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Procainamide

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1041. Psychosis induced by sustained-release procainamide. (PubMed)

Psychosis induced by sustained-release procainamide. 6498664 1984 12 28 2018 11 13 0008-4409 131 10 1984 Nov 15 Canadian Medical Association journal Can Med Assoc J Psychosis induced by sustained-release procainamide. 1188, 1190 Schubert D S DS Gabinet L L Hershey L A LA eng Case Reports Letter Canada Can Med Assoc J 0414110 0008-4409 L39WTC366D Procainamide AIM IM Aged Humans Male Procainamide adverse effects Psychoses, Substance-Induced etiology 1984 11 15 1984 11 15 0 1 1984 11 15 0 0

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1984 Canadian Medical Association Journal

1042. Procaine and procainamide (PubMed)

Procaine and procainamide 18610401 2010 06 25 2010 06 25 0007-0769 67 2 1992 Feb British heart journal Br Heart J Procaine and procainamide. 143 Hollman A A eng Journal Article England Br Heart J 0370634 0007-0769 1992 2 1 0 0 1992 2 1 0 1 1992 2 1 0 0 ppublish 18610401 PMC1024743

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1992 British Heart Journal

1043. Treating activated CD4+ T cells with either of two distinct DNA methyltransferase inhibitors, 5-azacytidine or procainamide, is sufficient to cause a lupus-like disease in syngeneic mice. (PubMed)

Treating activated CD4+ T cells with either of two distinct DNA methyltransferase inhibitors, 5-azacytidine or procainamide, is sufficient to cause a lupus-like disease in syngeneic mice. Human antigen-specific CD4+ T cells become autoreactive after treatment with various DNA methylation inhibitors, including 5-azacytidine, procainamide, and hydralazine. This suggests a mechanism that could contribute to the development of some forms of autoimmunity. In this report we have asked whether T cells (...) treated with DNA methylation inhibitors can induce autoimmunity. Murine CD4+ T cells were treated with 5-azacytidine or procainamide and were shown to respond to syngeneic antigen-presenting cells, similar to CD4+ human T cell clones treated with these drugs. Functional characterization demonstrated that cells treated with either drug spontaneously lysed syngeneic macrophages and secreted IL-4, IL-6, and IFN-gamma. Adoptive transfer of 5-azacytidine- or procainamide-treated cells into unirradiated

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1993 Journal of Clinical Investigation

1044. Pulmonary thromboembolism associated with procainamide induced lupus syndrome and anticardiolipin antibodies. (PubMed)

Pulmonary thromboembolism associated with procainamide induced lupus syndrome and anticardiolipin antibodies. 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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1989 Annals of the Rheumatic Diseases

1045. Metabolites of procainamide and practolol inhibit complement components C3 and C4. (PubMed)

Metabolites of procainamide and practolol inhibit complement components C3 and C4. 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

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1988 Biochemical Journal

1046. Metabolism of procainamide to the cytotoxic hydroxylamine by neutrophils activated in vitro. (PubMed)

Metabolism of procainamide to the cytotoxic hydroxylamine by neutrophils activated in vitro. An almost universal side effect of long-term therapy with procainamide is the appearance of serum autoantibodies and less frequently a syndrome resembling lupus erythematosus. Previous studies demonstrated that procainamide-hydroxylamine (PAHA), a metabolite generated by hepatic mixed function oxidases, was highly toxic to dividing cells, but evidence that PAHA could be formed in the circulation (...) was lacking. This study examines the capacity of neutrophils to metabolize procainamide to reactive forms. Neutrophils activated with opsonized zymosan were cytotoxic only if procainamide was present, whereas N-acetyl procainamide, which does not induce autoimmunity, was inert in this bioassay. PAHA was detected by HPLC in the extracellular medium if ascorbic acid was present. Generation of PAHA and cytotoxic procainamide metabolites was inhibited by NaN3 and catalase but not by superoxide dismutase

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1989 Journal of Clinical Investigation

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