Objective: A beneficial role of antioxidants in hepatopathic obese individuals has hitherto been inferred only from uncontrolled pilot studies. The authors compared the effect of vitamin E and weight loss on transaminase values and on ultrasonographic bright liver in a controlled group of children with obesity-related liver dysfunction.
Methods: Twenty-eight children with obesity-related hypertransaminasemia and bright liver were randomly allocated to two single-blind groups: group 1 (n = 14) treated with a low-calorie diet associated with oral placebo for 5 months, and group 2 (n = 14) treated with a low-calorie diet associated with oral vitamin E (400 mg/d × 2 months, 100 mg/d × 3 months). Transaminase values and ultrasonographic liver brightness along with weight loss and vitamin E levels were monitored.
Results: Variations in transaminase levels and percentage of patients with normalized transaminase values were comparable in the two groups. The disappearance of bright liver was observed only in patients who lost weight and was twice as common in patients from group 1. Two subgroups of patients with complete normalization of transaminase values emerged as a consequence of controlled adherence to diet alone (n = 6; significant decrease of percent overweight:P = 0.0019 ) and to vitamin E alone (n = 7; unmodified percent overweight and significant increase of vitamin E/cholesterol ratio:P < 0.0001). Changes in treatment-induced alanine aminotransferase levels in these two subgroups were comparable at month 2, whereas values at month 5 were significantly lower in the subgroup adherent to diet alone (P = 0.04). In the subgroup adherent to vitamin E alone, after 2 months washout, transaminase remained stable in 5 patients and increased in 2; bright liver persisted in all.
Conclusions: Oral vitamin E warrants consideration in obesity-related liver dysfunction for children unable to adhere to low-calorie diets.
*Departments of Pediatrics and †Laboratory Medicine, University of Naples Federico II, and ‡European Laboratory for Food Induced Disease [ELFID], Naples, Italy.
Received January 31, 2003; accepted July 15, 2003.
Supported in part by Ministero dell'Université e della Ricerco Scientifice e Technologica (MURST).
Address correspondence and reprint requests to: Prof. Pietro Vajro, Department of Pediatrics, University of Naples “Federico II,” Via Pansini 5, 80131 Naples, Italy (e-mail: email@example.com).