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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The peptide hormones neurotensin (NT) and cholecystokinin (CCK) are commonly attributed with a physiological role in the stimulation of exocrine pancreatic secretion. However, on the other hand, little is known about the effect of diminished exocrine pancreatic function and of the resulting maldigestion on postprandial plasma levels of these two gastrointestinal peptides. We investigated, therefore, the effect of enzyme substitution therapy on the magnitude and time course of plasma concentrations of both hormones in patients suffering from severe chronic pancreatitis. Pancreatic insufficiency led to elevated NT-concentrations, in response to a standard meal, which could be reduced by enzyme replacement therapy. Prior to enzyme therapy, the mean integrated postprandial release of NT amounted to 2800 +/- 250 pg/ml after 60 min in patients with severe chronic pancreatitis. This amount was significantly reduced to 1250 +/- 150 pg/ml after 60 min after enzyme therapy, compared to 810 +/- 90 pg/ml after 60 min in healthy volunteers after the standard meal. The integrated postprandial CCK level in patients investigated was significantly lower (35 +/- 4.8 pmol/L after 60 min) without any substitution therapy, compared to the integrated peptide amount in healthy volunteers (145 +/- 13.5 pmol/L after 60 min). Enzyme therapy in patients suffering from chronic pancreatitis led to an increased postprandial CCK-level (80 +/- 9.6 pmol/L after 60 min). Elevated CCK-plasma concentrations have not been demonstrated in these patients with pancreatic insufficiency. We therefore suggest that CCK might not play a major role in feedback regulation in patients with chronic pancreatitis. However, in light of elevated NT plasma concentrations in patients with chronic pancreatitis, NT-mediated influence on the pancreas deserves further study.
Pancreas 1991 May
PMID:Plasma concentrations of neurotensin and CCK in patients with chronic pancreatitis with and without enzyme substitution. 171 70

Human pancreas contains two cholinesterase isoenzymes: acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). In the present study, binding potency of two organophosphates for human cholinesterases were compared by the Ellman method. Echothiophate was found to have much greater potency than iso-OMPA for both cholinesterases. Using Karnovsky histochemical stains on human pancreatic tissue, the same results were confirmed. Dose-response studies with acetylcholine were done on viable pancreas fragments from nine human donors, without pancreatic disease (group I). Cold-preservation time was less than 30 h. Pancreas was minced into fragments, after the technique of Scheele and Palade, placed in Eagle's medium, and gassed with O2. Amylase release was measured by the Phadebas Method and corrected for basal release. There was a dose-dependent response to acetylcholine at 1 and 2 h, with a shift in peak amylase release to the left, when fragments were preincubated in 10(-4) M echothiophate. This indicated a 100-fold increase in sensitivity to acetylcholine. In three patients with chronic pancreatitis (Group II), there were variable patterns of response of amylase release to acetylcholine, and higher basal outputs. In Group III, prolonged storage conditions of over 40 h were tested for 4 pancreas donor tissues. There was no response to acetylcholine. These studies show that for up to 30 h cold storage, fragments of pancreas from human organ donors respond to acetylcholine in dose-dependent manner. An organophosphate, echothiophate (10(-4) M) which inhibits both cholinesterases, increases pancreatic sensitivity to acetylcholine, and these results are similar to findings from canine pancreas fragments, which also showed increased sensitivity.
Pancreas 1991 Jul
PMID:Organophosphate increases the sensitivity of human exocrine pancreas to acetylcholine. 171 83

Although the etiology of pain in chronic pancreatitis remains uncertain, that symptom remains the most common indication for surgery in these patients. Current endoscopic and imaging techniques now permit accurate definition of the morphology of the disease. Thus, surgical intervention can be more selectively applied to address specific abnormalities. Pancreaticojejunostomy should be the first line of surgical therapy if the ductal system is dilated. When, in addition, the head of the pancreas is enlarged and inflamed, the operation should include a localized resection of the head, preserving the stomach and duodenum. If the duct is not dilated, some form of pancreatic resection is indicated. The resection should be limited to the most severely diseased part of the pancreas. Efforts should be made to preserve as much pancreatic tissue as possible, while maintaining normal gastrointestinal continuity. In this way, the nutritional and metabolic consequences of pancreatic resection will be minimized.
Pancreas 1991
PMID:New perspectives in the surgical management of chronic pancreatitis. 178 57

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.
Pancreas 1991 May
PMID:Pseudocysts in chronic pancreatitis: a morphological analysis of 57 resection specimens and 9 autopsy pancreata. 186 65

