Long-Term Gastrointestinal Outcomes in Children Exposed in Utero to Maternal Chronic Hypertension

Background: Maternal hypertension has been linked to adverse pregnancy and neonatal outcomes, but long-term effects on offspring, particularly gastrointestinal (GI) health, are less well studied. Chronic hypertension may impair uteroplacental perfusion and promote a pro-inflammatory intrauterine environment, potentially disrupting foetal gut development; however, its independent effect on offspring GI health has not been examined. Objectives: To evaluate whether in utero exposure to maternal chronic hypertension, independent of preeclampsia, is associated with long-term GI morbidity in offspring. Methods: This population-based retrospective cohort study included all singleton deliveries at a tertiary medical centre over a 30-year period (1991–2021). Offspring were followed until age 18 for GI diagnoses based on ICD-9 codes from hospital and outpatient records. The primary exposure was maternal chronic hypertension, and the primary outcome was the incidence of GI morbidity in offspring. Piecewise Poisson log-linear models estimated adjusted incidence rate ratios (IRR), controlling for maternal age, parity, ethnic origin, smoking, obesity, and pre-gestational diabetes. Results: Among 342,635 singleton deliveries, 3097 (0.9%) were to mothers with chronic hypertension. The median follow-up was 12.6 years (interquartile range 5.6, 18.0). GI incidence rates were 1903.0 and 1901.9 per 100,000 person-years among chronic hypertension and normotensive groups. Offspring of mothers with chronic hypertension showed lower GI risk in early childhood (adjusted IRR < 1 year: 0.34, 95% confidence interval [CI] 0.11, 1.05; 1–3 years: 0.46, 95% CI 0.29, 0.73), with estimates consistent with no difference in late adolescence (15–18 years: adjusted IRR 1.09, 95% CI 0.98, 1.21). All-cause mortality was low and similar between groups. Conclusions: The association between maternal chronic hypertension and offspring GI morbidity is time-varying and non-proportional, with lower risk in early childhood and no evidence of excess risk at later ages.