Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PANCREATITIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed2005

Duodenum preservation in pancreatic head resection to maintain pancreatic exocrine function (determined by pancreatic function diagnostant test and cholecystokinin secretion).

BACKGROUND/PURPOSE: Organ-preserving surgery, such as pylorus-preserving pancreatoduodenectomy (PPPD), duodenum-preserving pancreatic head resection (DPPHR), or medial pancreatectomy (MP), is one of the recent advances in pancreatic surgery. There was a previous report that preservation of the duodenum maintained pancreatic function. However, concerning the resected pancreas, patients were divided into two groups; one group included pancreatic head resections such as Whipple, PPPD, and complete DPPHR, and the other group included MP that removed only the pancreatic neck and preserved the pancreatic head and distal pancreas. The present study was designed to clarify the significance of duodenum preservation, in comparison with duodenum removal, in patients with pancreatic head resection, in terms of pancreatic function, determined by a pancreatic function diagnostant (PFD) test and cholecystokinin (CCK) secretion. METHODS: The subjects were 61 patients (10 with Whipple, 41 with PPPD, and 10 with complete DPPHR). PFD tests and postprandial plasma CCK secretion were used for evaluation. RESULTS: There was a significant difference between pre- and postoperative PFD values in the patients who received Whipple or PPPD; however, there was no difference in those who had complete DPPHR. Concerning the postoperative PFD value, complete DPPHR was superior to Whipple and PPPD. Regarding postprandial CCK secretion, the pre- and postoperative values were significantly different in the patients with Whipple or PPPD, but there was no difference in those with complete DPPHR. Comparing the three kinds of operations, complete DPPHR was superior to the other two procedures in its maintenance of pancreatic function. There was the significant correlation between CCK and PFD in our patients in the Spearman Rank Correlation (P < 0.0029) and Fisher's r to z (P < 0.0058). CONCLUSIONS: When pre- and postoperative pancreatic exocrine function and postprandial CCK secretion were measured in patients with pancreatic head resection, it was found that preservation of the entire duodenum was an important factor for maintaining pancreatic function.

Cholecystokinin↗
PubMed1992

Effect of short-termed pancreatic duct obstruction on the pancreatic subcellular organellar fragility and pancreatic lysosomal enzyme secretion in rabbits.

We studied the effect of short-term (3 h) pancreatic duct obstruction (PDO) on the exocrine pancreas and on the secretion of lysosomal enzymes into the pancreatic juice of rabbits during stimulation by pancreatic secretagogues. The following evaluations were made: serum amylase levels, pancreatic water content, pancreatic amylase, trypsinogen and cathepsin B content, and output of pancreatic enzymes and lysosomal hydrolases when stimulated by secretin and caerulein as well as the distribution of cathepsin B in subcellular fraction. Cellular fragility (LDH leakage from dispersed acini) and subcellular organellar fragility (cathepsin B leakage from lysosomes and malate dehydrogenase leakage from mitochondria) were also evaluated. PDO for 3 h plus secretin infusion caused a significant rise in serum amylase levels, pancreatic water content, and pancreatic amylase and trypsinogen content due to congestion of digestive enzymes during PDO. There was also a redistribution of cathepsin B from the lysosomal fraction to the zymogen fraction and increased cellular and subcellular organellar fragility. In normal rabbits and in those with only secretin infusion, caerulein stimulated the secretion of cathepsin B into pancreatic juice. Just after PDO, the secretion of cathepsin B, amylase and trypsinogen significantly decreased. By 24 h after PDO, the output of cathepsin B stimulated by caerulein and secretin had increased significantly. Amylase and trypsinogen output were also significantly increased at this stage, in both the secretin and caerulein fractions. These results indicate that the secretion of lysosomal enzymes into pancreatic juice is stimulated by gut hormones, such as caerulein, in the normal physiological state and in pathological states, such as PDO. These results also show an important role of increased cellular and subcellular organellar fragility in the pathogenesis of pancreatic injuries induced by PDO and augmented secretion of both lysosomal enzymes and pancreatic digestive enzymes in the recovery stage after PDO and their important roles at this stage. Lysosome enzymes also seem to play some physiological roles in the pancreatic ductal system in normal physiological states as well as their roles in pathological states, because cathepsin B can activate trypsinogen, and trypsin can activate many other enzymes.

Amylases↗
PubMed2006

Overexpression of c-met in the early stage of pancreatic carcinogenesis; altered expression is not sufficient for progression from chronic pancreatitis to pancreatic cancer.

