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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatic fibrosis was found in 23 of 31 cases of acute necrotising and haemorrhagic pancreatitis; however, in the cases with a history of six days or less neither the extent nor the frequency of fibrosis differed significantly from those in controls. There was no histological evidence that duct or vascular lesions are necessary for the disease to occur. The liver was examined in 26 cases and showed cholestasis in 12, including 10 of 20 cases without a biliary aetiology and only two of six cases with biliary tract disease. In no case did the liver show specific features of alcoholic damage.
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PMID:The liver and pancreas in acute necrotising pancreatitis. 69 Feb 44

Obstructive jaundice is a rare complication of alcoholic pancreatitis. In three patients with persistent jaundice, percutaneous transhepatic cholangiography demonstrated either stenosis and dislocation of the common bile duct due to pancreatic pseudocysts or stenosis due to pancreatic fibrosis. These stenoses were easily differentiated from obstructions due to tumours or common duct stones. We suggest that percutaneous transhepatic cholangiography is valuable in pancreatitis with jaundice.
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PMID:Obstructive jaundice in pancreatitis investigated by percutaneous transhepatic cholangiography. 70 54

Thirty-eight patients have been examined by ultrasound when symptoms or sign suggested the development of a pseudocyst following an attack of proven acute pancreatitis. Pseudocyst was diagnosed in 23 of the 38 cases. Five patients had multilocular cysts, four of which were shown to be communicating. Laparotomy was carried out on 14 of the 23 patients and surgical drainage was performed in 12 cases. The remaining nine cases were monitored and showed steady regression. Small cysts arising in the head of pancreas may give rise to recurrent or persistent pancreatitis and may be demonstrated pre-operatively by ultrasound but not readily by other means. A further 12 patients showed an area of irregular absorption of ultrasound interpreted as an inflammatory mass. Monitoring of these cases showed progressive resolution without cyst formation. Three of these cases subsequently required laparotomy-one developed an abscess and one necrosis of the body and tail of pancreas while a third developed severe pancreatic fibrosis of the area identified by ultrasound. The ability to distinguish between pseudocysts and inflammatory masses and to demonstrate communication between multiple cysts is of considerable value in pre-operative diagnosis.
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PMID:Ultrasound in the management of acute pancreatitis. 97 74

Jaundice occurring in patients with pancreatitis is usually due to hepatocellular injury or to associated biliary tract disease. Common duct obstruction is occasionally caused by pancreatic fibrosis, edema or pseudocyst in patients who have neither hepatocellular injury nor biliary tract disease. We have studied 7 patients with obstructive jaundice due to pancreatitis who demonstrated no other known cause for jaundice. The difficulty in making the differential diagnosis between benign and malignant disease in these patients, particularly when no pain is associated with obstructive jaundice, is discussed. In view of the fact that the terminal common duct traverses the pancreas, it is uncertain why obstructive jaundice associated with chronic pancreatitis does not occur more often unless the condition is sometimes transient and overlooked. Operative intervention is required in those patients in whom jaundice is persistent. Operation is intended to decompress the biliary tract and the pancreas. The approach used will be dictated by the operative findings in each patient.
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PMID:Obstructive jaundice in patients with pancreatitis without associated biliary tract disease. 121 86

The effect of repetitive inductions of pancreatitis by supramaximal doses of cerulein on pancreatic morphology and collagen content was studied in the rat. Pancreatitis was induced nine times at intervals of about 20 days; 3 days after the last injection of cerulein, pancreatitis was still observed, as indicated by pancreatic weight loss, increase of protein-bound hydroxyproline content, acinar-cell destruction, cellular infiltration, and deposition of collagen fibers. However, 6 weeks later, no differences in the parameters mentioned above were observed between control and cerulein-treated animals. Thus, repetitive induction of pancreatitis in the rat, according to the experimental protocol we used, did not result in pancreatic fibrosis.
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PMID:Repetitive cerulein-induced pancreatitis and pancreatic fibrosis in the rat. 159 61

Chronic pancreatitis is difficult to treat in patients with a nondilated duct. Patients experiencing intractable pain unresponsive to or judged untreatable by lesser procedures must decide between total pancreatectomy and resultant diabetes or a continuation of their pancreatitis. From 1977 through 1990, 26 patients underwent extensive pancreatectomy and dispersed pancreatic islet tissue autotransplantation for treatment of chronic pancreatitis pain and prophylaxis of surgical diabetes. Of these 26 patients, total (Whipple) or near-total (greater than 95%) pancreatectomy was performed in 24 patients. Of these 24 patients, pain relief could be assessed in 21 patients at 5 to 155 months (mean, 5.7 years), and 19 patients (90%) reported partial or complete remission. Of the patients who underwent total or near-total pancreatectomy, islets were injected intraportally in 22 patients and into the renal subcapsule in two patients. The latter two patients have required insulin since surgery. Of the other 22, one patient died from a complication of the pancreatectomy. Nine of the 21 evaluable recipients of intraportal islet autografts were insulin independent for at least several months after surgery. Five patients are currently insulin independent at 6 years, 4 years, 1.5 years, 9 months, and 5 months after surgery. Of the other four patients, one patient died insulin independent at 6 years, and three patients required insulin beginning 8 to 18 months after surgery. Insulin independence correlated with the number of islets recovered, which in turn correlated inversely with the degree of pancreatic fibrosis. Of our four most recent patients, three patients had mildly to moderately fibrotic glands, and higher numbers of islets were obtained. After total (Whipple) pancreatectomy, these three patients are insulin independent. A liver biopsy was performed in one patient 8 months after total pancreatectomy and islet autotransplantation; numerous clusters of islet cells staining strongly for insulin and glucagon were detected within portal triads on both wedge and needle biopsy specimens. Morbidity related to the intraportal-dispersed pancreatic islet tissue transplantation was low (no disseminated intravascular coagulation, significant portal hypertension, or hepatic dysfunction). Islet autotransplantation can be an effective and safe adjunct to extensive pancreatic resection for those patients who risk surgical diabetes for relief of their chronic pancreatitis pain.
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PMID:Autotransplantation of dispersed pancreatic islet tissue combined with total or near-total pancreatectomy for treatment of chronic pancreatitis. 185 51

