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Neopterin, PMN Elastase, and Complement Components as Monitoring Parameters in Women with the Syndrome of Hemolysis, Elevated Liver Enzymes and Low Platelet Count

Neopterin, PMN Elastase, and Complement Components as Monitoring Parameters in Women with the... Summary Preeclampsia is a pregnancy induced hypertensive disease with an incidence of about 5% in primigravida and it significantly contributes to maternal and neonatal morbidity and mortality. The primary cause remains unknown but might be immunologic. Our previous studies have shown that complement neutrophils and macrophages are activated in preeclampsia. The present study evaluated whether the extension of the macrophage, the neutrophil and the complement activation is related to the severity of preeclampsia. Patients with severe preeclampsia. complicated by the syndrome of hemolysis. elevated liver enzymes and low platelet count (HELLP) and women with preeclampsia were studied. Women with uncomplicated pregnancies were controls. To detect activation of macrophages and polymorphonuclear neutrophils (PMN), respectively. the formations of neopterin and PMN elastase were analyzed. For evaluation of complement activation. the biologically active components C5a and the terminal C5b-9 complement complex (TCC) were determined in plasma. Patients with the HELLP syndrome had significantly elevated plasma concentrations of neopterin and C5a at delivery compared to women with preeclampsia. and compared to the controls, the HELLP group had significantly raised plasma levels of neopterin. PMN elastase. C5a and TCC. Women with preeclampsia had significantly higher plasma concentrations of neopterin and TeC at delivery as compared to the controls. In preeclamptics and HELLP patients, the plasma concentrations at delivery of PMN elastase, C5a and TCC were normalized within one week. but the plasma levels of neopterin remained elevated after one week. Neopterin, PMN http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Pteridines de Gruyter

Neopterin, PMN Elastase, and Complement Components as Monitoring Parameters in Women with the Syndrome of Hemolysis, Elevated Liver Enzymes and Low Platelet Count

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References (26)

Publisher
de Gruyter
Copyright
Copyright © 1993 by the
ISSN
0933-4807
eISSN
2195-4720
DOI
10.1515/pteridines.1993.4.3.138
Publisher site
See Article on Publisher Site

Abstract

Summary Preeclampsia is a pregnancy induced hypertensive disease with an incidence of about 5% in primigravida and it significantly contributes to maternal and neonatal morbidity and mortality. The primary cause remains unknown but might be immunologic. Our previous studies have shown that complement neutrophils and macrophages are activated in preeclampsia. The present study evaluated whether the extension of the macrophage, the neutrophil and the complement activation is related to the severity of preeclampsia. Patients with severe preeclampsia. complicated by the syndrome of hemolysis. elevated liver enzymes and low platelet count (HELLP) and women with preeclampsia were studied. Women with uncomplicated pregnancies were controls. To detect activation of macrophages and polymorphonuclear neutrophils (PMN), respectively. the formations of neopterin and PMN elastase were analyzed. For evaluation of complement activation. the biologically active components C5a and the terminal C5b-9 complement complex (TCC) were determined in plasma. Patients with the HELLP syndrome had significantly elevated plasma concentrations of neopterin and C5a at delivery compared to women with preeclampsia. and compared to the controls, the HELLP group had significantly raised plasma levels of neopterin. PMN elastase. C5a and TCC. Women with preeclampsia had significantly higher plasma concentrations of neopterin and TeC at delivery as compared to the controls. In preeclamptics and HELLP patients, the plasma concentrations at delivery of PMN elastase, C5a and TCC were normalized within one week. but the plasma levels of neopterin remained elevated after one week. Neopterin, PMN

Journal

Pteridinesde Gruyter

Published: Aug 1, 1993

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