Introduction
Alcoholism represents one of the most serious worldwide socio-economic and health problems. An alcoholic is a person who consumes an amount of alcohol capable of producing pathological changes (Criteria Committee, 2002). Alcohol consumption is known for morbidity (diseases) and mortality (death) and has being serious health hazard of the world. It is one of the most serious worldwide socio-economic and health problems (National Council, 2009).
The amount of alcohol capable of producing disease depend on a variety of factors including genetic predisposition (Bailey et al., 2006), malnutrition (Menden, 2004) and concomitant viral infections of the liver (Hall, 2005). It has been reported that medically diagnosed alcoholics can be differentiated from non-alcoholics using clinical laboratory test.
Multiple organs defects can be involved like hepatobilliary system, cardiovascular system, central nervous system, haemapoitic system. Alcohol can lead to all types of anaemia with suppression of bone marrow. Many times this disease are left undetected and untreated which could progress to cardiac failure (National Council, 2009).
Acute and chronic alcohol abuses are common conditions in patients, admitted to hospitals. Alcohol has wide spread direct and indirect effects on the hematological system which can mimic and obscure other disorders. Leukocyte, erythrocyte and thrombolytic production and functions are affected directly (Lidenbaum, 1987).
The new trend of alcohol consumption among young and old Nigerians contributes to Nigerians ranking among thirty countries with highest per capita consumption of alcohol globally (world Health Organization, 2004). These ranking fail to account for the unrecorded production and consumption of alcohol (Jernigan & Obot, 2006). The 2009 report did not indicate a decline in consumption of alcohol rather revealed that Nigeria consumed 10.57 litres per head of the population (Toroyan, 2009). The corroborates (Gureje et al., 2007).
Findings also add that heavy episodic drinking, rather than moderate drinking is common among users of alcohol in Nigeria and that alcohol is the most commonly used drug among Nigerians.
Conceptual framework
Alcohol drinks have been consumed for thousands of years and the problems that can accompany excess alcohol intake have undoubtedly been around just as long. In moderation, alcohol can be the oil that makes a social occasion go with a bit more flow or helps a shy person overcome his inhibition (Flavin et al.,1992).
However, high level of alcohol consumption can lead to physical illness, physiological and social distress. Alcohol therefore, has always had an ambivalent position in society. Alcohol as a substance, legal or illegal, has a more paradoxical history than any other substance. It is undeniably one of the most widely and safely used mood altering substance in our society and cultural activities. It is also a potent and dangerous drug of abuse both from a physiological and psychological view point. Alcohol works to reduces social inhibition and to produce pleasure and a sense of well being. It also has some impressive positive medical effects.
However, it is debated whether it is consumed because of these psychological medical effects or because it is a product associated with youthfulness, sexuality, and positive social interactions.
Every effort to ban its use, from religious campaigns to constitutional amendment has failed. The right to drink is as basic to American value as the bill of rights. The Journal of the American Medical Association defines alcoholism as a primary chronic disease characterized by impaired control over drinking. Progressive disease like alcoholism and cancer persist over time and people with alcoholism experience physical, emotional and other changes in their lives and relationships.
If treatment specific to alcoholism is not retained, the extent of changes tends to increase often worsening life situations. Left untreated, alcoholism cause premature death though overdose and through chronic damage to the brain, liver, heart and many other organs. Excessive alcohol consumption is a leading contribution to suicide, motor vehicle crashes, violence and other traumatic events. People with untreated alcoholism often lose their jobs, their families and other relationship and freedoms that were once important to them.
Alcohol problem can often be prevented by early identification and brief intervention. The weak links in identifying problems early are the skill and competencies necessary for such an assessment and the experience to confidently move to more specific questions and “suggestions for change. Understanding the difficulties in assessing alcoholic will help the physician to update his/her skills set and master the core issues in moderate alcohol consumption and in alcohol consumption and in alcohol abuse problem and dependence detection, as well as in intervention.
History of alcohol
Although the exact date when alcohol was produced remain elusive, the discovery of late stone age beer Jugs’ has established the fact that intentionally fermented beverages existed as early as the Neolithic period. (Gaitley, 2009).
Wine has appeared in Egyptian pictographs around 4000 BC. Since prehistoric times a variety of alcohol beverage have been used in China. The Babylonians considered beer as one of their major beverages. The Samarians have engraved the art of making beer pictorially. The art of wine making reached the Hellenic peninsula around 2000 BC.(Dietler, 2006).