AIM: To investigate c-met expression during early pancreatic carcinogenesis. METHODS: We used 46 bulk tissues and 36 micro-dissected samples, including normal pancreas, chronic pancreatitis, and pancreatic cancer, for quantitative real-time reverse transcription-polymerase chain reaction. RESULTS: In bulk tissue analyses, pancreatic cancer tissues expressed significantly higher levels of c-met than did chronic pancreatitis and normal pancreas tissues. c-met levels did not differ between chronic pancreatitis and normal pancreas tissues. In microdissection-based analyses, c-met was expressed at higher levels in microdissected pancreatic cancer cells and pancreatitis-affected epithelial cells than in normal ductal epithelial cells (both, P < 0.01). Interestingly, pancreatitis-affected epithelial cells expressed levels of c-met similar to those of pancreatic cancer cells. CONCLUSION: Overexpression of c-met occurs during the early stage of pancreatic carcinogenesis, and a single alteration of c-met expression is not sufficient for progression of chronic pancreatitis-affected epithelial cells to pancreatic cancer cells.

Biomarkers, Tumor↗
PubMed1990

Immunochemical characterization and quantitative distribution of pancreatic stone protein in sera and pancreatic secretions in pancreatic disorders.

A fluorometric immunoassay has been established to quantitate pancreatic stone protein providing a sensitivity for concentrations from 0.015 to 0.5 micrograms/mL. When concentrations of pancreatic stone protein were determined from pancreatic secretions obtained either from patients suffering from chronic pancreatitis (n = 31) [including the calcifying forms (n = 10)], pancreatic cancer (n = 22), or nonpancreatic diseases (n = 17), no significant differences were found. In contrast, increased concentrations were found in serum samples from patients with chronic (39/66) and acute pancreatitis (16/20) compared with control patients. The differences between these diagnostic groups and controls were highly significant (P less than 0.0001) and independent of pancreatic enzyme activity. Immunochemical analyses of serum pancreatic stone protein showed an isoelectric point (pH 9) similar to that reported for the pancreatic thread protein. With respect to recent communications, these data do not support the etiopathogenic role postulated for pancreatic stone protein in chronic pancreatitis and chronic calcifying pancreatitis by other investigators.

Adult↗
PubMed1981

Interdigestive canine pancreatic juice composition and pancreatic reflux and pancreatic sphincter anatomy.

Canine and human exocrine pancreatic secretion into the duodenum during fasting is cyclical and related to intestinal motility. To characterize the composition of pure pancreatic juice during the cyclically recurring sequence of propagated motor events (interdigestive motor complex) and to establish whether pancreatic reflux occurs, dogs were prepared with three permanent indwelling duodenal catheters and a pancreatodochal cutaneous catheter. The duodenal catheters were used to record duodenal pressures and measure pancreatic secretion of trypsin, lipase, and bicarbonate, based on the recovery of a constantly perfused marker, [14C]PEG. Pancreatic duct pressures or pancreatic juice concentrations of [14C]PEG, trypsin, lipase, or bicarbonate (done separately in each of five dogs throughout one interdigestive cycle on 4 different days) were related to duodenal motor activity. Finally, the pancreatic duct orifice of freshly sacrificed dogs was examined by light and electron microscopy. During fasting, (1) pancreatic volume secretion increased 10-fold during phases II, III, and IV (P less than 0.001), and bicarbonate concentration increased during phases III and IV (P less than 0.05) compared with phase I, while trypsin and lipase concentrations did not change; (2) reflux of duodenally perfused [14C]PEG into the pancreatic duct occurred in two of five dogs and was minimal (less than 0.1%); and (3) a positive mean pressure gradient from duodenum to pancreatic duct occurred only during phase III (7.4 +/- 4.1 cm H2O). Anatomic studies of the pancreatic duct opening showed a specialized papillary mucosa and an independent crescentic sphincter muscle. We conclude that during fasting, pancreatic juice composition is intimately linked to the different phases of interdigestive intestinal motor activity and that an efficient antireflux mechanism exists.

Animals↗
PubMed1989

Extrahepatic portal venous obstruction of different pathogenesis in pancreatic diseases: reports of 4 autopsy cases with chronic pancreatitis and pancreatic carcinoma.

