| ANA | acetylneuraminic acid; American Narcolepsy Association; American Neurological Association; American ... |
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| ANF | alpha-naphthoflavone; American Nurses' Foundation; antineuritic factor; antinuclear factor; atrial n... |
| ANuA | antinuclear antibody |
| FANA | fluorescent antinuclear antibody |
| LSANA | leukocyte-specific antinuclear antibody |
| ANAs | Antinuclear antibodies |
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| FANA | Fluorescent antinuclear antibodies |
| AEA | A-anti-endomysium antibodies |
| ANCA | Anti-Neutrophil Cytoplasmic Antibodies |
| ACA | Anti-cardiolipin antibodies |
| antibodies, antinuclear | See: Antinuclear antibodies. (12 Dec 1998) |
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| antinuclear | Having an affinity for or reacting with the cell nucleus. (05 Mar 2000) |
| antinuclear antibody | <immunology> Antinuclear antibody is an antibody that react against components of the cell nucleus such as DNA, RNA, histone or non-histone proteins. These antibodies are present in a variety of immunologic or autoimmune diseases including systemic lupus erythematosus, systemic sclerosis, scleroderma, Sjogren's syndrome, rheumatoid arthritis, polymyositis, dermatomyositis and in persons taking hydralazine, procainamide or isoniazid. A serologic measurement for antinuclear antibodies can aid in the diagnosis of unexplained arthritis, rashes or chest pains. Acronym: ANA (12 Jan 1998) |
| antinuclear factor | A factor, usually antibodies, present in serum with strong affinity for nuclei and detected by fluorescent antibody technique; present in lupus erythematosus, rheumatic arthritis, and certain other autoimmune conditions; may also be present at lower levels in normal individuals. (05 Mar 2000) |
| fluorescent antinuclear antibody test | FANA test, a test for antinuclear antibody components; used, in particular, for the diagnosis of collagen-vascular diseases. (05 Mar 2000) |
| acetylcholine receptor antibodies | <neurology, investigation> A test used to measure the amount of antibodies to acetylcholine receptors on nerve endings. This is a diagnostic test for myasthenia gravis. A normal value is no antibodies in the bloodstream. Acetylcholine receptor (AChR) binding autoantibodies (i.e. Antibodies reactive with several epitopes other than the binding site for acetylcholine or alpha-bungarotoxin) are present in approximately 88% of patients with generalised myasthenia gravis, 70% of ocular myasthenia and in approximately 80% of myasthenia gravis in remission. Although serum concentrations of AChR binding autoantibodies do not in general correlate well with severity of weakness, there is typical decrease in concentration as weakness improves with immunosuppressive therapy. AChR blocking autoantibodies (i.e., antibodies reactive with the AChR binding site) are present in about 50% of patients with myasthenia gravis, 30% with ocular myasthenia gravis and 20% of myasthenia gravis in remission, AChR blocking autoantibodies are the only AChR autoantibodies present in about 1% of myasthenia gravis. AChR modulating autoantibodies (i.e., autoantibodies which cross-link AChRs and cause their removal from muscle membrane surfaces) are present in more than 90% of myasthenia gravis and occasionally are the only AchR autoantibodies detectable in mild, recent onset or ocular-restricted myasthenia gravis. Results for AChR modulating autoantibodies can be transiently false-positive due to curare-like drugs used during general anesthesia. AChR autoantibodies of one or more types are found in at least 80% of ocular myasthenia gravis. Although generally absent in neurological conditions other than myasthenia gravis(and consequently unlikely to cause confusion in neurodiagnosis), false-positive results for AChR autoantibodies occasionally occur in primary biliary cirrhosis, tardive dyskinesia, autoimmune thyroiditis, the elderly, amyotrophic lateral sclerosis patients treated with cobra venom and patients with thymoma in the absence of myasthenia gravis. Approximately 1% of patients with rheumatoid arthritis treated with D-penicillamine develop AChR autoantibodies and myasthenia gravis, both of which disappear when the drug is discontinued. Babies born to ~10% of myasthenia gravis mothers have a transient neonatal form of myasthenia gravis that responds well to anticholinesterase therapy and usually remits within 1 month as maternal IgG disappears. (29 Dec 1997) |
| antibodies | Any of numerous protein molecules produced by the B-cells as a primary immune defense. (16 Dec 1997) |
| antibodies, anticardiolipin | Antiphospholipid antibodies found in association with systemic lupus erythematosus (lupus erythematosus, systemic), antiphospholipid syndrome, and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase immunoassay employing the purified phospholipid antigen cardiolipin. (12 Dec 1998) |
| antibodies, anti-idiotypic | Antibodies which react with the individual structural determinants (idiotopes) on the variable region of other antibodies. (12 Dec 1998) |
| antibodies, antineutrophil cytoplasmic | Autoantibodies directed against cytoplasmic constituents of polymorphonuclear leukocytes and/or monocytes. They are used as specific markers for wegener's granulomatosis and other diseases, though their pathophysiological role is not clear. Anca are routinely detected by indirect immunofluorescence with three different patterns: c-anca (cytoplasmic), p-anca (perinuclear), and atypical anca. (12 Dec 1998) |
| antibodies, antiphospholipid | Autoantibodies directed against phospholipids. These antibodies are characteristically found in patients with systemic lupus erythematosus (lupus erythematosus, systemic), antiphospholipid syndrome, related autoimmune diseases, some non-autoimmune diseases, and also in healthy individuals. (12 Dec 1998) |
| antibodies, archaeal | Immunoglobulins induced by substances elaborated by archaea that have an antigenic activity. (12 Dec 1998) |
| antibodies, bacterial | Immunoglobulins induced by substances elaborated by bacteria that have an antigenic activity. (12 Dec 1998) |
| antibodies, bispecific | Antibodies, often monoclonal, in which the two antigen-binding sites are specific for separate antigenic determinants. They are artificial antibodies produced by chemical crosslinking, fusion of hybridoma cells, or by molecular genetic techniques. They function as the main mediators of targeted cellular cytotoxicity and have been shown to be efficient in the targeting of drugs, toxins, radiolabelled haptens, and effector cells to diseased tissue, primarily tumours. (12 Dec 1998) |
| antibodies, blocking | Antibodies that inhibit the reaction between antigen and other antibodies or sensitised T-lymphocytes (e.g., antibodies of the IgG class that compete with IgE antibodies for antigen, thereby blocking an allergic response). Blocking antibodies that bind tumours and prevent destruction of tumour cells by cytotoxic T-lymphocytes have also been called enhancing antibodies. (12 Dec 1998) |
| antinuclear antibodies |
ABBR: ANA. A group of autoantibodies that react against normal components of the cell nucleus. These antibodies are present in a variety of immunologic diseases, including systemic lupus erythematosus, progressive systemi
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