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      Fosfolipasa A2-II sérica durante el ciclo menstrual, embarazo y puerperio


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          Objetivo: Evaluar los niveles circulantes de fosfolipasa A2-II durante el ciclo menstrual normal y determinar sus alteraciones en las concentraciones maternas circulantes durante el ciclo menstrual, el embarazo y el puerperio. Método: Las concentraciones séricas de fosfolipasa A2-II se compararon entre 28 mujeres no embarazadas con ciclo menstruales normales, 57 embarazadas normales y 11 mujeres en el séptimo día del posparto normal. También se cuantificó en 8 pacientes con amenaza de parto pretérmino. Los niveles de fosfolipasa A2-II antes y después del parto se cuantificaron para determinar las diferencias en 8 neonatos obtenidos por vía vaginal y 8 por cesárea selectiva. Se tomó una muestra de sangre de 10 mL en la mañana y se realizó una prueba inmunorradiométrica, usando la combinación de dos anticuerpos monoclonales, para determinar la fosfolipasa A2-II en el suero. Resultados: Las concentraciones séricas de fosfolipasa A2-II en la fase lútea fueron significativamente menores que en la fase menstrual o folicular (p< 0,05). No hubo diferencias significativas en los niveles séricos de fosfolipasa A2-II entre las mujeres con embarazos normales y las pacientes con amenaza de parto pretérmino. Sus concentraciones séricas fueron significativamente mayores en mujeres en el séptimo día del posparto que en aquel1as con embarazos normales (p< 0,05) Conclusión: Estos resultados sugieren que puede existir un mecanismo regulatorio de fosfolipasa A2-II durante el ciclo menstrual normal y el puerperio.

          Translated abstract

          Objective: To evaluate phospholipaseA2-II circulating levels during normal menstrual cycle and determine alterations in maternal circulating phospholipaseA2-II concentrations during menstrual cycle, pregnancy and puerperium. Method: Serum phospholipaseA2-II concentrations were compared among 28 non-pregnant women with normal menstrual cycle, 57 normal pregnant women and 11 women at seventh day of puerperium. Also were measured in 8 patients with threatened premature labor. phospholipaseA2-II levels before and after delivery were made to determine differences in 8 neonates delivered vaginally and 8 neonates delivered by cesarean section. A 10-mL blood sample was obtained in the morning and an immunoradiometric assay, using two monoclonal antibodies, to determine serum phospholipaseA2-II. Results: Serum phospholipaseA2-II concentrations at luteal phase were significantly lower than those at menstrual o follicular phase (p< 0,05). There was no significant difference in serum phospholipasA2-II levels between normal pregnant women and patients with threatened premature labor. Serum phospholipaseA2-II concentrations at seventh day post-partum were significantly higher than those in normal pregnant women. Conclusions: These results suggest that a regulatory mechanism of phospholipaseA2-II may exist during the normal menstrual cycle and at puerperium.

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          Extracellular phospholipases A2 in relation to systemic inflammatory response syndrome (SIRS) and systemic complications in severe acute pancreatitis.

