Effects Of Alcohol On Some Biochemical Parameters Of Alcoholics
This work was aimed at finding the effects of alcohol on some biochemical parameters. A total of one hundred and eighty (180) apparently healthy, nonhypertensive male alcoholics were used for the study. Forty (40) non-consumers of alcohol were used as control. The activity of alanine aminotransferase (ALT) in the control was 10.50±2.00 IU/L while it was 16.50±1.50 IU/L; 17.50±2.00 IU/L and 18.31±2.00 IU/L in alcoholics who showed preference for palmwine, beer and distilled spirit respectively. Also, the activity of aspartate aminotransferase (AST) in the control was 9.51±0.35 IU/L while it was 18.44±0.40 IU/L, 19.21±0.19 IU/L, 20.32±0.64 IU/L in alcoholics who showed preference for palmwine, beer and distilled spirit respectively. The ALT and AST activities of alcoholic subjects who showed preference for distilled spirit was significantly higher (p < 0.05) than those who showed preference for palmwine and beer.
The activities of alcoholics who showed preference for palmwine was the lowest. Furthermore, the serum total bilirubin concentration of the alcoholics was significantly higher (p < 0.05) compared with the control. The serum total bilirubin concentrations were 18.65±2.10 µmol/l, 19.40±1.50 µmol/l and 22.75±1.60 µmol/l for alcoholics who showed preference for palmwine, beer and distilled spirit respectively. The serum total bilirubin of the control was 8.30 ± 2.00 µmol/l. The alkaline phosphatase (ALP) activity of the alcoholic subjects was significantly higher (p<0.05) compared with the control. The ALP activity of the control was 61.50 ± 30.00 IU/L while the ALP activity was 174.20±2.50 IU/L, 175.10±1.50 IU/L and 177.40±1.00 IU/L in the three categories of alcoholics who showed preference for palmwine, beer and distilled spirit respectively. Moreover, the urine total protein concentration of the alcoholics was significantly higher (p<0.05) compared with the control. Alcoholics who showed preference for distilled spirit had urine total protein of 153.96±0.43 mg/dl followed by alcoholics who showed preference for beer and palmwine who had urine total protein of 152.74±0.42 mg/dl and 151.34±0.60 mg/dl respectively.
The urine total protein of the control was 56.40±0.40 mg/dl. Furthermore, the urine specific gravity, serum urea and creatinine of the alcoholics were significantly higher (p < 0.05) compared with the control. However, the plasma sodium, potassium and creatinine clearance of the alcoholics were significantly lower (p < 0.05) compared with the control. The body mass index (BMI) of the three groups of alcoholics fell within the range of 18.50 to 24.90. The blood pressure of both the alcoholic and control subjects were normal (below 140/90 mmHg). This work therefore shows that chronic alcohol use could induce both hepatic and renal dysfunctions in the alcoholics which manifested in form of adverse variations in some biochemical parameters of prognostic and diagnostic utility
Introduction
Generally, alcohol designates a class of compounds that are hydroxyl derivatives of aliphatic hydrocarbons. However, in this study, the term alcohol used without additional qualifications refers specifically to ethanol. A variety of alcoholic beverages have been consumed by man in the continuing search for euphoria producing stimuli. Among some people, alcohol enjoys a high status as a social lubricant that relieves tension, gives self confidence to the inadequate, blurs the appreciation of uncomfortable realities and serves as an escape from environmental and emotional stress.
Alcohol has been loved and hated at different times by different people. Alcohol has been celebrated as healthful especially to the heart (red wine) and most pleasant to the taste buds; and then dismissed as “demon’s rum” and “devil in solution” depending on the prevalent view.
In spite of the apparent divergent and sometimes conflicting opinions about alcohol, the consensus shared by drinkers and non drinkers alike is that excessive and chronic consumption of alcohol is a disorder. Like any other chronic disorder, it develops insidiously but follows a predictable course. The first or pre-alcoholic symptomatic phase begins with the use of alcohol to relieve tensions. The second (or prodromal) phase is marked by a range of behaviours including preoccupation with alcohol, surreptitious drinking and loss of memory (Hock et al., 1992). In the third (or crucial) phase, the individual loses control over his drinking. This loss of control is the beginning of the disease process of addiction. The individual starts drinking early in the morning and stays up drinking till late in the night. Impairment in biochemical activities becomes manifest as the organs of the alcoholic begin to deteriorate. Other medical problems develop by the time the alcoholic gets into the final (chronic phase). Prolonged intoxications become the rule. Alcoholic psychosis develops, thinking is impaired, and fear and tremors become persistent (Klemin and Sherry, 1981). A previously responsible individual may be transformed into an inebriate – stereotype alcoholic.
