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• W2128582073 abstract "BackgroundThe pathogenesis of chronic pancreatitis (CP) remains poorly understood. Recently, molecular biology has identified the genetic background for many patients with hereditary CP. In addition, a number of studies have focused on the detection of proto‐oncogenes and tumour suppressor gene mutations in the pathogenesis of CP. So far, the use of these mutations (with the exception of mutations causing hereditary CP), as diagnostic and prognostic markers is still controversial.DiscussionIt is well known that the risk of pancreatic cancer in patients with CP, especially the hereditary form, is high. At present, there is insufficient evidence to show a clear relationship between the development of pancreatic cancer and certain mutations. New biotechnological methods, such as DNA array expression analysis, expand our knowledge of the molecular pathogenesis of this disease and may help to develop specific diagnostic, prognostic and therapeutic tools. However, until long‐term studies examine the safety and efficacy of certain genetic markers, long‐term follow‐up of patients with CP who harbour mutations is needed. The pathogenesis of chronic pancreatitis (CP) remains poorly understood. Recently, molecular biology has identified the genetic background for many patients with hereditary CP. In addition, a number of studies have focused on the detection of proto‐oncogenes and tumour suppressor gene mutations in the pathogenesis of CP. So far, the use of these mutations (with the exception of mutations causing hereditary CP), as diagnostic and prognostic markers is still controversial. It is well known that the risk of pancreatic cancer in patients with CP, especially the hereditary form, is high. At present, there is insufficient evidence to show a clear relationship between the development of pancreatic cancer and certain mutations. New biotechnological methods, such as DNA array expression analysis, expand our knowledge of the molecular pathogenesis of this disease and may help to develop specific diagnostic, prognostic and therapeutic tools. However, until long‐term studies examine the safety and efficacy of certain genetic markers, long‐term follow‐up of patients with CP who harbour mutations is needed. Chronic pancreatitis (CP) is characterised by progressive inflammatory destruction of the functional parenchyma of the pancreas, resulting in severe exocrine and endocrine insufficiency. Morphologically, prominent features of CP include necrosis, acinar cell destruction and regeneration, severe widespread (intralobular) fibrosis, dysplastic ducts, variable pancreatic duct lesions, foci of proliferating ductal cells, ductular hyperplasia and ductal stones, as well as infiltration of inflammatory cells and alterations of nerves [1Kloppel G. Maillet B. Pathology of acute and chronic pancreatitis.Pancreas. 1993; 8: 659-670Crossref PubMed Scopus (248) Google Scholar, 2Kloppel G. Progression from acute to chronic pancreatitis. A pathologist's view.Surg Clin North Am. 1999; 79: 801-814Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar]. The incidence of CP is increasing in industrialised countries, and the disease affects 3.5–10 per 100 000 inhabitants in Western countries [3Etemad B. Whitcomb D.C. Chronic pancreatitis: diagnosis, classification, and new genetic developments.Gastroenterology. 2001; 120: 682-707Abstract Full Text Full Text PDF PubMed Scopus (1014) Google Scholar, 4Lankish P.G. Assmus D. Pfchthofer D. Maisonneuve P. Lowenfels A.B. The burden of pancreatic disease in a well‐defined population.Gastroenterology. 1998; 114: A24Google Scholar, 5Copenhagen Pancreatitis Study Group. Copenhagen Pancreatitis StudyAn interim report from a prospective epidemiological multicentre study.Scand J Gastroenterol. 