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At least 19 recordsLinked to original sources
PubMed1999

Antirheumatic agents and leukocyte recruitment. New light on the mechanism of action of oxaceprol.

Most anti-inflammatory agents used in the treatment of joint diseases exert inhibitory effects on leukocyte infiltration. Methotrexate, a disease-modifying drug, and corticosteroids also inhibit leukocyte accumulation during inflammation. However, the mechanisms of action of these different compounds on leukocytes vary and in the case of non-steroidal anti-inflammatory drugs (NSAIDs) the mechanism(s) may be indirect. No current drug for inflammatory or degenerative joint disease has been proposed to act specifically by an inhibitory action on neutrophilic leukocytes. Oxaceprol is an amino acid derivative that has been used for several years for the treatment of osteoarthritis and rheumatoid arthritis, ameliorating pain and stiffness and showing good gastrointestinal safety, particularly in comparison with NSAIDs. Recent experimental studies have shown that oxaceprol does not inhibit the synthesis of prostaglandins in vitro, but markedly inhibits neutrophil infiltration into the joints of rats with adjuvant arthritis. These results support earlier screening data showing inhibition by oxaceprol of leukocyte infiltration into sites of acute inflammation. In studies on surgical ischemia reperfusion in hamsters in vivo, oxaceprol was an effective inhibitor of leukocyte adhesion and extravasation. It is proposed that oxaceprol represents a therapeutic agent for degenerative and inflammatory joint diseases, which acts predominantly by inhibiting leukocyte adhesion and migration.

Anti-Inflammatory Agents↗
PubMed1989

Relationships between knowledge and experience in the use of disease-modifying antirheumatic agents. A study of primary care practitioners.

The timely dissemination of new medical information is a complex and often faulty process. We surveyed primary care physicians to determine their knowledge and use of disease-modifying antirheumatic agents for the treatment of rheumatoid arthritis. Only 26.2% of patients hospitalized for rheumatoid arthritis had been treated with disease-modifying antirheumatic agents in the past, and 13.9% were presently receiving them. When responding to a clinical vignette on rheumatoid arthritis, only 12% (10/84) of practitioners would implement therapy with disease-modifying antirheumatic agents, while the majority would refer the patient to a rheumatologist. Experience with similar patients was clearly the factor that led to initiation of therapy. While 73% of practitioners were aware of the value of disease-modifying antirheumatic agents, only 14% prescribed them in the last year. These findings suggest that dissemination of information concerning disease-modifying antirheumatic agents has been successful, but the problems inherent in their use result in referral rather than initiation of therapy.

Adult↗
PubMed1981

Studies on type II collagen-induced polyarthritis in rats. Effect of antiinflammatory and antirheumatic agents.

The effect of a variety of antiinflammatory and antirheumatic agents on both developing and established lesions of type II collagen induced polyarthritis in rats was examined. Administration of the nonsteroidal antiinflammatory agents indomethacin or phenylbutazone suppressed the paw inflammation associated with the disease without affecting type II collagen antibody titers. Radiographic analysis of the joints showed suppression of several parameters related to joint destruction. This was most probably related to the antiinflammatory properties of the two drugs. Administration of prednisolone, a steroidal antiinflammatory agent, suppressed paw inflammation; type II collagen antibody titers were significantly decreased in the developing lesion, but the drug had no effect on antibody titers in the established lesion. Radiographic analysis of the joints showed decreases in several parameters of joint destruction. Cyclophosphamide, an immunosuppressive agent, completely suppressed the inflammation associated with the developing lesion but had only minimal effect against the established disease. Collagen antibody titers were decreased and an improvement in only one radiologic parameter (periostitis) was detected. Treatment with antirheumatic agents such as gold thioglucose or levamisole enhanced severity of inflammation in the established lesion and caused increases in collagen antibody titers. Radiographic analysis of the joints indicated that while gold had no effect, levamisole enhanced joint destruction. Treatment with D-penicillamine had no effect on paw inflammation, despite increases in collagen antibody titers. Radiographic analysis of the joints indicated an improvement in all parameters related to joint destruction in animals treated with penicillamine.

Animals↗
PubMed1983

[Recently discovered mechanisms of action of non-steroidal antirheumatic agents: possible, not only symptomatic therapeutic effects].

