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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 9 (2015) 180–182
Contents lists available at ScienceDirect
Diabetes & Metabolic Syndrome: Clinical Research & Reviews journal homepage: www.elsevier.com/locate/dsx
Original Article
Relationships between the smoking status and plasma fibrinogen, white blood cell count and serum C-reactive protein in Japanese workers Tomoyuki Kawada * Department of Hygiene and Public Health, Nippon Medical School, Japan
A R T I C L E I N F O
A B S T R A C T
Keywords: Fibrinogen White blood cell count C-reactive protein Smoking
Objective: Confirmation of the association between smoking status and biological inflammatory or anticoagulant markers is required in the field of occupational therapy to promote anti-smoking education. The associations between the smoking status and biological markers were clarified. Methods: The study was performed in 5102 working men aged 30–60 years old. The author measured the plasma fibrinogen, white blood cell count (WBC) and serum high-sensitivity C-reactive protein (CRP) as biomarkers of the smoking status. Results: After adjustment for age, the mean plasma fibrinogen level in never-smokers was significantly lower than that in current smokers. The mean WBC count was also significantly lower in the neversmokers than that in current smokers and ex-smokers who had quit within the previous 1 year. Furthermore, the mean log-transformed serum CRP value in never-smokers was significantly lower than that in current smokers smoking 20 cigarettes daily. Spearman’s rank correlation coefficients between the plasma fibrinogen and the serum CRP and WBC were 0.561 and 0.243, respectively. The mean plasma fibrinogen, serum CRP and WBC count in the ex-smokers showed a trend toward decreasing as the duration of abstinence became longer. Conclusion: Among the three biomarkers, the plasma fibrinogen was the most strongly associated with the smoking status, its value being to be the highest in current smokers smoking 20 cigarettes daily. The same trend was also observed for the WBC count. ß 2015 Diabetes India. Published by Elsevier Ltd. All rights reserved.
1. Introduction Plasma fibrinogen plays an essential role in blood coagulation, and is reported to be associated with the development of coronary, peripheral and cerebral vascular disease [1–3]. According to some epidemiological studies, increased plasma fibrinogen concentration is an independent risk factor for future cardiovascular events [4–7] and stroke [8,9]. Serum C-reactive protein (CRP) has been used as a surrogate marker of CVD [10,11], and combination of serum CRP and plasma fibrinogen has been shown to be associated with all-cause mortality and CVD mortality [12]. Cigarette smoking is one of the known risk factors for coronary heart disease [13] and stroke [14], especially in women [15]. No
* Correspondence to: Department of Hygiene and Public Health, Nippon Medical School, 1-1-5 Sendagi, Bukyo-Ku, Tokyo 113-8602, Japan. Tel.: +81 3 3822 2131; fax: +81 3 5685 3065. E-mail address: [email protected] http://dx.doi.org/10.1016/j.dsx.2015.02.010 1871-4021/ß 2015 Diabetes India. Published by Elsevier Ltd. All rights reserved.
interaction has been reported between age and plasma fibrinogen [16]. In this study, the plasma fibrinogen, serum CRP and WBC count in non-smokers, ex-smokers and current smokers were compared, with special emphasis on the number of cigarettes smoked per day in current smokers and the duration of abstinence in ex-smokers. It was expected that the results would contribute to health education for smoking cessation. 2. Subjects and methods 2.1. Study population A total of 5862 male workers of a car-manufacturing company in Japan who attended an annual health examination in 2014 were enrolled in the study. A self-administered questionnaire was used to record the history of tobacco smoking. Smoking status was categorized as ‘‘never-smoker’’, ‘‘past smoker’’ or ‘‘current smoker’’. Subjects with
T. Kawada / Diabetes & Metabolic Syndrome: Clinical Research & Reviews 9 (2015) 180–182
181
Table 1 Body mass index and biological markers in subjects categorized according to the smoking status. Variables
Never
Past <1 year
Past 1–6 year
Past 6 year
Current <20/day
Current 20/day
Number BMI CRP (mg/L) Fibrinogen (mg/dL) WBC (count/cmm)
1512 24.2 0.09 0.35 1.03 244.4 1.12 6037 45.8
61 23.6 0.47 0.45 1.15 248.6 5.52 6820 226.9*
695 23.6 0.14* 0.34 1.04 242.6 1.64 5989 67.3
205 23.2 0.26* 0.34 1.08 236.5 3.08 5766 126.8
1492 23.3 0.10* 0.36 1.03 249.4 1.13* 7053 46.4*
1266 23.8 0.10 0.41 1.03* 255.7 1.22* 7786 50.1*
Data presented are means and standard deviations. BMI, body mass index; WBC, white blood cell count; CRP, C-reactive protein. Data for CRP were presented as geometric mean and geometric standard error. * p < 0.05 against never smokers.
