Key result
Cigarette smoking significantly increased plasma fibrinogen levels and atherogenic lipid profiles compared to non-smokers in Sudanese men.
Why the study?
Cigarette smoking is a leading preventable risk factor for cardiovascular diseases, prompting the assessment of fibrinogen and lipid parameters in Sudanese tobacco smokers.
Does cigarette smoking increase plasma fibrinogen and alter lipid profiles in adult males?
Case-Control (n=155)
No
Does cigarette smoking increase plasma fibrinogen and alter lipid profiles in adult males?
Absolute Event Rate: 423.44% vs 284.98%
p-value: p=<0.0001
Cigarette smoking in Sudanese adult males is associated with significantly elevated plasma fibrinogen and an atherogenic lipid profile, increasing cardiovascular risk.
Smoking linked to higher fibrinogen and atherogenic lipids in Sudanese men; hypothesis-generating, requiring prospective confirmation before practice implications.
Background: Cigarette smoking is a leading preventable risk factor for the development and progression of cardiovascular diseases (CVDs). Epidemiologic studies in smokers confirm the association between the alteration in lipid profile levels and CVDs risk. Fibrinogen, an acute phase reactant with active involvement in endothelial function, thrombosis and inflammation. It is signified as a systemic marker of carotidatherosclerosis. The purpose of this study was to assess the level of fibrinogen and lipid parameters in Sudanese tobacco smokers. Methods: This case-control study included 55 adult male of a current smoking status; their ages ranged between 18 and 54 years, and 100 non-smokers considered as controls. We evaluated the effect of cigarette smoking on plasma fibrinogen and serum lipid profile. The American Heart Association guidelines and reference ranges were used to identify the smokers with increased risk of coronary heart disease. Results: Our study revealed an increase in the levels of fibrinogen, total cholesterol, and low-density lipoprotein cholesterol (LDL-C) among smokers than controls, whereas the mean level of and triglycerides did not differ. The levels of highdensity lipoprotein cholesterol HDL-C demonstrated decrement. Further, smokers were classified according to the atherogenic risk index LDL-C/HDL-C ratio, the studied parameters fibrinogen, total cholesterol, and triglycerides were significantly increased in those who have ratio 4.5 and more (p = 0.001, p = 0.018, p = 0.007, respectively). Smokers with atherogenic index ≥ 4.5 were more likely to have ≥ 300 mg/dl fibrinogen level (odds ratio (OR) 3.96, 95% confidence interval (95%CI) 1.14– 13.73, p = 0.026). Moreover, the level of the fibrinogen can be predicted by linear regression equation: Fibrinogen level = 19.49 + 79.08 (the ratio of LDL-C ⁄HDL-C), r = 0.37, p = 0.008, 95%CI 21.20–136.95. Conclusion: Increased fibrinogen, LDL-C, and LDLC/HDL-C ratio may potentiate the development of cardiovascular disease in smokers.
No takes yet. Share an insight, caveat, or question.
Zaki et al. (2018) conducted a case-control in Tobacco smoking (n=155). Cigarette smoking vs. Non-smokers was evaluated on Plasma fibrinogen level (mg/dl) (p=<0.0001). Cigarette smoking significantly increased plasma fibrinogen levels and atherogenic lipid profiles compared to non-smokers in Sudanese men.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: