Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A Cameroonian affected with massive Loa loa infection developed febrile arthritis with involvement of both knees and the left ankle. Although the patient was first seen by us after one month of treatment with Indomethacin, at this time the joints were still inflamed and microfilariae of Loa loa were found in the synovial fluid. No other etiological mechanism was identified. Following the articular puncture and treatment with Ketoprofen, the arthritis subsisted within a week. This is the first case to be studied in which arthritis during loasis has been explicitly documented by the presence of intra-articular microfilariae.
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PMID:Microfilarial polyarthritis in a massive Loa loa infestation. A case report. 2 59

In the experimental model of streptococcal CFE-induced arthritis, PGE and PGF concentrations rise significantly. This is due to an increase both in the substrate concentration and the enzyme activity for PG biosynthesis. Indomethacin therapy inhibited PG synthesis and diminished some of the gross, but not the histological, features of the inflammatory response. These results lend further support to the contention that the beneficial effect of indomethacin in arthritis is due to inhibition of PG biosynthesis.
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PMID:The role of prostaglandins in experimental arthritis in the rat. 19 64

Human peripheral neutrophils generated superoxide radicals as assessed by ferricytochrome C reduction in response to activation by the synthetic chemotactic factor, N-formyl-methionyl-leucyl-phenylalanine. Superoxide generation was inhibited by 2-deoxy-D-glucose (ID50 4 X 10(-5)M), 2-iodoacetate (ID50 5 X 10(-5)M), and N-ethyl-maleimide (ID50 5 X 10(-6)M), suggesting a dependence on anaerobic glycolysis and sulfhydryl groups. Ouabain, microtubule-disrupting agents, inhibitors of respiration, oxidative phosphorylation, and protein and nucleic acid synthesis were without appreciable effects. Indomethacin (ID50 1 X 10(-4)M), ibuprofen (ID50 9 X 10(-4)M, and phenylbutazone (ID50 1 X 10(-5)M) all caused dose-dependent inhibition of superoxide generation at concentrations approximating those plasma and tissue levels obtained in human beings at therapeutic doses. Acetylsalicylic acid (125-500) microgram/ml) and aurothioglucose (10(-3)-10(-6)M) were without appreciable effects. Superoxide generation was inhibited only by relatively high concentrations of hydrocortisone (ID50 greater than 10(-3)M). Because superoxide radicals have been implicated in the pathogenesis of tissue injury in several forms of inflammation and arthritis in vivo, these studies suggest that the production of a potential cytotoxic factor may be subject to pharmacologic manipulation and that at least some of the antiphlogistic effects of the nonsteroidal antiinflammatory agents may be mediated through effects on superoxide production.
Arthritis Rheum 1979 Jul
PMID:Chemotactic factor-induced generation of superoxide radicals by human neutrophils: effect of metabolic inhibitors and antiinflammatory drugs. 22

In the management of rheumatic diseases, the use of corticosteroids should be reserved for active arthritis. Phenylbutazone (Butazolidin) is probably the drug of choice for acute gout and is also effective in ankylosing spondylitis, Reiter's syndrome, and psoriatic arthritis. Indomethacin (Indocin) also is useful in these conditions. Ibuprofen (Motrin) is only slightly more efficacious than aspirin. Aspirin is still the preferred treatment for rheumatoid arthritis and should be tried before ibuprofen. Osteoarthritis of the cervical or lumbar spine calls for a full program of physical therapy. Experimental procedures for total replacement of joints other than hip and knee show promise.
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PMID:Rheumatic diseases. 2. Therapeutic considerations. 108 14

