Dexamethasone (4-8 mg/m2 body surface area) was given orally or intravenously to six normal volunteers. The maximum neutrophil count occurred 4-6 h after oral or intravenous administration of dexamethasone and was due almost entirely to an increase in mature neutrophils; concomitantly there was a lymphocytopenia. A second rise in the neutrophil count occurred 24 h after oral ingestion of dexamethasone, coinciding with a lymphocytosis. Neutrophil alkaline phosphatase (NAP) activity during development fell as the neutrophil count rose. Other haematological values were unchanged except for small increments in erythrocyte sedimentation rate (ESR). Sodium concentration in serum and urine remained normal but urinary potassium excretion and urine volume increased after the intravenous dose. There was a direct relationship between plasma concentration of dexamethasone and the rise in neutrophil count following intravenous but not oral administration. The concentration of dexamethasone in plasma fell to half its peak value in 2-6 h. Dexamethasone-induced neutrophilia was similar to that induced by other corticosteroids. Dexamethasone in a dose of 6 mg/m2 produced minimal discomfort while inducing an adequate neutrophilia in the volunteers.

Gross elevation of the serum lactate dehydrogenase (S.L.D.) in megaloblastic anaemia was first reported by Hess and Gehm (1955) who found values from 5 to 21 times the upper limit of normal in 16 cases of pernicious anaemia. They also noted an inverse correlation between the serum enzyme activity and the peripheral red blood cell count. The rise in the S.L.D. has since been confirmed by Lührs and Negelein (1955), Cintrön‐Rivera, Acosta‐Martienzo and Diaz‐Rivera (1956), Zimmerman, West and Heller (1958), Heller, West and Zimmerman (1959), Gordin and Enari (1959), Levitan, Wasserman and Wróblewski (1959), Amelung (1960), Grönvail (1961), Elliott and Wilkinson (1963) and Goldfarb and Papp (1963), but there are conflicting reports concerning the relation between the degree of S.L.D. elevation and the severity of the anaemia. While Gordin and Enari (1959) reported that the S.L.D. activity correlated inversely with the serum vitamin B12 level, but not with either the blood haemoglobin concentration or the peripheral red cell count, in patients with pernicious anaemia or Diphyllobothrium latum infections, Levitan et al. (1959) found S.L.D. elevations in Addisonian anaemia only and not in megaloblastosis due to other causes. However, Amelung (1960) and Grönvall (1961) have suggested that the occurrence of extremely high S.L.D. activities might be diagnostic of megaloblastosis, and Fleming and Elliott (1964) have recently reported high levels of S.L.D. and of serum 2‐hydroxybutyrate dehydrogenase (S.H.B.D.) in folic acid‐deficient Nigerian patients with macrocytic anaemia of pregnancy. Similar elevation of the S.H.B.D. in pernicious anaemia had previously been reported by Elliott and Wilkinson (1963) who also observed a rise in the S.H.B.D./S.L.D. ratio during specific therapy. The present investigation was carried out to assess the reliability of S.L.D. and S.H.B.D. determinations in the diagnosis of megaloblastic anaemia and as indicators of the response to treatment. The enzyme levels have also been compared with the results of haematological investigations.

A reduction of donor effects during centrifugal plateletpheresis with the Haemonetics Blood Processor was achieved by reducing the concentration of the citrate anticoagulant. Serum citrate and ionized calcium levels, immediately and 1 h post-pheresis, were affected to a lesser extent by using 5.0 g total ionized citrate (TIC) THAN WITH EITHER 8.0 G OR 11.0 G. Total calcium, bicarbonate, prothrombin time, partial thromboplastin time, ECG, and platelet counts were affected to a similar degree by all three TIC formulations. The total number of platelets collected per litre of blood processed was not significantly different among the three TIC formulations. In vitro studies employing the screen filtration pressure (SFP) technique showed no evidence of platelet aggregates in whole blood collected into either 0.01 M or 0.005 M citrate and agitated or left stationary at room temperature for 5 h. The use of different citrate concentrations in plateletpheresis is discussed.

Summary Two methods for the determination of glutathione peroxidase (GSH‐Px) activity have been compared and the overall superiority of a linked‐enzyme system has been confirmed. The erythrocyte GSH‐Px activity was measured in 120 newborn infants and compared with older children and adults. A definite deficiency of the enzyme was found in the former group, but could not be related to evidence of haemolysis. A relationship between serum tocopherol levels and erythrocyte GSH‐Px was found and the possible implications are discussed.

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