Morphological And Morphometric State Of The Gastrointestinal Tract In Offspring Born Under Conditions Of Maternal Chronic Toxic Hepatitis

Abstract

Chronic toxic hepatitis (CTH) in pregnant women represents a significant risk factor for impaired fetal development due to the liver’s central role in metabolic regulation and detoxification. The gastrointestinal tract (GIT), which undergoes complex morphogenesis during gestation, is particularly vulnerable to disruptions in maternal homeostasis. This study investigates the morphological and morphometric alterations in the GIT of offspring born to mothers with experimentally induced CTH, aiming to elucidate the potential mechanisms and long-term consequences of such exposure.

Using a controlled animal model, pregnant rats were subjected to chronic carbon tetrachloride (CCl₄)-induced hepatotoxicity to simulate maternal CTH. Postnatal offspring were examined at day 21, with comparative histological and morphometric analyses conducted on gastric, small intestinal, and colonic tissues. Histopathological evaluation revealed significant structural abnormalities, including mucosal atrophy, glandular degeneration in the stomach, shortened and widened intestinal villi, and reduced crypt depth in the colon. Morphometric assessments demonstrated a statistically significant decrease in villus height (control: 450 ± 25 µm vs. CTH: 320 ± 30 µm, p < 0.01), crypt depth (control: 120 ± 10 µm vs. CTH: 85 ± 8 µm, p < 0.05), and overall mucosal thickness (control: 200 ± 15 µm vs. CTH: 150 ± 12 µm, p < 0.01), indicating compromised epithelial integrity and absorptive capacity.

These findings suggest that maternal CTH disrupts normal GIT development in offspring, likely due to a combination of metabolic disturbances, oxidative stress, and impaired nutrient exchange. The observed changes may predispose affected individuals to gastrointestinal dysfunction, malabsorption syndromes, and increased susceptibility to enteric infections later in life. This study highlights the need for further research into therapeutic strategies to mitigate the developmental impact of maternal liver disease on fetal organ systems.