Disease relevance of Pancreatitis, Chronic

• Elevated PAP-H levels were observed in patients with acute pancreatitis and in some patients with chronic pancreatitis [1].
• When concentrations of pancreatic stone protein were determined from pancreatic secretions obtained either from patients suffering from chronic pancreatitis (n = 31) [including the calcifying forms (n = 10)], pancreatic cancer (n = 22), or nonpancreatic diseases (n = 17), no significant differences were found [2].
• CONCLUSIONS: The findings suggest the involvement of TGF-beta 1 in the development of fibrosis in chronic pancreatitis and the important role of inflammatory cells [3].
• BACKGROUND & AIMS: Nonalcoholic chronic pancreatitis is usually idiopathic and often associated with cystic fibrosis gene (CFTR) mutations [4].
• RESULTS: Serum antibodies against carbonic anhydrase I and II were detected in 7 and 11 of 33 patients with idiopathic chronic pancreatitis, respectively, and in 8 and 13 of 21 patients with Sjögren's syndrome, respectively [5].
• Annexin A2 and insulin-like growth factor-binding protein 2 were overexpressed in cancer but not in chronic pancreatitis, making them promising biomarker candidates for pancreatic cancer [6].

Psychiatry related information on Pancreatitis, Chronic

• Since MLI is known to initiate the formation of the interdigestive migrating motor complexes, diminished motilin release secondary to pancreatic exocrine deficiency may result in disordered gastrointestinal motor activity in patients with chronic pancreatitis [7].
• METHODS: We compared the racial status of 1883 patients discharged with a first-listed diagnosis of two diseases strongly related to alcohol abuse: 433 patients with chronic pancreatitis (ICD 5771) and 1450 patients with alcoholic cirrhosis (ICD 5712) [8].
• Phorbol ester-induced O2- and H2O2 production in neutrophils of patients with acute and chronic pancreatitis was greater than in controls, but these differences, except of superoxide anion production by neutrophils of patients with chronic pancreatitis, were not statistically significant because of large individual differences [9].

High impact information on Pancreatitis, Chronic

• Our results indicate that mutations in SPINK1 are associated with chronic pancreatitis [10].
• Mutations in the gene encoding the serine protease inhibitor, Kazal type 1 are associated with chronic pancreatitis [10].
• Immunohistologic studies of pancreatic-biopsy specimens from three patients with negative tests for glutamic acid decarboxylase autoantibodies and low glycosylated hemoglobin values revealed T-lymphocyte-predominant infiltrates in the exocrine pancreas but no insulitis and no evidence of acute or chronic pancreatitis [11].
• RESULTS: Ten patients with idiopathic chronic pancreatitis (37 percent) had at least one abnormal CFTR allele [12].
• Cimetidine plus propantheline for chronic pancreatitis [13].

Chemical compound and disease context of Pancreatitis, Chronic

• Seven patients (six male, one female; mean age 49.9 years) with chronic pancreatitis complicated by pseudocysts and persistent pain were treated with the pancreatic anti-secretory drug octreotide for 2 weeks [14].
• Using fluorescein angiography, we studied the prevalence and characteristics of diabetic retinopathy in 40 patients with chronic pancreatitis complicated by diabetes and in 40 type 1 diabetics with comparable duration of diabetes [15].
• We assessed the effects of lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, on spontaneously occurring chronic pancreatitis [16].
• Papaverine increased blood flow in control and chronic pancreatitis cats without altering tissue pressure, suggesting that despite the reduced basal blood flow, the ability to increase blood flow was preserved in chronic pancreatitis [17].
• BACKGROUND & AIMS: In both pancreatic cancer and chronic pancreatitis, there is enhanced expression of mitogenic growth factors and their tyrosine kinase receptors, which have the capacity to activate mitogen-activated protein kinase (MAPK) [18].

