RESUMEN
BACKGROUND: Pre-eclampsia (PE) remains a disease of theories despite extensive research into its etiology. Alteration in the production of vascular endothelial growth factor (VEGF), a biomarker of endothelial dysfunction, is associated with pre-eclampsia although conflicting reports have been reported. The aim of the study was to determine and compare maternal serum levels of VEGF among pre-eclamptics, normotensive non pregnant and pregnant women. This was a cross-sectional study involving 100 women with pre-eclampsia, 102 women with normotensive pregnancy and 75 normotensives who were not pregnant. The study was carried out at Korle Bu Teaching Hospital (KBTH) from April to June in 2011. Basic socio-demographic and obstetric data were obtained by means of structured questionnaire. Following venesection, about 5mls of blood was sampled from the participants for the various tests. Enzyme Linked Immunosorbent Assay was used to determine the maternal serum levels of free VEGF. Data analysis was performed using SPSS version 20. RESULTS: Significant reduction in median serum levels of free VEGF was seen in both, normal pregnant [84.06 pg/ml (IQR: 78.90-99.67)] and pre-eclamptic women [4.71 pg/ml, (IQR: 3.41-7.93)] compared to the non-pregnant (395.85 pg/ml, IQR 234.93-625) with p < 0.001; the reduction was far greater in the pre-eclamptic group compared to that of normotensive pregnant group (p < 0.001). Early-onset pre-eclampsia had significantly more severe reduction in free VEGF levels (3.89, IQR: 2.60-5.67 pg/ml) compared to that of late onset PE (5.23, IQR: 3.78-16.97 pg/ml) with p<0.001 indicating a severer endothelial damage in former. CONCLUSIONS: Endothelial dysfunction contributes significantly to the pathogenesis of pre-eclampsia as demonstrated by profound decrease in maternal serum VEGF levels in PE compared to normotensive pregnancy and non-pregnancy state. The pathophysiology of early-onset pre-eclampsia may be partly explained by marked reduction in free serum VEGF levels with resultant severe endothelial dysfunction.
Asunto(s)
Presión Sanguínea/fisiología , Preeclampsia/fisiopatología , Factor A de Crecimiento Endotelial Vascular/sangre , Adolescente , Adulto , Edad de Inicio , Anciano , Biomarcadores/sangre , Estudios Transversales , Femenino , Ghana , Humanos , Persona de Mediana Edad , Preeclampsia/diagnóstico , Embarazo , Adulto JovenRESUMEN
BACKGROUND: Preeclampsia (PE) is still a disease of theories as the exact cause remains uncertain. Widespread vascular endothelial cell dysfunction is thought to mediate the generalized vasospasm and hypertension characteristic of PE. Altered nitric oxide (NO) production has been associated with the endothelial dysfunction in the pathogenesis of PE but conflicting results have emerged from previous studies. OBJECTIVES: To determine maternal serum levels of NO, a biomarker of endothelial function, in nonpregnant, normal pregnant, and preeclamptic women. MATERIALS AND METHODS: This was a cross-sectional case-control study of 277 women comprising 75 nonpregnant, 102 normal pregnant, and 100 preeclamptic women conducted at the Korle Bu Teaching Hospital between April and June 2011. About 5 mL of venous blood was obtained from the participants for the various investigations after meeting the inclusion criteria and signing to a written consent. Serum levels of NO were determined by Griess reaction. The data obtained were analyzed with SPSS version 20. RESULTS: The study showed significantly elevated serum levels of NO in preeclamptic women (82.45±50.31 µM) compared with normal pregnant (33.12±17.81 µM) and nonpregnant (16.92±11.41 µM) women with P<0.001. The alteration in maternal serum NO levels was significantly more profound in early-onset (severe) PE (119.63±45.860 µM) compared to that of late-onset (mild) disease (62.44±40.44 µM) with P<0.001, indicating a more severe vascular endothelial cell dysfunction in the early-onset disease. CONCLUSION: This study has determined a profound NO upregulation in PE evidenced by significant elevation of NO metabolite levels compared to normal pregnancy. This might be due to deranged endothelial function with dysregulated production of NO to restore the persistent hypertension characteristic of PE.