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. 2026 Jul 31;105(31):e49906. doi: 10.1097/MD.0000000000049906

The causal association between inflammatory bowel disease and pancreatitis: A 2-sample Mendelian randomization study

Zetian Gao a, Xie Zhang a, Dihui Cai a, Yufei Song a, Jingyu Kang a, Qiubo Zhang a,*
PMCID: PMC13433129  PMID: 42536580

Abstract

Clinical studies showed a relationship between inflammatory bowel disease (IBD) and pancreatitis. Nonetheless, the causal relationship between IBD and pancreatitis has yet to be established. We employed Mendelian randomization (MR) to determine potential causal associations between IBD and pancreatitis. Genome-wide association study data on IBD were acquired from the International Inflammatory Bowel Disease Genetics Consortium. Summary statistics for pancreatitis were from the FinnGen database and BioBank Japan. Inverse-variance weighting (IVW) was used to perform a 2-sample MR analysis. Heterogeneity tests, horizontal pleiotropy tests, and sensitivity analyses were used to ensure the consistency and accuracy of our results. In the European population, the incidence of acute pancreatitis (AP) in IBD populations was a 6.3% higher risk than in the control population (odd ratio [OR]: 1.063, 95% confidence interval [CI]: 1.008–1.121, IVW P = .023), while chronic pancreatitis (CP) was elevated by 7.5% (OR: 1.075, 95% CI: 1.004–1.153, IVW P = .039). The incidence of AP (OR: 1.056, 95% CI: 1.010–1.105, IVW P = .017) and CP (OR: 1.070, 95% CI: 1.009–1.135, IVW P = .024) in Crohn disease (CD) populations were higher than in the control population. AP incidence in ulcerative colitis (UC) populations was a 7.0% higher risk than in the control population (OR: 1.070, 95% CI: 1.007–1.137, IVW P = .030), and AAP incidence was elevated by 18.9% (OR: 1.189, 95% CI: 1.009–1.135, IVW P = .024). In the East Asian population, UC has a causality relationship with CP (OR: 1.290, 95% CI: 1.119–1.487, IVW P = .0004). In the European population, IBD and its 2 types have potential causality with AP; IBD and CD have potential causality with CP. In the East Asian population, UC has a causal association with CP.

Keywords: causal association, inflammatory bowel disease, Mendelian randomization, pancreatitis

1. Introduction

Inflammatory bowel disease (IBD) is a subset of chronic nonspecific intestinal inflammation, which contains ulcerative colitis (UC) and Crohn disease (CD).[1] The etiology of IBD is unknown; it is believed to be related to intestinal abnormalities and immune imbalances caused by the interaction of environmental, genetic, and intestinal microecological regulators. Under the influence of environmental factors and intestinal microorganisms, genetically susceptible individuals develop intestinal immune imbalances and damage to the intestinal mucosal barrier, leading to inflammatory damage of the intestinal mucosa.[2] IBD has become a global public health challenge, especially in Europe and North America.[3] In developed countries, the incidence of IBD has stabilized; however, the prevalence remains high. In contrast, in developing countries, the incidence of IBD rises yearly.[4]

Acute pancreatitis (AP) is an inflammatory disease caused by the self-digestion of pancreatic tissue. AP is characterized by pancreatic edema, hemorrhage, and necrosis. Chronic pancreatitis (CP) is a chronic, progressive, inflammatory pancreatic disease. CP is characterized by irreversible damage to the internal and external secretory functions of the pancreas. IBD is a multisystem disease; most patients have extraintestinal manifestations, adversely affecting daily life.[5] Excessive alcohol intake is a cause of AP and CP.[6,7] Therefore, pancreatitis can be classified as alcohol-induced AP (AAP) or alcohol-induced CP (ACP). Pancreatic inflammation is a general extraintestinal manifestation of IBD, which includes AP and CP.[8] Clinical studies showed that IBD was closely related to pancreatic disease, primarily acute pancreatitis,[2] chronic pancreatitis, and autoimmune pancreatitis. In recent years, an increasing number of case reports and clinical studies have indicated that AP is more prevalent in IBD; however, the number of population-based studies remains limited, and consequently, robust evidence supporting this association is also scarce.

