Parenchymal Disruption of Thyroid Gland in Rat Offspring Following Maternal Khat Exposure

Maternal consumption of khat has been associated with adverse neonatal outcomes like preterm birth and low birth weight. These effects resemble those seen in neonatal hypothyroidism, suggesting that khat disrupts thyroid function in the fetus. There is, however, limited data on the microscopic alterations in the thyroid gland of offspring following maternal consumption of khat. We examined the same in rat offspring whose mothers were exposed to khat during pregnancy as the suitable animal model.

Female rats were acquired and randomized into groups receiving khat extract (200 or 500 mg/kg) or distilled water. Maternal khat consumption was started 7 days before mating and continued throughout pregnancy. From the offspring born, 28 thyroid glands were harvested and processed for histological analysis with hematoxylin and eosin and Ki-67 staining. Data on the follicle density and diameter, follicular cell epithelia, follicular cell nuclear-cytoplasmic index, and expression of proliferation marker Ki-67 were collected. These were analyzed using SPSS and key findings presented in tables and photomicrographs.

Compared to controls, khat-treated groups exhibited parenchymal disruption evidenced by a dose-dependent epithelial shift of follicular cells from columnar to cuboidal, reduced follicular diameter, reduced follicular density, and increased nuclear-cytoplasmic index. There was also suppressed proliferative activity evidenced by a reduction in cells expressing Ki-67. Infiltration of follicular cells into colloid was observed in treated groups.

The observed parenchymal insult of the fetal thyroid gland following maternal exposure to khat could partially explain the adverse birth outcomes seen in the offspring.