Why the study?
Does vitamin A and E supplementation cause liver fibrosis in patients with familial homozygous hypobetalipoproteinaemia?
Does vitamin A and E supplementation cause liver fibrosis in patients with familial homozygous hypobetalipoproteinaemia?
Vitamin A and E supplementation may cause liver fibrosis in patients with familial homozygous hypobetalipoproteinaemia, highlighting the need for regular liver function monitoring.
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May warrant monitoring during vitamin A/E supplementation in hypobetalipoproteinaemia; leaves open causality and need for prospective data.
A case of apolipoprotein B-related disorder is reported in which liver fibrosis developed without long term administration of medium chain triglycerides, previously incriminated in the pathogenesis of this lesion. The patient was a young woman in whom the diagnosis of familial homozygous hypobetalipoproteinaemia was made at the age of 21. A first liver specimen taken at diagnosis revealed steatosis, hypertrophic Golgi apparatus and proliferating smooth endoplasmic reticulum. The patient was treated with vitamin A and E supplementation only. Two years later, a second liver biopsy, carried out because of increased serum alanine aminotransferase concentrations, showed fibrosis, mild cytolysis and marked mitochondrial alterations. Hepatic level of vitamin A was increased. This finding supports the hypothesis that liver disease observed in our patient might be an adverse effect of vitamin supplementation. Our observation underlines the importance of including liver function tests in the follow up of patients with apolipoprotein B-related disorders.
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Scoazec et al. (1992) studied this question.
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