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Parietalzellhypertrophie und Drüsenkörperzysten

Ursachen und Management

Parietal cell hypertrophy and fundic gland polyps

Causes and management

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Der Gastroenterologe Aims and scope

Zusammenfassung

Eine Parietalzellhypertrophie ist Folge des trophischen Effekts der Hypergastrinämie. Die häufigste Ursache für die Entstehung einer Parietalzellhypertrophie ist die Einnahme von Protonenpumpenhemmern (PPI). Weitere Ursache einer Hypergastrinämie mit Parietalzellhypertrophie ist die Atrophie der oxyntischen Magenschleimhaut durch eine Autoimmungastritis und eine Helicobacter (H.)-pylori-Infektion sowie ein Zollinger-Ellison-Syndrom (ZES). Bei Patienten mit Parietalzellhypertrophie unter PPI-Therapie oder im Rahmen eines ZES kommt es nach abruptem Absetzen einer PPI-Therapie zu einem Säurerebound, worunter säureassoziierte Symptome rezidivieren oder de novo entstehen können. So empfiehlt sich nach einer Langzeiteinnahme das langsame Absetzen der PPI-Therapie. Drüsenkörperzysten wurden lange vor der Ära der PPI beschrieben. Der Zusammenhang mit kolorektalen Neoplasien gerade bei familiärer adenomatöser Polyposis (FAP), aber auch bei sporadischen kolorektalen Neoplasien wurde ebenfalls durch den Erstbeschreiber Kurt Elster belegt. Aus diesem Grund werden Drüsenkörperzysten in Deutschland auch Elster-Drüsenkörperzysten genannt. Die molekularen Unterschiede zwischen sporadischen und FAP-assoziierten Drüsenkörperzysten sind immer noch nicht bis zur Gänze aufgeklärt. Die Entartungswahrscheinlichkeit selbst bei Patienten mit FAP und Adenomen oberhalb der Drüsenkörperzysten ist sehr gering. Bei sporadischen Drüsenkörperzysten ist das Risiko noch wesentlich kleiner. So können routinemäßige Biopsien aus Drüsenkörperzysten nicht empfohlen werden. Die Assoziation von Drüsenköperzysten mit kolorektalen Neoplasien wird kontrovers diskutiert. Anhand der aktuellen Literatur empfehlen die Autoren die leitliniengerechte Vorsorgekoloskopie unabhängig von dem Vorliegen von Drüsenkörperzysten.

Abstract

Parietal cell hypertrophy is related to the trophic effect of hypergastrinaemia. Long-term therapy with proton pump inhibitors (PPI) is the most common cause of parietal cell hyperplasia. Further causes of hypergastrinaemia with parietal cell hypertrophy are atrophy of the oxyntic gastric glands following autoimmune gastritis or Helicobacter pylori infection, as well as the Zollinger–Ellison syndrome (ZES). In patients with parietal cell hypertrophy as a result of long-term PPI therapy or ZES, abrupt withdrawal of a PPI induces an acid-rebound that can lead to acid-related symptoms or their relapse. Therefore, patients on long-term PPI therapy should taper down PPI slowly. Fundic gland polyps were described long before PPI became available. Kurt Elster also first described their association with colorectal neoplasms in both patients with familial adenomatous polyposis (FAP) and those with sporadic colorectal neoplasias, which is why fundic gland polyps are called Elster’s fundic gland polyps in Germany. The molecular differences between sporadic and FAP-associated fundic gland polyps are still not completely elucidated. The risk of malignant progression is very low even among FAP patients with adenomas in the apical part of fundic gland polyps, and even lower among subjects with sporadic fundic gland polyps. Thus, routine biopsy examination for fundic gland polyps in regular gastric biopsy protocols is not recommended. The association of fundic gland polyps with colorectal neoplasms, even if not confirmed in some studies, justifies the recommendation to perform a colonoscopy. The association between fundic gland polyps and colorectal neoplasia is controversial. According to the current literature the authors recommend preventive colonoscopy according to current guidelines regardless of the presence of fundic gland polyps.

