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

The ability of the pancreas to regenerate and the effects of trophic hormones on regeneration of the pancreas after partial pancreatectomy are not completely understood. We investigated the effects of the trypsin inhibitor FOY-305 (an agent that stimulates endogenous cholecystokinin) on pancreatic regeneration after partial pancreatectomy in rats. FOY-305 or water was administered for either 13 days or 27 days by gavage feeding, after sham operation or partial pancreatectomy (n = 6 to 8 animals per group). FOY-305 stimulated hypertrophy of the pancreatic remnant at 13 days; prolonged treatment for 27 days produced both hypertrophy and hyperplasia. The magnitude of pancreatic growth after FOY-305 administration was significantly greater at 27 days in the pancreatic remnant than growth of the equivalent pancreatic segment (duodenal and parabiliary) in sham-operated rats treated with FOY-305. Our results suggest that endogenous cholecystokinin released by FOY-305 stimulates regeneration after partial pancreatectomy. The pancreatic remnant is more sensitive to trophic stimulation in comparison to the normal pancreas. FOY-305 may be a useful agent in the treatment of pancreatic insufficiency after extensive subtotal pancreatectomy or chronic pancreatitis.
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PMID:Pancreatic regeneration after partial pancreatectomy. 170 41

Factors influencing the effectivity of replacement therapy with Panpur and Creon were controlled by in vivo and in vitro investigations. Both enteric coated preparations were equally acid protected, they even seemed to be more effective in hyperacid than in anacid chronic pancreatitis patients. Thus the uneven results of Panpur treatment in pancreatic steatorrhea cannot be explained by acid inactivation of the enzymes. Creon dose-dependently ameliorated the steatorrhea as well as vitamin B12 absorption while crushed but not the intact Panpur has only some insignificant effect. Good mixing of pancreatin with the B12-intrinsic factor - R protein complex and with the protein containing meal seems to be important for digestion of protein as well as fat. Unbound, overflowing trypsin activity of Panpur resulted in fast proteolytic inactivation of lipase. This could be diminished by soybean trypsin inhibitor which increased the in vivo effectiveness of the preparate. In summary Creon fulfilled two important factors of replacement therapy more successfully than Panpur: good mixing with meals and stability of lipase against proteolytic splitting, that is why it proved to be more effective for replacement therapy of pancreatic insufficiency.
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PMID:[Requirements for successful pancreatic enzyme replacement therapy (comparative study of Kreon and Panpur)]. 230 64

Pancreatic secretory trypsin inhibitor (PSTI) is a 6000-dalton peptide, that occurs in high concentrations in the pancreas and in pancreatic juice. It is thought to be synthesized by pancreatic acinar cells. We have recently reported the findings of an identical trypsin inhibitor at high concentrations in the urine of patients with gynecological malignancy. Therefore, we have named the inhibitor tumor-associated trypsin inhibitor (TATI). We have now studied patients who have undergone total pancreatoduodenectomy for pancreatic cancer or chronic pancreatitis. By radioimmunoassay (RIA), we found normal levels of this inhibitor in the serum and urine of pancreatectomized patients. The absence of pancreas was confirmed by measuring serum trypsin. By gel filtration and HPLC it was found that PSTI/TATI occurring in pancreatectomized patients was indistinguishable from that found in connection with pancreatitis and ovarian cancer.
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PMID:Pancreatic secretory trypsin inhibitor-like immunoreactivity in pancreatectomized patients. 393 45

In this study we looked for the occurrence of immunoglobulin E (IgE) in feces from healthy individuals and determined the total daily excretion and day-to-day variation in IgE in feces from patients with allergy, as well as the correlation between concentrations of IgE in small samples of feces and the total amounts of IgE in feces collected over a longer period. Concentrations of IgE in extracts of small samples of dry feces correlated well with the total daily amounts of IgE in feces collected over a 3-day period. Thus, single small samples of feces can be used to measure the excretion of IgE with feces at that time. In 3 children, studied over a 5-week period, the IgE excretion varied somewhat from one day to another, but was largely within a certain range of concentrations. Addition of trypsin inhibitor to fresh feces had no influence on the IgE concentrations of the resulting fecal extracts. Less than 10% of 88 presumably healthy infants, children, and adults had detectable IgE in their feces, while 21 of 40 children with various kinds of allergy had measurable fecal IgE. Only 3 of 13 individuals who were suffering from infectious acute gastroenteritis had IgE-positive fecal extracts. This was also the case for 6 of 25 adult patients in clinical remission of ulcerative colitis or Crohn's disease. Seven of 14 adult patients with chronic pancreatitis had measurable IgE in feces, and the concentrations were up to ten times the upper limit of IgE found in healthy individuals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The excretion of IgE with feces from healthy individuals and from others with allergy and diseases affecting the intestinal tract. 394 13

The concentrations of pancreatic amylase, immunoreactive trypsin, and immunoreactive pancreatic specific trypsin inhibitor have been studied in serum drawn from 258 patients before an endoscopic retrograde cholangiopancreatography (ERCP) examination, in which both ducts were successfully filled. The results are correlated to the morphology of the ducts and the diagnosis given at the ERCP examination. One third of the patients with normal morphology of both ducts showed an abnormal concentration of at least one of the measured specific pancreatic proteins. Sixteen out of 38 patients with changes suggestive of chronic pancreatitis and 6 out of 23 patients with changes suggestive of pancreatic cancer showed normal levels of all variables measured. The sensitivity and specificity for pancreatic disease evident by ERCP were around 0.40 and 0.80, respectively, for all three proteins.
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PMID:Correlation between serum concentrations of three specific exocrine pancreatic proteins and pancreatic duct morphology at ERCP examinations. 620 96

