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

The etiology, pathophysiology, clinical presentation, dietary management, and drug therapy of maldigestion associated with pancreatic insufficiency are reviewed. Maldigestion can occur in a number of conditions that lead to pancreatic insufficiency but is seen most frequently in patients with alcohol-related chronic pancreatitis or cystic fibrosis. Destruction of pancreatic tissue and obstruction of the ducts that lead into the small intestine prevent pancreatic secretions from reaching the small intestine and result in weight loss, anorexia, abdominal distention, and changes in the appearance and frequency of stools. The goal of dietary intervention in patients with maldigestion is to provide sufficient calories and protein to maintain weight while limiting fat intake to an amount tht the patient can tolerate. Medium-chain triglycerides can be substituted for dietary fat in patients whose symptoms continue despite dietary fat restriction. Drug therapy involves supplementing deficient pancreatic enzymes with pancreatin or pancrelipase. Regimens must be individualized for each patient because of problems with gastric inactivation of orally administered enzymes, lack of standardization of commercially available preparations, and large interpatient variation in response. In selecting an enzyme supplement preparation, the amount of available enzyme activity, dosage form, number of dosage units needed per dose, dosage schedule, and product cost must be considered. When enzyme supplementation alone does not adequately control the symptoms of maldigestion, a histamine H2-receptor antagonist or antacids may be added to the therapeutic regimen. Although complete resolution of the symptoms of maldigestion is difficult to achieve, a regimen of dietary modification and pancreatic-enzyme replacement can improve patients' quality of life.
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PMID:Management of maldigestion associated with pancreatic insufficiency. 398 14

The name juvenile tropical pancreatitis syndrome (JTPS) is proposed for a disease which affects young people of both sexes in certain parts of the tropics and which is characterised by abdominal pain, diabetes, steatorrhoea, and pancreatic calcification. The condition seems to start with blockage of the pancreatic ducts by laminated secretions or inspissated mucus plugs which later calcify. Chronic pancreatitis follows. The hypothesis is that plugs are the result of pancreatic stasis due to prolonged lack of food in the stomach and/or gastroenteritis and dehydration. Most plugs are probably dislodged during convalescence when protein-containing foods are eaten and stimulate vigorous flow of pancreatic juice. The sluggish pancreatic flow produced by very-low-protein diets may not dislodge plugs. Repeated infection and anorexia can enlarge the plugs which ultimately calcify. JTPS therefore occurs in Third-World areas with a high rate of childhood infections, and where low-protein staples are taken. Cereal staples seem to reduce the incidence of JTPS in endemic areas because of their protein content.
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PMID:Pathogenesis of juvenile tropical pancreatitis syndrome. 610 87

Intramural hematoma of the intestine caused intestinal obstruction in three dogs. Two dogs were examined because of vomiting and anorexia of several weeks' duration. In one of these, an intramural hematoma of the duodenum was associated with chronic pancreatitis. A cause was not found in the second dog. The third dog, which had clinical and radiographic evidence of gastric dilatation, was found at surgery to have hemoperitoneum associated with a ruptured intramural intestinal hematoma. In 1 dog, the hematoma was evacuated through a serosal incision. In the other 2 dogs, the problem was resolved by resection of the involved segment of intestine, followed by anastomosis. All 3 dogs recovered without complications.
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PMID:Intramural intestinal hematoma causing obstruction in three dogs. 669 51

A 56 years old male with chronic pancreatitis complained of intractable abdominal pain, anorexia, emaciation and peripheral edema. Medical treatment initiated only partial improvement in the general condition and hypoproteinemia. Endoscopic retrograde cholangiopancreatography revealed multiple filling defects in the dilated main pancreatic duct. Endoscopic aspiration of pure pancreatic juice yielded numerous protein plugs. The endoscopic removal of protein plugs from the pancreatic duct resulted in remarkable improvement in symptoms, laboratory findings and ERCP findings. We consider this procedure to be an important new treatment of chronic pancreatitis.
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PMID:A case of chronic pancreatitis successfully treated by endoscopic removal of protein plugs. 673 Oct 27

