Abstract
Background: Delayed gastric emptying with prolongation of gastrointestinal transit time resulting in nausea and vomiting of pregnancy (NVP) which is the most common disorder during the first trimester of pregnancy with significant mor-bidity and adverse birth outcomes, few percentage of women develop a severe form of NVP called hyperemesis gravidarum (HG). The mechanism of NVP remains unclear with wide controversy, Several observational studies have suggested that NVP are related to the high levels of human chorionic gonadotropin (hCG), others relate it to hCG induced transient hyperthyroidism that commonly occur during pregnancy, these studies did not ascertain the possible relationship and mech-anism either which hormone is the direct responsible?.
Aim of the Study: To investigate the effect of hCG treatment and thyroid hormone changes on gastric transit in hCG treated female rats.
Material and Methods: This study was done on 18 female Wister albino rats, were divided to 3 groups (n=6): Control group (I) treated with saline, hCG treated group (II), and hCG + Methimazole treated group (III). After 2 weeks, at the end of the study, in all group, serum levels of Thyriod stimulating hormone (TSH), free (thyroxine) T4, hCG, estrogen and progesterone were estimated and gastric empting time was calculated. Groups comparison were done by applying one way analysis of variance (ANOVA) and the relationship between various parameters was evaluated by calculating coefficient of correlation, "r".
Results: Gastric emptying time was significantly decreased in both hCG treated groups and correlate negatively with hCG levels. Free serum T4 was significantly increased and TSH levels was significantly decreased in hCG treated group (II) in comparison to both control (I) and Methimazole treated (III) groups. Estrogen and progesterone levels showed no significant changes in both hCG treated groups when compared to control.
Conclusion: Our results are confirmative of the involve-ment of hCG in the pathogenesis of NVP and HG through a mechanism involving delaying gastric emptying time with no implication of hCG induced hyperthyroidism in this patho-genesis.