Z Gastroenterol 2018; 56(05): 469-478
DOI: 10.1055/s-0043-123881
Originalarbeit
© Georg Thieme Verlag KG Stuttgart · New York

Prevalence of inflammatory bowel disease in alcoholic, non-alcoholic and autoimmune pancreatitis

Inflammatory bowel disease in pancreatitisPrävalenz chronisch entzündlicher Darmerkrankungen bei alkoholischer, nicht-alkoholischer und autoimmuner PankreatitisChronisch entzündliche Darmerkrankungen bei Pankreatitis
Alexander Schneider
1   Department of Medicine II, University Medical Center Mannheim, Medical Faculty of the University of Heidelberg, Mannheim, Germany
,
Michael Hirth
1   Department of Medicine II, University Medical Center Mannheim, Medical Faculty of the University of Heidelberg, Mannheim, Germany
,
Christel Weiss
2   Department of Medical Statistics, University Medical Center Mannheim, Medical Faculty of the University of Heidelberg, Mannheim, Germany
,
Philip Weidner
1   Department of Medicine II, University Medical Center Mannheim, Medical Faculty of the University of Heidelberg, Mannheim, Germany
,
Christoph Antoni
1   Department of Medicine II, University Medical Center Mannheim, Medical Faculty of the University of Heidelberg, Mannheim, Germany
,
Anne Thomann
1   Department of Medicine II, University Medical Center Mannheim, Medical Faculty of the University of Heidelberg, Mannheim, Germany
,
Wolfgang Reindl
1   Department of Medicine II, University Medical Center Mannheim, Medical Faculty of the University of Heidelberg, Mannheim, Germany
,
Matthias P. Ebert
1   Department of Medicine II, University Medical Center Mannheim, Medical Faculty of the University of Heidelberg, Mannheim, Germany
,
Roland H. Pfützer
1   Department of Medicine II, University Medical Center Mannheim, Medical Faculty of the University of Heidelberg, Mannheim, Germany
› Author Affiliations
Further Information

Publication History

19 May 2017

22 November 2017

Publication Date:
07 May 2018 (online)

Abstract

Objectives Patients with inflammatory bowel disease (IBD) frequently reveal features of pancreatic inflammation. However, the prevalence of IBD in patients with alcoholic pancreatitis (AP) and nonalcoholic pancreatitis (NAP) has not yet been determined, and the prevalence of IBD in patients with autoimmune pancreatitis (AiP) from Germany is unknown.

Aims Thus, we aimed, first, to determine the prevalence of IBD in AP, NAP, and AiP from a tertiary center in Germany and, second, to characterize patients with AiP and IBD.

Methods We performed a retrospective cross-sectional study to determine the prevalence of IBD in patients with different forms of pancreatitis presenting to our clinic.

Results Compared to the general population and to a control group with viral hepatitis from our clinic, we observed the most significant increase of IBD in patients with AiP (n = 3/28; p < 0.0001 vs. general population, binomial proportion test; p = 0.0112 vs. hepatitis group, Fisher’s exact test), followed by a significant increase in subjects with NAP (n = 11/278; p < 0.0001 vs. general population, binomial proportion test; p = 0.0338 vs. hepatitis group, Fisher’s exact test). A review of previous studies on the prevalence of IBD among patients with AiP revealed a combined prevalence of 12 % (n = 43/355). Type 2 AiP is significantly more often associated with IBD than type 1 AiP (n = 28/48, 58 % vs. n = 7/129, 5 %; combined patient cohort, p < 10E − 12; Fisher’s exact test).

Conclusions Immune-mediated mechanisms related to IBD may participate in the development of AiP, especially AiP type 2, and may also increase the risk for the development of other forms of pancreatic inflammation.

Zusammenfassung

Fragestellung Patienten mit chronisch entzündlicher Darmerkrankung (CED) entwickeln häufig morphologische Pankreasveränderungen. Die Prävalenz von CED bei Patienten mit alkoholischer Pankreatitis (AP) und nicht-alkoholischer Pankreatitis (NAP) wurde bislang nicht untersucht, und die Prävalenz von CED bei Patienten mit autoimmuner Pankreatitis (AiP) aus Deutschland ist ebenfalls unbekannt.

Ziel Die Ziele der Arbeit waren, die Prävalenz von CED bei Patienten mit AP, NAP und AiP in einem tertiären Versorgungszentrum in Deutschland zu bestimmen, und die Patienten mit CED und AiP zu charakterisieren.

Methoden Wir bestimmten in einer retrospektiven Querschnittsstudie die Prävalenz von CED bei Patienten mit verschiedenen Formen der Pankreatitis, die sich in unserer Klinik vorstellten.

Ergebnisse Wir beobachteten im Vergleich zur Allgemeinbevölkerung und zu einer Kontrollgruppe mit viraler Hepatitis unserer Klinik die deutlichste signifikante Häufung von CED bei Patienten mit AiP (n = 3/28; p < 0.0001 versus Allgemeinbevölkerung, Binomial Proportion Test; p = 0.0112 versus Hepatitisgruppe, Fisher’s exact Test). Wir sahen ebenfalls eine signifikante Häufung von CED bei Patienten mit NAP (n = 11/278; p < 0.0001 versus Allgemeinbevölkerung, Binomial Proportion Test; p = 0.0338 versus Hepatitisgruppe, Fisher’s exact Test). Ein Review unter Berücksichtigung aller vorangegangenen Studien ergab eine kombinierte Prävalenz der CED bei Patienten mit AiP von 12 % (n = 43/355). Die Typ 2 AiP war signifikant häufiger mit CED assoziiert als die Typ 1 AiP (n = 28/48, 58 % versus n = 7/129, 5 %; kombinierte Patientengruppe, p < 10E - 12; Fisher’s exact Test).

Schlussfolgerung Mit CED assoziierte immunologische Mechanismen beteiligen sich möglicherweise bei der Entwicklung der AiP, insbesondere der Typ 2 AiP, und tragen eventuell auch zur Entstehung anderer entzündlicher Pankreaserkrankungen bei.