Alcohol drinks were an intricate part of most civilization ranging from china and India and Western Asia to Europe. In India alcohol beverages appeared, during the Indus valley civilization. In Hindie Ayurvedic texts both the beneficial and detrimental effects of alcohol have been outlined distilled spirits originated in India and China around 800BC. The distillation process emerged in Europe around the eleventh century. (Dasgupta and Amitava, 2011).
Alcohol use in Nigeria dates far back in history as far the colonial period. Alcoholic beverages in the pre-colonial period consisted mainly of palm wine (or distillate of palm wine e.g. ogogoro) and fermented cereal, such as guinea corn. Elaborate alcohol consumption by the local community priest and pouring of libations formed essential parts of many religious ceremonies and rituals, similar to the Kofyar people near Jos (Netting, 1964). Carnival drinking during important social events was characteristics of many traditional Nigerian Communities (Odejide and Olatawura, 1977). The Greeks worshipped the god Bacchus the god of wine and the Romans worshipped the same god under a different name Dionysus. Around 55BC, the Romans introduced beer to the Europeans. Wine became part of rituals with the rise of Christianity. There was a simultaneous spread of viticulture and Christianity in Europe. It reached the Americans from Europe. Although by then the natives in American were quite adept at developing their local versions (Dineley and Dineley, 2000).
The pattern and extent of drinking changed radically as trading contacts were made with European colonists led to an upsurge in alcohol consumption in Africa. According to her “Alcohol was part and parcel of the commerce which for centuries constituted the basic tie between Europe and Africa. It was an article of the barters system through which European goods were exchanged for African slaves. During the middle ages, wine was the preferred beverage and the consumption of alcohol began to spread to all parts of the world. Today, it is widely consumed by people all over the world (Bert and Valle, 1998).
Alcohol production and products
Alcohol is a colourless flammable liquid, obtained by the fermentation of sugar and starch. It is used either in its pure or denature form as a solvent in drugs, explosives, cleaning solution or intoxicating beverages (Dietler, 2006). Alcohol can be made by fermenting fruits or gains with yeast. Ethanol is produced through fermentation in the production of fuel. Alcohol is classified according to the relation between the carbon atoms in it. The most commonly used primary alcohols are methanol and ethanol. As methanol was formerly obtained from the distillation of wood, it is also known as wood alcohol. Surgical spirits is a form of ethanol. Ethanol’s is used in the industrial solvent. The simplest secondary alcohol is isopropanol, while butanol is a simple tertiary alcohol.
Other uses of alcohol
Alcohol is used in industries as reagents, solvents and fuels. The primary alcohol methanol and ethanol burn more efficiently than diesel or gasoline ethanol is used as a solvent in medical drugs and perfumes.
Alcohol doses and absorption
Consumption in large doses can cause acute respiratory failure or death and with chronic use has medical repercussion. About 20 percent of alcohol is absorbed by the stomach and 80 percent by the small intestine. The alcohol then enters the blood stream and dissolved in the blood. The blood circulates the alcohol throughout the body, leading to intoxication (Alcohol and Public Health, 2012).
Body response to alcohol
The human body responds to alcohol in stages, initially a person consuming alcohols experiences a state of euphoria, where he may become more self-confident and appear flushed. Later, he reaches a stage of excitement and is unable to react swiftly to natural situation. This is followed by a sense of stupor where he does not respond to stimuli. Excessive consumption of alcohol leads to coma or death (WHO, 2007).
Human vices connected with alcohol
Most are aware that drugs are major factor in our biggest social problems, violence, crime, poverty, aids, family disintegration, but many do not think of alcohol as a drug at all, only as social beverage. Even with the recent cases of EVD (Ebola Virus Disease) which can be contracted by close contact, at the stage of alcohol intoxication, contact can be made unknowingly and uncontrollably leading to transfer of the disease. We shall agree that alcohol causes immunes problems, of which alcoholism is only one.
The facts about alcohol are distorted by our emotionally charged attitude toward drinking, drunkenness and alcoholism. Those attitudes are the result of many factors: family situation, social-cultural experience, biological differences, prohibition, differing religious and political economic and personal feelings unique to each individual (National Council, 2009).
Epidemiology
According to WHO one-third of the world consume alcohol, although two-thirds of American adult’s drinks alcohol, only a minority are problem drinkers. Never the less, the number of alcoholics in the United State is estimated to be 14 million (National Council, 2009).
