Official Journals By StatPerson Publication
Table of Content - Volume 12 Issue 1 - October 2019
Comparison of lipid profiles in alcoholic and non-alcoholic patients attending a tertiary care hospital
Banubadi Anil Kishore1, Chand Basha Sk Y2*
1,2Assistant Professor, Department of Biochemistry. Apollo Institute of Medical Sciences and Research. Chittoor. Email: yaseenchandbasha@gmail.com
Abstract Background: Alcohol has many effects on lipid metabolism, including inducing de novo fatty acid synthesis and inhibiting fatty acid oxidation in the liver. The most common effect of alcohol is to increase plasma triglyceride levels. The coronary heart disease has been reported to decrease with moderate drinking in both sexes, but such benefit disappears with high consumption. Heavy alcohol consumption for prolonged periods result in marked perturbation of the lipid transport system, reflecting both effects of alcohol on lipid metabolism in hepatic and extra hepatic tissue, as well as its marked toxic effects on liver function. This present study was undertaken to compare lipid profiles in alcoholics and non-alcoholics patients attending tertiary care center. Material and Methods: Present study was comparative, observational study. Among selected 80 male patients, from age group 41-50 years of age, 40 were alcoholic and 40 males who did not consume alcohol or do not have history of alcohol consumption were included in the study. Results: We analysed Total Cholesterol, HDL, Triglyceride, LDL and VLDL values from 80 male patients, from age group 41-50 years. Among them 40 were alcoholic and 40 were non-alcoholic. Results are displayed in table 1. Overall raised total cholesterol, serum triglyceride, VLDL, LDL values and lowered HDL were noted in alcoholic group as compared to non-alcoholic group. Statistically significant values were noted in HDL and LDL values. Rest total cholesterol, serum triglyceride, VLDL values were not significant. Conclusion: Moderate to severe alcoholism causes profound dyslipidemia, increases risk of spectrum of Atherosclerotic cardiovascular diseases such as stroke, myocardial infarction, along with alcoholic liver disease. Key Words: Alcohol, Lipid Profile, cardiovascular risk
INTRODUCTION The liver plays an important role in lipid metabolism and several stages of synthesis, transportation and degradation of lipoprotein. The liver is the principal site for formation and clearance of lipoproteins. So, the liver contributes to both the exogenous and endogenous cycles of lipid metabolism and transport of lipids through plasma1. Hypertriglyceridemia can be due to genetically determined disturbances in lipid metabolism or secondary to conditions such as obesity, diabetes mellitus, hypothyroidism, the nephrotic syndrome, steroids, diuretics, oestrogens, immunosuppressants and antiviral drugs2. Alcohol has many effects on lipid metabolism, including inducing de novo fatty acid synthesis and inhibiting fatty acid oxidation in the liver. The most common effect of alcohol is to increase plasma triglyceride levels. A leading protective mechanism has been suggested by alcohol’s ability to produce changes in plasma lipoproteins especially HDL and LDL. Increase in plasma level of HDL is often associated with decrease in the prevalence of coronary artery disease. The coronary heart disease has been reported to decrease with moderate drinking in both sexes, but such benefit disappears with high consumption3. Heavy alcohol consumption for prolonged periods result in marked perturbation of the lipid transport system, reflecting both effects of alcohol on lipid metabolism in hepatic and extra hepatic tissue, as well as its marked toxic effects on liver function4. Until 2025, total alcohol per capita consumption (15+ years) is expected to increase in half of the WHO regions, the highest increase is expected in the South-East Asia Region, with an increase of 2.2 litres alone in India which represents a large proportion of the total population in this region5. The causal relationship of alcohol consumption and liver diseases is well established, and alcohol has been shown to have an ability to cause hepatocellular damage through ethanol metabolism-associated mechanisms and malnutrition6. This present study was undertaken to compare lipid profiles in alcoholics and non-alcoholics patients attending tertiary care center.
MATERIAL AND METHODS Present study was conducted in XXX hospital, XXXX . The study period was from Jan 2019 to June 2019. Study was comparative, observational study. Approval was taken from local institutional ethics committee. A written informed consent was obtained from all participants. In our local population alcohol consumption is rare amongst females. So, study was proceeded in male subjects only. For comparison of lipid profiles in alcoholics and non-alcoholics patients, we selected 80 male patients, from age group 41-50 years of age for the study. Among them 40 were alcoholic and 40 males who did not consume alcohol or do not have history of alcohol consumption were included in the study. Alcoholic patients were heavy drinkers (consuming 5 or more drinks on the same occasion on each of 5 or more days in the past 3 years). Patients of known cases of liver, cardiovascular or renal disorders , diabetes mellitus, and who did not give the consent were excluded from the study.Blood sample of 5 ml was withdrawn following overnight fasting of 12 hours. The sample was processed in Biochemistry lab of our hospital. Total Cholesterol, HDL, Triglyceride, Low density lipoprotein cholesterol (LDL) and very low-density lipoprotein cholesterol (VLDL) values were estimated. Values were collected and statistical analysis was performed by using SSPS version 21.
RESULTS We analysed Total Cholesterol, HDL, Triglyceride, LDL and VLDL valuesfrom 80 male patients, from age group 41-50 years. Among them 40 were alcoholic and 40 were non-alcoholic. Results are displayed in table 1. Overall raised total cholesterol, serum triglyceride, VLDL, LDL values and lowered HDL were noted in alcoholic group as compared to non-alcoholic group. Statistically significant values were noted in HDL and LDL values. Rest total cholesterol, serum triglyceride, VLDL values were not significant.
Table 1: Comparison of lipid profile among the three groups
DISCUSSION The harmful use of alcohol ranks among the top five risk factors for disease, disability and death throughout the world7. Socially and financially, resources spent on alcohol would be subtracted from more productive uses in the long run, and the harms from drinking often include impoverishment as well as ill-health8. Atherosclerotic cardiovascular diseases in India are rising alarmingly high and a major cause of concern. Indians are not only at high risk of developing atherosclerotic cardiovascular diseases, they usually get the disease at an early age, have a more severe form of the disease and have poorer outcome as compared to the western populations9. Dyslipidemia is an easily correctable factor, which is a highest population attributable risk for myocardial infarction, both because of its high prevalence and also because of its direct pathogenic association with atherosclerosis10.‘Global Burden of Metabolic Risk Factors Study’ reported trends in total cholesterol levels in different countries and world regions from the years 1980 to 2008. It was concluded that total cholesterol levels increased in India and other low-income and lower middle-income countries over this period. The levels declined in most high income countries11,12. Alcohol consumption may introduce a cardiovascular benefit by improving an individual’s lipid profile, including an effect on HDL-c levels, HDL particle concentration, and HDL-c subfractions13. But , the observed association between alcohol use and lipids can be confounded by demographic, social and behavioural factors, as well as access to health care, and health-related conditions14. Using genetic variants that influence alcohol consumption may better capture the role of life-long alcohol use. A limited number of Mendelian randomization studies have been conducted to evaluate the relationship between alcohol consumption and lipid levels, and the results have been largely inconclusive15. Numerous mechanisms have been proposed to explain the benefit that light-to-moderate alcohol intake has on the heart, including an increase of HDL-C, reduction in plasma viscosity and fibrinogen concentration, increase in fibrinolysis, decrease in platelet aggregation, improvement in endothelial function, reduction of inflammation, and promotion of antioxidant effects16. Results from observational studies, where alcohol consumption can be linked directly to an individual’s risk of CHD, provide strong evidence that moderate amounts of all alcoholic drinks are linked with lower risk. Thus, a substantial portion of the benefit is from alcohol rather than other components of each type of drink17. In initial stages of alcoholism, these are packaged with apolipoproteins and exported as very-low-density lipoproteins(VLDL). Increased concentrations of VLDL and hence of serum triglycerides are often present in early stages of alcoholic liver disease. As the liver disease progresses, there is failure to produce apolipoproteins and export the fat as VLDL, thus accumulation of TG ensues. Consumption of alcohol, up to 4 drinks per day in men and 2 drinks per day in women, was inversely associated with total mortality in the western population. Heavy drinking was associated with an increase in mortality, hypertension, alcoholic cardiomyopathy, cancer, and cerebrovascular events, including cerebrovascular hemorrhage. The mechanism responsible for reduction of triglyceride level in patients with chronic alcoholism, might be poor nutrition and the reduced metabolism of free fatty acids due to chronic liver disease causing decreased reserve of liver parenchyma. The significant reduction in the level of serum HDL in chronic alcoholics when compared to healthy normal is consistent with other studies. Subhan et al observed that in patients with chronic liver parenchymal disease without cholestasis, HDL levels decline and become worse as the disease progresses18. The decrease in HDL in patients with cirrhosis can be attributed to decreased hepatic synthesis of HDL. This could be due to LCAT deficiency. Liver is the only source of this enzyme (LCAT) and serum levels of this enzyme are decreased in liver disorders. The decreased LCAT results in impairment of conversion of nascent HDL to mature HDL19. A cross sectional study by Roy et al. suggests that alcohol use is not protective against CHD in Indian men. Rather, it is associated with possible harm. Hence, alcohol intake even in moderation should be avoided by Indians20. Expert Consensus Panel, Lipid Association of India Expert Consensus Statement on Management of Dyslipidemia in Indians 20168, recommends that “Patients with atherosclerotic cardiovascular diseases who do not consume alcohol should not be encouraged to start regular drinking. However, for patients who drink, alcohol should not exceed 1 drink per day for women or up to 2 drinks per day for men.”
CONCLUSION Moderate to severe alcoholism causes profound dyslipidemia, increases risk of spectrum of Atherosclerotic cardiovascular diseases such as stroke, myocardial infarction, along with alcoholic liver disease.
REFERENCES
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