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)

Pancreatic polypeptide, a 36-amino peptide, is released from the pancreas by a variety of stimuli, including intravenous Boots secretin. Studies in a generalized destructive and inflammatory process such as chronic pancreatitis have revealed a markedly diminished response to stimulation. To assess whether pancreatic polypeptide release in response to Boots secretin provides a useful measure of pancreatic destruction in cystic fibrosis, 41 patients with proven cystic fibrosis, aged 14 months-23 years, and seven control subjects, aged 18-24 years were studied. Serum pancreatic polypeptide, measured by radioimmunoassay, rose from a basal of 18.5 +/- 2.7 pmol/liter to a peak of 35.6 +/- 4.3 pmol/liter at 5 min in cystic fibrosis, and from a basal of 10.8 +/- 2.8 pmol/liter to a 5-min peak of 109 +/- 27.7 pmol/liter in control subjects. The basal levels of both groups were similar but the cystic fibrosis patients had a significantly lower peak response than controls (P less than 0.05). The peak over basal pancreatic polypeptide ratio was calculated and was less than five in 93% of cystic fibrosis patients, whereas all control subjects had a ratio greater than five. Pancreatic polypeptide measurements in response to secretin may be a convenient and useful means of following the course of pancreatic disease in a chronic illness such as cystic fibrosis.
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PMID:Pancreatic polypeptide secretion. A marker for disturbed pancreatic function in cystic fibrosis. 661 99

Pancreatic size and pancreatic echo amplitude were examined to determine their value for distinguishing chronic pancreatitis from normal. Using patients with cystic fibrosis as a model for chronic pancreatitis, a prospective study was performed comparing 16 patients with this disease and 16 normals. Absolute measurements of the pancreatic body and the ratio of pancreatic size to vertebral body size were determined. Pancreatic echo amplitude was both measured clinically from the B-scan and evaluated in a blind review by seven observers. The pancreases of cystic fibrosis could be distinguished on the basis of echo amplitude with sensitivity and specificity of 94 per cent and 100 per cent for direct B-scan echo amplitude measurements and 74 per cent and 88 per cent for reviewers. Pancreatic size was of no value as a distinguishing characteristic, probably because as the diseased pancreas increases in echo amplitude by fat and fibrous tissue replacement, it blends imperceptibly with the peripancreatic soft tissues. Measurement of pancreatic size in chronic pancreatitis is therefore inaccurate and probably overestimated.
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PMID:Chronic pancreatitis: the diagnostic significance of pancreatic size and echo amplitude. 674 40

An increased proportion of ductulelike structures, sometimes dilated, occurs in association with pancreatic adenocarcinoma, chronic pancreatitis, cystic fibrosis, and pancreatic ectasia associated with conditions such as uremia. This frequently is interpreted as ductular proliferation, implying origin in ductal elements. Recent animal studies have provided an altered view of pancreatic architecture that is consistent with acinar dedifferentiation leading to the ductulelike structures, or tubular complexes. The architecture of pancreas from organ donors was studied by light and scanning electron microscopy and by wax reconstruction of serial sections. It is concluded that the zymogen granule-containing cells of normal human exocrine pancreas are arranged as branching tubules that vary in diameter and curve acutely. The tubules frequently end blindly to form acinar structures; less frequently they anastomose. This arrangement is consistent with the interpretation that tubular complexes associated with pancreatic disease result from dedifferentiative changes in acinar cells. Tubular complexes may reflect a defect or defects common to pancreatic disease rather than ductular proliferation specific to each one.
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PMID:Architecture of human pancreas: implications for early changes in pancreatic disease. 685 61

Radioimmunoassays for plasma pancreatic enzymes, especially cationic trypsin, are good tools to diagnose pancreatic pathology. The trypsin assay is very sensitive. Its detection limit is 300 pg/ml. The plasma level of this enzyme appears to be representative of pancreatic function. This assay was shown to be valuable in the diagnosis of acute pancreatitis, and to follow the course of the disease. In chronic pancreatitis, it enables assessment of residual function of the organ. In the terminal stage of this disease, very low values were found. Used as a screening test, the assay allowed early detection of cystic fibrosis.
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PMID:Clinical usefulness and methodology of immunological assay of pancreatic enzymes. 686 35

A number of human diseases with intestinal adaptation have been investigated, including acute infective diarrhoea, intestinal resection, jejuno-ileal bypass, coeliac disease, tropical sprue, chronic pancreatitis and cystic fibrosis. In all, the newly isolated hormone enteroglucagon appeared to be elevated in proportion to the degree of adaptation. In rats after gut resection and cold adaptation, enteroglucagon was also elevated and the degree of elevation correlated closely with the crypt cell production rate (CCPR). Chronic administration of somatostatin suppressed both enteroglucagon and CCPR, while bombesin stimulated both. A crude preparation of enteroglucagon was found to directly stimulate DNA synthesis in enterocyte cultures. It is thus concluded that, at present, the most likely candidate for the humoral component of intestinal adaptation is the hormonal peptide enteroglucagon.
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PMID:The hormonal pattern of intestinal adaptation. A major role for enteroglucagon. 695 45