          The pathophysiology of severe acute pancreatitis (AP) resembles other conditions with systemic inflammatory response syndrome (SIRS) such as sepsis predisposing to remote organ failure. Because extracellular phospholipases A2 (PLA2) have been implicated in AP, their serum concentrations were analyzed with respect to SIRS and systemic complications in patients with severe AP. The serum samples were collected daily for 12 days in 57 patients with severe AP. SIRS, early organ complications, local complications, and outcome of AP were recorded. Time-resolved fluoroimmunoassays were used for group I and group II PLA2 measurements. Thirty-nine (68.4%) patients fulfilled the criteria of SIRS within 12 days from admission. Pancreatic necrosis was detected in 43 (75.4%) patients. Infected necrosis was found preoperatively or at operation in five (8.8%) patients. Twenty-six (45.6%) and eight (14.0%) patients had respiratory or renal failure, respectively. Seven (12.3%) patients died of their disease. All patients with systemic complications fulfilled the criteria of SIRS. The increasing number of positive SIRS criteria was associated with increased frequency of systemic complications. Pancreatic necrosis was not significantly associated with SIRS. The serum concentration of group II PLA2 was significantly higher in patients with SIRS (p < 0.05) compared with patients without from day 7 onward. The concentration of group II PLA2 increased (p < 0.01) in patients with SIRS but decreased in patients without. The serum concentration of group II PLA2 did not differ significantly with respect to systemic complications. The concentration of group I PLA2 decreased (p < 0.05) similarly in patients with and without SIRS or systemic complications during follow-up, respectively. Early systemic complications of severe AP are associated with SIRS with increasing frequency as the number of positive SIRS criteria increases. Group II PLA2 but not group I PLA2 may have pathophysiologic importance in severe AP-associated SIRS. Increasing serum concentration of group II PLA2 seems to reflect the ongoing systemic inflammation in severe AP-associated SIRS.
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            Interleukin-1 and tumor necrosis factor stimulate arachidonic acid release and phospholipid metabolism in human myometrial cells.

            Our aim was to evaluate the effects of the cytokines interleukin-1 and tumor necrosis factor on arachidonic acid release in human myometrial cells. Primary monolayer cultures of human myometrial cells prelabeled with tritiated arachidonic acid were exposed to interleukin-1 or tumor necrosis factor for varying periods and the release of tritiated arachidonic acid and its loss from phospholipids were measured by radiochromatography. To gain some information on the biologic action of interleukin-1 the contractile response to oxytocin was measured in myometrial strips preincubated with this cytokine. Data were statistically evaluated with analysis of variance or Student's test. Both cytokines caused a dose-dependent increase in tritiated arachidonate release that was suppressed by the protein synthesis inhibitor cycloheximide. Tritiated arachidonic acid release was maximal after 24 hours of stimulation with interleukin-1. Both interleukin-1 and tumor necrosis factor stimulated the release of the isotopically labeled fatty acid from phosphatidylcholine. In addition, interleukin-1 also increased the loss of arachidonic acid from phosphatidic acid and significantly potentiated the oxytocin-evoked myometrial contractility. Both interleukin-1 and tumor necrosis factor enhance arachidonic acid release, probably by inducing the synthesis of phospholipase A2 and possibly other enzymes involved in the metabolism of phospholipids. In turn, arachidonic acid itself may act as a second messenger, synergizing with other uterotonic agents, as well as serving as the precursor for prostaglandins and various other bioactive eicosanoids.
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              Immunohistologic detection of non-pancreatic phospholipase A2 (type II) in human placenta and its possible involvement in normal parturition at term.

              Placenta is one of the richest sources of non-pancreatic phospholipase A2 (npPLA2) (type II) in the human body, and the enzyme is the key enzyme releasing unsaturated fatty acids from membrane phospholipids. Prostaglandins (PGs) play a critical role in the initiation and progression of parturition. Cytokines are presumed to play a central role in the initiation of normal labor at term, and cytokines are also found to regulate both synthesis and secretion of npPLA2 enzyme. In an attempt to resolve the physiologic function of the npPLA2 enzyme in placental tissue, immunohistologic localization and enzymatic activity measurements of npPLA2 enzyme were performed. NpPLA2 protein was detected in vascular smooth muscle, endothelial cells and connective tissue cells in placenta and umbilical cord, and the protein was weakly stained in trophoblast cells in placenta. Enzymatic activity was not increased in sera from mother nor child compared to sera from healthy individuals, but the activity in amniotic fluid was considerably higher. Our findings support the candidacy for npPLA2 in enzymatic arachidonic acid release from foetal membranes.

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                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 )
                July 2003
                : 63
                : 3
                : 129-133
                [1 ] Hospital Central Dr. Urquinaona



                SciELO Venezuela

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

                Obstetrics & Gynecology
                Phospholipase A2,Menstrual Cycle,Pregnancy,Puerperium,Fosfolipasa A2,Ciclo menstrual,Embarazo,Puerperio


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