Abstract

GARCIA, Ronald et al. Increased PRC and IL6 concentrations and lower early flow-mediated vasodilatation in gestation help predict the developement of pregnancy-induced hypertension. Acta Med Colomb [online]. 2005, vol.30, n.3, pp.92-99. ISSN 0120-2448.

Background: endothelial dysfunction has been involved in the development of pre-eclampsia. Recently, there has been an increasing interest in the role of infection-inflammation as a key factor of endothelial dysfunction. The purpose of this study was to investigate whether endothelial dysfunction is associated with inflammation that precedes the clinical and biochemical manifestations of pregnancy induced hypertension (PIH). Methods: two hundred and twenty six normotensive primigravidae pregnant women under 25 years of age, at 20-30 weeks of gestation, were included in a nested case-control study. Flow-mediated dilation in the brachial artery was measured using a 7.5MHz transducer (Aloka, vario-view SDD2200, Tokyo, Japan). Plasma concentrations of interleukin-6 and C-reactive protein were determined (IMMULITE 1000, DPC, Los Angeles, CA). Results: ten women developed PIH and 216 remained normotensive. Twenty 20 normal pregnant women were selected as matched controls. The women who subsequently developed PIH had lower flow-mediated dilation (17.65% [SD 9.33] vs 24.81% [SD 5.30]; p=0.01), and higher plasma concentrations of C- reactive protein (3.6 ± 2.32 mg/dL vs 1.99 ± 1.2 mg/dL, p=0.02), interleukin-6 (2.06 ± 0.55 pg/dL vs 1.64 ± 0.28 pg/dL, p=0.02) and leukocyte counts (11.7 ± 2.2 (x10⁶/L) vs 8,1 ± 1.9 (x10⁶/L) , p=0.02). Conclusions: maternal endothelial dysfunction associated with inflammation is present in early stages of gestation in women who subsequently develop PIH. This impairment occurs before the onset of clinical symptoms and laboratory alterations. Flow mediated dilation and inflammatory markers can be useful methods to screen women at risk of developing PIH.

Keywords : pregnancy induced hypertension; pre-eclampsia; endothelium; nitric oxide; cytokines; inflammation.

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