Non-steroidal antirheumatic agents are assumed to exert their therapeutic effects by inhibiting biosynthesis of prostaglandins at the level of cyclo-oxygenase. This effect leads to a reduction of inflammatory symptoms caused or potentiated by prostaglandins. Recently, some new further effects (partly also induced by inhibition of prostaglandin synthesis) of non-steroidal antirheumatic drugs have been discovered. These effects influence functions and interactions of white blood cells involved in pro-inflammatory and immunological processes, and appear to be causal rather than symptomatic. Furthermore, there are differences in the mode of action of some antirheumatic agents, in particular with regard to inhibition of generation of inflammatory superoxide anions.

Anti-Inflammatory Agents↗
PubMed1981

Results of a double-blind study with indomethacin and indoprofen, a new non-steroidal antirheumatic agent.

Indoprofen, a new non-steroidal antirheumatic agent, was tested in a controlled, double-blind, cross-over study versus indomethacin and placebo, in 30 patients with rheumatoid arthritis. The study consisted of three fourteen-day treatment periods. At the end of the trial 14 patients expressed a preference for the indoprofen therapy (200 mg q.i.d.), 10 patients for indomethacin (25 mg q.i.d.) and 5 patients decided in favour of the placebo. Judging from the patients' assessment of spontaneous pain, a complete analgesic effect was observed in 44% of the patients under indoprofen, in 26% under indomethacin and in 13% under placebo. Indoprofen showed good efficacy on all the other parameters measured (Ritchie's index, morning stiffness, number of painful and swollen joints, and grip strength) and good clinical and biological safety.

Adult↗
PubMed1996

Effects of antirheumatic agents on cytokines.

A review of the literature concerning the effects of traditional antirheumatic drugs on cytokines and the cytokine and anticytokine approaches already used in the therapy of rheumatoid arthritis (RA) is presented. Many antirheumatic drugs are capable of cytokine modulation in vitro. Corticosteroids inhibit the transcription of a broad spectrum of genes including those encoding monocyte, T cell-derived cytokines and several hemopoietic growth factors, whereas drugs such as cyclosporin A and D-penicillamine interfere with T cell activation more specifically by suppressing interleukin 2 (IL-2) production. The in vivo effects of drug therapy on cytokines in RA patients are less well established. Gold compounds reduce circulating IL-6 levels and the expression of monocyte-derived cytokines, such as IL-1, tumor necrosis factor (TNF), and IL-6, in the rheumatoid synovium. Decreases in circulating IL-6, soluble IL-2 (sIL-2R), and TNF receptors and in synovial fluid IL-1 levels have been reported with methotrexate. Reductions in circulating IL-6 and sIL-2R concentrations have also been observed with cyclosporin and corticosteroids, whereas azathioprine reduces IL-6 but not sIL-2R. Studies on sulfasalazine are conflicting and the in vivo effects of D-penicillamine and antimalarials have not been studied yet. Interferon gamma therapy is not effective in RA but may prove a useful antifibrotic for systemic sclerosis. Colony stimulating factors improve the granulocytopenia associated with Felty's syndrome or drug toxicities but can induce arthritis flares and should be reserved to treat infectious complications. Promising results are being obtained with selective antagonism of TNF and IL-1 in RA, and combinations of anticytokine strategies with traditional antirheumatic drugs have been already envisaged. These should preferably be based in a broader knowledge of the effects of antirheumatic agents on the cytokine network.

Antirheumatic Agents↗
PubMed1999

Possible factor for nonlinear pharmacokinetics of TAK-603, a new antirheumatic agent, in rats.