Rat peritoneal macrophages stimulated in vivo by group A streptococcal peptidoglycan-polysaccharide (PG-APS) resorb bone as measured by solubilization of 45Ca from radiolabeled, devitalized bone chips. Activity was strain-dependent and correlated with the susceptibility of rat strains to PG-APS-induced arthritis. PG-APS-stimulated macrophages from the resistant Buf rat strain were not induced to resorb bone, but ingested equivalent concentrations of PG-APS compared to bone-resorbing macrophages from the arthritis-susceptible Lew strain. Resorptive activity peaked at three to five days and decreased to background levels by 10 days after injection. PG-APS-stimulated macrophages from congenitally athymic Lew rats were as effective as macrophages from heterozygous littermates at resorbing bone. Lew macrophages were also responsive to small, nonarthropathic PG-APS polymers generated by mutanolysin digestion. Resident peritoneal macrophages did not respond to stimulation by PG-APS in vitro. Indomethacin at a concentration of 10 micrograms/ml was an effective blockade against PG-APS-induced macrophage bone resorption in vitro, but catalase was ineffective. These results indicate that expression of rat macrophage bone-resorbing activity reflects genetic regulation of the response to PG-APS rather than a defect in ingestion of these polymers and imply that PG-APS-stimulated, bone-resorbing macrophages may contribute to early, initial bone destruction that occurs in inflammatory arthritis.
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PMID:Bone-resorbing activity is expressed by rat macrophages in response to arthropathic streptococcal cell wall polymers. 142 23

Polymorphonuclear leukocytes (PMN) are involved in inflammatory reactions. It is thought that oxygen-derived free radicals released from activated PMN may participate in tissue damage during inflammation. We have shown that flosulide (6-(2,4-difluorophenoxy)-5-methylsulfonylamino-1-indanone ), a novel highly potent anti-inflammatory compound, inhibits superoxide production induced by N-formyl-Met-Leu-Phe (FMLP), C5a and PMA without impairing bacterial killing or chemotaxis. Flosulide (10(-5)-10(-7) M) was more potent in inhibiting the FMLP-induced respiratory burst of PMN than the structurally related compound nimesulide. FMLP-induced superoxide generation was also inhibited by two human flosulide metabolites. A good correlation between this in vitro effect and in vivo anti-inflammatory potency in rat adjuvant arthritis was found for flosulide and its metabolites. Indomethacin, piroxicam and ibuprofen did not inhibit the respiratory burst at 10(-5) M. FMLP receptor number was decreased by 36% in the presence of 10(-5) M flosulide. However, a 250-fold molar excess of flosulide could not displace labeled FMLP from the receptor. Inhibition of degranulation of primary and secondary granules was a common effect of all anti-inflammatory compounds tested. At a concentration of 10(-5) M, all drugs inhibited degranulation to about the same degree, independent of their in vivo anti-inflammatory activity.
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PMID:Influence of the anti-inflammatory compound flosulide on granulocyte function. 166 Feb 71

SK&F 105685 (N,N-Dimethyl-8,8-dipropyl-2-azaspiro[4.5]decane-2-propanamine+ ++ dihydrochloride) is a novel azaspirane with beneficial activity in animal models of autoimmune diseases such as adjuvant-induced arthritis and experimental autoimmune encephalomyelitis in the Lewis rat and lupus-like disease in the MRL mouse. The effect of SK&F 105685 on the proliferation of rat lymphoid cells was examined in vitro. The compound inhibited the proliferative response of spleen, thymus and lymph node cells to the mitogen concanavalin A (Con A) in a dose-dependent manner but had little or no effect on the mitogenic response of peripheral blood lymphocytes. Although less potent than cyclosporin A, SK&F 105685 was able to inhibit the proliferation of spleen cells stimulated with PMA and ionomycin or the mitogens phytohemagglutinin (PHA), Con A and pokeweed mitogen (PWM). Relatively early event(s) in cell proliferation were affected by SK&F 105685 since delaying addition of the drug by 24 to 48 hours after Con A stimulation of rat spleen cells resulted in reduced levels of suppression. The mode of action of SK&F 105685 appeared to differ from that of cyclosporin A or rapamycin. Unlike cyclosporin A, SK&F 105685 did not affect IL-2 production by Con A-stimulated spleen cells or the IL-2-producing Jurkat cell line, but, like rapamycin, the compound significantly reduced the IL-2-induced proliferation of rat ConA blasts. These results suggest that inhibition of lymphocyte proliferation by SK&F 105685 may require the activity of an intermediate effector cell(s) present in susceptible populations such as cells from the spleen, thymus, lymph nodes and Con A blast preparations but absent or present in low numbers in resistant populations such as peripheral blood cells. Indomethacin and NG-monomethyl-L-arginine (NGMMA), a competitive inhibitor of nitric oxide synthase, were both unable to relieve SK&F 105685-induced suppression of splenic Con A responses thereby ruling out a role for the production of prostaglandins or nitric oxide by macrophages as an intermediate in drug-mediated suppression. In summary, SK&F 105685 was unable to inhibit lymphoproliferative responses by a mechanism distinct from that of cyclosporin A or rapamycin and which appears to involve regulation of cellular interactions rather than a direct effect on responding lymphocytes.
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PMID:Inhibition of lymphoproliferative responses by SK&F 105685, a novel anti-arthritic agent. 166 43

