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

Urinary excretion of lactulose, mannitol, and 3-0-methylglucose, following oral administration (5 g, 5 g, and 2 g, respectively, in 100 ml H2O; 80 ml/m2), has been measured in subjects with cystic fibrosis (CF) (22), Shwachman syndrome (3), chronic pancreatitis (3), and normal controls (46). Mean lactulose excretion was increased 10-fold in CF (p less than 0.001), and two-fold in other disorders associated with pancreatic insufficiency (PI) (p less than 0.05). Mean mannitol excretion was 1.6 times greater in CF (p less than 0.001), compared with controls, but was reduced in other forms of PI (p less than 0.03). The mean lactulose/mannitol excretion ratio was increased in all types of PI (p less than 0.001). There were no significant differences in 3-0-methylglucose excretion. This study confirms the large increase in lactulose absorption recently reported in CF and also demonstrates increased absorption of mannitol; these changes are different than those in other forms of PI. This study provides further evidence for a specific abnormality of the mucosal barrier to the absorption of passively absorbed, water soluble molecules in CF.
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PMID:Active and passive sugar absorption in pancreatic insufficiency. 249 12

The dietary treatment of steatorrhea requires knowledge of the cause of the disease associated with the steatorrhea. Once the cause is established, then an approach to the dietary management can be adopted. Guidelines for treatment are reviewed in this article. Recommendations for either the treatment of the primary disease, limitation of fat intake, nutritional support, or pancreatic-enzyme replacement are made depending on the disease process. The most common disease entities causing steatorrhea are discussed in detail. Specific recommendations are made for the treatment of steatorrhea in cystic fibrosis of the child and adult, pancreatic insufficiency caused by chronic pancreatitis, gluten enteropathy, and the short-bowel syndrome. Emphasis is placed on the fact that each patient must be managed by correlating the cause of the steatorrhea with specific modalities of therapy.
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PMID:Dietary therapy of steatorrhea. 250 53

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

Enzyme replacement therapy is a vital aspect of the management of patients with chronic pancreatic insufficiency. However, pharmaceutical technology in the manufacture of enzyme products has advanced significantly only in the last decade. In the late 1970s, Johnson & Johnson scientists developed novel pH-sensitive enteric-coated microspheres of pancrelipase (Pancrease) that could be encapsulated for convenient administration. The increased efficiency of the formulation allowed lower daily doses than had been required with conventional enzyme products. In vitro studies indicate that the microspheres disintegrate at a pH appropriate for patients with cystic fibrosis and chronic pancreatitis. Clinical studies of Pancrease in chronic pancreatitis demonstrate a significant improvement in fecal fat excretion, fat utilization, stool weight, and stool frequency, as well as significant weight gain and improved quality of life of patients. Pancrease represents a major advance in the clinical management of chronic pancreatic insufficiency.
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PMID:Development of pancreatic enzyme microsphere technology and US findings with Pancrease in the treatment of chronic pancreatitis. 270 48

The association between asymptomatic primary sclerosing cholangitis and exocrine pancreatic disease was underlined by the findings in a patient with cystic fibrosis and in another with chronic pancreatitis. In each case hepatocytes showed extensive microvesicular steatosis and studies of drug metabolism suggested hepatic enzyme induction: biliary or serum analysis, or both, disclosed raised concentrations of a lipid-based marker of free radical oxidation. These findings suggest that toxic metabolites of oxygen or other chemicals may have a role in the pathogenesis of the bile duct lesion.
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PMID:Sclerosing cholangitis with hepatic microvesicular steatosis in cystic fibrosis and chronic pancreatitis. 273 40

