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Untitled - D Ank Unlimited

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antipapillomavirus antibody 67 anti-PM/Scl autoantibodies<br />

antipapillomavirus antibody<br />

A rabbit antibody against papillomavirus. The structural<br />

antigens on this virus can be detected in a variety of proliferative<br />

squamous lesions. Only 50 to 60% of lesions caused<br />

by papillomavirus will express the structural antigens. This<br />

antibody staining is predominantly intranuclear in a focal<br />

or diffuse pattern, although perinuclear cytoplasmic staining<br />

of koilocytotic cells may also be seen.<br />

antiparathyroid hormone (PTH) antibody<br />

A polyclonal antibody against parathyroid hormone (PTH).<br />

PTH controls the concentration of calcium and phosphate<br />

ions in the blood. A decrease in blood calcium stimulates<br />

the parathyroid gland to secrete PTH, which acts on cells<br />

of bone, increasing the number of osteoclasts and leading<br />

to absorption of the calcified bone matrix and the release<br />

of calcium into the blood. Hyperparathyroidism may be<br />

caused by adenomas, rarely by carcinomas, and by ectopic<br />

PTH production. PTH is released by renal adenocarcinomas<br />

and by squamous cell cancers of the bronchi.<br />

Anti-PCNA antibodies.<br />

anti-PCNAs<br />

Antibodies present in the sera of 3% of systemic lupus<br />

erythematosus (SLE) patients. Epitope mapping reveals that<br />

the antibodies bind conformational epitopes of this antigen.<br />

antiphospholipid antibodies<br />

A heterogeneous group of immunoglobulins directed<br />

against negatively charged phospholipids, protein–phospholipid<br />

complexes, and plasma proteins. Antiphospholipid<br />

antibodies occur in autoimmune disease; bacterial, fungal,<br />

and viral infections; and malignant tumors, or they may<br />

result from use of specific medications or appear in normal,<br />

healthy people. They are associated with both venous and<br />

arterial thrombosis. They occur in systemic lupus erythematosus<br />

(SLE), rheumatoid arthritis, Sjögren’s syndrome,<br />

Reiter’s syndrome, and possibly scleroderma and polyarteritis.<br />

They may appear as a result of HIV, Lyme disease,<br />

ornithosis, adenovirus, rubella and chicken pox, smallpox<br />

vaccination, or syphilis. Refer also to anticardiolipin antibody<br />

syndrome and to lupus anticoagulant.<br />

antiphospholipid syndrome (APS)<br />

An autoimmune disorder characterized by autoantibodies<br />

against constituents of the prothrombin activator complex<br />

requisite for the blood coagulation cascade. A condition with<br />

four common clinical features: venous thrombosis, arterial<br />

thrombosis, pregnancy loss, or thrombocytopenia. Fifty<br />

percent of patients present with primary APS (not associated<br />

with systemic disease), and the remaining 50% have secondary<br />

APS associated with such diseases as systemic lupus<br />

erythematosus (SLE), other connective tissue diseases, HIV<br />

or other infections, malignancy, and drug use. APS is a leading<br />

cause of hypercoagulability and thrombosis. Thrombosis<br />

is the most common presentation of APS. Anticardiolipin<br />

(ACA)-positive APS and lupus anticoagulant (LA)-positive<br />

APS are the two syndromes. ACA-APS is more common<br />

than LA-APS, with a relative prevalence of 5 to 2. Both are<br />

associated with thrombosis, fetal wastage, and thrombocytopenia.<br />

ACA-APC is associated with both arterial and<br />

venous thrombosis including deep vein thrombosis and pulmonary<br />

embolism, premature coronary artery disease, and<br />

premature cerebrovascular disease. By contrast, LA-APS is<br />

more commonly associated with venous thrombosis involving<br />

mesenteric, renal, hepatic, and portal veins and vena<br />

cava. Antiphospholipid antibodies (aPL) are demonstrated<br />

by either prolongation of a phospholipid-dependent coagulation<br />

test (lupus) or by their reactivity to anticoagulant (LA<br />

anionic phospholipids [PL]) in a solid-phase immunoassay.<br />

To diagnose APS, at least one of the above clinical features<br />

and a positive test are required.<br />

Placental alkaline phosphatase (PLAP)⎯placenta.<br />

antiplacental alkaline phosphatase antibody<br />

Placental alkaline phosphatase (PLAP) is normally produced<br />

by syncytiotrophoblasts after the 12th week of pregnancy.<br />

Human placental alkaline phosphatase is a member<br />

of a family of membrane-bound alkaline phosphatase<br />

enzymes and isoenzymes. It is expressed by both malignant<br />

somatic and germ-cell tumors. PLAP immunoreactivity can<br />

be used in conjunction with epithelial membrane antigen<br />

(EMA) and keratin to differentiate between germ cell and<br />

somatic tumor metastases. Germ cell tumors appear to be<br />

universally reactive for PLAP, whereas somatic tumors<br />

show only 15 to 20% reactivity.<br />

antiplatelet antibodies<br />

Autoantibodies that may be induced by drugs such as<br />

amphotericin B, cephalothin, methicillin, pentamidine,<br />

trimethoprim-sulfamethoxizole, and vancomycin.<br />

anti-PM/Scl autoantibodies<br />

Myositis-associated autoantibodies specific for the nucleolar<br />

antigen PM/Scl found among many patients with overlap<br />

syndrome with features such as scleroderma and polymyositis/dermatomyositis<br />

(25%). This autoantibody is found in<br />

a few patients with pure polymyositis or scleroderma. It is<br />

A

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