1981; 16: 305-312Crossref PubMed Scopus (102) Google Scholar, 6Ammann R.W. A clinically based classification system for alcoholic chronic pancreatitis: summary of an international workshop on chronic pancreatitis.Pancreas. 1997; 14: 215-221Crossref PubMed Scopus (178) Google Scholar, 7Lowenfels A.B. Maisonneuve P. Cavellini G. Ammann R.W. Prognosis of chronic pancreatitis, an international multicenter study.Am J Gastroenterol. 1994; 89: 1567-1571Google Scholar], with alcohol abuse being the predominant cause. Although different forms of CP result from different initiating causes, there is evidence to suggest a common pathophysiological pathway in all forms [8Comfort M. Steinberg A. Pedigree of family with hereditary chronic relapsing pancreatitis.Gastroenterology. 1952; 21: 54-63Abstract Full Text PDF PubMed Scopus (332) Google Scholar, 9Perrault J. Hereditary pancreatitis.Gastroenterol Clin North Am. 1994; 23: 743-752Abstract Full Text PDF PubMed Google Scholar, 10Sossenheimer M.J. Aston C.E. Preston R.A. Clinical characteristics of hereditary pancreatitis in a large family, based on high risk haplotype.Am J Gastroenterol. 1997; 92: 1113-1116PubMed Google Scholar, 11Whitcomb D.C. Genetic predisposition to acute and chronic pancreatitis.Med Clin North Am. 2000; 84: 531-547Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar, 12Whitcomb D.C. Hereditary pancreatitis: new insights into acute and chronic pancreatitis.Gut. 1999; 45: 317-322Crossref PubMed Scopus (242) Google Scholar, 13Bruno M.J. Current insights into the pathogenesis of acute and chronic pancreatitis.Scand J Gastroenterol. 2001; 36: 103-108Crossref Scopus (12) Google Scholar, 14Braganza J.M. Schofield D. Snehalatha C. Mohan V. Micronutrient antioxidant status in tropical compared with temperate‐zone chronic pancreatitis.Scand J Gastroenterol. 1993; 28: 1098-1104Crossref PubMed Scopus (86) Google Scholar, 15Narendranathan M. Cheriyan A. Lack of association between cassava consumption and tropical pancreatitis syndrome.J Gastroenterol Hepatol. 1994; 9: 282-285Crossref PubMed Scopus (25) Google Scholar, 16Bhatia E. Choudhuri G. Sikora S.S. Tropical calcific pancreatitis: strong association with SPINK1 trypsin inhibitor mutations.Gastroenterology. 2002; 123: 1020-1025Abstract Full Text Full Text PDF PubMed Scopus (181) Google Scholar, 17Schneider A. Suman A. Rossi L. SPINK1/PSTI mutations are associated with tropical pancreatitis and type II diabetes mellitus in Bangladesh.Gastroenterology. 2002; 123: 1026-1030Abstract Full Text Full Text PDF PubMed Scopus (127) Google Scholar, 18Kino‐Ohsaki J. Nishimori I. Morita M. Serum antibodies to carbonic anhydrase I and II in patients with idiopathic chronic pancreatitis and Sjögren's syndrome.Gastroenterology. 1996; 110: 1579-1586Abstract Full Text Full Text PDF PubMed Scopus (220) Google Scholar, 19Frulloni L. Bovo P. Brunelli S. Elevated serum levels of antibodies to carbonic anhydrase I and II in patients with chronic pancreatitis.Pancreas. 2000; 20: 382-388Crossref PubMed Scopus (43) Google Scholar, 20Lönnerholm G. Selking Ö. Wistrand P.J. Amount and distribution of carbonic anhydrases CA I and CA II in the gastrointestinal tract.Gastroenterology. 1985; 88: 1151-1161Abstract Full Text PDF PubMed Scopus (75) Google Scholar, 21Gu Z.Y. Zhang K.H. Chronic pancreatitis in China: etiology and management.World J Surg. 1990; 14: 28-31Crossref PubMed Scopus (14) Google Scholar, 22Misra S.P. Dwivedi M. Do gallstones cause chronic pancreatitis.Int J Pancreatol. 1991; 10: 97-102PubMed Google Scholar, 23Friess H. Büchler M.W. Müller C. Malfertheiner P. Immunopathogenesis of chronic pancreatitis.Gastroenterology. 