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Literatur

  1. Annibale B, Lahner E, Fave GD (2011) Diagnosis and management of pernicious anemia. Curr Gastroenterol Rep 13:518–524

    Article  PubMed  Google Scholar 

  2. Dockray GJ, Varro A, Dimaline R et al (2001) The gastrins: their production and biological activities. Annu Rev Physiol 63:119–139

    Article  CAS  PubMed  Google Scholar 

  3. Dimaline R, Varro A (2014) Novel roles of gastrin. J Physiol 592:2951–2958

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  4. Lundell L, Vieth M, Gibson F, Nagy P, Kahrilas PJ (2015) Systematic review: the effects of long-term proton pump inhibitor use on serum gastrin levels and gastric histology. Aliment Pharmacol Ther 42:649–663

    Article  CAS  PubMed  Google Scholar 

  5. Hunt RH, Camilleri M, Crowe SE, El-Omar EM, Fox JG, Kuipers EJ, Malfertheiner P, McColl KE, Pritchard DM, Rugge M, Sonnenberg A, Sugano K, Tack J (2015) The stomach in health and disease. Gut 64(10):1650–1668

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  6. Lamberts R, Brunner G, Solcia E (2001) Effects of very long (up to 10 years) proton pump blockade on human gastric mucosa. Digestion 64(4):205–213

    Article  CAS  PubMed  Google Scholar 

  7. Cats A, Schenk BE, Bloemena E, Roosedaal R, Lindeman J, Biemond I, Klinkenberg-Knol EC, Meuwissen SG, Kuipers EJ (2000) Parietal cell protrusions and fundic gland cysts during omeprazole maintenance treatment. Hum Pathol 31:684–690

    Article  CAS  PubMed  Google Scholar 

  8. Reimer C, Søndergaard B, Hilsted L, Bytzer P (2009) Proton-pump inhibitor therapy induces acid-related symptoms in healthy volunteers after withdrawal of therapy. Gastroenterology 137(1):80–7, 87.e1

    Article  CAS  PubMed  Google Scholar 

  9. Malfertheiner P, Kandulski A, Venerito M (2017) Proton-pump inhibitors: understanding the complications and risks. Nat Rev Gastroenterol Hepatol 14(12):697–710

    Article  CAS  PubMed  Google Scholar 

  10. Falconi M, Eriksson B, Kaltsas G, Bartsch DK, Capdevila J, Caplin M, Kos-Kudla B, Kwekkeboom D, Rindi G, Klöppel G, Reed N, Kianmanesh R, Jensen RT, Vienna Consensus Conference participants (2016) ENETS consensus guidelines update for the management of patients with functional pancreatic neuroendocrine tumors and non-functional pancreatic neuroendocrine tumors. Neuroendocrinology 103:153–171

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Ojeaburu JV, Ito T, Crafa P et al (2011) Mechanism of acid hypersecretion post curative gastrinoma resection. Dig Dis Sci 56:139–154

    Article  PubMed  Google Scholar 

  12. Okano A, Takakuwa H, Matsubayashi Y (2007) Parietal-cell hyperplasia mimicking sporadic fundic gland polyps in the atrophic mucosa of autoimmune gastritis. Gastrointest Endosc 66:394–395

    Article  PubMed  Google Scholar 

  13. Venerito M, Varbanova M, Röhl FW, Reinhold D, Frauenschläger K, Jechorek D, Weigt J, Link A, Malfertheiner P (2016) Oxyntic gastric atrophy in helicobacter pylori gastritis is distinct from autoimmune gastritis. J Clin Pathol 69:677–685

    Article  CAS  PubMed  Google Scholar 

  14. Venerito M, Radünz M, Reschke K, Reinhold D, Frauenschläger K, Jechorek D, Di Mario F, Malfertheiner P (2015) Autoimmune gastritis in autoimmune thyroid disease. Aliment Pharmacol Ther 41(7):686–693

    Article  CAS  PubMed  Google Scholar 

  15. Elster K, Eidt H, Ottenjann R, Rösch W, Seifert E (1977) The glandular cyst, a polypoid lesion of the gastric mucosa (author’s transl). Dtsch Med Wochenschr 102:183–187

    Article  CAS  PubMed  Google Scholar 

  16. Sipponen P, Siurala M (1978) Cystic “hamartomatous” epithelial polyps of the stomach. Acta Hepatogastroenterol (Stuttg) 25:380–383

    CAS  Google Scholar 

  17. Eidt S, Stolte M (1989) Gastric glandular cysts—investigations into their genesis and relationship to colorectal epithelial tumors. Z Gastroenterol 27:212–217

