Objective: Nonalcoholic fatty liver disease has been associated with the development of gestational diabetes (GDM). We sought to determine whether abnormal liver enzyme levels and indices of hepatic steatosis and fibrosis in an entire pregnant population are associated with GDM development. Methods: A retrospective cohort study was conducted on adult women (≥18 years) who delivered at 2 teaching hospitals in Sydney Australia from January 2016 to December 2017. Liver enzymes (aspartate aminotransaminase (AST), alanine aminotransaminase (ALT), gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), albumin (ALB) and bilirubin (BIL)) obtained 12 months pre-gravid, or during pregnancy but prior to GDM screening, were extracted from the hospital pathology database and linked with oral glucose tolerance test results. The Fibrosis-4 (FIB-4) and Hepatic Steatosis Index (HSI) were calculated. Univariate analysis was undertaken to determine the association between deranged liver enzymes, FIB-4, HSI and GDM. Multiple logistic regression, with adjustment for age, ethnicity, pre-gravid body mass index (BMI), parity, prior GDM and family history of diabetes, was conducted to determine if any of these were independent predictors of GDM. Results: Over 2 years, 1429 women had liver enzymes collected. As per IADPSG (2010) criteria, 255 had diagnosed GDM, of which 82 (32.2%) were obese (BMI >30kg/m2), 243 (82.4%) were multiparous, and 223 (87.5%) had prior GDM. Elevated GGT (>35IU/L, p=0.006) and HSI (p=0.005) were associated with development of GDM, whilst low ALB (<35g/L) and elevated ALP (>110IU/L), ALT (>35IU/L), AST (>35IU/L), BIL (>19umol/L) and FIB-4 were not. On adjustment for confounders, elevated GGT (AOR 1.1, 95% CI 0.32-3.8, p=0.88) and HSI (AOR 0.6, 95% CI 0.26-1.3, p=0.21) were not independent predictors of GDM. Conclusions: Our results indicate deranged liver enzymes or clinical indices of hepatic steatosis and fibrosis were not associated with GDM. Disclosure T. Y. L. Chai: None. D. Pasupathy: None. J. George: None. N. Cheung: None.
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