1. Concentrations of ascorbic acid (ascorbic and dehydro-ascorbic; A+D; measured by the 2,4-dinitrophenylhydrazine method) of nearly three times those of plasma are present in gastric juice samples from patients with normal gastric histology. 2. A significant reduction in gastric juice ascorbic acid (A+D) was observed in patients with chronic gastritis. This reduction in concentration was independent of the grade of gastritis. 3. Concentrations of ascorbic acid (A+D) in gastric biopsy specimens were consistently higher in the antrum than in the body of the stomach. 4. These data demonstrate that considerable quantities of ascorbic acid (A+D) are normally ‘secreted’ into the stomach. 5. Ascorbic acid (ascorbic only; A; measured by h.p.l.c.) was present predominantly in its biologically active form in the patients with normal gastric histology. However, in patients with gastritis, independent of grade, ascorbic acid was present predominantly in its oxidized, biologically inactive form.

1. The measurement of the intestinal metabolism of the nitrogen moiety of glutamic acid has been investigated by oral ingestion of l -[ 15 N]glutamic acid and sampling of arterialized blood. 2. Measurements have been made in six normal adults weighing an average of 72.8 kg ingesting 100 mg of l -[ 15 N]glutamic acid after an overnight fast. 3. Measurement of the enrichment of arterial glutamic acid, glutamine and alanine was by gas chromatography–mass spectrometry. Isotopic enrichment of the amino acids was followed for 150 min after the ingestion of the amino acid. 4. Arterialized venous blood amino acid concentrations, measured by h.p.l.c., demonstrated no significant changes during the course of the experiment. 5. From the observed appearance of label in arterialized glutamic acid, alanine and glutamine, little luminal glutamic acid reaches the extracellular pool. The majority of the administered nitrogen label appears in the arterial alanine and glutamine components.

1. Gas–liquid chromatography and a radioreceptor assay were used to measure plasma γ-aminobutyric acid (GABA) in patients with liver disease and hepatic encephalopathy. 2. There was a significant correlation between the results obtained by the two methods, and compared with controls plasma GABA was elevated. 3. These findings suggest that the increased GABA binding inhibitory activity of plasma of these patients is probably due to GABA itself.

1. Serum vitamin A, retinol binding protein, prealbumin and transferrin have been studied in chronic renal failure patients receiving maintenance haemodialysis and after renal transplantation. 2. Vitamin A and retinol binding protein were uniformly raised in haemodialysis patients and this was unrelated to the period on dialysis. There was a molar excess of retinol binding protein to both vitamin A and prealbumin as compared with normal individuals. 3. Renal transplantation significantly reduces serum vitamin A and retinol binding protein concentrations but has no effect on prealbumin concentrations. The reduction in vitamin A and retinol binding protein is variable in individual patients and cannot be predicted either by the allograft function or time since transplantation. 4. Several years after transplantation, with normal serum creatinine, both serum vitamin A and retinol binding protein levels may still be greatly increased. Despite the very high vitamin A and retinol binding protein concentrations, the close correlation between the two seen in normal individuals is well maintained. 5. The continuing high vitamin A and retinol binding protein levels in patients with satisfactorily functioning transplants is unexplained.

1. Erythrocytes with membrane abnormalities seen on interference contrast microscopy (‘pitted erythrocytes’) were counted in venous blood samples from patients with treated coeliac disease and dermatitis herpetiformis, and from control subjects and patients who had had an elective splenectomy. 2. The percentage of ‘pitted erythrocytes’ was compared with the 99m Tc-labelled heat-damaged erythrocyte clearance, and with the splenic size computed from scintiscans. 3. There was a significant correlation between percentage ‘pitted erythrocytes’ and the above methods of measuring splenic function and size. Increase in the percentage of ‘pitted erythrocytes’ above the control range indicated splenic hypofunction. 4. The number of coeliac patients with percentage ‘pitted erythrocytes’ above the control range increased with increasing age at which they started a gluten-free diet. 5. Counting of ‘pitted erythrocytes’ is a simple and sensitive method of assessing splenic hypofunction in treated coeliac disease. It avoids radiation exposure, and is applicable to all ages and repeatable without risk. 6. The incidence of splenic hypofunction in coeliac patients may be related to the duration of untreated disease.

1. Fat malabsorption caused by bile-salt deficiency is not easily corrected by standard therapy. It has been shown in rats with bile-salt deficiency that non-ionic detergents can replace bile salts and improve fat absorption. A careful assessment of the place of synthetic detergents such as Tween in human therapy has not been reported. 2. The effects of Tween were studied in 13 patients with bile-salt-deficient steatorrhoea, eight of whom received Tween 80 and five Tween 20. 3. Tween therapy reduced steatorrhoea in 10/13 patients; a mean decrease in faecal fat of 33% was achieved with best effect seen in patients with severe steatorrhoea. 4. In the five patients given Tween 20, duodenal/jejunal intubation was conducted using meals with or without added Tween. Jejunal bile salt concentrations were low in all subjects and Tween had no effect on bile-salt output. 5. With Tween addition micellar free fatty acids and phospholipids were increased in four out of the five patients (mean increases 100% and 260% respectively). The mean ratio of fatty acid to bile salt increased from 1·26 to 3·53 and of phospholipid to bile salt from 0·09 to 0·21 in the presence of Tween. 6. The results suggest that in steatorrhoea due to bile-salt deficiency Tween causes increased micellization of ingested fat and improvement in fat absorption. 7. Tween and other non-ionic detergents may, therefore, find a place in therapy of bile-salt deficiency.

1. Control, vitamin E-deficient, vitamin E-supplemented (deficient with added ‘normal’ intake) and vitamin E-treated rats were given paracetamol at a dose of 25.5 mmol (4 g)/kg body weight. Control rats were also given paracetamol with or without simultaneous vitamin E. 2. Plasma aspartate aminotransferase and alanine aminotransferase activities increased to very high values (mean 2842 and 1241 i.u./l respectively) in the control group, and even higher (mean 8220 and 2320 i.u./l respectively) in the vitamin E-deficient group. 3. In the vitamin E-supplemented group the rises in activity were similar but rather less than in the control group (mean 2417 and 815 i.u./l) and in the vitamin E-treated group only very small rises (mean 177 and 98 i.u./l) were seen. 4. Histological evidence of hepatic necrosis correlated closely with plasma enzyme activities. 5. It appears that paracetamol-induced hepatic necrosis is potentiated in vitamin E deficiency and reduced by prior treatment with α-tocopherol. 6. Vitamin E administered simultaneously with paracetamol at 12.8 or 19.2 mmol/kg also greatly reduced the expected rise in serum enzyme activities. 7. These observations may shed some light on the mechanism of paracetamol-induced hepatic necrosis, and may form a basis for preventing or reducing this lesion in man.