A double-blind, between-patient, placebo controlled trial was carried out to investigate the effects of methylcysteine hydrochloride in patients with chronic obstructive bronchitis. After a 2-week washout period on placebo, 30 patients were allocated at random to treatment for 6 weeks with either methylcysteine (1200 mg daily in Week 1, 800 mg daily in Week 2, then 600 mg daily) or with identical placebo tablets on the same regimen. During the post-treatment period, all patients returned to a single-blind placebo regimen (6 tablets daily) for a further 14 days. Assessments were made at the start, at regular intervals during the trial, and at the end of the post-treatment period, of subjective and objective measures of clinical response, and measurements of pulmonary function and certain physico-chemical properties of sputum. The results showed that methylcysteine increased sputum volume, reduced the viscidity of sputum, and significantly improved the subjective assessments of ease of expectoration and severity and frequency of cough, leading to a definite improvement in the patients' clinical state. No side-effects of clinical significance were reported and no abnormalities were found in any of the haematological, hepatic and renal function tests carried out.

No abstract

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to circulating proteins:this phenomenon was not observed when alclofenac, sodium aurothiomalate or D-penicillamine were withdrawn.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.

No abstract

It has been proposed (McArthur, Dawkins & others, 1971) that human connective tissue diseases may arise from modifications in the binding characteristics of the plasma proteins. McArthur, Smith & Freeman (1972) presented evidence that human serum contains a substance that possesses anti‐inflammatory activity and is bound to circulating proteins. Furthermore, it has been suggested that, in patients with active rheumatoid arthritis, the anti‐inflammatory substance is bound to an abnormal extent to the plasma proteins and that the clinically useful antirheumatic drugs act by re‐establishing the bound: free ratio to that in the normal subject (Smith & Dawkins, 1971). There is evidence that the behaviour of L‐tryptophan mimics that of the hypothetical substance which protects susceptible tissues against chronic inflammatory insults. All the clinically useful antirheumatic agents were found to displace L‐tryptophan from human plasma in vitro (McArthur, Dawkins & Smith, 1971) but not so other drugs which bind to plasma proteins to an equivalent extent but have no demonstrable antirheumatic effects (Smith, Dawkins & McArthur, 1971). In patients with rheumatoid arthritis receiving drug therapy the percentage of L‐tryptophan bound to plasma proteins is significantly reduced but increases when drug administration is stopped (McArthur, Dawkins & others, 1971).