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Soluble P-selectin (soluble + p-selectin)
Selected AbstractsThe effects of maximal treadmill graded exercise testing on haemorheological, haemodynamic and flow cytometry platelet markers in patients with systolic or diastolic heart failureEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2008I. Chung ABSTRACT Background, Acute exercise has been associated with activation of thrombosis, and this risk may be accentuated in patients with heart failure. Given the relation of platelets to atherothrombosis, we tested the hypothesis that acute exercise would adversely affect platelet indices and platelet activation markers in patients with systolic and diastolic heart failure. Materials and methods, We studied 20 patients with systolic heart failure (17 men, 3 women; mean age 64 ± 10 years, all with ejection fraction (EF) , 40%) and 20 patients with diastolic heart failure (14 men, 6 women; mean age 64 ± 8 years, mean EF = 66%) who were exercised to maximal intensity, who were compared to 13 healthy controls (6 men, 7 women; mean age 60 ± 4 years, mean EF = 73%). We measured platelet indices (platelet volume, mass and component) and platelet activation markers (platelet-bound CD62P%G, CD63%G and CD40L%G using flow cytometry, as well as plasma sCD40L and soluble P-selectin (sP-sel) levels). Results, Baseline Mean Platelet Volume (MPV), sP-sel, CD40L%G and CD63%G levels were significantly higher in patients with systolic and diastolic heart failure, when compared with controls. The mean exercise duration and VO2 peak in patients with systolic and diastolic heart failure were not significantly different, but lower than that seen in healthy controls. Following exercise, mean haematocrit, CD62P%G, and CD63%G significantly increased in all three subject groups (all P < 0·05). The proportional change in CD62P%G and CD63%G were not significantly different between healthy controls and heart failure patients (P > 0·05). Conclusion, Acute maximal graded exercise increases platelet activation markers, with no disproportionate differences between heart failure patients and healthy controls, despite the former group having a lower exercise tolerance and VO2 peak. [source] Prognostic value of interleukin-6, plasma viscosity, fibrinogen, von Willebrand factor, tissue factor and vascular endothelial growth factor levels in congestive heart failureEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 11 2003B. S. P. Chin Abstract Background, Congestive heart failure (CHF) carries a poor prognosis with a high mortality rate, frequent hospitalizations and increased risk of thrombotic complications such as stroke. Cytokines may contribute to the progression and prothrombotic state of CHF, including the pro-inflammatory interleukin-6 (IL-6) and the pro-angiogenic vascular endothelial growth factor (VEGF), both of which are raised in CHF. The procoagulant properties of both cytokines may be mediated via tissue factor (TF), a potent clotting activator. We hypothesized that plasma levels of these markers, as well as levels of plasma viscosity, fibrinogen, soluble P-selectin and von Willebrand factor (markers of abnormal rheology, clotting, platelet activation, and endothelial damage, respectively) will be useful in predicting morbidity and mortality in chronic stable CHF. Methods and results, One hundred and twenty consecutive out-patients with chronic stable CHF (92 males; mean [SD] age 64 [11] years, mean [SD] left ventricular ejection fraction of 29 [6]%) were recruited and followed for 2 years during which 42 patients reached a clinical end-point of all-cause mortality and cardiovascular hospitalizations, including stroke and myocardial infarction. Plasma IL-6 (P = 0·003) and TF (P = 0·013) levels, but not other research indices, were higher in those who suffered events compared with those without events. Predictors of end-points were high (, median) TF (P = 0·011), and IL-6 (P = 0·023) levels, as well as the lowest quartile of a left ventricular ejection fraction (P = 0·007). A strong correlation was present between TF and IL-6 levels (r = 0·59; P < 0·0001) and with VEGF levels (r = 0·43; P < 0·0001). Conclusion, IL-6 and TF are predictors of poor prognosis in chronic CHF, raising the hypothesis that IL-6 may contribute to the progression and thrombotic complications of CHF via its actions on TF expression. Although VEGF did not