Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pleural involvement in drug-induced lupus erythematosus is not uncommon. Lupus erythematosus cells were found in vivo in the pleural of an elderly patient who had received procainamide (Pronestyl) hydrochloride (2 gm daily) for nine months. Patients who initially have pleural effusions while receiving drugs capable of inducing lupus erythematosus should have the fluid analyzed for lupus erythematosus cells to help clarify the cause of the effusion.
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PMID:Drug-induced lupus erythematosus with in vivo lupus erythematosus cells in pleural fluid. 7 54

Sera from 11 (65%) of 17 patients with newly diagnosed procainamide-induced lupus contained cold-reactive lymphocytotoxic antibodies to normal human lymphocytes in titres of 1/2 to 1/128. In contrast, only 3 of 15 patients on long-term procainamide therapy without lupus and 3 of 65 normal men had serum lymphocytotoxic antibodies, none at a titre higher than 1/2. Antibody levels in the lupus patients declined quickly after procainamide was stopped, in parallel with their clinical improvement. Procainamide (3.75 x 10(-3) mol/l) suppressed by more than 80% in-vitro phytohaemagglutinin-induced 3H-thymidine incorporation by normal human blood lymphocytes. At 3.75 x 10(-4) mol/l, procainamide enhanced the mitogenic response to 160 +/- 20% of normal. Thus procainamide may interact with the lymphocyte membrane, possibly producing a lupus syndrome directly, by altering lymphocyte function, or indirectly, by generating autoantibodies reactive with normal membrane structures.
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PMID:Lymphocyte alteration by procainamide: relation to drug-induced lupus erythematosus syndrome. 9 Sep 17

The existence of iatrogenic lupus is now well-established and seems to be on the increase. A number of drugs must take the blame for these outbreaks: Hydrazine derivatives (Hydralazine, I.N.H.), anticonvulsants, Procainamide, psychotropics, antibiotics, antalgics, contraceptives. Clinically, these drugs can: --either mimic L.E. without showing any visceral or biological signs; --or aggravate a chronic L.E., or a systemic L.E. during a remission with biological symptoms appearing; --or trigger a true L.E.: all the various clinical symptoms of idiopathic L.E. may be encountered, certain articular, cutaneous symptoms predominating, renal symptoms rarely appearing. The discovery of HARGRAVES cells is the only certain biological sign to confirm systemic lupus, the existence of antinuclear antibodies or antinuclear factors merely serving as a guide to the collecting of a whole gamut of clinical and biological symptoms.
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PMID:[Iatrogenic lupus-like syndromes]. 13 11

Procainamide, a frequently sued antiarrhythmic agent, may produce a syndrome clinically indistinguishable from idiopathic lupus erythematosis. Pericarditis with or without effusion is occasionally a prominent manifestation of the disease, but cardiac tamponade is exceptional. The patient described had a clinically evident and laboratory confirmed drug-induced syndrome complicated by an unusually severe pericarditis with effusion and tamponade necessitating pericardiocentesis. Treatment with prednisone produced impressive amelioration of the pericarditis with no recurrence of the lupus erythematosis syndrome during a prolonged period of observation following cessation of corticosteroid therapy. Prompt initation of steroid treatment in drug-induced lupus erythematosus complicated by massive pericardial effusion is strongly suggested by this experience.
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PMID:Pericardial tamponade. A presenting manifestation of procainamide-induced lupus erythematosus. 112 94

Procainamide is the commonest cause of a drug induced lupus syndrome. Long term administration of this compound may induce a variety of immunological abnormalities, including antinuclear antibodies. Uncommonly, 'lupus anticoagulants' have been demonstrated in the absence of other evidence of drug induced lupus. Details of a 67 year old man who developed not only drug induced lupus but also antiphospholipid antibodies which were associated with multiple pulmonary thromboemboli after the administration of procainamide are recorded.
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PMID:Pulmonary thromboembolism associated with procainamide induced lupus syndrome and anticardiolipin antibodies. 249 58

Systemic lupus erythematosus (SLE) is known to cause various forms of ocular problems, including severe retinal vaso-occlusive disease. Procainamide is one of many drugs that may cause a lupus-like syndrome which resembles SLE but can be distinguished through clinical features and laboratory studies. Presented is a patient with severe vaso-occlusive retinopathy on high-dose procainamide therapy. Associated clinical, laboratory, and pathologic findings suggest the diagnosis of drug-induced lupus and exclude other vasculitic or inflammatory etiologies. This represents the first documented case of retinal disease attributed to procainamide-induced lupus.
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PMID:Severe retinal vaso-occlusive disease secondary to procainamide-induced lupus. 258 49

