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)

Cell-mediated immune responses of cultured synovial mononuclear cells against ureaplasmal, chlamydial, Mycoplasma hominis and mumps antigens were measured by the 3H-thymidine uptake method. Specific responses against ureaplasmal or chlamydial antigens were found in 3 of 4 patients with venereally-acquired Reiter's syndrome, but not in 3 patients with arthritis after episodes of diarrhea and 4 patients with rheumatoid arthritis.
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PMID:Cell-mediated immune responses of synovial mononuclear cells in Reiter's syndrome against ureaplasmal and chlamydial antigens. 616 Feb 48

The therapeutic efficacy of N-(2,6-dichloro-m-tolyl)anthranilic acid, sodium salt (meclofenamate sodium, Meclomen) in the management of rheumatoid arthritis was clearly established in four large, double-blind, controlled multicenter studies in 757 patients. In one study, 200 mg/day of meclofenamate sodium was compared with 300 mg/day and placebo for six weeks. Another compared meclofenamate sodium, 300 mg/day, with acetylsalicylic acid (ASA), 3.6 g/day, for eight weeks. Two other long-term studies compared meclofenamate sodium and ASA, 300 mg/day and 3.6 g/day, respectively, for six months; in one, the patients were allowed to receive concomitant gold salts or steroids, while in the other, they were not. Both objective and subjective measures showed that meclofenamate sodium was as effective as ASA and superior to placebo. Gastrointestinal reactions, most commonly diarrhea, were seen more often with meclofenamate sodium than with ASA or placebo, but withdrawal for adverse reactions did not differ significantly between treatment groups. ASA-associated side effects such as tinnitus and deafness were not experienced by the patients receiving meclofenamate sodium. Meclofenamate sodium is a safe, effective agent for the treatment of rheumatoid arthritis.
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PMID:Double-blind multicenter studies with meclofenamate sodium in the treatment of rheumatoid arthritis in the United States and Canada. 634 46

A case of fulminant watery diarrhea after therapy with 485 mg of gold thioglucose in a 78-yr-old woman suffering from rheumatoid arthritis is presented. Evaluation failed to reveal evidence of infection, malabsorption, or mucosal inflammation. Treatment, after stopping therapy, was supportive over several months and the patient recovered completely. A comparison with other presentations of gold induced diarrhea is made through a review of all known cases reported in the literature. Although these cases have many points in common, it is apparent that there is a spectrum of disease from fatal hemorrhagic diarrhea to nonexudative diarrhea. Any diarrhea in a patient receiving gold salt therapy must be thoroughly investigated before continuing therapy.
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PMID:Nonexudative diarrhea after gold salt therapy: case report and review of the literature. 640 89

A case of gold-induced enterocolitis in a 69-year-old female with rheumatoid arthritis who had received the new gold compound by oral administration (Auranofin (AF) for 4 weeks) is reported. Mild diarrhoea is a commonly described side effect accompanying AF, but in this case a severe colitis developed. The course of this case is very similar to those reported regarding Myochrysin. The pathogenesis is discussed. It might be a direct toxic effect on the mucosa of the bowel, evidenced by the relatively high excretion of oral gold with faeces.
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PMID:Auranofin (SK + F 39162) induced enterocolitis in rheumatoid arthritis. A case report. 641 80

The oral gold salt auranofin, 6 mg per day, was compared with oral d-penicillamine, 500 mg per day, in a single-blind trial in 40 patients suffering with definite or classic rheumatoid arthritis. The patients were randomly allocated into the two therapeutic regimens (19 patients auranofin; 21 patients d-penicillamine) and monitored at a minimum of four-week intervals during the first year of treatment. Significant diminution in rheumatoid disease activity, as assessed by numerous clinical and laboratory parameters, was observed in both the auranofin- and penicillamine-treated groups. No significant differences existed for these parameters between the two groups, either initially or at the end of the trial period. Ten patients were lost from the trial over the 52-week period. Three subjects were withdrawn from the auranofin-treated group (increasing severity of rheumatoid arthritis at four weeks; severe diarrhea at four weeks; probable drug-related erosive gastritis at 40 weeks). Seven subjects were permanently withdrawn from the penicillamine-treated group (four, skin rashes four to eight weeks; one, heavy proteinuria at 24 weeks; one, therapeutic failure at 32 weeks; one, compliance failure at eight weeks), and treatment was temporarily withheld in three further patients because of thrombocytopenia (two) and proteinuria (one). We conclude that both drugs are effective in rheumatoid arthritis and that the lesser toxicity with auranofin will make it a valuable addition to our therapeutic armamentarium.
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PMID:A 12-month comparative trial of auranofin and D-penicillamine in rheumatoid arthritis. 641 96

