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Das Spektrum der chronischen Pankreatitis

Auf dem Weg zur ätiologischen Klassifikation

Spectrum of chronic pancreatitis

On the way to etiological classification

Zusammenfassung

Die chronische Pankreatitis ist eine Erkrankung mit entzündlich-fibrosierender Genese, die durch Schädigungen der interstitiellen, duktalen und/oder azinären Zellen ausgelöst wird. Die wichtigsten Ursachen hierfür sind Alkoholabusus, Genmutationen, autoimmune Reaktionslage, anatomische Besonderheiten und Gangobstruktionen. Das morphologische Spektrum der chronischen Pankreatitisformen, welche sich mit den genannten Ätiologien verbinden, zeigt Unterschiede, die in zunehmendem Maße eine ursächliche Zuordnung gestatten. Für die Abgrenzung der chronischen Pankreatitis vom duktalen Adenokarzinom des Pankreas wird ein Katalog, der fünf Kriterien umfasst, vorgestellt.

Abstract

Chronic pancreatitis is a fibroinflammatory disease that is induced by injuries to the interstitial, ductal, and/or acinar cells. The most important causes are alcohol abuse, gene mutations, autoimmune processes, special anatomic changes, and obstructive duct lesions. The morphologic spectrum of the various types of chronic pancreatitis related to the above causes shows features that increasingly allow an etiological distinction and categorization to be made. A catalog of five criteria is presented for distinguishing chronic pancreatitis from ductal adenocarcinoma of the pancreas.

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Literatur

  1. 1.

    Abraham SC, Leach S, Yeo CJ et al. (2003) Eosinophilic pancreatitis and increased eosinophils in the pancreas. Am J Surg Pathol 27: 334–342

    Article  PubMed  Google Scholar 

  2. 2.

    Allen-Mersh TG (1985) What is the significance of pancreatic ductal mucinous hyperplasia? Gut 26: 825–833

    CAS  PubMed  Google Scholar 

  3. 3.

    Ammann RW, Heitz PU, Klöppel G (1996) Course of alcoholic chronic pancreatitis: a prospective clinicomorphological long-term study. Gastroenterology 111: 224–231

    CAS  PubMed  Google Scholar 

  4. 4.

    Apte MV, Haber PS, Darby SJ et al. (1999) Pancreatic stellate cells are activated by proinflammatory cytokines: implications for pancreatic fibrogenesis. Gut 44: 534–541

    CAS  PubMed  Google Scholar 

  5. 5.

    Ebert M, Kasper HU, Hernberg S et al. (1998) Overexpression of platelet-derived growth factor (PDGF) B chain and type β PDGF receptor in human chronic pancreatitis. Dig Dis Sci 43: 567–574

    Article  CAS  PubMed  Google Scholar 

  6. 6.

    Ectors N, Maillet B, Aerts R et al. (1997) Non-alcoholic duct destructive chronic pancreatitis. Gut 41: 263–268

    Google Scholar 

  7. 7.

    Etemad B, Whitcomb DC (2001) Chronic pancreatitis: diagnosis, classification, and new genetic developments. Gastroenterology 120: 682–707

    CAS  PubMed  Google Scholar 

  8. 8.

    Fléjou JF, Potet F, Molas G, Bernades P, Amouyal P, Fékété F (1993) Cystic dystrophy of the gastric and duodenal wall developing in heterotopic pancreas: an unrecognized entity. Gut 34: 343–347

    PubMed  Google Scholar 

  9. 9.

    Hruban RH, Adsay NV, Albores-Saavedra J et al. (2001) Pancreatic intraepithelial neoplasia. A new nomenclature and classification system for pancreatic duct lesions. Am J Surg Pathol 25: 579–586

    Article  CAS  PubMed  Google Scholar 

  10. 10.

    Kawaguchi K, Koike M, Tsuruta K, Okamoto A, Tabata I, Fujita N (1991) Lymphoplasmacytic sclerosing pancreatitis with cholangitis: variant of primary sclerosing cholangitis extensively involving pancreas. Hum Pathol 22: 387–395

    Article  CAS  PubMed  Google Scholar 

  11. 11.

    Kimura W, Nagai H, Kuroda A, Muto T, Esaki Y (1995) Analysis of small cystic lesions of the pancreas. Int J Pancreatol 18: 197–206

    CAS  PubMed  Google Scholar 

  12. 12.

    Klöppel G (1998) Chronic pancreatitis. Etiology, pathophysiology, and pathology. In: Howard J, Idezuki Y, Ihse I, Prinz R (eds) Surgical diseases of the pancreas, 3rd edn. Williams & Wilkins, Baltimore/MD, pp 321–328

  13. 13.

