Peri-appendiceal inflammation is associated with appendiceal orifice stenosis and appendiceal body thickening in ulcerative colitis: A case

Abstract

Objective

This case–control study aimed to investigate whether peri-appendiceal inflammation is associated with orifice stenosis and appendiceal body thickening in patients with ulcerative colitis.

Methods

Data from patients with ulcerative colitis—including demographics, symptoms, medications, clinical signs, diagnosis, laboratory tests, colonoscopy findings, and abdominal computed tomography—were recorded and analyzed. Orifice stenosis was defined as apparent narrowing or disappearance of the appendiceal orifice compared with the nearest cecal fold. A thickened appendiceal body was defined as an appendiceal >6 mm with or without surrounding inflammatory changes on computed tomography. The severity of peri-appendiceal inflammation was scored using the Mayo endoscopic score.

Results

A total of 169 patients with ulcerative colitis were included, of whom 17.2% (29/169) had appendiceal orifice stenosis. Appendiceal orifice stenosis was associated with age (odds ratio: 1.042, P = 0.008) and the peri-appendiceal inflammation score (odds ratio: 3.382, P < 0.001). Among 42 patients who underwent abdominal computed tomography, 69.0% (29/42) had appendiceal body thickening. None of these 29 patients had a positive McBurney sign or a flare of acute appendicitis. Appendiceal width was associated with the peri-appendiceal inflammation score (odds ratio: 4.172, P = 0.006).

Conclusions

Appendiceal orifice stenosis and appendiceal body thickening are prevalent in patients with ulcerative colitis. Peri-appendiceal inflammation is associated with the severity of stenosis and appendiceal width, suggesting it may serve as an indirect indicator of appendiceal inflammation related to ulcerative colitis.

Keywords

Peri-appendiceal inflammation appendiceal orifice stenosis appendiceal body thickening ulcerative colitis ulcerative colitis-related appendiceal inflammation

Introduction

Ulcerative colitis (UC) is a subtype of inflammatory bowel disease (IBD) characterized by continuous mucosal inflammation extending from the rectum to the proximal colon.¹ However, the concept of continuous mucosal involvement may be misleading. Several studies have reported independent inflammation of the appendix in patients with UC.^2,3 In 1993, Saitoh et al. first described peri-appendiceal orifice inflammation and peri-appendiceal red patch (PARP) on endoscopy.⁴ Subsequent reports have described appendiceal peri-orifice inflammation or PARP in UC, observed in up to 70% of patients with proctitis or left-sided colitis.^5–7 This inflammation may even precede the clinical onset of UC.⁸ The peri-appendiceal inflammation demonstrates the same endoscopic characteristics as UC, including erythema, erosions, loss of vascular pattern, and mucosal bleeding.⁹

In surgically resected appendiceal specimen, appendiceal inflammation has been reported in 60%–80% of patients with UC.^3,10,11 The pathological characteristics of appendiceal inflammation in UC are similar to those observed elsewhere in the colon but differ from those of acute appendicitis.¹² Unlike the transmural inflammation typical of acute appendicitis, UC-related appendiceal inflammation shows chronic mucosal inflammation, crypt abscesses, goblet cell depletion, and Paneth cell metaplasia. Appendectomy has been shown to improve UC, suggesting that the appendix may be a “critical organ” in the pathogenesis of UC and a potential initiating site of immune dysregulation and dysbiosis.^2,8,13

The clinical diagnosis of UC-related appendiceal inflammation is challenging. Because of the narrow lumen of the appendix, endoscopic observation is often difficult. Clinically, we have noted that in some patients with UC and PARP, the appendiceal orifice is narrowed, making ultra-thin endoscopic observation impossible. In addition, we observed that in some patients with UC and PARP, abdominal computed tomography (CT) revealed thickening of the appendix. These findings suggest that peri-appendiceal inflammation or PARP may serve as a diagnostic indicator of UC-related appendiceal inflammation. Therefore, the aim of this study was to investigate whether peri-appendiceal inflammation is associated with orifice stenosis and appendiceal body thickening (ABT) in patients with UC.