Reactive arthritis is the leading cause of arthritis in Papua New Guinea, followed probably by gonococcal arthritis. Indomethacin and local hydrocortisone acetate are useful in the treatment of reactive arthritis. Refractory cases of reactive arthritis may be helped by weekly low-dose oral methotrexate or by long courses of doxycycline. When Neisseria gonorrhoeae is thought to be involved treatment should cover penicillinase-producing strains. Infective arthritis due to Staphylococcus aureus and Mycobacterium tuberculosis is less common but should be considered in all patients because prompt and specific treatment is required to avoid permanent damage.
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PMID:The diagnosis and management of common forms of arthritis in adults in Papua New Guinea. 175 Feb 56

In previous studies we observed an enhanced anti-inflammatory activity of MPEG-SOD derivatives in acute inflammation in rat. To assess the activity in chronic inflammation we tested the compound with longer half-life (MPEG-SOD 18) in complete adjuvant arthritis in rat. According to the prophylactic schedule of treatment (i.m. administration at alternative days of 10 mg/kg from day 3 to day 21), the MPEG-SOD derivative reduced arthritic lesions in a significant way (P less than 0.01 at 14th, 21st, 28th day). Indomethacin, administered i.m. daily at the dose of 1.5 mg/kg according to the same schedule, significantly inhibited adjuvant arthritis each time it was considered (% of inhibition are 66.5% at 14th day, 58.3% at 21st day and 50.8% at 28th day). Native SOD and inactivated enzyme, administered from day 3 to day 21 did not show any anti-inflammatory properties. According to the therapeutic schedule of treatment (from day 14 to day 28), neither MPEG-SOD nor native SOD showed antiarthritic activity.
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PMID:Anti-inflammatory activity of monomethoxypolyethylene glycol superoxide dismutase on adjuvant arthritis in rats. 204 60

Rats were sensitized by i.d. injection in the base of the tail with Freund's complete adjuvant (FCA) and were challenged i.d. in the dorsal skin with mycobacterial antigen. The 24 hour dermal delayed-type hypersensitivity (DTH) response increased up to 10 days after FCA injection followed by a decrease by day 15 which coincided with the development of adjuvant arthritis (AA). Drug studies were performed, using a 4-day dosing schedule, on optimal DTH elicited on day 10, suboptimal DTH elicited on day 15, and AA (day 16). Cyclosporine, leflunomide and prednisolone significantly inhibited day 10 DTH and AA with no effect on day 15 DTH. Indomethacin and tiaprofenic acid significantly inhibited AA with no effect on either DTH response. Chloroquine, levamisole, D-penicillamine, diazepam and RU38468 had no significant effect on DTH or AA. These findings suggest a complex temporal relationship between AA, DTH and drug actions.
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PMID:Drug actions on delayed-type hypersensitivity in rats with developing and established adjuvant arthritis. 233 72


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