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Glucagon-like peptide 1 receptor agonist use is associated with reduced risk for glaucoma
  1. Jacob Sterling1,2,
  2. Peiying Hua3,
  3. Joshua L Dunaief1,
  4. Qi N Cui1,
  5. Brian L VanderBeek1,4,5
  1. 1Department of Ophthalmology, University of Pennsylvania, Philadelphia, Pennsylvania, USA
  2. 2Medical Scientist Training Program, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA
  3. 3Center for Preventative Ophthalmology and Biostatistics, Department of Biostatistics and Epidemiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA
  4. 4Center for Clinical Epidemiology and Biostatistics, Department of Biostatistics & Epidemiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA
  5. 5Leonard Davis Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA
  1. Correspondence to Dr Brian L VanderBeek, Department of Ophthalmology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA; brian.vanderbeek{at}pennmedicine.upenn.edu

Abstract

Background/aims Glucagon-like peptide-1 receptor (GLP-1R) agonists regulate blood glucose and are commonly used to treat type 2 diabetes mellitus. Recent work showed that treatment with the GLP-1R agonist NLY01 decreased retinal neuroinflammation and glial activation to rescue retinal ganglion cells in a mouse model of glaucoma. In this study, we used an insurance claims database (Clinformatics Data Mart) to examine whether GLP-1R agonist exposure impacts glaucoma risk.

Methods A retrospective cohort of patients who initiated a new GLP-1R agonist was 1:3 age, gender, race, classes of active diabetes medications and year of index date matched to patients who initiated a different class of oral diabetic medication. Inverse probability of treatment weighting (IPTW) was used within a multivariable Cox proportional hazard regression model to test the association between GLP-1R agonist exposure and a new diagnosis of primary open-angle glaucoma, glaucoma suspect or low-tension glaucoma.

Results Cohorts were comprised of 1961 new users of GLP-1R agonists matched to 4371 unexposed controls. After IPTW, all variables were balanced (standard mean deviation <|0.1|) between cohorts. Ten (0.51%) new diagnoses of glaucoma were present in the GLP-1R agonist cohort compared with 58 (1.33%) in the unexposed controls. After adjustment, GLP-1R exposure conferred a reduced hazard of 0.56 (95% CI: 0.36 to 0.89, p=0.01), suggesting that GLP-1R agonists decrease the risk for glaucoma.

Conclusions GLP-1R agonist use was associated with a statistically significant hazard reduction for a new diagnosis of glaucoma. Our findings support further investigations into the use of GLP-1R agonists in glaucoma prevention.

  • glaucoma
  • degeneration
  • inflammation
  • intraocular pressure
  • treatment medical

Data availability statement

Data are available upon reasonable request.

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Data availability statement

Data are available upon reasonable request.

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Footnotes

  • QNC and BLV are joint senior authors.

  • Twitter @jacobksterling, @cuilab

  • Contributors JS and QNC were responsible for study design and conception, data analysis and interpretation, writing manuscript, manuscript revision, final approval and agreement to be accountable. PH helped in data acquisition, data analysis and interpretation, manuscript revision, final approval and agreement to be accountable. JLD helped in study design and conception, data analysis and interpretation, manuscript revision, final approval and agreement to be accountable. BLVB was responsible for study design and conception, data acquisition, data analysis and interpretation, writing manuscript, manuscript revision, final approval and agreement to be accountable.

  • Funding National Institutes of Health-National Eye Institute K23 Award (K23EY025729), National Institutes of Health-National Eye Institute K12 Award (K12EY015398; PI: Joshua L Dunaief), National Institutes of Health-National Eye Institute K08 Award (K08EY029765), National Institutes of Health-National Eye Institute Vision Training Grant (T32EY007035; PI: Diego Contreras), National Institutes of Health-National Eye Institute F30 Award (F30EY032339) and the University of Pennsylvania Core Grant for Vision Research (P30EYEY001583). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. Additional funding was provided by Research to Prevent Blindness (no grant/award number) and the Paul and Evanina Mackall Foundation. Funding from each of the above sources was received in the form of block research grants to the Scheie Eye Institute or University of Pennsylvania Perelman School of Medicine. None of the funding organisations had any role in the design or conduct of the study.

  • Competing interests Patent pending (Penn Center for Innovation; JS, JLD and QNC).

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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