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[Autotransplantion of Langerhans islets after total duodeno-pancreatectomy in a patient with chronic pancreatitis (author's transl)].

Total duodenopancreatectomy was performed in a 36-year-old man because of global chronic pancreatitis. Islets cells were isolated by collagenase digestion from the resected pancreas and re-implanted into the liver via the portal vein. Until the sixth postoperative day the amount of insulin required fell from 54 IU initially to 10 IU per day. Serial insulin determination demonstrated secretion by the implanted cells.

Adult↗

Progressive loss of sensitivity of the A cell to insulin in geese made diabetic by subtotal pancreatectomy.

The effects of insulin deficiency on pancreatic A cell responsiveness to glucose was studied in subtotally depancreatized geese. In geese operated for 3 to 5 days and receiving insulin therapy (I.M.: 0.5-1.0 U/kg/24 h), A cell response to glucose (I.V. injection: 0.5 g/kg) was abolished, but could be restored to normal range by insulin (I.V. injection: 0.025-0.2 U/kg) together with glucose. After 5 weeks of therapy, A cell sensitivity declined: the physiological amount of insulin (0.025 U/kg) was insufficient to suppress glucagon during the glucose load, whereas the large dose (0.2 U/kg) partially restored A cell response. In addition, daily insulin treatment prevented a severe increase of fasting plasma glucose and glucagon. Geese receiving no insulin therapy showed "total blindness" to glucose, even when given insulin at the time of the test. These data suggest a progressive loss of sensitivity of the A cell to insulin. Endocrine and/or panacrine insulin deficiency may play a role on the dysfuncion of the glucose-glucagon feedback mechanism.

Animals↗

The pancreatic duct and its arteriovenous relationship: an underutilized aid in the diagnosis and distinction of pancreatic adenocarcinoma from pancreatic intraepithelial neoplasia. A study of 126 pancreatectomy specimens.

Pancreatic intraepithelial neoplasia (PanIN) may be difficult to differentiate from isolated glands of pancreatic adenocarcinoma. We studied the normal relationship between the pancreatic ducts and the pancreatic muscular blood vessels in 126 pancreata, 64 of which were removed for pancreatic adenocarcinoma and 62 for other diagnoses. We also examined the effects that atrophy and PanIN have on this relationship. In normal pancreatic parenchyma and in mild to moderate atrophy, blood vessels are guideposts of the interlobular space. The pancreatic acinar parenchyma ensheathes the pancreatic ductal system and separates it from the muscular pancreatic vasculature. Since these blood vessels do not accompany the pancreatic ducts, the presence of a well-differentiated duct-like structure, which may resemble PanIN, located adjacent to a pancreatic blood vessel should be a clue to the infiltrative and hence malignant nature of that gland. Ducts showing PanIN appear to resist atrophy. Since lobular outlines and vascular landmarks are ultimately lost in severe atrophy, they cannot be relied on to aid in the distinction between PanIN and invasive carcinoma. However, it is unusual to see PanIN1 in such severe atrophy (2%), and although the normal vascular landmarks are no longer there to aid in the interpretation, the presence of well-differentiated duct-like structures resembling PanIN1 in this background should be viewed with suspicion for well-differentiated adenocarcinoma.

Adenocarcinoma↗