Four autopsy cases of extrahepatic portal venous obstruction associated with pancreatic diseases, 1 case of pancreatitis and 3 cases of pancreatic carcinoma, are presented. The pathogenesis of portal obstruction was different in each case; old thrombosis with recanalization due to chronic pancreatitis with pseudocysts formation in 1 case, fresh thrombosis due to intraportal venous catheterization for pancreatic carcinoma in 1 case, fresh thrombosis probably due to pancreatitis accompanying pancreatic carcinoma in 1 case, and direct invasion of pancreatic carcinoma into the portal vein in the remaining 1 case. Morphologic evidence for portal hypertension was present in each case. In the pancreatitis case and one pancreatic carcinoma case with portal tumor invasion, both of which had chronic portal obstruction, there were many thin-walled vascular channels (cavernous transformation) around the occluded portal vein. Their endothelia were positive for factor VIII-related antigen and Ulex europaeus lectin I, implying that these vessels were hepatopetal blood vascular collaterals. It was shown that pancreatic diseases resulted in portal venous obstruction by several different mechanisms and chronic portal obstruction in pancreatic diseases led to the formation of hepatoperal blood vascular collaterals.

Adenocarcinoma↗
PubMed2002

Differences in the expression of glutathione S-transferases in normal pancreas, chronic pancreatitis, secondary chronic pancreatitis, and pancreatic cancer.

INTRODUCTION: In our previous study, glutathione S-transferase-pi (GST-pi), a phase II drug metabolizing enzyme, was found to be expressed in pancreatic ductal and ductular cells but not acinar cells of the normal pancreas, chronic pancreatitis, and secondary pancreatitis caused by pancreatic cancer. A greater percentage of the cells expressing GST-pi was shown in the islets of chronic pancreatitis specimens compared with the normal pancreas and secondary pancreatitis. AIMS AND METHODOLOGY: To examine whether the increased number of islet cells expressing GST-pi and the absence in the acinar cells are compensated for by other GST isozymes, we investigated the expression of GST-alpha and GST-mu in the same specimens. RESULTS: Unlike the distribution of GST-pi, the distribution of GST-alpha and GST-mu in islets did not show marked differences between the three groups. However, in four of 18 primary chronic pancreatitis specimens, more islet cells (approximately 25%) expressed GST-alpha than in the normal pancreas and secondary chronic pancreatitis (both approximately 10%). The reactivity of cancer cells to GST-alpha, GST-mu, and GST-pi was similar to the ductal cells in the normal pancreas, chronic pancreatitis, and secondary chronic pancreatitis. Contrary to the expression of GST-pi, no statistically significant differences were found in the distribution of GST-alpha and GST-mu in the normal pancreas, chronic pancreatitis, and secondary chronic pancreatitis. CONCLUSION: The expression of the other GSTs does not compensate for the variation of expression of GST-pi. There was no specimen in each group that did not express at least one GST isozyme in islet, acinar, and ductal cells.

Adolescent↗
PubMed2004

A highly sensitive and quantitative telomerase activity assay with pancreatic juice is useful for diagnosis of pancreatic carcinoma without problems due to polymerase chain reaction inhibitors: analysis of 100 samples of pancreatic juice from consecutive patients.

BACKGROUND: Early detection of pancreatic carcinoma is difficult even with current diagnostic tools. Novel biomarkers and detection techniques are urgently needed. Telomerase activity is a promising diagnostic marker. However, the conventional telomeric repeat amplification protocol (TRAP) assay is not suitable for clinical application because of its complexity, time-consuming nature, and the effects of polymerase chain reaction (PCR) inhibitors in samples leading to difficulties in quantification. METHODS: The authors used a hybridization protection assay in combination with TRAP (TRAP/HPA) to investigate the effects of PCR inhibitors in pancreatic juice on quantification of telomerase activity. They analyzed 117 consecutive samples of pancreatic juice to determine the feasibility of TRAP/HPA for diagnosis of pancreatic carcinoma. RESULTS: The authors found that TRAP/HPA was 1000-fold more sensitive than the conventional TRAP assay, and that the effects of PCR inhibitors could be avoided by diluting samples. In a large analysis of pancreatic juice samples with TRAP/HPA, 17 samples were excluded from the final analysis because of insufficient follow-up periods or inadequate treatment of the samples. Relative telomerase activity (RTA) in samples from patients with pancreatic carcinoma was significantly higher in comparison to samples from patients with pancreatitis and 13 (61.9%) of 21 samples from patients with pancreatic carcinoma showed high RTA (> 4 U). Meanwhile, high RTAs were observed in 4 of 35 (11.4%) samples from patients with intraductal papillary mucinous tumor and in 1 of 40 samples (2.5%) fom patients without malignant disease. CONCLUSIONS: TRAP/HPA accurately evaluated weak telomerase activity in pancreatic juice samples without the problem due to PCR inhibitors. This large analysis of nonselected pancreatic juice samples suggested that TRAP/HPA is a promising approach for the diagnosis of pancreatic carcinoma.

