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      Perfil lipídico y malonilaldehído en preeclámpticas

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          Abstract

          Objetivo: Determinar las concentraciones séricas de lípidos, lipoproteínas, apolipoproteínas y malonilaldehído en preeclámpticas. Métodos: Estudio descriptivo y prospectivo. Setenta pacientes que asistieron a la emergencia de obstetricia fueron seleccionadas y divididas en dos grupos mediante un muestreo no probabilístico. Ambos grupos consistieron en preeclámpticas (grupo A) y embarazadas normotensas (grupo B), consideradas como controles. Se midieron las concentraciones de colesterol total, triglicéridos, apolipoproteína A-I y B, lipoproteínas de alta densidad (HDL-C), baja densidad (LDL-C), muy baja densidad (VLDL) y malonilaldehído. Ambiente: Hospital Central “Dr. Urquinaona”. Maracaibo, Estado Zulia. Resultados: No se encontraron diferencias en la edad materna y en el promedio de peso materno entre las preeclámpticas y los controles (P = ns). Se evidenciaron diferencias estadísticamente significativas en la edad gestacional al momento del estudio, presión arterial sistólica y diastólica, peso del recién nacido y presencia de proteinuria (P < 0,05). Se encontraron diferencias estadísticamente significativas en las concentraciones de triglicéridos, lipoproteinas de alta densidad y de muy baja densidad, apolipoproteína B y malonilaldehído (P < 0,05). No se encontraron diferencias estadísticamente significativas en las concentraciones plasmáticas de colesterol, lipoproteínas de baja densidad y apolipoproteína A-I (P = ns). Se observaron correlaciones significativas negativas en las preeclámpticas entre las concentraciones de lipoproteínas de alta densidad y de muy baja densidad y entre las concentraciones de lipoproteínas de alta densidad y apolipoproteína B (P < 0,05). Conclusión: Existen diferencias significativas en las concentraciones de triglicéridos, lipoproteínas de alta densidad y de muy baja densidad, apolipoproteína B y malonilaldehído en las preeclámpticas.

          Translated abstract

          Objective: To determine lipids, lipoproteins, apolipoproteins and malonilaldehyde concentrations in preeclamptic and normotensive patients. Method: Seventy patients who assisted to obstetric emergency were selected and divided in two groups using a non-probabilistic sampling method. Both groups consisted in preeclamptic patients (group A) and normotensive pregnant women (group B), considered as controls. Plasma total cholesterol, triglycerides, apolipoproteins A-I and B, high density lipoprotein (HDL-C), low density (LDL-C), very low density (VLDL) and malonilaldehyde were measured. Settings: Hospital Central "Dr. Urquinaona". Maracaibo, Estado Zulia. Results: There were not significant statically differences in mean maternal age and weight between preeclamptic patients and controls (P = ns) There were found significant differences in gestational age at the moment of delivery, systolic and diastolic blood pressure, newborn weight and presence of proteinuria (P > 0.05). There were statically significant differences in concentrations of triglycerides, HDL-C, VLDL, apolipoprotein B and malonilaldehyde (P < 0.05). There were not found significant differences in plasma concentrations of cholesterol, LDL-C and apolipoprotein A-I (P = ns). There were negative significant correlations in preeclamptic between HDL-C and LDL-C and between HDL-C and apolipoprotein B (P < 0,05). Conclusions: There are significant differences in triglycerides, HDL-C, VLDL, apolipoprotein B and malonilaldehyde in preeclamptic patients.

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          Most cited references51

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          Endovascular trophoblast invasion: implications for the pathogenesis of intrauterine growth retardation and preeclampsia.

          Maternal uteroplacental blood flow increases during pregnancy. Altered uteroplacental blood flow is a core predictor of abnormal pregnancy. Normally, the uteroplacental arteries are invaded by endovascular trophoblast and remodeled into dilated, inelastic tubes without maternal vasomotor control. Disturbed remodeling is associated with maintenance of high uteroplacental vascular resistance and intrauterine growth restriction (IUGR) and preeclampsia. Herein, we review routes, mechanisms, and control of endovascular trophoblast invasion. The reviewed data suggest that endovascular trophoblast invasion involves a side route of interstitial invasion. Failure of vascular invasion is preceded by impaired interstitial trophoblast invasion. Extravillous trophoblast synthesis of nitric oxide is discussed in relation to arterial dilation that paves the way for endovascular trophoblast. Moreover, molecular mimicry of invading trophoblast-expressing endothelial adhesion molecules is discussed in relation to replacement of endothelium by trophoblast. Also, maternal uterine endothelial cells actively prepare endovascular invasion by expression of selectins that enable trophoblast to adhere to maternal endothelium. Finally, the mother can prevent endovascular invasion by activated macrophage-induced apoptosis of trophoblast. These data are partially controversial because of methodological restrictions associated with limitations of human tissue investigations and animal studies. Animal models require special care when extrapolating data to the human due to extreme species variations regarding trophoblast invasion. Basal plates of delivered placentas or curettage specimens have been used to describe failure of trophoblast invasion associated with IUGR and preeclampsia; however, they are unsuitable for these kinds of studies, since they do not include the area of pathogenic events, i.e., the placental bed.
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            Reaction conditions affecting the relationship between thiobarbituric acid reactivity and lipid peroxides in human plasma.