a serum CRP of 10.0 mg/L (n = 82) were excluded based on the possible presence of occult inflammatory or infectious disorder. After excluding such patients, the data of 5102 male workers were analyzed in this study. Body mass index (BMI) was calculated as weight (in kilograms) divided by height (in meters)2. Informed consent was obtained from each of the study participants. A research protocol was reviewed and received ethics clearance through ethical committee. 2.2. Biochemical analysis Fasting blood samples were obtained from each subject. Serum high-sensitivity CRP was measured by a latex turbidimetry assay (Mitsubishi Kagaku Iatron, Tokyo, Japan) using the Hitachi 7700 auto-analyzer. The lower detection limit of this assay is 0.1 mg/L. The intra-assay CVs for repeated measurements ranged from 0.84% to 2.54%. Plasma fibrinogen was measured by the lightscattering method using CA-1500 (Sysmex Inc, Kobe, Japan) with light scattering method. The lower detection limit of this assay is 250 mg/L. The intra-assay CV for repeated measurements ranged from 3.26% to 6.99%. White blood cell count was measured with the XE-2100 or XE-5000 (Sysmex Inc, Kobe, Japan) auto-analyzer. The intra-assay CV for repeated measurements was 1.7%. 2.3. Statistical analysis The serum CRP values were log-transformed, and the log mean value was transformed back and presented as geometric means. Differences in the mean values among the smoking categories were tested by Bonferroni’s multiple comparison after adjusting for age. SPSS, version 21.0 for windows was used for the analysis. Statistical significance was set at p < 0.05. 3. Results The subjects ranged in age from 30 to 60 years, with a mean age standard deviation of 43.1 7.1 years. The mean values of the biological markers and BMI of the subjects are listed in Table 1. After adjustment for age, the mean Table 2 Spearman’s rank correlation coefficients among the three biomarkers, age and BMI. Variables Age BMI
BMI
CRP ***
0.081 n = 5543
Fibrinogen ***
0.064 n = 5543 0.406*** n = 5543
CRP (mg/L) Fibrinogen (mg/dL) Abbreviations were listed in Table 1. * p < 0.05, ** p < 0.01, *** p < 0.001.
***
0.242 n = 5522 0.250*** n = 5522 0.561*** n = 5522
WBC (count/cmm) 0.030* n = 5543 0.159*** n = 5543 0.300*** n = 5543 0.243*** n = 5522
plasma fibrinogen level in never-smokers was significantly lower than that in current smokers. The mean WBC count in neversmokers was significantly lower than that in current smokers and ex-smokers who had quit within the previous 1 year. Furthermore, the mean log-transformed serum CRP value in never-smokers was significantly lower than that in current smokers who smoked 20 cigarettes daily. In contrast, the mean BMI in never-smokers was significantly higher than that in current smokers who smoked <20 cigarettes daily and ex-smokers who had quit 1 year ago. Spearman’s rank correlation coefficients (rs) between the plasma fibrinogen and serum CRP and WBC were 0.561 and 0.243, respectively (Table 2). In addition, the rs between the BMI and the serum CRP, plasma fibrinogen and WBC count were 0.406, 0.250 and 0.159, respectively.