independently predict outcome in chronic CHF, the possibility arises that it may act with IL-6 to induce TF expression. [source] The use of platelet density and volume measurements to estimate the severity of pre-eclampsiaEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2000P. Järemo This study evaluated whether it is possible to estimate the severity of pre-eclampsia through in vitro measurements of platelet and granulocyte parameters. Eighteen pre-eclamptic women in the third-trimester of pregnancy and 11 women in the third-trimester of normal pregnancies were included in the study. Three to 12 months after delivery, 15 patients with pre-eclampsia and all the subjects with normal pregnancies were re-examined. Before delivery, peak platelet density was determined using a specially designed apparatus. Before and 3,12 months after delivery the following were measured: platelet counts, mean platelet volume and neutrophil and monocyte counts. Furthermore, circulating P-selectin, interleukin-6 and myeloperoxidase were determined to estimate platelet, monocyte and granulocyte activities, respectively. Compared to their results after delivery, pre-eclamptic females demonstrated lower platelet counts (P < 0·001) and raised mean platelet volumes (P < 0·01). Both pre-eclamptic women (P < 0·01) and normal pregnancies (P < 0·05) demonstrated elevated soluble P-selectin at pregnancy. Then pre-eclamptic women had advanced neutrophil counts (P < 0·01) but normal pregnancies showed a similar phenomenon (P < 0·001). Interleukin-6 remained normal during pregnancy. Plasma myeloperoxidase levels were lower both in pre-eclampsia (P < 0·05) and in normal pregnancies (P < 0·001). In pre-eclampsia elevated blood pressure was related to higher mean platelet volumes (P < 0·05). Furthermore, a group of pre-eclamptic females whose platelets had disturbed density distribution displayed elevated mean platelet volumes (P < 0·01). The present work demonstrates considerable platelet alterations in pre-eclampsia. We failed to show granulocyte involvement in the pathogenesis of the disease. Severe pre-eclampsia is related to elevated mean platelet volumes. The latter parameter is associated with disturbed density distribution. It appears possible to estimate disease severity from measurements of platelet density and volume. [source] Effects of Helicobacter pylori Eradication on Platelet Activation and Disease Recurrence in Patients with Acute Coronary SyndromesHELICOBACTER, Issue 6 2004J. Ignasi Elizalde ABSTRACT Background., Platelet activation is consistently observed in animal models of Helicobacter pylori infection and could help to explain the alleged epidemiological association between H. pylori and coronary heart disease. Materials and Methods., Ninety-two patients with recent acute coronary syndromes were enrolled. Helicobacter pylori -positive patients were randomized to receive a 7-day course of omeprazole, amoxycillin and metronidazole or placebos. Two months later, H. pylori status was reassessed and baseline parameters, including soluble P-selectin and platelet surface expression of CD62P, CD63 and CD41, were measured again. Patients were followed-up for 1 year or until death or readmission. Results., No baseline differences were observed between H. pylori -positive and -negative cases. Among H. pylori -positive patients, 18 received placebo and 31 received active medication resulting in eradication in 21 cases. No differences were observed in inflammatory parameters or platelet activation markers between patients with persistent or resolved H. pylori infection. However, coronary events recurred at 6 and 12 months, respectively, in 35% and 55% of patients with persisting H. pylori infection compared with 10% and 25% of patients in whom H. pylori was either absent or eradicated (p = .01). Only final H. pylori status [RR 3.07 (95% CI 1.35,98)] and number of coronary risk factors [RR 2.58 (95% CI 1.51,4.41)] were independent predictors of recurrence. Conclusions., Infection with H. pylori does not induce significant platelet activation in patients treated for coronary disease. Helicobacter pylori -infected patients, however, may have an increased risk of recurrence of coronary events. [source] Changes in serum concentrations of tumor necrosis factor , and adhesion molecules in normal pregnant women and those with pregnancy-induced hypertensionJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 