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)

Clinical and immunological parameters in 14 patients with rheumatoid arthritis (RA) receiving sulphasalazine (SASP) were evaluated, to determine whether their clinical response was reflected by any quantitative changes in their peripheral blood lymphocytes after 12 weeks. Whilst disease activity markers fell significantly, no such changes were noted in the percentage or absolute numbers of lymphocytes or their subsets. The lymphocytes of a further 21 patients before and after receiving SASP for 12 weeks were then studied qualitatively. The suppression mediated by in vitro SASP on ex vivo PHA stimulated lymphocytes showed a decrease at 12 weeks. This change was more marked and reached statistical significance only in those patients who showed a good clinical response. It is postulated that this may in some way be related to expression of activation markers and concomitant SASP binding.
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PMID:Sulphasalazine therapy in rheumatoid arthritis: qualitative changes in lymphocytes and correlation with clinical response. 134 99

The influence of acetylator status on the therapeutic efficacy and the toxicity of sulphasalazine (SASP) was assessed in 106 patients with rheumatoid arthritis (RA). Changes of indices of disease activity after 6 months, and progression of erosions after 2 years of SASP treatment were similar in fast and slow acetylators. Incidence and nature of withdrawals and side-effects, and requirement for intra-articular steroid injections or combination therapy due to poor response to SASP were almost identical in the two groups. A significant increase of the hepatic enzyme aspartate transaminase was noted mainly in slow acetylators, but was not associated with clinical disease. These results suggest that acetylator status does not relate significantly to either the efficacy or the toxicity of SASP in RA. It is possible that hepatic metabolism is affected by SASP, particularly in slow acetylators, but this does not lead to clinically identifiable problems.
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PMID:Influence of acetylator status on sulphasalazine efficacy and toxicity in patients with rheumatoid arthritis. 135 35

Cholera toxin was orally administered to mice concurrently receiving sulphasalazine (SASP) dissolved in L-lysine, or a control substance (L-lysine alone). Circulating antibodies to cholera toxin of IgM, IgG and IgA class were determined by direct ELISA at day 7, 14, 21 and 28. Although both groups made a significant antibody response to the antigen, mice receiving SASP tended to produce lower levels. These were significant for IgA on day 21 (P = 0.013), and for days 7-28 (P = 0.009), and 14-28 (P = 0.007). Overall, considering all antibody classes together from day 7 to 28, there was a significant effect in the SASP treated group (P = < 0.04). It appears that SASP exerts a mild immunomodulatory effect on the mucosal immune system. Further work is obviously required to substantiate these findings. The effect on the gut mucosal immune system of a drug known to ameliorate rheumatoid arthritis may offer an insight into the aetiopathogenesis of this disease.
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PMID:Effect of sulphasalazine on antibody response to oral antigen. 136 Aug 61

Low dose pulse methotrexate (MTX, 5-7.5mg/week) was administered to fifty one patients with severe and active rheumatoid arthritis (RA) who did not respond to the various disease modifying antirheumatic drugs (DMARDs). The follow-up period ranged from 2 to 30 months. As to efficacy rate and probability of patients continuing therapy, the results of MTX were compared with those of the other DMARDs (131 cases of bucillamine (BU), 163 of D-penicillamine (DP), 98 of salazopyrin (SASP), 126 of auranofin (AF), 55 of lobenzarit (CCA)). The patients treated with MTX showed remarkable improvement within 1 or 2 months in Lansbury's index items, CRP, immunoglobulin levels and rheumatoid factor values. But OKT4/8 ratio remained unchanged throughout the study period. As to the adverse reactions due to MTX an elevation of serum transaminase occurred most frequently (41.2%). MTX treatment was, however, tolerable to the most cases with its transient discontinuance or its dose reduction. The efficacy rate of MTX (71.4%) was the best among above mentioned DMARDs at the end of 6 months treatment. After treatment of 24 months, the probability of still taking MTX (70.1%) proved to be about the same with that of DP and better than that of BU, SASP, AF and CCA. In conclusion low dose pulse MTX turned out to be effective in the treatment of severe and active rheumatoid arthritis.
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PMID:[The treatment of rheumatoid arthritis with low dose pulse methotrexate--comparative study with other disease modifying antirheumatic drugs]. 160 14

To study the role of the superoxide radical (O2-) in the pathogenesis of rheumatoid arthritis (RA), both the O2- generation of peripheral blood (PB) polymorphonuclear cells (PMN) and the superoxide scavenging activity (SSA) of PB-PMN, plasma, joint fluid (JF) and PB- or JF-mononuclear cells (MNC) were measured in forty-five patients with RA using the highly sensitive and specific 2-methyl-6-methoxyphenyl-3,7-dihydroimidazo[1,2-alpha] pyrazin-3-one dependent chemiluminescence and the electron paramagnetic resonance/spin trapping methods, respectively. Since many drugs, particularly the slow-acting anti-rheumatic drugs (SARDs) used in RA, may alter O2- metabolism, the effects of SARDs on SSA were also studied. The basal O2- release and opsonized zymosan- or phorbol myristate acetate-stimulated O2- generation by PB-PMN from RA patients were significantly increased, while the SSA of PMN was decreased as compared to those from healthy controls. In addition, the SSA of PMN showed a negative correlation with their O2- generation rates. The JF-PMN showed lower SSA levels than PB-PMN. A negative correlation was also found between the SSA of the plasma and the erythrocyte sedimentation rates. The SSA of the plasma, PB-PMN, JF and JF-PMN were significantly higher in patients treated with SARDs than those without. In cell-free systems, sulfasalazine (SAP) and its metabolite, 5-amino-salicylic acid, had a direct SSA within a millimolar range. The other metabolites of SASP and D-penicillamine had an indirect SSA, since they affected the O2- generating system. Auranofin and bucillamine had no SSA. However, none of the SARDs examined could scavenge O2- at concentrations reported in patients' plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association of enhanced superoxide generation by neutrophils with low superoxide scavenging activity of the peripheral blood, joint fluid, and their leukocyte components in rheumatoid arthritis: effects of slow-acting anti-rheumatic drugs and disease activity. 164 12

