ArticleCureus2026
Glucagon-Like Peptide-1 (GLP-1) Receptor Agonist Treatment After Liver Transplantation: A Hypothesis-Generating Case Report.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
2 authors.
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Abstract
Glucagon-like peptide-1 receptor agonists (GLP1RAs) are widely used for the management of type 2 diabetes (T2D) and obesity, yet their safety profile in liver transplant recipients remains insufficiently characterized. We report a case of a 59-year-old liver‑retransplanted man with metabolic dysfunction-associated steatohepatitis (MASH) who developed acute disorientation and vomiting four days after initiation of dulaglutide therapy. Although a low tacrolimus trough level (2.1 µg/L) was measured upon admission to our hospital, this reflected temporary discontinuation of the drug for four days prior to sampling. Tacrolimus concentration during symptomatic episodes was not measured. Brain imaging showed cortical atrophy without evidence of posterior reversible encephalopathy syndrome (PRES) or acute ischemia. The patient had multiple risk factors for calcineurin inhibitor neurotoxicity, including hypomagnesemia (0.68 mmol/L), chronic kidney disease (glomerular filtration rate (GFR) 49 mL/min), and extensive portal-systemic shunting. Symptoms resolved after supportive therapy and adjustment of immunosuppression. This case raises the hypothesis that GLP1RAs might alter tacrolimus pharmacokinetics through delayed gastric emptying, but our case does not prove this mechanism due to the absence of contemporary tacrolimus measurement and the presence of multiple alternative explanations. We recommend enhanced monitoring when initiating GLP1RAs in transplant recipients with predisposing risk factors for neurotoxicity. Prospective pharmacokinetic studies are needed to validate this hypothesis.
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