4. Discussion This study confirmed that the plasma fibrinogen was the highest in current smokers and that in ex-smokers, a tendency was observed toward lower plasma fibrinogen levels as the duration of abstinence increased. The same tendency was observed for the WBC count, but not for the serum CRP. All of the data were obtained after adjusting for age. Yasue et al. reported that the plasma mean fibrinogen levels in ex-smokers were intermediate between those of current-smokers and never-smokers [17]. As they did not divide smokers into current and ex-smokers, the effect of smoking cessation with the duration of abstinence and the amount of smoking in current smokers on the plasma fibrinogen and other biomarkers could not be elucidated. The trend toward decrease of the plasma fibrinogen in exsmokers according to the duration of abstinence has been reported in the past. Wannamethee et al. reported that the serum CRP level in heavy cigarette smokers did not decrease to the level seen in never-smokers until at least 20 years after quitting [18], which has also been corroborated by other studies [19,20]. Similar observations have been reported for the WBC count [21]. Lao et al. reported that the serum CRP decreased to the level seen in never-smokers after 20 years of abstinence, and that the WBC count retuned to the level seen in never-smokers within 5 years of abstinence [22]. On this point, the author observed that the plasma fibrinogen and serum CRP levels in ex-smokers showed no significant differences from those recorded in never-smokers, and that the WBC count in ex-smokers returned to the level seen in never-smokers by 1 year after cessation of smoking. Our result was not in concordance with the past report that the serum CRP level in ex-smokers did not decrease within 1 year after cessation of smoking [23]. However, the number of ex-smokers with shorter periods of abstinence than 1 year was 61, and loss of statistical power should be considered. The author conducted a cross-sectional study, therefore, the causality could not be determined; however, the results do indicate that the plasma fibrinogen level is a useful marker for detecting the effects of smoking cessation.
T. Kawada / Diabetes & Metabolic Syndrome: Clinical Research & Reviews 9 (2015) 180–182
182
Conflict of interest I declare that there is no conflict of interest in this study. Acknowledgments I wish to express my appreciation to the study participants. This study was supported by Grant-in-Aid for Scientific Research (C) (24590763). References [1] Kakafika AI, Liberopoulos EN, Mikhailidis DP. Fibrinogen: a predictor of vascular disease. Curr Pharm Des 2007;13:1647–59. [2] Fibrinogen Studies Collaboration. Collaborative meta-analysis of prospective studies of plasma fibrinogen and cardiovascular disease. Eur J Cardiovasc Prev Rehabil 2004;11:9–17. [3] Fibrinogen Studies Collaboration, Kaptoge S, White IR, Thompson SG, Wood AM, Lewington S, et al. Associations of plasma fibrinogen levels with established cardiovascular disease risk factors, inflammatory markers, and other characteristics: individual participant meta-analysis of 154,211 adults in 31 prospective studies: the fibrinogen studies collaboration. Am J Epidemiol 2007;166:867–79. [4] Maple-Brown LJ, Cunningham J, Nandi N, Hodge A, O’Dea K. Fibrinogen and associated risk factors in a high-risk population: urban Indigenous Australians, the DRUID Study. Cardiovasc Diabetol 2010;9:69. [5] De Stavola BL, Meade TW. Long-term effects of hemostatic variables on fatal coronary heart disease: 30-year results from the first prospective Northwick Park Heart Study (NPHS-I). J Thromb Haemost 2007;5:461–71. [6] St-Pierre AC, Cantin B, Bergeron J, Pirro M, Dagenais GR, Despre´s JP, et al. Inflammatory markers and long-term risk of ischemic heart disease in men: a 13-year follow-up of the Quebec Cardiovascular Study. Atherosclerosis 2005;182:315–21. [7] Scarabin PY, Arveiler D, Amouyel P, Dos Santos C, Evans A, Luc