Methods

Case selection

A retrospective case–control study was conducted. The clinical files of 186 consecutive patients who were initially diagnosed with UC from March 2015 to June 2022 were reviewed in detail by two senior physicians with expertise in IBD. Discrepancies were resolved through discussion. Inclusion criteria were as follows: (a) age 18–80 years (both sexes); (b) a confirmed diagnosis of UC verified by two IBD specialists; and (c) complete clinical and endoscopic records available for retrospective review. Exclusion criteria were as follows: (a) unclear or indeterminate diagnosis of UC; (b) inadequate bowel preparation; (c) failure to achieve cecal intubation during colonoscopy; and (d) missing or incomplete clinical data. Twelve cases were excluded due to uncertain diagnosis, one due to a final diagnosis of Crohn’s disease, three due to incomplete insertion of the colonoscope into the cecum, and one due to unsatisfactory bowel preparation. Ultimately, 169 patients with UC were included in the analysis (Figure 1). The reporting of this study conforms to the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines.¹⁴

Figure 1.

Flow chart of patient selection. The clinical files of 186 patients initially diagnosed with UC were reviewed by two IBD experts. After excluding patients with uncertain diagnosis, Crohn’s disease, or unsatisfactory colonoscopic examinations, 169 patients with UC were included in the analysis. IBD: inflammatory bowel disease; UC: ulcerative colitis.

Information and data extraction

Electronic medical records, including medical history, laboratory tests, imaging examinations, and colonoscopy findings, were reviewed. Data on demographics, symptoms, medications, clinical signs, diagnosis, complete blood cell counts, blood biochemistry tests, C-reactive protein levels, erythrocyte sedimentation rate (ESR), colonoscopy findings, and abdominal CT scans were recorded and entered into an Excel spreadsheet. The Montreal classification was used to evaluate the extend of colitis.¹⁵ The Mayo score and Mayo endoscopic score were used to assess disease severity.¹⁶ All patient data used in this retrospective study were de-identified before analysis; no patient-identifiable information is included in the manuscript or any supplementary files. All procedures involving human participants were conducted in accordance with the Declaration of Helsinki (1975; revised in 2024) and approved by the Ethics Committee of Beijing Tsinghua Changgung Hospital (No 23380-6-01).

Definition of appendiceal internal orifice stenosis

As this was a retrospective study, quantitative measurement of the appendiceal internal orifice was not feasible. Instead, a relative and qualitative assessment was used. In the colonoscopic images, the maximal width of the appendiceal internal orifice was compared with the maximal width of the nearest cecal fold. In patients with UC and no cecal involvement, the maximal width of the appendiceal internal orifice is remarkably wider than that of the nearest cecal fold; this was defined as “no stenosis” (stenosis severity score = 0) (Figure 2(a)). Apparent narrowing of the appendiceal internal orifice compared with the cecal fold was defined as “moderate stenosis” (stenosis severity score = 1) (Figure 2(b)). A “severe stenosis” was defined as the absence of a recognizable appendiceal internal orifice (stenosis severity score = 2) (Figure 2(c)).

Figure 2.

Different severities of AOS in patients with UC. (a) No stenosis (score = 0). The internal orifice (yellow dashed line) is wider than the nearest cecal fold (white dashed line). (b) Moderate stenosis (score = 1). The internal orifice (yellow dashed line) is narrower than the nearest cecal fold (white dashed line). Peri-appendiceal inflammation was noted and (c) severe stenosis (score = 2). The internal orifice is barely visible. Peri-appendiceal inflammation is more prominent. AOS: appendiceal orifice stenosis; UC: ulcerative colitis.

Definition of ABT

ABT was evaluated using abdominal CT scans. The width of the appendiceal body was measured (Figure 3(a) and 3(b)), and inflammatory stranding of the surrounding mesenteric fat was recorded. A thickened appendiceal body was defined as a width >6 mm, with or without surrounding inflammatory changes. Typically, a maximum diameter greater than 6 mm is considered a significant suspicious sign of acute appendicitis.

