Pathobiology of experimental acute pancreatitis.

Pancreatic duct obstruction, even in the absence of biliary obstruction and/or bile reflux into the pancreatic duct, can trigger acute hemorrhagic necrotizing pancreatitis. The earliest changes are seen within acinar cells. Early derangements in acinar cell biology include inhibition of digestive enzyme secretion and the co-localization of lysosomal hydrolases with digestive enzyme zymogens. Under appropriate conditions, this co-localization could lead to digestive enzyme activation within acinar cells.     

Patterns of incidence in acute pancreatitis.

A review of acute pancreatitis occurring over a 20-year period in the Bristol clinical area is reported. A total of 590 cases were available for analysis. The yearly incidence was 53-8 per million population at risk, with a mortality of 9-0 per million. This compares favourably with 11-4 deaths per million for England and Wales as a whole during the same period but the difference is not statistically significant. When the deaths occurring in the Bristol clinical area were expressed in terms of case mortality rate the figure was 17%. In contrast the mortality for recurrent acute pancreatitis was only 1-5%, and the benign nature of this second condition is confirmed. Aetiological factors and age and sex distribution were also analysed in relation to each other and to mortality. An increase in acute pancreatitis secondary to chronic alcoholism was confirmed and steroid pancreatitis also emerged as a definite entity in this survey. The pattern of recurrence in patients with idiopathic pancreatitis was studied in detail and is analysed on an actuarial basis.     

Familial benign hypercalcaemia (FBH; McK. No. 14598, 1983): Linkage studies in a large Dutch family

Summary By screening 27 hypercalcaemic and 21 normocalcaemic subjects in a large Dutch pedigree with familial benign hypercalcaemia (FBH; McK. No. 14598) (McKusick 1983) for more than 35 genetic markers, it was found that linkage of FBH can be excluded at about 25 centimorgans (cM) from GM, 20 cM from ABO, 15 cM from MNS and HLA, 10cM from JK and PI, and 5cM each from ACP1, AK1, ADA, GPT1, and PGP.     

Paraneoplastic hypercalcaemia in ovarian carcinoma.

Five patients were seen in whom a raised serum calcium concentration was associated with ovarian carcinoma (clear cell in two cases, cystadenocarcinoma in three). None showed evidence of metastases in bone. The hypercalcaemia occurred as a paraneoplastic phenomenon, but biochemical studies suggested the production of a parathyroid-hormone-like substance. One patient remained free of symptoms of her hypercalcaemia throughout. Paraneoplastic hypercalcaemia due to ovarian carcinoma may be more common than generally recognised and present as a life threatening condition requiring urgent treatment.