G, et al. Plasma fibrinogen explains much of the difference in risk of coronary heart disease between France and Northern Ireland. The PRIME study. Atherosclerosis 2003;166:103–9. [8] Rudnicka AR, Mt-Isa S, Meade TW. Associations of plasma fibrinogen and factor VII clotting activity with coronary heart disease and stroke: prospective cohort study from the screening phase of the Thrombosis Prevention Trial. J Thromb Haemost 2006;4:2405–10. [9] Sato S, Iso H, Noda H, Kitamura A, Imano H, Kiyama M, et al. Plasma fibrinogen concentrations and risk of stroke and its subtypes among Japanese men and women. Stroke 2006;37:2488–92. [10] Emerging Risk Factors Collaboration, Kaptoge S, Di Angelantonio E, Lowe G, Pepys MB, Thompson SG, et al. C-reactive protein concentration and risk of
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coronary heart disease, stroke, and mortality: an individual participant metaanalysis. Lancet 2010;375:132–40. Yousuf O, Mohanty BD, Martin SS, Joshi PH, Blaha MJ, Nasir K, et al. Highsensitivity C-reactive protein and cardiovascular disease: a resolute belief or an elusive link? J Am Coll Cardiol 2013;62:397–408. Ahmadi-Abhari S, Luben RN, Wareham NJ, Khaw KT. Seventeen year risk of allcause and cause-specific mortality associated with C-reactive protein, fibrinogen and leukocyte count in men and women: the EPIC-Norfolk study. Eur J Epidemiol 2013;28:541–50. Nakamura K, Nakagawa H, Sakurai M, Murakami Y, Irie F, Fujiyoshi A, et al. Influence of smoking combined with another risk factor on the risk of mortality from coronary heart disease and stroke: pooled analysis of 10 Japanese cohort studies. Cerebrovasc Dis 2012;33:480–91. Mannami T, Iso H, Baba S, Sasaki S, Okada K, Konishi M, et al. Cigarette smoking and risk of stroke and its subtypes among middle-aged Japanese men and women: the JPHC Study Cohort I. Stroke 2004;35:1248–53. Peters SA, Huxley RR, Woodward M. Smoking as a risk factor for stroke in women compared with men: a systematic review and meta-analysis of 81 cohorts, including 3,980,359 individuals and 42,401 strokes. Stroke 2013;44:2821–8. Nascetti S, Elosua R, Pena A, Covas MI, Senti M, Marrugat J, et al. Variables associated with fibrinogen in a population-based study: interaction between smoking and age on fibrinogen concentration. Eur J Epidemiol 2001;17: 953–8. Yasue H, Hirai N, Mizuno Y, Harada E, Itoh T, Yoshimura M, et al. Low-grade inflammation, thrombogenicity, and atherogenic lipid profile in cigarette smokers. Circ J 2006;70:8–13. Wannamethee SG, Lowe GD, Shaper AG, Rumley A, Lennon L, Whincup PH. Associations between cigarette smoking, pipe/cigar smoking, and smoking cessation, and haemostatic and inflammatory markers for cardiovascular disease. Eur Heart J 2005;26:1765–73. Lowe GD, Yarnell JW, Rumley A, Bainton D, Sweetnam PM. C-reactive protein, fibrin D-dimer, and incident ischemic heart disease in the Speedwell study: are inflammation and fibrin turnover linked in pathogenesis? Arterioscler Thromb Vasc Biol 2001;21:603–10. Fro¨hlich M, Sund M, Lo¨wel H, Imhof A, Hoffmeister A, Koenig W. Independent association of various smoking characteristics with markers of systemic inflammation in men: results from a representative sample of the general population (MONICA Augsburg Survey 1994/95). Eur Heart J 2003;24: 1365–72. Smith MR, Kinmonth AL, Luben RN, Bingham S, Day NE, Wareham NJ, et al. Smoking status and differential white cell count in men and women in the EPIC-Norfolk population. Atherosclerosis 2003;169:331–7. Lao XQ, Jiang CQ, Zhang WS, Adab P, Lam TH, Cheng KK, et al. Smoking, smoking cessation and inflammatory markers in older Chinese men: the Guangzhou Biobank Cohort Study. Atherosclerosis 2009;203:304–10. Crook MA, Scott DA, Stapleton JA, Palmer RM, Wilson RF, Sutherland G. Circulating concentrations of C-reactive protein and total sialic acid in tobacco smokers remain unchanged following one year of validated smoking cessation. Eur J Clin Invest 2000;30:861–5.
