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      Plaquetas e hipertensión arterial durante el posparto


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          Objetivo: Determinar el contaje plaquetario posparto en preclampsia, eclampsia e hipertensión arterial crónica con preeclampsia sobreañadida. Método: Se cuantificaron las plaquetas pre y posparto de las gestantes ingresadas se repitieron cada 12 horas hasta normalizarse el reporte de trombocitopenia (< 150 000 x mm3). Ambiente: Maternidad del Hospital Central "Dr. Urquinaona". Maracaibo, Estado Zulia. Resultados: Hubo 85 pacientes admitidas; 21 con preeclampsia severa, 10 con eclampsia y 19 con hipertensión arterial crónica con preeclampsia sobreañadida. Ventiún pacientes presentaron trombocitopenia preparto, a las 12, 24, 36 y 48 horas posparto el contaje plaquetario continuaba bajo en 13, 9, 3 y 2 pacientes respectivamente, no hubo trombocitopenia a las 60 horas. Conclusión: La trombocitopenia asociada a la preeclampsia, eclampsia e hipertensión arterial crónica con preeclampsia sobreañadida se normalizó a las 48 horas posparto, por lo que se sugiere practicar controles de contajes plaquetarios cada 12 horas posparto, para vigilar la evolución y determinar el pronóstico de estas pacientes

          Translated abstract

          Objective: To determine the postpartum platelet count in preeclampsia, eclampsia and chronic hypertension with superimposed preeclampsia. Method: Prepartum and postpartum platelet counts were investigated; when thrombocytopenia was reported (< 150 000 x mm3), it was monitored every 12 hours until reaching normal values. Setting: Hospital Central "Dr. Urquinaona", Maracaibo - Zulia. Results: Eighty five patients were studied. There were 21 patients with mild preeclampsia, 35 with severe preeclampsia, 10 with eclampsia and 19 with chronic hypertension with superimposed preeclampsia. Twenty one patients presented prepartum thrombocytopenia; at 12, 24, 36 and 48 hours postpartum the levels remained low in 13, 9, 3 and 2 patients respectively, there was no thrombocytopenia at 60 hours. Conclusion: The thrombocytopenia associated with preeclampsia, eclampsia and chronic hypertension with superimposed preeclampsia was normalized at 48 hours postpartum. We recommend platelets counts every 12 hours to follow up its evolution and the prognosis of these patients

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          Endothelial dysfunction in preeclampsia.

          Several years ago the hypothesis was advanced that alterations of endothelial function could explain much of the pathophysiology of preeclampsia. Since that time, extensive data have been generated to support the hypothesis. Markers of endothelial activation can be demonstrated in women with overt preeclampsia. More importantly, many of these markers precede clinically evident disease and disappear with resolution of the disease. The original postulate was that materials produced by the poorly perfused placenta, which is characteristic of preeclampsia, entered the systemic circulation and altered endothelial cell activity. This was proposed to change vascular sensitivity to circulating pressors, activate coagulation, and reduce vascular integrity resulting in the pathophysiological changes of preeclampsia. As data have accumulated it has become increasingly evident that the insult to the endothelium is neither toxicity nor nonspecific injury but rather can better be characterized as endothelial activation. Candidate molecules have been suggested but not established. It seems likely that the responsible agent(s) will not be unique molecules but rather usual molecules present in excessive amounts. The hypothesis has been expanded to invoke involvement of the maternal constitution in the generation of endothelial injury and injurants. This concept is stimulated by the observation that reduced placental perfusion per se is not sufficient to generate the maternal syndrome. Women with growth-restricted fetuses frequently are not preeclamptic. Placental bed biopsies from not only growth-restricted but also prematurely born infants demonstrate failure of the physiological remodeling of decidual vessels responsible for the reduced placental perfusion of preeclampsia. This has led to the concept that preeclampsia is secondary to an interaction of reduced placental perfusion and maternal factors. Interestingly these maternal factors, obesity, insulin resistance, black race, hypertension, and elevated plasma homocysteine concentration are all risk factors for atherosclerosis in later life.
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            Guía práctica par el embarazo y el parto de alto riesgo

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              Pregnancy complicated by preeclampsia-eclampsia with the syndrome of hemolysis, elevated liver enzymes, and low platelet count: how rapid is postpartum recovery?

              The rapidity of postpartum disease recovery for severe preeclampsia associated with hemolysis, elevated liver enzymes, and low platelet count (HELLP syndrome) has not been well studied. Between January 1980 and March 1989, 158 pregnancies with preeclampsia-eclampsia complicated by HELLP syndrome were managed at the University of Mississippi Medical Center. The 70 patients with platelet nadir below 50,000/microL (class 1 HELLP syndrome) required as long as 11 days for all members to achieve a platelet recovery concentration of more than 100,000/microL, whereas all 88 gravidas with platelet nadir between 50,000-100,000/microL (class 2 HELLP syndrome) exceeded this platelet concentration by the sixth postpartum day, a statistically significant difference (P less than .0001). The interval between delivery and the onset of diuresis (mean +/- SD) was significantly longer in class 1 than in class 2 patients with milder disease (22.7 +/- 18.9 compared with 15.9 +/- 11.1 hours). Significantly more postpartum days were required in class 1 than in class 2 HELLP parturients for the lactic dehydrogenase (LDH) concentration to decrease below 500 IU/L (4.2 +/- 4.9 compared with 3.2 +/- 2.7 days). No women in the class 2 group required plasma exchange therapy to effect disease arrest and reversal, but 11 of 58 severely ill women in class 1 were treated with this modality. We conclude that the platelet count and LDH serum concentration, as indicators of HELLP severity and recovery, are clinically useful tools and that a more protracted postpartum recovery period should be expected for progressively severe expressions of HELLP syndrome.

                Author and article information

                Role: ND
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                Revista de Obstetricia y Ginecología de Venezuela
                Rev Obstet Ginecol Venez
                Sociedad de Obstetricia y Ginecología de Venezuela (Caracas )
                September 2001
                : 61
                : 4
                : 239-244
                [1 ] Hospital Dr. Manuel Noriega Trigo
                [2 ] Universidad del Zulia



                SciELO Venezuela

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

                Obstetrics & Gynecology
                Pregnancy,Platelets counts,Preeclampsia,Thrombocytopenia,Embarazo,Posparto,Contaje plaquetario,Trombocitopenia


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