Adult↗
PubMed1989

Effects of a newly synthesized pancreatic protease inhibitor (PATM) on pancreatic microcirculation in experimental acute pancreatitis.

Pancreatic inschemia, especially due to pancreatic microcirculation disturbance, has been considered to trigger and aggravate acute pancreatitis. In this work experimental acute pancreatitis was produced by autologous bile and trypsin in mongrel dogs to study the time-course changes in systemic and local hemodynamics in association with disease progress. In addition, the effects of a new synthetic pancreatic protease inhibitor (PATM, 3 mg/kg/hr, i.v.) on systemic and local circulation were examined. In animals with untreated pancreatitis the mean baseline pancreatic microflow was 55.6 +/- 17.0 ml/min/100g before the onset of pancreatitis and this decreased by 22% and 52% at 1 hr and 5 hr, respectively. The femoral arterial pressure and cardiac index also decreased during the 5 hr experiment at period in comparison with the respective preoperative levels. The portal venous flow showed a sharp reduction immediately after the onset of pancreatitis, staying at a low level thereafter. The pancreatic microflow was significantly improved by PATM treatment for the first 60 min and the portal venous flow for the first 120 min. PATM treatment prevented the decrease in femoral arterial pressure, although it failed to exert any appreciable effect upon the cardiac index. These findings suggest that intravenous administration of PATM might be of value for improving the pancreatic microflow and portal venous flow, at least in the early stage of experimental acute pancreatitis in dogs.

Acute Disease↗
PubMed1999

Does bile of patients with acute gallstone pancreatitis cause pancreatic inflammatory lesions? A study of the pancreatic toxicity of choledochal secretions collected at ERCP.

BACKGROUND: Bile flow into the pancreatic duct has been proposed as the cause of acute biliary pancreatitis. However, the pancreatic toxicity of choledochal bile from patients with acute gallstone pancreatitis has not been studied. METHODS: Bile was collected endoscopically from the common bile ducts of 21 patients with acute gallstone pancreatitis within 72 hours after the onset of disease. The bile samples were instilled into the pancreatic duct of rabbits, and light microscopic examination of the pancreas morphology was performed to assess the toxicity of human bile. Microbiologic quantitative analysis of the aerobic and anaerobic bacterial bile flora was performed. RESULTS: Bile of six patients with acute gallstone pancreatitis (29%) induced interstitial inflammation in the rabbit pancreas. Choledochal bile of these patients harbored more than 10(4) CFU/mL bacteria (Proteus vulgaris, n = 1; Klebsiella pneumoniae, n = 1; Escherichia coli, n = 2; enterococci, n = 2). After sterilization, the bile samples did not induce acute pancreatitis. In 15 patients (71%), bile did not cause acute pancreatitis in the rabbit pancreas. These choledochal secretions were sterile or contained less than 10(4) CFU/mL. CONCLUSIONS: Reflux of infected bile may be a potential cause of acute pancreatitis in the minority of patients with bacterobilia. In most patients with gallstone pancreatitis, bile is neither infected nor harmful to the pancreas, and its flow into the gland is unlikely to be the cause of inflammation.

Acute Disease↗
PubMed2004

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↗
PubMed1999

Differential diagnosis between tumor-forming pancreatitis and pancreatic cancer by percutaneous transhepatic portography and selective direct pancreatic venography.

In 32 patients with tumor-forming pancreatitis and 109 patients with pancreatic cancer, the usefulness of percutaneous transhepatic portography (PTP) and selective pancreatic venography (SPV) for differential diagnosis of the two diseases was evaluated. The PTP images were type I in 53.1%, type II in 21.9%, type III in 12.5%, and type IV in 12.5% of the patients with tumor-forming pancreatitis and type I in 20.2%, type II in 23.9%, type III in 37.6%, and type IV in 18.3% of the patients with pancreatic cancer. Advanced images (type III or type IV) were observed in more than half the patients with pancreatic cancer. Mild images classified as type II were observed slightly more frequently in the patients with pancreatic cancer, but the differential diagnosis of the two diseases was difficult in patients showing type II PTP images. SPV findings were primarily hypervascularization (78.1%) and vasodilation (68.8%) in the patients with tumor-forming pancreatitis. Although encasement (smooth encasement) was noted in 31.3%, obstruction was found in only 3.1%. In the patients with pancreatic cancer, obstruction was observed in 85.3%, and encasement (irregular encasement) was noted in 78.9%. However, hypervascularization or vasodilatation was infrequent, and the tumor was characteristically imaged as a hypovascular area. PTP and SPV were considered to be useful for the differential diagnosis of tumor-forming pancreatitis and pancreatic cancer.

