Biologic response modifiers in primary immunodeficiency disorders
Article Abstract:
Immunity is the complicated mechanism by which the human body protects itself from infectious and malignant diseases. The immune system involves the actions of white blood cells, specifically the B-cells which produce antibodies (proteins that have immune functions), and the T-cells which aid the B-cells and other cells in their immune functions. A number of diseases exist in which there are defects in some aspect of the immune system's ability to fight infection. One of these is severe combined immunodeficiency, SCID, which is caused by defects in both B- and T-cells, and results in severe and often fatal infections in the first few months of life. The most common primary immune deficiency disorder in adults is selective IgA deficiency, in which the antibody Immunoglobulin A is present at reduced levels. While many people with this disorder have few symptoms, others have a high incidence of upper respiratory infections, asthma, and allergies. Another disorder that is characterized by defective T-cells is chronic mucocutaneous candidiasis, which manifests itself in fungal infections of the skin, nails, and mucous membranes. Biologic response modifiers are agents that are given to attempt to modify the immune system's functions, or in the cases of these diseases, the immune system's dysfunctions. Biologic response modifiers include: gammaglobulin, a purified preparation of antibodies that can fight infection and promote other immune processes; H-2 receptor blockers, which block the effects of histamine, a substance active in many immune responses; and retinoids, which are related to vitamin A, and can be given to patients with immune abnormalities due to vitamin A deficiency. Other biologic response modifiers are interferon and interleukin-2, which have been extensively studied in certain cancers and AIDS. One new technique being explored is gene therapy. Immunodeficiency disorders may be caused by the absence of a particular gene. In some cases, these genes have been identified and fused with viruses, which are then injected into the patient. As the immune system is understood, biologic response modifiers will include the treatment of previously untreatable diseases. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Annals of Internal Medicine
Subject: Health
ISSN: 0003-4819
Year: 1991
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Drug-induced disorders of glucose tolerance
Article Abstract:
Many drugs may cause the development of glucose tolerance disorders. Glucose tolerance disorders are a group of disorders that affect glucose metabolism. A survey of studies published in the medical literature since 1966 found that many commonly used drugs can affect glucose metabolism. These drugs can affect glucose metabolism by causing abnormalities in the function of the pancreas, liver or peripheral blood vessels. Drugs that affect glucose metabolism may cause both hypoglycemia or hyperglycemia depending on a different factors at the time of usage. Certain drugs can cause the development of diabetes in patients suffering from impaired glucose tolerance. Drug-induced glucose tolerance disorders can sometimes mimic other disorders and lead to costly and fruitless diagnostic efforts. Discontinuation of treatment with the drug often results in the restoration of normal glucose metabolism.
Publication Name: Annals of Internal Medicine
Subject: Health
ISSN: 0003-4819
Year: 1993
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DNA and the immune system
Article Abstract:
Results from recent studies suggest that the genetic coding material called deoxyribonucleic acid (DNA) may also play a role in triggering the immune response. Different forms of antibodies to certain bacterial DNA have been found in patients with systemic lupus erythematosus that are not found in healthy volunteers. These findings may have implications for how lupus is treated, how future vaccines against other conditions are formulated, and how the immune system pathways are understood.
Publication Name: Annals of Internal Medicine
Subject: Health
ISSN: 0003-4819
Year: 1997
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