A 29-yr-old man with cystic fibrosis had a 4-yr history of recurrent episodes of obstructive jaundice. Endoscopic retrograde cholangiography revealed a common bile duct smoothly narrowed in its intrapancreatic portion, with dilatation above. A choledochojejunostomy was performed, but the patient died of septic complications. At autopsy, extensive pancreatic fibrosis caused compression of the distal bile duct in a manner which is analogous to that seen in chronic pancreatitis. This complication of cystic fibrosis, not previously reported, may become more prevalent as more patients with cystic fibrosis are living into adulthood.
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PMID:Intrapancreatic common bile duct compression causing jaundice in an adult with cystic fibrosis. 745 Apr 4

Clinical conditions in which secondary maldigestion associated with exocrine pancreatic insufficiency occur include chronic pancreatitis, cystic fibrosis, pancreatic cancer, partial or total gastrectomy, and pancreatic resection. Maldigestion can cause serious weight loss, nutritional deficiencies, and subjective complaints associated with steatorrhea. The various causes of exocrine pancreatic insufficiency may be associated with cause-related changes in gastrointestinal physiology, such as changes in gastrointestinal intraluminal pH, bile acid metabolism, gastric emptying, and intestinal motility. Therefore, to optimize the efficacy of treatment, the management of exocrine pancreatic insufficiency must be individually tailored to account for both the underlying cause and any associated disturbance in gastrointestinal physiology. In addition, the properties of the pancreatic enzyme preparations and adjuvant drugs need to be taken into consideration. This paper reviews the pathophysiological mechanisms of maldigestion in exocrine pancreatic insufficiency, discusses the efficacy of different therapy regimens, and gives guidelines for a cause-related and patient-tailored treatment with respect to both drug therapy and dietary counselling.
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PMID:Maldigestion associated with exocrine pancreatic insufficiency: implications of gastrointestinal physiology and properties of enzyme preparations for a cause-related and patient-tailored treatment. 766 Nov 55

The 'naked' islets of Langerhans (NIL) in randomly selected autopsy cases and in cases of chronic alcoholic pancreatitis, cystic fibrosis, and pancreatic carcinoma were studied histopathologically. The NIL were found in 55 of 164 randomly selected cases, with age-related frequency, in 21 of 30 cases of chronic alcoholic pancreatitis, in 2 of 2 cases of cystic fibrosis, and in 25 of 32 cases of pancreatic carcinoma. The NIL were frequently accompanied by ductal alterations: epithelial metaplasia and hyperplasia in randomly selected cases, protein plugs in chronic alcoholic pancreatitis, mucus plugs in cystic fibrosis, and obliterated ducts in pancreatic carcinoma. The NIL in randomly selected cases may have been formed by ductal alterations that caused stenosis of the lumen, those in chronic alcoholic pancreatitis and cystic fibrosis were the result of protein or mucus plugging, and those in pancreatic carcinoma were a result of neoplastic involvement of the distal pancreatic duct. Therefore, the common factor in the development of NIL is thought to be obstruction of the pancreatic duct system, and in cases of NIL that have a multilobular distribution and interinsular fibrosis, a diagnosis of chronic pancreatitis can usually be made.
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PMID:A morphologic analysis of 'naked' islets of Langerhans in lobular atrophy of the pancreas. 795 49

Pancreatic enzyme extracts have been used for several decades to decrease maldigestion of macro- and micronutrients due to pancreatic insufficiency and to alleviate various abdominal symptoms, including the pain of alcohol-induced chronic pancreatitis and distal intestinal obstruction. Decreasing nutrient maldigestion and malabsorption in pancreatic insufficiency is of additional critical importance because improvement in nutritional status reduces morbidity and mortality. For example, pancreatic sufficient patients with cystic fibrosis (CF) demonstrate a slower decline in pulmonary function. In spite of the recognized importance of pancreatic enzymes, several problems exist with current preparations, and as newer enzyme preparations are marketed, proper evaluation becomes critical. There is a clear need to optimize the constituents of enzyme preparations, improve manufacturing processes, and find better sources of enzymes. Other issues that need addressing include standardization of the ratios of enzymes (lipase, amylase, protease) in these products; the stability of the enzymes at room temperature; the shelf life of the finished product; whether there are significant batch-to-batch differences; and the need for a USP reference standard.
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PMID:Enzyme therapy for pancreatic insufficiency: present status and future needs. 810 63

Pancreatic transplantation for endocrine replacement is well-established for insulin-dependent diabetes mellitus. Exocrine pancreatic function after pancreas transplantation has been maintained after orthotopic cluster transplants for malignancy, and restoration of adequate exocrine function in a previously deficient patient has been reported in a patient with chronic pancreatitis who developed labile diabetes and steatorrhea after pancreatectomy. We performed a triple organ transplant (pancreas, liver and kidney) in a patient with exocrine pancreatic insufficiency and insulin-dependent diabetes related to cystic fibrosis (CF) after he developed hepatic and renal failure. Pancreatic exocrine secretions were drained enterically to the jejunum. At 24-month follow-up, malabsorption is absent. The 3-day stool fat, stool trypsin and chymotrypsin are normal. Serum carotene is within the normal range. Exocrine pancreatic insufficiency in CF patients can be corrected by pancreas transplantation. However, routine use in CF is precluded by the risks of surgery and immunosuppression. For diabetic patients with pancreatic exocrine insufficiency who require another organ transplant (e.g., lung, liver, or kidney), simultaneous pancreas transplantation with the exocrine secretions directed into the upper gastrointestinal tract should be considered.
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PMID:Restoration of exocrine pancreatic function following pancreas-liver-kidney transplantation in a cystic fibrosis patient. 813 59


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