Biological context of Pancreatitis, Chronic

• Altered frequencies of alpha 1 antitrypsin phenotypes have been reported in patients with chronic pancreatitis, suggesting a possible genetic basis for individual susceptibility to this disease [19].
• Mucin (MUC) gene expression in human pancreatic adenocarcinoma and chronic pancreatitis: a potential role of MUC4 as a tumor marker of diagnostic significance [20].
• To confirm correlation between function and histology of the exocrine pancreas in chronic pancreatitis, we compared exocrine pancreatic function, as estimated by cholecystokinin secretin test (CST), with histological findings in 108 patients [21].
• METHODS: In the present study DNA from 80 samples of tissue from patients with chronic pancreatitis was isolated and subjected to single-strand conformation polymorphism (SSCP) analysis of p53 exons 5-9 and restriction fragment length polymorphism analysis of K-ras (codon 12) [22].
• To identify a pancreatitis-associated gene, we performed a quantitative trait locus (QTL) analysis for the traits of chronic pancreatitis and diabetes mellitus in WBN/Kob rats [23].

Anatomical context of Pancreatitis, Chronic

• RESULTS: PG-I was overexpressed in the ECM of pancreatic cancer samples compared with normal pancreas or chronic pancreatitis tissues [24].
• Diseases that may present with similar symptoms include gastroesophageal reflux, biliary tract disease, chronic pancreatitis, and irritable bowel syndrome [25].
• Pancreatic adenocarcinoma is the fifth leading cause of cancer death in the United States. Mutations in the K-ras oncogene occur in 85% of pancreatic adenocarcinomas and have also been identified in 75% of pancreatic ducts with mucinous cell hyperplasia seen in association with chronic pancreatitis [26].
• CONCLUSIONS: We show for the first time the presence of PSR in chronic pancreatitis on pancreatic cells other than macrophages in regions with high apoptotic activity [27].
• The number of requests is growing, owing to the increasingly wide range of recognized CFTR gene diseases (cystic fibrosis, congenital bilateral absence of the vas deferens, disseminated bronchiectasis, allergic bronchopulmonary aspergillosis and chronic pancreatitis), and the availability of efficient molecular tools for detecting mutations [28].

Gene context of Pancreatitis, Chronic

• METHODS: We tested 39 patients with idiopathic chronic pancreatitis (mean age at diagnosis, 33 years) for common mutations of CFTR and of genes encoding a trypsin inhibitor (PSTI) and trypsinogen (PRSS1) [4].
• CCK1 receptor proteins were found occasionally in small-sized pancreatic nerves, whereas acini expressed a low density of CCK2 receptors in a few cases of chronic pancreatitis [29].
• CONCLUSIONS: The observed differential expression of distinct chemokine genes in pancreatic parenchyma and infiltrates from patients with chronic pancreatitis strongly suggests an involvement of distinct chemokines in the initiation and perpetuation of disease [30].
• Transgenic mice overexpressing TGF-alpha develop tissue changes in the pancrease resembling changes found in chronic pancreatitis [31].
• In this study we investigated the potential role of aFGF and bFGF in chronic pancreatitis (CP), a fibrotic condition associated with acinar cell dedifferentiation and atrophy, and fibroblastic proliferation [32].

Analytical, diagnostic and therapeutic context of Pancreatitis, Chronic

• The TDH result was 41.6 +/- 31.7% (SD) in a group of chronic pancreatitis patients (n = 22) and 91.5 +/- 4.8% in the control group (n = 47) [33].
• By immunohistochemistry, the EGF receptor, TGF alpha, and PLC gamma 1 were found to be expressed at high concentrations in pancreatic ductal and acinar cells from chronic pancreatitis patients [34].
• Northern blot analysis showed that, by comparison with normal controls, 19 of 27 chronic pancreatitis tissues exhibited a 5.7-fold increase in EGF receptor mRNA concentrations, and 20 of 27 chronic pancreatitis tissues exhibited a sixfold increase in TGF alpha mRNA concentrations [34].
• By in situ hybridization, areas with ductal metaplasia in chronic pancreatitis exhibited intense PLA2 type IV mRNA signals [35].
• The response of serum immunoreactive gastric inhibitory polypeptide (IR-GIP), gastrin (IRG) and insulin (IRI) to a mixed standard meal was measured in 15 controls, 6 patients with coeliac disease, 26 patients with chronic pancreatitis and partial duodenopancreatectomy (Whipple's procedure) [36].

References