[Congenital duodenal stenosis in adulthood]. / Kongenitale Duodenalstenose im Erwachsenenalter.

A high-grade duodenal stenosis in adults can, in rare cases, be congenital, and its cause is found in an intraduodenally sited membrane. The anamnesis reveals growth disorders with vomiting and meteorism and abdominal complaints. A perforation opening in this membrane is the reason for survival into adulthood. The X-ray appearance and deep duodenoscopy make the diagnosis easy. Volvulus in cases of malrotation, Ladd's ligaments, annular pancreas, and compression of the duodenum by mesenteric vessels must be considered in the differential diagnosis. When the intraduodenal membrane is resected it is most important to expose the papilla Vateri, since this not uncommonly ends in the area of the septum. If necessary, a duodenoduodenostomy is performed. If the windsock web abnormality is present the duodenum should be opened at the point of attachment of the diaphragm. The construction of a gastrojejunostomy should be avoided.

Improvement of oral glucose tolerance in the dog by feeding trypsin inhibitor. Role of the enteroinsular axis.

The influence of oral trypsin inhibitor (TI) or vehicle (V) during 4 weeks on oral glucose tolerance (OGT) and on the enteroinsular axis (EIA) of insulin, CCK, and gastrin was studied in five beagles. TI improved OGT throughout the 180-min test period. Incremental areas of insulin and gastrin did not differ from 0 to 60 min after TI and V treatment, but both increased significantly from 60 to 180 min after TI. From 0 to 60 min CCK decreased significantly in the TI group, whereas the differences (delta) in hormone changes (insulin, CCK, gastrin) observed during oral and intravenous glucose showed a decrease for their incremental areas during this period. During the 60- to 180-min period this hormone spectrum was reversed into a non-significant increase. We suggest that TI pretreatment improves oral glucose tolerance, possibly owing to decreased intestinal glucose absorption (early test period), augmentation of the incretin effect (later test period), or some unidentified factor.