The total cost of alcohol abuse is about $185 billion annually, most of which are related to lost productivity and motor vehicle accidents. Alcoholic liver disease also is a major health care problem, accounting for 40% of deaths from cirrhoses and more than 30% of cases of hepatocellular carcinoma in the United States (National Council, 2009; Robert and Daniel, 1998).
Comparable statistics have two decades in Nigeria according to the survey done by WHO 2004 has shown an increase in abstinence and decrease in consumption. In 2010 the worldwide total consumption was equal to 6.2 litres of pure alcohol per person 15 years and older unrecorded consumption account for 25% of the worldwide total consumption. With a population of 160,000,000 of 15 years and older from 1961 – 2010 there has been a reduction in alcohol intake in Nigeria. (WHO: GENASICS, 2010).
Gender difference
Statistics show an extreme gender difference in consumption patterns. Prevalence among women has consistently been rated as less than 10% but is much higher in the urban area. Significantly higher use has been recorded among tribal, rural and lower social-economic urban sections.
A study conducted by the WHO GENACIS drew a general conclusion from alcoholic relatively high ranking as a risk factor for death and disability (Ezzati et al.,2002) is that a major effort to strengthen alcohol policies is needed on a global basis. The need is particularly strong; it would seem in some of the countries of the world. Women in Nigeria have lower report of alcohol problem than the men (WHO, 2010).
Statistics of alcohol
- More than 100,000 US deaths are caused by excessive alcohol consumption each year. Direct and indirect causes of death include drunken driving, cirrhosis of the liver falls, cancer, and stroke.
- At least once a year the guideline for low risk drinking is exceeded by an estimated 74% of male drinkers and 72% of female drinkers aged 21 and older.
- Nearly 14 million American meet diagnostic criteria for alcohol use disorders.
- Youth who drink alcohol are 50 times more likely to will hard drugs than those who never drink alcohol.
- Among current adult drinkers, more than half say they have a blood relative who is or was an alcoholic or a problem drinker.
- Across people of all ages, males are four times a likely as females to be heavy drinkers.
- Traffic crash are the greatest single cause of death for persons aged 6-33. About 45% of these fatalities are in alcohol related crashes.
- Alcohol is most commonly used drug among young people.
- Problem drinkers average four times as many days in the hospital as non-drinkers. Mostly because of drinking related injuries.
- Alcohol kills 61/2 time more youth than all other illicit drugs combined. (Gowda, 2010).
Genetics
Pattern of alcohol drinking are inherited, however, a specific genetic abnormality is involved in susceptibility has not been identified Rates of alcohol elimination varies as much as three fold among individuals. Prevalence of alcoholism is greater among monozygotic than dixygotic twins, suggesting an inherited defect. Different rates of alcohol estimation may be related to genetic polymorphism of enzyme system. Individuals with different alcohol dehydrogenase (ADH) isoenzymes have different alcohol elimination rates.
Polymorphism of ADH2 and ADH3 which are more active forms, may be protective as faster acetaldehyde accumulation leads lower tolerance to alcohol. However, if such persons do imbibe, more acetaldehyde is produced so increasing the risk of liver disease. The microsomal, ethanol inducible cytochrome P450-11E1 (CYP2E1) is the key in non-ADH oxidation of ethanol which produces acetaldehyde. However, there is little or no association between polymorphisms in the CYP2E1 gene and the incidence of alcoholic liver disease. Inactive ALDH2 is found in 50% of Japanese and Chinese and this explains the aldehyde flush reaction when they consume alcohol. This inhibits Orientals from taking alcohol and is a negative risk for the development of alcoholic liver disease. Polymorphism in tumour necrosis factor promoters associated with susceptibility to alcoholic steato-hepatitis(Smith et al., 2005).
Metabolism of alcohol
Alcohol cannot be stored and obligatory oxidation must take place, predominantly in the liver. The healthy individual cannot metabolize more than 160 – 180g/ day. Alcohol induces enzymes used in its catabolism and the alcoholic at least while the liver is relatively unaffected may be able to metabolize more(Chalmers et al., 2009).
The haematological complications of alcoholism
Alcoholism has numerous adverse effects on the various blood cells and their functions, for example heavy alcohol consumption can cause generalized suppression of blood cell production and precursors that cannot mature into functional cells. Alcoholics frequently have defective red blood cells that are destroyed prematurely possibly resulting in anaemia. Alcohol also interferes with the production and function of white blood cells, especially those that defend the body against invading bacteria. Consequently, alcoholics frequently suffer from bacterial infections (Ballard, 1989).
