Disturbed release of cholecystokinin in pregnant women with hyperemesis gravidarum Ebru Biberoglu 1 , Ayse Kirbas 1 , Cantekin Iskender 1 , Aylin Dirican 1 , Halil Daglar 1 , Canan Demirtas 2 , Beyza Doganay 3 , Dilek Uygur 1 and Kutay Biberoglu 4 1 Department of Obstetrics and Gynecology, High Risk Pregnancy Unit, Dr. Zekai Tahir Burak Women’s Health Care, Education and Research Hospital, 2 Department of Biochemistry, 4 Department of Obstetrics and Gynecology, Gazi University Medical School and 3 Department of Biostatistics, Ankara University Medical School, Ankara, Turkey Abstract Aims: We aimed to investigate cholecystokinin (CCK) release in pregnant women with and without hyper- emesis gravidarum (HG). Material and Methods: In this case–control study including 40 pregnant women with HG and 40 women with healthy uncomplicated pregnancies, serum CCK levels in addition to hematological, biochemical and hor- monal parameters were investigated. Results: Serum CCK values were found to be significantly lower in pregnant women with HG (P < 0.001). Additionally, while serum blood urea nitrogen and free thyroxine levels were significantly higher, sodium, potassium, and thyroid stimulating hormone levels were significantly lower in women with HG than in control women. No correlation was detected between CCK and other parameters like ketonuria and thyroid function tests. Conclusions: CCK release has been found to be halved in pregnant women with HG, which supports the hypothesis that gastrointestinal motility is increased in pregnant women with HG. A causal effect remains to be confirmed. Key words: gastrointestinal motility, gut hormone, pathogenesis of hyperemesis gravidarum, thyroid func- tion tests. Introduction Hyperemesis gravidarum (HG) is a condition of intrac- table vomiting in pregnancy, typically in the first tri- mester, resulting in dehydration and ketonuria that in some cases may be severe enough to justify hospital admission and require parenteral fluid therapy. Although investigators have tried to relate psychologi- cal factors, infections, immunological, metabolic, and anatomical factors 1,2 to the pathogenesis of HG, the etiopathology is still elusive. 3 Cholecystokinin (CCK) is a neuropeptide that binds to its CCK2 receptors in several brain regions, such as the brainstem or hypothalamus 4 and is also a gut hormone, which binds to CCK1 receptors in peripheral tissues, including the gallbladder, pancreas and the smooth muscle cells of the gastrointestinal tract. It is released primarily in response to fat and protein intake and inhibits food intake. 5–8 Alimentary CCK delays gastric emptying, modulates gastric sensory function, increases the rate of meal-induced esophageal sphinc- ter relaxations and affects small bowel and colonic Received: April 24 2014. Accepted: August 6 2014. Reprint request to: Professor Kutay Biberoglu, Obstetrics and Gynaecology, Gazi University Medical School,Ankara 06500, Turkey. Email: kobiber@gmail.com doi:10.1111/jog.12562 © 2014 The Authors Journal of Obstetrics and Gynaecology Research © 2014 Japan Society of Obstetrics and Gynecology 505 J. Obstet. Gynaecol. Res. Vol. 41, No. 4: 505–511, April 2015