Glucagon-like peptide 1 receptor agonist use is associated with reduced risk for glaucoma.
Br J Ophthalmol
; 107(2): 215-220, 2023 Feb.
Article
em En
| MEDLINE
| ID: mdl-34413054
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 13 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.Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Glaucoma de Ângulo Aberto
/
Diabetes Mellitus Tipo 2
Idioma:
En
Ano de publicação:
2023
Tipo de documento:
Article