Abstract TU280: Endometriosis subtypes and risk of type 2 diabetes: advancing research in cardiovascular health and endometriosis study (ARCHES) retrospective cohort study

M Maggie Fuzak (George Mason University, Fairfax, Virginia, United States) B Bin Yan (Institute of Genetics and Developmental Biology, Chinese Academy of Sciences) K Karen Schliep (UNIVERSITY UTAH, Salt Lake City, Utah, United States) L Leslie Farland (University of Arizona, Tucson, Arizona, United States) M Michael Varner (UNIVERSITY UTAH, Salt Lake City, Utah, United States) J Jenna Krall (George Mason University, Fairfax, Virginia, United States) A Anna Pollack (George Mason University, Fairfax, Virginia, United States)

Abstract

Endometriosis is a chronic inflammatory condition that affects ~11% of reproductive-aged women and is characterized by growth of endometrial-like tissue outside the uterus. Chronic inflammation contributes to the development of type 2 diabetes (T2D) by impairing insulin sensitivity and glucose uptake. Despite overlapping inflammatory pathways, prior studies have reported inconsistent associations between endometriosis and T2D. We conducted a population-based retrospective cohort study using the Utah Population Database (UPDB), a statewide, multigenerational resource that links electronic health records, vital records, and administrative data. The cohort included women born in or after 1935 with documented Utah residency between 1996 and 2021 (N = 2,939,380). Endometriosis diagnoses (n = 99,978) were ascertained from International Classification of Diseases (ICD-9/10) codes and categorized as superficial peritoneal (SE), ovarian (OE), deep infiltrating (DE), adenomyosis, or other site (OS; including scar, bladder, umbilicus, and lung). T2D diagnoses were identified using ICD-9 codes 250.x0 and 250.x2 and ICD-10 codes E11. We fit Cox proportional hazards models with time-varying endometriosis exposure and calendar time as the time scale to estimate adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) for incident T2D, adjusting for birth year, birth state, race/ethnicity, age, and body mass index (BMI) at cohort entry. Women with endometriosis had a 46% higher risk of developing T2D compared with women without endometriosis (aHR = 1.46; 95% CI: 1.43, 1.50). Elevated hazards were observed across all subtypes: SE (aHR = 1.67; 95% CI: 1.61, 1.74), OE (aHR = 1.61; 95% CI: 1.53, 1.68), and DE (aHR = 1.45; 95% CI: 1.24, 1.69). The strongest association was for OS endometriosis (aHR = 2.00; 95% CI: 1.90, 2.10); adenomyosis was also associated with increased risk (aHR = 1.34; 95% CI: 1.20, 1.38). These findings underscore the importance of understanding the metabolic consequences of chronic inflammatory conditions such as endometriosis.

Article Details

Journal Circulation
Volume / Issue Vol. 153, Issue Suppl_1
Published March 24, 2026
ISSN 0009-7322
Publisher Lippincott Williams & Wilkins

Journal Info

Circulation

Lippincott Williams & Wilkins

ISSN: 0009-7322 Health Sciences

Authors (7)

M

Maggie Fuzak

George Mason University, Fairfax, Virginia, United States

B

Bin Yan

Institute of Genetics and Developmental Biology, Chinese Academy of Sciences

K

Karen Schliep

UNIVERSITY UTAH, Salt Lake City, Utah, United States

L

Leslie Farland

University of Arizona, Tucson, Arizona, United States

M

Michael Varner

UNIVERSITY UTAH, Salt Lake City, Utah, United States

J

Jenna Krall

George Mason University, Fairfax, Virginia, United States

A

Anna Pollack

George Mason University, Fairfax, Virginia, United States