6 2003Keiichi Matsubara Abstract Aim:, To study whether serum tumor necrosis factor , gene (TNF,) and adhesion molecule levels are indicators of the onset of pregnancy-induced hypertension (PIH), we compared levels of these molecules between normal pregnant women and PIH patients from the first to the third trimester. Methods:, We serially measured serum concentrations of TNF,, soluble intercellular adhesion molecule-1 (sICAM-1), soluble E-selectin (sE-selectin), soluble vascular cell adhesion molecule-1 (sVCAM-1) and soluble P-selectin (sP-selectin) using enzyme immunoassay kits in 10 normal pregnant women and 10 pregnant women who developed PIH late in gestation. Results:, Serum TNF,, sICAM-1 and sE-selectin levels in PIH affected women were significantly higher from the first trimester compared with those in normal pregnancy. sVCAM-1 and sP-selectin levels were not significantly changed. Conclusion:, Serum TNF,, sE-selectin and sICAM-1 levels might be effective indicators of the onset of PIH. [source] Platelet turnover, coagulation factors, and soluble markers of platelet and endothelial activation in essential thrombocythemia: Relationship with thrombosis occurrence and JAK2 V617F allele burden,AMERICAN JOURNAL OF HEMATOLOGY, Issue 2 2009Eduardo Arellano-Rodrigo Patients with essential thrombocythemia (ET) have an increased frequency of thrombosis, but the relationship of both thrombosis and JAK2 V617F allele burden with platelet turnover, acquired activated protein C resistance (aAPCR), and levels of coagulation factors and soluble markers of platelet, and endothelial activation is not well known. In 53 ET patients (26 with a history of thrombosis), reticulated platelets (RP) percentage, aAPCR, platelet tissue factor (TF) expression, and plasma levels of TF, coagulation factors, soluble P-selectin (sP-selectin), soluble CD40 ligand (sCD40L), von Willebrand factor antigen (VWF:Ag), soluble thrombomodulin (sTM), D -dimer and prothrombin fragment 1 + 2 were compared with those in matched healthy individuals and correlated with thrombosis occurrence and JAK2 mutational load. ET patients with thrombosis had significantly higher values for RP percentage, aAPCR, and levels of factors V and VIII, VWF:Ag, sP-selectin, and sCD40L than patients without thrombosis and controls. At multivariate study, RP percentage, factor V levels, and aAPCR were independently associated with an increased risk of thrombosis. Patients with JAK2 mutation had significantly lower levels of free protein S (PS) and higher levels of TF, sP-selectin, sCD40L, VWF:Ag, and sTM than those with wild-type allele. A mutant allele dosage effect (, 12%) was observed for TF, sP-selectin, sCD40L, VWF:Ag, and PS levels. These results support a role for platelet turnover, factor V, and aAPCR in the thrombosis of ET as well as the association between JAK2 V617F allele burden and either decreased free PS or increased TF and soluble markers of platelet and endothelial activation. Am. J. Hematol., 2009. © 2008 Wiley-Liss, Inc. [source] SOLUBLE BIO-MARKERS IN VASCULAR DISEASE: MUCH MORE THAN GAUGES OF DISEASE?CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2005Kevin J Woollard SUMMARY 1.,In recent years demonstration of a direct association between slightly elevated serum levels of soluble proteins including the acute phase response proteins, selectins and intercellular adhesion molecules and the risk of developing vascular disease have been widely reported. These studies may provide the clinician with an insight into disease diagnosis, prognosis and disease activity. 2.,The simplest interpretation of this data is that soluble proteins are just sensitive markers of inflammation. However, they may in fact be modulating inflammation directly through interaction with circulating cells. 3.,Recent work has shown that these soluble proteins do indeed remain active and can bind to functional ligands expressed by circulating leucocytes. The current review focuses on the soluble proteins C-reactive protein and soluble P-selectin and describes previous studies characterizing their interaction with immune cells to modulate the pathogenesis of vascular disease. 4.,The current review focuses on the soluble proteins C-reactive protein and soluble P-selectin and describes previous studies characterizing their interaction with immune cells to modulate the pathogenesis of vascular disease. [source] | ||||||||||