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Biomedical subjects

M Aylward

Publications and source records attributed to M Aylward.

At least 37 records · Page 2Linked to original sources
PubMed1976

Evaluation of tolmetin in the treatment of arthritis: open and controlled double-blind studies.

In a 6-week open study in 24 patients with rheumatoid arthritis, tolmetin was shown to have analgesic and anti-inflammatory activity at daily doses in excess of 1200 mg per day and produced statistically significant reductions in overall joint pain, walking time and articular index. The drug was well tolerated, but 2 patients were withdrawn because of persistent indigestion and 1 because of an urticarial type rash. In a double-blind crossover comparison against indomethacin and placebo in 22 patients, 1400 mg tolmetin daily showed efficacy comparable with that of 150 mg indomethacin daily. Few side-effects were reported and did not necessitate any patients being withdrawn.

Adult↗
PubMed1975

Long-term study of indomethacin and alclofenac in treatment of rheumatoid arthritis.

Indomethacin and alclofenac were compared for 13 months under double-blind conditions in 109 patients with active, classical, or definite rheumatoid arthritis at a relatively early stage of the disease. Both indomethacin and alclofenac were clearly effective: most patients either improved or remained as well controlled as on entry. Alclofenac proved the more effective drug, however, producing a significantly greater reduction in morning stiffness, articular index, and erythrocyte sedimentation rate, and only in the alclofenac-treated group did functional capacity improve and latex-agglutination titres diminish. Comprehensive laborabory tests showed no significant deviation from normal which could have been attributed to either drug.

Administration, Oral↗
PubMed1975

A study of the influence of various antirheumatic drug regimens on serum acute-phase proteins, plasma tryptophan, and erythrocyte sedimentation rate in rheumatoid arthritis.

In patients with rheumatoid arthritis neither indomethacin nor aspirin influenced the levels of the erythrocyte sedimentation rate (e.s.r) or serum acute-phase proteins fibrinogen, haptoglobin, C-reactive protein and alphaI acid-glycoprotein). Treatment with D-penicillamine, sodium aurothiomalate, or alclofenac produced a significant reduction both in acute-phase protein levels and in e.s.r. Each of the drugs displaced L-tryptophan from plasma proteins in vivo but withdrawal of indomethacin and aspirin was followed immediatley by excessive binding of this amino acid to circulating proteins:this phenomenon was not observed when alclofenac, sodium aurothiomalate or D-penicillamine were withdrawn. It has been demonstrated that disease activity in rheumatoid arthritis is reflected in acute-phase protein concentrations and in the extent to which L-tryptophan is bount to plasma protein. It is suggested that drugs which profoundly affect these parameters provide not only symptomatic relieft but also possible beneficial effects upon the disease process itself.

Adult↗
PubMed1975

A review of possible mechanisms of action of the antirheumatic drug, alclofenac.

A number and variety of hypotheses have been proposed to explain the primary mechanism of action of the antirheumatic drugs. A critical review is made of the biochemical and pharmacological parameters which, on current evidence, parallel the clinical activity of the drugs. The numerous chemical mediators of the inflammatory response are discussed, as is the possible role of endoenous anti-inflammatory substances. Particular attention is paid to the plasma protein-binding effects of antirheumatic drugs and the competitive displacement theory of drug action is examined in the light of recent work on the behaviour of L-tryptophan binding in vitro and in vivo. It is suggested that antirheumatic drugs can be differentiated by their influence on the acute-phase protein response and their effects on tryptophan binding. Clinical findings are reviewed to support the proposal that drugs such as alcofenac, which both inhibit the acute-phase response and exert prolonged influence on the binding of tryptophan to plasma proteins, reduce inflammatory activity more profoundly than those drugs which produce symptomatic relief alone. They are capable, therefore, of altering the course of the disease.

Animals↗
PubMed1975

Clinical studies on alclofenac in the treatment of rheumatic diseases: a drug in question.

The potential advantage to patients with chronic rheumatic diseases of an effective, non-steroidal analgesic/anti-inflammatory drug which causes insignificant gastric bleeding was a decisive factor leading to the introduction of alclofenac. Short-term double-blind trials showed that alclofenac has analgesic/anti-inflammatory activities equivalent to phenylbutazone, indomethacin and aspirin, but superior to the fenemates and propionic acid derivatives. Long-term controlled studies, ranging from 5 months to 3-1/2 years and using reliable, objective measures revela, however, that patients with rheumatoid arthritis improve in functional status and graduate to less severe classes of disease activity, a phenomenon not observed with either indomethacin or aspirin administered to matched patients over the same periods of time. So far, clinical improvement on alclofenac has been matched only by treatment with gold, D-penicillamine and the immunosuppressive anti-proliferative drugs. This clinical improvement on alclofenac is reflected in haematological and serological indices, and research shows that alclofenac, like these other antirheumatoid drugs, has a pronounced effect upon the acute-phase protein response and the extent to which L-tryptophan is bound to plasma protein. The clinical data reviewed suggest that alclofenac represents an advance in the therapy of the rheumatic diseases.

Arthritis, Rheumatoid↗
PubMed1975

The influence of alclofenac treatment on acute-phase proteins, plasma tryptophan, and erythrocyte sedimentation rate in patients with rheumatoid arthritis.

Alclofenac and D-penicillamine were compared under controlled, double-blind conditions in the treatment of 35 patients with active rheumatoid arthritis over a period of 26 weeks. The principal aim of the study was to investigate any relationships between changes in clinical status and changes in concentrations of three serum acute-phase proteins (fibrinogen, C-reactive protein, and haptoglobin), plasma free and protein-bound L-tryptophan, and the erythrocyte sedimentation rate. Both alclofenac and D-penicillamine were clearly effective: all patients showed steady improvement on the seven clinical indices of response employed. Drug management was easiest with alclofenac. Both drugs produced a significant reduction in acute-phase proteins, E.S.R. and protein-bound plasma tryptophan. Since it has previously been established that the course of rheumatoid arthritis is reflected in the acute-phase protein levels and the extent to which L-tryptophan is bound to plasma protein, it is suggested that drugs, such as D-penicillamin and alclofenac which profoundly affect these parameters, provide not only symptomatic relief but also possible beneficial effects on the disease process itself.

Arthritis, Rheumatoid↗
PubMed1975

Simultaneous pharmacokinetics of benorylate in plasma and synovial fluid of patients with rheumatoid arthritis.

Twenty patients with definite or classical rheumatoid arthritis and chronic knee effusions were each given an oral dose of 4 g benorylate as the 40% suspension. Synovial fluid and plasma samples were obtained up to 9 hours after drug administration and assayed for their salicylate and benorylate content. A mean peak benorylate plasma level of 2.18 +/- 0.19 mug/ml occurred 30 min after drug administration but declined rapidly and benorylate was virtually undetectable in the plasma 90 min later. The mean peak benorylate synovial fluid level of 0.74 +/- 0.21 mug/ml occurred 3 hours after drug administration but the concentration remained steady for at least a further 9 hours. A mean peak plasma salicylate level of 119 +/- 14.2 mug/ml and mean peak synovial fluid salicylate level of 78 +/- 13.6 mug/ml occurred 3 hours after benorylate administration. Both levels declined slowly over some hours. This study shows that benorylate per se readily enters the synovial fluid in patients with rheumatoid arthritis and continues to accumulate there even when undetectable in the plasma. It is possible that the lipophilic nature of the benorylate molecule facilitates its uptake by the inflamed synovial tissue.

Arthritis, Rheumatoid↗