Finally alcohol adversely affects the platelets and other component of the blood clotting system. Heavy alcohol consumption thus may increase the drinkers’ risk of suffering a stroke. Alcohol’s adverse effects on the body building or hematopoietic system are both direct and indirect. The direct consequences of excessive alcohol consumption include toxic effects on the bone marrow; the blood cell precursors; and the mature red blood cells (RBC’s) white blood cells (WBC’s) and platelets. Alcohol’s indirect effects include nutritional deficiencies that impair the production and function of various red blood cells. (Pellegriniet al., 1996).
This direct and indirect effect of alcohol can result in serious medical problems for the drinkers, for example, anaemia resulting from diminished RBC production and impaired RBC metabolism and function can cause fatigue. Shortness of breath, light-headedness and even reduced mental capacity and abnormal hearts beats. A decrease in the number and function of WBC’s increase the drinker’s risk of serious infection and impaired platelet production and function interfere with blood clothing leading to symptoms ranging from a simple nose bleed to bleeding in the brain (i.e. hemorrhagic stroke). Finally, alcohol indirect abnormalities in the plasma proteins that are required for blood clotting can lead to the formation of blood clots (i.e. thrombosis)(Seppaet al.,2005).
Alcohol’s effects on the bone marrow and on RBC production
Alcohol is the most commonly used drug whose consequences include the suppression of blood cell production, or haematopoiesis, because its toxic effects are those dependent, however, significantly impaired haematopoiesis usually occurs only in people with severe alcohol who also may suffer from nutritional deficiencies of folic acid and other vitamin that play a role in blood cell development. Chronic excessive alcohol ingestion reduces the number of blood cell precursors in the bone marrow and causes characteristics structural abnormalities in the cells, resulting in fewer than normal or non-functional mature red blood cells. As a result alcoholics may suffer from moderate anaemia, characterized by enlarged, structurally abnormal RBC’s, mildly reduced numbers of WBC’s especially of neutrophils and moderately to severely reduced numbers of platelets. Although this generalized in the blood cell numbers (i.e. pancytopenia) usually is not progressive of fatal and is reversible with abstinence, complex operations of haematopoiesis can develop overtime that may cause death (Ballard,1993).
Many bone marrow abnormalities occurring in severe alcoholics affect the RBC precursor cells. These abnormalities most prominently include precursors containing fluid-filled. Alcohol’s effect on iron Metabolism in addition to interfering with proper absorption of iron into the haemoglobin molecules of red blood cells (RBC’s), alcohol use can lead to either iron deficiency or excessively high level of iron in the body because iron is essential to RBC functioning, iron deficiency which is commonly caused by excessive blood loss can result in anaemia. In many alcoholic patients, blood loss and subsequent iron deficiency are caused by gastro intestinal bleeding. Iron deficiency in alcoholics often is difficult to diagnose however because it may be masked by symptoms of other nutritional deficiencies (i.e. folic acid deficiency or by co-existing) liver disease and other alcohol related inflammatory conditions. For an accurate diagnosis, the physician must therefore exclude folic acid deficiency and evacuate the patient’s iron (Ballard,1993).
Conversely, alcohol abuse can increase iron levels in the body for example, iron absorption from the food in the gastrointestinal tract may be elevated in alcoholics. Iron levels can rise from excessive ingestion of iron-containing alcoholic beverages, such as red wine. The increased iron levels can cause hemochromatosis a condition characterized by the formation of iron deposits throughout the body (e.g. in the liver, pancreas, heart, joint and gonads). Moreover, patients whose chronic alcohol consumption and hemochromatosis have led to liver cirrhosis are at increased risk for liver, cancer.
Development of vacuoles in RBC precursor
The most striking indication of alcohol toxic effects on bone marrow cells in the appearance of numerous large vacuoles in early RBC precursor cells. It is unknown whether these vacuoles affect the cells function and thus the drinker’s health; however, their appearance generally is considered an indicator of excessive alcohol consumption. The vacuoles usually appear in the pronormoblastics 5 to 7 days following the initiation of heavy alcohol consumption. Moreover the vacuoles on average disappear after 3 to 7 days of abstinence, although in some patients they persist for up to 2 weeks(Ballard,1993).