Copper and zinc are both secreted by the pancreas but are necessary for pancreatic secretion. We have studied the effects of a 4- or 8-week zinc or copper-deficient diet associated with or without lipid or protein deficiency on rat pancreatic secretion after stimulation by secretin, cerulein, or intraduodenal oleic acid. Twenty animals were in the control group; 40 rats were fed a copper-deficient diet (20 copper-deficient only and 20 copper- plus lipid-deficient). Ninety rats were deprived of zinc (30 of zinc-deficient only, 30 zinc-plus protein-deficient, 30 of zinc- plus lipid-deficient). Only the zinc- plus lipid-deficient diet for 8 weeks decreased basal bicarbonate and basal protein secretion (-42 and -70%, respectively, of the control values). Stimulated secretion was not markedly altered by copper deficiency while zinc deficiency, zinc plus protein deficiencies, and zinc plus lipid deficiencies suppressed almost responses to hormonal stimulation: After 8 weeks, the maximal protein response to oleic acid was reduced to 19.00 +/- 3.40, 18.58 +/- 3.00, and 12.04 +/- 2.91 microgram/30 min/g body weight in zinc- zinc and protein-; and zinc- and lipid-deficient diet, respectively, versus 39.87 +/- 6.33 microgram/30 min/g body weight (p less than 0.05) in controls. In all types of stimulation, lipid deficiency potentiated the deleterious effect of zinc deficiency on pancreatic secretion. This might be paralled with an extremely low level of lipid in the diet of people living in countries in which nutritional pancreatitis is observed and with the relative risk of developing an alcoholic chronic pancreatitis being increased by a low fat diet.
Pancreas 1991 May
PMID:Effects of zinc and copper deficiency associated with protein or lipid deficiency on rat exocrine pancreatic secretion. 186 68

Pancreas transplantation is usually performed in patients with denovo type I diabetes, who have advanced secondary complications. We report a case in which whole pancreaticoduodenal transplantation, with enteric drainage, was performed to correct both endocrine and exocrine deficiencies in a patient with hyperlabile diabetes and steatorrhea, unresponsive to oral enzyme replacement therapy, following staged total pancreatectomy for idiopathic or familial chronic pancreatitis. The transplant was performed one year after completion of native pancreatectomy and immediately established an insulin-independent euglycemic state, with normal oral and intravenous glucose tolerance test results and correction of steatorrhea. Beginning one year posttransplant, the patient had intermittent episodes of steatorrhea, associated with mild elevation of blood sugar levels, which were presumed to be due to rejection and, indeed, responded to antirejection treatment with antilymphocyte globulin and temporary increases in steroids dosages. At 20 months posttransplant, steatorrhea did not respond to antirejection treatment and an acute abdomen developed. Laparotomy revealed a perforated graft duodenum, which was resected; pathology showed transmural necrosis secondary to chronic rejection. The pancreas graft itself was left in situ, disconnected from the intestinal tract. The patient remained normoglycemic after graft duodenectomy but resumed oral enzyme replacement therapy in an attempt to combat recurrence of severe steatorrhea. However, his overall situation remained improved compared to pretransplant, since the exocrine deficiency was tolerable in the absence of a diabetic state. Ten months postgraft duodenectomy (38 months posttransplant), elevations in blood sugar levels were treated with another course of antirejection treatment and levels temporarily declined. At 14 months postgraft duodenectomy (42 months posttransplant), graft endocrine function again declined and exogenous insulin was resumed. Six months later, four years after the original transplant, a new enteric-drained pancreaticoduodenal graft was placed, once again resulting in an insulin-independent, steatorrheafree state. With improvements in immunosuppression, pancreas transplantation could be offered to selected patients with hyperlabile diabetes, following total pancreatectomy for benign disease; if the enteric drainage technique is used, in the absence of rejection, exocrine deficiency could be corrected as well.
Pancreas 1991 Jul
PMID:Pancreaticoduodenal transplantation with enteric drainage following native total pancreatectomy for chronic pancreatitis: a case report. 187 4

We have examined the possibility that selenium deficiency may underlie one or more of the following peculiarities of chronic pancreatitis in tropical as compared to temperate zones: much higher prevalence, propensity for pancreatic calculi, and high frequency of diabetes. Selenium was measured by graphite furnace atomic absorption spectrometry in sera from 20 healthy volunteers, 36 patients with chronic pancreatitis (calcific 35, diabetic 32), and 23 patients with primary forms of diabetes, from Madras, South India; results were compared with data from 41 controls and 37 patients with chronic pancreatitis (calcific 13, diabetes 8) from Manchester, North West, England. We conclude that (a) bioavailability of selenium is equally high in each geographic area; (b) decrement in serum selenium (p less than 0.001) is of a similar order in Manchester and Madras patients, which denies a connection with calculi formation or pancreatic exocrine failure (since the incidence of these two problems was substantially higher in the Madras series); and (c) selenium levels do not account for accelerated course to diabetes in tropical chronic pancreatitis.
Pancreas 1991 Sep
PMID:Selenium and diabetes in the tropics. 194 9

