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Antinuclear antibody

Activated partial thromboplastin time, anticardiolipin antibody,° antinuclear and other autoantibodies... [Pg.175]

In addition to the toxic effects indicated for propranolol, acebutolol may produce hair loss and elevate antinuclear antibody titers (32). [Pg.119]

Oxyphenbutazone (712), y-hydroxyphenylbutazone and kebuzone (715) are metabolites of phenylbutazone in liver. The first cited is an equally potent antiinflammatory agent but slightly less toxic. Compounds (711) and (712) are rarely used as analgesics and antipyretics because of their toxicities. The first one is used in therapy of rheumatoid disorders characterized by a lack of detectable antiglobulin and antinuclear antibodies in the serum. The y-hydroxyphenylbutazone has marked uricosuric activity but little antirheumatic effect. Kebuzone (715) is an antiinflammatory agent still widely used in Europe. [Pg.296]

Hydantoln anticonvulsants may cause the appearance of positive L.E. cells and methemoglobinemia. Chloropromazlne has been Implicated In causing a syndrome like systemic lupus erythematosus with accompanying positive tests for L.E. cells and antinuclear antibodies (6). [Pg.275]

Kilbum KH, Warshaw RH. 1992. Prevalence of symptoms of systemic lupus erythematosus (SLE) and of fluorescent antinuclear antibodies associated with chronic exposure to trichloroethylene and other chemicals in well water. Environ Res 57 1-9. [Pg.273]

A 5. 5-year-oId male has recurrent ventricular arrhythmias after an Ml, for which he is given an antiarrhythmic agent that blocks Na+ channels and prolongs the action potential. One year later, a blood, test is positive for circulating antinuclear antibodies. [Pg.115]

The answer is c. (Hardman, p 868. Katzung, pp 231—232) Procainamide blocks open Na+ channels. Long-term therapy can result in drug-induced lupus syndrome, identified by circulating antinuclear antibodies. Many patients may develop a facial rash and joint pains. Pericarditis can occur, but renal involvement is rare. [Pg.130]

In selected circumstances and secondary headache presentation, serum chemistries, urine toxicology profiles, thyroid function tests, lyme studies, and other blood tests, such as a complete blood count, antinuclear antibody titer, erythrocyte sedimentation rate, and antiphospholipid antibody titer may be considered. [Pg.614]

Woosley, R.L. et al., Effect of acetylator phenotype on the rate at which procainamide induces antinuclear antibodies and the lupus syndrome, New Engl. J. Med., 298, 1157, 1978. [Pg.464]

Monestier, M., Novick, K.E., and Losman, M.J., D-penicillamine- and quinidine-induced antinuclear antibodies in A.SW (H-2s) mice Similarities with autoantibodies in spontaneous and heavy metal-induced autoimmunity. Eur. J. Immunol., 24, 723, 1994. [Pg.483]

Robinson, C.J., Balazs, T., and Egorov, I.K., Mercuric chloride-, gold sodium thiomalate-, and D-penicillamine-induced antinuclear antibodies in mice. Toxicol. Appl. Pharmacol., 86, 159, 1986. [Pg.483]

In the circulation of the BN rat there is a simultaneous and transient presence of antiglomerular basement membrane antibodies and circulating immune complexes [175]. Another characteristic is a striking increase in total and antigen-specific IgE level [190], which also has been found in Hooded Lister rats [ 191 ], as well as anti-single-stranded DNA antibodies [ 181] in the BN rat. In PVG/C rats [192, 193], mercuric chloride also induced glomerulopathi and antinuclear antibodies directed against non-histone nucleoprotein. [Pg.202]

Perry, H.M., Tane, M. and Camody, S. (1970). Relationship of acetyl transferase activity to antinuclear antibodies and toxic symptoms in hypertensive patients treated with hydralazine. J. Lab. Clin. Med. 76 114-125. [Pg.593]

Weeping, J.J., Fleuren, G.J. and Hoedemaeker, J. (1978). Demonstration of antinuclear antibodies in mercuric chloride-induced glomerulopathy in the rat. Lab. Invest. 39 405-411. [Pg.594]

The prolonged administration often leads to the development of a positive antinuclear antibody (ANA) test, with or without symptoms of a lupus erythematosus-like syndrome. If a positive ANA titer develops, assess the benefit/risk ratio related to continued procainamide therapy. [Pg.427]

Perform complete blood counts and antinuclear antibody (ANA) titer determinations before and during prolonged therapy, even in the asymptomatic patient. These studies also are indicated if the patient develops arthralgia, fever, chest pain, continued malaise, or other unexplained signs or symptoms. If the ANA titer reaction is positive, carefully weigh benefits to be derived from hydralazine. [Pg.565]

