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)

To test the validity of the putative association between Raynaud's syndrome and rheumatoid arthritis (RA) 277 patients with rheumatic disorders were questioned about cold-induced colour reactions in the extremities. The time to recover digital temperature after brief immersion in ice water was used to confirm the presence of Raynaud's syndrome. The prevalence of Raynaud's syndrome in the 148 patients with RA and the 59 patients with osteoarthritis was 2.7% and 5.1% respectively. It is concluded that Raynaud's syndrome is not a frequent accompaniment of RA, and it is suggested that in view of the close association between Raynaud's syndrome and certain other disorders, such as mixed connective tissue disease and scleroderma, when patients present with polysynovitis and Raynaud's syndrome special consideration should be given to these conditions.
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PMID:The prevalence of Raynaud's syndrome in rheumatoid arthritis. 733 76

The water-soluble gold preparation aurothiomalate, which contains gold as Au(I), is frequently prescribed for patients with rheumatoid arthritis as a disease-modifying agent. We report that aurothiomalate negatively modulates glucocorticoid hormone action; it represses the ligand- and DNA-binding activities and the transactivation function of the glucocorticoid receptor. We suggested the existence of endogenous titrating activities of Au(I) because otherwise administration of aurothiomalate to a patient with rheumatoid arthritis would be expected to result in peripheral insensitivity to glucocorticoids and worsen the patient's status. Focusing on metal ions that are present in vivo, we found that Zn(II) counteracts the inhibitory effect of Au(I) on glucocorticoid receptor function. This complementary effect of Zn(II) was observed at physiological concentrations. We suggest that Zn(II) preserves glucocorticoid receptor function in target tissues and maintains hormone responsiveness, even with chrysotherapy.
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PMID:Zinc ions antagonize the inhibitory effect of aurothiomalate on glucocorticoid receptor function at physiological concentrations. 747 25

The feasibility of extracting neuropeptides from rat knee joints for quantitation by radioimmunoassay was tested. The investigation, based on 25 adult Lewis rats, focused on substance P, calcitonin gene-related peptide, neuropeptide Y, and vasoactive intestinal polypeptide. The relative recovery of the peptides in different extraction media was assessed Both knee joints including the articulating epiphysis were dissected and cut into small pieces. The series was divided into five subgroups, 10 joints in each, for extraction in five different media: 1) 1 M acetic acid in 4% EDTA, 2) 2 M acetic acid in 4% EDTA, 3) neutral water in 4% EDTA, 4) 2 M acetic acid in 4% EDTA and 95% alcohol, and 5) 2 M acetic acid without EDTA. Measureable concentrations of the four neuropeptides were reproducibly assessed by RIA. Although all extraction media provided measurable concentrations, 2 M acetic acid in 4% EDTA was found to give the highest overall yield of the four neuropeptides analyzed. Reverse-phase HPLC confirmed that the immunoreactivities assessed by RIA corresponded to the four neuropeptides of interest. Experimental and clinical evidence suggest a neurogenic involvement in the pathophysiology of inflammatory joint disease, e.g., rheumatoid arthritis. The extraction procedure described offers a means of determining neuropeptide concentrations in joint tissue under normal and pathologic conditions by RIA.
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PMID:Extraction of neuropeptides from joint tissue for quantitation by radioimmunoassay. A study in the rat. 751 57

Adjuvant-induced arthritis is a model of chronic inflammation that exhibits several pathological changes similar to those occurring in rheumatoid arthritis, an autoimmune disease in humans characterized by chronic inflammation of the joints. We have examined the role of inducible nitric oxide synthase in producing the pathological changes associated with adjuvant-induced arthritis. Plasma nitrite concentrations were maximally elevated 14 days following adjuvant administration compared to untreated control animals. Arthritic changes in the paw were first observed between days 10-12 and were maximally elevated 21 days following adjuvant administration. Inducible nitric oxide synthase immunoreactivity was found localized in the synovial tissue from adjuvant-treated rats, while untreated controls exhibited no inducible nitric oxide synthase staining. Two selective inducible nitric oxide synthase inhibitors, aminoguanidine and N-iminoethyl-L-lysine, suppressed the increase in plasma nitrite levels and joint inflammation associated with adjuvant-induced arthritis in a dose-dependent manner. N-Iminoethyl-L-lysine attenuated the inducible nitric oxide synthase immunoreactivity in adjuvant-treated rats. Blood pressure was not affected by the highest dose of N-iminoethyl-L-lysine administered in the drinking water, indicating a lack of inhibition of constitutive nitric oxide synthase.
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PMID:Suppression of adjuvant-induced arthritis by selective inhibition of inducible nitric oxide synthase. 753 78

The Chinese herbal formula suching-huo-hsuei-tang (SHT) was studied to evaluate its efficacy and possible mechanism on adjuvant-induced arthritis (AIA) in rats. SHT was extracted with water, butanol and chloroform into 5 different layers. The top 3 layers of SHT showed a significant suppression of AIA and writhing reaction; the top 2 layers suppressed neutrophil chemotaxis and platelet aggregation. The results suggest that SHT is very promising in the treatment of rheumatoid arthritis (RA) by way of its anti-inflammatory and analgesic action. The possible mechanisms for arthritis are multifactorial.
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PMID:Efficacy and possible mechanisms of the Chinese herbs suching-huo-hsuei-tang in the treatment of adjuvant-induced arthritis in rats. 769 52

