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)

Biochemical, histological, and crystallographic studies were carried out on basal pancreatic secretion of 4 dogs fed alcohol for 12-15 months and 11 control dogs. The results in alcohol-fed dogs when compared to normals showed that: (1) protein concentration was higher, (2) fluid was decreased; (3) conductivity was decreased leading to differences in ionic distribution: Cl- and H+ ion concentrations increased, HCO3 concentrations and output decreased, total Ca, Mg, and Zn soluble in the juice did not change and therefore Ca, Mg, and Zn to protein ratios decreased. In the basal secretion of alcoholic dogs, numerous plugs were found of which three components were identified: (1) cells mostly of ductal origin; (2) calcium already crystallized; (3) protein material in the center of these plugs. Thus a change in Donan equilibrium led to modifications of protein and calcium solubilities with formation of precipitates. These findings are relevant to the study of chronic pancreatitis due to alcohol consumption.
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PMID:Pancreatic basal secretion in alcohol-fed and normal dogs. 728 45

Pancreatic stone protein (PSP) has been argued to play a crucial role in intraductal pancreatic stone formation in chronic pancreatitis. PSP was initially reported to inhibit calcium carbonate precipitation from human pancreatic juice and to be decreased in pancreatic secretions from patients with chronic pancreatitis. Recent clinical investigations have further demonstrated elevation of PSP in the serum and urine of patients with renal disease as well as pancreatic disease. However, the PSP reduction in pancreatic secretion in chronic pancreatitis remains controversial. Therefore, we review the current concept of PSP.
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PMID:Current status of pancreatic stone protein. 789 66

A 51-year-old man had repeated admissions and discharges from the hospital for alcohol dependence and alcoholic hepatitis. Thereafter, with a diagnosis of chronic pancreatitis, he was examined on an outpatient basis. He presented with right hypochondriac pain as the chief complaint, and was admitted to the hospital because of a suspected acute exacerbation of chronic pancreatitis. Pyrexia and jaundice were present from about the 5th hospital day, and he was admitted to Kurume University Hospital with a diagnosis of obstructive icterus. Percutaneous transhepatic biliary tract drainage (PTBD) was immediately performed. A roentgenogram revealed moderate dilatation of the extrahepatic bile ducts and stricture of the intrapancreatic common bile duct. No calculi were observed in the gallbladder or bile ducts by ultrasonography of the abdominal region. The main pancreatic duct was dilated to 10 mm, and a strong echo, probably a calculus, was observed in the main pancreatic duct. Pancreatoduodenectomy was performed with a diagnosis of stricture of the common bile duct due to chronic pancreatitis with a pancreatic stone. Examination of the excised specimens revealed a rigid pancreatic head; and when the common bile duct was incised, no stricture was observed. A milk-white calculus about 10 mm in diameter was observed in the common channel of the lower portion of the common bile duct. The orifice of the pancreatic duct was also observed at the same site. The common channel was about 20 mm long, and malfusion of the pancreatobiliary ducts was observed. The obstructive icterus was due to an impaction of the pancreatic stone at the confluence of the pancreatobiliary ducts. The calculus was composed of calcium carbonate, and the histopathological findings in the pancreas showed chronic pancreatitis.
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PMID:A case of obstructive icterus caused by incarceration of a pancreatic stone in the common channel of the pancreatobiliary ducts. 870 63

Aberrant membrane transport caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene is associated with a wide spectrum of respiratory and digestive diseases as well as cystic fibrosis. Using a gene scanning method, we found 11 polymorphisms and mutations of the CFTR gene in the Korean population. Individual variants at these sites were analyzed by conventional DNA screening in 117 control and 75 patients having bronchiectasis or chronic pancreatitis. In a haplotype determination based on a Bayesian algorithm, 15 haplotypes were assembled in the 192 individuals tested. Several haplotypes, especially with Q1352H, IVS8 T5, and E217G, were found to have disease associations in a case-control study. Notably, a common polymorphism of M470V appears to affect the intensity of the disease association. Among the two haplotypes having IVS8 T5, the T5-V470 haplotype showed higher disease association than the T5-M470 haplotype. In addition, a Q1352H mutation found in a V470 background showed the strongest disease association. The physiological significances of the identified mutations were rigorously analyzed. Non-synonymous E217G and Q1352H mutations in the M470 background caused a 60-80% reduction in CFTR-dependent Cl(-) currents and HCO3(-) -transport activities. Surprisingly, the additional M470V polymorphic variant with the Q1352H mutation completely abolished CFTR-dependent anion transport activities. These findings provide the first evidence on the importance of CFTR mutations in the Asian population. Importantly, the results also reveal that interactions between multiple genetic variants in cis affect the final function of the gene products.
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PMID:A haplotype-based molecular analysis of CFTR mutations associated with respiratory and pancreatic diseases. 1295 61

