title: Study of factor VII, tissue factor pathway inhibitor and monocyte tissue factor in noninsulin-dependent diabetes mellitus.
abstract: Changes in plasma tissue factor (TF)-activated factor VII (FVIIa) and plasma tissue factor pathway inhibitor (TFPI) in type II diabetes mellitus are assessed, vascular complicated and noncomplicated patients compared, and whether these novel hemostatic activity markers predict vascular complications in diabetic patients, improving risk assessment, is determined. Fifty type II diabetic patients and 20 healthy controls (age, sex and body mass matched) underwent medical history and examination, fasting plasma glucose level, glycosylated hemoglobin (HbA1c), lipid profile, hemostatic parameters, plasma TF activity, and TFPI and TF expression on blood monocytes. Mean TF, TF activity, TFPI, and FVIIa significantly increased among hyperlipidemic compared with normolipidemic diabetic patients, and normolipidemic diabetic patients compared with controls. Mean percentage TF-positive monocytes with and without lipopolysaccharide, plasma TF activity, TFPI and FVIIa were significantly higher among complicated than noncomplicated diabetic patients. Mean percentage TF-positive monocytes without and with lipopolysaccharide, plasma TF activity, plasma TFPI and FVIIa were higher among diabetic patients with macrovascular compared with microvascular complications. High significant correlation occurred between HbA1c, triglycerides and percentage TF-positive monocytes with and without lipopolysaccharide stimulation, plasma TF activity and both FVIIa and TFPI. High activity levels of plasma TF and FVIIa with increased circulating TF-positive monocytes occurred in type II diabetic patients, especially with vascular complications. Results reflect high procoagulant activity possibly involved in diabetic vascular complications. Elevated TFPI levels were observed, but were not sufficient to balance high procoagulant activity. Correlation of procoagulant activity markers with HbA1c reinforces the importance of optimal glycemic control in type II diabetes.
authors.affiliation: Department of Clinical Pathology, National Research Center, Cairo, Egypt. elghorouryeman@yahoo.com
authors.forename: Eman A
authors.initials: EA
authors.lastname: El-Ghoroury
authors.forename: Hesham Gamal
authors.initials: HG
authors.lastname: El-Din
authors.forename: Mona
authors.initials: M
authors.lastname: Abdel-Kader
authors.forename: Shadia
authors.initials: S
authors.lastname: Ragab
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D048909:Diabetes Complications / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D015942:Factor VIIa / Q000378:metabolism*; D005260:Female; D006442:Glycated Hemoglobin; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications; D008074:Lipoproteins / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000502:physiology*; D013925:Thromboplastin / Q000378:metabolism*
chemical_list: D015942:Factor VIIa; D006442:Glycated Hemoglobin; D008074:Lipoproteins; D013925:Thromboplastin; C051928:lipoprotein-associated coagulation inhibitor