Abstract This is a prospective cohort study aimed to compare women treated due to hyperemesis gravidarum (HG) (n = 24) to women with normal pregnancy attending regular antenatal outpatient care (n = 22) in… Click to show full abstract
Abstract This is a prospective cohort study aimed to compare women treated due to hyperemesis gravidarum (HG) (n = 24) to women with normal pregnancy attending regular antenatal outpatient care (n = 22) in terms of fasting and post-prandial cholecystokinin (CCK) levels, and gallbladder (GB) functions. The Pregnancy-Unique Quantification of Emesis (PUQE) scores, fasting and postprandial CCK levels, and ultrasonographic GB parameters were recorded at admission before any treatment. The median PUQE score in the study group was 8. There were no statistically significant differences in GB parameters (p>.05), and fasting and postprandial CCK levels between the groups (p=.851, p=.395, respectively). Fasting CCK levels were positively correlated with postprandial GB volume (PGv) (p=.022, r = 0.464). Although GB contractility is compromised during pregnancy, HG does not cause further GB impairment. The positive correlation between fasting CCK levels and PGv requires further evaluation. Impact Statement What is already known on this subject? The pathophysiology of hyperemesis gravidarum (HG) remains poorly understood. Altered cholecystokinin (CCK) levels may have potential consequences on gastric emptying, which may be related to nausea and vomiting. In this context, alterations in CCK secretion in women diagnosed with HG have been previously reported, and alterations in CCK levels lead to impaired gallbladder (GB) functions. What do the results of this study add? CCK levels and GB functions in pregnant women with HG are not statistically significantly different from those in healthy pregnant women. What are the implications of these findings for clinical practice and/or further research? Further studies designed in patients with different severities of HG and larger sample sizes are required for a better understanding of HG pathophysiology.
               
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