1998; 115: 1018-1022Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar, 24DiMagno E.P. A short, eclectic history of exocrine pancreatic insufficiency and chronic pancreatitis.Gastroenterology. 1993; 104: 1255-1262PubMed Google Scholar, 25Steer M.L. Waxman I. Freedman S. Chronic pancreatitis.N Engl J Med. 1995; 332: 1482-1490Crossref PubMed Scopus (587) Google Scholar, 26Braganza J.M. A framework for the aetiogenesis of chronic pancreatitis.Digestion. 1998; 59: 1-12Crossref PubMed Scopus (78) Google Scholar, 27Okazaki K. Uchida K. Ohana M. Autoimmune‐related pancreatitis is associated with autoantibodies and a Th1/Th2‐type cellular immune response.Gastroenterology. 2000; 118: 573-581Abstract Full Text Full Text PDF PubMed Scopus (496) Google Scholar, 28Chiari H. Ueber die Selbstverdauung des menschlichen Pankreas.Zeitschrift für Heilkunde. 1896; 17: 69-96Google Scholar]. Recently, developments in molecular biology have revealed genetic causes of hereditary CP. Mutations of the cationic trypsinogen gene (PRSS1), as well as of the pancreatic secretory trypsin inhibitor (SPINK‐1) gene, seem to predispose people to CP through enhancement of intra‐pancreatic trypsin activity and lowering of the threshold for inhibiting trypsin activity [29Rinderknecht H. Activation of pancreatic zymogens. Normal activation, premature intrapancreatic activation, and protective mechanisms against inappropriate activation.Dig Dis Sci. 1986; 31: 314-321Crossref PubMed Scopus (269) Google Scholar, 30Jansen J.B.M.J. te Morsche R. van Goor H. Drenth J.P.H. Genetic basis of chronic pancreatitis.Scand J Gastroenterol. 2002; 37: 91-94Crossref Google Scholar, 31Whitcomb D.C. Gorry M.C. Preston R.A. Hereditary pancreatitis is caused by a mutation in the cationic trypsinogen gene.Nat Genet. 1996; 14: 141-145Crossref PubMed Scopus (1323) Google Scholar, 32Whitcomb D.C. Preston R.A. Aston C.E. A gene for hereditary pancreatitis maps to chromosome 7q35.Gastroenterology. 1996; 110: 1975-1980Abstract Full Text Full Text PDF PubMed Scopus (276) Google Scholar, 33Le Bodic L. Bignon J.D. Raguenes O. The hereditary pancreatitis gene maps to long arm of chromosome 7.Hum Mol Genet. 1996; 5: 549-554Crossref PubMed Scopus (179) Google Scholar, 34Rowen L. Koop B.F. Hood L. The complete 685 kilo‐base DNA sequence of the human beta T‐cell locus.Science. 1996; 272: 1755-1762Crossref PubMed Scopus (375) Google Scholar, 35Gorry M.C. Gabbaizedeh D. Furey W. Mutations in the cationic trypsinogen gene are associated with recurrent acute and chronic pancreatitis.Gastroenterology. 1997; 113: 1063-1068Abstract Full Text Full Text PDF PubMed Scopus (400) Google Scholar, 36Antonarakis S.E. the Nomenclature WorkgroupRecommendations for a nomenclature system for human gene mutations.Hum Mutat. 1998; 11: 1-3Crossref PubMed Scopus (852) Google Scholar, 37Witt H. Luck W. Becker M. A signal peptide cleavage site mutation in the cationic trypsinogen gene is strongly associated with chronic pancreatitis.Gastroenterology. 1999; 117: 7-10Abstract Full Text Full Text PDF PubMed Scopus (232) Google Scholar, 38Witt H. Luck W. Hennies H.C. Mutations in the gene encoding the serine protease inhibitor Kazal type 1 are associated with chronic pancreatitis.Nat Genet. 2000; 25: 213-216Crossref PubMed Scopus (844) Google Scholar, 39Jansen J.B.M.J. te Morsche R. van Goor H. Drenth J.P.H. Genetic basis of chronic pancreatitis.Scand J Gastroenterol. 2002; 37: 91-94Crossref Scopus (10) Google Scholar, 40Pfötzer R.H. Barmada M.M. Brunskill A.P. SPINK1/PSTI polymorphisms act as disease modifiers in familial and idiopathic chronic pancreatitis.Gastroenterology. 