A Comparative study of Lipid Profile among Smokers and non Smokers

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1 ORIGINAL ARTICLE A Comparative study of Lipid Profile among Smokers and non Smokers Kavita *, Priyanka Gohel 2, M. G. Nanavati 3, R.N.Gonsai 4 3 nd Year Resident, 2 Tutor, 3 Associate professor, 4 Professor & Head, Department Of Pathology, B. J. Medical College, Ahmedabad, Gujarat. ABSTRACT BACKGROUND: Smoking is one of the major risk factors in the genesis of coronary atherosclerosis and development of coronary heart disease. Smoking which is recognized as a major risk factor for the development of ischemic heart disease may lead to alter the normal plasma lipoprotein pattern. Aims: ) Comparative study of lipid profile in and non-. 2). to study variable patterns of lipid profile in terms of duration and severity of smoking. 3) To study the effect of lipid profile in healthy. MATERIALS AND METHODS: Prospective study was carried out to find percentage of dyslipidemia among in comparison with non total 00 patients admitted to civil Hospital and were included in this study. Serum lipid profile was analysed in all the subjects. CONCLUSION: Increase in total cholesterol, triglycerides and low density lipoproteins were noted in all age groups with history of smoking. Amount and duration of smoking also influences dyslipidemia. Increased amount of smoking causes more of dyslipidemia. The rapid reduction in risks of cardiac events after cessation of smoking implies that policies that prevent and reduce smoking will have large benefits for reducing cardiovascular mortality. Key Words: lipid profile,, non-smoker. INTRODUCTION Cigarette smoking is the single most preventable cause of preventable diseases and premature deathstobacco smoking is one of the most potent and prevalent addictive habits, influencing behaviour of human beings. Smoking is now increasing rapidly throughout the developing world and is one of the biggest threats to currents and future world health. Furthermore, while the prevalence of tobacco use has declined among men in some high income countries, it is still increasing among young people and women. Cigarette smoking is the most common type of tobacco use. Tobacco continues to be the second major cause of death in the world. 2 By 2030, if current trends continue smoking will kill more than 9 million people annually. 3 It has been practiced by people all over the *Corresponding Author Dr. Kavita R/3 Golden nagar society Vyara, Tal - vyara, Dist - Tapi Mob no ID: drkavitagamit@gmail.com world from centuries. Coronary artery disease (CAD) is the most common form of heart disease and the single most important cause of death in the young. Ischemic heart disease is a result of either reduced blood supply to the heart or an increased myocardial demand. The reduced blood supply is the main cause and it occurs as a result of coronary atherosclerosis. Among the many risk factors associated with the development of atherosclerosis, the principle cause is dyslipidemia. Various studies have shown that Low Density Lipoprotein (LDL) and Very Low Density Lipoprotein (VLDL) are atherogenic and High Density Lipoprotein (HDL) is a protective factor against it. HDL has got the ability to mobilize cholesterol from peripheral tissues to the liver, which excretes it. The aim of study is to make aware, the hazards of smoking and discourage tobacco usage in any form. To study the effect of smoking on lipid profile of healthy. To compare the lipid profile of both and non-. To study the effect of severity and duration of smoking on lipid profile. 76 Int J Res Med. 204; 3(4);76-8 e ISSN: p ISSN:

2 Objectives. Comparative study of lipid profile in and non-. 2. To study variable patterns of lipid profile in terms of duration and severity of smoking. 3. To study the effect of lipid profile in healthy MATERIALS AND METHODS The were defined as those who had smoked at least once every week for last one year. The non- were defined as those who had never smoked.the and non- were comparable in age, sex and socioeconomic status. The inclusion and exclusion criteria were as follows: Inclusion Criteria: () Age: > 2 years; (2) Control: Who never smoked; (3) Subjects: Who smoked at least once every week for a year or more and are nonsymptomatic. Mild : subjects smoking 5 to 0 cigarette and/or biddies per day Moderate : subjects smoking 0-5 cigarettes and/or biddies per day Severe : subjects smoking more than 5 cigarettes/biddies per day Exclusion Criteria: () Diabetes and endocrine Disorder: Both itself can lead to dyslipidemia or oxidation of LDL. Diabetes is a known risk factor for coronary heart disease as it increases vascular reactivity and microvascular disease. (2) Hypertension: It is a known risk factor for coronary heart disease as it promotes atherosclerosis by increasing vascular permeability or endothelial injury that promotes oxi LDL. (3) Renal Disorder: It leads to altered lipid profile by itself. (4) Coronary Artery Disease; (5) History of Drug intake: β-blockers, Lipid lowering drugs, Steroids; (6) History of Alcohol Intake/Drug abuse A detailed history was taken. Subjects were explained in detail about the study and written informed consent was taken. Blood Sample was collected after overnight fasting under all aseptic precautions and sample was centrifuged at 2000rpm for one minute. Lipid profile estimation which includes serum cholesterol, serum triglyceride, High density lipoprotein, low density lipoprotein and very low density lipoprotein The present study was carried out in 00 patients. All the subjects were those who attended civil hospital from December 202 to August 20 RESULTS Table: lipid profile of and non Lipid parameter Smokers (mg/dl) TG ± TC ±37.6 HDL ±6.90 LDL ±2.40 VLDL ±9.39 Non 5.9± ± ± ± ±9. 75 P value = P value statically significant Table: 2 lipid profile in different group of Lipid parameter Mild (mg/dl) TG 63± TC 85± HDL 45.6± 7.7 LDL 00.5± 9.87 VLDL 32.58±.7 Moderate Heavy 72.50± 86.2± ± 205.5± ± 46.43± ± 0.8± ± ± 8.83 Table: 3 lipid profile in different group of Lipid parameter Smokers Non P value (mg/dl) smoker Tg Mild 63± 5.9± < Moderate 72.50± 5.9± < Severe 86.2± 5.9± < Tc Mild 85± < ± 28.7 Moderate 92.2± ± 28.7 Severe 205.5± ± 28.7 Hdl Mild 45.6± ± 9.87 Not signific Moderate 46.75± 53.58± < Severe 46.43± ± < Ldl Mild 00.5± 78.36± 77 Int J Res Med. 204; 3(4);76-8 e ISSN: p ISSN:

3 Moderate 07.8± ± 2.74 Severe 0.8± 78.36± Vldl Mild 32.58± 23.8± Moderate 34.5± 23.8± Severe 37.26± 23.8± P value <O.05 Statically significant and highly Significant. The present study comprises of comparison of lipid profile of 50 healthy male with 50 healthy male non. The study was carried out in the period extending from December 202 to August 203.All of them belonged to middle or lower socioeconomic status. DISSCUSION Serum Triglycerides The mean serum triglycerides levels in non- and were 5.9 ± mg/dl and ± mg/dl respectively. These findings are similar to those observed by Wynder et al (7) and Rustogi et al (2). The mean values of s. triglycerides were significantly higher in those subjects smoking 0-5 cigarettes/bidis per day as compared to those smoking 5-0 cigarettes/ bidis per day and even higher in case of those who smoked >5 cigarettes/bidis per day. These findings are similar to those of Rustogi et Recent studies have suggested that triglyceride levels are the most important factor leading to CHD.(6) Triglyceride as a risk factor has been suggested by various research workers.[7] The reduced Lipoprotein lipase activity in as observed by Freeman et al (5) may explain impaired triglyceride metabolism and higher triglyceride levels. Serum Cholesterol The mean serum total cholesterol in non was ± 28.7 mg/dl while it was significantly higher in, i.e., ± 37.6 mg/dl. The total cholesterol values in subjects smoking 5-0 cigarettes/bidis per day was 85.6 mg/dl and those smoking 0-5 cigarettes/bidis per day was 92.2 and > 5 cigarettes/bidis per day was mg/dl. al.(2) These findings are in accordance with those of Muscat JE et al (4), NS Neeki et al 8. Increased cholesterol levels and CHD are observed in cigarette.(9) Higher level of cholesterol are associated with CHD 20 Cigarette smoking substantially increases the risk of coronary heart disease. According to Zamir et al. nicotine causes increase cholesterol level 25. HDL It was observed that HDL-cholesterol level was decreased in when compared with non-. The mean HDL-C in non- was ± 9.87 and ± 6.90 in respectively (p value 2). This finding is similar to that of Rosenson2 who reported that there is fall in HDL-C level by 3-5 mg/dl in. The fall in oestrogen level that occurs due to smoking further results in decreased HDL cholesterol.[8] These findings are in conformity with the work of Zamir et al (25) and scrot. Direct relationship of smoking towards CHD has been mentioned by MRFIT (26) who described that increase in HDL level by mg/dl was associated with decrease in the risk of CHD by 3%. Further, the subjects smoking 5-0 cigarettes/biddies per day had significantly higher HDL-C (48.6 mg/dl) as compared to those who smoked 0-5 cigarettes/biddies per day, mg/dl and mg/dl in those who smoked > 5 cigarettes/biddies per day. Similar findings have been reported by Brischetto et al.22s LDL & VLDL On the other hand, LDL & VLDL levels were also significantly increased in than non- and are in agreement with results of Kesaneimi and Grundy.27 The mean LDL-C VLDL-C values in non- were ± 2.74 mg/dl and 23.8 ± 9.75 mg/dl respectively. But these values were significantly higher in subjects with severe smoking than that of mild and moderate. These observations are also similar to those of Rustogi et al 2 It has been described that nicotine contained in cigarette increased the circulatory pool of atherogenic LDL through accelerated transfer of lipids from HDL and impaired clearance of LDL from 78 Int J Res Med. 204; 3(4);76-8 e ISSN: p ISSN:

