Abstract
OBJECTIVE: The aim of the study was to evaluate the levels of adipokines such as adiponectin and leptin as well as soluble intercellular adhesion molecule-1 (sICAM-1) and endogenous NOS inhibitor-asymmetric dimethylarginine (ADMA), as the endothelium dysfunction markers in pregnant women with gestational hypertension (GH). PATIENTS AND METHODS: Adiponectin, leptin, sICAM-1, and ADMA concentrations were measured in a group of 34 patients with GH and in 32 healthy pregnant women between the 24(th) and 34(th) week of gestation with ELISA tests. RESULTS: The patients with GH compared with healthy ones were characterized by significantly higher BMI (28.09 ± 7.90 vs. 22.34 ± 4.21 kg/m(2), p=0.016) and higher concentrations of leptin (45.89 ± 35.91 vs. 24.09 ± 24.40 ng/mL, p=0.006). sICAM-1 levels were also higher in the GH group but without the statistical significance (264.51 ± 50.99 vs. 232.56 ± 43.3 ng/ml, p=0.057). There were no significant differences between groups in adiponectin (8.79 ± 8.67 vs. 7.90 ± 3.71 μg/mL, p=0.46, NS) and ADMA (0.57 ± 0.26 vs. 0.60 ± 0.24 μmol/L, p=0.68, NS) levels. The significant correlation between leptin levels and BMI value was observed only in patients with GH (R = 0.56, p=0.02). CONCLUSIONS: The higher levels of leptin in pregnant women with gestational hypertension may be suggestive of the role of leptin in GH development. As the patients in the GH group had higher BMI, hyperleptinemia may link obesity with gestational hypertension. The significance of leptin as the predictive marker of GH development could be implied. It could be postulated that the higher levels of sICAM-1 in the GH patients, although not statistically significant, could reflect some impairment of the endothelium function occurring in GH regardless of BMI. The comparable adiponectin levels in GH and healthy pregnant patients and the lack of its correlation with BMI may indicate the occurrence of a protective mechanism in pregnancy maintaining its concentration and preserving from the consequences of the decrease in its levels in overweight and obese patients. Since ADMA levels were similar in GH and healthy pregnant women, ADMA seems not to be involved in GH pathogenesis, suggesting that NO synthesis is not impaired in this pregnancy complication. As the data on the gestational hypertension pathogenesis and its correlations with adipokines and markers of the endothelium dysfunction are limited, further studies on this issue are warranted.