Assessment of Plasma Fibrinogen Level and Lipid Profile in Sudanese Smokers


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 carotid
atherosclerosis. 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.

[1] Moran, A. E., Roth, G. A., Narula, J., et al. (2014). 1990-2010 Global Cardiovascular Disease Atlas. Global Heart, vol. 9, no. 1, pp. 3–16. DOI: 10.1016/j.gheart.2014.03.1220.

[2] WHO. (2015). WHO report on the global tobacco epidemic, 2015. Raising taxes on tobacco, pp. 11–12.

[3] Ray, K. K., Kastelein, J. J., Boekholdt, S. M., et al. (2014). The ACC/AHA 2013 guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular disease risk in adults: The good the bad and the uncertain: a comparison with ESC/EAS guidelines for the management of dyslipidaemias 2011. European Heart Journal, vol. 35, no. 15, pp. 960–968. DOI: 10.1093/eurheartj/ehu107.

[4] Jousilahti, P., Patja, K., and Salomaa, V. (2002). Environmental tobacco smoke and the risk of cardiovascular disease. Scandinavian Journal of Work, Environment & Health, vol. 28, no. 2, pp. 41–51.

[5] Ansari, R., Khosravi, A., Bahonar, A., et al. (2012). Risk factors of atherosclerosis in male smokers, passive smokers, and hypertensive nonsmokers in central Iran. ARYA Atherosclerosis, vol. 8, no. 2, pp. 90–95.

[6] Marano, K. M., Kathman, S. J., Jones, B. A., et al. (2015). Study of cardiovascular disease biomarkers among tobacco consumers. Part 3: evaluation and comparison with the US National Health and Nutrition Examination Survey. Inhalation Toxicology, vol. 27, no. 3, pp. 167–173. DOI: 10.3109/08958378.2015.1009196.

[7] Hammett, C. J., Prapavessis, H., Baldi, J. C., et al. (2007). Variation in blood levels of inflammatory markers related and unrelated to smoking cessation in women. Preventive Cardiology, vol. 10, no. 2, pp. 68–75.

[8] Waters, D., Lesperance, J., Gladstone, P., et al. (1996). Effects of cigarette smoking on the angiographic evolution of coronary atherosclerosis. A Canadian Coronary Atherosclerosis Intervention Trial (CCAIT) Substudy. CCAIT Study Group. Circulation, vol. 94, no. 4, pp. 614–621.

[9] Kiechl, S., Werner, P., Egger, G., et al. (2002). Active and passive smoking, chronic infections, and the risk of carotid atherosclerosis: prospective results from the Bruneck Study. Stroke: A Journal of Cerebral Circulation, vol. 33, no. 9, pp. 2170– 2176.

[10] Tosetto, A., Prati, P., Baracchini, C., et al. (2011). Association of plasma fibrinogen, C-reactive protein and G-455>A polymorphism with early atherosclerosis in the VITA Project cohort. Thrombosis and Haemostasis, vol. 105, no. 2, pp. 329–335. DOI: 10.1160/TH10-08-0522.

[11] Zhang, Q., Zhou, S., and Zhou, J. (2015). Tigecycline treatment causes a decrease in fibrinogen levels. Antimicrobial Agents and Chemotherapy, vol. 59, no. 3, pp. 1650–1655. DOI: 10.1128/AAC.04305-14.

[12] Song, B., Shu, Y., Xu, Y. N., et al. (2015). Plasma fibrinogen lever and risk of coronary heart disease among Chinese population: a systematic review and meta-analysis. International Journal of Clinical and Experimental Medicine, vol. 8, no. 8, pp. 13195– 13202.

[13] Kotbi, S., Mjabber, A., Chadli, A., et al. (2016). Correlation between the plasma fibrinogen concentration and coronary heart disease severity in Moroccan patients with type 2 diabetes. Prospective study. Annales d’Endocrinologie, vol. 77, no. 5, pp. 606–614. DOI: 10.1016/j.ando.2015.02.004.

[14] Lawlor, D. A., Davey Smith, G., Rumley, A., et al. (2005). Associations of fibrinogen and C-reactive protein with prevalent and incident coronary heart disease are attenuated by adjustment for confounding factors. British Women’s Heart and Health Study. Thrombosis and Haemostasis, vol. 93, no. 5, pp. 955–963. DOI:

[15] Kawada, T. (2015). Relationships between the smoking status and plasma fibrinogen, white blood cell count and serum C-reactive protein in Japanese workers. Diabetes & Metabolic Syndrome: Clinical Research & Reviews, vol. 9, no. 3, pp. 180– 182. DOI: 10.1016/j.dsx.2015.02.010.

[16] Ramanathan, G., Araujo, J. A., Gornbein, J., et al. (2014). Cigarette smoking is associated with dose-dependent adverse effects on paraoxonase activity and fibrinogen in young women. Inhalation Toxicology, vol. 26, no. 14, pp. 861–865. DOI: 10.3109/08958378.2014.965559.

[17] Cho, H. M., Kang, D. R., Kim, H. C., et al. (2015). Association between fibrinogen and carotid atherosclerosis according to smoking status in a Korean male population. Yonsei Medical Journal, vol. 56, no. 4, pp. 921. DOI: 10.3349/ymj.2015.56.4.921.

