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)

Two cases with different and not previously described fatal renal complications during treatment with penicillamine are reported. A man with seronegative rheumatoid arthritis with features of systemic lupus erythematosus was treated with penicillamine for six months and developed a mild membranous glomerulonephritis and a severe renal vasculitis leading to uremia and death. A woman with primary biliary cirrhosis was treated with penicillamine for nine months and developed a nephrotic syndrome, the renal biopsy showing minimal change glomerulonephritis. The nephrotic syndrome responded to prednisone but the patient died, probably from septicemia. Penicillamine may thus cause glomerular damage without deposition of immune complexes. A restricted use of the drug is recommended.
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PMID:Fatal renal vasculitis and minimal change glomerulonephritis complicating treatment with penicillamine. Report on two cases. 76 Apr 1

A female patient with IgM RF seropositive rheumatoid arthritis according to criteria of the American Rheumatism Association was treated for 133 months with Penicillamine and for 17 months also with Sulfasalazine. Both types of treatment were discontinued because the patient developed symptoms meeting diagnostic criteria of systemic lupus erythematosus, as defined by the same society. Early recognition of this diagnosis was made possible by regular follow up of clinical and laboratory data (ANA, anti DNP, anti dsDNA, C3, C4 and others). Marked improvement, incl. improvement of the nephropathy, was recorded after pulsed treatment with methylprednisolone.
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PMID:[Rheumatoid arthritis developing into systemic lupus erythematosus during long-term treatment with penicillamine and sulfasalazine]. 168 Feb 56

Penicillamine is the drug of choice for the treatment of Wilson's disease, whatever the stage of the illness. Toxic manifestations may preclude the use of this life-saving drug in some patients and discontinuation of penicillamine therapy usually leads to death. We report our experience with Trientine in seven patients, aged 13 to 33 years, with Wilson's disease who developed toxic manifestations with penicillamine that required discontinuation of therapy. These include two with nephrosis, one with neutropenia, two with thrombocytopenia, and one each with a SLE-like and a Henoch-Schonlein-like syndrome. The patients were treated for periods from 6 weeks to 16 years with a dose of 0.5 to 2 g/day. Trientine proved to be an effective alternative copper chelating agent in the treatment of Wilson's disease in patients with penicillamine-induced neutropenia, thrombocytopenia, SLE, and nephrosis. No serious untoward side effects were noted.
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PMID:Treatment of Wilson's disease with triethylene tetramine hydrochloride (Trientine). 232 83

The capacity of D-Penicillamine (DP) to induce or to potentiate the production of antinuclear antibodies (ANA), detected by immunofluorescence (IF), was investigated in vitro, using peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE) and normal individuals. Except in one patient with SLE, DP did not enhance ANA synthesis when using unseparated PBMC. In contrast, when B cells were cocultured with irradiated T cells or irradiated enriched T4+ subset, DP induced or potentiated the production of ANA. These results indicate that DP acts by stimulating T4+ helper cells to promote ANA synthesis in the absence of radio-sensitive suppressor T cell function contained within the T4+ population.
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PMID:The induction of human antinuclear antibodies by D-penicillamine: activation of inducer helper T cells in the absence of irradiation sensitive suppressor T cells. 293 56

D-Penicillamine is effective in the treatment of Wilson's disease, cystinuria and rheumatoid arthritis. However, it may have adverse side-effects by inducing a spectrum of diseases such as myasthenia gravis, lupus-like disease, IgA deficiency and pemphigus vulgaris. A case of D-penicillamine-induced pemphigus is presented. The clinical aspects, pathogenesis, immunology and therapy of D-penicillamine-induced diseases are discussed.
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PMID:[Penicillamine-induced pemphigus]. 331 68

The effect of D-Penicillamine (DP) on the in vitro production of anti-DNA antibodies by peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE) and from healthy individuals was studied. Anti-DNA antibodies were measured in culture supernatants using a sensitive microenzyme-linked immunoassay technique. The results of this investigation suggest that DP can act as an immunomodulator capable of potentiating or initiating anti-DNA antibodies synthesis as well as suppressing it. Although PBMC from both SLE patients and controls were responsive to this thiol compound, our results indicate that PBMC from patients with SLE were more susceptible to the enhancing effect of DP than did PBMC from controls. The cellular mechanism by which this drug can modulate anti-DNA antibodies production is discussed.
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PMID:D-penicillamine: a modulator of anti-DNA antibodies production. 348 66

