Autoantibodies in alcoholic liver disease
Article Abstract:
Autoimmune diseases are disorders in which immune cells and factors attack body tissues. Chronic active hepatitis (CAH), the chronic inflammation of the liver, and systemic lupus erythematosus (SLE), a chronic inflammatory disease of connective tissue, are autoimmune diseases with similar immunological characteristics. Autoantibodies are abnormal immune proteins that specifically bind and attack tissues and body factors such as the genetic material of the cell, deoxyribonucleic acid (DNA), or components of the cell nucleus. Autoantibodies to DNA and to nuclear elements have been detected in both CAH and SLE. Antinuclear antibodies have been identified in patients with liver disease due to alcohol abuse. The role of autoimmunity in the pathogenesis, or disease process, of alcoholic liver disease (ALD) was assessed in 47 patients with ALD. Autoimmunity was assessed by the presence of antibodies to lymphocytes, which are immune cells, and by the degree of lymphocytotoxicity, or adverse effects on lymphocytes. The results were compared with measurements from 20 alcoholics without ALD and 28 patients with autoimmune CAH. Antinuclear antibodies were identified in 22 percent of patients with ALD and 71 percent of patients with CAH. Antibodies to DNA were detected in 60 percent of patients with ALD, which was slightly more than in patients with CAH. The presence of a particular antibody, immunoglobulin M (IgM), against lymphocytes serves as a marker of autoimmunity. Antilymphocyte antibodies were detected in 72 percent of patients with CAH and 59.6 percent of patients with ALD. Lymphocytotoxicity was present in 90 percent of blood samples from ALD and CAH patients. All three types of autoantibodies to nuclear elements, DNA, and lymphocytes were detected in 32 percent of patients with CAH and 25.5 percent of patients with ALD. These findings are consistent with a role of autoimmunity in the pathogenesis of ALD in some patients. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
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The lung mucosa: a critical environmental battleground
Article Abstract:
The mucous membranes that form the inner lining of the lung air passages are constantly exposed to dust particles, gases, and vapors that are present in the air. These membranes are covered with small tube-like structures called cilia. The cilia wave back and forth and clear excess mucous and dust particles out of the lungs. When the cilia become damaged, as they do in certain types of obstructive lung diseases, it becomes difficult to clear mucous and dust from the lungs. This means that people with lung disease are more sensitive to environmental air pollutants. The ability of dust particles to enter the lungs depends on their size. Particles between 10 and 100 microns in diameter become trapped in the nose, but particles less than 5 microns can pass directly into the lungs. Recent studies have reported that ozone can have adverse effects on the lungs. Ozone is formed in the air when sunlight interacts with hydrocarbon aerosols. Some of the cities located in the sunbelt region have ozone levels that are three times higher than the established federal standards. Ozone has been reported to cause more mucous to be produced in the lungs, which may limit the flow of air in the lungs. This can have serious consequences for people with asthma or other forms of lung disease. Several studies have reported that inhaling air containing large amounts of ozone, as may occur during certain exercise, reduces the ability of the lungs to function and reduces exercise performance. Also, ozone has been shown to reduce lung function during exercise in patients with asthma and obstructive lung disease. Further studies are needed to define the exact relationship between atmospheric ozone and lung function in people with and without lung disease. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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Myocardial infarction, cardiomyopathy, and interstitial lung disease in a 38-year-old man
Article Abstract:
A case is described of a 38-year-old man who developed cardiomyopathy (disease of the heart muscle) and pulmonary infiltrates (accumulation of fluid within the lung). The patient had a heart attack in March 1988 and was shown to have narrowing of the left main coronary artery. The function of the left ventricle was depressed and the heart was enlarged. Coronary bypass surgery was performed, which is an operation to restore blood flow to the heart, and the patient was placed on therapy with steroids to prevent inflammation of the aorta and pericardium (a membrane that surrounds the heart). A biopsy of heart tissue taken during surgery revealed fibrosis, the formation of fiber-like tissue. In September 1988, the man developed heart failure and did not improve despite treatment with antibiotics for possible infection of the lungs. He had an enlarged heart and persistent infiltrates in the right mid-lung area. The patient was diagnosed with fibrosing mediastinitis, the inflammation of the mediastinum (the mass of tissue including the heart and associated blood vessels that separate the lungs). The mediastinitis was associated with fibrosis, and resulted in heart attack, cardiomyopathy, congestive heart failure, and pulmonary infiltration. The pathologic findings and X-ray studies are reviewed. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
User Contributions:
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