A new antirheumatic, TAK-603, shows nonlinear pharmacokinetics in both animals and humans. To elucidate the mechanism of these nonlinear pharmacokinetics, in vivo and in vitro metabolism of 14C-labeled TAK-603 ([14C]TAK-603) was studied using rats as these resemble humans in their metabolic profiles. After intravenous injection of [14C]TAK-603 to rats at doses of 1, 5, and 15 mg kg(-1), the total body clearance of unchanged drug decreased significantly with increasing dose, whereas the apparent distribution volume did not alter remarkably. Thus, saturation in the elimination processes was considered to be a factor responsible for the nonlinear pharmacokinetics. The disappearance of unchanged drug from the circulation, however, followed a dose-dependent first-order process, indicating that the nonlinearity observed was not merely due to saturation of the elimination capacity. In vitro studies using rat liver microsomes showed that TAK-603 competitively inhibited CYP-catalysed nifedipine oxidation and also that the demethylated metabolite M-I, the major metabolite in rats and humans, competitively inhibited the oxidation of nifedipine. These results suggested that inhibition by M-I of the metabolism of the parent drug (i.e. product-inhibition) may be the most likely factor responsible for the nonlinear pharmacokinetics of TAK-603.

Administration, Oral↗
PubMed2002

[Gastropathies caused by non-steroidal antirheumatic agents].

Non-steroid antirheumatics are among very frequently prescribed drugs. They can be, however, associated with the development of serious and undesirable effects on the digestive tract. Therefore at present therapeutic procedures are sought which will restrict the negative effect of drugs on the mucous membranes of the stomach, duodenum and gut in general, incl. new forms of non-steroid antirheumatics with a "sparing" effect on the gastroduodenal mucous membranes. This group of drugs includes preparations with a so-called preferential or specific effect on cyclooxygenase 2 (COX-2). This enzyme is of fundamental importance for the development of mucosal lesions and its inhibition is the basis of safe medication with non-steroid antirheumatics. Other possible alternative therapy is the combined administration of non-steroid antirheumatics with drugs which inhibit the secretion of gastric hydrochloric acid. These drugs include above all proton pump blocking agents. The principle of medication with non-steroid antirheumatics should, of course, be careful and correct indication, knowing possible complications of treatment, and in particular knowledge which groups of subjects may be threatened by treatment with non-steroid antirheumatics. Preference of drugs on the basis of COX-2 inhibition is a necessity in these subjects.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1985

Effect of antirheumatic agents on the mitogen response of arthritic rat spleen cells.

Splenic lymphoid cells from rats with adjuvant induced polyarthritis show a diminished response to the T-cell mitogens Con A and PHA. This report describes the in vitro effects of various antirheumatic agents on the mitogen induced proliferative response of normal (NSC) and arthritic (ASC) rat spleen cells. Indomethacin enhanced only the arthritic responses. Other PG synthesis inhibitors such as ibuprofen and naproxen enhanced the arthritic as well as the normal spleen cell proliferative responses. Gold sodium thiomalate augmented arthritic but not normal blastogenesis. Penicillamine significantly enhanced only the Con A response of arthritic cells at 10(7)M. Levamisole produced a significant increase in the PHA response of arthritic cells and the Con A NSC response. Chloroquine diphosphate enhanced the Con A response of normal cells at 10(-5)M and 10(-6)M; both chloroquine and tilorone suppressed blastogenesis of arthritic spleen cells at 10(-4)M and 10(-5)M. When classifying antirheumatic agents as stimulator or suppressors of immune function, one must account for their effects on arthritic as well as normal lymphoid cells at the predicted pharmacologic plasma levels.

Animals↗
PubMed1990

Pulmonary disease due to antirheumatic agents.

Drug-induced lung disease presents several diagnostic and therapeutic problems to the clinician. This is especially true in the case of lung disease associated with antirheumatic agents in which pulmonary disease may be due to the underlying disorder. Unfortunately, no specific markers exist to differentiate drug-induced lung disease from other pathologic processes. In addition, the numerous drugs often used simultaneously or in close sequence in rheumatic disorders make assignment of toxicity to a specific agent difficult. Six groups of drugs used as anti-inflammatory/antirheumatic agents have been discussed in association with pulmonary damage penicillamine, gold, methotrexate, salicylates, NSAIDs, and colchicine. The major clinical syndromes ascribed to these drugs include hypersensitivity pneumonitis and chronic alveolitis/fibrosis (penicillamine, gold, methotrexate, NSAIDs), pulmonary-renal syndrome (penicillamine), bronchiolitis obliterans (penicillamine, gold), and noncardiogenic pulmonary edema (salicylates, colchicine). Unfortunately, treatment options remain limited. Withdrawal of the offending drug and supportive care are the mainstays of therapy. In cases in which active inflammation causes significant derangement of gas exchange, corticosteroids are warranted. More aggressive management using immunosuppressive drugs has been recommended in cases of refractory PABO and PAGS, but these recommendations are at present based only on isolated case reports.