An alcoholic, 67-year old retired male nurse complained of abdominal pain, loss of appetite and weight loss of 10 kg within one year. Based on elevated serum enzyme levels, ultrasonography and computed tomography examinations, an acute attack of chronic pancreatitis with several pancreatic pseudocysts was diagnosed. Ultrasonographically, an 1.8 cm phi, echo-free, pulsatile, space-occupying lesion, suggestive of a pancreatic pseudoaneurysm, was found at the right lateral margin of an almost echo-free pseudocyst measuring 6.8 x 5.6 x 5.0 cm in the head of the pancreas. Shortly before the planned discharge when the patient felt well, he developed acute abdominal pain. An immediate ultrasound examination showed an inhomogenous and echo-dense pseudocyst, in short, an acute hemorrhage. Rupture of the pseudoaneurysm of the Arteria gastroduodenalis was suspected and later confirmed by angiography and laparotomy. After proximal an distal ligation of the vessel and fibrin sealing of the inner surface of the cyst, the patient recovered and, under alcohol abstinence, has been free of symptoms since one year.
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PMID:Acute abdominal pain in chronic pancreatitis: hemorrhage from a pseudoaneurysm? 757 59

There are (at least) two types of receptor for cholecystokinin (CCK)/gastrin peptides. Highly potent specific antagonists are available for both types. The CCKA-receptor mediates classical CCK-like effects on the gut. Antagonists given to man inhibit pancreatic enzyme secretion and generally shorten gastrointestinal transit times. Potential clinical indications include anorexia, gastro-paresis, pseudo-paresis, pseudo-obstruction, severe constipation and chronic pancreatitis. However gallbladder contraction is markedly inhibited and this led to gallstone formation in baboons. This will obviously have to be avoided if CCKA antagonists are to be used in man. CCKB-receptors mediate the effects of gastrin on the gut and the effects of CCK in the brain. They inhibit gastrin-stimulated acid secretion. If used in acid-peptic disease they might inhibit the trophic effects of gastrin on enterochromaffin cells. CCKB-antagonists can also inhibit the growth of some gastrin-dependent tumours, including certain human colonic cancer cell lines which produce gastrin. CCKB-antagonists have a potent anxiolytic-like effect in animals, and this effect might become their main clinical application.
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PMID:CCK/gastrin antagonists--clinical perspectives. 826 65

The diagnosis of pancreatic cancer usually depends upon symptoms; consequently it is late when there is no chance for cure. At this point, pain, anorexia, early satiety, sleep problems and weight loss are present. Back pain also may be prominent, which predicts unresectability and shortened survival after resection. However, earlier recognition of symptoms of pancreatic cancer might improve early detection of the cancer. For example, 25% of patients have symptoms compatible with upper abdominal disease up to 6 months prior to diagnosis and 15% of patients may seek medical attention more than 6 months prior to diagnosis. These symptoms erroneously may be attributed to problems such as irritable syndrome. Symptoms, however, may be less common. For example a quarter of patients with pancreatic cancer may have no pain at diagnosis, and half, particularly those with pancreatic head tumors, may have little pain compared with patients with body-tail tumors. However, if the tumor is suspected because of predisposing conditions, earlier diagnosis may be possible. These conditions include diseases such as chronic pancreatitis, intraductal papillary mucinous tumor (IPMT), and recent onset of diabetes mellitus, particularly if the diabetes occurs during or beyond the sixth decade. In addition inherited syndromes also are associated with an increased risk of pancreatic cancer including familial pancreatic cancer, hereditary pancreatitis, familial adenomatous polyposis syndrome (FAP) and familial atypical multiple mole melanoma (FAMMM) syndrome (hereditary dysplastic nevus syndrome). Of these conditions, recent onset of diabetes may be the best clue and should be included in a clinical profile of patients prior to the onset of symptoms to identify a high-risk group to apply screening strategies for detection of early disease. Contrary to a clinical aphorism that pancreatic cancer patients are elderly, lean and recently may have developed diabetes, we found that patients who develop pancreatic cancer are overweight prior to onset of symptoms compared to controls (body mass index, 28 vs 25). Forty percent had the diagnosis of diabetes made at the time of diagnosis of pancreatic cancer and more patients with a resectable tumor had diabetes (58%) compared to patients with locally unresectable or metastatic disease (37%). Perhaps, screening overweight persons who have new-onset diabetes may lead to a diagnosis of asymptomatic, early, resectable pancreatic cancer.
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PMID:Pancreatic cancer: clinical presentation, pitfalls and early clues. 1043 7