To a lesser extent, vacuoles also develop in the granulocyte precursors of alcoholics. This finding is not specifically alcohol related, however because other events that interfere with WBC production (e.g. infection) may induce similar structural changes in the granulocyte precursors.
The precise mechanism underlying vacuoles development in blood cell precursors currently is unknown. Microscopic analysis of early blood cell precursors grown in tissue culture suggest that when the cells are exposed to a wide range of alcohol concentrations, the membrane surrounding each cell is damaged. These alterations in membrane structure may play an influential role in vacuole formation.
Sideroblastic Anaemia
One component of RBC’s is haemoglobin and non-containing substance that is essential for oxygen transport. Sometimes, however the iron is not incorporated properly into the haemoglobin molecules. Instead, it is converted into a storage form called ferritin, which can accumulate in RBC precursor of ten forming granules that encircle the cell’s nucleus. These ferritin-containing cells, which are called ringed sideroblast cannot mature further into functional RBC’s. As a result, the number of RBC’s in the blood declines and patients develop anaemia. Many patients also have some circulating RBC’s that contain ferritin granules called pappenheimer bodies. The presence of these cells in the blood serves as an indicator of sideroblastic anaemia and can prompt the physician to perform a bone marrow examination to confirm the diagnosis. Sideroblastic anaemia is a common complication in severe alcoholics. Approximately one-third of these patients contain ringed sideroblasts in their bone marrow. (Savage and Lidenbaum, 1986)
Alcohol may cause sideroblastic anaemia by interfering with the activity of an enzyme that mediates a critical step in haemoglobin synthesis. Abstinence can reverse this effect: the ringed sideroblasts generally disappear from the bone marrow within 5 to 10 days and RBC production resumes. In fact excess numbers of 4 reticulocytes can accumulate temporarily in the blood, indicating higher than normal RBC production (Savage and Lidenbaum, 1986).
Magaloblastic anaemia
Blood cell precursors require folic acid and other B vitamins for their continued production under conditions of folic acid deficiency, precursor cells cannot divide properly and immature and non functional cells (i.e megaloblasts) accumulate in the bone marrow as well as in the blood stream. This impaired hematopoises affects mainly RBC’s, but also WBC’s and platelets. The results (i.e. pancytopenia) has numerous adverse consequences for the patient including weakness and pallor from anaemia infections resulting from reduced neutrophil numbers, and bleeding as a result of the lack of platelets. (Savage and Lidenbaum, 1986)
Megaloblasts occur frequently in the bone marrow of alcoholics; they are particularly common among alcoholics with symptoms of anaemia, affecting up to one-third of these patients. These alcohol generally also have reduced folic acid levels in their RBCs. The most common causes of this deficiency is a direct spoor in folic acid, a frequent complication in alcoholics who often have poor nutritional habits. In addition, alcohol injection itself may accelerate the development of folic acid deficiency by altering the desorption of folic acid from food (Savage, and Lidenbaum, 1986).
Alcohol effect on WBCs
Since the 1920s, clinicians have noted on association between excessive alcohol ingestion and the development of infection. These observations suggest that alcohol interferes with the normal production from the body’s defense against microorganisms and other foreign substances. Because infection, much research has focused on alcohol’s effects on neutrophils, the primary cell of defense against bacterial invasion. However, alcohol also impairs the function of monocytes and macrophages which attack bacteria and other micro organism and of lymphocytes which mediate the immune response. Alcohol-induce impairment of neutrophils and monocytosis discussed in the following sections (Ballard, 1989).
Neutrophils
When severe bacterial infection occurs, the body’s responses usually include an increase in the number of WBC’s especially neutrophils. In the blood, a condition called leukocytosis, in contrast alcoholics suffering from bacterial infections often exhibit a reduced number of neutrophils in the blood (i.e neutropenia) for example in a study of 10 alcoholics with severe bacterial pneumonia or other bacterial infections, neutropenia was present in 5 patients within 24 to 48 hours (Macfarland and Libre,1963). The neutropenia was transient, however and in several patients a rebound leukocytosis occurred between 5 and 10 days after hospital admission.
The observed neutropenia may be related to impaired neutrophil development in the bone marrow. Thus, bone marrow analysis of alcoholic patients during the neutropenic stage demonstrated that virtually none of the neutrophil precursor had matured beyond on early developmental stages.