    CAS  PubMed  Google Scholar 

  18. Rohner HG, Frommhold H, Kühr J, Koischwitz D, Lelbach WK (1977) Corrosive lesions of the upper intestinal tract in gastrectomized patients. Leber Magen Darm 7:376–379 (author’s translation)

    CAS  PubMed  Google Scholar 

  19. Pilichowska ME, Borchard F (1994) Drüsenkörperzysten des Magens zeigen eine Epithel-Proliferation und eine räumlich gestörte Differenzierung (foveoläre Metaplasie). Verh Dtsch Ges Pathol 78:507

    Google Scholar 

  20. Graham JR (1992) Gastric polyposis: onset during long-term therapy with omeprazole. Med J Aust 157(4):287–288

    CAS  PubMed  Google Scholar 

  21. Choudhry U, Boyce HW Jr, Coppola D (1998) Proton pump inhibitor–associated gastric polyps: a retrospective analysis of their frequency, and endoscopic, histologic, and ultrasound characteristics. Am J Clin Pathol 110:615–621

    Article  CAS  PubMed  Google Scholar 

  22. Vieth M, Stolte M (2001) Fundic gland polyps are not induced by proton pump inhibitor therapy. Am J Clin Pathol 116(5):716–720

    Article  CAS  PubMed  Google Scholar 

  23. Iida M, Yao T, Watanabe H, Itoh H, Iwashita A (1984) Fundic gland polyposis in patients without familial adenomatosis coli: its incidence and clinical features. Gastroenterology 86(6):1437–1442

    CAS  PubMed  Google Scholar 

  24. Domizio P, Talbot IC, Spigelman AD, Williams CB, Phillips RK (1990) Upper gastrointestinal pathology in familial adenomatous polyposis: results from a prospective study of 102 patients. J Clin Pathol 43(9):738–743

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Bianchi LK, Burke CA, Bennett AE, Lopez R, Hasson H, Church JM (2008) Fundic gland polyp dysplasia is common in familial adenomatous polyposis. Clin Gastroenterol Hepatol 6(2):180–185. https://doi.org/10.1016/j.cgh.2007.11.018

    Article  PubMed  Google Scholar 

  26. Wu TT, Kornacki S, Rashid A, Yardley JH, Hamilton SR (1998) Dysplasia and dysregulation of proliferation in foveolar and surface epithelia of fundic gland polyps from patients with familial adenomatous polyposis. Am J Surg Pathol 22(3):293–298

    Article  CAS  PubMed  Google Scholar 

  27. Coffey RJ Jr, Knight CD Jr, van Heerden JA, Weiland LH (1985) Gastric adenocarcinoma complicating Gardner’s syndrome in a North American woman. Gastroenterology 88:1263–1266

    Article  PubMed  Google Scholar 

  28. Hofgärtner WT, Thorp M, Ramus MW, Delorefice G, Chey WY, Ryan CK, Takahashi GW, Lobitz JR (1999) Gastric adenocarcinoma associated with fundic gland polyps in a patient with attenuated familial adenomatous polyposis. Am J Gastroenterol 94:2275–2281

    Article  PubMed  Google Scholar 

  29. Zwick A, Munir M, Ryan CK, Gian J, Burt RW, Leppert M, Spirio L, Chey WY (1997) Gastric adenocarcinoma and dysplasia in fundic gland polyps of a patient with attenuated adenomatous polyposis coli. Gastroenterology 113:659–663

    Article  CAS  PubMed  Google Scholar 

  30. Garrean S, Hering J, Saied A, Jani J, Espat NJ (2008) Gastric adenocarcinoma arising from fundic gland polyps in a patient with familial adenomatous polyposis syndrome. Am Surg 74:79–83

    PubMed  Google Scholar 

  31. Zwick A, Munir M, Ryan CK, Gian J, Burt RW, Leppert M, Spirio L, Chey WY (1997) Gastric adenocarcinoma and dysplasia in fundic gland polyps of a patient with attenuated adenomatous polyposis coli. Gastroenterology 113:659–663

    Article  CAS  PubMed  Google Scholar 

  32. Jalving M, Koornstra JJ, Götz JM, van der Waaij LA, de Jong S, Zwart N, Karrenbeld A, Kleibeuker JH (2003) High-grade dysplasia in sporadic fundic gland polyps: a case report and review of the literature. Eur J Gastroenterol Hepatol 15:1229–1233

