AIM: The purpose of this study was to determine the levels of inhibin A simultaneously in the maternal serum and placental extract in preeclampsia (PE) with or without small-for-gestational-age (SGA) and normal controls at term, and to evaluate the relationship among changes in serum and placental inhibin A according to the severity of PE and PE with or without SGA. MATERIAL AND METHODS: This study involved 40 pregnant women; normal (n = 20), and PE (n = 20), the latter of who were classified into (i) mild (n = 10) and severe PE (n = 10); (ii) PE with SGA (n = 7) and without SGA (n = 13). Inhibin A concentrations were quantified by enzyme-linked immunosorbent assay (ELISA) in the maternal serum and placental extract. Inhibin-α subunit in the placenta was stained by immunohistochemistry (IHC), and its intensity was graded by a semiquantitative scoring method. RESULTS: There was a positive correlation in inhibin A concentrations between the serum and placental extract (r = 0.57, P < 0.001). Both maternal serum and placental inhibin A in PE groups were significantly higher than in controls, but there was no severity-dependent increase of inhibin A when compared with mild and severe PE. There was no difference in inhibin A levels between PE with and without SGA. Moreover, the inhibin-α subunit was predominantly abundant in the cytoplasm of the syncytiotrophoblasts, where the PE groups showed higher staining intensity than the controls (P < 0.000). CONCLUSION: Serum inhibin A level might be a useful biomarker for diagnosis and monitoring of PE.
AIM: The purpose of this study was to determine the levels of inhibin A simultaneously in the maternal serum and placental extract in preeclampsia (PE) with or without small-for-gestational-age (SGA) and normal controls at term, and to evaluate the relationship among changes in serum and placental inhibin A according to the severity of PE and PE with or without SGA. MATERIAL AND METHODS: This study involved 40 pregnant women; normal (n = 20), and PE (n = 20), the latter of who were classified into (i) mild (n = 10) and severe PE (n = 10); (ii) PE with SGA (n = 7) and without SGA (n = 13). Inhibin A concentrations were quantified by enzyme-linked immunosorbent assay (ELISA) in the maternal serum and placental extract. Inhibin-α subunit in the placenta was stained by immunohistochemistry (IHC), and its intensity was graded by a semiquantitative scoring method. RESULTS: There was a positive correlation in inhibin A concentrations between the serum and placental extract (r = 0.57, P < 0.001). Both maternal serum and placental inhibin A in PE groups were significantly higher than in controls, but there was no severity-dependent increase of inhibin A when compared with mild and severe PE. There was no difference in inhibin A levels between PE with and without SGA. Moreover, the inhibin-α subunit was predominantly abundant in the cytoplasm of the syncytiotrophoblasts, where the PE groups showed higher staining intensity than the controls (P < 0.000). CONCLUSION: Serum inhibin A level might be a useful biomarker for diagnosis and monitoring of PE.
Authors: C Emily Kleinrouweler; Miranda van Uitert; Perry D Moerland; Carrie Ris-Stalpers; Joris A M van der Post; Gijs B Afink Journal: PLoS One Date: 2013-07-12 Impact factor: 3.240