 
  • References

  • 1 Dignass A, Eliakim R, Magro F. et al. Second European evidence-based consensus on the diagnosis and management of ulcerative colitis part 1: definitions and diagnosis. J Crohns Colitis 2012; 6: 965-990
  • 2 Van Assche G, Dignass A, Panes J. et al. The second European evidence-based consensus on the diagnosis and management of Crohn’s disease: definitions and diagnosis. J Crohns Colitis 2010; 4: 7-27
  • 3 Kostic AD, Xavier RJ, Gevers D. The microbiome in inflammatory bowel disease: current status and the future ahead. Gastroenterology 2014; 146: 1489-1499
  • 4 Neurath MF. Cytokines in inflammatory bowel disease. Nat Rev Immunol 2014; 14: 329-342
  • 5 Khor B, Gardet A, Xavier RJ. Genetics and pathogenesis of inflammatory bowel disease. Nature 2011; 474: 307-317
  • 6 Larsen S, Bendtzen K, Nielsen OH. Extraintestinal manifestations of inflammatory bowel disease: epidemiology, diagnosis, and management. Ann Med 2010; 42: 97-114
  • 7 Pitchumoni CS, Rubin A, Das K. Pancreatitis in inflammatory bowel diseases. J Clin Gastroenterol 2010; 44: 246-253
  • 8 Navaneethan U, Shen B. Hepatopancreatobiliary manifestations and complications associated with inflammatory bowel disease. Inflamm Bowel Dis 2010; 16: 1598-1619
  • 9 Czako L, Gyokeres T, Topa L. et al. Autoimmune pancreatitis in Hungary: a multicenter nationwide study. Pancreatology 2011; 11: 261-267
  • 10 Ikeura T, Manfredi R, Zamboni G. et al. Application of international consensus diagnostic criteria to an Italian series of autoimmune pancreatitis. United European Gastroenterol J 2013; 1: 276-284
  • 11 Maire F, Le BaleurY, Rebours V. et al. Outcome of patients with type 1 or 2 autoimmune pancreatitis. Am J Gastroenterol 2011; 106: 151-156
  • 12 Park SH, Kim D, Ye BD. et al. The characteristics of ulcerative colitis associated with autoimmune pancreatitis. J Clin Gastroenterol 2013; 47: 520-525
  • 13 Ravi K, Chari ST, Vege SS. et al. Inflammatory bowel disease in the setting of autoimmune pancreatitis. Inflamm Bowel Dis 2009; 15: 1326-1330
  • 14 Nahon UzanK, Levy P, O’Toole D. et al. Is idiopathic chronic pancreatitis an autoimmune disease?. Clin Gastroenterol Hepatol 2005; 3: 903-909
  • 15 Oracz G, Cukrowska B, Oralewska B. et al. Is chronic pancreatitis in children an autoimmune disease?. Clin Gastroenterol Hepatol 2006; 4: 802
  • 16 von Elm E, Altman DG, Egger M. et al. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement: guidelines for reporting observational studies. J Clin Epidemiol 2007; 147: 573-577
  • 17 Schneider A, Löhr JM, Singer MV. The M-ANNHEIM classification of chronic pancreatitis: introduction of a unifying classification system based on a review of previous classifications of the disease. J Gastroenterol 2007; 42: 101-119
  • 18 Shimosegawa T, Chari ST, Frulloni L. et al. International consensus diagnostic criteria for autoimmune pancreatitis: guidelines of the International Association of Pancreatology. Pancreas 2011; 40: 352-358
  • 19 Okazaki K, Kawa S, Kamisawa T. et al. Clinical diagnostic criteria of autoimmune pancreatitis: revised proposal. J Gastroenterol 2006; 41: 626-631
  • 20 Kim KP, Kim MH, Kim JC. et al. Diagnostic criteria for autoimmune chronic pancreatitis revisited. World J Gastroenterol 2006; 12: 2487-2496
  • 21 Otsuki M, Chung JB, Okazaki K. et al. Asian diagnostic criteria for autoimmune pancreatitis: consensus of the Japan-Korea Symposium on Autoimmune Pancreatitis. J Gastroenterol 2008; 43: 403-408
  • 22 Chari ST, Smyrk TC, Levy MJ. et al. Diagnosis of autoimmune pancreatitis: the Mayo Clinic experience. Clin Gastroenterol Hepatol 2006; 4: 1010-1016
  • 23 Chari ST, Takahashi N, Levy MJ. et al. A diagnostic strategy to distinguish autoimmune pancreatitis from pancreatic cancer. Clin Gastroenterol Hepatol 2009; 7: 1097-1103
  • 24 Frulloni L, Scattolini C, Falconi M. et al. Autoimmune pancreatitis: differences between the focal and diffuse forms in 87 patients. Am J Gastroenterol 2009; 104: 2288-2294