The chemistry, pharmacology, pharmacokinetics, clinical use and efficacy, adverse effects, and dosage of auranofin, an oral chrysotherapeutic agent used in treatment of rheumatoid arthritis, are reviewed. Auranofin is lipid-soluble and is monomeric in solution. It has a modulatory effect on both the humoral and cellular immune systems. Auranofin may be a condition-dependent immunoregulating agent rather than an immunosuppressive agent. It inhibits (1) monocyte-mediated antibody-dependent cellular toxicity, (2) release of enzymes from polymorphonuclear leukocytes that may contribute to the pathogenesis of rheumatoid arthritis, and (3) neutrophil activity. In patients with rheumatoid arthritis, 15-33% of an oral dose of auranofin 6 mg is absorbed. Peak plasma gold concentrations are achieved in one to two hours. Gold is highly protein bound. Elimination occurs through the feces and urine; 73-100% of auranofin gold is excreted. Plasma half-life is three weeks. Patients receiving auranofin 3 mg twice daily for rheumatoid arthritis reported improvement after five weeks of therapy; improvement has also been reported with lower doses. Diarrhea, rashes, and pruritus were the most common adverse effects. Auranofin is safe and effective for short- and long-term treatment of patients with rheumatoid arthritis. Its relative safety and potency compared with injectable gold salts and other drugs need further study.
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PMID:Review of auranofin, an oral chrysotherapeutic agent. 642 43

Auranofin is the first orally active gold compound for the treatment of rheumatoid arthritis. Like other chrysotherapeutic agents, its exact mechanism of action is unknown, but it probably acts via immunological mechanisms and alteration of lysosomal enzyme activity. Although long term clinical experience with auranofin is limited, its efficacy appears to approach that of sodium aurothiomalate. Further comparative studies with aurothioglucose, hydroxychloroquine and D-penicillamine are required before definitive statements can be made regarding the relative efficacy of auranofin and these agents. While patients have demonstrated clinical remission of rheumatoid arthritis in response to auranofin therapy, radiological studies have been inconclusive regarding its effect on the occurrence or progression of erosive lesions. Auranofin is relatively well tolerated in most patients, but diarrhoea, skin rash, and pruritus are sometimes troublesome, and thrombocytopenia and proteinuria are potentially serious side effects which may occur during therapy. Whereas mucocutaneous side effects are more frequent with injectable gold compounds, gastrointestinal reactions are the most common adverse effect seen with auranofin. The frequency of side effects has been similar with auranofin and sodium aurothiomalate, but they are generally less severe with auranofin. While some of the side effects are controlled by a reduction in dosage, temporary or permanent withdrawal of auranofin may be necessary. Auranofin is clearly a useful addition to the limited list of agents with disease-modifying potential presently available for the treatment of rheumatoid arthritis. It will doubtless generate much interest as its final place in therapy becomes better defined through additional well-designed studies and wider clinical experience.
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PMID:Auranofin. A preliminary review of its pharmacological properties and therapeutic use in rheumatoid arthritis. 642 23

Forty patients with rheumatoid arthritis were randomly allocated to treatment with auranofin 3 mg b.d. or hydroxychloroquine 200 mg b.d. Twenty patients received each drug. Efficacy was analysed by comparing patients with available data at weeks 12, 24, 36 and 48 with baseline within each treatment group, and between treatment groups at each of these same time points. There were statistically significant improvements in all measured parameters of clinical efficacy among hydroxychloroquine treated patients, and in all efficacy parameters except one (time to onset of fatigue) in the auranofin treatment group. There were no significant differences between the treatment groups for any parameter of clinical efficacy. Of the laboratory parameters measured, only auranofin treatment produced statistically significant decreases in the concentration of IgA, IgG and IgM, with significant differences between treatments being detected in the case of IgA and IgG. Eight auranofin-treated and three hydroxychloroquine-treated patients were withdrawn because of adverse reactions before completing 48 weeks treatment. The commonest reason for stopping auranofin treatment was diarrhoea (5 cases). Three hydroxychloroquine-treated and two auranofin-treated patients were withdrawn from the study because of inefficacy of the trial drug. Auranofin had a more 'potent' biochemical profile than hydroxychloroquine, although more patients tolerated one year of treatment with the latter drug.
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PMID:A single-blind comparative study of auranofin and hydroxychloroquine in patients with rheumatoid arthritis. 643 15

There are few drugs available with purported disease-modifying or healing effects in rheumatoid arthritis. The two agents that have gathered the most support in favor of these effects are parenteral gold and cyclophosphamide; however, both can produce intolerable toxicity. A new oral gold compound (auranofin; Ridaura) is being investigated in rheumatoid arthritis. Available studies suggest that auranofin may be slightly less effective than parenteral gold, but is significantly less toxic, the main side effect being diarrhea. There is evidence to suggest auranofin slows radiologic progression of the disease, but further studies are indicated. If further studies demonstrate a healing effect of the drug, comparable with data suggesting this effect for parenteral gold, auranofin may become a first-line agent in rheumatoid arthritis.
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PMID:Oral gold in arthritis. 643 87

Auranofin (Ridaura SK and F 39 162) was tested in an open multicenter study with regard to its anti-inflammatory effect in 166 patients suffering from rheumatoid arthritis. The time for treatment lasted for one or two years. The therapeutic effect of the drug was judged by its influence on pain, joint swelling, morning stiffness, grip strength, blood-sedimentation rate and rheumatoid factor etc. The serum gold concentration was measured regularly. With Auranofin the majority of the patients achieved a lasting improvement of the condition. The therapeutical effect was observed gradually. Side-effects were frequent but removal from the therapy was rare. Most of the side-effects were diarrhea, rash, pruritus and conjunctivitis. Regular laboratory controls revealed in some cases toxic organic reactions.
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PMID:[Auranofin in the treatment of chronic polyarthritis. Results of an open multicenter study]. 644 53


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