4 plasma compartment, and hence LDL cholesterol in the arterial wall increased.(2,7) The results shows that smoking influences the lipid profile negatively hence causing dyslipidemia in. Smoking results in increase in oxidized LDL-cholesterol level which plays a key role in the development of atherosclerosis, and also raising the cardiovascular disease risk8. Therefore, it could be probably deduced that smoking is very dangerous to health and should be discouraged. Duration of Smoking and Lipid Profile The values of serum triglycerides, cholesterol and VLDL were higher in those subjects smoking cigarettes/ biddies for more than 5 years as compared to those who smoked for 0-5 years, 5-0 years and -5 years. A rising trend of mean values was seen with increase in duration of smoking but the differences were not statistically significant. It clearly shows that duration of smoking directly affects lipoprotein value in suggesting increase in cardiovascular risk. The mean values of HDL were lower in who had history of smoking for more than 5 years as compared to to 5 years of smoking. The differences were not statistically significant. A larger sample size could probably give more accurate results. Cigarette and Bidi Smoking Difference in mean values for cigarette and bidi were not statistically significant which is similar to the observation of Rustogi et al 2 but the mean value of HDL was lower in bidi than in cigarette smoker. This could be due to higher nicotine, hydrogen cyanide and carbon monoxide 0, contents of bidi Also, bidi smoke delivers three times amount of nicotine and carbonmonoxide and five times the amount of tar compared to cigarette smoke.2 Probably a larger sample size would help to establish statistically significant effect of bidi smoking on lipid profile. Table: 4 Comparison of present study with other studies Lipid parameter (mg/dl) Present study Ns neeki et al (8) Zamir et al (25) TG 73.4± ± ± 44.2 TC 99.06± ± ± 3.03 HDL 47.32± ± ± 6.08 LDL 03.06± ± ± VLDL 34.69± ± ± 8.83 The above table shows that the findings of the present study are more in accordance with that of NS Nekki than Zamir CONCLUSION The total serum cholesterol, LDL, VLDL and Triglyceride values were higher in as compared to Non-. These values increased with increase in number of Cigarette/ bidis smoked. Serum levels of HDL are lower in than the same in non-. Serum HDL levels decrease with increase in number of Cigarette/ bidis smoked. Association of HDL had inverse relationship with cigarettes/bidis smoked per day. Increase in duration of smoking adversely affects lipid profile. Bidi smoking has more adverse effects HDL than cigarette smoking although statistically significant results were not obtained. It shows that serum anti-atherogenic HDL- C level is significantly low in chronic irrespective of the number of cigarettes smoked. The serum level of total cholesterol, LDL-C and VLDL-C and TG are significantly increased with the severity of smoking. To conclude smoking causes alteration in lipid profile and increased risk of cardiovascular disease. Amount and duration of smoking also influences dyslipidemia. Increased amount of smoking causes more of dyslipidemia. The rapid reduction in risks of cardiac events after cessation of smoking implies that policies that prevent and reduce smoking will have large benefits for reducing cardiovascular mortality. Intense education programme should be undertaken through all means including 79 Int J Res Med. 204; 3(4);76-8 e ISSN: p ISSN:

5 audio visual media to the public and to students through their curriculum. REFEREANCES. Sontag S, Graham DY, Belsito A, Weiss J, Farley A, Grunt R, et al. Cimetidine, cigarette smoking, and recurrence of duodenal ulcer. N Engl J Med. 984;3(): Terry PD, Rohan TE, Franceschi S, Weiderpass E. cigarette smoking and the risk of endometrial cancer. Lancet Oncol. 2002;3(8): Terry PD, Rohan TE. Cigarette smoking and the risk of breast cancer in women: a review of the literature. Cancer Epidemiol Biomarkers Prev. 2002;(0 Pt ): Fujieda M, Yamazaki H, Saito T, Kiyotani K, Gyamfi MA, Sakurai M, et al. Evaluation of CYP2A6 geneticpolymorphisms as determinants of smoking behavior and tobaccorelated lung cancer risk in male Japanese. Carcinogenesis. 2004;25(2): Ishizaka N, Ishizaka Y, Toda E, Nagai R, Koike K, Hashimoto H, et al. Relationship between smoking, white blood cell count and metabolic syndrome in Japanese women. Diabetes Res Clin Pract. 2007;78(): Kannel WB. Update on the risk of cigarette smoking in coronary artery disease. Am Heart J 98; 0: Wynder EL, Harris et al. Population screening for plasma cholesterol. Community based results from Connecticut. Am Heart J 989; 7: Wilhelmsen L. Coronary heart disease. Epidemiology of smoking & intervention studies of smoking. Am Heart J 988; 5: Mc Gill HC. Cardiovascular pathology of smoking. Am Heart J 988; 5: Carlson LA, Bottiger LE, Ahfeldt PE. Risk factors for myocardial infarction in the Stockholm prospective study: A 4 year followup on focusing on the role of plasma triglycerides and cholesterol. Acta Med Scand 979; 206: Mjøs OD. Lipid effects of smoking. Am Heart J 988; 5: Rastogi R, Shrivastava SS, Mehrotra TN, Singh VS, Gupta MK. Lipid profile in. J Assoc Physicians India. 989;37(2): Austin MA. Plasma triglycerides and coronary heart disease. Arterio Throm 99; : Muscat JE, Harris RE et al. Cigarette smoking and plasma cholesterol. Am Heart J 99; 2: Freeman DJ, Griffin BA, Murray E, Lindsay GM, Gaffney D, Packard CJ, et al. Smoking and plasma lipoproteins in man: effects on low density lipoprotein cholesterol levels and high density lipoprotein subfraction distribution. Eur J Clin Invest. 993;23(0): Chary TM, Sharma HO. Practical Biochemistry for medical and Dental Student. st ed. New Delhi: Jaypee Brothers: 2004, Carlson LA, Böttiger LE. Ischaemic heart-disease in relation to fasting values of plasma triglycerides and cholesterol. Stockholm prospective study. Lancet. 972;(7756): Neki NS. lipid profile in chronic. JIACM. 2002;3: White PD. Coronary disease & coronary thrombosis in youth. J Med Soc. 935:32: Goldbourt U, Holtlman Ev Neufeld HN. Total & high density lipoprotein cholesterol in the serum & risk of mortality. Br Med J (Clin Res Ed). 985; 290(6477): Rosenson RS. Low level of HDLcholesterol (Hypoalphalipoproteinemia). An approach to management. Arch Intern Med 993; 53(3): Brischetto CS, Connor WE et al. Plasma lipid and lipoprotein profile of cigarette from randomly selected families. Enhancement of hyperlipidaemia and depression of HDL. Am J Cardiol 983; 52: Int J Res Med. 204; 3(4);76-8 e ISSN: p ISSN:

6 23. Michael A, Jonas, John AO et al. Statement on smoking and cardiovascular disease for health care professionals. AHA Medical/Scientific statement. Circulation 992;86: Krishna Swami S, Richard J, Prasad NK et al. Association between cigarette smoking and coronary artery disease in patients in India. How quantitative is it? An assessment by selective coronary arteriography. Intern J Cardiol 99; 3: Zamir MAA, Muhammad SB, Muhammad S Lipid Profile in smoking. JAMC. 2000;2 (3): Publication Information Directorate. Tobacco products - the wealth of India. In: Industrial products Part IX. New Delhi: Council of Scientific and Industrial Research. 976; Kesaniemi YA, Grundy SM. Significance of low density lipoprotein production in the regulation of plasma cholesterol level in men. J Clin Invest. 982; 70(): Padmavathi P, Reddy VD, Varadacharyulu N. Influence of chronic cigarette smoking on serum biochemical profile in male human volunteers. J Health Sci. 2009;55(2): Neil E. Grunberg. Smoking cessation and weight gain. New Eng J Med 99; 324 (): Yanbaeva DG, Dentener MA, Creutzberg E. Systemic Effects of Smoking. Chest journal of the American College of Chest Physician.2007;3: Kshitisk K, SinhaR,Bhattacharjee J A study of smoking on lipid and vitamin C metabolism International Journal of pharma and Bio Sciences.200;(4):0 8 Int J Res Med. 204; 3(4);76-8 e ISSN: p ISSN:

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