Contents lists available at ScienceDirect
Diabetes & Metabolic Syndrome: Clinical Research & Reviews journal homepage: www.elsevier.com/locate/dsx
Original Article
Relationships between the smoking status and plasma fibrinogen, white blood cell count and serum C-reactive protein in Japanese workers Tomoyuki Kawada * Department of Hygiene and Public Health, Nippon Medical School, Japan
A R T I C L E I N F O
A B S T R A C T
Keywords: Fibrinogen White blood cell count C-reactive protein Smoking
Objective: Confirmation of the association between smoking status and biological inflammatory or anticoagulant markers is required in the field of occupational therapy to promote anti-smoking education. The associations between the smoking status and biological markers were clarified. Methods: The study was performed in 5102 working men aged 30–60 years old. The author measured the plasma fibrinogen, white blood cell count (WBC) and serum high-sensitivity C-reactive protein (CRP) as biomarkers of the smoking status. Results: After adjustment for age, the mean plasma fibrinogen level in never-smokers was significantly lower than that in current smokers. The mean WBC count was also significantly lower in the neversmokers than that in current smokers and ex-smokers who had quit within the previous 1 year. Furthermore, the mean log-transformed serum CRP value in never-smokers was significantly lower than that in current smokers smoking 20 cigarettes daily. Spearman’s rank correlation coefficients between the plasma fibrinogen and the serum CRP and WBC were 0.561 and 0.243, respectively. The mean plasma fibrinogen, serum CRP and WBC count in the ex-smokers showed a trend toward decreasing as the duration of abstinence became longer. Conclusion: Among the three biomarkers, the plasma fibrinogen was the most strongly associated with the smoking status, its value being to be the highest in current smokers smoking 20 cigarettes daily. The same trend was also observed for the WBC count. ß 2015 Diabetes India. Published by Elsevier Ltd. All rights reserved.
1. Introduction Plasma fibrinogen plays an essential role in blood coagulation, and is reported to be associated with the development of coronary, peripheral and cerebral vascular disease [1–3]. According to some epidemiological studies, increased plasma fibrinogen concentration is an independent risk factor for future cardiovascular events [4–7] and stroke [8,9]. Serum C-reactive protein (CRP) has been used as a surrogate marker of CVD [10,11], and combination of serum CRP and plasma fibrinogen has been shown to be associated with all-cause mortality and CVD mortality [12]. Cigarette smoking is one of the known risk factors for coronary heart disease [13] and stroke [14], especially in women [15]. No
* Correspondence to: Department of Hygiene and Public Health, Nippon Medical School, 1-1-5 Sendagi, Bukyo-Ku, Tokyo 113-8602, Japan. Tel.: +81 3 3822 2131; fax: +81 3 5685 3065. E-mail address: [email protected] http://dx.doi.org/10.1016/j.dsx.2015.02.010 1871-4021/ß 2015 Diabetes India. Published by Elsevier Ltd. All rights reserved.
interaction has been reported between age and plasma fibrinogen [16]. In this study, the plasma fibrinogen, serum CRP and WBC count in non-smokers, ex-smokers and current smokers were compared, with special emphasis on the number of cigarettes smoked per day in current smokers and the duration of abstinence in ex-smokers. It was expected that the results would contribute to health education for smoking cessation. 2. Subjects and methods 2.1. Study population A total of 5862 male workers of a car-manufacturing company in Japan who attended an annual health examination in 2014 were enrolled in the study. A self-administered questionnaire was used to record the history of tobacco smoking. Smoking status was categorized as ‘‘never-smoker’’, ‘‘past smoker’’ or ‘‘current smoker’’. Subjects with
T. Kawada / Diabetes & Metabolic Syndrome: Clinical Research & Reviews 9 (2015) 180–182
181
Table 1 Body mass index and biological markers in subjects categorized according to the smoking status. Variables
Never
Past <1 year
Past 1–6 year
Past 6 year
Current <20/day
Current 20/day
Number BMI CRP (mg/L) Fibrinogen (mg/dL) WBC (count/cmm)
1512 24.2 0.09 0.35 1.03 244.4 1.12 6037 45.8
61 23.6 0.47 0.45 1.15 248.6 5.52 6820 226.9*
695 23.6 0.14* 0.34 1.04 242.6 1.64 5989 67.3
205 23.2 0.26* 0.34 1.08 236.5 3.08 5766 126.8
1492 23.3 0.10* 0.36 1.03 249.4 1.13* 7053 46.4*
1266 23.8 0.10 0.41 1.03* 255.7 1.22* 7786 50.1*
Data presented are means and standard deviations. BMI, body mass index; WBC, white blood cell count; CRP, C-reactive protein. Data for CRP were presented as geometric mean and geometric standard error. * p < 0.05 against never smokers.
