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Two automated counters, the H1 (Technicon) and the H6000 (Technicon), which count 10,000 cells per sample, were compared and used to examine the clinical relevance of the additional haematological information now provided to the rheumatologist in three groups of patients--38 with rheumatoid arthritis (RA), 41 with ankylosing spondylitis (AS), and 35 with systemic lupus erythematosus (SLE). The two machines agreed in their estimations of the main indices (haemoglobin, red blood cell count, and white blood cell count), but estimations of platelet count and volume were significantly lower on the H6000 machine, as were mean cell haemoglobin and monocyte count, whereas packed cell volume and red cell distribution width were higher. As expected, both machines identified pancytopenia among the group with SLE, while low haemoglobin and high platelet count were found particularly among patients with RA and AS respectively. Additional information available from these counters showed marked variability in red cell size in SLE, and also of haemoglobin content, which is only measured on the newer H1 machine. Flags for microcythaemia, anisochromasis, and white cell noise (usually due to nucleated red cells) were all more common in SLE. Interpretation of results was complicated by the inevitable difference in age and sex distribution among the disease groups, and identification of active disease was also limited by the effect of drugs. In conclusion, the increasingly widespread use of automated counters as part of the routine haematological service may provide the rheumatologist with useful information, but, as always, care should be taken in the interpretation of indices in patients receiving non-steroidal or second line agents, and also in extrapolating results from one machine to another when they are updated or when patients are monitored at more than one centre.

When fresh rabbit aorta is incubated with plasma, prostacyclin, a potent inhibitor of platelet aggregation, is normally released. Plasma obtained from 2 patients with systemic lupus erythematosus (SLE) inhibited prostacyclin activity, while plasma from 22 other patients with SLE and 40 normal control subjects showed normal activity. Absence of prostacyclin activity did not appear to correlate with the clinical severity of the underlying disease. The possible association of this finding and the presence of thrombotic lesions in both patients is discussed.

Using a whole blood technique we assessed neutrophil migration, phagocytosis, and killing in a group of 20 patients with systemic lupus erythematosus (SLE) and in 8 patients with other connective tissue disorders. In the untreated cases of SLE neutrophil migration was significantly depressed, but it was usually normal in the treated group. This may be attributable either to an intrinsic neutrophil abnormality or to a humoral factor. Although isolated abnormalities of phagocytosis and killing were observed in SLE, these functions were normal when the patients were considered as a group. The treated patients with other collagen diseases showed enhanced migration in both autologous and control plasma, normal phagocytosis, and enhanced killing in autologous plasma only. The small group of untreated, non-SLE patients showed some depression of all 3 functions. There was no correlation between neutrophil function and clinical activity of disease. In the SLE patients there was no correlation between neutrophil function and circulating immune complexes.

Eight out of 10 patients studied longitudinally received benefit from plasmapheresis. The patients were used as their own controls, being treated in a steady state as far as was possible. Levels of circulating complexes did not bear a close relationship with clinical results. On the evidence plasma exchange alone does not appear to represent an important part of the long-term management of patients with systemic lupus erythematosus but may well be of value in combination with other therapy.