Diagnosis, Differential↗
PubMed1981

Pancreatic oncofetal antigen in pancreatic juices. Partial chemical characterization and diagnostic application of a pancreatic cancer-associated antigen.

Antisera were raised in rabbits to an antigenic structure present in fetal pancreas tissue, pancreatic tumor tissue, and pancreatic juices and in sera obtained from pancreatic cancer patients. The first chemical data indicate that this pancreatic oncofetal antigen is distinct from CEA, NCA, and NCA2 and is not glycolipid in nature. Immunoelectrophoretic analyses demonstrate that pancreatic oncofetal antigen is a protein or a glycoprotein, which displays microheterogeneity. The apparent molecular weight of the basic unit of pancreatic oncofetal antigen is estimated to about 40 K. So far 234 pancreatic juices have been investigated for pancreatic oncofetal antigen. Pancreatic oncofetal antigen was detected within the pancreatic juices from 59 of 74 (80%) pancreatic carcinoma patients but could be traced in only 16%-26% of samples obtained from patients with other diseases.

Adult↗
PubMed1983

Comparative evaluation of the therapeutic efficacy of a pH-sensitive enteric coated pancreatic enzyme preparation with conventional pancreatic enzyme therapy in the treatment of exocrine pancreatic insufficiency.

The therapeutic efficacy of a pH-sensitive enteric coated pancreatic enzyme preparation was compared with conventional pancreatic enzyme preparations in 6 adult patients with exocrine pancreatic insufficiency. Fecal fat excretion and postprandial duodenal recovery of orally ingested pancreatic enzymes were evaluated after ingestion of each preparation. Fecal fat excretion decreased significantly (p less than 0.005) on treatment with pH-sensitive and conventional pancreatic enzyme preparations. Postprandial concentration and delivery of trypsin and lipase in samples aspirated from duodenojejunal junction were higher after ingestion of conventional pancreatic enzyme preparation as compared to the pH-sensitive enteric coated preparation. The difference, however, did not reach statistical significance. Our observations suggest that the pH-sensitive enteric coated pancreatic enzyme preparation is only as effective as conventional pancreatic enzyme preparations in controlling fat malabsorption in patients with exocrine pancreatic insufficiency. Failure of pH-sensitive enteric coated preparation to deliver greater quantities of pancreatic enzymes at duodenojejunal junction is most likely related to the impaired release of enzymes from microspheres due to low intraluminal pH in the upper small intestine in pancreatic insufficiency.

Adult↗
PubMed2003

Pancreatic regeneration after ethionine-induced acute pancreatitis in rats lacking pancreatic CCK-A receptor gene expression.

BACKGROUND: We examined the effects of cholecystokinin (CCK) on the development of ethionine-induced pancreatitis and pancreatic recovery. We used Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model lacking pancreatic CCK-A receptor gene expression. METHODS: Ethionine-induced pancreatitis was induced in the 7-week-old male OLETF rats and in a control group that does not lack the pancreatic CCK-A receptor, Long-Evans Tokushima Otsuka (LETO) rats. The two groups were maintained on a low-protein diet for 11 days. During the last 4 days of the low-protein diet, dl-ethionine 20 mg/100 g body weight was administered intraperitoneally once daily. Histologic and biochemical examinations of the pancreas were performed, and plasma CCK concentrations were measured on days 1, 4, and 7 after the last ethionine administration. RESULTS: Pancreatic histologic scores for inflammation, hemorrhage, and necrosis in the LETO and OLETF rats were highest on days 1 and 4, respectively. Pancreatic weight, DNA content, and protein level per DNA content in both groups decreased during the low-protein diet, and recovery signs were delayed in the OLETF rats. The highest plasma CCK concentrations in the LETO and OLETF rats were reached on days 1 and 4, respectively. CONCLUSIONS: Ethionine-induced pancreatitis developed in the OLETF rats, and their pancreatic regeneration was delayed in comparison to that in the LETO rats. Our results suggested that CCK plays an important role in the development of pancreatitis as well as in the pancreatic repair process.