Hereditary Pancreatitis (HP), is an autosomal dominant trait, which presents with recurrent attacks of abdominal pain, and is the most common cause of chronic relapsing pancreatitis in children. In addition to recurring episodes of intense epigastric pain, patients have nausea, vomiting, and anorexia, and typically show elevated serum amylase levels during the acute episode that can rapidly decline in convalescence. Complications of long-standing disease include features of chronic pancreatitis, such as pancreatic pseudo-cyst, exocrine and endocrine failure, parenchymal calcification, and pancreatic cancer. A large family from Virginia, which was originally studied by Katwinkle and Lapey in 1973, was re-ascertained through a new proband. Linkage studies in this family mapped the gene to the 7q35 region, with similar results being reported simultaneously by two other groups. A pathogenic G to A transition mutation in exon 3 of the cationic trypsinogen (CT) gene, which had previously been mapped to this region, was found both in our family as well as other families from North America. Many other conditions can produce abdominal symptoms that are often mis-attributed to the disease in HP families. An affected member of our family in whom the mutation was confirmed by direct sequencing of exon 3 of the cationic trypsinogen gene requested diagnostic testing on his 4-year-old son because of onset of severe abdominal pain and vomiting. Screening for the mutation in this child did not reveal the pathogenic G to A change. These results prevented unnecessary invasive diagnostic procedures and treatment in this child. The pre-symptomatic testing of high risk individuals could, thus, have a significant impact on the well being of both affected and normal family members.
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PMID:Implications of molecular diagnostic testing in families with hereditary pancreatitis. 1046 47

Hereditary tyrosinemia results from an inborn error in the final step of tyrosine metabolism. Neurological manifestations have been reported in nearly half of patients during illness to have characteristics of altered consciousness, weakness, anorexia, vomiting, and pain in the extremities and abdomen. His physical findings and laboratory results pointed out acute pancreatitis. There have been some reports of acute and chronic pancreatitis in patients with metabolic diseases; however, this is the first case with tyrosinemia type I who exhibited clinical and biochemical findings of acute pancreatitis during neurological crisis. The presented case suggests the possibility that the pancreas is affected in neurological crisis. The determination of amylase concentration both in serum and urine samples of further cases will clarity the association between pancreatitis and neurological crisis.
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PMID:Neurological crisis mimicking acute pancreatitis in tyrosinemia type I. 1077 Jan 19

There are various potential explanations for weight-loss and poor physical performance in patients with chronic pancreatitis: In severe chronic pancreatitis the decline in enzyme secretion is an important cause for the malassimilation syndrome frequently seen in these patients. Occasionally, difficulties may arise in establishing this decline and in quantifying the secretory capacity of the gland. Many patients limit their food intake because of the pain caused by eating. In untreated patients with diabetes, glucosuria may contribute to their malnutrition. Insufficient funds for food due to alcoholism and anorexia may also be of some significance. Concomitant gastrointestinal diseases and malabsorption following gastrointestinal surgery are frequently found in patients with chronic pancreatitis. Neurological complications and traumatic lesions after accidents - often in connection to the underlying alcoholism - are joined by physical inactivity and thus contribute to the development of muscular atrophy and decreased physical performance. Consequently, rehabilitation of patients with chronic pancreatitis is challenging: They not only need expert medical treatment of both the symptoms of chronic pancreatitis and the concomitant disorders. Therapy must also include dietary support, careful physical training, and - in cases caused by alcoholism - psycho-social support. So far, the multi-professional competence required for these purposes can only be expected in a specialized rehabilitation centre.
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PMID:[Chronic pancreatitis: weight loss and poor physical performance - experience from a specialized rehabilitation centre]. 1174 23


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