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Hepatotoxicity of dietary supplements containing Garcinia gummi-gutta (L.) N. Robson
Hepatotoxicity of dietary supplements containing Garcinia gummi-gutta (L.) N. Robson
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Hepatotoxicity of dietary supplements containing Garcinia gummi-gutta (L.) N. Robson
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Hepatotoxicity of dietary supplements containing Garcinia gummi-gutta (L.) N. Robson
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Hepatotoxicity of dietary supplements containing Garcinia gummi-gutta (L.) N. Robson
Hepatotoxicity of dietary supplements containing Garcinia gummi-gutta (L.) N. Robson
Journal Article

Hepatotoxicity of dietary supplements containing Garcinia gummi-gutta (L.) N. Robson

2025
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Overview
Botanical dietary supplements derived from the fruit of the tree (L.) N. Robson (commonly known as or ) are used to support weight loss but are increasingly linked to adverse events and case reports of liver injury. Clinical case reports of liver injury associated with dietary supplements were reviewed that had prompted the United States Pharmacopeia (USP) to revise the USP family of dietary ingredient monographs to include a cautionary statement regarding potential risk of liver damage. The terms ' ,' ' ,' or ' ' were searched in multiple databases of adverse events. PubMed and Google Scholar were searched for peer-reviewed papers describing preclinical and clinical studies of toxicity. More than 200 adverse events of liver injury resulting from consumption were identified. A total of 34 case reports of hepatotoxicity indicated one death and nine liver transplants, with 17 cases receiving CIOMS/RUCAM scores that indicated possible to highly probable causality due to dietary supplements. In one case, causality was confirmed by rechallenge with . toxicity was consistent with drug-induced liver injury and included elevated serum liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase with a high ratio of ALT to alkaline phosphatase. Proposed mechanisms of toxicity include genetic predisposition to immune-mediated reactions involving the human leucocyte antigen HLA-B*35:01 allele, induction of hepatocyte oxidative stress and inflammation, and hepatocyte apoptosis caused by the active constituent, hydroxycitric acid, which inhibits mitochondria ATP-citrate lyase.