    Klöppel G (1999) Progression from acute to chronic pancreatitis. A pathologist’s view. Surg Clin North Am 79: 801–814

    PubMed  Google Scholar 

  14. 14.

    Klöppel G, Maillet B (1992) The morphological basis for the evolution of acute pancreatitis into chronic pancreatitis. Virchows Arch A Pathol Anat 420: 1–4

    Google Scholar 

  15. 15.

    Klöppel G, Lüttges J, Löhr M, Zamboni G, Longnecker D (2003) Autoimmune pancreatitis: pathological, clinical, and immunological features. Pancreas 27: 14–19

    Article  PubMed  Google Scholar 

  16. 16.

    Klöppel G, Detlefsen S, Feyerabend B (2004) Fibrosis of the pancreas: the initial tissue damage and the resulting pattern. Virchows Arch 445: 1–8

    Google Scholar 

  17. 17.

    Luttenberger T, Schmid-Kotsas A, Menke A et al. (2000) Platelet-derived growth factors stimulate proliferation and extracellular matrix synthesis of pancreatic stellate cells: implication in pathogenesis of pancreas fibrosis. Lab Invest 80: 47–55

    CAS  PubMed  Google Scholar 

  18. 18.

    Lüttges J, Stigge C, Pacena M, Klöppel G (2004) Rare ductal adenocarcinoma of the pancreas in patients younger than age 40 years. An analysis of its features and a literature review. Cancer 100: 173–182

    Article  PubMed  Google Scholar 

  19. 19.

    Notohara K, Burgart LJ, Yadav D, Chari S, Smyrk TC (2003) Idiopathic chronic pancreatitis with periductal lymphoplasmacytic infiltration: clinicopathologic features of 35 cases. Am J Surg Pathol 27: 1119–1127

    Article  PubMed  Google Scholar 

  20. 20.

    Schmitz-Moormann P, Hein J (1976) Changes of the pancreatic duct system associated with ageing. Virchows Arch A Pathol Anat 371: 145–152

    Article  CAS  Google Scholar 

  21. 21.

    Solcia E, Capella C, Klöppel G (1997) Tumors of the pancreas. AFIP Atlas of tumor pathology, 3rd series, fascicle 20. Armed Forces Institute of Pathology, Washington/DC

  22. 22.

    Stolte M, Weiss W, Volkholz H, Rösch W (1982) A special form of segmental pancreatitis: „groove pancreatitis“. Hepatogastroenterology 29: 198–208

    CAS  PubMed  Google Scholar 

  23. 23.

    Weber SM, Cubukcu-Dimopulo O, Palesty JA, Suriawinata A, Klimstra D, Brennan MF, Conlon K (2003) Lymphoplasmacytic sclerosing pancreatitis: inflammatory mimic of pancreatic carcinoma. J Gastrointest Surg 7: 129–139

    Article  PubMed  Google Scholar 

  24. 24.

    Witt H, Luck W, Hennies HC et al. (2000) Mutations in the gene encoding the serine protease inhibitor, Kazal type 1 are associated with chronic pancreatitis. Nat Genet 25: 213–216

    Article  CAS  PubMed  Google Scholar 

  25. 25.

    Wreesmann V, Eijck CH van, Naus DC, Velthuysen ML van, Jeekel J, Mooi WJ (2001) Inflammatory pseudotumour (inflammatory myofibroblastic tumour) of the pancreas: a report of six cases associated with obliterative phlebitis. Histopathology 38: 105–110

    Article  CAS  PubMed  Google Scholar 

  26. 26.

    Zamboni G, Lüttges J, Capelli P et al. (2004) Histopathological features of diagnostic and clinical relevance in autoimmune pancreatitis: a study on 53 resection specimens and 9 biopsy specimens. Virchows Arch 445: 552–563

    Google Scholar 

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Correspondence to G. Klöppel.

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Klöppel, G., Sipos, B. & Lüttges, J. Das Spektrum der chronischen Pankreatitis. Pathologe 26, 59–66 (2005). https://doi.org/10.1007/s00292-004-0733-2

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Schlüsselwörter

  • Alkohol
  • Hereditäre Genese
  • Autoimmunpankreatitis
  • Duodenalwandpankreatitis
  • Obstruktive Pankreatitis

Keywords

  • Alcohol
  • Hereditary origin
  • Autoimmune pancreatitis
  • Duodenal wall pancreatitis
  • Obstructive pancreatitis