The role of interleukin-17 in intrahepatic cholestasis of pregnancy


Kirbas A., Biberoglu E., Ersoy A. O., UĞRAŞ DİKMEN A., Koca C., Erdinc S., ...More

JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE, vol.29, no.6, pp.977-981, 2016 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 29 Issue: 6
  • Publication Date: 2016
  • Doi Number: 10.3109/14767058.2015.1028354
  • Journal Name: JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.977-981
  • Keywords: Bile acid, cholestasis, inflammation, interleukin 17, pregnancy, OBSTRUCTIVE-CHOLESTASIS, T(H)17 CELLS, LIVER-INJURY, INFLAMMATION, ACID, ASSOCIATION, MECHANISMS, DISEASE, IL-17A
  • Gazi University Affiliated: Yes

Abstract

Objective: Intrahepatic cholestasis of pregnancy (ICP) is the most common pregnancy-specific liver disease, is characterized by pruritus, abnormal liver function and elevated serum bile acid levels. The main cause of ICP has not yet been identified. We aimed to provide a new perspective to the pathogenesis of by investigating the possible association of circulating interleukin-17 (IL-17) that is a recently discovered proinflammatory cytokine levels with ICP.Materials and methods: In this controlled cross-sectional study, maternal venous blood samples were obtained from 33 consecutive pregnant women with ICP (15 with mild and 18 with severe forms of the disease) and 25 healthy women with uncomplicated pregnancies (as the control group) and IL-17 levels were compared among the groups.Results: Although serum IL-17 levels were significantly higher in the severe ICP group than in the control group (p=0.022), there were no significant differences between the mild and severe ICP groups or between the control and mild ICP groups.Conclusion: Explaining the mechanisms of hepatocyte injury might contribute to the existing therapeutic strategies for treating cholestatic diseases. Changes in IL-17 levels may shed light on the pathogenesis of ICP.