This article is an English translation of the original Czech publication. The translation was generated with the assistance of artificial intelligence and has been reviewed and approved by the authors. The original version remains the authoritative source.

Introduction

According to epidemiological data published by Iang et al., 2,814,972 cases of acute pancreatitis were registered worldwide in 2019, with a total of 115,972 deaths from this disease confirmed [1]. In recent years, the incidence of acute pancreatitis has continued to increase, including mortality in younger populations [2,3]. The induction, development, and further course of acute pancreatitis correlate significantly with coinciding immunological factors. On the other hand, gastrointestinal tract involvement in various autoimmune diseases (e.g., immune complex vasculitis) can also manifest as acute pancreatitis, the clinical course of which is often more severe compared to individuals without coinciding autoimmunity.

Idiopathic inflammatory bowel disease (IBD) are diseases that may be associated with symptoms of acute or chronic pancreatitis. These include clinical manifestations of pain, weight loss, possibly diarrhea and intestinal dyspepsia, which may be caused by exocrine pancreatic insufficiency or morphological abnormalities of the pancreatic duct, with laboratory findings in the form of elevated

CRP levels and hyperamylasemia. A relatively common form of chronic pancreatitis in patients with IBD is type 2 autoimmune pancreatitis [4]. The incidence of acute pancreatitis is higher in people with IBD than in the general population. In patients with Crohn's disease, the incidence is 4.1 times higher, and in patients with ulcerative colitis, it is 2.6 times higher than in individuals without these intestinal diseases [5]. Various autoimmune conditions can initiate the onset of acute pancreatitis or cause exacerbation of pancreatitis and also have the ability to modulate inflammatory processes in the pancreas by affecting lymphocyte function and cytokine production [7]. In summary, patients with IBD have an increased risk of developing acute pancreatitis [8].

Inflammatory bowel diseases and acute pancreatitis

The incidence and prevalence of IBD is increasing not only worldwide but also in the Czech Republic, probably due to many external influences such as stress, antibiotic use, a diet higher in highly processed foods, lower physical activity, and increasing urbanization [9]. There are also a number of specific causes of acute pancreatitis in people suffering from IBD. In such cases, pancreatitis is classified as an extraintestinal manifestation or associated disease of IBD [10,11]. Significant causes of acute pancreatitis in IBD include drug therapy, especially azathioprine and mesalazine [12,13], or an associated form of the disease in the form of autoimmune pancreatitis [14,15]. In a South Korean study from the ASAN Medical Center in Seoul involving a total of 3,307 patients with ulcerative colitis, the authors demonstrated an incidence of acute pancreatitis in 1.5% of cases [8]. These were patients with associated type 2 autoimmune pancreatitis (13 patients), ten cases of pancreatitis indicated by mesalazine, and 13 cases induced by thiopurines. All patients survived the attack of acute pancreatitis and made a full recovery. The course of ulcerative colitis was very similar in patients without pancreatitis and in patients with acute pancreatitis in terms of the need for colectomy, the extent of intestinal inflammation, and the need for biological treatment.

