Hyperfibrinogenemia and metabolic syndrome in type 2 diabetes: a population-based study

Background It has been hypothesized that fibrinogen clusters with several c omponents of the metabolic syndrome, thus increasing its cardiovascular ris k. The aims of the present study were to assess in a large population-based cohort of patients with type 2 diabetes (1) variables associated with fibr inogen and (2) the relationship between hyperfibrinogenemia, a number of co mponents of the metabolic syndrome, and coronary heart disease (CHD). Methods We identified a cross-sectional, population-based cohort of 1574 pa tients with type 2 diabetes using multiple sources of ascertainment. Compon ents of the metabolic syndrome were hypertension (systolic blood pressure g reater than or equal to 160 mmHg and/or diastolic blood pressure greater th an or equal to 95 mmHg and/or treatment with antihypertensive drugs), dysli pidemia (tryglicerides >2.82 mmol/l and/or HDL-cholesterol <1.03 mmol/l), h yperuricemia (uric acid > 416 mu mol/l) and increased albumin excretion rat e (AER greater than or equal to 20 mug/min). Results Fibrinogen increases with age, HbA(1c), smoking, hypertension and a number of components of the metabolic syndrome, even after adjustment for confounders. Prevalence of CHD increases linearly across quartiles of fibri nogen (from 26.1 to 40.6%, p = 0.046). However, in logistic regression, aft er adjustment for both confounders and known risk factors for CHD, the role of fibrinogen is no more significant, whereas ORs for HbA(1c) between 6.8 and 8.8% and >8.8% vs values <6.8% are, respectively, 1.91 (95% CI 1.36-2.6 9) and 1.56 (1.07-2.27). Conclusions This population-based study shows that fibrinogen increases wit h age, HbA(1c), smoking, hypertension and a number of components of the met abolic syndrome, independent of major confounders. We also found that poor blood glucose control was associated with CHD. Copyright (C) 2000 John Wile y & Sons, Ltd.