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Different Profile of Serum Leptin between Early Onset and Late Onset Preeclampsia

DOI: 10.1155/2014/628476

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Abstract:

Aim. This study was designed to clarify the role of leptin and adiponectin in preeclampsia (PE) pathogenesis and different subtypes of preeclampsia. Method. This case control study was performed in 45 PE patients and 45 healthy controls matched for age, BMI, and ethnicity. Serum leptin and adiponectin levels were determined by enzyme linked immunosorbent assay (ELISA). Results. Maternal serum leptin and adiponectin were significantly higher in PE women than controls. Serum leptin was elevated in early onset preeclampsia (EOPE) and late onset preeclampsia (LOPE) compared to controls. Among PE patients, serum leptin was higher in EOPE than LOPE women. However, serum adiponectin was not different between EOPE and LOPE women. The serum leptin was significantly higher in severe PE than mild PE. The serum adiponectin was significantly elevated in severe PE compared to controls. Significant positive correlation was observed between leptin and adiponectin and also between leptin and BMI in controls. Moreover significant positive correlation was observed between adiponectin and BMI in PE patients and controls. Conclusion. The present study showed that serum leptin level may play a significant role as a biomarker to differentiate early and late onset PE and also its relation to BMI and severity of disease. 1. Introduction Preeclampsia (PE) is a complication of pregnancy which is characterized by hypertension and proteinuria. It affects 2% to 5% of pregnancies and is a major contributor to fetal, neonatal, and maternal morbidity and mortality. PE symptoms might be revealed from 20 weeks of gestation up to six weeks postpartum and is considered early onset before 34 weeks of gestation [1]. Although PE has an unknown etiology, metabolic, placental, genetic, and immune factors have been concerned in its etiopathogenesis [2]. There is convincing evidence for the association between obesity related complications and preeclampsia [3]; however, the mechanism by which excess adipose tissue causes developing PE in pregnant women remains unknown. Adipose tissue is not only involved in energy storage but can also act as an endocrine tissue producing a wide range of cytokines and chemokines such as adiponectin and leptin. It is shown that these two adipokines play a role in normal pregnancy, as well as in complications of pregnancy, including PE [4]. Leptin is a 16?kDa protein hormone which plays an important role in modulating satiety, energy homeostasis, and reproductive biology. There are several studies showing that leptin serum concentration increases during pregnancy

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