Fecal pancreatic elastase 1 (PE-1) has been advocated as a noninvasive marker of pancreatic function and allows detection of moderate and severe exocrine insufficiency. Few studies have evaluated the utility of measuring PE-1 in duodenal fluid for the diagnosis of pancreatic insufficiency. Our purpose was (1) to determine the feasibility of measuring PE-1 concentrations in duodenal aspirates obtained through our endoscopic pancreatic function test (ePFT) in healthy subjects and patients with chronic pancreatitis (CP) and (2) to determine correlations between duodenal PE-1 concentrations and bicarbonate and lipase concentrations in duodenal fluid. Healthy subjects (HS) and CP patients underwent an ePFT with CCK or secretin. CP was defined as endoscopic retrograde pancreatography (ERP) Cambridge class III-IV, endoscopic ultrasound (EUS) score >5, or presence of pancreatic calcifications on CT scan. Duodenal fluid PE-1, lipase, and bicarbonate concentrations were measured in each study group. Duodenal lipase and bicarbonate concentrations were measured using an autoanalyzer (Roche Diagnostics, Indianapolis, IN). PE-1 was measured using an ELISA (Genova Diagnostics, Asheville, NC). Ten HS and 10 CP patients were studied. In the CCK test the median peak lipase for HS and CP was 1605 and 113 IU/L, respectively (P < 0.008). In the secretin test the median peak bicarbonate for HS and CP was 102 and 40 mEq/L, respectively (p < 0.008). Median PE-1 concentrations for HS and CP were 317 and 63 microg/ml, respectively, after CCK stimulation (p = 0.046) and 87 and 17 microg/ml, respectively, after secretin stimulation (p = 0.033). Statistically significant correlations were found between [PE-1] and peak [lipase] (r = 0.83, P < 0.001), as well as [PE-1] and peak [HCO3(3)-] (r = 0.65, P = 0.037). Conclusions are as follows: (1) PE-1 concentrations can be measured from duodenal fluid obtained by endoscopic aspiration. (2) Duodenal fluid PE-1 concentrations are decreased in CP compared to HS. (3) Duodenal fluid [PE-1] has an excellent correlation with [lipase] and therefore is a marker of acinar cell function. (4) Secretin-stimulated endoscopic function testing with measurement of bicarbonate and PE-1 may provide a simultaneous assessment of both ductal cell and acinar cell function.
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PMID:Analysis of pancreatic elastase-1 concentrations in duodenal aspirates from healthy subjects and patients with chronic pancreatitis. 1548 11

The direct measurement of pancreatic function remains the best tool for diagnosing chronic pancreatitis, especially if imaging tests are normal or inconclusive. The most effective means of measuring pancreatic function is the standard hormone stimulation test using secretin. Traditionally, direct pancreatic function testing involves the fluoroscopic placement of an oroduodenal tube and collection of duodenal fluid containing pancreatic secretions after administration of a standardized dose of secretin and/or CCK. The test is time-consuming and tedious to perform, and placement of the oroduodenal tube is often difficult for the person performing the test and uncomfortable for the patient. Bicarbonate concentration typically has been measured by back-titration, requiring specialized equipment no longer found in most hospital clinical chemistry laboratories. For these reasons, the direct testing of pancreatic function after secretin stimulation has become a much admired but rarely performed test, currently done in only a few centers in the United States. In this issue of the Journal, Stevens et al. report on a cross-over study of secretin-stimulated endoscopic pancreatic function test (ePFT) and dreiling tube pancreatic function test (D-PFT) in healthy subjects and demonstrate that the accuracy of the ePFT is comparable to that of the D-PFT (17). They have demonstrated the relative simplicity and reliability of ePFT, bringing it closer to the diagnostic armamentarium of the practicing physician. We may have lost the Dreiling tube but, in its place, gained a "gold standard" which will be more widely used.
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PMID:Where have all the dreiling tubes gone? 1645 42

The pancreatic duct stenting is now recognized as the treatment option for a number of pancreatic disorders. Although the stent-induced ductal changes may result, there is little information regarding the frequency of these stent-induced changes in chronic pancreatitis. Pancreatic stents may occlude with time, but there is only little information available on the nature of the clogging process. Although a short-term efficacy of endoscopic pancreatic duct stenting has been proved, the long-term efficacy continues to be controversial. The aim of this study was to report a case of chronic pancreatitis with pancreatolith after the incidental long-term pancreatic stenting for 3 years due to a pancreas divisum with acute pancreatitis. Also, this study described the analysis of the ultrastructural changes in the surface of an occluded pancreatic stent. A scanning and transmission electron microscopy showed an amorphous protein matrix in whole stent that arranged as a network in some areas but arranged as the layers in other areas. A variable number of bacteria of mixed species, calcium carbonate or calcium oxalate crystal, round leukocyte were scattered in the protein matrix. The yeast and plant material were seen in some part of the stent as well.
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PMID:[A case of the pancreatic duct change after a long-term pancreatic stenting in pancreas divisum and the fine structural analysis of occluded pancreatic polyethylene stent]. 1649 82

