Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003873 (rheumatoid arthritis)
 53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-six patients with rheumatoid arthritis, 22 receiving D-penicillamine and 2j alclofenac, took part in a 6-month single-bind external observer trial to compare the efficacy and toxicity of these drugs in the treatment of severe rheumatoid arthritis. Both drugs were active and similar in their efficacy at 6 months as judged by clinical and laboratory measurements. Penicillamine was active therapeutically by 3 months, one month before alclofenac. 9 patients, 8 on alclofenac and one on D-penicillamine, had to stop treatment because of lack of effect or toxic effects. Skin rashes within the first week of treatment were a major problem with alclofenac and led to 6 withdrawals.
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PMID:Alclofenac and D-penicillamine. Comparative trial in rheumatoid arthritis. 2 26

A 73-year-old woman with rheumatoid arthritis was treated with Levamisole, 150 mg per day, on 2 days a week. Her arthritis improved, but she developed a severely itching rash, and the treatment was stopped after 6 months. Penicillamine was subsequently given and tolerated without skin complications. 15 months after regular Levamisole was stopped, she was given a single dose of 150 mg which provoked fever of 40 degrees C and rash. Thirteen punch-biopsy specimens were examined by direct immunofluorescence microscopy. During the Levamisole treatment, granular deposits of IgG and C3 were found at the dermal--epidermal junction. Subsequently, the deposits disappeared, but reappeared after Levamisole challenge. The patient's leukocytes were exposed in vitro to Levamisole, and 36% of the total histamine content in the basophils was released. Our results provide further evidence that Levamisole can cause type-I as well as type-III hypersensitivity.
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PMID:Levamisole-induced hypersensitivity. 8 40

A case of dermatomyositis is reported in a 50-year-old woman receiving D-Penicillamine therapy for rheumatoid arthritis. There was no evidence of neoplasia on full investigation. Remission of dermatomyositis occurred on withdrawal of D-Penicillamine.
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PMID:Dermatomyositis induced by penicillamine. 9 19

In a series of 100 adult patients with definite rheumatoid arthritis of at most 3 years' duration and with no previous penicillamine, gold or systemic corticosteroid treatment, 50 patients were treated with D-penicillamine and 50 with gold for one yar. The dose of penicillamine was 600 mg daily. Sodium aurothiomalate was given 50 mg weekly up to a total of 13 mg/kg and thereafter 50 mg once a month. In both treatment groups a statistically significant decrease in the number of painful and/or swollen joints, an increase in haemoglobin and a decrease in ESR, serum ceruloplasmin-, alpha1-acid glycoprotein-, IgG-, IgM- and IgA levels was observed. All the changes in these clinical and laboratory tests were of the same degree in both treatment groups. In the penicillamine group 12 out of 20 seropositive patients became seronegative and in another 5 the Waaler-Rose titre dropped clearly. In the gold group, 7 out of 16 seropositive patients became seronegative, and the Waaler-Rose titre dropped in another 5. An equal increase in the number of eroded joints in hands and toes was seen in the penicillamine and the gold group. Penicillamine was discontinued because of side effects in 13 patients (26%), and gold treatment in 15 (30%). Proteinuria and/or haematuria were the most common causes of discontinuation in the penicillamine group.
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PMID:Comparison of penicillamine and gold treatment in early rheumatoid arthritis. 10 90

In order to evaluate clinical efficacy of D-penicillamine (DP) a double-blind study was conducted by the Metalcaptase Research Group consisting of forty-one rheumatological centers in Japan. A total of 179 patients with rheumatoid arthritis (RA) was divided into two groups; one treated with 5 mg (control group) and the other with 100 mg (drug group) of DP in capsule form. The trial lasted 24 weeks. Global judgment by physicians revealed that improvement was found in 27% in the controls and 65% in the drug group. Adverse reactions occurred in 34% of the controls and 49% of the drug group. Skin rashes, taste disturbances, gastrointestinal upset and proteinuria were frequent in the drug group, but severe or fatal reactions could not be seen in this trial.
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PMID:Clinical evaluation of D-penicillamine by multicentric double-blind comparative study in chronic rheumatoid arthritis. 14 7

