Serum isoamylase activities in diabetes mellitus.

Serum pancreatic isoamylase activities were used to assess exocrine pancreatic function in 39 patients with diabetes mellitus (21 on insulin, 12 on sulphonylureas, and six on biguanides or diet), and the results were compared with serum immunoreactive trypsin concentrations. Thirteen patients had decreased pancreatic isoamylase activity, the insulin-dependent diabetics showing the highest incidence of abnormality. This incidence of abnormality is similar to that previously described for serum immunoreactive trypsin, and the two procedures gave excellent overall correlation (r = 0.9). Our observations offer further evidence that pancreatic exocrine function is impaired in diabetes mellitus. Serum isoamylase determination provides a convenient, inexpensive, and rapid procedure for its detection.

Pancreatic exocrine function after truncal and highly selective vagotomy.

We have measured plasma glucose and immunoreactive trypsin concentrations and serum pancreatic amylase activities in single blood samples following truncal vagotomy (TV) in 13 patients and highly selective vagotomy (HSV) in 14 patients. Our results show that an increased incidence of exocrine pancreatic insufficiency occurs postoperatively regardless of the type of vagotomy. Glucose concentrations were significantly higher after TV, suggesting that HSV is preferable for patients at risk of or suffering from diabetes mellitus.

Serum immunoreactive trypsin in beta-thalassaemia major.

To assess the exocrine pancreatic function in beta-thalassemia major with iron overload, serum immunoreactive trypsin (IRT) was measured in 38 patients with this condition. In 23 (60%) patients' IRT was abnormal: it was subnormal in 16 patients and supranormal in seven. Whereas subnormal IRT concentrations were more frequent in patients of more than 12 years old, supranormal IRT concentrations were more frequent in younger patients. These data provide the first antemortem evidence of exocrine pancreatic damage in this condition. They also suggest that this acinar cell damage is initially associated with a rise in IRT which is followed by a fall in the serum concentration of this enzyme.

Hyperlipidaemia in untreated nephrotic syndrome, increased production or decreased removal?

The relative importance of increased lipoprotein synthesis and decreased lipoprotein catabolism is examined in 13 patients with untreated nephrotic syndrome by the use of intravenous fat tolerance tests analysed in relation to other parameters of lipid metabolism. Increased lipoprotein synthesis in nephrotic patients was indicated by the fact that at a given fractional clearance rate of Intralipid (K2), nephrotic patients had higher serum TG concentrations than did control subjects. A defect in lipoprotein catabolism was also suggested by the frequent finding of intermediate density lipoproteins on electrophoresis and the marginally low (p = 0.05) mean K2 in nephrotic patients. A highly significant (p less than 0.001) positive correlation between HDL-cholesterol concentrations and postheparin fractional clearance rates (K'2) of Intralipid led to the speculation that in the severe nephrotic state (albumin less than 20 g/l) the loss of high density lipoproteins may contribute to the hyperlipidaemia.

Plasma lecithin-cholesterol acyltransferase activities in uraemic patients.

Plasma lecithin-cholesterol acyltransferase (LCAT) activity was measured in 43 haemodialysis and 15 peritoneal dialysis (CAPD) patients. LCAT activities in both groups of patients were significantly lower than those of normal subjects and did not correlate with any of the other biochemical parameters studied. The effect of intravenous administration of 100 U/kg of heparin on LCAT activity was examined in 21 haemodialysis patients and 19 normal subjects. Heparin inhibited LCAT activity by increasing plasma free fatty acid concentrations. LCAT remained inhibited throughout a dialysis session and returned towards pre-dialysis levels an hour after haemodialysis was discontinued. The cause of the low LCAT activities in the patients was not certain, but did not appear to be due to the presence of inhibitors in the uraemic plasma. The significance of these findings is discussed.

Plasma LCAT activities in renal allograft recipients.

Plasma LCAT activities were measured in 51 renal allograft recipients as well in 18 patients before and after successful renal transplantation. The mean plasma LCAT activity of the 51 patients did not differ significantly from that of 27 normal subjects. When the patients were separated into two groups according to whether they had normal or impaired renal function, there was no significant difference in their mean LCAT activities. Plasma LCAT activities correlated significantly with total cholesterol and total triglyceride concentrations. The sequential study demonstrates that the low plasma LCAT activities in uraemic patients rose towards normal after successful transplantation. At the same time, total cholesterol and HDL-cholesterol concentrations also increased. The increase in LCAT activity after renal transplantation is due to increased concentrations of the enzyme and probably reflects increased turnover of triglyceride-rich lipoproteins.

Serum immunoreactive trypsin in cystic fibrosis.

Serum immunoreactive trypsin (IRT) concentrations were measured blind in sera from 33 patients with cystic fibrosis and in 32 age-matched controls. Thirty-two patients had abnormal trypsin concentrations. In 30 of these patients the level of IRT was very low whereas in the other two (the youngest of the group) it was extremely high. All 30 patients with low IRT concentrations had clinical or biochemical evidence of malabsorption. Serum IRT concentration may thus be a useful diagnostic test for cystic fibrosis. In view of the recent observation that neonates with cystic fibrosis consistently have raised IRT concentrations, and the fact that the youngest two patients in our series also had markedly increased IRT, it would appear that the initial elevation of IRT reflects early damage to the pancreas with release of enzyme/zymogen; this is thereafter superseded by a progressive destruction of the pancreas resulting in low IRT concentrations in adults with cystic fibrosis.