Significance of vitronectin and PAI-1 activity levels in carotid artery disease: comparison of symptomatic and asymptomatic patients.

AIM: Carotid atherosclerosis one of the main risk factors for ischemic stroke. Acute thrombosis after atherosclerotic plaque disruption is a major complication of primary atherosclerosis, leading to acute ischemic syndromes and atherosclerotic progression. PAI-1 is the most important and most rapidly acting physiological inhibitor of tissue-type (t-PA) and urokinase type (u-PA) plasminogen activators. Active PAI-1 form spontaneously converts to the latent with a half-life of ~1 h. Complex formation with vitronectin increases half life of PAI-1 by two- to four-folds. Thus, this inhibitor function of PAI-1 facilitated by Vn that binds the inhibitor and may regulate its activity by the stabilizing the active PAI-1 conformation. In addition, PAI-1/VN complexes may effect vascular structure and function. However, the exact role of these complexes in vascular remodelling are not completely clear. The aim of the present study was determining, correlating and comparing the plasma vitronectin, t-PA and PAI-1 activity levels in asymptomatic and symptomatic patients with carotid artery plaque. METHODS: A total of 37 carotid artery disease patients were included in this study. Blood samples were obtained from Cerrahpasa Medical School, Department of Heart and Vessel Surgery, University of Istanbul. Plasma vitronectin, tPA and PAI-1 activity levels were determined by ELISA. RESULTS: We found plasma PAI-1 activity levels were elevated in the asymptomatic group as compared with symptomatic group (P=0.038). We have also found a positive correlation between PAI-1 activity and vitronectin levels in symptomatic group (r=0.399, P=0.039). CONCLUSION: Decreased PAI-1 activity levels correlate with vitronectin in the symptomatic group; a) may be the consequence a compensatory mechanisms (due to possibilty in increased fibrinolytic activity and decreased vascular remodelling) against disease progression. b) or may be also cause progression of disease by increase of vascular remodelling.

Plasma Levels of Plasminogen Activator Inhibitor Type 1 and Vitronectin in Children With Cancer.

BACKGROUND: The plasminogen activator system controls intravascular fibrin deposition; besides, it also participates in a wide variety of physiologic and pathologic processes, including cancer. PROCEDURE: In this study, we examined the levels of plasminogen activator inhibitor 1 (PAI-1) and vitronectin in 32 newly diagnosed pediatric patients with malignancies, determined by enzyme-linked immunosorbent assay between January 2009 and January 2010 and compared them to 35 age-matched healthy children, using SPSS 16.0 software. RESULTS: The mean level of PAI-1 was 23.02 ± 15 (8.2-71.19) ng/mL and vitronectin was 83.10% ± 23.77% (12%-126%) in the tumor group. Thirty-five healthy children in the same age range were enrolled in the control group. The levels of PAI-1 and vitronectin were 23.63 ± 10.44 (11.67-58.85) ng/mL and 85% ± 20.85% (39%-126%), respectively. No significant difference was found between the 2 groups by independent sample t-test (P = .86 and P = .69). CONCLUSIONS: This is a preliminary study done in children with malignancies, investigating PAI-1 and vitronectin. Further study is needed, including larger trials and tumor tissue with histopathological examination as in adults.

Iron, nitric oxide, and myeloperoxidase in asthmatic patients.

Plasma nitric oxide (NO), myeloperoxidase (MPO), and iron (Fe) levels were determined in bronchial asthma. The relations among these parameters in different stages of asthma were interpreted. Their association with airway inflammation observed in patients with bronchial asthma as well as the roles and the contributions to the pathological processes were evaluated. A total of 62 individuals, 32 asthmatics and 30 controls, were included into the scope of this study. Plasma nitric oxide metabolites (NOx) and MPO and Fe levels were determined by the Griess reaction, ELISA, and the automated TPTZ (2,4,6-tri[2-pyridyl]-5-triazine) method, respectively. In the asthmatic individuals, plasma NOx, MPO, and Fe concentrations were 133 +/- 13 microM, 95 +/- 20 ng/ml, and 159 +/- 20 microg/dl, respectively; in the control group these values were 82 +/- 11 microM, 62 +/- 11 ng/ml, and 96 +/- 9 microg/dl. Increased values were detected for plasma MPO (p > 0.05), NOx (p < 0.01), and Fe (p < 0.01) concentrations in asthmatic individuals. Considering the facts that NO modulates the catalytic activity of MPO and induces the expression of heme oxygenase as important contributors to the mechanisms causing free Fe release, it is concluded that elevated NOx, MPO, and Fe levels observed in the asthmatic group act in a concerted manner and appear to be involved in the pathogenesis of asthma.