2000; 119: 615-623Abstract Full Text Full Text PDF PubMed Scopus (438) Google Scholar, 41Threadgold J. Greenhalf W. Ellis I. The N34S mutation of SPINK 1 (PSTI) is associated with a familial pattern of idiopathic chronic pancreatitis but does not cause the disease.Gut. 2002; 50: 675-682Crossref PubMed Scopus (175) Google Scholar, 42Drenth J.P.H. te Morsche R. Jansen J.B.M.J. Mutations in the serine protease inhibitor Kazal type 1 are strongly associated with chronic pancreatitis.Gut. 2002; 50: 687-693Crossref PubMed Scopus (143) Google Scholar, 43Chen J.M. Mercier B. Audrezet M.P. Mutational analysis of the human pancreatic secretory trypsin inhibitor (PSTI) gene in hereditary and sporadic chronic pancreatitis.J Med Genet. 2000; 37: 67-69Crossref PubMed Scopus (136) Google Scholar, 44Witt H. Hennies H. Becker C.M. SPINK1 mutations in chronic pancreatitis.Gasroenterology. 2001; 120: 1060-1061Abstract Full Text Full Text PDF PubMed Scopus (31) Google Scholar, 45Witt H. Luck W. Becker M. Mutation in the SPINK1 trypsin inhibitor gene, alcohol use, and chronic pancreatitis.JAMA. 2001; 285: 2716-2717Crossref PubMed Scopus (174) Google Scholar]. In addition, other mutations in several genes have been reported to be implicated in hereditary CP [46Cohn J.A. Friedman K.J. Noone P.G. Knowles M.R. Silverman L.M. Jowell P.S. Relation between mutations of the cystic fibrosis gene and idiopathic pancreatitis.N Engl J Med. 1998; 339: 653-658Crossref PubMed Scopus (805) Google Scholar, 47Sharer N. Schwarz M. Malone G. Mutations of the cystic fibrosis gene in patients with chronic pancreatitis.N Engl J Med. 1998; 339: 645-652Crossref PubMed Scopus (797) Google Scholar, 48Cohn J.A. Bornstei J.D. Jowell P.S. Cystic fibrosis mutations and genetic predisposition to idiopathic chronic pancreatitis.in: Whitcomb D.C. Cohn J.A. Ulrich II, C.D. The Medical Clinics of North America. WB Saunders, 2000: 621-632Abstract Full Text Full Text PDF Scopus (65) Google Scholar, 49Truninger K. Malik N. Ammann R.W. Mutations of the cystic fibrosis gene in patients with chronic pancreatitis.Am J Gastroenterol. 2001; 96: 2657-2661Crossref PubMed Google Scholar, 50Carey M.C. Fitzerald O. Hyperparathyroidism associated with chronic pancreatitis in a family.Gut. 1968; 9: 700-703Crossref PubMed Scopus (25) Google Scholar, 51Wilson D.D.E. Hata A. Kwong L.K. Mutations in exon 3 of the lipoprotein lipase gene segregating in a family with hypertriglyceridemia, pancreatitis and non‐insulin‐dependent diabetes.J Clin Invest. 1993; 92: 203-211Crossref PubMed Scopus (70) Google Scholar, 52Beil F.U. Fojo S.S. Brewer H.j. Greten H. Beisiegel U. Apolipoprotein C‐II deficiency syndrome due to apo C‐II Hamburg: clinical and biochemical features and HphI restriction enzyme polymorphism.Eur J Clin Invest. 1992; 22: 88-95Crossref PubMed Scopus (22) Google Scholar, 53Fojo S.S. Brewer H.B. Hypertriglyceridemia due to genetic defects in lipoprotein lipase and apolipoprotein C‐II.J Intern Med. 1992; 231: 669-677Crossref PubMed Scopus (102) Google Scholar]. The analysis of gene mutations and gene expression in pancreatic cancer and CP has identified several factors, which are commonly deregulated in both diseases [54Bos J.L. ras oncogenes in human cancer: a review.Cancer Res. 1989; 49: 4682-4689PubMed Google Scholar, 55Levi S. Urbano‐Ispizua A. Gill R. Multiple K‐ras codon 12 mutations in cholangiocarcinomas demonstrated with a sensitive polymerase chain reaction technique.Cancer Res. 1991; 51: 3497-3502PubMed Google Scholar, 56Lemoine N.R. Jain S. Hughes C. Ki‐ras oncogene activation in pre‐invasive pancreatic cancer.Gastroenterology. 