Fear-instilling but thought- provoking terms such as the “coming epidemic”, a “miserable trap”, have been used to show concern for the potential hazard of widespread alcoholism.
In its 1978 revision of the international classification of diseases, the World Health Organization defined alcoholism as “a state, psychic and usually also physical, resulting from taking alcohol, characterised by behavioural and other responses that always include a compulsion to take alcohol on a continuous or periodic basis in order to experience its psychic effects and sometimes to avoid the discomfort of its absence; tolerance may or may not be present. This definition emphasized the compulsive nature of drinking, the psychological and physical effects, and dependence (“discomfort of its absence”) (WHO, 1978).
The kidney and liver could be particularly vulnerable to the chemical assault resulting from alcohol abuse because they receive high percentage of the total cardiac output. Also, the liver is pivotal in intermediary metabolism; so ingested alcohol must come in contact with the liver and kidney. Alcohol could produce many of its damaging effects by the formation of dangerous, highly reactive intermediates such as acetaldehyde which may lead to glutathione depletion, free radical generation, oxidative stress and cell dysfunction.
Alcohol dehydrogenase in the presence of a hydrogen acceptor nicotinamide adenine dinucleotide (NAD) oxidizes ethanol to acetaldehyde. This is the initial obligatory biochemical event in alcohol induced hepatotoxic and nephrotoxic effects. Thus, it is important to find out in quantitative terms the effects of different types of alcohol drinks on some principal biochemical parameters of diagnostic utility.
Title
Declaration
Approval
Dedication
Acknowledgement
Abstract
Table of Content
Chapter One:
Introduction
1.1 Alcohol
1.2 Microanatomy of the kidney
1.3 Serum electrolyte and alcohol-induced renal
1.4 Alcohol induced pathological proteinuria
1.5 Urine specific gravity as an index of alcohol-induced renal dysfunction
1.6 Alteration in plasma urea concentration as a pointing indicator of renal dysfunction under the nephrotoxic assault of chronic and excessive alcohol abuse
1.7 Microanatomy of the human liver
1.8 The liver and alcohol metabolising system
1.9 The nature and metabolic roles of some alcohol metabolizing enzymes
1.10 Some alcohol-induced liver problems
1.11 Alcoholic liver diseases
1.12 Alcohol-induced liver degeneration and intracellular accumulation
1.13 Bilirubin metabolism and alcohol-induced liver dysfunction
1.14 Diagnosis of alcohol-induced liver problems
1.15 Justification of the study
1.16 Aim and objectives of the study
Chapter Two:
Materials And Methods
2.1 Materials
2.2 Methods
2.3 Statistical analysis
Chapter Three:
Results
3.1 Effect of alcohol consumption on urine total protein concentration in human subjects
3.2 Effect of alcohol consumption on urine specificgravity in human subjects
3.3 Effect of alcohol consumption on serum urea concentration in human subjects
3.4 Effect of alcohol consumption on serum creatinine concentration in human subjects
3.5 Effect of alcohol consumption on urine creatinine concentration in human subjects
3.6 Effect of alcohol consumption on creatinine clearance in human subjects
3.7 Effect of alcohol consumption on serum potassium concentration in human subjects
3.8 Effect of alcohol consumption on serum sodium concentration in human subjects
3.9 Effect of alcohol consumption on serum total bilirubin concentration in human subjects
3.10 Effect of alcohol consumption on serum alkaline phosphatase activity in human subjects
3.11 Effect of alcohol consumption on serum aspartate aminotransferase activity in human subjects
3.12 Effect of alcohol consumption on serum alanine aminotransferase activity in human subjects
3.13 Effect of alcohol consumption on gamma glutamyltransferase activities in humans subjects
3.14 Effect of alcohol consumption on body mass index in human subjects
3.15 Effect of alcohol consumption on blood pressure in human subjects
Chapter Four:
Discussion
4.1 Discussion
4.2 Conclusion
4.3 Suggestions for Further Research
References
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