Anti-Inflammatory Agents↗
PubMed1982

[Mechanism of action of non-steroidal antirheumatic agents].

Non-steroidal antirheumatic drugs permit a nonspecific, symptomatic therapy of inflammatory rheumatic processes and may also be given for a limited period of time in patients with so-called activated osteoarthrosis. Their mode of action is a complex one. More recent knowledge on mediators in inflammation such as prostaglandins, leukotriens and oxygen radicals have brought new insights on the mode of action of non-steroidal antirheumatic drugs.

Analgesia↗
PubMedDate not supplied

Effect of the antirheumatic agent Tenidap on CD3, CD4, and CD8 expression and interleukin-1 and leukotriene B4 secretion in human peripheral blood mononuclear cells.

Thymocytes that express the complete CD3-T-cell receptor (TCR) complex are CD4- and CD8-. The CD4+ T-cell population can be subdivided into at least two quite distinct subsets, TH1 and TH2 cells, based upon cytokine expression. Interleukin-1 (IL-1) appears to be required for optimal proliferation of T cells in response to antigen and it seems that in the absence of IL-1, TH2 clones proliferate less in response to antigen. Tenidap is an antirheumatic agent that has an inhibitory effect on IL-1 production. In these studies, we show that isolated human peripheral blood mononuclear cells (PBMCs) treated in vitro with Tenidap (15 micrograms/mL) for 48-h incubations significantly (p < 0.05) enhanced the present of CD4+ expression compared with untreated cells (control), as determined by cytofluorimetric analysis. Lipopolysaccharide and Bacillus Calmette-Guérin were used as positive controls. When the cells were tested for CD3 or CD8 receptor expression, no differences were found between the untreated PBMCs and the treated (15 micrograms/mL Tenidap) cells. No change was found when cells were incubated for 72 h. Moreover, our data show a strong dose-dependent inhibitory effect of Tenidap (15 micrograms/mL) on IL-1 alpha, IL-1 beta, and leukotriene B4 secretion in PBMCs treated overnight. The increased CD4+ expression by Tenidap in PBMCs may suggest an important role for this new antirheumatic agent in immunity and may hold future therapeutic promise for diseases involving IL-1 and leukotriene B4 as mediators.

Antigens, CD↗
PubMed1977

New antirheumatic agents: Fenoprofen calcium (Nalfon), naproxen (Naprosyn), and tolmetin sodium (Tolectin).

The new antirheumatic agents, fenoprofen calcium, naproxen, and tolmetin sodium, are effective in the management of rheumatoid arthritis. Their efficacy is comparable, but not superior, to that of aspirin in usual oral doses. These agents also may be useful in degenerative joint disease and ankylosing spondylitis and as analgesics and antipyretics; however, there are insufficient data available to establish their efficacy and dosages for these uses. The incidence of adverse reactions, including gastrointestinal bleeding, is lower with these agents than with aspirin; thus, these drugs may be useful substitutes in patients who cannot tolerate the gastrointestinal effects of aspirin.

Anti-Inflammatory Agents↗
PubMed2004

Separation methods for antibacterial and antirheumatism agents in plant medicines.

Traditional oriental medicines (TOM), with a very long history and many remarkable features, are very popular in Asian countries, especially in China, Japan and Korea. With the development of advanced analytical techniques, the modernization of traditional medicine has become a hot area in recent years and some herbal medicines have been increasingly accepted in western countries. Separation and determination of active components in various herbal medicines are considered to be critical for the modernization process. Antibacterial and antirheumatism agents are widely distributed in many medical plants and commonly used in clinical treatment. Therefore, the development of effective separation methods for the quality control of herbal medicines is absolutely important. In this article, the separation methods for the analysis of antibacterial and antirheumatism compounds in TOM were reviewed, including thin layer chromatography (TLC), gas chromatography (GC), supercritical fluid chromatography (SFC), high-performance liquid chromatography (HPLC), capillary electrophoresis (CE) and related hyphenation techniques. Sample preparation procedures and further development of these methods were also discussed.

Anti-Bacterial Agents↗