Figure 3.

Abdominal CT coronal images of the appendiceal body (yellow arrowhead) in patients with UC.

Statistical analysis

Collected data were analyzed using Statistical Package for the Social Sciences (SPSS) (version 26.0, IBM Corporation, US). Figures were created using GraphPad Prism 9.3 (San Diego, CA) and R 3.5.2 (ggplot2 package). After testing for normality (Shapiro–Wilk test) and homogeneity of variances (Levene’s test), continuous data were presented as mean ± SD or median (interquartile range, IQR) as appropriate, and categorical data were presented as n (%). Depending on data distribution, either the independent samples t-test or the Mann–Whitney U test was used for comparisons between two groups. Categorical data were compared using Fischer’s exact test. Correlation analysis was performed using the Spearman rank correlation test. Univariate analysis followed by multivariate logistic regression was conducted to identify risk factors. A two-sided P-value < 0.05 was considered statistically significant.

Results

Demographic information of the included UC patients

Among the 169 patients with UC included in the study, the median age (IQR) was 43 (33–56) years. There were 100 men and 69 women. The median (IQR) symptom duration was 24 (6–50) months. According to the Montreal classification, there were 62 E1 cases, 47 E2 cases, and 60 E3 cases. The median Mayo score (IQR) was 5 (4–7.5). Regarding extraintestinal manifestations, six patients had oral ulcers, six had arthritis, two had primary sclerosing cholangitis (PSC), and one had psoriasis. Regarding prior or ongoing medications, 163 patients received mesalazine, 24 received glucocorticoids, 2 received immunosuppressants, and 8 received biologics. Only one patient underwent colectomy. PARP was observed in 112 patients (66.3%).

Appendiceal internal orifice stenosis in UC patients

Twenty-nine patients (17.2%) were noted to have appendiceal orifice stenosis (AOS). As shown in Table 1, patients with AOS tended to be older (52.4 (37–63) vs. 42 (33–55) years, P = 0.027) and had more frequent E3 classification (55.2% vs. 31.4%, P = 0.024), higher disease activity (Mayo score 6 (5–9.5) vs. 5 (3.25–7), P = 0.038), more frequent PSC (6.9% vs. 0%, P = 0.029), and more frequent PARP (96.6% vs. 60.0%, P < 0.001). The peri-appendiceal endoscopic inflammation score was remarkably higher in patients with AOS (1 (1–2) vs. 1 (0–1), P < 0.001). Multivariate logistic regression analysis suggested that age (OR): 1.042, 95% confidence interval (CI): 1.011–1.074, P = 0.008) and peri-appendiceal inflammation score (odds ratio (OR): 3.382, 95% CI: 1.865–6.133, P < 0.001) were risk factors for AOS (Table 2). Furthermore, the severity of AOS was positively correlated with the peri-appendiceal inflammation score (Figure 4(a)), (R = 0.307, P < 0.001).

Table 1.

Comparison of clinical characteristics between UC patients with AOS and UC patients without AOS.

