Systemic lupus erythematosus procainamide

Procainamide Systemic lupus erythematosus, diarrhea, nausea, vomiting, TdP, aggravation of underlying HF, conduction disturbances or ventricular arrhythmias, agranulocytosis... 

Certain autoimmune syndromes can be induced by drugs. Examples include systemic lupus erythematosus following hydralazine or procainamide therapy, "lupoid hepatitis" due to cathartic sensitivity, autoimmune hemolytic anemia resulting from methyldopa administration, thrombocytopenic purpura due to quinidine, and agranulocytosis due to a variety of drugs. As indicated in other... 

Certain collagen-like diseases are caused by hypersensitivity reactions to drugs. Hydralazine, and particularly procainamide, may produce a clinical picture similar to systemic lupus erythematosus (43). A number of cases of polyarteritis nodosa have developed during treatment with guanethidine and after repeated exposure to the sulfonamides, penicillin, and iodides (44). Nephropathy has been reported following high doses of methicillin and benzylpenicillin (45). 

Collagen diseases (type II) and syndromes resembling them, e.g. systemic lupus erythematosus are sometimes caused by drugs, e.g. hydralazine, procainamide, isoniazid, sulphonamides. Adrenal steroid is useful. 

Agudelo CA, Wise CM, Lyles MF. Pure red cell aplasia in procainamide induced systemic lupus erythematosus. Report and review of the literature. J Rheumatol 1988 15(9) 1431-2. 

Procainamide is used in veterinary practice as an antiarrhythmic. Clinical effects seen in animals are similar to those seen in humans and include arrythmias, gastrointestinal complaints, and systemic lupus erythematosus-like syndrome. 

Procainamide may induce a syndrome similar to systemic lupus erythematosus. This syndrome consists of arthralgias, myalgias, pleurisy, rash, fever, and elevated nuclear antibodies. Patients who are slow acetylators are at increased risk for developing this syndrome. While some studies have reported that less than one in 500 on chronic procainamide therapy developed this syndrome, others have reported this syndrome in up to 30% of patients on long-term therapy. Other side effects with chronic use include development of neutropenia, thrombocytopenia, hemolytic anemia, agranulocytosis, liver failure, a myasthenia-like syndrome, and psychosis with hallucinations. 

Symptoms of intoxication include (1) bradycardia, (2) prolongation of the QRS interval, (3) atrioventricular block, and (4) induced arrhythmias. These symptoms occur at blood concentrations of procainamide and NAPA exceeding 30[ig/mL. Hypotension sometimes encountered in procainamide therapy is not related to excessive plasma concentration. The development of systemic lupus erythematosus associated with procainamide therapy is not related to plasma concentration but is associated with the acetyla-tor status of the patient slow acetylators predominate in the group in whom the syndrome develops. 

Glomerulonephritis is one of the most serious complications of systemic lupus erythematosus (SLE) and accounts for much of the morbidity and mortality of patients afflicted with the disease. The renal manifestations of lupus nephritis are variable and encompass a wide spectrum of histopathologic lesions. ° ° The underlying histopathology is associated with different prognoses and responses to therapy, which cannot be predicted solely based on clinical manifestations. A renal biopsy is therefore required to assess the severity of the disease and to predict the short-term and long-term outcomes associated with therapy. Drugs, such as hydralazine and procainamide, are known to precipitate a lupus syndrome however, they are unlikely to cause disease that affects the kidney. 

Acetylation genotypic variations (fast and slow). Drug-induced systemic lupus erythematosus (SLE) by slow acetylators with hydralazine > procainamide > isoniazid (INH). 

Certain drugs, such as hydralazine, procainamide, isoniazid, chlorpromazine, and minocycline, can provoke lupus-like manifestations (D Cruz, 2000). Clear differences between systemic lupus erythematosus and lupus syndrome can be identified — hence the recommended different terminology. Typical clinical features of the drug-induced lupus syndrome include arthralgias, arthritis, rash, and... 

A recently suggested mode of action of the induction of immune responsiveness as a result of drug exposure also involves interference with central tolerance induction in the thymus. It has been demonstrated that intrathymic injection of procainamide-hydroxyl-amine, a metabolite of procainamide, alters positive selection and results in systemic lupus erythematosus-like changes (appearance of antibodies to a histone [H2A-H2BJ-DNA complex) in C57BL/6 mice (Kretz-Rommel et al., 1997 Rubin Kretz-Rommel, 2001). 

Dubois EL Strain L (1972) Failure of procainamide to induce a systemic lupus erythematosus-like disease in animals. Toxicol Appl Pharmacol, 21(2) 253-259. 

Procainamide Ventricular tachyarrhythmia Hypotension, systemic lupus erythematosus... 

Since the original reports by Perry and Schroder (1954) and Dunstan et al. (1954) describing a lupus-like syndrome inducible with hydralazine, and by Ladd (1962) with procainamide, much attention has been paid to the relationship of drug-induced lupus with the established clinical entity - systemic lupus erythematosus. 

Hope RR, Bates LA (1972) The frequency of procainamide induced systemic lupus erythematosus. Med J Aust 2 298-301... 

Swerbrick ET, Grey IR (1973) Procainamide induced systemic lupus erythematosus. Rheumatol Rehabil 12 9 96... 

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