A recent European multicenter study, PANDORA, retrospectively evaluated results from 34 European centers in 69,989 patients with IBD [16]. The study found a prevalence of acute pancreatitis in 1.13% of cases; using the strict criteria of the Atlanta classification, the incidence was only 0.58% [17]. These were younger individuals with an average age of 36.6 years, predominantly women, with Crohn's disease diagnosed in 56.5% of cases. Acute pancreatitis was classified as mild in 87% of cases, with the edematous form of acute pancreatitis verified in 62.8% of them. An interesting finding is the age at which idiopathic intestinal inflammation was diagnosed in patients with acute pancreatitis. In 64% and 69% of patients with Crohn's disease and ulcerative colitis, respectively, the diagnosis of IBD was made in the 16–40 age group, corresponding to Montreal classification group A2. The group of patients falling into category A3 (aged over 40) at the time of diagnosis included 31.5% with Crohn's disease and 23% with ulcerative colitis. The proportion of patients with pancreatitis who regularly consumed alcohol or smoked cigarettes did not differ from IBD patients without pancreatitis. Similarly, the family history of IBD or pancreatitis did not differ between the two groups. Pancreatic involvement was statistically significantly associated with Crohn's disease compared to patients with ulcerative colitis. Acute pancreatitis within 1 year of IBD diagnosis was induced or associated with IBD drug therapy in 70% of cases. In patients with UC, the sequence of subsequent pancreatic disease was more frequent than in patients with CN. Etiologically, it was mainly drug-induced acute pancreatitis (55.3%) and biliary pancreatitis (14.8%). In 13.6% of acute pancreatitis cases, the etiology was not precisely determined. The alcoholic form of acute pancreatitis was identified in only 3.5% of cases. The most common drugs involved were 5-ASA (42%), 6-mercaptopurine (47%), and, in isolated cases, ustekinumab, ciprofloxacin, integrin inhibitors, vedolizumab, budesonide, or metronidazole. Of the clinical symptoms of acute pancreatitis, abdominal pain was reported in 90.6% of cases, and vomiting and nausea in 32.2% of cases. Using imaging methods, pancreatic findings were assessed as edematous pancreatitis in 71.6% of cases, while findings were described as normal in 23.5% of the examined individuals. Mendelian randomization is a method that allows the detection of potential causal relationships between risk factors and the resulting induced disease or course of the disease and minimizes the influence of bias factors [18]. According to epidemiological data from 2019, 2,814,972 individuals worldwide were diagnosed with acute pancreatitis, of whom 115,053 died. Retrospective monitoring has clearly shown that the onset and further course of acute pancreatitis is strictly linked to certain immunological factors, or rather the immune system. An Asian study by Zheng et al. [2] using Mendelian randomization demonstrated a significant association between genetically predicted IBD and an increased risk of acute pancreatitis. The influence of the intestinal microbiome was confirmed, whose alteration in patients with IBD can lead to impaired immune regulation and increased intestinal permeability [19]. Another study confirmed the relationship between genes conditioning the development of IBD and acute pancreatitis. The study also confirmed the beneficial effect of orally administered corticosteroids in reducing the risk of acute pancreatitis in individuals with IBD (HR 0.83; 95% CI 0.73–0.94), in contrast to the ineffective protection after the administration of antirheumatic drugs or TNF blockers [20]. A meta-analytical study by Chinese authors evaluated a total of 14 observational studies in terms of the prevalence and risk of developing hepato-pancreato-biliary lesions in individuals with IBD. A high association was found between the development of gallstones and acute pancreatitis; in addition, IBD was associated with an increase in the presence of portal system thrombosis [21]. Similarly, the prevalence of primary sclerosing cholangitis and non-alcoholic fatty liver disease (NAFLD), autoimmune hepatitis, and autoimmune pancreatitis was also increased compared to the general population.

Conclusion

Globally and in our domestic conditions, the incidence and prevalence of IBD is increasing significantly. Patients with ulcerative colitis and Crohn's disease have a higher risk of developing extraintestinal manifestations or associated diseases, including acute pancreatitis, which has several different causes in patients with IBD. Most often, it is a side effect of drug therapy, especially azathioprine and mesalazine, or it is autoimmune pancreatitis or pancreatitis induced by pancreatic duct involvement in primary sclerosing cholangitis. It is important to note the increased incidence of cholelithiasis, especially in patients after repeated ileocolonic resections, which may be responsible for the biliary form of acute pancreatitis. Some studies have found a link between the risk of developing acute pancreatitis and the severity of intestinal disease.

ORCID autorů

P. Ditě 0000-0002-1882-3051,
D. Solil 0009-0004-3343-3424,
M. Uvírová 0000-0002-2783-5724,
T. Kupka 0000-0001-5510-8498,
M. Konečný 0000-0002-7119-8881,
J. Dolina 0000-0002-4204-4082,
B. Kianička 0000-0003-0988-5928.

Doručeno/Submitted: 12. 12. 2025
Přijato/Accepted: 22. 12. 2025

Korespondenční autor prof. MUDr. Petr Dítě, DrSc.
Interní gastroenterologická klinika
LF MU a FN Brno
Jihlavská 20
625 00 Brno
Pdite.epc@gmail.com

