| immune serum globulin | A sterile solution of globulin's that contains many antibodies normally present in adult human blood; a passive immunizing agent frequently used for prophylaxis against hepatitis A. (05 Mar 2000) |
|---|---|
| testosterone-oestrogen-binding globulin | A glycoprotein migrating as a beta-globulin. Its molecular weight, 52,000 or 95,000-115,000, indicates that it exists as a dimer. The protein binds testosterone, dihydrotestosterone, and estradiol in the plasma. Changes in its concentration significantly affect the ratio of unbound (biologically active) testosterone to estradiol in plasma. (12 Dec 1998) |
| tetanus immune globulin | <protein> A protein antibody to tetanus toxin, given as passive immunity for those lacking any prior tetanus vaccination. (27 Sep 1997) |
| thyroid binding globulin | <protein> Thyroid binding globulin (TBG) is a plasma protein which binds the majority of thyroid hormone in the bloodstream. Bound thyroid hormone is inactive, only the unbound fraction (0.3%) is considered active. Birth control pills and pregnancy can lead to increased TBG levels in the plasma. Androgens can decrease TBG levels in the plasma. (27 Sep 1997) |
| thyroxine-binding globulin | An alpha-globulin of blood with a strong binding affinity for thyroxine; triiodothyronine is bound to it much less firmly; a deficiency or excess of this protein may occur as a rare benign X-linked disorder. Synonym: thyroxine-binding protein. (05 Mar 2000) |
| zoster immune globulin | A globulin fraction of pooled plasma from individuals who have recovered from herpes zoster; used prophylactically and therapeutically for varicella. (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, antinuclear | See: Antinuclear antibodies. (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) |