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

We report a patient with primary sclerosing cholangitis and associated pancreatitis. She had exocrine and endocrine pancreatic insufficiency.
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PMID:Primary sclerosing cholangitis with chronic pancreatitis. 225 18

Comparative studies of pancreatic enzymes carbohydrate antigen 19-9 (CA 19-9) and carcinoembryonic antigen (CEA) were performed in various pancreatic disease. In acute pancreatitis as well as during acute exacerbation of chronic pancreatitis, all pancreatic enzymes were abnormally high. In chronic pancreatitis, they did not have any diagnostic sensitivity for pancreatic insufficiency. In pancreatic carcinoma, serum elastase levels may have a diagnostic value compared with other pancreatic enzymes. In studies of CEA and CA 19-9, both tumor markers were within normal range in benign pancreatitis but 27.7% of CEA and 30.7% of CA 19-9 in acute pancreatitis were above normal. In pancreatic carcinoma, although most of these patients had advanced disease, both tumor markers were extremely high and 61% for CEA and 71% for CA 19-9 were above normal. In patients with resected pancreatic carcinoma, serum CEA was slightly higher than normal CA 19-9 was much higher than normal. The sensitivity of CEA and CA 19-9 in this group were 33 and 77.7%, respectively. The results indicate that the CA 19-9 assay is a useful adjunct in the diagnosis of pancreatic carcinoma, possibly in the resectable stage especially combined measurement of serum elastase and CEA.
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PMID:Evaluation of serum pancreatic enzymes, carbohydrate antigen 19-9, and carcinoembryonic antigen in various pancreatic diseases. 241 Nov 25

The diagnostic value of a new enzyme immunoassay for lipase (IRL) was evaluated in controls (n = 65), in acute pancreatitis (n = 11) and in extrapancreatic hyperamylasemia (n = 15) by comparing IRL with serum amylase (TA), pancreatic isoamylase (PA) and lipase (turbidimetrically: TL). IRL and immunoreactive trypsin (IRT) of 60 patients with alcoholic chronic calcified pancreatitis were also studied and correlated with duration of disease and degree of pancreatic insufficiency (based on fecal chymotrypsin test: FCT). IRL was constantly elevated in patients with acute pancreatitis. In extrapancreatic hyperamylasemia IRL was mainly normal, in contrast to PA, which was elevated in 7 patients with macroamylasemia. In 56.7% of all patients with chronic pancreatitis, IRL was pathologically low; in association with advanced insufficiency (FCT less than 20 micrograms/g) this figure was 74%, and after duration of disease of greater than or equal to 15 years 77%. For IRT comparable results were found in 79% and 77% respectively. This new lipase test thus seems to be useful for the diagnosis of acute pancreatitis, the differential diagnosis of extrapancreatic hyperamylasemia and the detection and monitoring of severe chronic pancreatitis.
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PMID:[Significance of immunoreactive lipase in the diagnosis of pancreatic diseases]. 241 82

Serum isoamylases were determined prospectively in dogs with pancreatic and extrapancreatic diseases. Mean serum isoamylase determinations were significantly different (p less than 0.05) between normal dogs and dogs with pancreatitis and exocrine pancreatic insufficiency. The sensitivity of serum isoamylase determination exceeded that of total amylase activity for the diagnosis of pancreatitis. Serum isoamylase determinations were less influenced by extrapancreatic diseases compared to total amylase activity when used in the diagnosis of pancreatic disease. Neither serum isoamylase determination nor total amylase activity had adequate sensitivity to support their use in the diagnosis of exocrine pancreatic insufficiency. There were significant (p less than 0.05) linear correlations between isoamylase determinations, total amylase activity, and trypsin-like immunoreactivity concentration.
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PMID:Sensitivity and specificity of canine serum total amylase and isoamylase activity determinations. 246 94

This is a report on five patients who had acute attacks of pancreatitis (three cases complicated by pseudocysts). They all showed pancreatic calcifications on plain abdominal X-ray (n = 5), computed tomography (n = 3), or at postmortem examination (n = 1). Despite calcifications, the exocrine pancreatic function, as tested with the secretin-pancreozymin test and fecal fat analysis, was either normal or returned to normal. The conclusion is that pancreatic calcifications do not indicate severe exocrine pancreatic insufficiency and the necessity for pancreatic enzyme substitution. Calcifications are not necessarily a sign of chronic pancreatitis. They may result rather from scars following acute pancreatitis.
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PMID:Pancreatic calcifications in patients with normal pancreatic function. 247 21

We report the case of a 60 year old lady suffering from celiac disease and autoimmune cirrhosis who developed exocrine pancreatic insufficiency with canalicular lesions consistent with chronic pancreatitis. Celiac disease is known to be associated with either pancreatic insufficiency or liver disease, but association of all three diseases has not yet been described. We suggest that chronic pancreatitis be added to the list of idiopathic inflammatory pancreatitis of possible autoimmune origin, enabling to explain the pathophysiology of all three disorders with one hypothesis.
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PMID:[Celiac disease, autoimmune cirrhosis, chronic pancreatitis: apropos of a triple association]. 262 89