Endosonography (EUS) has emerged as a major diagnostic tool in pancreatic imaging. Direct tests of pancreatic function are considered the most sensitive and accurate method to establish a diagnosis of chronic pancreatitis (CP), particularly when imaging studies are inconclusive. The aim of this study was to compare current EUS CP criteria with our newly described, purely endoscopic, secretin-stimulated pancreatic function test (ePFT). Fifty-six patients (25 male, mean age = 44 years) who were referred for evaluation/treatment of chronic abdominal pain with or without CP underwent both EUS and ePFT. The EUS protocol included the following: (1) EUS images were obtained in a standardized fashion from both gastric and duodenal stations, and (2) EUS images were scored independently by one of three therapeutic endoscopists for 0--9 parenchymal/ductal criteria as follows: 0-3 = normal, 4-5 = equivocal, >/=6 = definite CP. Endoscopic pancreatic function test (ePFT) protocol included the following: (1) upper endoscopy, (2) intravenous synthetic porcine secretin (0.2 mcg/kg, ChiRhoClin, Inc.) after test dose, (3) duodenal fluid aspirated every 15 min for 1 h, and (4) autoanalyzed for [HCO3] cutpoint of 80 mEq/L. According to EUS, 33 were normal, 13 equivocal, and 10 definite for CP. The mean peak [HCO3 -] range (in mEq/L) for each group was normal CP (83.7, range = 58-118), equivocal CP (68, range = 30-88), and definite CP (56, range=19-84). Using a peak [HCO3 -] of </=80 mEq/L as diagnostic for CP, the referent values (sensitivity%/specificity%) for EUS in the diagnosis of CP were normal (60/72), equivocal (36/94), and definite (26/100), respectively. An EUS score or greater than 5 had the best specificity (100%) and negative predictive value (100%). We conclude that endoscopic pancreatic function testing with secretin confirms that as EUS score increases, the peak pancreatic fluid bicarbonate decreases. We also conclude that EUS has excellent statistical inferences for diagnosing CP when at least 6 or more criteria are present. EUS as a screening test in patients with chronic abdominal pain and equivocal imaging studies may be of limited value.
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PMID:Comparison of endoscopic ultrasound chronic pancreatitis criteria to the endoscopic secretin-stimulated pancreatic function test. 1738 11

HCO3- -rich fluid in the pancreatic juice (2-3 L/day) is secreted by epithelial cells lining the pancreatic duct tree, while digestive enzymes are secreted by acinar cells with a small amount of Cl- -rich fluid. Ductal HCO3- secretion is not only regulated by gastrointestinal hormones and cholinergic nerves but is also influenced by luminal factors: intraductal pressure, Ca2+ concentration, pathological activation of protease and bile reflux. The maximum HCO3- concentration of the juice under secretin stimulation reaches 140-150 mM. Thus pancreatic duct cells secrete HCO3- against a approximately 7-fold concentration gradient. HCO3- secretion critically depends on the activity of CFTR, a cAMP-dependent anion channel localized in the apical membrane of various epithelia. In the proximal part of pancreatic ducts close to acinar cells HCO3 secretion across the apical membrane is largely mediated by SLC26A6 CI- -HCO3- exchanger. In distal ducts where the luminal HCO3- concentration is already high, most of the HCO3- secretion is mediated by HCO3- conductance of CFTR. CFTR is the causative gene for cystic fibrosis. Loss of function due to severe mutations in both alleles causes typical cystic fibrosis characterized by dehydrated, thick, and viscous luminal fluid/mucus in the respiratory and gastrointestinal tract, pancreatic duct, and vas deferens. A compound heterozygote of mutations/polymorphisms (causing a mild dysfunction of CFTR) involves a risk of developing CFTR-related diseases such as chronic pancreatitis. In cystic fibrosis and certain cases of chronic pancreatitis, the pancreatic duct epithelium secretes a small amount of fluid with neutral-acidic pH, which causes an obstruction of the duct lumen by a protein plug or viscous mucus.
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PMID:Physiology and pathophysiology of bicarbonate secretion by pancreatic duct epithelium. 2251 7

Ductal epithelial cells of the exocrine pancreas secrete HCO3(-) rich, alkaline pancreatic juice, which maintains the intraluminal pH and washes the digestive enzymes out from the ductal system. Importantly, damage of this secretory process can lead to pancreatic diseases such as acute and chronic pancreatitis. Intracellular Ca(2+) signaling plays a central role in the physiological regulation of HCO3(-) secretion, however uncontrolled Ca(2+) release can lead to intracellular Ca(2+) overload and toxicity, including mitochondrial damage and impaired ATP production. Recent findings suggest that the most common pathogenic factors leading to acute pancreatitis, such as bile acids, or ethanol and ethanol metabolites can evoke different types of intracellular Ca(2+) signals, which can stimulate or inhibit ductal HCO3(-) secretion. Therefore, understanding the intracellular Ca(2+) pathways and the mechanisms which can switch a good signal to a bad signal in pancreatic ductal epithelial cells are crucially important. This review summarizes the variety of Ca(2+) signals both in physiological and pathophysiological aspects and highlight molecular targets which may strengthen our old friend or release our nasty enemy.
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PMID:Calcium signaling in pancreatic ductal epithelial cells: an old friend and a nasty enemy. 2460 4


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