title: Haemostasis, cytoadhesive molecules (sE-selectin and sICAM-1) and inflammatory markers in non-insulin dependent diabetes mellitus (NIDDM).
abstract: Non-insulin dependent diabetes mellitus (NIDDM) is connected with a higher incidence of macrovascular atherosclerotic disorders. The aim of the study was to detect any difference in levels of "cardiovascular risk factors"--fibrinogen, PAI-1 and inflammation response (documented by an increase of protein of acute phase orosomucoid) and of soluble cytoadhesive molecule sE-selectin and sICAM-1 (as markers of endothelial dysfunction) in blood plasma of 118 patients with NIDDM in comparison to the levels in blood plasma of 59 healthy persons as a control group. We observed higher levels of fibrinogen (fibrinogen level was 3.44 +/- 1.02 g/l in NIDDM pts versus 2.44 +/- 0.55 g/l in control group, p < 0.01) and PAI-1 Ag concentration was 159.7 +/- 110.3 ng/ml in NIDDM pts versus 51.43 +/- 24.64 ng/ml in control group, p < 0.01) together with an increase of acute phase protein orosomucoid as a "inflammatory response marker" (orosomucoid concentration was 0.85 +/- 0.23 g/l in NIDDM pts versus 0.54 +/- 0.18 g/l in control group, p < 0.01) in patients with NIDDM. The increase of these "cardiovascular risk factors" levels will be probably induced by higher activity of inflammatory cytokines IL-1 beta and/or TNF alpha in NIDDM patients, because both are inducers of orosomucoid fibrinogen and PAI-1 synthesis. This hypothesis is also supported by observation of higher levels of soluble cytoadhesive molecules sE-selectin (sE-selectin level was 64.25 +/- 26.8 ng/ml in NIDDM pts versus 46.64 +/- 29.57 ng/ml in control group, p < 0.01) and sICAM-1 (sICAM-1 level was 307.71 +/- 86.2 ng/ml in NIDDM pts versus 255.6 +/- 58.0 ng/ml in control group, p < 0.01) in patients with NIDDM. Both cytoadhesive molecules are produced by endothelial cells which are influenced by IL-1 beta and/or TNF alpha. According to these findings we suppose that an "inflammation" plays an important role in the evolution of atherosclerotic process at NIDDM together with the known influence of glucose and lipid metabolism pathology.
authors.affiliation: Department of Clinical Haematology, 1st Faculty of Medicine, Charles University, Prague, Czech Republic. kvasnic@okhvfn.anet.cz
authors.forename: J
authors.initials: J
authors.lastname: Kvasnicka
authors.forename: J
authors.initials: J
authors.lastname: Skrha
authors.forename: J
authors.initials: J
authors.lastname: Perusicová
authors.forename: T
authors.initials: T
authors.lastname: Kvasnicka
authors.forename: M
authors.initials: M
authors.lastname: Marková
authors.forename: A
authors.initials: A
authors.lastname: Umlaufová
authors.forename: L
authors.initials: L
authors.lastname: Pecen
mesh_terms: D002318:Cardiovascular Diseases / Q000209:etiology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications; D019040:E-Selectin / Q000097:blood*; D006487:Hemostasis; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008875:Middle Aged; D009961:Orosomucoid / Q000032:analysis*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012307:Risk Factors
chemical_list: D019040:E-Selectin; D018836:Inflammation Mediators; D009961:Orosomucoid; D017395:Plasminogen Activator Inhibitor 1; D018799:Intercellular Adhesion Molecule-1