Background: Women with gestational diabetes (GDM) have an increased risk of adverse perinatal outcomes and future type 2 diabetes (T2D). Gestational glucose intolerance (GGI, abnormal initial GDM screen) without GDM has been linked to adverse perinatal outcomes but is not a recognized T2D risk factor. We tested whether GGI without GDM is associated with incident T2D.

Methods: Using clinical data from women seen at our US medical center for prenatal and primary care (1998-2018), we assessed risk of T2D (defined using validated laboratory and outpatient diagnoses) according to GGI/GDM status during pregnancy. We defined GGI as 1-hr glucose loading test (GLT) ≥ 140 mg/dl at ≥ 24 weeks gestation. We subcategorized GGI by 3-hr oral glucose tolerance test (OGTT) result. We used Cox proportional-hazard models with time-varying exposures/covariates to assess T2D risk after delivery, adjusting for age, race/ethnicity, parity, insurance type, marital status, BMI, and blood pressure. Women were followed from 1st delivery until diagnosed with T2D or censored at time of last primary care visit.

Results: Among 13988 women, 17109 pregnancies had normal glucose tolerance (NGT, GLT < 140mg/dL). Among 3619 GGI pregnancies (GLT ≥ 140 mg/dl), 2076 had a normal OGTT, 699 had 1 abnormal OGTT value, and 844 had GDM (≥ 2 abnormal OGTT values). Over a median of 8.3 years of follow-up, 2.2% (N=304 women) developed T2D. In our primary comparison, women with GGI without GDM (16% of pregnancies) had increased T2D risk compared to women with NGT (HR 2.1 [1.5-2.9], p<0.001). Among women with GGI, T2D risk increased with the number of abnormal OGTT values (normal OGTT: HR 1.8; 1 abnormal OGTT value: HR 2.8; GDM: HR 11.7; p≤0.01 for all compared to NGT).

Conclusions: Pregnant women with GGI without GDM have a two-fold increased risk of future T2D compared to those with NGT. Clinical data universally available during pregnancy identifies a large, previously unrecognized group of women who may benefit from T2D screening and prevention.

Disclosure

D. J. Selen: None. T. Thaweethai: None. S. Hsu: None. K. James: None. A. Kaimal: None. J. B. Meigs: Consultant; Self; Quest Diagnostics. C. E. Powe: None.

Funding

National Institutes of Health (2T32DK007028-46, K23DK113218); Robert Wood Johnson Foundation; Massachusetts General Hospital

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at http://www.diabetesjournals.org/content/license.