Pancreatic secretory profiles for 11 pancreatic enzymes and proteins were established in nine patients with cancer of the pancreas by analysis of minute-to-minute collections of pure pancreatic juice after sequential administration of secretin and cholecystokinin. Aspiration of pancreatic fluid sufficient for this study was successful in less than one quarter of the patients investigated because of ductal obstruction and/or the effect of the disease on pancreatic exocrine function. Flow rates in patients generally were lower than in healthy individuals, and secretion of total protein, trypsin inhibitor, and activity of digestive enzymes were in the lowest part of or below the normal range. Normal flow rates in four patients precluded ductal obstruction as the sole cause of impaired enzyme secretion. Activity of lysosomal hydrolases in pancreatic juice of these patients, in contrast to that of digestive enzymes, remained within or rose above the normal range. The tumor appeared to have a diametrically opposite effect on the two different groups of enzymes. This is illustrated most dramatically in the form of ratios of lysosomal to digestive enzymes. Virtually all of 10 such ratios were far above the normal average in all patients, and none was below. In an analogous investigation of 25 patients with chronic pancreatitis only three exhibited the ratio pattern characteristic of pancreatic cancer patients. Pancreatic secretory profiles appear to be capable of discriminating between cancer of the pancreas and chronic pancreatitis in a high percentage of cases. Extension and refinement of this approach may facilitate early detection of cancer of the pancreas.
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PMID:Abnormalities in pancreatic secretory profiles of patients with cancer of the pancreas. 682 32

The activity of trypsin, common trypsin inhibitor and elastase was evaluated in the blood serum of children with chronic diseases of the digestive organs. The activity of trypsin and its inhibitor was shown to be elevated in most children with both concomitant pancreatitis and without it. Increased activity of the trypsin inhibitor reflects a positive compensatory response of the body to excess trypsin supply to the blood. The activity of serum elastase rises only with exacerbation of chronic pancreatitis.
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PMID:[Change in proteolytic enzymatic activity in the blood serum in children with chronic diseases of the digestive organs]. 699 29

The serum values of tumour-associated trypsin inhibitor (TATI) were measured in a prospective series of 97 patients with jaundice, 36 patients with unjaundiced cholestasis and 21 patients with suspicion of chronic pancreatitis or a pancreatic tumour, to assess its value in diagnosing pancreatic cancer. There were altogether 15 patients with cancer of the pancreas and 2 patients with cancer of the papilla of Vater. The highest serum TATI values were noticed in patients with choledocholithiasis, and raised values were also seen in patients with malignant disease of the liver or bile ducts. In the patients with pancreatic cancer, chronic pancreatitis or benign liver disease, the serum TATI values showed lower levels. The sensitivity of TATI in diagnosing pancreatic cancer was 41.1% with a specificity of 63.5% and an efficiency of 61.0%. In comparison to carcinoembryonic antigen (CEA), carbohydrate antigens CA 50, CA 242, tissue polypeptide antigen and tissue polypeptide-specific antigen, TATI showed a lower diagnostic value. When TATI was analysed in combination with the other markers (two tests positive), the combination of CEA with TATI reached the highest specificity (95.6%), efficiency (89.6%) and positive likelihood ratio (9.3). The results suggest that the diagnostic value of TATI is inferior to that of the established markers, but because of its different nature, it may be of help when used in combination as a complementary serum tumour marker in the diagnosis of pancreatic cancer.
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PMID:Tumour-associated trypsin inhibitor in the diagnosis of pancreatic carcinoma. 820 49

Chronic pancreatitis (CP) is a continuing or relapsing inflammatory disease of the pancreas. In approximately one-third of all cases, no aetiological factor can be found, and these patients are classified as having idiopathic disease. Pathophysiologically, autodigestion and inflammation may be caused by either increased proteolytic activity or decreased protease inhibition. Several studies have demonstrated mutations in the cationic trypsinogen gene (PRSS1) in patients with hereditary or idiopathic CP. It is thought that these mutations result in increased trypsin activity within the pancreatic parenchyma. Most patients with idiopathic or hereditary CP, however, do not have mutations in PRSS1 (ref. 4). Here we analysed 96 unrelated children and adolescents with CP for mutations in the gene encoding the serine protease inhibitor, Kazal type 1 (SPINK1), a pancreatic trypsin inhibitor. We found mutations in 23% of the patients. In 18 patients, 6 of whom were homozygous, we detected a missense mutation of codon 34 (N34S). We also found four other sequence variants. Our results indicate that mutations in SPINK1 are associated with chronic pancreatitis.
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PMID:Mutations in the gene encoding the serine protease inhibitor, Kazal type 1 are associated with chronic pancreatitis. 1083 40

Summary. The understanding of the pathogenesis of chronic pancreatitis is limited. Several theories (i. e. obstruction hypothesis) were suggested in the past but could not be confirmed by experimental data. As a formal description of the course of the disease, the necrosis-fibrosis concept seems to be very attractive. According to this theory, there is no significant difference in the pathogenesis of acute and chronic pancreatitis. A major step was the identification of mutations of the cationic trypsinogen, the secretory trypsin inhibitor (SPINK 1) and the cystic-fibrosis protein (CFTR) in some patients. Investigation of these mutations may significantly contribute to a better understanding of the pathogenesis of chronic pancreatitis.
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PMID:[Pathogenetic concepts of chronic pancreatitis]. 1175 98


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