While D-Penicillamine is effective in the treatment of rheumatoid arthritis, its mechanism of action is unknown. In this study, effects of D-Penicillamine on collagenase production by adherent rheumatoid synovial cells were investigated. D-Penicillamine did not directly affect the synovial collagenase production. However, lymphocyte-free-supernatant (LFS) recovered from lymphocytes exposed to D-Penicillamine in vivo and in vitro significantly reduced collagenase production by adherent synovial cells. LFS from lymphocytes of normal subjects and from non-D-Penicillamine treated rheumatoid patients stimulated collagenase production. These investigations indicate that D-Pencillamine indirectly affects collagenase production by cultured synovial cells and suggests beneficial effects on controlling the primary disease process.
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PMID:Effects of D-penicillamine on lymphocyte modulation of synovial collagenase production. 22 82

Penicillamine (beta1 beta2 dimethylcysteine) is the drug of choice in the therapeutic management of Wilson's disease and cystinuria and has been used in the treatment of some heavy-metal intoxications. Recent studies have shown that it is efficacious in patients with rheumatoid arthritis. Side effects include sensitivity reactions, nephrotoxicity, bone-marrow suppression, hypogeusia, skin lesions, and the formation of autoantibodies. Two cases are described with the features of pemphigus which were attributed to penicillamine therapy.
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PMID:D-penicillamine-induced mucocutaneous lesions with features of pemphigus. 27 88

The term proliferative lesion refers to the increase in the amount of connective tissue and in the number of small blood vessels and mesenchymal cells with both phagocytic and synthetic functions, characterizing the rheumatoid synovium. This type of lesion is probably responsible for most of the joint destruction and synovial tissue fibrosis seen in this disease. In vitro data indicate that not only factors inducing bone resorption, for instance osteoclast activating factor and prostoglandins, but also connective tissue-degrading enzymes, can be produced locally in the joint, which suggests that these factors play a role in the destruction of articular structures. D-Penicillamine suppresses the immuno-inflammatory process of rheumatoid arthritis, which indirectly may lead to a depression of the stimuli perpetuating the proliferative lesion. As yet, there are no unequivocal clinical data indicating that D-Penicillamine has a direct suppressive effect on the proliferative lesion.
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PMID:Proliferative lesion of arthritis: a target for therapy? 29 34

Characteristics of patients on penicillamine therapy for rheumatoid arthritis were correlated with the occurrence of different side-effects. Patients developing proteinuria tended to have lower sheep-cell agglutination test titres prior to therapy, but no other correlations were found. It is postulated that rheumatoid factor reacts with immune complexes, causing their precipitation and reducing renal glomerular deposition and therefore the incidence of proteinuria. Penicillamine would surely be the first choice of anti-rheumatic therapy if it were not for its side-effects. It is capable of controlling the disease, but in many cases treatment must be interrupted because of some potentially serious side-effects, such as thrombocytopenia, rash or nephropathy. Understanding the mode of action of a drug may lead to the development of new and better compounds. Similarly, understanding the mechanism of the side-effects may lead to their elimination. This survey was designed to identify factors which influenced the development of particular side-effects in patients receiving penicillamine for rheumatoid arthritis.
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PMID:Factors affecting the development of penicillamine side-effects. 31 May 74

D-Penicillamine treatment in rheumatoid arthritis resulted in a fall in plasma alfa-1-antitrypsin-IgA complexes which was significantly more pronounced among responders than among non-responders. Plasma free cystine levels also fell during D-penicillamine treatment, the fall being dose dependent up to a daily dose of 500 mg. Higher doses did not result in further lowering, and no difference was detected between responders and non responders. The dominating sulphur containing aminoacid excreted in the urine was penicillamine-cysteine disulphide, the concentration of which did not correlate to either toxicity or clinical effectiveness, but showed much individual variation. The slow kinetics of change in the complex concentration taken together with in vitro experiments, suggest that the effect of D-penicillamine is more likely to be on the de novo formation of the complexes, rather than on their reduction.
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PMID:D-penicillamine treatment in rheumatoid arthritis monitored by plasma alfa-1-antitrypsin-IgA complexes and plasma and urinary sulphur containing aminoacids. 31 74


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