Alcoholic Liver Diseases

Another article in this encyclopedia discusses the relationship between alcohol and the liver in great detail. In any article dealing with the effects of drugs on the liver, however, alcohol must be addressed.

The gamut of alcoholic liver diseases and their interrelationship is illustrated in Figure 1.

Alcoholic Fatty Liver. Fat accumulation in the liver is an almost universal response to excessive alcohol consumption. It occurs in the majority of heavy drinkers. How and why fat accumulates in liver cells is complicated and not completely understood; but we know for sure that it happens. If you examine a piece of biopsied liver tissue from an alcoholic under the microscope, you see that many liver cells are loaded with big bubbles consisting of fat, almost totally occupying the cell. In most cases, this fatty change does not matter too much as far as the patient s health is concerned. It is an almost invariable response to too much alcohol consumption and an early warning. The person who has nothing worse than an alcoholic fatty liver may not feel sick at all, and only if a biopsy is done can the fatty liver be diagnosed. The doctor may feel an enlarged liver by palpation, which may be a bit tender. The laboratory test may show a slight elevation in the blood of some liver enzymes, best known by their initials: SGOT (or AST) and SGPT (or ALT). These enzymes are elevated because some of them tend to leak out of the fatty liver cells into the blood.

If a person stops drinking, the fat disappears from the liver cells, the swelling subsides and the AST and ALT levels become normal. The two-way arrow in the diagram of Figure 1 indicates that fatty liver is reversible with abstinence, and the condition may fluctuate back and forth between normal and fatty liver with abstinence and drinking, respectively. Thus, this, per se is not likely a serious situation; it is an early warning that ''your liver does not like alcohol'' and that possibly worse things might yet come. There was a time when fatty liver was regarded as the precursor of the end-stage liver disease called cirrhosis (indicated by the broken arrow and question mark on Figure 1), but in the 1990s, most physicians do not believe that this direct connection exists.

Alcoholic Hepatitis. This is a potentially more serious form of alcoholic liver disease. A certain proportion of alcoholics, in addition to accumulating fats in their livers when drinking, will develop inflammation (hepatitis means liver in-flammation)-consisting of an accumulation of white blood cells, the death (necrosis) of some of the liver cells, and the presence of some very char-

Normal Liver

Normal Liver

Alcoholic Cirrhosis Liver Uss

Alcoholic Hepatitis

Figure 1

Interrelationships between Various Forms of Alcoholic Liver Disease

Alcoholic Hepatitis i

Death acteristic material (called Mallory bodies). Again, all this can be seen under the microscope in a biopsied piece of tissue.

The clinical picture of alcoholic hepatitis can be very variable. At one extreme is the person who feels perfectly well and only the biopsy could tell that something is wrong. At the other extreme is the patient with a swollen and painful liver, yellow jaundice (a yellowing of the entire body from bile pigment leaking into the blood), fever, and disturbed consciousness—who dies. Between these extremes are people with varying degrees of seriousness of the illness; for example, with or without some jaundice, with or without pain and fever, etc. The blood's white cell count is usually elevated. The bilirubin (bile pigment) level may be elevated in patients who are yellow (apale to deep mustard). The liver enzymes are higher than normal in the blood, because they leak out of the inflamed liver cells. However, these values are not as high as in viral hepatitis and, characteristically, in alcoholic hepatitis AST (SGOT) is higher than ALT (SGPT), which helps to distinguish alcoholic hepatitis from viral hepatitis (difficult to do at times). In viral hepatitis not only are the absolute enzyme values higher, but the ratio is reversed: ALT is higher than AST.

Thus, the outcome of alcoholic hepatitis can be death (worst scenario) or recovery (best scen-ario)-as shown on Figure 1. Repeated episodes of drinking and alcoholic hepatitis, however, even if the patient does not die in a given episode, can lead to the endstage of alcoholic liver disease: cirrhosis.

Alcoholic Cirrhosis. In terms of histology (tissue damage) this indeed is an end-stage disease: a cirrhotic liver cannot become normal; in Figure 1, there is no arrow between cirrhosis and normal liver. Clinically, cirrhosis is a serious disease, potentially fatal, but not inevitably so. Alcoholism is not its only cause, but it is by far the most common.

Under the microscope a cirrhotic liver shows a disorganized architecture: the dead (necrotic) liver cells have been replaced by scar tissue. The liver tries to repair itself: In a somewhat haphazard fashion it attempts to produce new liver tissue in the form of nodules, which are separated from each other by scar. These newly formed liver nodules may indeed sustain liver function and thus life for a time, but at a price: the liver's blood circulation is mechanically compressed. Thus, the pressure increases in the blood vessels leading to the liver.

Some of these overloaded blood vessels, especially those on the border of the stomach and esophagus (called esophageal varices), can rupture any time, causing a major hemorrhage.

Those who develop the cirrhotic stage of alcoholic liver disease present their symptoms in various ways. Some of them look quite normal and only the biopsy will reveal the presence of cirrhosis. Others are jaundiced, the yellow color coming from bile pigment leaking out of the damaged liver into the blood, thus staining the skin and the whites of the eyes. Still others have large fluid accumulations in their extremities (edema) or in their abdominal cavity (ascites); the latter may make these patients—men or women—look like they are nine months pregnant. Some may vomit blood, because of the hemorrhaging. In most advanced cases, there is just not enough functioning liver tissue left; the liver no longer can perform its ''laboratory'' function, and the person slips into a coma and may die.

