期刊
JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
卷 32, 期 7, 页码 1219-1223出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/14767058.2017.1400006
关键词
Pre-eclampsia; gestational hypertension; chronic hypertension; blood pressure determination; autoantibodies
资金
- Poznan University of Medical Sciences, Poland [502-14-02218346-50637]
Introduction: The etiology and pathogenesis of pregnancy-related hypertensive disorders is complex and multifactorial. The aim of our study is the investigation of the differences in the autoantibodies against angiotensin II type 1 receptor (AT1-AA) titers among pregnant patients with chronic hypertension, gestational hypertension, and preeclampsia compared to the healthy pregnant women. Patients and methods: We created three study groups (preeclampsia [n = 16], chronic hypertension [n = 13], gestational hypertension [n = 17]) and the control group consisting of 17 healthy pregnant women. Every compared group was matched for mother's age, parity, prepregnancy BMI, and gestational age at time of recruitment into study. The autoantibodies titer were assessed using commercially available ELISA kit. Results: We found a statistically higher AT1-AA titer in the group of patients with gestational hypertension (GH) and preeclampsia (PE) compared to healthy normotensive pregnant women (median 9.6 versus 7.8 ng/ml, p = .01 and 10.9 ng/ml versus 7.8 ng/ml, p = .02, respectively). There was no correlation between blood pressure values and AT1-AA titer in any group. We found no correlation in group with preeclampsia between urinary protein excretion and AT1-AA titer (p = .23, R = 0.32). Conclusions: We assume that pregnancy-related hypertensive disorders might be autoimmune diseases and AT1-AA contribute to the pathophysiology of the disease. Our study may have some therapeutic implications and shows the necessity of new research into the mechanisms involved in the production of AT1-AA. Such investigations might enable to inhibit the formation of these autoantibodies or elaborate another method for AT1-AA removal.
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