a serum CRP of 10.0 mg/L (n = 82) were excluded based on the possible presence of occult inflammatory or infectious disorder. After excluding such patients, the data of 5102 male workers were analyzed in this study. Body mass index (BMI) was calculated as weight (in kilograms) divided by height (in meters)2. Informed consent was obtained from each of the study participants. A research protocol was reviewed and received ethics clearance through ethical committee. 2.2. Biochemical analysis Fasting blood samples were obtained from each subject. Serum high-sensitivity CRP was measured by a latex turbidimetry assay (Mitsubishi Kagaku Iatron, Tokyo, Japan) using the Hitachi 7700 auto-analyzer. The lower detection limit of this assay is 0.1 mg/L. The intra-assay CVs for repeated measurements ranged from 0.84% to 2.54%. Plasma fibrinogen was measured by the lightscattering method using CA-1500 (Sysmex Inc, Kobe, Japan) with light scattering method. The lower detection limit of this assay is 250 mg/L. The intra-assay CV for repeated measurements ranged from 3.26% to 6.99%. White blood cell count was measured with the XE-2100 or XE-5000 (Sysmex Inc, Kobe, Japan) auto-analyzer. The intra-assay CV for repeated measurements was 1.7%. 2.3. Statistical analysis The serum CRP values were log-transformed, and the log mean value was transformed back and presented as geometric means. Differences in the mean values among the smoking categories were tested by Bonferroni’s multiple comparison after adjusting for age. SPSS, version 21.0 for windows was used for the analysis. Statistical significance was set at p < 0.05. 3. Results The subjects ranged in age from 30 to 60 years, with a mean age standard deviation of 43.1 7.1 years. The mean values of the biological markers and BMI of the subjects are listed in Table 1. After adjustment for age, the mean Table 2 Spearman’s rank correlation coefficients among the three biomarkers, age and BMI. Variables Age BMI
BMI
CRP ***
0.081 n = 5543
Fibrinogen ***
0.064 n = 5543 0.406*** n = 5543
CRP (mg/L) Fibrinogen (mg/dL) Abbreviations were listed in Table 1. * p < 0.05, ** p < 0.01, *** p < 0.001.
***
0.242 n = 5522 0.250*** n = 5522 0.561*** n = 5522
WBC (count/cmm) 0.030* n = 5543 0.159*** n = 5543 0.300*** n = 5543 0.243*** n = 5522
plasma fibrinogen level in never-smokers was significantly lower than that in current smokers. The mean WBC count in neversmokers was significantly lower than that in current smokers and ex-smokers who had quit within the previous 1 year. Furthermore, the mean log-transformed serum CRP value in never-smokers was significantly lower than that in current smokers who smoked 20 cigarettes daily. In contrast, the mean BMI in never-smokers was significantly higher than that in current smokers who smoked <20 cigarettes daily and ex-smokers who had quit 1 year ago. Spearman’s rank correlation coefficients (rs) between the plasma fibrinogen and serum CRP and WBC were 0.561 and 0.243, respectively (Table 2). In addition, the rs between the BMI and the serum CRP, plasma fibrinogen and WBC count were 0.406, 0.250 and 0.159, respectively.