When cirrhotic patients are examined by doctors, their livers do not feel smooth on palpation, but bumpy from all those nodules that formed. At first the liver may be swollen and enlarged, but at the later stages it shrinks. The ultrasound picture suggests a patchy, disorganized architecture of the liver. The spleen may enlarge from the increased pressure in the blood vessels. The liver enzymes (AST and ALT) may be moderately elevated as in other forms of alcoholic liver disease, but this has no prognostic importance. More ominous signs pointing toward severely compromised liver functions are the following: a decrease in blood level of albumin (an important protein manufactured by the liver), deficiency in blood-clotting factors that are also made in the liver, and the presence of anaemia (low hemoglobin and red blood cell count).

What Can Kill a Cirrhotic Patient? Ascites (fluid accumulation in the abdomen) is very uncomfortable and unsightly but, by itself, usually does not kill—unless it gets spontaneously infected, which is always a threat. Generally, cirrhosis compromises the immune system, rendering cirrhotic alcoholics susceptible to all sorts of potentially overwhelming infections. Portal hypertension is a serious complication of the cirrhotic fibrosis. The obstruction to portal vein flow through the liver results in the development of other vein channels to accommodate the return of blood from the abdominal organs which comprise the blood in the portal vein. The result is the development of varices (enlarged, engorged veins) in the stomach and esophagus. These enlarged, thin-walled veins are prone to rupture leading to one of the most serious complications of cirrhosis of the liver—bleeding varices. This constitutes an emergency and calls for immediate intervention in the form of measures to control the bleeding. A variety of therapies are available, all of which have all been employed with a varying degree of success that depends on the severity of the hemorrhage and the skill and experience of the physician. Once the bleeding has been controlled, the patient should be considered for an appropriate permanent venous shunt procedure whereby venous blood bypasses the liver. Finally, total decompensation of liver-cell function may cause coma and death.

The good news is that even when there is irreversible cirrhosis at the tissue level, death may not be inevitable. Survival depends mainly on two factors: luck and alcohol abstinence. Abstaining alcoholics with cirrhosis can stabilize and survive on what's left of their liver tissue without necessarily and relentlessly progressing to one of the fatal outcomes. A famous Yale University study many years ago showed clearly the correlation between abstinence and survival in cirrhosis.

Who Gets Which Alcoholic Liver Disease? There are still no certain answers to this question. Fatty liver is an almost universally predictable response to heavy alcohol consumption, but this by itself is seldom a serious problem. A smaller number of people develop alcoholic hepatitis and still fewer (variously estimated in different populations between 5 to 25% of alcoholics) end up with cirrhosis. Considering the large number of alcoholics in our society, the minority who develop cirrhosis still represents huge numbers; cirrhosis is one of the leading causes of all deaths.

Still, why do some alcoholics develop alcoholic hepatitis and cirrhosis, while others who drink equally heavily do not? The amount of alcohol consumption and the length of time of heavy drinking is certainly one risk factor. Gender may be another: Women's livers generally are more vulnerable to the effects of alcohol than those of men, given equal alcohol exposures. Finally, there may be a genetically determined (but still unclarified) individual susceptibility, which may explain why some people never get cirrhosis, why some do after many years of alcoholism, and why still others get cirrhosis at a young age or after a relatively short drinking career.

Prognosis and Treatment. The issues of prognosis and treatment cannot be separated from each other. The cornerstone of treatment is complete abstinence from alcohol; achieving abstinence can arrest the progression of liver disease, even in established cirrhosis. Continued drinking leads to deterioration and death.

One therapeutic issue relating to alcoholism itself, should be addressed here because it is relevant to liver disease. The drug DISULFIRAM (Antabuse) is sometimes prescribed to reinforce abstinence: its unpleasant, sometimes severe interaction with alcohol is used as a deterrent against drinking. Since disulfiram (as so many other drugs) has been occasionally reported to produce liver toxicity of its own, the presence of alcoholic liver disease is sometimes regarded as a relative contraindication against the prescription of disulfiram. The liver toxicity caused by alcohol far outweighs any risk that may be caused by disulfiram.

Are there any other treatment techniques available beyond abstinence that can help the recovery from alcoholic liver damage? In the late 1980s, a Toronto research group reported the beneficial effect of propylthiouracil (PTU). This is a drug normally used for the treatment of thyroid disease, but by reducing oxygen demand in the body (including in the liver), it might help to repair the damage caused by alcohol. The early results were promising but it is still not a widely accepted treatment. Other drugs, such as corticosteroids (to decrease inflammation) or colchicine (to decrease scar formation) have dubious value.

There are relatively effective treatments available for some of the complications of alcoholic liver disease so that the patient may survive and thus begin his or her abstinence program. The fluid accumulation in the extremities (edema) or in the abdomen (ascites) can he helped by diet modifications (salt restriction), water removing drugs (diuretics), albumin infusion, or tapping the abdomen. Infections can be treated with antibiotics. The brain syndrome of liver failure (so-called hepatic encephalopathy or, in severe cases, hepatic coma) can improve with dietary means (protein restriction) or some drugs (e.g., neomycin, lactulose). The potentially or actually bleeding esophageal varicose veins can be obliterated by certain injections through a gastroscope (so-called sclerotherapy), and the bleeding risk can be lessened by beta-blocking drugs or some surgical procedures to decrease pressure.

Finally, in the 1990s we have the possibility of liver transplantation. If all else fails, a successful liver transplant cures alcoholic liver disease. Apart from the general problems of donor matching and supply, some people have raised objections on ethical grounds to offering transplantation for alcoholic (i.e., "self-inflicted") liver disease. This is not an acceptable objection and goes against medical ethics. Well-motivated recovering alcoholics are entitled, as much as anybody else, to a life-saying procedure. In fact, studies have shown that the very dramatic and heroic nature of this operation may be an extremely powerful motivator for future abstinence by liver recipients. Numerous successful transplants have been carried out on alcoholics.

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