Mendelian randomization (MR) analysis is an epidemiological instrument that uses genetic instrumental variables (IVs) to produce conclusions regarding causality. Genetic variants are randomly allocated when inherited from parents to offspring. Single nucleotide polymorphisms (SNPs) can infer causal relationships between exposure and outcomes, minimizing confounding and reverse causality.[9]

Nevertheless, the causal relationship between IBD and pancreatitis has not been explored in an MR study. Therefore, we used the MR method to identify the causal inference between IBD and pancreatitis.

2. Materials and methods

2.1. Data source and study design

The genome-wide association study data for IBD were acquired from the International Inflammatory Bowel Disease Genetics Consortium, a public network devoted to the genetics of IBD, including 65,642 European participants (31,665 diagnosed with IBD and 33,977 controls) and 6543 East Asian participants (2,824 diagnosed with IBD and 3719 controls).[10] The CD subtype included 51,874 European participants (17,897 CD cases and 33,977 control cases) and 5409 East Asian participants (1,690 diagnosed with CD and 3719 controls). The UC subtype contained 27,432 European participants (6,968 UC cases and 20,242 control cases) and 4853 East Asian participants (1,134 diagnosed with UC and 3719 controls). To avoid sample size overlap, we collected summary statistics for AP, CP, AAP, and ACP from the FinnGen database (https://risteys.finngen.fi). The FinnGen database contains 3022 AP cases and 1,95,144 controls, 1737 CP cases and 1,95,144 controls, 457 AAP cases, 2,18,335 controls, 977 ACP cases, and 2,17,815 controls. We also collected 827 AP cases and 1,77,471 controls, and 457 CP cases and 1,77,471 controls in the East Asian population.[11] Summary statistics are displayed in Table S1, Supplemental Digital Content 2.

Due to the data in the study from the publicly available GWASs, the necessity for obtaining approval from the ethical committee was exempted.

Three assumptions were adopted in the MR analysis: IVs have a tight relationship with exposure (IBD, CD, and UC); IVs have no relationship with potential confounders (smoking, drinking, body mass index, and diabetes); IVs have no direct relationship with the outcome and only affect the outcome (AP, CP, AAP, and ACP) by associated exposure (Fig. 1).

Figure 1.

Figure 1.

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Design of this Mendelian randomization study. This study was performed with independent cancer genome-wide association study (GWAS) datasets from the International Inflammatory Bowel Disease Genetics Consortium, FinnGen and other international consortiums. AAP = alcohol-induced acute pancreatitis, ACP = alcohol-induced chronic pancreatitis, AP = acute pancreatitis, CD = Crohn disease, CP = chronic pancreatitis, IBD = inflammatory bowel disease, IV = instrumental variable, IVW = Inverse-variance weighting, MR = Mendelian randomization, SNP = single nucleotide polymorphism, UC, ulcerative colitis.

2.2. Selection of IVs

SNPs at the genome-wide significance threshold (P < 5 × 10−8) were selected as IVs. To guarantee the independence between each SNP, the linkage disequilibrium threshold for grouping was set to r2 < 0.001, and genetic distance was set to 10,000 kb (Table S2, Supplemental Digital Content 3). Each included SNP was searched in PhenoScanner. SNPs strongly associated with confounders (smoking, drinking, body mass index, and diabetes) were excluded (P < 5 × 10−6). The details of removed SNPs were listed in Table S3, Supplemental Digital Content 4. F-statistics (F = beta2/se2) were calculated to avoid the weak instrument bias of the included IVs. F-statistics < ten explained that the included IVs were weakly associated with exposure, and these IVs had been eliminated.

