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A double-blind randomized controlled trial compared the effectiveness of prophylactic oral trimethoprim/sulfamethoxazole (cotrimoxazole) to a placebo in preventing peritonitis in continuous ambulatory peritoneal dialysis (CAPD) patients. A daily trimethoprim/sulfamethoxazole dose of 160/800 mg gives a steady state dialysate concentration of 1.07/4.35 mg/L in the final dwell of each dosing interval. Identification of a 40% reduction in peritonitis probability with 80% statistical power and a type 1 error probability of 0.05 required 52 subjects per group. With stratification by previous peritonitis, 56 were allocated to cotrimoxazole and 49 to placebo. For cotrimoxazole there were five deaths and seven catheter losses. For placebo there were three deaths and nine catheter losses. There were 20 withdrawals from cotrimoxazole and 9 from the placebo group. With respect to time to peritonitis, there was no statistically significant difference between cotrimoxazole and placebo groups (p = 0.19). At 6 months, 64.1% of cotrimoxazole and 62.5% of placebo were peritonitis free; at 12 months 41.9% of cotrimoxazole and 35% of placebo were peritonitis free. There was no effect (p > 0.05) of age, sex, catheter care technique, spike or luer, or dialysate additives. Previous peritonitis increased the risk of peritonitis by 2.06 (95% CI, 3.61–1.18) while frequent (six weekly) extension tubing changes increased the risk of by 1.79, (95% CI, 3.04–1.02) when compared to six monthly changes. Cotrimoxazole appears ineffective in prevention of CAPD peritonitis.

1. The sodium concentration within the erythrocytes of 159 subjects was found to be 7·35 ± 1·25 (SD) mmol/litre of cells. 2. In 157 normal subjects, the erythrocyte potassium concentration was 99·08 ± 5·3 (SD) mmol/litre of cells. 3. In the erythrocytes from twenty-seven normal subjects there was a striking linear correlation between the rate constant for active sodium efflux and resting sodium concentration. 4. It is concluded that these studies confirm the assumption that the resting concentration of sodium within a cell is determined by the activity of the sodium pump. What is not known is the mechanism by which this precise control is maintained.

1. Intracellular cation composition has been measured in the red cells from twenty patients with hyperthyroidism. The mean concentration of sodium was 11·18 m-mole/l red cells; in sixty normal control subjects the mean red cell sodium level was 7·04 m-mole/l. The difference between these two groups was highly significant. There was no measurable difference between the potassium concentration and water content of red cells from thyrotoxic and control groups. 2. Measurements of active sodium efflux were carried out in red cells from ten hyperthyroid subjects and their matched controls. The rate constant for active sodium efflux was significantly lower in the patients than the control group. 3. The total amount of sodium actively pumped from red cells in 1 hr was significantly higher in the patients than the controls. 4. The total amount of sodium moving out of the red cells, both actively and by exchange diffusion, matched the total influx of sodium. This was true for control subjects and those with hyperthyroidism and this would support the view that the intracellular sodium concentration is constant and represents the result of a balance between influx and efflux. In hyperthyroidism this balance persists, but with an abnormally high intracellular sodium concentration. 5. There was a linear relationship between the cell sodium content and the active transport of sodium from the cell in control and hyperthyroid subjects. 6. Triiodothyronine did not produce any change in sodium transport by normal red cells in vitro. 7. It is concluded that there is a depression of the activity of the sodium pump in the red cells of hyperthyroid subjects. This allows the resting intracellular sodium concentration to rise until a new steady state is reached. Evidence is given that these changes are reversed when hyperthyroidism is corrected.

1. Acute oral administration of metoprolol and propranolol to ten normal males resulted in equal reduction in heart rate both supine and after passive tilting to 60°. 2. Tilted systolic blood pressure was reduced by both agents but metoprolol alone reduced supine systolic blood pressure. 3. Tilted but not supine diastolic blood pressure was reduced by both agents. 4. Metoprolol and propranolol both reduced the rise in plasma renin activity induced by tilting. 5. No effect of tilting was observed on plasma aldosterone.