Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Obstructive jaundice in patients with pancreatitis without associated biliary tract disease. 121 86

According to the 1988 Marseilles-Rome classification inflammatory pancreatic diseases are represented by acute (AP) and chronic pancreatitis (CP), pancreatic fibrosis and abscesses (due to infection of cystic cavities). Each form is defined by specific etiological, pathomorphological, functional and evolutive aspects. In our experience with 348 AP cases, gallstones and chronic alcohol abuse, alone or together, represent the major causative factors (over 70% of cases). Mortality observed in necrotizing AP only, varies from 26% of idiopathic to 8% of biliary cases. Ductal scars, exocrine and endocrine impairment were observed in about 45% and 20% respectively as sequelae of necrotizing AP, whatever the etiology. As far as CP is concerned, the main etiological factor is chronic alcohol consumption (82% of cases). The clinical evolution of CP may be roughly divided in two phases, the earlier (within 5 years from onset) characterized by frequently recurrent pain, calcifications and cystic cavities and the later when pain spontaneously regresses and steatorrhea and diabetes tend to appear. Heavy alcohol intake, smoking and frequent relapses are related to a less favourable course. About 60% of the patients underwent surgery within 5 years from onset. Pain relief was achieved in the large majority. Reduction in alcohol intake and the natural tendency of the disease to burn out, probably aid pain relief. Mortality in CP is due to diseases secondary to alcohol and smoking abuse (cardiovascular and neoplastic) more than to CP alone. We believe that multiple parameters are required for a complete definition of each pancreatic patient.
 ...
PMID:Acute and chronic pancreatitis: an up-date. 174 47

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.
 ...
PMID:Autotransplantation of dispersed pancreatic islet tissue combined with total or near-total pancreatectomy for treatment of chronic pancreatitis. 185 51

The pathology of chronic pancreatitis is reviewed in order to study the histology and incidence of pseudocysts in relation to the degree of pancreatic fibrosis and calcification. The series consisted of 57 resection specimens (49 partial pancreatectomy specimens and 8 total pancreatectomy specimens) and 9 autopsy pancreata. The histology of cystic lesions observed in the specimens was found to be identical to that of pseudocysts in acute pancreatitis. In 19 of 57, there was concomitant occurrence of focal autodigestive (fat) necrosis and pseudocysts. Pseudocysts were more common in specimens with focal fibrosis and few calcifications (13/25) than in those with diffuse advanced fibrosis and numerous calcifications (15/41). The findings indicate that sequelae of acute pancreatitis are frequently present in chronic pancreatitis, particularly in an early stage when fibrosis is still focal and calcification rare. This suggests that chronic pancreatitis may result from relapses of severe acute pancreatitis. A pathogenetic concept that relates acute pancreatitis with chronic pancreatitis is proposed.
 ...
PMID:Pseudocysts in chronic pancreatitis: a morphological analysis of 57 resection specimens and 9 autopsy pancreata. 186 65

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.
 ...
PMID:Serum apolipoprotein A-I in alcoholic patients with chronic calcifying pancreatitis. 212 44

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.
 ...
PMID:Pancreatic structure and glucose tolerance in a longitudinal study of experimental pancreatitis-induced diabetes. 247 67

Previous studies on pancreatic calculi (PC) from alcoholic pancreatitis and our recent studies on calculi from tropical pancreatitis have shown them to consist mainly of CaCO3 with minute quantities of Mg. However, no attempt was made to look for other elements in PC. This is because of the difficulty in obtaining adequate samples of PC, coupled with the technical limitations in analyzing multi-elements from small samples. In this study, our aim was to analyze the major, minor and trace elements of PC from different parts of the world. DC plasma emission spectroscopy, a modern method that permits determination of multiple elements from small samples, was used in elemental analysis. We identified 17 elements in addition to calcium. Selenium was looked for but was absent. It was interesting that the elemental composition of PC in four patients from different geographical areas with divergent etiological factors remained the same. Absence of Se is of interest, as Se deficiency is associated with pancreatic fibrosis in experimental animals and it is often noted in chronic alcoholics and the malnourished. This preliminary study emphasizes the need for analysis of the elemental composition of pancreatic juice in normals and in conditions predisposing to chronic pancreatitis, to understand lithogenesis and possibly also the etiology of, at least, some types of pancreatitis.
 ...
PMID:DC plasma emission spectroscopic analysis of pancreatic calculi. 368 Oct 37

The changes in the residual function of the exocrine pancreas before and after the operation for chronic pancreatitis were examined with N-benzoyl-L-tyrosyl-p-aminobenzoic acid (NBT-PABA test) in 15 patients. The results of the NBT-PABA test classified by the surgical formula proved that no significant difference was found between the pancreatectomized group (pancreaticoduodenectomy and distal pancreatectomy) and the decompression group (pancreatojejunostomy and transduodenal exploration of the pancreatic duct), and no improvement on the outcome of the postoperative NBT-PABA test, as compared with the outcome of the preoperative test, was noted in both groups. When the state of the fibrosis of the pancreas was classified by the grade for comparison, it was observed that the outcome of the NBT-PABA test of grade 1, in which little fibrosis was made, was better than the outcome of the test of grade 3 before operation (p less than 0.01) and after operation (p less than 0.01). In each of the grades, however, no difference was found between the outcome of the preoperative NBT-PABA test, and that of the postoperative test. It was presumed from these findings that the residual function of the exocrine pancreas after operation was dependent largely on the degree of pancreatic fibrosis at operation.
 ...
PMID:Residual function of exocrine pancreas after operation for chronic pancreatitis by N-benzoyl-L-tyrosyl-p-aminobenzoic acid test (NBT-PABA test). 633 64

Necrotic lesions are rarely observed in chronic pancreatitis, but its presence in a few patients has been misinterpreted in the diagnosis of acute pancreatitis. In this series, 12 patients (11.2%) of 107 operated for chronic alcoholic pancreatitis, presented with acute pancreatic necrosis associated with pancreatic fibrosis characteristic of chronic pancreatitis. Ten patients were treated by pancreatic debridement and drainage and two by distal pancreatic resections. Postoperative complications included five pancreatic fistulas and two pancreatic abscesses. Despite the severity of the pancreatic lesions which led to several complications, all the patients survived. The occurrence of pancreatic necrosis in patients with chronic pancreatitis is demonstrated.
 ...
PMID:Acute pancreatic necrosis in chronic alcoholic pancreatitis. 674 31

Of 114 patients with chronic pancreatitis, 19 (16.7%) has gastric or duodenal ulcers. Patients with moderate pancreatic exocrine dysfunction tended to show high acid output and low serum gastrin levels, while those with severe dysfunction had slightly lower acid output and higher serum gastrin levels. The higher the degree of pancreatic fibrosis, the higher tended to be the acid output and serum gastrin levels. Not all patients with ulcers developed hypergastrinemia. The mechanism of acid hypersecretion and ulcer formation in patients with chronic pancreatitis cannot be explained solely by pancreatic deterioration, fibrosis or gastrin release; a decrease in the production and release of gastric inhibitory hormone should be taken into consideration.
 ...
PMID:Gastric acid secretion and serum gastrin levels in chronic pancreatitis. 722 67


1 2 3 4 5 6 7 8 9 10 Next >>