We report the case of a patient with myotonic dystrophy who developed tachypnea and severe dyspnea without respiratory failure. Myotonia of inspiratory muscles was diagnosed on the grounds of marked prolongation of transdiaphragmatic pressure (Pdi) decay during sniffs. In view of the recognized sensory role of inspiratory muscles in dyspnea, it was hypothesized that antimyotonic therapy might relieve dyspnea in this patient. Procainamide therapy induced a decrease in half relaxation time of Pdi during sniffs and yielded a striking clinical improvement with cessation of tachypnea and dyspnea. Later, this beneficial effect was maintained by tocainide after procainamide was stopped because of a lupus syndrome. We conclude that myotonia of respiratory muscles can cause severe dyspnea that can be improved by antimyotonic therapy.
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PMID:Procainamide for dyspnea in myotonic dystrophy. 281 10

The specific factors predisposing to thrombosis in patients with LAs have not been resolved. With extensive cross-reactivity, and several proposed sites of action, LAs and their effects may be heterogeneous. While the risk of thrombosis with phenothiazine-induced LAs is probably low, the incidence of thrombosis in association with procainamide-induced LAs is uncertain. Procainamide is a commonly used antiarrhythmic drug associated with the induction of autoantibodies, and occasionally with a lupus-like syndrome. Serologic and coagulation profile monitoring may be required to detect patients in whom LAs develop since these individuals may be at increased risk for thrombosis. Monitoring may be especially important in patients who are receiving procainamide and who have atherosclerosis and cardiac disease, since they may be at increased risk for thrombosis of coronary and other arteries. Future prospective studies are needed to investigate whether the development of lupus anticoagulants during procainamide therapy increases the risk of thrombosis.
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PMID:Procainamide-induced lupus anticoagulants and thrombosis. 312 75

Procainamide is a widely used antiarrhythmic that is fraught with therapeutic limitations such as a short half-life, production of autoimmune antibodies and a lupus-like syndrome, and complex pharmacokinetics. We synthesized the congeners of procainamide possessing one or two methyl substituents ortho to the 4-amino moiety (compounds 4 and 5, respectively), in order to sterically encumber the 4-amino substituent and prevent or diminish the rate of metabolic N-acetylation. Moreover, we anticipated that this structural alteration might eliminate the autoimmune toxicities associated with procainamide. Like procainamide, the two methylated analogues significantly reduced the rate of rise and amplitude of the action potential when studied in isolated canine Purkinje fibers. Whereas procainamide caused no significant change in action potential duration (APD), both methylated congeners significantly reduced APD at 70% and 95% repolarization. Moreover, the dimethylated congener was significantly more efficacious than procainamide in reducing ERP (effective refractory period) and increasing the ERP/APD70. The ability of these compounds to block ouabain-induced arrhythmias was studied in anesthetized dogs. Addition of two methyl groups ortho to the amine produced an increase in potency: The conversion doses for procainamide and the monomethyl and dimethyl congeners were 19.0, 18.3, and 14.3 mg/kg, respectively, following iv administration. After iv administration to rats, procainamide was extensively metabolized to N-acetylprocainamide and displayed a half-life of 0.4 h. In contrast, dimethylprocainamide was not metabolized by N-acetylation, had a half-life of 1.4 h, and provided greater peak plasma concentrations. Thus, addition of methyl substituents ortho to the 4-amino group of procainamide alters the electrophysiological characteristics of the compound, increases its potency against ouabain-induced arrhythmias in vivo, increases its plasma half-life, and prevents N-acetylation.
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PMID:Electrophysiologic and antiarrhythmic activities of 4-amino-N-[2-(diethylamino)ethyl]-3,5-dimethylbenzamide, a sterically hindered procainamide analogue. 338 24

Procainamide-induced lupus is a well-recognized syndrome, but the events leading up to clinical symptoms are obscure. In the present study, serologic changes in a 69-year-old man were monitored during his treatment with procainamide and after discontinuation of procainamide because of symptoms of drug-induced lupus. Antihistone antibodies of unique specificity and in vivo complement activation were detected after one year of procainamide therapy during a period prior to development of significant clinical symptoms. Antihistone antibodies and complement activation substantially increased during a full-blown episode of lupus-like symptoms. Progressive return to normal laboratory findings occurred after procainamide was discontinued. The antihistone/complement profile may be useful in the diagnosis of drug-induced lupus and warn of impending clinical deterioration in patients with minimal symptoms.
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PMID:Serologic changes during induction of lupus-like disease by procainamide. 370 85


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