[18] Kawase Ishihara, K., Kokubo, Y., Yokota, C., et al. (2015). Effect of plasma fibrinogen, high-sensitive C-reactive protein, and cigarette smoking on carotid atherosclerosis: The suita study. Journal of Stroke and Cerebrovascular Diseases, vol. 24, no. 10, pp. 2385–2389. DOI: 10.1016/j.jstrokecerebrovasdis.2015.06.039.

[19] Martin, S. S., Abd, T. T., Jones, S. R., et al. (2014). 2013 ACC/AHA cholesterol treatment guideline: What was done well and what could be done better. Journal of the American College of Cardiology, vol. 63, no. 24, pp. 2674–2678. DOI: 10.1016/j.jacc.2014.02.578.

[20] Zhang, X. and Long, Q. (2017). Elevated serum plasma fibrinogen is associated with advanced tumor stage and poor survival in hepatocellular carcinoma patients. Medicine (Baltimore), vol. 96, no. 17, pp. e6694. DOI:

[21] Rao, Ch. S. and Subash, Y. E. (2013). The effect of chronic tobacco smoking and chewing on the lipid profile. Journal of Clinical and Diagnostic Research: JCDR, vol. 7, no. 1, pp. 31–34. DOI: 10.7860/JCDR/2012/5086.2663.

[22] Tuut, M. and Hense, H. W. (2001). Smoking, other risk factors and fibrinogen levels. evidence of effect modification. Annals of Epidemiology, vol. 11, no. 4, pp. 232–238.

[23] Kawada, T. (2015). Relationships between the smoking status and plasma fibrinogen, white blood cell count and serum C-reactive protein in Japanese workers. Diabetes & Metabolic Syndrome. DOI: 10.1016/j.dsx.2015.02.010.

[24] van Dijk, W. D., Akkermans, R., Heijdra, Y., et al. (2013). The acute effect of cigarette smoking on the high-sensitivity CRP and fibrinogen biomarkers in chronic obstructive pulmonary disease patients. Biomarkers in Medicine, vol. 7, no. 2, pp.211–219. DOI: 10.2217/bmm.12.112.

[25] Sinha, S., Luben, R. N., Welch, A., et al. (2005). Fibrinogen and cigarette smoking in men and women in the European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) population. The European Journal of Cardiovascular Prevention & Rehabilitation, vol. 12, no. 2, pp. 144–150.

[26] Hozeifa, H. and Mahdi, H. (2014). The effect of cigarette smoking and smoking cessation on fibrinogen level in Sudan. International Journal of Current Research, vol. 6, no. 4, pp. 6307–6309.

[27] Hunter, K. A., Garlick, P. J., Broom, I., et al. (2001). Effects of smoking and abstention from smoking on fibrinogen synthesis in humans. Clinical Science, vol. 100, no. 4, pp. 459–465.

[28] Vitorino de Almeida, V., Silva-Herdade, A., Calado, A., et al. (2015). Fibrinogen modulates leukocyte recruitment in vivo during the acute inflammatory response. Clinical Hemorheology and Microcirculation, vol. 59, no. 2, pp. 97–106. DOI: 10.3233/CH-121660.

[29] Kovesdy, C. P., Norris, K. C., Boulware, L. E., et al. (2015). Association of race with mortality and cardiovascular events in a large cohort of US veterans clinical perspective. Circulation, vol. 132, no. 16, pp. 1538–1548. DOI: 10.1161/circulationaha.114.015124.

[30] Kawase Ishihara, K., Kokubo, Y., Yokota, C., et al. (2015). Effect of plasma fibrinogen, high-sensitive C-reactive protein, and cigarette smoking on carotid atherosclerosis: The suita study. Journal of Stroke and Cerebrovascular Diseases: The Official Journal of National Stroke Association. DOI: 10.1016/j.jstrokecerebrovasdis.2015.06.039.

[31] Zhang, Y., Zhu, C. G., Guo, Y. L., et al. (2014). Higher fibrinogen level is independently linked with the presence and severity of new-onset coronary atherosclerosis among Han Chinese population. PloS One, vol. 9, no. 11, p. e113460. DOI: 10.1371/journal.pone.0113460.

[32] Paramo, J. A., Beloqui, O., Roncal, C., et al. (2004). Validation of plasma fibrinogen as a marker of carotid atherosclerosis in subjects free of clinical cardiovascular disease. Haematologica, vol. 89, no. 10, pp. 1226–1231.

[33] Bazzano, L. A., He, J., Muntner, P., et al. (2003). Relationship between cigarette smoking and novel risk factors for cardiovascular disease in the United States. Annals of Internal Medicine, vol. 138, no. 11, pp. 891–897.

[34] Mammas, I. N., Bertsias, G. K., Linardakis, M., et al. (2003). Cigarette smoking, alcohol consumption, and serum lipid profile among medical students in Greece. European Journal of Public Health, vol. 13, no. 3, pp. 278–282.

[35] Sliwinska-Mosson, M., Mihulka, E., and Milnerowicz, H. (2014). [Assessment of lipid profile in non-smoking and smoking young health persons]. Przeglad lekarski, vol. 71, no. 11, pp. 585–587.

[36] Messner, B. and Bernhard, D. (2014). Smoking and cardiovascular disease: Mechanisms of endothelial dysfunction and early atherogenesis. Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 34, no. 3, pp. 509–515. DOI:10.1161/atvbaha.113.300156.