  • 25 Schneider A, Löhr JM. Autoimmune Pankreatitis. Der Internist 2009; 50: 318-330
  • 26 Schneider A, Löhr JM, Singer MV. Comparison of the Mannheim diagnostic criteria of autoimmune pancreatitis with other diagnostic criteria systems (Abstract Joint Meeting of the 14th Meeting of the International Association of Pancreatology (IAP) and the 41st Annual Meeting of the Japan Pancreas Society (JPS), Fukuoka, Japan). Pancreatology 2010; 10: 101-102
  • 27 Schneider A, Michaely H, Rückert F. et al. Diagnosing autoimmune pancreatitis with the Unifying-Autoimmune-Pancreatitis-Criteria. Pancreatology 2017; 17: 381-394
  • 28 Dignass A, Preiss JC, Aust DE. et al. Updated German guideline on diagnosis and treatment of ulcerative colitis, 2011. Z Gastroenterol 2011; 49: 1276-1341
  • 29 Preiss JC, Bokemeyer B, Buhr HJ. et al. Updated German clinical practice guideline on “Diagnosis and treatment of Crohn’s disease” 2014. Z Gastroenterol 2014; 52: 1431-1484
  • 30 Loftus Jr EV. Clinical epidemiology of inflammatory bowel disease: Incidence, prevalence, and environmental influences. Gastroenterology 2004; 126: 1504-1517
  • 31 Lowe AM, Roy PO, B-Poulin M. et al. Epidemiology of Crohn’s disease in Quebec, Canada. Inflamm Bowel Dis 2009; 15: 429-435
  • 32 Molodecky NA, Soon IS, Rabi DM. et al. Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology 2012; 142: 46-54
  • 33 Timmer A. Epidemiologie der CED. In: Hoffmann J, Kroesen A, Klump B. eds Chronisch entzündliche Darmerkrankungen – Handbuch für die Praxis. Stuttgart, New York: Georg Thieme Verlag; 2009: 8-24
  • 34 Ball WP, Baggenstoss AH, Bargen JA. Pancreatic lesions associated with chronic ulcerative colitis. Arch Pathol (Chic) 1950; 50: 347-358
  • 35 Seyrig JA, Jian R, Modigliani R. et al. Idiopathic pancreatitis associated with inflammatory bowel disease. Dig Dis Sci 1985; 30: 1121-1126
  • 36 Barthet M, Hastier P, Bernard JP. et al. Chronic pancreatitis and inflammatory bowel disease: true or coincidental association?. Am J Gastroenterol 1999; 94: 2141-2148
  • 37 Barthet M, Lesavre N, Desplats S. et al. Frequency and characteristics of pancreatitis in patients with inflammatory bowel disease. Pancreatology 2006; 6: 464-471
  • 38 Ebert MP, Ademmer K, Müller-Ostermeyer F. et al. CD8+CD103+ T cells analogous to intestinal intraepithelial lymphocytes infiltrate the pancreas in chronic pancreatitis. Am J Gastroenterol 1998; 93: 2141-2147
  • 39 Hunger RE, Mueller C, Z’Graggen K. et al. Cytotoxic cells are activated in cellular infiltrates of alcoholic chronic pancreatitis. Gastroenterology 1997; 112: 1656-1663
  • 40 Saurer L, Reber P, Schaffner T. et al. Differential expression of chemokines in normal pancreas and in chronic pancreatitis. Gastroenterology 2000; 118: 356-367
  • 41 Clemens DL, Wells MA, Schneider KJ. et al. Molecular mechanisms of alcohol associated pancreatitis. World J Gastrointest Pathophysiol 2014; 5: 147-157
  • 42 Pezzilli R, Pagano N. Pathophysiology of autoimmune pancreatitis. World J Gastrointest Pathophysiol 2014; 5: 11-17
  • 43 Okazaki K, Uchida K, Sumimoto K. et al. Autoimmune pancreatitis: pathogenesis, latest developments and clinical guidance. Ther Adv Chronic Dis 2014; 5: 104-111
  • 44 Löhr JM, Faissner R, Koczan D. et al. Autoantibodies against the exocrine pancreas in autoimmune pancreatitis: gene and protein expression profiling and immunoassays identify pancreatic enzymes as a major target of the inflammatory process. Am J Gastroenterol 2010; 105: 2060-2071
  • 45 Seibold F, Mork H, Tanza S. et al. Pancreatic autoantibodies in Crohn’s disease: a family study. Gut 1997; 40: 481-484
  • 46 Stocker W, Otte M, Ulrich S. et al. Autoimmunity to pancreatic juice in Crohn’s disease. Results of an autoantibody screening in patients with chronic inflammatory bowel disease. Scand J Gastroenterol Suppl 1987; 139: 41-52