            The thiobarbituric acid (TBA) reactivity of human plasma was studied to evaluate its adequacy in quantifying lipid peroxidation as an index of systemic oxidative stress. Two spectrophotometric TBA tests based on the use of either phosphoric acid (pH 2.0, method A) or trichloroacetic plus hydrochloric acid (pH 0.9, method B) were employed with and without sodium sulfate (SS) to inhibit sialic acid (SA) reactivity with TBA. To correct for background absorption, the absorbance values at 572 nm were subtracted from those at 532 nm, which represent the absorption maximum of the TBA:MDA adduct. Method B gave values of TBA-reactive substances (TBARS) 2-fold higher than those detected with method A. SS lowered TBARS by about 50% with both methods, indicating a significant involvement of SA in plasma TBA reactivity. Standard SA, at a physiologically relevant concentration of 1.5 mM, reacted with TBA, creating interference problems, which were substantially eliminated by SS plus correction for background absorbance. When method B was carried out in the lipid and protein fraction of plasma, SS inhibited by 65% TBARS formation only in the latter. Protein TBARS may be largely ascribed to SA-containing glycoproteins and, to a minor extent, protein-bound MDA. Indeed, EDTA did not affect protein TBARS assessed in the presence of SS. TBA reactivity of whole plasma and of its lipid fraction was instead inhibited by EDTA, suggesting that lipoperoxides (and possibly monofunctional lipoperoxidation aldehydes) are involved as MDA precursors in the TBA test. Pretreatment of plasma with KI, a specific reductant of hydroperoxides, decreased TBARS by about 27%. Moreover, aspirin administration to humans to inhibit prostaglandin endoperoxide generation reduced plasma TBARS by 40%. In conclusion, reaction conditions affect the relationship between TBA reactivity and lipid peroxidation in human plasma. After correction for the interfering effects of SA in the TBA test, 40% of plasma TBARS appears related to in vivo generated prostaglandin endoperoxides and only about 60% to lipoperoxidation products. Thus, the TBA test is not totally specific to oxidant-driven lipid peroxidation in human plasma.
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              The role of placental oxidative stress and lipid peroxidation in preeclampsia.

              Preeclampsia is a complex multisystem disorder exclusively seen in human species that is characterized by hypertension and proteinuria. This disorder has the highest maternal and fetal morbidity and mortality of all pregnancy-related complications. Growing evidence suggests that placental oxidative stress is involved in the etiopathogenesis of preeclampsia. Reduced perfusion as a result of abnormal placentation leads to ischemia reperfusion injury to the placenta. Placental oxidative stress, which results from the ischemia reperfusion injury, is being increasingly reported to be involved in the etiopathogenesis of preeclampsia. It has been proposed as a promoter of lipid peroxidation and the endothelial cell dysfunction that is commonly seen in this condition. Although preeclampsia is characterized by increased lipid peroxidation and diminished antioxidant capacity, there is no consensus regarding causality of lipid peroxidation in preeclampsia. In this article, we address the question of the biologic association of lipid peroxidation and preeclampsia. Lipid peroxidation and leukocyte activation may play a pivotal role in endothelial cell dysfunction. We also review the different factors that have been proposed to cause endothelial cell dysfunction in preeclampsia, trials investigating the role of antioxidant supplementation in preeclampsia, and the lack of consensus among the trials. Additional longitudinal studies are necessary to determine if the various oxidative stress biomarkers estimated early in pregnancy can be narrowed to a single marker for predicting preeclampsia. Obstetricians & Gynecologists, Family Physicians. After completion of this article, the reader should be able to recall that placental oxidative stress is involved in the etiopathogenesis of preeclampsia, state that placental oxidative stress results from ischemic reperfusion injury, and explain that ischemic reperfusion injury is a promoter of lipid peroxidation and endothelial cell dysfunction seen in preeclampsia.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                og
                Revista de Obstetricia y Ginecología de Venezuela
                Rev Obstet Ginecol Venez
                Sociedad de Obstetricia y Ginecología de Venezuela (Caracas )
                0048-7732
                March 2012
                : 72
                : 1
                : 28-33
                Affiliations
                [1 ] Hospital Central Dr. Urquinaona
                Article
                S0048-77322012000100005
                81f9fc6d-1155-4a96-a4ff-7a505e0d4e0b

                http://creativecommons.org/licenses/by/4.0/

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                SciELO Venezuela

                Self URI (journal page): http://www.scielo.org.ve/scielo.php?script=sci_serial&pid=0048-7732&lng=en
                Categories
                OBSTETRICS & GYNECOLOGY

                Obstetrics & Gynecology
                Preeclampsia,Triglycerides,Lipoproteins,Apolipoproteins,Malonilaldehyde,Lípidos,Lipoproteínas,Apolipoproteínas,Malonilaldehído

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