Characteristic	UC patients with AOS (N = 29)	UC patients without AOS (N = 140)	P-value
Age, median (IQR), years	52.4 (37–63)	42 (33–55)	0.027
Sex, male:female	18:11	82:58	0.837
Symptom duration, median (IQR), months	13 (7–96)	24 (6–50)	0.477
Montreal classification, n (%)
E1	5 (17.2)	57 (40.7)	0.024
E2	8 (27.6)	39 (27.9)
E3	16 (55.2)	44 (31.4)
Backwash ileitis, n (%)	4 (13.8)	9 (6.4)	0.241
Mayo score, median (IQR)	6 (5–9.5)	5 (3.25–7)	0.038
Mayo endoscopic score, median (IQR)	3 (2–3)	2 (2–3)	0.124
Extraintestinal manifestations, n (%)
Oral ulcer	1 (3.4)	5 (3.6)	1.000
Arthritis	1 (3.4)	5 (3.6)	1.000
Psoriasis	1 (3.4)	0	0.172
Cholangitis	2 (6.9)	0	0.029
Laboratory tests
WBC, median (IQR), 10⁹/L	5.9 (4.8–7.7)	6.4 (4.9–7.8)	0.367
Hemoglobin, median (IQR), g/L	134 (114.5–147)	141 (127.3–151)	0.123
CRP, median (IQR), mg/L	6.5 (1.1–40)	4 (1.3–12)	0.169
ESR, median (IQR), mm/h	15 (7–33.3)	10.5 (5–20)	0.108
Albumin, median (IQR), g/L	45 (38–46.7)	45 (41.1–47.1)	0.441
PARP, n (%)	28 (96.6)	84 (60)	<0.001
Peri-appendiceal inflammation score, median (IQR)	1 (1–2)	1 (0–1)	<0.001
Width of appendiceal body on CT scan, median (IQR), mm	7 (4.8–7.9)	6.5 (5.7–7.9)	0.913
Previous or following treatment, n (%)
Mesalamine	25 (86.2)	138 (98.6)	0.008
Glucocorticoids	9 (31.0)	15 (10.8)	0.008
Immunosuppressant	2 (6.9)	0	0.029
Biologics	4 (13.8)	4 (2.9)	0.030
Surgery	1 (3.4)	0	0.172

UC: ulcerative colitis; AOS: appendiceal internal orifice stenosis; IQR: interquartile range; WBC: white blood cells; CRP: C-reactive protein; ESR: erythrocyte sedimentation rate; CT: computed tomography; PARP: peri-appendiceal red patch.

Table 2.

Risk factors for AOS in UC: multivariable logistic regression analysis.

Parameter	Multivariable
Parameter	B	SE	OR (95% CI)	P-value
Age	0.041	0.015	1.042 (1.011–1.074)	0.008
Peri-appendiceal inflammation score	1.229	0.303	3.418 (1.887–6.194)	<0.001

AOS: appendiceal orifice stenosis; UC: ulcerative colitis; SE: standard error; OR: odds ratio; CI: confidence interval.

Figure 4.

Positive correlation of peri-appendiceal inflammation score with (a) severity of AOS and (b) appendiceal width. AOS: appendiceal orifice stenosis.

In addition, patients with AOS were less likely to be on mesalazine and more likely to be on glucocorticoids, immunosuppressants, or biologics (all P < 0.05).

ABT in UC patients

A total of 42 patients underwent abdominal CT scans. The median width of the appendiceal body (IQR) was 6.5 (5.3–7.8) mm. Among these patients, ABT was observed in 29 cases (69.0%), and 3 patients (7.1%) had surrounding inflammatory changes. None of the patients exhibited a positive McBurney sign. During a median follow-up time period of 18 (8–37) months, none of the patients developed symptoms of acute appendicitis or underwent appendectomy.

As shown in Table 3, patients with ABT were more likely to have a PARP (86.2% vs. 46.2%, P = 0.019). The peri-appendiceal endoscopic inflammation score was remarkably higher in patients with ABT (2 (1–2) vs. 0 (0–1) mm, P = 0.003). Univariate logistic regression analysis indicated that the peri-appendiceal inflammation score was a risk factor for ABT (OR: 4.172, 95% CI: 1.511–11.523, P = 0.006) (Table 4). Furthermore, the severity of ABT was positively correlated with the peri-appendiceal inflammation score (Figure 4(b)), (R = 0.493, P = 0.001).

Table 3.

Comparison of the clinical characteristics of UC patients with and without ABT.