The mechanism leading to exocrine pancreatic disease in children differs from those encountered in adult patients: I. In acute pancreatitis autodigestion of the gland by proteolytic enzymes may occur and two mechanisms may play a role. 1. Reflux of biliary secretions (e.g. in malformations of the duct system) facilitates activation of trypsinogen by enteropeptidase and leads to the presence of active proteolytic enzymes in the gland (exogenous activation). 2. Lysosomal enzymes may play a role in the intracellular activation of zymogens if inflammation leads to a fusion of lysosomes with zymogen granules (endogenous activation). II. In chronic relapsing and hereditary pancreatitis malformations of the pancreatico-biliary duct system must be sought because surgery may be indicated (common channel syndrome and choledochal cysts). III. Among the hereditary diseases leading to pancreatic insufficiency cystic fibrosis (CF) plays the main role. Haplotype analysis has shown that two genetically different types of CF exists (PS and PI). The pancreas shows manifest insufficiency only in the PI-types which occur in more than 70% of cases but the distribution of haplotypes is different in different ethnic groups. In spite of the recent discovery of the cystic fibrosis gene the exact mechanism leading to exocrine pancreatic dysfunction in CF is not clear, but diminished chloride and bicarbonate secretion, may be the result of a disturbance in the regulation of chloride channels, on acinar or ductular level. In the Shwachman-Diamond syndrome a very severe type of exocrine insufficiency with unknown etiology is encountered at birth.
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PMID:[Physiopathology of the exocrine pancreas in children]. 269 2

The goals of treatment with pancreatic extracts in patients with chronic relapsing pancreatitis are twofold: pain relief and control of maldigestion caused by exocrine pancreatic insufficiency. Experience with the use of pancreatic enzymes for analgesic purposes suggests that the less severe the pain, the greater the analgesic effect of these enzymes. However, the number of trials, as well as the number of patients treated, is fairly small and more studies in larger patient populations are needed. The use of pancreatic enzymes for maldigestion owing to exocrine pancreatic insufficiency which is secondary to chronic pancreatitis, pancreatectomy, cystic fibrosis, or GI bypass surgery incurs several problems. These problems are primarily caused by gastric inactivation of the enzymes, low enzyme activity of many commercial preparations and/or poor patient compliance. Treatment with conventional enzyme products (powdered extracts, enteric-coated tablets or capsules) has been disappointing. At best, results were inconsistent, showing a high degree of individual variation. The introduction of enzyme preparations in the form of pH-sensitive enteric-coated microspheres in hard gelatin capsules represents a significant advance. These microspheres are superior to conventional enzyme preparations in improving the symptoms of pancreatic insufficiency, particularly steatorrhea, where low doses of microspheres are as effective as large doses of conventional enzyme preparations. Steatorrhea, however, is rarely completely resolved. In cases refractory to therapy, treatment with the combination of pH-sensitive enteric-coated microspheres and H2-antagonists or prostaglandins has met with some success.
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PMID:Management of chronic pancreatitis. Focus on enzyme replacement therapy. 270 47

Three cats were thin despite eating well. Steatorrhoea was confirmed in each by 72-hour fat assimilation tests. Fat digestibility in all 3 increased twofold when the diet was supplemented with pancreatic enzymes, suggesting the possibility of exocrine pancreatic insufficiency. However, examination of stained faecal smears gave evidence of both maldigestion and malabsorption of fat, without maldigestion of starch, and only one case had indications of protein maldigestion. In the latter cat, fat digestibility normalised with pancreatic enzyme supplementation and exocrine pancreatic insufficiency was considered likely. However, at post-mortem examination enteropathy and pancreatitis, but not exocrine pancreatic insufficiency, were found. The cause of fat malassimilation in these cats was unknown. The evaluation of malassimilation in cats is difficult because investigative tests used in other species are either unsuitable or have not been evaluated in cats.
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PMID:Fat malassimilation in three cats. 273 Apr 75

The list of extraintestinal manifestations of inflammatory bowel diseases does not classically include pancreatitis and pancreatic insufficiency. We report here six cases of unexplained pancreatitis associated with inflammatory bowel disease (five patients with Crohn's disease, one with indeterminate colitis). None of the classical etiologies for pancreatitis was found in our patients; moreover none of them had duodenal localization of Crohn's disease or sclerosing cholangitis, two conditions in which pancreatitis associated with inflammatory bowel disease has been previously described. Pancreatitis was painless (or was associated with moderate and atypical abdominal pain) in four of our six cases; no pancreatic calcification was found in any case; in three patients a total or subtotal exocrine pancreatic insufficiency was evidenced. Endoscopic retrograde pancreatography performed in four subjects showed normal or minimally altered pancreatic ducts even in those with severe pancreatic insufficiency. These cases emphasize the existence of a probably nonfortuitous association of inflammatory bowel disease with pancreatitis. Its recognition could make a significant contribution in the management of inflammatory bowel disease.
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PMID:Idiopathic pancreatitis associated with inflammatory bowel disease. 286 72


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