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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aplastic anemia is a rare but usually fatal complication of gold salt therapy for rheumatoid arthritis. This report describes 3 patients who developed aplastic anemia while receiving gold salts, and a fourth patient who developed aplastic anemia after receiving gold and then cytotoxic agents. These patients failed to respond to conventional therapy for aplastic anemia and subsequently received bone marrow transplants from HLA-matched siblings. Engraftment occurred in all 4 patients. One patient is alive 2 years after transplantation, and 3 patients died of complications following transplantation.
Arthritis Rheum 1977 Jun
PMID:Bone marrow transplantation in patients with gold-induced marrow aplasia. 32 60

Renal biopsy specimens from 20 patients, 14 women and 6 men, with rheumatoid arthritis (RA) of at least 6 months' duration were studied by direct immunofluorescence microscopy for the presence of immune deposits. Pathological changes were most prominent in patients with longstanding or malignant disease and in patients previously on gold salt therapy. Staining for IgG and C3 was negative in 4 patients with an arthritis of 2 year's duration or less. Fifteen patients had glomerular deposits containing IgG or C3, or both. In 6 of these patients staining was also positive for IgM and in 3 for IgA. In 8 patients C3 was distributed in irregular deposits along the tubular basement membrane. These results suggest that in patients with RA, immunological processes have an untoward effect on the kidneys. The long-term effects of these processes might contribute, moreover, to the development of late renal complications. There is no evidence, however, that the renal immune deposits documented so frequently in this study derive from the rheumatoid disease itself.
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PMID:Immunofluorescence study of renal biopsies in chronic rheumatoid arthritis. 39 46

Two doses of gold sodium thiomalate were compared for their effect on rheumatoid arthritis. Thirty-seven patients with active disease for longer than 6 months were treated with 25 mg of gold sodium thiomalate for an average of 29.6 weeks, then at biweekly or monthly intervals to complete 2 years of treatment. Thirty-eight patients were given more than twice as much gold salt at the same intervals on a flexible dose schedule that produced serum gold levels which averaged 332 microgram/dl during the weekly injection phase. No differences were observed in the therapeutic responses of the two groups. Therefore the minimal dose of gold sodium thiomalate required to induce a response in rheumatoid arthritis is 25 mg or less per week. Serum gold levels in the steady state varied between 95 and 386 microgram/dl and were not related to response. Serum half-life for gold was calculated for patients who had an excellent response and for those who were treatment failures. The rate at which gold disappeared from serum was not related to therapeutic responses.
Arthritis Rheum
PMID:Comparison of two dosage schedules of gold salts in the treatment of rheumatoid arthritis. Relationship of serum gold levels to therapeutic response. 40 13

In albino rats with adjuvant arthritis, the metabolism of skin collagen was studied. This skin samples were taken from 21 to 49 days after the injection of Freund's adjuvant. Glycine-1-C14 was given 5h before sacrifice of the animals. The analyses of skins showed that compared to uninflammed skins, the adjuvant arthritis group had an increase in neutral-salt soluble collagen and acid soluble collagen contents. But the total and insoluble collagen contents were found to be decreased. The incorporation of C14 glycine into skin collagen and the free glycine content of skins were also decreased. There was no significant change in the total nitrogen, RNA and DNA contents of skins. The analyses of urine at weekly intervals showed an increased value of urinary total, free and non-dialysable hydroxyproline in arthritic group. The results suggest that there is an alteration in the metabolism of collagen.
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PMID:Effect of adjuvant-arthritis on collagen metabolism. 73 57

Glucocorticosteroids and mineralocorticosteroids were tested for their capacity to inhibit the nonphagocytic discharge of two lysosomal enzymes--a cartilage matrix-degrading neutral protease and beta-glucuronidase--from highly purified human neutrophils. Lysosomal enzyme discharge from neutrophils adherent to nonphagocytizable, immobilized, heat-aggregated IgG was inhibited by the four glucocorticosteroids--methylprednisolone sodium succinate, triamcinolone acetonide hemisuccinate, para methasone acetate, and hydrocortisone sodium succinate. These glucocorticoids also inhibited zymosan-induced release of beta-glucuronidase from neutrophils that had been pretreated with cytochalasin B in order to completely prevent the onset of phagocytosis. Inhibition by the glucocorticoids of lysosomal enzyme discharge provoked by a soluble divalent cation ionophore was also observed. Neither desoxycorticosterone acetate nor aldosterone hemisuccinate, two mineralocorticosteroids, inhibited lysosomal enzyme release. Similarly, the salt moieties of some of the steroids tested, such as sodium succinate and sodium acetate, failed to elicit an effect on enzyme release. Therefore interference with lysosomal enzyme discharge was restricted to the glucocorticosteroid ring structure. Because interference either with the adherence of neutrophils to immune reactants or with the activities of the discharged lysosomal enzymes by the glucocorticoids could be interpreted as inhibition of lysosomal enzyme release, steroidal effects on these parameters were examined. None of the glucocorticoids tested elicited any significant effects on neutrophil adherence or lysosomal enzyme activity. Thus it appears that glucocorticosteroids are capable of inhibiting directly the nonphagocytic discharge of lysosomal enzymes from human neutrophils.
Arthritis Rheum
PMID:Glucocorticosteroid inhibition of nonphagocytic discharge of lysosomal enzymes from human neutrophils. 83 39

