Circulating immune complexes have been measured using the (125I)C1q binding test in 216 sera from 135 children with acute lymphoblastic leukaemia. Increased circulating immune complexes were detectable in 10.7% of the sera and 10.4% of the children. There was no correlation between the presence of circulating immune complexes and prognosis, but a strong correlation with a history of recent infection.
comment on the apparent decrease in turnover rate in one patient after allopurinol treatment: did he mean that this was during allopurinol treatment and that this decrease in turnover rates was due to allopurinol? DR. ScoTr: The second study in the patient taking allopurinol was carried out while he was taking the drug -about 6 months after starting. Associated with the fall in plasma and urinary uric acid caused by xanthine oxidase inhibition there was a reduction in the exchangeable pool size and daily turn-over rate of uric acid. The pattern of decline in urinary specific activity now indicated the presence of a single-compartment rather than the two-compartment system before treatment. Indomethacin was used either alone or in combination with other drugs in 26 of the 48 patients; 24 received aspirin at some time during the study and because of its wide usage before admission to hospital the effects of this drug were difficult to assess. Systemic steroids were used in eight cases, intra-articular injection of steroids in five, phenylbutazone in two, and Biogastrone in one.
Influence of Gold Salts onChanges in synovial fluid cell cytology and in serology were observed after treatment. Neither synovial fluid cell count nor differential count showed any significant change with treatment; however, the staining reactions of cell smears showed marked differences. These differences were best seen with the PAS stain, there being marked diminution of staining following treatment. Similar results were obtained using enzyme histochemical techniques to demonstrate the lysosomal enzymes such as acid phosphatase and N-acetyl-,B-glucosaminidase.Serologically seven of thirty patients showed positive anti-nuclear factor, eighteen showed positive reticulin antibody, and five demonstrated a positive smooth muscle antibody. Changes in antinuclear factor staining were seen after treatment in three cases, and changes were seen in four out of five patients with a positive smooth muscle antibody. Little change was observed with the reticulin antibody.
Intra-articular inflammation is associated with a reduction in viscosity of synovial fluid which is due to changes in hyaluronic acid rather than in the protein component of the fluid (Kulonen, 1951;Sundblad, 1953). Hyaluronic acid is a polymer of molecular weight greater than 1 x 106 made up from repeating units of N-acetyl-D-glucosamine and D-glucuronic acid. It is present in concentrations of about 0 1 g. per cent. or less in rheumatoid synovial fluids, compared with 0 3 g. per cent. in normal fluids. Synovial fluid shows anomalous viscosity, i.e. the viscosity decreases with increasing rate of shear, typical of a non-Newtonian fluid. The relative viscosity of a solution of synovial fluid, defined as the viscosity of the solution divided by the viscosity of the solvent, decreases with age (Jebens and Monk-Jones, 1959) and that of rheumatoid synovial fluid is usually lower than normal (Ropes, Robertson, Rossmeisl, Peabody, and Bauer, 1947;Ragan and Meyer, 1949). However, only slight reductions have been found when normal and rheumatoid fluids have been diluted to the same low concentration (0 06 g. per cent.) of hyaluronic acid (Hamerman and Schuster, 1958); this suggests that it is the amount rather than the nature of the hyaluronic acid which determines the relative viscosity. Measurements of intrinsic viscosity, determined by extrapolation of the specific viscosity (i.e. relative viscosity -1) to zero concentration of solute, and anomalous viscosity give a more accurate picture of the state of hyaluronic acid in solution.The lower values of both these parameters for rheumatoid fluids have been attributed to a low mean degree of polymerization of hyaluronic acid in rheumatoid disease (Seppala, 1964;Brimacombe and Webber, 1964). Changes similar to those found in
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