    Article  PubMed  Google Scholar 

  33. Abraham SC, Singh VK, Yardley JH, Wu TT (2001) Hyperplastic polyps of the stomach: associations with histologic patterns of gastritis and gastric atrophy. Am J Surg Pathol 25(4):500–507

    Article  CAS  PubMed  Google Scholar 

  34. Sekine S, Shibata T, Yamauchi Y, Nakanishi Y, Shimoda T, Sakamoto M, Hirohashi S (2002) Beta-catenin mutations in sporadic fundic gland polyps. Virchows Arch 440:381–386

    Article  CAS  PubMed  Google Scholar 

  35. Watson SA (2001) Oncogenic targets of beta-catenin-mediated transcription in molecular pathogenesis of intestinal polyposis. Lancet 357:572–573

    Article  CAS  PubMed  Google Scholar 

  36. Abraham SC, Montgomery EA, Singh VK, Yardley JH, Wu TT (2002) Gastric adenomas: intestinal-type and gastric-type adenomas differ in the risk of adenocarcinoma and presence of background mucosal pathology. Am J Surg Pathol 26:1276–1285

    Article  PubMed  Google Scholar 

  37. Wei J, Chiriboga L, Yee H, Mizuguchi M, Li E, Sidhu GS, West AB (2002) Altered cellular distribution of tuberin and glucocorticoid receptor in sporadic fundic gland polyps. Mod Pathol 15:862–869

    Article  PubMed  Google Scholar 

  38. Jalving M, Koornstra JJ, Götz JM, van der Waaij LA, de Jong S, Zwart N, Karrenbeld A, Kleibeuker JH (2003) High-grade dysplasia in sporadic fundic gland polyps: a case report and review of the literature. Eur J Gastroenterol Hepatol 15:1229–1233

    Article  PubMed  Google Scholar 

  39. Elster K, Eidt H, Ottenjann R, Rösch W, Seifert E (1977) The glandular cyst, a polypoid lesion of the gastric mucosa. Dtsch Med Wochenschr 102:183–187

    Article  CAS  PubMed  Google Scholar 

  40. Jung A, Vieth M, Maier O, Stolte M (2002) Fundic gland polyps (Elster’s cysts) of the gastric mucosa. A marker for colorectal epithelial neoplasia? Pathol Res Pract 198(11):731–734

    Article  CAS  PubMed  Google Scholar 

  41. Hwang SM, Kim BW, Chae HS, Lee BI, Choi H, Ji JS, Choi KY, Chung IS, Maeng LS (2011) Gastric fundic gland polyps and their relationship to colorectal neoplasia in Koreans: a 16-year retrospective study. Korean J Gastroenterol 58:20–24

    Article  PubMed  Google Scholar 

  42. Teichmann J, Weickert U, Riemann JF (2008) Gastric fundic gland polyps and colonic polyps – is there a link, really? Eur J Med Res 13:192–195

    PubMed  Google Scholar 

  43. Lee HS, Choi Y, Jung JY, Sung YJ, Ahn DW, Jeong JB, Kim BG, Lee KL, Koh SJ, Kim JW (2016) Do we need colonoscopy verification in patients with fundic gland polyp? Intest Res 14:172–177

    Article  PubMed  PubMed Central  Google Scholar 

  44. Genta RM, Schuler CM, Robiou CI, Lash RH (2009) No association between gastric fundic gland polyps and gastrointestinal neoplasia in a study of over 100,000 patients. Clin Gastroenterol Hepatol 7:849–854

    Article  PubMed  Google Scholar 

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Authors and Affiliations

  1. Klinik für Gastroenterologie, Hepatologie und Infektiologie, Medizinische Fakultät, Otto-von-Guericke-Universität, Leipzigerstr. 44, 39120, Magdeburg, Deutschland

    M. Venerito & A. Canbay

  2. Institut für Pathologie, Klinikum Bayreuth, 95445, Bayreuth, Deutschland

    M. Vieth

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  1. M. Venerito
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M. Venerito, A. Canbay und M. Vieth geben an, dass kein Interessenkonflikt besteht.

Dieser Beitrag beinhaltet keine von den Autoren durchgeführten Studien an Menschen oder Tieren.

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M. Ebert, Mannheim

M. Müller-Schilling, Regensburg

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Venerito, M., Canbay, A. & Vieth, M. Parietalzellhypertrophie und Drüsenkörperzysten. Gastroenterologe 13, 90–97 (2018). https://doi.org/10.1007/s11377-018-0235-z

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