The effects of sulfasalazine (SASP) and its metabolites sulfapyridine (SP) and 5-aminosalicylic acid (5-ASA) were investigated on release of prostaglandins (PG) and leukotrienes (LT) from synovial tissue of 37 patients with osteoarthritis, chondrocalcinosis and rheumatoid arthritis. Calcium ionophore A23187 significantly increased the release of PGE2, 6-keto-PGF1 alpha, LTB4, and LTC4 from human synovial tissue irrespective of the underlying joint disease. SASP inhibited release of LTC4 and increased release of PGE2. On the other hand, 5-ASA and SP inhibited the release of all eicosanoids measured. The effective concentrations of SASP and SP were found to be in the range which can be reached during SASP therapy. On the other hand, blood and synovial fluid levels of 5-ASA are considerably lower than those which inhibit eicosanoid synthesis in vitro. While nonsteroidal anti-inflammatory drugs, which are used for symptomatic therapy of rheumatoid arthritis, inhibit cyclooxygenase only, SP, the active metabolite of the second line anti-rheumatic drug SASP, inhibits both PG and LT release. Inhibition of LT synthesis by SASP and SP could contribute to the second line efficacy of SASP therapy in rheumatoid arthritis.
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PMID:[Effect of sulfasalazine and its metabolites on prostaglandin and leukotriene liberation from human synovial tissue]. 167 14

Presented is a case story of a woman with classical rheumatoid arthritis, who during introduction of sulphasalazine (SASP) therapy developed a severe and lasting psoriasis-like skin reaction.
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PMID:Psoriasis-like skin reaction in a patient with rheumatoid arthritis after sulphasalazine therapy. 168 May 96

Salazosulfapyridine (salazopyrin) (SASP) is effective basic treatment for rheumatoid arthritis (RA) after failure or intolerance of antimalarials or gold salts. Sulfapyridine is the active part of the molecule. Its mechanism of action probably involves anti-inflammatory activity as well as effects on cells participating in immune reactions. Adverse reactions occur in approximately one third of cases, in the majority of instances during the first three months of treatments. Simple digestive upsets are the commonest, but SASP may be responsible for sometimes severe cutaneous, hematological and hepatic reactions. The sometimes delayed onset of intolerance reactions justifies continuous monitoring of laboratory parameters. Results obtained with SASP are sometimes prolonged and therapeutic maintenance rates are similar to those seen with other basic treatment for RA. The use of SASP in RA should be tried before methotrexate in relatively early forms of the disease.
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PMID:[Treatment of rheumatoid spondylarthritis with salazosulfapyridine]. 134 66

Abnormalities in serum immunoglobulin levels (Igs) are documented in a series of 350 patients with rheumatoid arthritis (RA) and other inflammatory joint diseases treated with sulphasalazine (SASP) for up to 10 years. Low Ig levels occurred in just over 10% of patients after therapy. Three per cent developed selective IgA deficiency between 8 and 20 weeks after starting SASP. Low IgG levels occurred in 2% at 4-52 weeks and low IgM levels in 5% after 3-7 months. One per cent developed panhypogammaglobulinaemia (hypo gamma) 3-7 months after commencing therapy. Most immunodeficiencies were not accompanied by other toxic reactions and SASP was continued in all but one patient with a rash and thrombocytopenia. A good clinical response was observed in most patients particularly those with selective IgA deficiency and hypo gamma. Two patients with hypo gamma developed chest infections which responded to antibiotics. A low level of individual Igs is not usually an indication to stop SASP unless accompanied by other reactions. Panhypo gamma is potentially serious and should be monitored carefully and replacement therapy should be considered in these patients if infections occur.
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PMID:Immunodeficiencies associated with sulphasalazine therapy in inflammatory arthritis. 168 24

Sulphasalazine (SASP) is now accepted as an effective slow-acting antirheumatic drug for treating active rheumatoid arthritis (RA), but has not been previously evaluated in psoriatic arthritis. An earlier open study suggested that it was well tolerated and potentially beneficial. The present double-blind placebo-controlled trial of 30 patients has now confirmed its efficacy. Greater improvement occurred in those patients on active treatment than on placebo, with more benefit being detected in those patients with the symmetrical polyarticular but seronegative pattern of arthritis associated with a high acute-phase response. SASP was stopped in 26% because of side-effects but these were mild. No exacerbation or remission of psoriasis was observed. Further studies are in progress to determine the degree of efficacy of SASP in different clinical subgroups of psoriatic arthritis.
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PMID:Sulphasalazine in psoriatic arthritis: a double-blind placebo-controlled study. 197 14


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