The clinical features and investigations of 17 patients were analysed. Thirteen of them were Chinese and the rest Indians. Their ages at presentation ranged from 8 to 63 years (mean 18.35 years). Thirteen patients (76%) were symptomatic; 8 with predominantly hepatic manifestations and 5 with neurological features. Four were asymptomatic siblings. At diagnosis, however, 10(59%) had features of liver involvement singly, 3 (18%) had neurological involvement alone and 4 (27%) had mixed presentations. Family histories were available in 15 patients; 26.9% of siblings had Wilson's Disease. Serum ceruloplasmin was low in 82% of the patients. 24-hour urinary copper was measured in 16 patients and was raised in all of them. About half the patients (41%) had evidence of concomittant renal tubular dysfunction with hypouricaemia and aminoaciduria. Three patients (18%) had joint involvement at presentation. All 17 patients were treated with Penicillamine. Complications due to therapy included pemphigus in one and toxic epidermal necrolysis and later a lupus like syndrome in another. The features of clinical improvement included fading of K-F rings, improvement of neurological signs and the normalisation of serum transaminases. One patient developed primary hepatocellular carcinoma 5 years after presentation. Delay in diagnosis was encountered in half of the patients reviewed. Being a treatable condition, Wilson's Disease, although rare, should always be thought of in patients with haemolysis, liver diseases or extrapyramidal disorders.
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PMID:Wilson's disease revisited in the tropics. 375 94

Penicillamine is the drug of choice in Wilson's disease and a therapeutic alternative in rheumatoid arthritis. Autoimmune complications associated with penicillamine include cases resembling systemic lupus erythematosus and Goodpasture's syndrome. We report a case of diffuse pulmonary hemorrhage associated with prolonged penicillamine use in a patient with Wilson's disease with evidence of circulating immune complexes and complement activation, but without serologic or morphologic evidence of systemic lupus erythematosus, Goodpasture's syndrome or renal disease.
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PMID:Penicillamine associated pulmonary hemorrhage. 382 Feb 9

Eighty four patients with classical rheumatoid arthritis were treated with 300-1 200 mg/day of D-Penicillamine. During follow-up, attention was paid to various clinical and biological parameters including the antinuclear factor (ANF) and anti-deoxyribonucleic acid (DNA) antibodies. Before therapy the ANF was greater than or equal to 1/50 in 22 patients (26 p. 100); it increased significantly in treated patients (p less than or equal to 0.01). In addition, positive ANF were found in 22 of the 62 patients (35.5 p. 100) who had negative ANF before D-Penicillamine therapy. There was no correlation between the appearance of ANF or the increase in ANF levels and the initial clinical and biological status, tolerance of therapy, the percentage of cases in which D-Penicillamine was effective. Anti-DNA antibodies were found in 5 patients but no clinical signs of lupus disease were observed despite treatment periods of up to 3.5 years in one case. Anti-SM antibodies were also found in one female patient. The disappearance of anti-DNA antibodies after reducing the dosage of D-Penicillamine (1 case) or withdrawal of therapy (2 cases) is an argument in favour of the inducing role of the drug. The incidence, signification and consequences of these observations are analysed and compared with previously reported results.
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PMID:[Lupus biology: incidence and development in 84 rheumatoid polyarthritis patients treated with D-penicillamine]. 633 65

A 69-year-old woman with classical rheumatoid arthritis developed a severe dermato-myopathy during treatment with penicillamine. Remission occurred on withdrawal of the drug. Penicillamine (dimethylcysteine) is a pharmacological agent used for its chelating properties in the treatment of Wilson's disease and heavy metal poisoning, and in cysteinuria because of soluble disulphide formation. Within the last 17 years penicillamine has been increasingly applied in the treatment of rheumatoid arthritis, the mechanism of action still being unknown. A great number of side effects have been reported, including less common auto-immune disorders such as drug-induced systemic lupus erythematosus, myasthenia gravis and polymyositis. These and other possible side effects have been well reviewed by others (1, 2). To our knowledge only a few earlier cases of dermatomyositis as a complication to penicillamine treatment of rheumatoid arthritis have been reported (3, 4, 5). We describe here another case.
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PMID:Penicillamine-induced dermatomyositis. A case history. 665 98


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