Does a perturbation in visfatin homeostasis participate in the phenotype definition of preeclampsia and SGA?

Abstract
Objective: Women with preeclampsia (PE) and those who delivered a small for gestational age (SGA) neonate share several mechanisms of disease including: chronic uteroplacental ischemia and failure of physiologic transformation of the spiral arteries. However, the clinical manifestation of these obstetrical syndromes is remarkably different. It has been proposed that an altered maternal metabolic state, as well as a unique circulating cytokines milieu, predispose women to develop either PE or SGA (Ness&Sibai AJOG 2006;195:40). Compelling evidence suggests that adipose tissue orchestrates both metabolic pathways and immunological responses via the production of adipokines. Visfatin is a novel adipocytokine with metabolic and immunomodulating properties. The objective of this study was to determine whether PE and SGA are associated with alterations in maternal circulating visfatin concentrations. Methods: This cross-sectional study included 255 pregnant women in the following groups: 1) normal pregnancy (n = 158); 2) patients with PE (n = 43) of which 32 had an AGA and 11 had an SGA neonate; and 3) patients who delivered an SGA neonate without PE (n = 54). Maternal plasma visfatin concentrations were measured by ELISA. Non-parametric tests and multiple linear regression analysis were used. Results: 1) Women who delivered an SGA neonate had higher median maternal plasma visfatin concentration than those with normal pregnancy (median: 20.0ng/ml, interquartile range: 17.2–24.6 vs. 15.2 ng/ml, 12.1–19.2, respectively; p. Conclusion: 1) Mothers with SGA, but not with PE, had a higher maternal plasma visfatin concentration than those with a normal pregnancy; 2) This finding suggests differential involvement of adipokines in SGA and PE; 3) We propose that perturbation of adipokine homeostasis may be implicated in the phenotypic definition and distinction of PE and SGA
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