2.3. Statistical analysis

A 2-sample MR analysis (R 4.3.0 and TwoSampleMR package 0.6.29) was performed to verify the causality between IBD (including CD and UC) and pancreatitis (AP, CP, AAP, and ACP). Causality between exposure and outcome was confirmed using inverse-variance weighting (IVW). This method is the most credible and is often the first option. We also performed MR-Egger regression and weighted median analysis to minimize the confounding factor produced by heterogeneity and horizontal pleiotropy.[12] We calculated the odds ratio (OR) and 95% confidence interval (CI) for MR results. The heterogeneity among the IVs was calculated using Cochran Q test.[13] If the p of heterogeneity > 0.05, the fixed effects model was used; otherwise, the multiplicative random effects model was used.[14] We also employed I2 (I2 = (Q–Q_df)/Q) to further evaluate heterogeneity, with I2 < 25% indicating no significant heterogeneity. Horizontal pleiotropy was assessed using MR-Egger intercept analysis.[15] MR-pleiotropy residual sum and outlier were applied to locate outliers in IVW linear regression and correct MR estimates after removing outliers.[12] The leave-one-out method was performed to confirm the influence of a single SNP on the causal association. Power calculations were conducted to validate the reliability of our results (shiny.cnsgenomics.com). We performed a reverse causality analysis to determine reverse causality.

3. Results

3.1. Selection of instrumental variables

In the European population, we identified 117, 111, and 34 SNPs for IBD, CD, and UC, respectively. All IBD, CD, and UC SNPs met three criteria, whose detailed characteristics are displayed in Tables S4–S6, Supplemental Digital Content 5. No weak tool bias was found in exposure factors, as F statistics for all SNPs of exposure were higher than 10.

In East Asian population, we identified 7, 12, and 10 SNPs for IBD, CD, and UC (Tables S7–S9, Supplemental Digital Content 6). No weak tool bias was found in exposure factors, as F statistics for all exposure SNPs were higher than 10.

3.2. Causal effects of IBD, UC, or CD on pancreatitis

Bonferroni correction (corrected P = .05/12 = 0.004) was used to address the issue of multiple testing. P values ranging from .004 to .05 were deemed to indicate potential causality between the exposures and the outcomes, while P values <.002 were interpreted as signifying a significant causal relationship. We performed power analysis in Table S10, Supplemental Digital Content 7.

In European population, the genetically predicted results between IBD and pancreatitis are shown in Figure 2. The IVW analysis revealed that the incidence of AP in IBD populations was a 6.3% higher risk than in the control population (OR: 1.063, 95% CI: 1.008–1.121, IVW P = .023, statistical power = 72%). The CP incidence in IBD populations was a 7.5% higher risk than in the control population (OR: 1.075, 95% CI: 1.004–1.153, IVW P = .039, statistical power = 65%). There was inadequate evidence to suggest that IBD had a causal association with AAP (OR: 1.121, 95% CI: 0.982–1.281, IVW P = .092, statistical power = 47%) or ACP (OR: 0.982, 95% CI: 0.896–1.077, IVW P = .697, statistical power = 7%). Based on the IVW approach (Fig. 3), AP incidence in CD populations was approximately a 5.6% higher risk than in the control population (OR: 1.056, 95% CI: 1.010–1.105, IVW P = .017, statistical power = 76%). The CP incidence in CD populations was approximately a 7.0% higher risk than in the control population (OR: 1.070, 95% CI: 1.009–1.135, IVW P = .024, statistical power = 71%). There was inadequate evidence to suggest that CD had a causal relationship with AAP (OR: 1.076, 95% CI: 0.961–1.205, IVW P = .205, statistical power = 28%) or ACP (OR: 1.045, 95% CI: 0.967–1.130, IVW P = .266, statistical power = 24%). As shown in Figure 4, AP incidence in UC populations was a 7.0% higher risk than in the control population (OR: 1.070, 95% CI: 1.007–1.137, IVW P = .030, statistical power = 81%). The AAP incidence in UC populations was an 18.9% higher risk than in the control population (OR: 1.189, 95% CI: 1.009–1.135, IVW P = .024, statistical power = 84%). There is no evidence that UC had a causal association with CP (OR: 1.048, 95% CI: 0.967–1.134, IVW P = .253, statistical power = 34%) and ACP (OR: 1.015, 95% CI: 0.913–1.129, IVW P = .778, statistical power = 6%). The MR-Presso and weighted median were consistent with the IVW analysis. Given the insufficient sample sizes of AAP and ACP in the European population, the result of MR analysis may be limited. In the European population, our research has found that IBD and its 2 types have potential causality with AP, and IBD and CD have potential causality with CP.