A 65-year-old female with severe aplastic anemia induced by gold salt, whose hematopoietic recovery was initiated by rhGM-CSF therapy, was reported. The patient has been given a total of 500 mg of gold-sodium thiomalate for treatment of her rheumatoid arthritis. Two months after the final administration of it, she was admitted to our hospital with complaints of palpitation and shortness of breath. The hemogulobin was 5.9 g/dl, the platelet count was 0.5 x 10(4)/microliter, and the leukocyte count was 800/microliters with 19% neutrophils. Her bone marrow showed aplasia, and both of Ham and sugar-water tests were positive. Three times of bolus-methylprednisolone treatment, with or without methenolone acetate, resulted in no definite improvement of peripheral pancytopenia and marrow aplasia. Subsequent subcutaneous rhGM-CSF, 300 micrograms daily for 28 days with oral prednisolone 5 mg and methenolone acetate 40 mg daily, initiated hematopoietic recovery of all three cell lineages in both peripheral blood and bone marrow. The same doses of prednisolone and methenolone acetate were continued after rhGM-CSF administration, and three months later peripheral cytopenia and positive Ham and sugar-water tests disappeared completely.
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PMID:[Initiation of hematopoietic recovery by recombinant human granulocyte-macrophage colony-stimulating factor in a case of severe aplastic anemia induced by gold salt]. 771 74

The neutral metalloproteinase collagenase is known to be, among others, one of the key enzymes promoting joint destruction in patients with rheumatoid arthritis. Because inflammatory cytokines, e.g., interleukin-1 and tumor necrosis factor-alpha, are considered to activate collagenase gene expression through activation of the transcription factor activator protein-1, we examined whether the water-soluble gold compound aurothiomalate (AuTM) influenced collagenase gene expression, using phorbol ester-treated human fibroblasts. However, AuTM did not prevent phorbol ester-mediated activation of activator protein-1 DNA-binding activity and subsequent induction of collagenase gene expression. In contrast, AuTM counteracted the repressive effects of glucocorticoids on collagenase gene expression and restored collagenase mRNA levels. The molecular target of this paradoxical AuTM action was suggested to be the glucocorticoid receptor.
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PMID:Paradoxical derepression of collagenase gene expression by the antirheumatic gold compound aurothiomalate. 780 28

The aim of this work was to compare and validate seven different methods for estimating changes in fat free mass, in patients suffering from rheumatoid arthritis. Measurements were made of fat and fat free mass before and after 12 weeks on an energy restricted, protein rich diet and physical training. The subjects were sixteen female and three male overweight out-patients (mean body mass index at baseline: 30 kg/m2) suffering from rheumatoid arthritis, according to the criteria of the American Rheumatism Association. Fat free mass was estimated by eight different body composition methods (a four-compartment model, total body water, total body potassium, impedance, near infrared interactance, creatinine excretion, body mass index and skinfold measurements). Mean weight loss was 2.7 kg fat and 1.7 kg fat free mass. There was no difference between measurements of mean change in fat free mass by the four-compartment model and the other methods, except for the creatinine method (P = 0.03). Compared to the four-compartment method, the total body water method gave the most accurate estimate of individual fat free mass changes (residual Mean Square: 0.4 kg), second to this method, the impedance method, seemed most valid (residual Mean Square: 0.8 kg). Accuracies of the other methods were lower (residual Mean Square between 4.2 and 8.2 kg [corrected]). Of eight methods for estimating changes in FFM, the TBW method gave the most accurate estimate of individual FFM changes, compared to a four-compartment model used as reference.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in fat free mass in overweight patients with rheumatoid arthritis on a weight reducing regimen. A comparison of eight different body composition methods. 789 20

1. Mice, whose drinking water contained sulphasalazine, sulphapyridine or 5-amino-salicylic acid, received an antigenic challenge by cholera toxin administered either orally or systemically. 2. Sulphasalazine treated mice made less specific antibody of IgA class provided the antigen also was administered orally (P = 0.009 for days 7-28). When the antigen was administered systemically, there was a vigorous anti-cholera toxin antibody response of IgG class, and a lesser IgM but only a weak IgA response. The effect of sulphasalazine in this case was confined to the IgG response, which was significantly suppressed on day 28 (P = 0.008). 3. Sulphapyridine and 5-amino salicylic acid had no significant effect on the anti-cholera toxin (CT) responses of all three classes. 4. It therefore appears that in this model, only sulphasalazine is capable of influencing the humoral immune system, the antibody class affected depending on the route of entry of antigen. This may have implications for conditions such as rheumatoid arthritis and chronic inflammatory bowel disease, for which sulphasalazine has been found useful.
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PMID:Comparison of the effect of oral sulphasalazine, sulphapyridine and 5-amino-salicylic acid on the in vivo antibody response to oral and systemic antigen. 809 1

Chenodeoxycholate (3 alpha, 7 alpha-dihydroxy-5 beta-cholanic acid) is a primary bile acid directly synthesized from cholesterol. It is an amphipathic molecule, possessing both a hydrophobic side and a polar hydrophilic side, giving it the ability to solubilize lipids in a water environment. Bile acids are necessary for the absorption of fats and fat soluble vitamins. Chenodeoxycholate inhibits the rate-limiting step of cholesterol synthesis, the formation of hydroxymethyl-glutaryl-coenzyme A. It was first reported to be useful in the dissolution of cholesterol gallstones in 1972. Today, chenodeoxycholate has other medicinal uses and is used for the management of cerebrotendinous xanthomatosis, hypertriglyceremia, congenital liver diseases, rheumatoid arthritis, and constipation. This article details some finer points of chenodeoxycholate biochemistry and physiology and discusses in some detail the current and past clinical uses of chenodeoxycholate. This is not an exhaustive discussion on gallstone dissolution therapies, but an overview of some of the lesser-known uses for this drug.
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PMID:Chenodeoxycholate: the bile acid. The drug. a review. 829 9


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