Do viruses contribute to the development of Sjogren's syndrome?
Article Abstract:
Primary Sjogren's syndrome (SS) is an autoimmune disease, the type of disease in which immune cells and factors attack the body's own tissues. SS is characterized by chronic inflammation and has similar symptoms to those of Hashimoto's thyroiditis (characterized by an enlarged thyroid gland and abnormally decreased activity of the thyroid) and systemic lupus erythematosus (a chronic inflammatory disease of the connective tissue). Patients with SS have: various types of abnormal immune proteins called autoantibodies; overgrowth of lymphocytes, a type of immune cell; and defective function of immune T-cells. Some patients with SS develop cancers of the immune B-cells. The cause of SS may be related to genetic and viral factors. Studies have attempted to define the genes located in the major histocompatibility complex (MHC) that enhance the immune responses and activate the formation of autoantibodies in patients with SS. Some studies have shown an increased incidence of DNA or antigens, elements that provoke an immune response, from Epstein-Barr virus (EBV) in patients with SS. In addition, the EBV has been shown to activate immune B cells. EBV, which infects immune B cells, may promote lymphocyte proliferation and thereby help in the maintenance and progression of SS. Evidence suggests that patients with SS may also be infected with A-type retrovirus. A-type retrovirus may infect immune T-cells. Studies and animal models support a relationship between retroviral infection and autoimmunity. The interaction between MHC and other genes and a virus or viruses is thought to be involved in the pathogenesis of SS, and requires further investigation. (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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Nephrotic syndrome in a 76-year-old man
Article Abstract:
A case is described of a 76-year-old man who was admitted to the hospital for treatment of nephrotic syndrome. This condition results from damage to the walls of the small blood vessels (capillaries) in the glomerulus, the portion of the kidney that filters blood. The patient had proteinuria, or protein in the urine, and edema, or the accumulation of fluid in the tissues, which persisted despite treatment with the drugs furosemide and prednisolone. Chest X-rays revealed mild cardiomegaly, or slight enlargement of the heart, leakage of fluid into the lung cavity, areas of lung collapse, and cell and fluid accumulation in the lung. Tests to monitor the electrical activity of the heart showed abnormal heart rhythms. The patient was suspected of having amyloid based on abnormalities of the heart, including its enlargement; disorders of the kidney; proteinuria (which occurs in 82 percent of patients with amyloid); and urinary excretion of light chains, which are portions of immunoglobulin, a type of immune protein (a finding in 72 percent of patients with amyloid). Tissue microscopic examination of the kidney confirmed the diagnosis of amyloidosis of the kidney. Amyloidosis is a metabolic disorder characterized by the deposition of a starch-like substance called amyloid in several tissues. The disease is thought to result from abnormalities in the production of immunoglobulins, and may or may not be associated with a chronic disease. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
User Contributions:
Comment about this article or add new information about this topic:
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