Literatura

1. Iang W, Du Y, Xiang C et al. Age period – cohort analysis of pancreatitis epidemiological trends from 1990 to 2019 and forecasts 2044: a systematic analysis from global Burden of Disease Study 2019. Front Publ Health 2023; 11: 1118888. doi: 10.3389/fpubh.2023.1118888.
2. Zheng F, Li J, Ma L et al. Acute pancreatitis risk in the diagnosis and management of inflammatory bowel disease: a critical focus. Open Med 2025; 20(1): 20251189. doi: 10.1515/med-2025-1189.
3. Cai QY, Tan K, Zhang XL et al. Incidence, prevalence and comorbidities of chronic pancreatitis: s 7-year population-based study. World J Gastroenterol 2023; 29(30): 4671–4384. doi: 10.3748/wjg.v29.i30.4671.
4. Schneider S, Hirth M, Weiss C et al. Prevalence of inflammatory bowel disease in alcoholic, non-alcoholic and autoimune pancreatitis. Z Gastroenterol 2018; 56(5): 469–478. doi: 10.1055/s-0043-123881.
5. Tél B, Stubnya B, Gede N et al. Inflammatory bowel disease elevate the risk of developing acute pancreatitis: a meta-analysis. Pancreas 2020; 49(9): 1174–1186. doi: 10.1097/MPA.0000000000001650.
6. Lee H, Lee E, Do GY et al. Histone deacetylase inhibitor MGCD00103 protects the pancreas from streptozotocin-induced oxidative and beta-cells death. Biomed Pharmacother 2019; 109: 921–929. doi: 10.1016/j.biopha.2018.10.163.
7. Venkatesh K, Glenn H, Delaney A et al. Fire in the belly: a scoping review of the imunopathological mechanisms of acute pancreatitis. Front Immunol 2022; 13: 1077414. doi: 10.3389/fimmu.2022.1077414.
8. Kim JW, Hwang SW, Park SH et al. Clinical course of ulcerative colitis in patients who develop acute pancreatitis. World J Gastroenterol 2017; 23(19): 3505–3512. doi: 10.3748/wjg.v23.i19.3505.
9. Ng WK, Wong SH, Ng SC et al. Changing epidemiological tends of inflammatorybowel disease in Asia. Intest Res 2016; 14(2): 111–119. doi: 10.5217/ir.2016.14.2.111.
10. Barthet M, Hastier P, Bernard JP et al. Chronic pancreatitis an inflammatory bowel disease: true or coincidental association? Am J Gastroent 1999; 94(8): 2141–2148. doi: 10.1111/j.1572-0241.1999.01287.x.
11. Rothfuss KS, Stange EF, Herrlinger KR. Extraintestinal manifestations and complications in inflammatory bowel diseases. World J Gastroenterol 2006; 12(30): 4819–4831. doi: 10.3748/wjg.v12.i30.4819.
12. Bernejo F, Lopez Sanroman A, Taxonera C et al. Acute pancreatitis in inflammatory bowel disease with special reference to azathioprine-induced panreatitis. Aliment Pharmacol Ther 2008; 28(5): 623–628. doi: 10.1111/j.1365-2036.2008.03746.x.
13. Inoue H, Shiraki K, Okano H et al. Acute pancreatitis in patients with ulcerative colitis. Dig Dis Sci 2005; 50(6): 1064–1067. doi: 10.1007/s10620-005-2705-7.
14. Ueki T, Kawamoto K, Otsuka Y et al. Prevalence and clinicopathological features of autoimmune pancreatitis in Japanese patients with inflammatory bowel disease. Pancreas 2015; 44(3): 434–440. doi: 10.1097/MPA.0000000000000261.
15. Park SH, Kim D, Ye BD et al. The characteristics of ulcerative colitis associated with autoimmune pancreatitis. J Clin Gastroenterol 2013; 47(6): 520–525. doi: 10.1097/MCG.0b013e31827fd4a2.
16. Bellocchi MC, Mottes MC, Blesl A et al. Acute pancreatitis in inflammatory bowel disease: results from the European Pandora Study. Medicina 2025; 61(9): 1532. doi: 10.3390/medicina6091532.
17. Banks PA, Bollen TE, Dervenis C et al. Classification of acute pancreatitis – 2012: revision of the Atlanta classification and definition by international consensus. Gut 2013; 62(1): 102–111. doi: 10.1136/gutjnl-2012-302779.
18. Sanderson E, Glymour MM, Holmes MV et al. Mendelian randomization. Nat Rev Methods Primers 2022; 2: 6. doi: 10.1038/43586-021-00925-5.
19. Lei Y, Zang L, Liu S et al. Parabacteroides produces acetate to alleviate heparanase-exacerbate acute pancreatitis through reducing neutrophil infiltration. Microbiome 2021; 9(1): 115. doi: 10.1186/s40168-021-01065-2.
20. Chang CC, Chiou CS, Lin HL et al. Increased risk of acute pancreatitis in patients with rheumatoid arthritis: a population-based cohort study. PLoS One 2015; 10(8): e0135187. doi: 10.1371/journal.pone.0135187.
21. Hong R, Li Z, Li M et al. Hepatobiliary and pancreatic manifestations in inflammatory bowel disease: an umbrella review of metaanalyses. Ther Adv Gastroenterol 2025; 18: 17562848241311165. doi: 10.1177/17562848241311165.