The phagocytosis of killed Staphylococcus epidermidis by neutrophilic leukocytes was inhibited in vitro by indomethacin in a concentration of 3 × 10‐4M, and by hydrocortisone, phenylbutazone, and paracetamol in a concentration of 10‐3M. Phagocytosis was slightly stimulated by 10‐7M phenylbutazone. Acetylsalicylic acid, mefenamic acid, and phenacetin had no effect. The bactericidal activity of leukocytes against live Staphylococcus epidermidis was reduced by 10‐4M phenacetin, 5 × 10‐4M mefenamic acid, and 10‐3M phenylbutazone and indomethacin, whereas concentrations of 10‐5M and above of paracetamol enhanced bacterial killing by leukocytes. Hydrocortisone and acetylsalicylic acid were ineffective. It is probable that concentrations of anti‐inflammatory agents sufficient to affect phagocytosis and bacterial killing by neutrophils are as a rule not attained in the organism during treatment, although inhibition may occur locally, for example in inflamed tissue, as a consequence of a low pH, which potentiates the effect of acid anti‐inflammatory drugs. This inhibition may be a factor in the mechanism of action of anti‐inflammatory compounds.

Calcitonin gene methylation at CCGG sites were determined in 39 chronic myeloid leukemia patients by isoschizomeric restriction endonuclease analysis. A total of 27 patients were analyzed while still in the chronic phase: 20 patients had a normal gene, and seven had a hypermethylated gene. There were 12 patients initially studied in accelerated or blastic phases. All but one patient showed gene hypermethylation, suggesting a good correlation between gene methylation and disease stage. All five patients who, while still in the chronic phase, had a major 3.1-kb hypermethylated calcitonin gene fragment, accelerated within 2 to 27 months. In consecutively analyzed patients, the initially normal calcitonin gene changed to a hypermethylated state as the disease escalated. The hypermethylation predicted disease acceleration with a median lead time of 6 months before any morphologic or clinical signs of disease progression were seen. The disease progressed in 8 of 27 patients initially studied in the chronic phase: in only two patients this occurred without predictive methylation changes. The results suggest that the assessment of calcitonin gene methylation status may be a promising tool for monitoring chronic myeloid leukemia disease escalation.

We have examined the mononuclear cell fraction from 35 individuals, 18 with hematologic malignancies and 17 healthy controls for the presence of cell surface-associated plasminogen activator (PA) activity. PA activity was found on the cell surface of 10 out of 12 samples from patients with acute leukemia. In addition to active urokinase (uPA) found on the cell surface in four out of five acute myeloid leukemia patients, tissue-type PA activity was detected in the same samples (3 of 5). Two out of four samples from acute lymphoid leukemia displayed only uPA activity and three out of three samples from biphenotypic leukemia were also clearly uPA-positive. Plasmin activity was not detected in any of the samples. PA activity was not found on the surface of mononuclear cells from either patients with chronic lymphoid leukemia or healthy controls and, in this respect, the cell surface- bound uPA activity behaved as a marker for acute leukemia. The finding of PA activity on the cell surface in acute leukemia suggests that there may be continuous generation of plasmin with consequent consumption of plasma plasmin inhibitors.

In a study of neutrophil functions in haematological disorders using in vitro techniques, a heat‐stable inhibitor of chemotaxis and phagocytosis was demonstrated in the plasma and serum of a 64‐year‐old woman with reticulum cell sarcoma. In partial purification by chromatography, the inhibitory activity could not be separated from IgG. Clinically the patient did not exhibit abnormal susceptibility to infections.