We comment the case of a 25-year-old woman, diagnosed since the age of 7 as cystic fibrosis, who presented acute pancreatitis, an exceptional complication of the underlying disease. In the ultrasonographic exploration and endoscopic retrograde cholangiopancreatography was appreciated dilation of the pancreatic ducts, with mobile echoes and filling defects, respectively, compatible with mucus plugs. The etiopathogenesis of this type of acute pancreatitis and the procedure for reaching an etiological diagnosis are discussed. Although the patient presented moderate grade pancreatic failure, there is presently no agreement as to whether pancreatitis secondary to cystic fibrosis can be considered as chronic pancreatitis.
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PMID:[Acute pancreatitis: an infrequent complication of cystic fibrosis (mucoviscidosis)]. 276 30

Many approaches have been proposed to differentiate between steatorrhea due to pancreatic insufficiency and intestinal disease. Bo-Linn and Fordtran recently suggested that fecal fat concentration (FFC) is a useful screening test for this distinction. Our aim was to validate their result in a large group of patients. Fecal fat concentrations were calculated for 613 fecal fat tests in 538 patients. Included were 88 patients with pancreatic steatorrhea (13 pancreatic carcinoma, 6 cystic fibrosis, and 69 chronic pancreatitis) and 525 with nonpancreatic steatorrhea. The mean FFC of patients with pancreatic disease (15.0 +/- 1.9 g%, mean +/- SEM) was significantly higher than that of patients with other diseases causing malabsorption (8.9 +/- 0.3 g%, p less than 0.001). Forty-two percent of patients with pancreatic steatorrhea had an FFC below 10 g%. The overlapping of the FFC of steatorrhea due to pancreatic disease and that produced by celiac disease, gastric resection, and other conditions suggests that this approach does not differentiate between pancreatic and intestinal steatorrhea.
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PMID:Fecal fat concentration in the differential diagnosis of steatorrhea. 291 27

In the treatment of disorders of the pancreas, artificial nutrition must satisfy nutritional requirements while avoiding stimulation of exocrine pancreatic juice observed during oral feeding. Although total parenteral nutrition (PN) induces pancreatic hyposecretion or weak pancreatic stimulation, enteral nutrition (EN) whether elementary or semi-elementary type stimulates pancreatic secretion and the release of CCK, with weaker stimulation in case of intrajejunal feeding. In acute pancreatitis, semi-elemental EN by jejunal feeding has successfully been used in the treatment of moderately serious cases, once the acute phase of the disease has been passed. Although PN remains the best indication for the treatment of pancreatic fistula, several studies have reported the closure of pancreatic fistulas during elementary enteral feeding administered by jejunal route. In the treatment of chronic pancreatitis, EN especially provides nutritional support for very undernourished patients, most often in the preoperative context. Finally, in children suffering from cystic fibrosis of the pancreas, prolonged sessions of EN provide marked improvement in the nutritional and respiratory status of these patients.
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PMID:[Indications of enteral nutrition in pancreatic disorders]. 314 4

Polyethylene glycol (PEG) 4000 is one of numerous substances used as non-absorbable markers to correct for variable faecal output when assessing daily faecal losses of nutrients. The introduction of enteric coated micro-encapsulated pancreatic enzyme (EMPE) preparations has greatly improved the control of fat malabsorption in cystic fibrosis and chronic pancreatitis patients. Unfortunately, these enzyme preparations contain significant quantities of PEG 4000 or polyvinyl pyrrolidine (PVP) as components of the enteric coating and thus PEG 4000 cannot be used either as a faecal marker, or in intubation studies, if these enzyme preparations are being used.
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PMID:Markers for faecal fat estimation in monitoring steatorrhoea in cystic fibrosis. 319 6

Secretin and cholecystokinin-pancreozymin had no effect on the secretion of human gastric lipase, in contrast to pentagastrin, which increased the gastric lipase output but not the enzyme concentration in gastric juice. The secretion of gastric lipase was not significantly different in patients with duodenal ulcer or chronic pancreatitis and in controls. In contrast, basal gastric lipase concentration was significantly lower in children with cystic fibrosis than in normal children. This shows that neither in adults nor in children is there a compensation for a decreased lipase secretion by an increased gastric lipase secretion.
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PMID:Human gastric lipase: variations induced by gastrointestinal hormones and by pathology. 324 86


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