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.
Yurukova et al. (2026) studied this question.