Bupropion Use in Patients With Glaucoma
Bupropion (Wellbutrin) has no well-established, guideline-level contraindication for patients with glaucoma based on high-quality prospective data. [1] Bupropion has been associated with rare episodes of acute angle-closure glaucoma via secondary mechanisms (uveal effusion), which can precipitate angle closure in susceptible patients. [2],[3]
Evidence on Glaucoma-Type Risk
Narrow-angle glaucoma (anatomically predisposed angle closure) is the glaucoma phenotype most classically associated with drug-triggered acute angle closure through mechanisms such as pupillary block or other precipitating events. [1] Bupropion-associated angle closure has been reported as secondary angle closure with diffuse uveal effusions and shallow anterior chambers, with gonioscopy showing appositional closure. [2],[3] This mechanism is not limited to patients who already carry a narrow-angle diagnosis, because the drug-associated process can physically narrow the angle through uveal effusion and anterior rotation of the ciliary body. [3] Open-angle glaucoma has not shown a consistent, high-certainty signal of medication-induced risk in the available review evidence, with the principal published concern for bupropion focused on rare events affecting angle closure through other pathways. [1]
Medication Safety Summary for Practical Decision-Making
Bupropion should be considered a low-frequency risk medication for angle-closure phenomena in clinical contexts where any patient-specific ocular risk factor for angle narrowing exists. [2],[3] Caution is appropriate because published reports describe acute bilateral angle-closure presentations temporally associated with bupropion use and resolution after discontinuation and treatment. [2],[3] The presence of known narrow-angle anatomy increases clinical concern for any agent that could precipitate angle closure. [1]
Initiation and Monitoring Considerations
Bupropion should be avoided or discontinued when signs of acute angle closure occur, because case reports describe marked intraocular pressure elevation and shallow anterior chambers at presentation with recovery after stopping the drug. [2],[3] Patients should receive urgent ophthalmic evaluation for symptoms consistent with acute angle closure, including sudden ocular pain, headache, blurred vision, halos around lights, and nausea/vomiting, because these presentations require rapid pressure-lowering and angle-closure-specific therapy. [3]
Key Evidence Supporting This Recommendation
A 2025 case report described presumed bupropion-associated acute bilateral angle-closure with uveal effusions, with intraocular pressures reported as 40 mmHg (right eye) and 45 mmHg (left eye), uniformly shallow anterior chambers, gonioscopy demonstrating 360° appositional closure, and resolution after discontinuation and treatment. [3] A 2012 report described bilateral uveal effusion and angle-closure glaucoma associated with bupropion use. [2] A 2020 review of systemic medications summarized that bupropion is among drugs discussed with respect to glaucoma risk modulation, with angle-closure–increasing drug classes in that review emphasizing categories such as anticholinergics and certain antidepressants rather than establishing bupropion as a common precipitant. [1]
Common Pitfalls to Avoid
Assuming that open-angle glaucoma eliminates the possibility of acute angle-closure syndromes caused by mechanisms other than pupillary block leads to missed recognition of rare drug-associated secondary angle closure. [3] Under-recognizing that bupropion has published case associations with uveal-effusion–mediated angle closure can delay discontinuation when acute symptoms develop. [2],[3]
Target Goals for Clinical Outcome
The clinical goal during suspected acute angle closure is rapid recognition and urgent treatment to prevent optic nerve injury from elevated intraocular pressure. [3] The clinical goal for medication management is prevention of recurrence by stopping the suspected offending agent after drug-associated angle-closure is suspected, as supported by reported recovery after discontinuation. [2],[3]