Lupus erythematosus Certain patients will develop a positive antinuclear antibody (ANA) test and some may show a lupus erythematosus-like syndrome similar to other drug-induced lupus, but it is not associated with hypocomplementemia and may be present without nephropathy. A positive ANA test does not mandate drug discontinuance however, a lupus erythematosus-like syndrome may develop later. Sensitivity reactions Once instituted for Wilson s disease or cystinuria, continue treatment with penicillamine on a daily basis. Interruptions for even a few days have been followed by sensitivity reactions after reinstitution of therapy. [Pg.653]

Antinuclear antibodies negative at 1 10 dilution of serum negative at 1 10 dilution of serum... [Pg.2119]

CNS toxicity occurs because isoniazid has structural similarities to pyridoxine (vitamin Be) and can inhibit its actions. This toxicity is dose-related and more common in slow acetylators. Manifestations include peripheral neuropathy, optic neuritis, ataxia, psychosis and seizures. The administration of pyridoxine to patients receiving INH does not interfere with the tuberculostatic action of INH but it prevents and can even reverse neuritis. Hematological effects include anaemia which is also responsive to pyridoxine. In some 20% of patients antinuclear antibodies can be detected but only in a minority of these patients drug-induced lupus erythematosus becomes manifest. [Pg.417]

This syndrome is characterized by proteinuria >3.5 g/day, hypoalbuminuria <3 g/dl, hyperlip-idaemia with an elevation of serum cholesterol, edema and oval fat bodies and fatty casts in the urinary sediment. A variety of disorders may produce nephrotic syndrome but, in the majority of cases, no cause is found. It is appropriate to define the selection of studies from the history and physical examination. Tests to order are antinuclear antibody, rheumatoid factor, cryoglobulins, serum complement, HBsAg VDRL serology (syphilis), protein electrophoresis of the serum and urine and HIV. If the cause is unclear a renal biopsy is done to define the glomerular lesion as treatment may on the underlying glomerular lesion. [Pg.613]

Skin rashes have been reported, as has an increase in the titer of antinuclear antibodies. Despite the latter observation, the appearance of a systemic lupus syndrome is rare. Labetalol also has been reported to interfere with chemical measurements of catecholamines and metabolites. [Pg.117]

Long-term drug use leads to increased antinuclear antibody titers in more than 80% of patients more than 30% of patients receiving long-term procainamide therapy develop a clinical lupus erythematosus-like syndrome. The symptoms may disappear within a few days of cessation of procainamide therapy, although the tests for antinuclear factor and lupus erythematosus cells may remain positive for several months. [Pg.173]

The most common adverse reaction to etanercept is mild to moderate erythema, pain, or pruritus at the injection site (37%). Headaches and abdominal pain can also occur. New positive autoantibodies, such as antinuclear antibodies (ANA), anti-dsDNA antibodies, and anticardiolipin antibodies, can develop in patients treated with etanercept. Although there is so far no association between this and the development of autoimmune diseases or malignancies, long-term studies have yet to be done. Rare cases of pancytopenia may be associated with this drug. Although clinical trials showed no increased risk of infection with etanercept treatment, postmarketing reports of serious infections, sepsis, and associated fatalities exist. [Pg.435]

Injection site reactions characterized by mUd to moderate erythema, itching, burning, and/or pain occur in approximately one-third of patients but rarely necessitate drug discontinuation. The impact of etanercept on the host s response to new or chronic infections is not fully understood. Serious infections and sepsis, including fatalities, have been reported in patients treated with etanercept. Increased levels of autoantibodies, including antinuclear antibodies and anti-double-stranded DNA antibodies, have also been reported, but the clinical significance of this observation is unknown. [Pg.495]


See other pages where Antinuclear antibody is mentioned: [Pg.644]    [Pg.2019]    [Pg.808]    [Pg.778]    [Pg.644]    [Pg.2019]    [Pg.808]    [Pg.778]    [Pg.241]    [Pg.957]    [Pg.1545]    [Pg.1553]    [Pg.274]    [Pg.46]    [Pg.55]    [Pg.444]    [Pg.455]    [Pg.203]    [Pg.556]    [Pg.559]    [Pg.384]    [Pg.191]    [Pg.552]    [Pg.347]    [Pg.1370]   
See also in sourсe #XX -- [ Pg.597 ]




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Antinuclear antibodies, drug-induced

Antinuclear antibodies, drug-induced autoimmunity

Antinuclear antibody lupus erythematosus

Antinuclear antibody procainamide

Minocycline antinuclear antibody

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