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Long-Term Gastrointestinal Outcomes in Children Exposed in Utero to Maternal Chronic Hypertension
Nir Roguin1, Gil Gutvirtz1, Gali Pariente1
1Department of Obstetrics and Gynaecology, Soroka University Medical Centre, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Insights
Maternal chronic hypertension was linked to reduced gastrointestinal (GI) issues in early childhood for offspring. However, this protective effect diminished over time, with no significant difference in GI morbidity observed in late adolescence.
Area of Science:
- Obstetrics and Gynecology
- Pediatric Gastroenterology
- Public Health
Background:
- Maternal hypertension is a known risk factor for adverse pregnancy outcomes.
- Long-term effects on offspring gastrointestinal (GI) health are not well understood.
- Chronic hypertension may impact fetal gut development via uteroplacental insufficiency and inflammation.
Purpose of the Study:
- To determine if maternal chronic hypertension, independent of preeclampsia, is associated with long-term GI morbidity in offspring.
- To investigate the temporal relationship between maternal hypertension and offspring GI health outcomes.
Main Methods:
- Population-based retrospective cohort study (1991-2021) of singleton deliveries.
- Offspring followed up to age 18 for GI diagnoses using ICD-9 codes.
- Piecewise Poisson log-linear models used to estimate adjusted incidence rate ratios (IRR), controlling for confounders.
Main Results:
- Among 342,635 deliveries, 0.9% involved mothers with chronic hypertension.
- Offspring exposed to maternal chronic hypertension showed reduced GI risk in early childhood (adjusted IRR < 1 year: 0.34; 1-3 years: 0.46).
- No significant difference in GI risk was observed in late adolescence (15-18 years: adjusted IRR 1.09).
Conclusions:
- The association between maternal chronic hypertension and offspring GI morbidity is time-varying.
- A protective effect on GI risk is observed in early childhood, which is not sustained into adolescence.
- No long-term excess GI risk was identified in offspring exposed 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.
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