1992; 102: 230-236Abstract PubMed Google Scholar, 57Almoguera C. Shibata D. Forrester K. Martin J. Arnheim N. Perucho M. Most human carcinomas of the exocrine pancreas contain mutant c‐K‐ras genes.Cell. 1988; 53: 549-554Abstract Full Text PDF PubMed Scopus (1903) Google Scholar]. Detection of mutations in the K‐ras proto‐oncogene and p53 tumour suppressor gene in specimens obtained by needle aspiration, from pure pancreatic juice, duodenal juice, serum or stool, may be clinically useful diagnostic markers for early detection of pancreatic malignancy [58Solmi L. Gandolfi L. Muratori R. Echo‐guided fine‐needle biopsy of pancreatic masses.Am J Gastroenterol. 1987; 82: 744-748PubMed Google Scholar, 59Hartner L.P. Moss A.A. Goldberg H.I. Gross B.H. CT‐guided fine‐needle aspirations for diagnosis of benign and malignant diseases.Am J Roentgenol. 1983; 140: 363-367Crossref PubMed Scopus (111) Google Scholar, 60Tada M. Komatsu Y. Kawabe T. Quantitative analysis of K‐ras gene mutation in pancreatic tissue obtained by endoscopic ultrasonography‐guided fine needle aspiration: clinical utility for diagnosis of pancreatic tumor.Am J Gastroenterol. 2002; 97: 2263-2269Crossref PubMed Google Scholar, 61Sawada Y. Gonda H. Hayashida Y. Combined use of brushing cytology and endoscopic retrograde pancreatography for the early detection of pancreatic cancer.Acta Cytol. 1989; 33: 870-874PubMed Google Scholar, 62Kubota Y. Takaoka M. Tani K. Endoscopic transpapillary biopsy for diagnosis of patients with pancreaticobiliary ductal strictures.Am J Gastroenterol. 1993; 88: 1700-1704PubMed Google Scholar, 63Pugliese V. Pujic N. Saccomanno S. Pancreatic intraductal sampling during ERCP in patients with chronic pancreatitis and pancreatic cancer: cytologic studies and k‐ras‐2 codon 12 molecular analysis in 47 cases.Gastrointest Endosc. 2001; 54: 595-599Abstract Full Text Full Text PDF PubMed Scopus (80) Google Scholar, 64Iguchi H. Sugano K. Fukayama N. Analysis of Ki‐ras codon 12 mutations in the duodenal juice of patients with pancreatic cancer.Gastroenterology. 1996; 110: 221-226Abstract Full Text PDF PubMed Scopus (106) Google Scholar, 65Theodor L. Melzer E. Sologov M. Bar‐Meir S. Diagnostic value of K‐ras mutations in serum of pancreatic cancer patients.Ann NY Acad Sci. 2000; 906: 19-24Crossref PubMed Scopus (7) Google Scholar, 66Fernandez E. La Vecchia C. Porta M. Negri E. D'Avanzo B. Boyle P. Pancreatitis and the risk of pancreatic cancer.Pancreas. 1995; 11: 185-189Crossref PubMed Scopus (103) Google Scholar, 67Flanders T.Y. Foulkes W.D. Pancreatic adenocarcinoma: epidemiology and genetics.J Med Genet. 1996; 33: 889-898Crossref PubMed Scopus (73) Google Scholar, 68Berndt C. Haubold K. Wenger F. K‐ras mutations in stool and tissue samples from patients with malignant and nonmalignant pancreatic diseases.Clin Chem. 1998; 44: 2103-2107PubMed Google Scholar, 69Wenger F.A. Zieren J. Peter F.J. Jacobi C.A. Muller J.M. K‐ras mutations in tissue and stool samples from patients with pancreatic cancer and chronic pancreatitis.Langenbecks Arch Surg. 1999; 384: 181Crossref PubMed Scopus (35) Google Scholar, 70Caldas C. Hahn S.A. Hruban R.H. Redston M.S. Yeo C.J. Kern S.E. Detection of K‐ras mutations in the stool of patients with pancreatic adenocarcinoma and pancreatic ductal hyperplasia.Cancer Res. 1994; 54: 3568-3573PubMed Google Scholar]. Although these mutations are considered critical and early events in pancreatic oncogenesis, the role of K‐ras and p53 mutations in CP as a precancerous disorder is not completely known. Furthermore, the role of other tumour suppressor genes in the multi‐step carcinogenesis remains uncertain. Epidemiological studies indicate that CP may be associated with pancreatic cancer. Therefore, having a resection procedure before pancreatic cancer develops seems to be more necessary than ever, especially since resection of early pancreatic cancer is the only chance of cure. Thus it is of major importance to identify genetic markers that help to stratify the risk of malignant transformation in CP. Genome‐wide