% normalized levels during a 22-month follow-up; no clinical liver disease signs observed.
- Liver histology in 46 patients revealed metabolic alterations (65%) more frequently than inflammation (13%).
Conclusions:
- Liver histology is informative in diagnosing idiopathic chronic hypertransaminasemia in children.
- Metabolic alterations are common findings, suggesting a need for targeted investigations.
- Histologic evaluation should be considered in the diagnostic workup for these patients.
Abstract:
The elevation of aminotransferase serum levels is frequently encountered in pediatric practice. We have retrospectively evaluated the clinical patterns of 108 patients with chronic, so called "idiopathic", alterations of aminotransferases, by sending a questionnaire to 11 Italian Pediatric Centers. The average period of follow-up was 22 months. Patients, whose ages ranged through all pediatric ages, were mostly asymptomatic and with a rather insignificant physical examination. The average rise of aminotransferases value was generally limited within 2 times the upper normal level and the highest value, during the period of follow-up, never exceeded 5 times the upper normal level. Other liver function tests did not result generally altered significant. Just 25,9% of the patients normalized aminotransferases serum level during the follow-up period. All maintained good physical status with no clinical signs of liver disease. A muscular cause of hyper-transaminasemia was excluded in all the cases. Possible infective causes (HBV and HCV) autoimmune hepatitis, Wilson disease, alfa1 antitripsine deficiency and hyperammoniemia were excluded. Ultrasound investigation did not seem to be a sensitive investigation, resulting negative in 54/82. Histologic liver examination was more informative. This evaluation, performed in 46/108 patients, showed infarct metabolic alterations (steatosis, nucleus glucogenic degeneration, cytoplasmatic clarification) in 65% of cases and inflammatory findings in only 13% of cases. In conclusion, our results suggest the opportunity to enclose liver histologic study in the diagnostic approach of children with hepatic idiopathic chronic hypertransaminasemia. This approach may address the clinician, in a more aimed way, towards further investigations.