Figure 2.

Figure 2.

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Causal relationship between IBD and pancreatitis in the European population. AAP = alcohol-induced acute pancreatitis, ACP = alcohol-induced chronic pancreatitis, AP = acute pancreatitis, CI = confidence interval, CP = chronic pancreatitis, IBD = inflammatory bowel disease, IVW = Inverse-variance weighting, MR = Mendelian randomization, OR = odds ratio.

Figure 3.

Figure 3.

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Causal relationship between CD and pancreatitis in the European population. AAP = alcohol-induced acute pancreatitis, ACP = alcohol-induced chronic pancreatitis, AP = acute pancreatitis, CD = Crohn disease, CI = confidence interval, CP = chronic pancreatitis, IVW = Inverse-variance weighting, MR = Mendelian randomization, OR = odds ratio.

Figure 4.

Figure 4.

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Causal relationship between UC and pancreatitis in the European population. AAP = alcohol-induced acute pancreatitis, ACP = alcohol-induced chronic pancreatitis, AP = acute pancreatitis, CI = confidence interval, CP = chronic pancreatitis, IVW = Inverse-variance weighting, MR = Mendelian randomization, OR = odds ratio, UC = ulcerative colitis.

In the East Asian population, we have not discovered the GWAS data for AAP and ACP. The results show that UC has a causal association with CP (OR: 1.290, 95% CI: 1.119–1.487, IVW P = .0004, statistical power = 100%). The incidence of CP in UC populations is 29% higher than in the control population. We found no causal association between IBD and AP (OR: 1.071, 95% CI: 0.926–1.240, IVW P = .357, statistical power = 21%), IBD and CP (OR: 1.105, 95% CI: 0.908–1.345, IVW P = .318, statistical power = 24%), CD and AP (OR: 1.050, 95% CI: 0.972–1.135, IVW P = .215, statistical power = 5%), CD and CP (OR: 1.000, 95% CI: 0.901–1.111, IVW P = .995, statistical power = 17%), or UC and AP (OR: 0.940, 95% CI: 0.846–1.045, IVW P = .252, statistical power = 28%) in the East Asian population (Fig. 5). The sample size of East Asian populations is generally smaller than European populations, which may render the MR results unreliable.

Figure 5.

Figure 5.

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Causal relationship between IBD, CD, UC, and pancreatitis in the East Asian population. AP = acute pancreatitis, CD = Crohn disease, CI = confidence interval, CP = chronic pancreatitis, IBD = inflammatory bowel disease, IVW = Inverse-variance weighting, MR = Mendelian randomization, OR = odds ratio, UC = ulcerative colitis.

3.3. MR sensitivity analysis

All Cochran Q tests and I2 showed that heterogeneity was not significant (P > .05); the fixed effects model was used (Table 1). Based on the MR-Egger intercept test results, MR pleiotropy residual sum, and outlier MR-PRESSO global test, we confirmed no evidence of horizontal pleiotropy (Table 1). There were no MR-pleiotropy residual sum and outlier analyses revealing outliers to influence MR results of IBD, CD, and UC, demonstrating the reliability of the causal relationship. The leave-one-out method confirmed that no single SNP influenced the causal association of all IVs (Supplementary Material 1 and 2, Supplemental Digital Content 1). Scatter plots demonstrated the causal effects of IBD, UC, or CD on pancreatitis risk (Supplementary Material 3 and 4, Supplemental Digital Content 8).

Table 1.

