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Hyperfibrinogenemia and metabolic syndrome in type 2 diabetes: a population-based study.
Diabetes Metab Res Rev 2001 Mar-Apr; 17(2):124-30DM

Abstract

BACKGROUND

It has been hypothesized that fibrinogen clusters with several components of the metabolic syndrome, thus increasing its cardiovascular risk. 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 fibrinogen and (2) the relationship between hyperfibrinogenemia, a number of components of the metabolic syndrome, and coronary heart disease (CHD).

METHODS

We identified a cross-sectional, population-based cohort of 1574 patients with type 2 diabetes using multiple sources of ascertainment. Components of the metabolic syndrome were hypertension (systolic blood pressure > or = 160 mmHg and/or diastolic blood pressure > or = 95 mmHg and/or treatment with antihypertensive drugs), dyslipidemia (tryglicerides >2.82 mmol/l and/or HDL-cholesterol <1.03 mmol/l), hyperuricemia (uric acid >416 micromol/l) and increased albumin excretion rate (AER > or = 20 microg/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 fibrinogen (from 26.1 to 40.6%, p=0.046). However, in logistic regression, after 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 1.36-2.69) and 1.56 (1.07-2.27).

CONCLUSIONS

This population-based study shows that fibrinogen increases with age, HbA(1c), smoking, hypertension and a number of components of the metabolic syndrome, independent of major confounders. We also found that poor blood glucose control was associated with CHD.

Authors+Show Affiliations

Department of Internal Medicine, University of Turin, Turin, Italy. graziella.bruno@katamail.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11307177

Citation

Bruno, G, et al. "Hyperfibrinogenemia and Metabolic Syndrome in Type 2 Diabetes: a Population-based Study." Diabetes/metabolism Research and Reviews, vol. 17, no. 2, 2001, pp. 124-30.
Bruno G, Cavallo-Perin P, Bargero G, et al. Hyperfibrinogenemia and metabolic syndrome in type 2 diabetes: a population-based study. Diabetes Metab Res Rev. 2001;17(2):124-30.
Bruno, G., Cavallo-Perin, P., Bargero, G., Borra, M., D'Errico, N., Macchia, G., & Pagano, G. (2001). Hyperfibrinogenemia and metabolic syndrome in type 2 diabetes: a population-based study. Diabetes/metabolism Research and Reviews, 17(2), pp. 124-30.
Bruno G, et al. Hyperfibrinogenemia and Metabolic Syndrome in Type 2 Diabetes: a Population-based Study. Diabetes Metab Res Rev. 2001;17(2):124-30. PubMed PMID: 11307177.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hyperfibrinogenemia and metabolic syndrome in type 2 diabetes: a population-based study. AU - Bruno,G, AU - Cavallo-Perin,P, AU - Bargero,G, AU - Borra,M, AU - D'Errico,N, AU - Macchia,G, AU - Pagano,G, PY - 2001/4/18/pubmed PY - 2001/7/6/medline PY - 2001/4/18/entrez SP - 124 EP - 30 JF - Diabetes/metabolism research and reviews JO - Diabetes Metab. Res. Rev. VL - 17 IS - 2 N2 - BACKGROUND: It has been hypothesized that fibrinogen clusters with several components of the metabolic syndrome, thus increasing its cardiovascular risk. 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 fibrinogen and (2) the relationship between hyperfibrinogenemia, a number of components of the metabolic syndrome, and coronary heart disease (CHD). METHODS: We identified a cross-sectional, population-based cohort of 1574 patients with type 2 diabetes using multiple sources of ascertainment. Components of the metabolic syndrome were hypertension (systolic blood pressure > or = 160 mmHg and/or diastolic blood pressure > or = 95 mmHg and/or treatment with antihypertensive drugs), dyslipidemia (tryglicerides >2.82 mmol/l and/or HDL-cholesterol <1.03 mmol/l), hyperuricemia (uric acid >416 micromol/l) and increased albumin excretion rate (AER > or = 20 microg/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 fibrinogen (from 26.1 to 40.6%, p=0.046). However, in logistic regression, after 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 1.36-2.69) and 1.56 (1.07-2.27). CONCLUSIONS: This population-based study shows that fibrinogen increases with age, HbA(1c), smoking, hypertension and a number of components of the metabolic syndrome, independent of major confounders. We also found that poor blood glucose control was associated with CHD. SN - 1520-7552 UR - https://www.unboundmedicine.com/medline/citation/11307177/Hyperfibrinogenemia_and_metabolic_syndrome_in_type_2_diabetes:_a_population_based_study_ DB - PRIME DP - Unbound Medicine ER -