Serum apolipoprotein A-I measurement was compared in alcoholic patients according to presence or absence of chronic pancreatitis and liver fibrosis. Among alcoholic patients without liver disease, apolipoprotein A-I was significantly lower in patients with chronic pancreatitis (157 +/- 70 mg/dl) than in patients without pancreatitis (209 +/- 74 mg/dl, p less than 0.001). In cirrhotic patients, apolipoprotein A-I was lower in patients with chronic pancreatitis (82 +/- 35 mg/dl) than in patients without pancreatitis (102 +/- 45 mg/dl), but this difference was not significant. The decrease of serum apolipoprotein A-I was independent of nutritional parameters whether or not there was cirrhosis. Immunohistochemical study of pancreatic samples with chronic pancreatitis showed that apolipoprotein A-I was located in the pancreatic fibrosis whereas lobules were unstained. This study suggests that apolipoprotein A-I is trapped by the pancreatic extracellular matrix and that this sequestration might explain, in part, the decrease of the serum apolipoprotein A-I.
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PMID:Serum apolipoprotein A-I in alcoholic patients with chronic calcifying pancreatitis. 212 44

Serum and urinary amylase level are different between in cases with carcinoma of the pancreas head and in those with carcinoma of body or tail of the pancreas. In this study the relationship between elevation in serum and urinary amylase level and the portion of obstructed pancreatic duct by tumor was analysed in cases with pancreatic carcinoma was analysed and also this was investigated in experimental model of pancreatic duct ligated dog. In patients with carcinoma of the pancreas and periampullary region, the site of obstruction of the main pancreatic duct was estimated by ERP and serum and urinary amylase level were measured. The values of serum amylase level were different according to the site of obstruction of the pancreatic duct by the tumor and in cases with highly elevated serum amylase levels the main pancreatic duct was obstructed within 5cm from the duodenal papilla. Pathology of these cases revealed pancreatic fibrosis derived from pancreatitis accompanied by tumor was closely related to serum and urinary amylase level. In pancreatic ligated dogs similar findings were observed. These data suggested that elevated serum amylase level is due to the pancreatic duct obstruction in cases with carcinoma of the periampullary duodenum.
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PMID:[Clinical and experimental studies on serum and urine amylase levels in carcinoma of the pancreas and periampullary region]. 241 41

Chronic pancreatitis is associated with glucose intolerance and resultant pancreatogenic diabetes. Using the canine pancreatic duct-ligated model of pancreatitis, we serially evaluated pancreatic histology and electron microscopy, tolerance to intravenous and oral glucose, and insulin response to glucose loading. Pancreatic duct ligation caused microscopic evidence of acute pancreatitis at 1 week, progressing to acinar loss and fibrosis consistent with chronic pancreatitis at time periods up to 6 months. The islets of Langerhans showed degranulation early and appeared to be structurally preserved late. Calculated K values indicated a progressive significant deterioration in intravenous glucose tolerance, falling significantly from 3.46 +/- 0.23 basally to 1.51 +/- 0.17 at 6 months after duct ligation (p less than 0.0001). Oral glucose tolerance deteriorated significantly, with the integrated glucose response rising from 23.7 +/- 1.2 g/dl.minute basally to 32.3 +/- 2.8 g/dl.minute at 6 months after duct ligation (p less than 0.05). Integrated insulin response to both intravenous and oral glucose deteriorated with pancreatitis. Pancreatitis-induced glucose intolerance is a consistent feature of this duct-ligated model. Glucose intolerance stabilizes between 4 and 6 months after duct ligation and is associated with pancreatic acinar fibrosis and pancreatic endocrine structural preservation. While the mechanism of altered glucose tolerance may involve mechanical, neural, humoral, or vascular events, our data clearly support the conclusion that pancreatic ductal stenosis with resultant pancreatic fibrosis and chronic pancreatitis is associated with abnormal islet responsiveness leading to circulating insulin deficiency and glucose intolerance, despite histologic and ultrastructural evidence of intact islets of Langerhans.
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PMID:Pancreatic structure and glucose tolerance in a longitudinal study of experimental pancreatitis-induced diabetes. 247 67

The residual pancreatic exocrine function before and after pancreaticoduodenectomy (PD) for periampullary carcinoma was studied clinically as well as experimentally. In clinical instances (n = 35), the N-Benzoyl-L-Tyrosil-p-Aminobenzoic Acid test (BTPABA test) before and within two months after PD revealed reduction of the function compared with those in the control study. However, the test result one year after PD was improved compared with those before and within two months after operation, without differences from that of the control group. In new canine PD models in which drainage of the pancreatic duct, 50 per cent pancreatectomy and duodenojejunectomy were performed after three months of pancreatic duct obstruction, fibrosis surrounding the pancreatic duct was disclosed. However, the results of examination five months after PD revealed a milder degree of pancreatic fibrosis without aggravation of the lesion. The aforementioned findings indicated that the exocrine pancreas before PD was impaired due to obstructive pancreatitis and that the postoperative pancreatic function was well preserved at the level close to that in the control group even after approximately 50 per cent resection of the pancreas, if pancreatic duct drainage was effectively performed.
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PMID:Clinical and experimental study of pancreatic exocrine function after pancreaticoduodenectomy for periampullary carcinoma. 325 31


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