Sensitivity analysis of MR.

Population Exposures Outcomes Heterogeneity Pleiotropy
Cochran Q P I 2 MR-Egger intercept P MR-PRESSO global test P
European IBD AP .795 0.00% .452 .822
CP .112 14.12% .309 .121
AAP .526 0.00% .13 .528
ACP .698 0.00% .503 .735
CD AP .847 0.00% .803 .858
CP .259 7.78% .895 .289
AAP .579 0.00% .441 .562
ACP .444 1.29% .741 .528
UC AP .994 0.00% .354 .999
CP .119 24.00% .287 .115
AAP .961 0.00% .74 .96
ACP .153 21.05% .462 .122
East Asian IBD AP .688 0.00% .824 .737
CP .995 0.00% .679 .998
CD AP .641 0.00% .477 .644
CP .983 0.00% .605 .984
UC AP .874 0.00% .789 .934
CP .359 9.24% .468 .372
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AAP = alcohol-induced acute pancreatitis, ACP = alcohol-induced chronic pancreatitis, AP = acute pancreatitis, CD = Crohn disease, CP = chronic pancreatitis, IBD = inflammatory bowel disease, MR = Mendelian randomization, UC = ulcerative colitis.

3.4. Reverse MR analysis

We performed reverse 2-sample MR analysis to investigate the bidirectional causal relationship between pancreatitis and IBD. Given the limited number of available SNPs, we relaxed the significance threshold to 5 × 10-6 when analyzing pancreatitis as exposure factors. The results show no significant association between pancreatitis and UC in European populations (Tables S11–S14, Supplemental Digital Content 9). However, constrained by the sequencing depth of IBD and its subtypes within the GWAS data, we were unable to identify sufficient SNPs for MR analysis in the outcome data for IBD and CD in European populations, or for IBD, CD, and UC in Asian populations.

4. Discussion

IBD is characterized by inflammation caused by an excessive host immune response and mucosal barrier disruption.[16] The gut harbors a substantial community of commensal microorganisms. Most of these bacteria are beneficial and contribute to food metabolism, immune response, and the elimination of pathogens.[17] However, some bacteria can promote pathological changes and disease development in specific environmental or genetic conditions.[17] Several defense mechanisms of the gut defend against IBD-induced intestinal inflammation. The pancreas also exerts a significant role in fighting intestinal inflammation. The pancreas performs digestive and endocrine functions. The pancreas secretes secretory phospholipase A2, pancreatic lipase, and glycoprotein 2 to protect the gut and maintain the flora through bacterial lysis.[18] Conversely, the gut can influence pancreatic endocrine function through vasoactive intestinal peptides such as secretin, glucagon-releasing peptide, and growth inhibitor.[19]

Dysbiosis of the intestinal flora due to IBD can affect pancreatic function and increase the risk of pancreatic disease. Previous studies showed that IBD patients have a higher risk of pancreatitis,[20] pancreatic cancer,[21] and type II diabetes.[22] In addition, intestinal bacteria can be transferred to the pancreas under pathologic conditions.[23] Increased intestinal microorganisms and weakened epithelial barrier function in IBD can cause or exacerbate pancreatitis and even contribute to acute necrotizing pancreatitis.[24] Various proteases released by the pancreas can maintain gut homeostasis. Neurons activated by gut microbes also regulate pancreatic function. Intestinal disruption is critical for the development of pancreatitis. IBD can contribute to irreversible intestinal dysfunction and exacerbate the risk of pancreatitis. IBD patients with suspected pancreatic dysfunction should be evaluated to rule out concurrent pancreatic disease.

