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Ibuprofen reduced human plasma melatonin (MT) after 2 h when administered orally (400 mg) at 2400 h. Increasing plasma concentrations correlated well with increasing inhibition of serum MT levels during this time. Maximum plasma ibuprofen coincided with minimum plasma MT in 3 out of 4 volunteers. Although two volunteers exhibited a partial recovery in MT levels, concentrations after 6 h were significantly less than 0600 h values in drug-free volunteers. Administration of ibuprofen (400 mg) at 1800 h delayed the nocturnal surge of plasma MT. When a slow release preparation of indomethacin (75 mg) was administered at 1800 h, the dark phase rise of plasma MT was completely prevented. Thus the longer acting cyclooxygenase inhibitor exhibited a longer lasting inhibition of plasma MT concentration.

Groups of 15 patients with active rheumatoid arthritis were treated for 24 weeks with zinc sulphate, trien, captopril, clozic in two doses or a combination of D-penicillamine and hydroxychloroquine. Serum histidine levels were monitored along with measures of disease activity including C-reactive protein, plasma viscosity, articular index, grip strength and early morning stiffness. Zinc sulphate and trien were found to be ineffective while the other drugs all showed evidence of second-line action. Serum histidine was found to improve during successful therapy. The possible cause of low serum histidine and its response to therapy is discussed.

Caeruloplasmin (Cp), prealbumin and alpha 2-macroglobulin (alpha 2-M) concentrations in serum were compared in rheumatoid arthritis (RA), osteoarthrosis, ankylosing spondylitis, psoriatic arthritis, Reiter's syndrome, Behçet's syndrome, SLE and normal controls. Cp was significantly elevated (p less than 0.01) in all disease groups except for Reiter's syndrome and SLE. Prealbumin was only significantly depressed (p less than 0.01) in RA. The most notable elevation in alpha 2-macroglobulin occurred in Reiter's syndrome. However, these differences were generally still within the normal range, and hence these proteins are unlikely to offer alternative indices of disease activity suitable for monitoring the the progress of seronegative arthropathies.