gene expression analysis by DNA arrays provides new insights into gene function and seems to be another promising diagnostic technique. Increased ethanol consumption is considered to be the most common cause of CP in the Western world. The mortality rate in alcoholic CP approaches 50% within 20–25 years due to malnutrition, severe infections, diabetes, other CP‐associated complications, and alcohol‐ and nicotine‐related diseases [6Ammann R.W. A clinically based classification system for alcoholic chronic pancreatitis: summary of an international workshop on chronic pancreatitis.Pancreas. 1997; 14: 215-221Crossref PubMed Scopus (178) Google Scholar, 7Lowenfels A.B. Maisonneuve P. Cavellini G. Ammann R.W. Prognosis of chronic pancreatitis, an international multicenter study.Am J Gastroenterol. 1994; 89: 1567-1571Google Scholar]. Hereditary CP, first described by Comfort and Steinberg in 1952, includes diagnostic criteria such as age of onset <20 years and a history of pancreatitis in at least two family members [8Comfort M. Steinberg A. Pedigree of family with hereditary chronic relapsing pancreatitis.Gastroenterology. 1952; 21: 54-63Abstract Full Text PDF PubMed Scopus (332) Google Scholar, 9Perrault J. Hereditary pancreatitis.Gastroenterol Clin North Am. 1994; 23: 743-752Abstract Full Text PDF PubMed Google Scholar]. HCP is characterised by an autosomal dominant model of inheritance, with approximately 80% penetrance and variable expression [10Sossenheimer M.J. Aston C.E. Preston R.A. Clinical characteristics of hereditary pancreatitis in a large family, based on high risk haplotype.Am J Gastroenterol. 1997; 92: 1113-1116PubMed Google Scholar, 11Whitcomb D.C. Genetic predisposition to acute and chronic pancreatitis.Med Clin North Am. 2000; 84: 531-547Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar]. Whereas the onset of symptoms is usually in childhood, presentation of the disease may occur from infancy to the fifth or sixth decade of life. Acute attacks range from mild abdominal discomfort to life‐threatening episodes, with pancreatic necrosis, splenic vein thrombosis and death [10Sossenheimer M.J. Aston C.E. Preston R.A. Clinical characteristics of hereditary pancreatitis in a large family, based on high risk haplotype.Am J Gastroenterol. 1997; 92: 1113-1116PubMed Google Scholar, 12Whitcomb D.C. Hereditary pancreatitis: new insights into acute and chronic pancreatitis.Gut. 1999; 45: 317-322Crossref PubMed Scopus (242) Google Scholar]. Cystic fibrosis (CF) is the most common autosomal recessive inherited disorder in Caucasians. It presents early in life and is associated with severe chronic progressive pulmonary disease, maldigestion and a shortened life expectancy. Pancreatic duct obstruction induced by a defective chloride channel, as a result of mutations in the cystic fibrosis transmembrane regulator (CFTR) gene, is the cause of pancreatic insufficiency in patients with CF [13Bruno M.J. Current insights into the pathogenesis of acute and chronic pancreatitis.Scand J Gastroenterol. 2001; 36: 103-108Crossref Scopus (12) Google Scholar]. Tropical pancreatitis is reported in tropical belts of the world. It occurs independently of alcohol, nutrition and environment [14Braganza J.M. Schofield D. Snehalatha C. Mohan V. Micronutrient antioxidant status in tropical compared with temperate‐zone chronic pancreatitis.Scand J Gastroenterol. 1993; 28: 1098-1104Crossref PubMed Scopus (86) Google Scholar, 15Narendranathan M. Cheriyan A. Lack of association between cassava consumption and tropical pancreatitis syndrome.J Gastroenterol Hepatol. 