Characteristic	UC patients with ABT (N = 29)	UC patients without ABT (N = 13)	P-value
Age, median (IQR), years	46 (31–62)	55 (41.5–65.5)	0.122
Sex, male:female	20:9	6:7	0.187
Symptom duration, median (IQR), months	13 (7–43)	14 (2–48)	0.788
Montreal classification, n (%)
E1	4 (13.8)	2 (15.4)	0.802
E2	8 (27.6)	2 (15.4)
E3	17 (58.6)	9 (69.2)
Backwash ileitis, n (%)	7 (24.1)	1 (7.7)	0.398
Mayo score, mean ± SD	7.0 ± 3.7	7.0 ± 3.6	1.000
Mayo endoscopic score, median (IQR)	3 (2–3)	3 (2–3)	0.648
Extraintestinal manifestations, n (%)
Oral ulcer	0	0	NA
Arthritis	2 (6.9)	0	1.000
Psoriasis	1 (3.4)	0	1.000
Cholangitis	1 (3.4)	1 (7.7)	0.528
Laboratory tests
WBC, median (IQR), 10⁹/L	6.4 (5.2–9.4)	6.2 (4.9–7.9)	0.407
Hemoglobin, mean ± SD, g/L	131.1 ± 21.8	114.9 ± 29.8	0.053
CRP, median (IQR), mg/L	17.3 (2.3–65.4)	9.5 (2.8–28.9)	0.613
ESR, mean ± SD, mm/h	32.2 ± 22.6	33.2 ± 20.9	0.906
Albumin, median (IQR), g/L	41.5 (31.1–47.2)	42.2 (33–43.7)	0.572
PARP, n (%)	25 (86.2)	6 (46.2%)	0.019
Peri-appendiceal inflammation score, median (IQR)	2 (1–2)	0 (0–1)	0.003
Appendiceal internal orifice stenosis, n (%)	9 (31.0)	4 (30.8)	1.000
Previous or following treatment, n (%)
Mesalamine	23 (79.3)	13 (100)	0.153
Glucocorticoids	9 (31.0)	3 (23.1)	0.722
Immunosuppressant	2 (6.9)	0	1.000
Biologics	6 (20.7)	0	0.153
Surgery	1 (3.4)	0	1.000

UC: ulcerative colitis; ABT: appendiceal body thickening; IQR: interquartile range; WBC: white blood cells; CRP: C-reactive protein; ESR: erythrocyte sedimentation rate; PARP: peri-appendiceal red patch.

Table 4.

Risk factors for ABT in UC: univariate logistic regression analysis.

Parameter	Univariate
Parameter	B	SE	OR (95% CI)	P-value
Peri-appendiceal inflammation score	1.428	0.518	4.172 (1.511–11.523)	0.006

ABT: appendiceal body thickening; UC: ulcerative colitis; SE: standard error; OR: odds ratio; CI: confidence interval.

Discussion

The appendix was once considered a vestigial part of the cecum in mammals, but it is now recognized as a host for gut microbiota and plays a role in immune regulation.^17,18 It is also considered to play a role in the pathogenesis of IBD.^2,5,6 In our study, 69.0% of patients with UC were found to have ABT on CT scans, possibly reflecting UC-related appendiceal inflammation. This percentage is higher than that reported in a recent study (43%) using abdominal ultrasound.¹⁹ Notably, the patients included in our study did not exhibit typical symptoms or signs of acute appendicitis and did not require surgery. Therefore, UC-related appendiceal inflammation appears to be distinct from acute appendicitis and should be differentiated clinically and pathologically.

Although the prevalence of UC-related appendiceal inflammation is high, it remains difficult to observe appendiceal inflammation under endoscopy due to the narrow lumen of the appendix. Peri-appendiceal inflammation or PARP may serve as an indicator of UC-related appendiceal inflammation. Maud et al. reported that UC patients with PARP had higher histopathological inflammation, as measured by Robarts histopathology index, in resected appendices (14 with PARP vs. 7 without PARP).⁹ In an ultrasound study by Reijntjes et al., the appendix was not significantly wider in UC patients with PARP (6.1 mm vs. 5.3 mm).⁶ Similarly, in our study, UC-related appendiceal inflammation detected by CT was significantly more prevalent in patients with PARP, and appendiceal width was positively correlated with the Mayo endoscopic score of peri-appendiceal inflammation (Figure 4(b)). These findings support the hypothesis that peri-appendiceal inflammation or PARP may represent a continuous extension of UC-related appendiceal inflammation.

