Вы находитесь на странице: 1из 1

Zofia Szczeklik-Kumala, Magorzata Bernas

OtyO JAKO stAN PROzAKRzEPOWy


ObEsIty As thE PROthROMbOtIC stAtE
Katedra i Klinika Chorb Wewntrznych i Diabetologii WUM. Chair and Department of Internal Diseases and Diabetology, Warsaw Medical University.

Background and aims. Disturbances in thrombosis and fibrinonolysis constitute one of the independent risk factors of atherosclerosis and embolism. They create a specific challenge in the management of obesity. The clinical significance of the thrombosis and fibrinolysis markers in obesity is, however, not sufficiently established. Therefore a study was undertaken. As the direct aim of research, the comparative determination and analysis of correlations in a general population group divided into 2 arms: a) with BMI < 29 kg/m2, and b) BMI 30 kg/m2 of: 1) phenotypic values; 2) pathophysiological parameters; 3) values and distribution of thrombosis and fibrinolysis markers; and 4) endothelial function indicator von Willebrand factor in venous plasma were studied. Material and methods. The whole group under study was composed of 269 persons above 19 years of age. They were selected by the proportional stratification method and represented the demographic profile of the general population of the city of Warsaw. This population was divided into 2 subgroups: 1) control with BMI between 19 and 29 kg/m2, fat body mass < 20% and, 2) the group with obesity BMI 30 kg/m2 and fat body mass > 20%. By allocating and comparing in these subgroups the results of the studies of thrombosis and fibrinolysis markers, the possibility of the prothrombotic risk of obesity could be assessed. In these 2 populations, the thrombosis, fibrinolysis and endothelial status markers were determined with methods as follows: 1) clinical phenotypic diagnostics: BMI, fat body mass bioimpedance, Bodystat 1500, W, WRR (WHO) accordingly to the WHO; 2) biochemical studies: plasma glucose glucose oxidase method, oral glucose tolerance test (WHO), serum insulin IRMA, Polatom RIA, C-peptide X Biodata set, insulin resistance, HOMA Mathew procedure; 3) thrombosis and fibrinolysis markers fibrinogen von Claus method, tissue plasminogen activator (t-PA) Biopol, reagents Immulyse, plasminogen activator inhibitor (PAI-l) Biopol set, von Willebrand factor Biopol set. Statistical analysis: ANOVA, SAS.

Results. The study is of comparative character. All results were divided into 2 subgroups: first characterizing the control group with BMI 19-29 kg/m2 and fat body mass < 20%, and the second the group with obesity. Persons with BMI 19-29 kg/m2 and fat body mass < 20% significantly differed from the subjects with obesity BMI 30 kg/m2 and fat body mass > 20% as follows: l) W (p < 0,01), WHR (p < 0,05); 2) fasting glycemia (p < 0,001), OGTT (p < 0,05), triglycerides (p < 0,02), plasma insulin (p < 0,006), C-peptide (p < 0,01), HOMA (p < 0,05); 3) coagulation markers: fibrinogen (p < 0,01), t-PA, PAI-I (p < 0,05); 4) von Willebrand factor (p < 0,05). Statistically valid differences were also found in the assessment of correlation between phenotypic and thrombosis markers. Conclusions. Obesity (BMI, fat body mass) associated with insulin resistance (W, WHR, fasting insulin, C-peptide, fasting glycemia, HOMA, triglycerides) is in a statistically significant manner, correlated to the increased levels of fibrinogen, t-PA and PAI-l. It points to a tendency toward increased thrombosis and fibrinolytic deficiency. These findings were significantly correlated with the augmentation of the von Willebrand factor. The results suggest the need for regular testing the individual prothrombotic risk in obesity for preventive purposes.

bIblIOGRAPhy
1. Tato J, Czech A, Bernas M: Otyo, zesp metaboliczny, Wyd. Lek. PZWL, Warszawa, 2007. 2. Tato J, Czech A, Opolski G, Zembala M (red.): Cukrzycowe choroby serca, Wyd. Via Medica, Gdask, 2005.
Adres do korespondencji: Z. Szczeklik-Kumala Klinika Chorb Wewntrznych i Diabetologii WUM 03-242 Warszawa, ul. Kondratowicza 8 e-mail: diabetologia@wum.edu.pl Nadesano: 10.07.2012 Zakwalifikowano do druku: 15.08.2012

Medycyna Metaboliczna, 2013, tom XVII, nr 1


www.medycynametaboliczna.pl

51

Вам также может понравиться