1994; 9: 282-285Crossref PubMed Scopus (25) Google Scholar]. It is characterised by pancreatic insufficiency, diabetes mellitus and recurrent attacks of pain, commonly with pancreatic calcifications [16Bhatia E. Choudhuri G. Sikora S.S. Tropical calcific pancreatitis: strong association with SPINK1 trypsin inhibitor mutations.Gastroenterology. 2002; 123: 1020-1025Abstract Full Text Full Text PDF PubMed Scopus (181) Google Scholar, 17Schneider A. Suman A. Rossi L. SPINK1/PSTI mutations are associated with tropical pancreatitis and type II diabetes mellitus in Bangladesh.Gastroenterology. 2002; 123: 1026-1030Abstract Full Text Full Text PDF PubMed Scopus (127) Google Scholar]. Children are commonly affected and often die in early adulthood from endocrine and exocrine dysfunction. In patients with CP, antibodies against carbonic anhydrase (CA) type I and II have been reported [18Kino‐Ohsaki J. Nishimori I. Morita M. Serum antibodies to carbonic anhydrase I and II in patients with idiopathic chronic pancreatitis and Sjögren's syndrome.Gastroenterology. 1996; 110: 1579-1586Abstract Full Text Full Text PDF PubMed Scopus (220) Google Scholar, 19Frulloni L. Bovo P. Brunelli S. Elevated serum levels of antibodies to carbonic anhydrase I and II in patients with chronic pancreatitis.Pancreas. 2000; 20: 382-388Crossref PubMed Scopus (43) Google Scholar]. Carbonic anhydrases are a family of zinc metal enzymes that catalyse the reversible conversion of carbon dioxide to bicarbonate and hydrogen ions. CA II antigens are present in the pancreatic ductal epithelium [20Lönnerholm G. Selking Ö. Wistrand P.J. Amount and distribution of carbonic anhydrases CA I and CA II in the gastrointestinal tract.Gastroenterology. 1985; 88: 1151-1161Abstract Full Text PDF PubMed Scopus (75) Google Scholar]; therefore, the presence of antibodies against this isoenzyme provides evidence of an immune reaction to a pancreatic target antigen. Moreover, non‐specific auto‐antibodies, such as antinuclear antibodies and antineutrophil cytoplasmic antibodies, have been found to be present in some patients with CP [19Frulloni L. Bovo P. Brunelli S. Elevated serum levels of antibodies to carbonic anhydrase I and II in patients with chronic pancreatitis.Pancreas. 2000; 20: 382-388Crossref PubMed Scopus (43) Google Scholar]. Biliary lithiasis represents the commonest cause of strictures that involve the main or the secondary pancreatic ducts, leading to stenosis of the papilla of Vater and concomitant progression of CP. However, the role of gallstone disease in the development of CP is still controversial [21Gu Z.Y. Zhang K.H. Chronic pancreatitis in China: etiology and management.World J Surg. 1990; 14: 28-31Crossref PubMed Scopus (14) Google Scholar, 22Misra S.P. Dwivedi M. Do gallstones cause chronic pancreatitis.Int J Pancreatol. 1991; 10: 97-102PubMed Google Scholar]. Nonetheless, recurrent attacks of acute pancreatitis due to gallstones or other causes represent an important and relatively common cause of CP. Less common causes of CP include nutritional factors (hyperlipoproteinaemia), metabolic disturbances (hypercalcaemia), congenital anomalies of the ductal system (pancreas divisum) and acquired pancreatic duct obstruction from strictures secondary to trauma, pseudocysts, mechanical or structural changes of the pancreatic duct sphincter or peri‐ampullary tumours, or other rare causes such as choledochal cysts [10Sossenheimer M.J. Aston C.E. Preston R.A. Clinical characteristics of hereditary pancreatitis in a large family, based on high risk haplotype.Am J Gastroenterol. 1997; 92: 1113-1116PubMed Google Scholar, 23Friess H. Büchler M.W. Müller C. Malfertheiner P. Immunopathogenesis of chronic pancreatitis.Gastroenterology. 1998; 115: 1018-1022Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar, 24DiMagno E.P. A short, eclectic history of exocrine pancreatic insufficiency and chronic pancreatitis.Gastroenterology. 