Document Type
Article
Publication Date
4-4-2024
Abstract
PURPOSE OF REVIEW: The purpose of this review is two-fold: (1) to discuss a case report of idiopathic intracranial hypertension (IIH) after abrupt cessation of a glucagon-like peptide-1 (GLP-1) receptor agonist with resultant rapid weight gain and (2) to review the literature regarding the potential role of GLP-1 receptor agonists in the treatment of IIH as well as potential pitfalls.
RECENT FINDINGS: GLP-1 receptor agonists have become widely used to treat obesity. Obesity is a known risk factor for the development of IIH, though the precise pathophysiology is unclear. GLP-1 receptor agonists may help treat IIH by promoting weight loss, lipolysis of adipose tissue, and potentially decreasing the secretion of CSF, as was seen in rat models. Abrupt cessation of GLP-1 receptor agonists can result in regaining lost weight rapidly. In the case that we present, the patient stopped duraglutide abruptly due to lack of insurance coverage and regained the weight she had lost within a month. She subsequently developed IIH.
SUMMARY: GLP-1 receptor agonists have the potential to help treat IIH; however, this class of medication needs to be used carefully, as cessation of the medication and resultant rapid weight gain can result in IIH.
Recommended Citation
Heckel, Brittany, "Idiopathic Intracranial Hypertension After Abrupt Cessation of Medication: A Case Report of Abrupt Glucagon-Like Peptide-1 (GLP-1) Receptor Agonist Cessation and Review of the Literature" (2024). Department of Jefferson Headache Center Papers and Presentations. Paper 23.
https://jdc.jefferson.edu/headache/23
Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 License.
Language
English


Comments
This article is the author’s final published version in Current Pain and Headache Reports, Volume 28, 2024, Pages 453-456.
The published version is available at https://doi.org/10.1007/s11916-024-01215-9. Copyright © The Author(s) 2024.
Publication made possible in part by support through a transformative agreement between Thomas Jefferson University and the publisher.