Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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-induced systemic lupus erythematosus (SLE) is a well recognized clinical syndrome believed to be characterized by normocomplementemia. However, in 7 cases of drug-induced SLE recorded in the literature, hypocomplementemia was found. The present report concerns a well documented case of procainamide-induce SLE with hypocomplementemia. The patient improved and complement values returned to normal after procainamide therapy was discontinued and replaced by digitalis and steroid therapy.
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PMID:Procainamide-induced systemic lupus erythematosus with hypocomplementemia. 85 6

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 and hydralazine inhibit T cell DNA methylation and induce autoreactivity in cloned CD4+ T cells. These drugs also induce an autoimmune syndrome, suggesting a possible relationship between DNA hypomethylation, T cell autoreactivity, and certain autoimmune diseases. To test this relationship, DNA methylation was studied in T cells from patients with rheumatoid arthritis and patients with systemic lupus erythematosus, and was found to be impaired. These results support a relationship between DNA hypomethylation and some forms of autoimmune disease.
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PMID:Evidence for impaired T cell DNA methylation in systemic lupus erythematosus and rheumatoid arthritis. 224 63

Quinidine, procainamide and disopyramide are antiarrhythmic drugs in the class 1A category. These drugs have a low toxic to therapeutic ratio, and their use is associated with a number of serious adverse effects during long term therapy and life-threatening sequelae following acute overdose. Class 1A agents inhibit the fast inward sodium current and decrease the maximum rate of rise and amplitude of the cardiac action potential. Prolonged Q-T interval and, to a lesser extent, QRS duration may be observed at therapeutic concentrations of quinidine. With increasing plasma concentrations, progressive depression of automaticity and conduction velocity occur. 'Quinidine syncope' (a transient loss of consciousness due to paroxysmal ventricular tachycardia, frequently of the torsade de pointes type) occurs with therapeutic dosing, often in the first few days of therapy. Extracardiac adverse effects of quinidine include potentially intolerable gastrointestinal effects and hypersensitivity reactions such as fever, rash, blood dyscrasias and hepatitis. Procainamide produces electrophysiological changes that are similar to those of quinidine, although Q-T interval prolongation with the former is less pronounced at therapeutic concentrations. Hypersensitivity reactions including fever, rash and (more seriously) agranulocytosis are associated with procainamide, and a frequent adverse effect requiring cessation of therapy is the development of systemic lupus erythematosus. Of the 3 drugs, disopyramide has the most pronounced negative inotropic effects, which are especially significant in patients with pre-existing left ventricular dysfunction. As with quinidine, unexpected 'disopyramide syncope' at therapeutic concentrations has been described. Anticholinergic side effects are common with this drug and may require cessation of therapy. Disopyramide therapy may unpredictably induce severe hypoglycaemia. Severe intoxication with the class 1A agents may result from acute accidental or intentional overdose, or from accumulation of the drugs during long term therapy. Acute overdose can result in severe disturbances of cardiac conduction and hypotension, frequently accompanied by central nervous system toxicity. Decreased renal function can cause significant accumulation of procainamide and its active metabolite acecainide (N-acetyl-procainamide), resulting in severe intoxication. Mild to moderate renal dysfunction is less likely to lead to quinidine or disopyramide intoxication, unless renal failure is severe or concurrent hepatic dysfunction is present. Management of acute intoxication with class 1A drugs includes gut decontamination with provision of respiratory support and treatment of seizures as needed. Hypertonic sodium bicarbonate, by antagonising the inhibitory effect of quinidine on sodium conductance, may reverse many or all manifestations of cardiovascular toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Poisoning due to class IA antiarrhythmic drugs. Quinidine, procainamide and disopyramide. 228 95

Drug-induced systemic lupus erythematosus arises from toxic side-effects of administration of hydralazine, isoniazid, procainamide and practolol. Hydralazine and isoniazid are nucleophilic drugs and inhibit the covalent binding reaction of complement components, C3 and C4, an effect likely to lead to deposition of immune complexes (a feature of systemic lupus erythematosus). Procainamide and practolol do not themselves inhibit C3 and C4. A range of metabolites and putative metabolites of procainamide and practolol were synthesized, and tested for their ability to inhibit the covalent binding reactions of C3 and C4. The highly nucleophilic hydroxylamine metabolite of procainamide was strongly inhibitory in both tests, as was a putative hydroxylamine metabolite of practolol. These studies indicate a potential role for the hydroxylamine metabolites in mediating the toxic side-effects of procainamide and practolol, and emphasize the need for adequate measurements of hydroxylamine metabolites in human tissue.
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PMID:Metabolites of procainamide and practolol inhibit complement components C3 and C4. 245 55

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


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