AP is one of the most prevalent pancreatic disorders in IBD.[25] The primary etiologies of AP in inflammatory bowel disease patients include medication and biliary stones, while endoscopic retrograde cholangiopancreatography (ERCP), alcohol,[26] hypercalcaemia, and hypertriglyceridemia appear to be less frequent causes.[27] Some APs caused by pathogenesis similar to IBD or systemic inflammation are also recognized as extraintestinal manifestations of IBD.[28] IBD and its 2 subtypes contribute to the risk of AP. A study of 11,909 patients with IBD and 47,636 patients without IBD showed that the overall incidence of AP was 3.56-fold higher in the IBD cohort than in the control cohort. After adjustment for multiple influencing factors, the adjusted hazard ratio in the IBD cohort was 2.93-fold higher.[29] In 1 study, 70 percent of EIMs occurred after the diagnosis of IBD, and very few EIMs occurred before the diagnosis.[30] A retrospective study of 3960 patients with IBD showed that only 0.3% had AP before being diagnosed with IBD.[31] A case report showed that presymptomatic CD was diagnosed in a 16-year-old child patient just after the onset of idiopathic acute pancreatitis, which was likely an EIM of CD.[32] Meanwhile, the prevalence of CP is more frequent in IBD patients than in the general population (5.75 and 0.56 per 10,000 person-years, respectively).[33] A study found that 56% of CD patients developed CP.[33] An autopsy study found that 53% of 86 UC patients had chronic interstitial pancreatitis.[34] Accumulating evidence from clinical studies and case reports has confirmed that the incidence of pancreatitis shows a notable rise after a definitive diagnosis of IBD is established. Meanwhile, it is well established that inflammatory bowel disease can raise the incidence of pancreatitis, which is attributed not only to the induction of systemic inflammatory reactions but also to the pharmacological interventions used in its clinical management. The incidence of pancreatitis among IBD patients is typically associated with IBD treatment, particularly with thiopurines, corticosteroids, and biological agents.[35] Azathioprine is more prone to induce drug-related acute pancreatitis, with its underlying mechanisms involving immune reactions and direct toxic effects; nevertheless, clinical conditions often show marked improvement after drug withdrawal.[26] Autoimmune pancreatitis is classified as type 1 or type 2 in adults, whereas pediatric autoimmune pancreatitis (AIP) shows similar features to type II AIP in adults. Approximately 30% of AIP is related to IBD or other autoimmune diseases. However, there is a lack of AIP-related genome-wide association data, and we did not validate it in MR analysis.

Myosin IXB mediates tight junction assembly and actin filament remodeling to regulate mucosal barrier function[36]; its gene is strongly related to intestinal permeability impairment and IBD.[36-38] Several subtypes are associated with UC, CD, and pancreatitis, predicting a solid association and similar mechanisms between IBD and pancreatitis.[39] Recent studies found an immune imbalance in both pancreatitis and IBD, as evidenced by abnormally elevated IL-1β, IL-6, and IL-10, which may contribute to the elevated risk of pancreatitis in IBD patients.[40] MUC1 is a transmembrane glycoprotein usually low-expressed on pancreatic ductal epithelia and over-expressed on colonic epithelium. MUC1-specific T cells in IBD mice migrated toward the colon and pancreas, increasing MUC1 expression in the pancreatic ductal epithelium. This result suggests that IBD can promote pancreatitis development through MUC1 in mice.[41]

IBD and pancreatitis are diseases with diversified pathogenesis. Genetic diversity may be central to identifying the genetic relationships among species. Clinical study revealed an association between IBD and pancreatitis; however, the findings may be affected by sample size and residual confounding.[42] Moreover, the underlying genetic risk remains unexplained. Our study first verified the causal relationship between IBD and pancreatitis using an MR method. In the European population, we found that IBD has potential causality with AP and CP. CD has potential causality with AP and CP. UC had a causal potential relationship with AP. In the East Asian population, UC has a causal association with CP. Several confidence intervals are very wide or close to including 1.0, which is constrained by sample size in analyses. The genetic instruments for IBD and its subtypes in our study were selected based on GWAS results with stringent thresholds (P < 5 × 10-8). All selected instruments had F-statistics > 10, meeting the criterion for avoiding weak instrument bias, which ensures the reliability of our causal inference despite the CI imprecision. These identical GWAS datasets have also been employed in prior MR studies, and no inter-dataset overlap existed in those analyses.[43] Moreover, all sensitivity analyses predicted no heterogeneity and horizontal pleiotropy, minimizing bias. Importantly, our study provides a theoretical foundation for preventing and treating pancreatitis in IBD patients. For patients with inflammatory bowel disease, the emergence of abdominal pain during treatment warrants vigilance for the development of pancreatitis.

