CureusOct 31, 2026

Lithium Poisoning After Starting Semaglutide in a Person With Bipolar Disorder

GLP-1 Therapies Weekly Brief ↗PubMed ↗DOI ↗

Updated Nov 2, 2026

Abstract

A 69-year-old woman with bipolar disorder experienced elevated lithium levels after starting semaglutide for weight management.

The patient presented with acute confusion, dysarthria, and expressive aphasia, prompting a stroke protocol.
Imaging studies revealed no acute infarct or hemorrhage.
Substantial weight loss, persistent nausea, intermittent vomiting, and reduced oral intake were reported after semaglutide initiation.
Elevated serum lithium levels were noted alongside a reduced estimated glomerular filtration rate and signs of volume depletion.
Renal function improved after halting lithium and administering intravenous fluids, leading to resolution of neurological deficits.
The case suggests the need for closer monitoring of lithium levels when starting GLP-1 receptor agonists.

Simplified

Glucagon-like peptide-1 (GLP-1) receptor agonists are increasingly prescribed for type 2 diabetes mellitus and obesity, including among patients with severe mental illness. Their effects on gastrointestinal motility, oral intake, and volume status raise concern for interactions with drugs with narrow therapeutic indices that are cleared almost entirely by the kidney, such as lithium. We describe a 69-year-old woman with bipolar disorder, stable for several years on lithium, who presented with acute confusion, dysarthria, and expressive aphasia. A stroke protocol was activated, and noncontrast head CT, CT angiography of the head and neck, and MRI of the brain showed no acute infarct or hemorrhage. Semaglutide had been initiated approximately one month earlier for weight management, and she had experienced substantial weight loss with persistent nausea, intermittent vomiting, and reduced oral intake. Serum lithium was elevated above the reference range, accompanied by a reduced estimated glomerular filtration rate and biochemical findings suggestive of volume depletion. Lithium was held, and intravenous fluids were administered; renal function improved and the neurologic deficits resolved. Lithium was subsequently resumed at a reduced dose without recurrence. In this patient, initiation of semaglutide was temporally associated with lithium toxicity in the setting of gastrointestinal intolerance, reduced oral intake, and suspected volume depletion. Although a single case cannot establish causality, this observation supports closer lithium monitoring when initiating GLP-1 receptor agonists and during dose escalation.

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Lithium Poisoning After Starting Semaglutide in a Person With Bipolar Disorder

Abstract

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