A new kit for radioimmunoassay of serum phospholipase A2 (PLA2) with monoclonal antibody (S-0932, Shionogi, Osaka, Japan) was used to examine PLA2 levels in patients with various diseases. Patients with acute pancreatitis showed significantly increased serum PLA2 levels. In patients with chronic pancreatitis, significant correlations were observed between the levels of factors evaluated by the secretin test and serum PLA2 levels. In patients with pancreatic cancer, serum PLA2 levels varied with disease severity. Serum PLA2 concentrations were within the normal range in patients with other malignant tumors, diabetes mellitus, and chronic liver diseases but were increased in patients with chronic renal failure. S-Sepharose column analysis of sera showed a small peak of pro-PLA2 and a large peak of PLA2 in sera from patients with severe acute pancreatitis, but a large peak of pro-PLA2 in healthy controls and patients with other diseases. On G-100 gel filtration, high-molecular-weight PLA2 immunoreactivity was detected in sera of patients with chronic renal failure, whereas a single peak of PLA2 immunoreactivity coinciding with that of standard PLA2 was detected in sera of patients with acute pancreatitis. These results suggest that (a) measurement of serum PLA2 is clinically useful for diagnosis and monitoring of pancreatitis, (b) active PLA2 in the circulation is dominant in severe acute pancreatitis, and (c) the kidney may be the main site of PLA2 degradation or excretion.
Pancreas 1991 Sep
PMID:Clinical usefulness of serum phospholipase A2 determination in patients with pancreatic diseases. 194 16

In an attempt to study the mechanisms leading to fibrosis in chronic pancreatitis, an in situ immunohistochemical investigation of lymphocytes and of class II major histocompatibility complex expression (HLA-DR) by epithelial cells has been designed. Samples of normal pancreas (n = 8), chronic calcifying pancreatitis (n = 4), chronic obstructive pancreatitis (n = 6), and diffuse fibrosing pancreatitis (n = 6) have been studied. In normal pancreas, T-lymphocytes were rare and were located in the epithelial layer of pancreatic ducts and in the periductal connective tissue. Duct cells were constantly HLA-DR negative. In chronic calcifying pancreatitis and chronic obstructive pancreatitis, T cells were numerous and were located around ducts and in the spreading areas of fibrous septa. In chronic obstructive pancreatitis, the duct cells strongly expressed the HLA-DR antigen. In diffuse fibrosing pancreatitis, fibrous tissue was devoid of lymphocytes and duct cells never expressed the HLA class II antigen. These results suggest that lymphocytes are involved in the fibrosing process occurring in chronic calcifying pancreatitis and chronic obstructive pancreatitis but not in diffuse fibrosing pancreatitis. The significance of de novo expression of HLA-DR antigen by duct cells is discussed.
Pancreas 1990 Jul
PMID:Lymphocyte subsets and HLA-DR expression in normal pancreas and chronic pancreatitis. 197 51

The aim of the present study is to assess the frequency of pancreas divisum and the features of patients with pancreas divisum in order to assess the role of this anomaly in the occurrence of pancreatitis. A total of 1049 endoscopic retrograde pancreatographies were studied between 1978 and 1988. Patients with pancreas divisum were studied in terms of their clinical findings and their disease (pancreatitis or not). Pancreas divisum was diagnosed in 62 patients (5.9%). No statistical differences with regard to age and sex were found between patients with and without pancreas divisum. The frequency of pancreas divisum was similar in the different groups of disease, especially chronic pancreatitis, acute pancreatitis, recurrent pancreatitis and idiopathic pancreatitis. The study of pancreatograms showed that dorsal ductal abnormalities alone were found as frequently as ventral alterations alone. Our results show that pancreas divisum cannot be directly implicated in the occurrence of pancreatitis, and should not prompt a systematic sphincterotomy of the accessory papilla. This treatment should only be considered in the rare cases of acute recurrent idiopathic pancreatitis with dorsal ductal dilatation and stenosis of the accessory papilla.
 ...
PMID:Pancreas divisum and pancreatitis: a coincidental association? 205 15


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