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Aspirin-induced hepatotoxicity in juvenile rheumatoid arthritis. A prospective study
Insights
Salicylate therapy can cause liver function abnormalities in children, particularly with higher serum salicylate levels. However, discontinuing aspirin is usually unnecessary unless bleeding occurs.
Area of Science:
- Pediatric Rheumatology
- Hepatology
- Pharmacology
Background:
- Biochemical alterations in liver function secondary to salicylate therapy have been reported.
- This study investigates these effects in children with various conditions.
Purpose of the Study:
- To prospectively evaluate liver function in children undergoing salicylate therapy.
- To correlate liver function test abnormalities with serum salicylate levels.
Main Methods:
- Serial monitoring of liver function tests (SGOT, SGPT, LDH, AP, bilirubin) and serum salicylate levels.
- Inclusion of children with juvenile rheumatoid arthritis, hip disease, and ulcerative colitis.
- Control group for comparison.
Main Results:
- 22/34 children with rheumatoid arthritis showed liver function abnormalities at serum salicylate levels of 7.0-18 mg%.
- 3 children experienced severe reactions (elevated liver enzymes, prolonged prothrombin time, epistaxis) at 18-43 mg% serum salicylate.
- 19 children had moderate changes (7.0-38.2 mg% serum salicylate), without prothrombin time prolongation.
Conclusions:
- Biochemical liver function abnormalities are common with chronic salicylate therapy in children.
- Severe reactions are rare and associated with higher serum salicylate levels and bleeding.
- Discontinuation of salicylates is generally not required unless bleeding occurs.
Abstract:
Recent reports of and our own experience with biochemical alterations of liver function secondary to salicylate therapy stimulated this prospective study. Thirty-four children with juvenile rheumatoid arthritis, 6 children with acute cartilagenous necrosis of the hipfollowing slipped capital femoral epiphysis, and 2 children with ulcerative colitis and hip disease who were on salicylates were followed over a period of 1-27 months with serial determinations of serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), lactic dehydrogenase (LDH), alkaline phosphatase (AP), bilirubin, and serum salicylate. Prothrombin time was measured in 14 children. Twenty-two of 34 children with rheumatoid arthritis and none of the 8 controls demonstrated abnormalities of various liver functions at serum salicylate levels between 7.0 and mg%. Three children demonstrated severe abnormalities characterized by marked elevation of SGOT, SGPT, LDH, and AP, prolongation of prothrombin time, and epistaxis. This type of reaction occurred within 5-14 days of initiation of aspirin therapy and occurred at serum salicylate levels between 18 and 43 mg%. Moderate changes in various liver function tests were observed in 19 other children. None of those children who were tested showed prolongation of prothrombin time. The serum salicylate level in this group varied between 7.0 and 38.2 mg%. The abnormal liver function tests returned to normal in 6 children upon withdrawal of aspirin and in 12 others even when salicylates were continued. Therefore, despite the occurrence of biochemical abnormalities following chronic salicylate therapy, it does not appear to be necessary to discontinue their use except in those children who develop bleeding.