4. Discussion This study confirmed that the plasma fibrinogen was the highest in current smokers and that in ex-smokers, a tendency was observed toward lower plasma fibrinogen levels as the duration of abstinence increased. The same tendency was observed for the WBC count, but not for the serum CRP. All of the data were obtained after adjusting for age. Yasue et al. reported that the plasma mean fibrinogen levels in ex-smokers were intermediate between those of current-smokers and never-smokers [17]. As they did not divide smokers into current and ex-smokers, the effect of smoking cessation with the duration of abstinence and the amount of smoking in current smokers on the plasma fibrinogen and other biomarkers could not be elucidated. The trend toward decrease of the plasma fibrinogen in exsmokers according to the duration of abstinence has been reported in the past. Wannamethee et al. reported that the serum CRP level in heavy cigarette smokers did not decrease to the level seen in never-smokers until at least 20 years after quitting [18], which has also been corroborated by other studies [19,20]. Similar observations have been reported for the WBC count [21]. Lao et al. reported that the serum CRP decreased to the level seen in never-smokers after 20 years of abstinence, and that the WBC count retuned to the level seen in never-smokers within 5 years of abstinence [22]. On this point, the author observed that the plasma fibrinogen and serum CRP levels in ex-smokers showed no significant differences from those recorded in never-smokers, and that the WBC count in ex-smokers returned to the level seen in never-smokers by 1 year after cessation of smoking. Our result was not in concordance with the past report that the serum CRP level in ex-smokers did not decrease within 1 year after cessation of smoking [23]. However, the number of ex-smokers with shorter periods of abstinence than 1 year was 61, and loss of statistical power should be considered. The author conducted a cross-sectional study, therefore, the causality could not be determined; however, the results do indicate that the plasma fibrinogen level is a useful marker for detecting the effects of smoking cessation.
T. Kawada / Diabetes & Metabolic Syndrome: Clinical Research & Reviews 9 (2015) 180–182
182
Conflict of interest I declare that there is no conflict of interest in this study. Acknowledgments I wish to express my appreciation to the study participants. This study was supported by Grant-in-Aid for Scientific Research (C) (24590763). References [1] Kakafika AI, Liberopoulos EN, Mikhailidis DP. Fibrinogen: a predictor of vascular disease. Curr Pharm Des 2007;13:1647–59. [2] Fibrinogen Studies Collaboration. Collaborative meta-analysis of prospective studies of plasma fibrinogen and cardiovascular disease. Eur J Cardiovasc Prev Rehabil 2004;11:9–17. [3] Fibrinogen Studies Collaboration, Kaptoge S, White IR, Thompson SG, Wood AM, Lewington S, et al. Associations of plasma fibrinogen levels with established cardiovascular disease risk factors, inflammatory markers, and other characteristics: individual participant meta-analysis of 154,211 adults in 31 prospective studies: the fibrinogen studies collaboration. Am J Epidemiol 2007;166:867–79. [4] Maple-Brown LJ, Cunningham J, Nandi N, Hodge A, O’Dea K. Fibrinogen and associated risk factors in a high-risk population: urban Indigenous Australians, the DRUID Study. Cardiovasc Diabetol 2010;9:69. [5] De Stavola BL, Meade TW. Long-term effects of hemostatic variables on fatal coronary heart disease: 30-year results from the first prospective Northwick Park Heart Study (NPHS-I). J Thromb Haemost 2007;5:461–71. [6] St-Pierre AC, Cantin B, Bergeron J, Pirro M, Dagenais GR, Despre´s JP, et al. Inflammatory markers and long-term risk of ischemic heart disease in men: a 13-year follow-up of the Quebec Cardiovascular Study. Atherosclerosis 2005;182:315–21. [7] Scarabin PY, Arveiler D, Amouyel P, Dos Santos C, Evans A, Luc G, et al. Plasma fibrinogen explains much of the difference in risk of coronary heart disease between France and Northern Ireland. The PRIME study. Atherosclerosis 2003;166:103–9. [8] Rudnicka AR, Mt-Isa S, Meade TW. Associations of plasma fibrinogen and factor VII clotting activity with coronary heart disease and stroke: prospective cohort study from the screening phase of the Thrombosis Prevention Trial. J Thromb Haemost 2006;4:2405–10. [9] Sato S, Iso H, Noda H, Kitamura A, Imano H, Kiyama M, et al. Plasma fibrinogen concentrations and risk of stroke and its subtypes among Japanese men and women. Stroke 2006;37:2488–92. [10] Emerging Risk Factors Collaboration, Kaptoge S, Di Angelantonio E, Lowe G, Pepys MB, Thompson SG, et al. C-reactive protein concentration and risk of
[11]
[12]
[13]
[14]
[15]
[16]
[17]
[18]
[19]
[20]
[21]
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