Our study has some limitations. First, the sample sizes of AAP and ACP are relatively modest, which may compromise the reliability of the study results in the European population. Although we investigated both European and East Asian populations, the relatively small sample size of the East Asian cohort led to divergent findings compared with the European group. Statistical power values for some results are below 80%, which compromises their reliability. We will expand the sample size in subsequent research to improve the reliability of these results. Secondly, the association between IBD patients and pancreatitis cases with distinct etiologies – specifically cholelithiasis, drug-related causes, and autoimmune diseases – was not examined in the current research. Lastly, a limitation of the present study is that we have neither clarified the biological mechanisms mediating the link between IBD and pancreatitis nor validated the corresponding signaling pathways. In subsequent experimental investigations, we intend to experimentally verify these potential biological mechanisms, with a specific focus on genetic loci, inflammatory signaling pathways (NF-κB, MAPK), and immune factors (IL-1β, IL-6, and IL-10).

5. Conclusion

In a nutshell, the present Mendelian randomization study demonstrates that in the European population, IBD and its 2 subtypes have a potential causality with AP, whereas IBD and CD are potentially causal for CP. In the East Asian population, a significant causal association was observed exclusively between UC and CP. Nevertheless, the pathophysiologic pathways and potential biological mechanisms associated with pancreatitis in IBD patients require further study.

Acknowledgments

We appreciate the previous studies and databases that accommodated our use of genome-wide association study summary data.

Author contributions

Conceptualization: Zetian Gao, Dihui Cai, Qiubo Zhang.

Data curation: Zetian Gao.

Formal analysis: Xie Zhang, Dihui Cai, Yufei Song.

Funding acquisition: Yufei Song.

Methodology: Dihui Cai.

Software: Zetian Gao, Xie Zhang, Jingyu Kang.

Supervision: Xie Zhang, Jingyu Kang, Qiubo Zhang.

Writing – original draft: Zetian Gao, Qiubo Zhang.

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Abbreviations:

AAP
alcohol-induced acute pancreatitis
ACP
alcohol-induced chronic pancreatitis.
AIP
autoimmune pancreatitis
AP
acute pancreatitis
CD
Crohn disease
CI
confidence interval
CP
chronic pancreatitis
ERCP
endoscopic retrograde cholangiopancreatography
IBD
Inflammatory bowel disease
MR
Mendelian randomization
UC
ulcerative colitis

The R code of this study is available upon reasonable request from the corresponding author.

This work was supported by the Zhejiang Natural Fund Project (Grant No. LQ21H090001) and the Ningbo Public Welfare Project (Grant No. 2021S183).

Owing to the data in the study being retrieved from the publicly available GWASs, the necessity for obtaining approval from the ethical committee was exempted. The research reported has adhered to the Declaration of Helsinki.

The authors have no conflicts of interest to disclose.

The datasets generated during and/or analyzed during the current study are publicly available.

Supplemental Digital Content is available in the online version of this article (http://dx.doi.org/10.1097/MD.0000000000049906).

How to cite this article: Gao Z, Zhang X, Cai D, Song Y, Kang J, Zhang Q. The causal association between inflammatory bowel disease and pancreatitis: A 2-sample Mendelian randomization study. Medicine 2026;105:31(e49906).

Contributor Information

Zetian Gao, Email: 2459962802@qq.com.

Xie Zhang, Email: ice_girl_sunny@163.com.

Dihui Cai, Email: caidihui@163.com.

Yufei Song, Email: 517582445@qq.com.

Jingyu Kang, Email: kangjinyu1222@163.com.

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medi-105-e49906-s001.pdf (153.5KB, pdf)
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