1993; 104: 1255-1262PubMed Google Scholar, 25Steer M.L. Waxman I. Freedman S. Chronic pancreatitis.N Engl J Med. 1995; 332: 1482-1490Crossref PubMed Scopus (587) Google Scholar, 26Braganza J.M. A framework for the aetiogenesis of chronic pancreatitis.Digestion. 1998; 59: 1-12Crossref PubMed Scopus (78) Google Scholar]. In 15–20% of cases, the cause of CP remains unclear [25Steer M.L. Waxman I. Freedman S. Chronic pancreatitis.N Engl J Med. 1995; 332: 1482-1490Crossref PubMed Scopus (587) Google Scholar, 27Okazaki K. Uchida K. Ohana M. Autoimmune‐related pancreatitis is associated with autoantibodies and a Th1/Th2‐type cellular immune response.Gastroenterology. 2000; 118: 573-581Abstract Full Text Full Text PDF PubMed Scopus (496) Google Scholar]. The mechanisms of tissue destruction and remodelling in CP are difficult to define in the early stages because structural changes are associated with moderate to advanced disease. The diagnostic accuracy of modern imaging techniques – i.e. ERCP, EUS, CT or MRI – has not yet been validated against histopathology as the gold standard [3Etemad B. Whitcomb D.C. Chronic pancreatitis: diagnosis, classification, and new genetic developments.Gastroenterology. 2001; 120: 682-707Abstract Full Text Full Text PDF PubMed Scopus (1014) Google Scholar]. The pancreas is not readily accessible for obtaining tissue specimens, and fine‐needle biopsies tend to yield false negative results because the primary lesions of early stage CP are usually focal. Therefore, a clinically definite diagnosis of CP will be deferred until the disease has reached an advanced stage in which surgical treatment is indicated or in which typical markers of CP, including pancreatic calcifications and/or persistent pancreatic dysfunction, are present. [6Ammann R.W. A clinically based classification system for alcoholic chronic pancreatitis: summary of an international workshop on chronic pancreatitis.Pancreas. 1997; 14: 215-221Crossref PubMed Scopus (178) Google Scholar]. Despite different causes and forms of CP, the phenotype of chronic pancreatitis is remarkably similar, suggesting a common underlying pathophysiological mechanism. The theory that inappropriate activation of pancreatic pro‐enzymes, especially trypsinogen, within the pancreatic parenchyma leads to auto‐digestion and acute attacks of pancreatitis was first reported in 1896 [28Chiari H. Ueber die Selbstverdauung des menschlichen Pankreas.Zeitschrift für Heilkunde. 1896; 17: 69-96Google Scholar]. Under normal conditions, multiple defence mechanisms are known to prevent uncontrolled activation of the digestive enzyme cascade within the pancreas [29Rinderknecht H. Activation of pancreatic zymogens. Normal activation, premature intrapancreatic activation, and protective mechanisms against inappropriate activation.Dig Dis Sci. 1986; 31: 314-321Crossref PubMed Scopus (269) Google Scholar, 30Jansen J.B.M.J. te Morsche R. van Goor H. Drenth J.P.H. Genetic basis of chronic pancreatitis.Scand J Gastroenterol. 2002; 37: 91-94Crossref Google Scholar]. These include: (a) synthesis of most digestive enzymes as inactive pro‐enzymes; (b) compartmentalisation and segregation of pro‐enzymes from other subcellular components, within distinct membrane‐bound compartments, to prevent their contact with vital cytosolic structures; (c) maintenance of an environmental state of low intracellular calcium; (d) appropriate release of pro‐enzymes from pancreatic acinar cells and their activation by intestinal enteropeptidase (this initial activating enzyme hydrolyses tr" @default.
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• W2128582073 title "Detection of oncogenes in chronic pancreatitis" @default.
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