Alcoholic liver disease
From Medical-Wiki
At one time, alcoholic liver disease was the leading cause of cirrhosis in the U.S. That role is now played by hepatitis C (HVC). It appears that the exact mechanism of this entity is a combination of genetic, environmental, nutritional, metabolic, and, more recently, immunologic factors as well as cytokines. The histology of alcohol damaged hepatocytes demonstrates centrilobular ballooning necrosis of hepatocytes, neutrophilic infiltration, megamitochondria, and Mallory hyaline inclusions.
Contents |
Etiology of alcoholic liver disease
Most alcoholics do not develop progressive liver injury. The fact that only a small percentage of alcoholics develop liver disease suggests that there is a genetic predisposition, but attempts to link a disease susceptibility to HLA groups and a variety of other factors have been unsuccessful.
There is a sex linked risk factor in that women are definitely more susceptible to developing alcoholic cirrhosis than are men.
Malnutrition also appears to play a role. This theory has been in and out of favor, but recent studies suggest that enteral or parenteral nutritional supplementation in patients with alcoholic hepatitis may improve survival.
Both ethanol and its metabolite acetaldehyde damage liver cell membranes. This damage appears to be the mechanism behind the megamitochondria, changes in membrane-bound enzymes and transport proteins, likely creates neoantigens that trigger immunologic injury. Further, it appears that ethanol plays a role in creating a state of hepatocyte hypermetabolism as well as generating free radicals. [1]
There also appears to be an immunologic component to alcoholic hepatitis. This is suggested by the fact that even after the insult of alcohol consumption is removed, active hepatitis continues and may even worsen. Further, levels of serum immunoglobulins, in particular immunoglobulin A class, are elevated with alcoholic hepatitis. This, plus the physical presence of B and T lymphocytes in the portal and periportal areas and the presence of autoantibodies in some patients lead to the conclusion that an immunologic component is an important part of the pathology in alcoholic liver disease.
Clinical course of alcoholic liver disease
The three phases of alcoholic liver disease closely follow those of nonalcoholic liver disease (NALD). Cirrhosis is the end stage; steatosis the initiating stage; and hepatitis the stage during which inflammation does the primary damage. The difference between the two is the inciting factors and the mechanisms that mediate this damage. In NALD it is those factors involved in the metabolic syndrome. In alcoholic liver disease it is ethanol and its metabolites.
These differences are not reflected in the end stage — cirrhosis is roughly equivalent between the two processes. Its clinical presentation with signs of portal hypertension and liver dysfunction, including such entities as esophageal varices and coagulopathies, are shared.
However, alcoholic liver disease has an added component of malnutrition and muscle wasting that is not a part of NALD. Korsakoff’s syndrome and Wernick’e encephalopathy, secondary to thiamine deficiency, are examples of two clinical states that are a reflection of vitamin deficiency that must be addressed in alcoholic hepatitis and not NALD.
Treatment options for alcoholic liver disease
Strict abstinence
Treatment for both conditions centers on avoiding the cause for their origin. In alcoholism, this means strict abstinence — a state that is exceedingly difficult to maintain. Most of the treatment programs for alcoholic liver disease are thus focused on alcoholism since without abstinence, the disease will continue at an accelerated rate.
Immunosuppression
Immunosuppressive therapy with glucocorticoids has been used in some patients with florid alcoholic hepatitis with some success. [2]
Unsubstantiated treatements
To this point, specific medical treatments such as the use of propriothiouricil because the hypermetabolism of alcoholic hepatitis appears to mirror that of thyrotoxicosis have yet to be substantiated as being efficacious. [3]
Keywords: ALCOHOLIC LIVER DISEASE alcoholic steatohepatitis, alcoholic steatonecrosis, sclerosing hyaline necrosis, subacute alcoholic cirrhosis, flapping tremor, nonalcoholic liver disease, NALD
