Cholangiocarcinoma is an infrequent complication of inflammatory bowel disease. Although increasing numbers of cholangiocarcinomas are being reported in association with ulcerative colitis, the occurrence of this disease in patients with Crohn's disease is rare. To understand this complication better, we have reported the case of a patient with Crohn's disease in whom cholangiocarcinoma subsequently developed and reviewed the literature.
Interest continues regarding the role ofinin peptides as humoral mediators in acute pancreatitis. Plasma is an ample substrate for kinin, which can be activated from its precursor state-bound to alpha 2 globulin-by either trypsin or kallikrein. These enzymes, in turn, are normally present in the pancreas and are activated during the cell necrosis of acute pancreatitis. Well-known pharmacologic actions of kinins include pain production, vasodilatation, increased vascular permeability, hypotension, smooth muscle stimulation, and leukocyte aggregation. All of these are characteristically found during the course of acute pancreatitis.Direct measurement of plasma kinin was extremely difficult and for this reason studies were carried out on the component parts of the kinin system. We previously reported the finding of increased kinin inhibitors during the course of experimental pancreatitis (1). Significant changes in the level of kinin precursors would add weight to the evidence indicating the kinin system in the pathologic physiology of acute pancreatitis.Method. Ten splenectomized mongrel dogs were anesthetized with sodium pentobarbital (30 mg/kg of body wt.) and both femoral veins were cannulated, one for the removal of blood and the other for injection of serum albumin x*lI. Splenectomy was carried out 2 weeks previously to decrease the influence of splenic sequestration on the circulating blood volume. Pancreatitis was induced by intraductal infusion at 40 cm water pressure of a 20 ml mixture of 4% sodium taurocholate and 400,000 units of trypsin, adjusted to pH 8. Trypsin was previously assayed on a benzyl arginine ethyl ester substrate. Plasma vol-~ ~ *Supported in part by a grant from the National 1 Present address: Karachi 18, Pakistan. 2 Present address: Manila, Philippines. Institutes of Health (AM 09050).ume was determined before operation and at 2, 4, and 6 hr after induction of pancreatitis using a Volemetron apparatus ( Ames Company, Elkhart, Indiana). Hematocrit was determined by the micromethod. Plasma kininogen was determined by the method of Dink and Carvalho (2) in which denatured plasma is exposed to an excess of trypsin, dried under pressure, and the residue resuspended in saline. Assays were carried out on an isolated, prepared, rat uterus. Isometric contraction was measured on a strain gauge and recorded on a direct writing oscillograph (Grass model no. 5DWCI).In three of the dogs, peritoneal fluid was collected at 2, 4, and 6 hr after the onset of pancreatitis. Volume was recorded, hematocrit was determined, and the kininogen content was measured by the same methods.Results. A devrease in the total circulating kininogen pool was demonstrated in all dogs during the first 6 hr of experimental pancreatitis. Circulating kininogen pool was calculated by multiplying the plasma volume by the kininogen concentration in micrograms per milliliter of plasma. Decrease varied from 11-48% with an average of 31.1% (Fig. 1). At the same time, plasma volume decreased an average of 28 % ( 17-41 % ) and blood vo...
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