Moreover the neutrophils store that are maintained in the bone marrow to allow in the body moreover, drugs that correlated the adherence defect in tissue – culture experience also improved neutrophil delivery in humans. The function of neutrophils, including their adheresion ability is regulated by hormone-like substances called leukotrines. Thus, the impaired neutrophil functioning observed after alcohol treatment could be attributable to reduced leukotrine production or to the neutrophils inability to respond to the leukotrines. Some research results indicate that alcohol can interfere with leukotrine productions. (MacFarland and Libre, 1963).
Alcohol’s effects on the blood clotting system
Blood clotting or coagulation, an important physiological process that ensures the integrity of the vascular system, involves the platelets or thrombocytes as well as several proteins dissolved in the plasma. When a blood vessel is injured, platelets are attracted to the site of the injury. Where they aggregate to form a temporary plug. The platelets secrete several proteins (i.e. clotting factors) that together will other proteins either secreted by surrounding tissue cells or present in the blood initiate a chain of events that results in the formation of fibrin(Pellegrini et al., 1996).
Fibrins a stringy protein that forms a tight mesh in the injured vessel; blood cells become trapped in this mesh, thereby plugging the wound. Fibrin dots; in turn can be dissolved by a process that helps prevent the development of thrombosis. (i.e. fibrinolysis),alcohol can interfere with these processes at several levels, causing for example abnormally low platelet numbers in blood (i.e. thrombocytopenia) impaired platelet function (i.e. thrombocytopathy) and diminished fibrinolysis. These effects can have serious medical consequences such as increase risk per strokes (Duarte et al.,1995).
Thrombocytopenia
Thrombocytopenia is a frequent complication of alcoholism, affecting 3-43 percent of non-acutely ill well nourished alcoholics and 14-81 percent of acutely ill hospitalized alcoholics. Thus apart from acquired immune deficiency syndrome (AIDS), alcoholism probably is the leading cause of thrombocytopenia. Except for the most severe cases. However, the patients generally do not exhibit manifestation of excessive bleeding. Moreover, alcohol related thrombocytopenia generally is transient and platelets counts usually return to normal within 1 week of abstinence. Therefore, patients generally require no therapeutic intervention other than that needed to ease alcohol withdrawal. Only in patient whose thrombocytopenia is severe and associated with excessive bleeding are platelet transfusion indicated (Duarte et al.,1995)
Thrombocytopathy
Alcohols affect not only platelet production but also platelet function. Thus patients who consume excessive amount of alcohol can exhibit a wide spectrum of platelet abnormalities. When admitted to a hospital, these abnormalities include impaired platelet aggregation, decreased secretion or activity of platelet derived proteins involved in blood clotting, and prolongation of bleeding in the absence of thrombocytopenia, because alcohol impairs the function of the normal blood clotting system, it also can adversely with over the counter and prescription medication, that prolong bleeding or prevent coagulation. For example, alcohol can potentiate the prolongation of bleeding time caused by aspirin and other no steroidal inflammatory drugs (NSAID) e.g. ibuprofen or indomethacin” particularly when alcohol ingestion, equivalent to about four drinks occurs with or following ingestion of normal close of these medications. As a result the concomitant use of alcohol and aspirin or NSAID’s greatly increase the patient’s risk for gastrointestinal bleeding. Similarly, alcohol can enhance aspirin induced fecal blood loss. To prevent such adverse reactions, health care professional should proactively counsel patients who regularly consume alcohol about the proper choice and safe use of aspirin and other over the counter USAID’s(Duarte et al., 1995).
Alcohol can also interact with anti-coagulants, prescription medication that prevent blood clotting and which are used to treat patients who are at increased risk of developing thrombosis or an embolism in the lung. One commonly used anticoagulant is warfarin. However warfarin treatment is not indicated for alcoholics patients, because alcohol ingestion can significantly interfere with the proper management of warfarin maintenance therapy(Pellegrini et al., 1996).
Fibrinolysis
The body’s ability to prevent excessive bleeding using the coagulation system is balanced by the fibrinolytic system, which helps ensure blood flow in peripheral organs and tissues by dissolving inappropriate fibrin clots. Alcohol’s effect on fibrinolysis is controversial. Whereas some older studies reported an increased in fibrinolytic activity after alcohol consumption more recent, better controlled studies have demonstrated that alcohol diminished fibrinolysis the day alcohol ingestion or during prolonged alcohol consumption. These actions suggest that alcoholics may be at increased risk for thrombosis(Duarte et al., 1995).
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