Autoimmunity and alcoholic liver disease

Article Abstract:

The relationship between chronic alcohol consumption and severe liver injury is not clear, although several mechanisms linking the liver disease process to alcohol consumption have been suggested. These include a direct toxic effect of ethanol; enhanced lipid peroxidation, a highly reactive and potentially damaging chemical reaction; the deprivation of oxygen in liver tissue; and malnutrition. Ethanol may also induce autoimmunity, an abnormal condition in which the body's natural defense system attacks the body's own tissues. However, liver injury often progresses despite discontinuation of alcohol intake, suggesting that other factors in addition to alcohol are causing the damage. There is a shorter period of time between resumption of alcohol abuse and recurrence of liver disease, suggesting that an alcohol-related process can be reactivated. In addition, alcoholic liver disease is associated with high levels of immunoglobulins, a type of immune protein, and immune complexes, which consist of antigen bound to antibody. Antigens are elements that provoke the production of antibodies, immune proteins that normally inactivate foreign particles. Alcoholic hepatitis is the inflammation of the liver characterized by the accumulation of various immune and inflammatory cells in the liver tissue. This condition is thought to be an intermediate step before the development of cirrhosis, an advanced liver disease characterized by abnormal structural changes in liver tissue. In addition to the high levels of immunoglobulins, autoantibodies or abnormal immune proteins that attack body factors such as elements of the cell nucleus and smooth muscle have also been detected. Other immune abnormalities include altered delayed hypersensitivity reactions; changes in the bodily distribution of T cells, a type of immune cell; toxic effects of immune cells on liver cells; and ability of naturally-occurring substances such as hyalin, liver-specific proteins, and acetaldehyde to act as antigens and trigger an immune response. Various aspects of the role of autoimmunity in alcoholic liver disease must be investigated further. (Consumer Summary produced by Reliance Medical Information, Inc.)

Analysis, Autoimmune diseases, Liver cirrhosis, editorial, Hepatitis, Alcoholic, Alcoholic hepatitis

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Consensus development conference: prophylaxis and treatment of osteoporosis

Article Abstract:

Osteoporosis is a condition that is characterized by a reduction in bone mass and an increased risk of fractures. It is estimated that osteoporosis is the cause of more than 1.3 million fractures per year in the United States, and affects one out of every three postmenopausal women. Hip fractures and spine fractures are leading causes of illness and death in the elderly. Approximately 12 to 20 percent of elderly patients with hip fracture die within one year of the injury. Those at greatest risk for developing osteoporosis are white and Asian women who are thin and have a family history of the disease. Other risk factors associated with osteoporosis include calcium deficiency, smoking, alcohol abuse, and sedentary lifestyle. The main cause of bone loss in postmenopausal women is a deficiency of the hormone estrogen. For diagnosis, bone mass can be measured using noninvasive techniques such as photon absorptiometry and computed tomography. Estrogen prevents bone loss and is the best therapy for osteoporosis. Also, calcitonin is used to reduce bone loss and to help ease the pain associated with bone fracture. Maintaining adequate dietary levels of calcium (at least 800 milligrams per day for adults) is important, but is not a substitute for estrogen therapy. Fluoride, anabolic steroids and parathyroid hormone are treatments that increase bone mass and may be beneficial in treating osteoporosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Bones, Diagnosis, Risk factors, Drug therapy, Fractures (Injuries)

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Ethanol reduces bone formation and may cause osteoporosis

Article Abstract:

Weakness of the bones in alcoholics (ethanol-associated osteopenia) is not fully understood. This paper explores the role that ethanol consumption may have in producing this condition in alcoholic patients with alcoholic liver disease. Twenty-eight patients who continued to drink alcohol, and 12 who claimed to have not consumed alcohol for at least 6 months were studied. Non-alcoholic control subjects (35) without evidence of liver disease were also included in this study. Various measurements of bone health were used (including biopsy and biochemical and endocrinologic tests). Bone mineral levels were significantly lower in alcoholic patients than in the controls. There was no difference between those which continued to drinking or those which had abstained for 6 months. However the drinkers had less bone formation than the abstainers. Both groups of drinkers had similar levels of bone resorption, a kind of bone loss. The authors conclude that ethanol may be responsible for a dysfunction resulting from a reduction in new bone formation and bone mineralization.

Alcohol, Ethanol

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