Animals↗
PubMed1995

Does acute pancreatitis progress to chronic pancreatitis? A microvascular pancreatitis model in the rat.

Ischemia as a causative factor for acute pancreatitis has been discussed for decades but has only recently gained wider acceptance. Chronic pancreatitis, however, has rarely been attributed to ischemic injury. While experimental evidence is available for the ischemic pathogenesis of acute pancreatitis, no studies have been reported about pancreatic ischemia as a single cause of chronic pancreatitis. Also, the progression from acute to chronic pancreatitis has been a very controversial issue. To address both questions we have injected polystyrene microspheres of 20-microns diameter into the pancreatic branches of the splenic artery of 36 rats. Thirteen more rats were sham operated and injected with saline. The animals were killed at 1, 2, 3, and 9 weeks after operation and macroscopically and histologically examined, and serum alpha-amylase and weight gain were determined. For the pancreas the following parameters were assessed using a score from 0 (no change) to 4 (severe change): atrophy, hemorrhage, edema, fat necrosis, acinar necrosis, polymorphonuclear infiltration, mononuclear infiltration, interstitial fibrosis, and ductal changes. While no difference between control and experiment was observed for serum alpha-amylase, weight gain, edema, and hemorrhage, persistent differences were evident for the parameters characteristic of chronic pancreatitis, most significantly for interstitial fibrosis, ductal changes, mononuclear infiltration, acinar necrosis, and atrophy. No spontaneous deaths occurred. The severity of the lesions remained stationary after the first week. Our work shows for the first time that pancreatic ischemia by microvascular hypoperfusion can cause histopathologic changes characteristic of chronic pancreatitis and that these changes follow acute necrotizing pancreatitis.

Acute Disease↗
PubMed1983

Postprandial release of gastric inhibitory polypeptide (GIP) and pancreatic polypeptide in dogs with pancreatic acinar atrophy. Correction of blunted GIP response by addition of pancreatic enzymes to a meal.

In order to evaluate the enteropancreatic hormone axis in dogs with pancreatic acinar atrophy, we measured the release of gastric inhibitory polypeptide and pancreatic polypeptide in response to a standard meal and a meal containing pancreatic enzymes in affected dogs and controls. Postprandial release of pancreatic polypeptide was normal in dogs with pancreatic atrophy and was not affected by addition of pancreatic enzymes to the food. Gastric inhibitory polypeptide was not released after a standard meal in affected dogs, but this blunted response was corrected by the addition of pancreatic enzymes to the food. Feeding the enzyme alone did not stimulate a gastric inhibitory polypeptide response. These results, in part, support similar observations previously reported in children with exocrine pancreatic insufficiency associated with cystic fibrosis. We conclude that dogs with idiopathic pancreatic acinar atrophy can be used as an animal model for future study of enteropancreatic hormonal abnormalities that occur in human beings with exocrine pancreatic insufficiency.

Animals↗
PubMed1995

Pancreatic stone protein and lactoferrin in human pancreatic juice in chronic pancreatitis.

Lactoferrin and pancreatic stone protein (PSP) are thought to be closely related to pancreatic stone formation in chronic pancreatitis. However, the results reported so far have not been conclusive. To reevaluate the pathological importance of PSP in chronic pancreatitis, compared to lactoferrin, levels of PSP were determined by applying an immunoassay specific to PSP to pure pancreatic juice taken from a total of 52 patients. The patients consisted of 16 controls, 19 chronic pancreatitis patients (13 noncalcified and 6 calcified), and 17 probable cases of pancreatitis. The monoclonal antibody PSP antagonist used in the study recognizes both forms of the protein, PSP S1 and S2-5, with equal effectiveness. No significant reduction of PSP was observed in either calcified (mean +/- SEM, 111 +/- 30 micrograms/mg and 24 +/- 3 micrograms/mg protein) or noncalcified (305 +/- 133 and 97 +/- 47) chronic pancreatitis patients compared with controls (85 +/- 23 and 34 +/- 16). PSP levels did not decrease, at least not in the complete forms of the protein found in chronic pancreatitis. PSP antibody and assay results indicated that a reduction of PSP S2-5 alone could not be ruled out in chronic pancreatitis either.

Adult↗