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

We evaluated the behavior of serum cationic trypsinogen (SCT), an enzyme of solely pancreatic origin, in 30 patients with chronic pancreatitis and 25 healthy subjects as a control, after secretin and bombesin stimulation. After both the stimulations, serum cationic trypsinogen is unable to distinguish between the healthy control subjects and the patients with chronic pancreatitis. On the other hand, after secretin, the enzyme is able to separate chronic pancreatitis patients with different levels of exocrine function insufficiency. It does so with a greater statistical significance than that obtained by the rapid injection of bombesin and equal to that of trypsin into the duodenal juice during duodenal intubation. For these reasons, as well as the absence of any side-effects, secretin is preferred to bombesin stimulation in the evaluation of the exocrine pancreatic function in patients with chronic pancreatitis.
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PMID:Different responses of serum cationic trypsinogen to secretin and bombesin in normal subjects and patients with chronic alcoholic pancreatitis. 343 9

Protein analysis of intraductal precipitates and calculi is important to elucidate the mechanism of stone formation in chronic pancreatitis. We revealed human cationic trypsin immunoreactivity in protein extracts of pancreatic stones from 11 of 13 patients with chronic calcified pancreatitis, ranging from 0 to 42.3 ng/micrograms protein. On gel filtration the immunoreactivity eluted as one peak, which is identical to that of human cationic trypsinogen. On immunostaining of pancreatic stone, using an immunogold technic and scanning electron microscopy, the immunoreactivity was observed more densely in the amorphous portion of the center of the stones than in the concentric laminar layer of the periphery. Only negligible activity was detected for elastase 1 or amylase in the stone extracts. These results suggest that the presence of trypsinogen in pancreatic stone is not due to coprecipitation or adsorption of pancreatic enzymes but that trypsinogen is more likely involved in an initial step of intraductal precipitate formation than in a subsequent step of stone formation. However, the absence of trypsinogen in the stones from two of the 13 patients also suggests that trypsinogen is not the sole protein initiating precipitate formation.
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PMID:Trypsin(ogen) content of pancreatic calculi in chronic calcified pancreatitis in man. 820 Feb 69

Pancreatic juice from most studied species contains two major forms of trypsin, one with anionic electrophoretic mobility and one with cationic mobility. They are referred to as anionic and cationic trypsin(ogen). The purpose of this study was to measure immunoreactive anionic trypsin (irAT) and immunoreactive cationic trypsin (irCT) in sera from patients with pancreatic cancer (n = 39) and chronic pancreatitis (n = 32) using two specific ELISA methods. Sera from 72 healthy persons were used as controls. Patients with pancreatic cancer showed significantly elevated serum levels of irAT median level 39 vs 20.5 micrograms/L in the control group (p < 0.001). No differences in irCT levels were found. The ratio between irAT and irCT in serum was significantly increased (p < 0.001). Patients with chronic pancreatitis showed a wide range of both irAT and irCT levels, but no significant differences compared to the control group. The ratio between irAT and irCT was, however, significantly increased also in this group of patients. The results suggest a nonparallel secretion of anionic and cationic trypsinogen in pancreatic disease. This is a pattern that has been observed in experimental forms of chronic "hyperCCKemia."
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PMID:Elevated serum levels of immunoreactive anionic trypsin (but not cationic trypsin) signals pancreatic disease. 896 71

Important advances in the understanding of pancreatic diseases have taken place through the application of molecular methods in the study of the inherited form of pancreatitis and pancreas cancer. Mutations of the cationic trypsinogen gene have been found to be causative for hereditary pancreatitis with important implications for the molecular pathogenesis of acute and chronic pancreatitis. A variety of cancer syndromes involving the P16 and BRCA2 genes, for example, also lead to pancreatic cancer, but the gene responsible for familial pancreatic cancer has not been identified so far. The establishment of a European Registry of Hereditary Pancreatitis and Pancreatic Cancer (EUROPAC) will facilitate future developments.
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PMID:Hereditary pancreatitis and familial pancreatic cancer. 943 3

The etiology of nonalcoholic chronic pancreatitis, occurring in tropical regions, is unknown. Although environmental factors may play a role in its pathogenesis, a specific genetic predisposition may be necessary. The genetic mutation responsible for hereditary pancreatitis was described recently. Unlike in patients with hereditary pancreatitis, we found a lack of the R117H mutation in the cationic trypsinogen gene in all patients with tropical pancreatitis from Bangladesh.
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PMID:Lack of R117H mutation in the cationic trypsinogen gene in patients with tropical pancreatitis from Bangladesh. 978 42

Cystic fibrosis is by far the commonest cause of chronic pancreatitis in children, but pancreatitis itself is only rarely its presenting feature. In this paper an hypothesis for the development of the pancreatic lesions is presented. Impaired activation of pancreatic proteases in the small intestine is perceived as the pivotal problem that leads to continual feedback release of cholecystokinin, thus, in effect, causing a chronic hyperstimulation pancreatitis with intra-acinar activation of zymogens and, when bicarbonate secretion falls, precipitation of 'Reg' and other proteins in the duct system. This position contrasts with that in hereditary pancreatitis in which a mutation in the cationic trypsinogen gene leads to a form of trypsin that resists degradation by mesotrypsin and enzyme Y. A survey of the literature suggests that oxidant stress is a plausible contributor to pancreatic injury in both these diseases and in several other conditions linked with childhood pancreatitis.
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PMID:Paediatric and hereditary aspects of chronic pancreatitis. 983 35

Hereditary pancreatitis is a rare form of chronic recurrent pancreatitis. A family, in which 11 members had chronic pancreatitis, five had diabetes, and two had pancreatic cancer, was studied, and hereditary pancreatitis was diagnosed in all patients by demonstrating the mutation in exon 3 of the cationic trypsinogen gene (R117H). The clinical implications of genotypic analysis in hereditary pancreatitis are discussed.
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PMID:Hereditary pancreatitis and mutation of the trypsinogen gene. 1020 58

Nine out of 48 (19%) patients referred to a pancreatic clinic with a presumed diagnosis of idiopathic chronic pancreatitis have been shown to have mutations in the cationic trypsinogen gene (PRSSI), consistent with a previously unsuspected diagnosis of hereditary pancreatitis.
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PMID:Mutations of the cationic trypsinogen gene in patients with chronic pancreatitis. 1052 Jun 63

Few risk factors for pancreatic cancer have emerged except for chronic pancreatitis. Recently, hereditary pancreatitis was estimated to carry a standardized incidence ratio of 53, a risk about 25 times higher than smoking. A review of the ongoing hereditary pancreatitis study of the Midwest Multicenter Pancreatic Study Group suggests that the risk of pancreatic cancer is related to long-standing pancreatitis rather than to the cationic trypsinogen mutations. No recommendations can be made on screening patients with hereditary pancreatitis for pancreatic cancer at this time. However, prospective data, serum, and pancreatic juice should be collected and banked on consenting patients at risk as part of prospective, multicenter trials so that evidence-based recommendations for hereditary pancreatitis and other types of chronic pancreatitis can be made in the future.
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PMID:Hereditary pancreatitis and pancreatic carcinoma. 1041 65

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


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