Prolactin secreted by rat anterior pituitary explants into organ culture medium was purified by salt fractionation and gel filtration. A yield of 22 mg/g was obtained, which clearly represented de novo synthesis and secretion of the hormone. Comparative characterization studies were performed on the secreted prolactin and pituitary extracted rat prolactin obtained from the National Institute of Arthritis, Metabolism and Digestive Disease. The biological and immunological activity estimates of both forms were comparable, although the specific activities of the secreted prolactin were somewhat lower than those of the pituitary prolactin. The secreted and extracted forms of prolactin appeared to be identical in primary structure as evidenced by similar amino acid compositions and identical NH2-terminal sequences. Circular dichroism spectra suggested that there may be differences in tertiary structure, since the positive tryptophan band at 292 nm, which eas observed with extracted hormone, was absent in the secreted prolactin.
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PMID:Comparison of secreted and extracted forms of rat pituitary prolactin. 95 31

Fenclorac (a,m-dichloro-p-cyclohexlphenylacetic acid, diethylammonium salt) is a potent nonsteroidal anti-inflammatory agent with significant analgesic and antipyretic activity. Fenclorac had an ED50 of 7.9 mg/kg in the carrageenan paw edema assay and had a duration of action of 18-22 hours. Comparative tests in the carrageenan paw edema assay in the rat indicated that the potency of fenclorac was 13 times that of aspirin, 3.4 times phenylbutazone, 3 times ibuprofen and 0.3 times indomethacin. Fenclorac was less potent than indomethacin, but more potent than phenylbutazone or aspirin in treatment of developing or established adjuvant arthritis. The anti-inflammatory effectiveness of fenclorac did not depend upon the integrity of the adrenopituitary axis and was not affected by the route of administration or sex of the test animal. Fenclorac was 77 times more potent than aspirin and more than twice as potent as indomethacin in reducing fever in rats rendered hyperthermic with brewer's yeast. Fenclorac did not affect normal body temperatures. Fenclorac did not interfere with cellular immune mechanisms as measured by its lack of effectiveness in experimental allergic encephalomyelitis. Antinociceptive testing indicated that fenclorac had peripheral but not central analgesic activity. Fenclorac had an acute oral LD50 in rats and mice of 285 and 430 mg/kg, respectively. The acute gastric lesion UD50 for fenclorac was 7 mg/kg in the fasted rat. Studies using 51Cr-tagged erythrocytes indicated that fenclorac did not produce significant fecal blood loss in the rat at twice the therapeutic ED50 dose for up to 12 days after dosing. Extensive and prolonged fecal blood loss was observed with a corresponding dose of indomethacin for up to nine days after administration. Comparison of the anti-inflammatory pharmacology, Therapeutic Ratio and the data obtained from the 51Cr-fecal blood loss studies indicated that fenclorac was well tolerated after acute or subacute administration to the rat.
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PMID:The antiphlogistic, antinociceptive and antipyretic properties of fenclorac. 100 19

The authors assess the efficacy of gold salt treatment for juvenile rheumatoid arthritis. The study was carried out on 16 children suffering from mono-pauciarticular, polyarticular and systemic arthritis. Treatment consisted of the administration of auranofin alone in a group of 8 children and auranofin associated to corticosteroids in a second group of 8 children. A marked improvement in clinical conditions was observed with slight transitory side effects at follow-up after 12 and 24 months.
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PMID:[Clinical assessment of a group of children with juvenile rheumatoid arthritis receiving long-term treatment with oral gold salt]. 136 92

Brown Norway rats injected with aurothiopropanolsulfonate sodium salt develop systemic autoimmunity. The aim of this study was to assess the influence of the sulfur-containing group in this experimental model of gold-induced autoimmunity. It was shown that the sulfur-containing group does not induce autoimmunity of itself, but potentiates the immunotoxic effects of gold.
Arthritis Rheum 1991 Dec
PMID:Effect of the thiol group on experimental gold-induced autoimmunity. 168 7

Approximately 60 million people in the United States have hypertension (BP greater than or equal to 140/90 mm Hg), 40 million have arthritis clinically suitable for nonsteroidal anti-inflammatory drug (NSAID) therapy, and millions take NSAIDs for nonarthritic conditions, creating considerable potential for concomitant administration of NSAIDs and antihypertensive agents. It is estimated that more than 20 million people are on concurrent therapy. Most NSAIDs produce mild elevations of normal blood pressure levels and can partially or completely antagonize the effects of many antihypertensive drugs. The effect on blood pressure can vary from no effect to hypertensive crisis. In pooled studies, the average increase in mean arterial pressure was 10 mm Hg, and duration was short-lived or chronic. Significant interactions occur in about 1% of patients per year. The risk is greatest in the elderly, blacks, and patients with low-renin hypertension. NSAIDs may block the antihypertensive effects of thiazide and loop diuretics, beta-adrenergic blockers, alpha-adrenergic blockers, and angiotensin-converting enzyme inhibitors. No interactions have been reported with centrally acting alpha agonists or the calcium channel blockers. The mechanism of the hypertensive effects of NSAIDs seem primarily related to their ability to block the cyclo-oxygenase pathway of arachidonic acid metabolism, with a resultant decrease in prostaglandin formation. The prostaglandins are important in normal modulation of renal and systemic vascular dilatation, glomerular filtration, tubular secretion of salt and water, adrenergic neurotransmission, and the renin-angiotensin-aldosterone system. Blockade of salutary effects of prostaglandins by NSAIDs results in a complex series of events culminating in attenuation of the effects of many antihypertensive agents. High-risk patients treated with NSAIDs should be identified and have blood pressure, renal function, and serum potassium frequently monitored.
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PMID:Nonsteroidal anti-inflammatory drugs and antihypertensives. 190 2


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