Interestingly, in most UC patients with PARP, the internal appendiceal orifice was narrowed. This observation arose from unsuccessful attempts to insert an ultra-thin (9 Fr) cholangioscope into the appendix of UC patients. Age and Mayo endoscopic score of peri-appendiceal inflammation were identified as risk factors associated with stenosis. Heuthorst et al. reported total fibrous obliteration and partial fibrous obliteration in the appendiceal lumen in 17.1% (12/70) and 25.7% (18/70) of UC patients who underwent appendectomy.¹¹ In our study, orifice stenosis was less common than luminal stenosis (17.2% vs. 42.8%), and the severity of orifice stenosis was positively correlated with the peri-appendiceal inflammation score (Figure 4(a)). Luminal fibrosis is generally considered a normal age-related change but can also result from chronic inflammation.²⁰ Both luminal fibrosis and swelling due to chronic peri-appendiceal inflammation may contribute to orifice stenosis.

UC-related appendiceal inflammation appears to be a distinct entity from acute appendicitis. Clinically, it does not present with typical symptoms or abdominal signs and can currently be observed only through imaging studies. The PARP may serve as an indirect indicator under colonoscopy. During follow-up, it does not appear to exacerbate or necessitate surgery. Pathologically, UC-related appendiceal inflammation is more likely to exhibit Paneth cell metaplasia, crypt branching and shortening, fibrous stenosis, and limited mucosal infiltration of neutrophils.¹¹ UC-related appendiceal inflammation is not directly associated with overall UC activity.⁷ Nevertheless, appendectomy can induce remission in selected refractory UC patients, possibly through immune modulation.¹³

However, this study has several limitations. First, the retrospective design precluded accurate measurement of the appendiceal orifice. We used a qualitative comparison between the orifice and adjacent cecal fold to define stenosis, and only severe stenosis could be detected. Second, the evaluation of orifice stenosis was performed by a single experienced endoscopist. Inter-observer agreement could not be assessed, which may introduce bias; however, the endoscopist was blinded to the patients’ clinical information. Future prospective studies including healthy controls with precise endoscopic measurements are warranted to define the cutoff values for stenosis. Finally, this is the first study evaluating both AOS and ABT, making direct comparison with existing literature challenging.

In conclusion, AOS and ABT are prevalent in patients with UC. Peri-appendiceal inflammation is positively associated with the severity of stenosis and ABT and may serve as an indirect indicator of UC-related appendiceal inflammation. The use of ultra-thin endoscopes in future studies may facilitate the investigation of mucosal inflammation in UC-related appendiceal inflammation.

Footnotes

Acknowledgments

We express our sincere gratitude to Ms Qiuxiang Lu, an endoscopic nurse, for her assistance in obtaining endoscopic data and to Dr Benqi Zhao, a radiologist, for his help in diagnosing appendicitis on abdominal computed tomography. No financial support was received for this study.

Author contributions

Concept: Ting Yi, Zejun Song, Hongliang Zhao, Qing Huang, Bo Jiang, Ruifeng Wang, and Yutang Ren.

Design: Ting Yi, Zejun Song, Hongliang Zhao, Qing Huang, Bo Jiang, Ruifeng Wang, and Yutang Ren.

Definition of intellectual content: Ting Yi, Qing Huang, Bo Jiang, Ruifeng Wang, and Yutang Ren.

Literature search: Ting Yi, Zejun Song, Hongliang Zhao, Ruifeng Wang, and Yutang Ren.

Clinical studies: Ting Yi, Zejun Song, Hongliang Zhao, Xiaojuan Guo, Yuan Tian, Shiming Zhou, Ruifeng Wang, and Yutang Ren.

Data acquisition: Ting Yi, Zejun Song, Hongliang Zhao, Xiaojuan Guo, Yuan Tian, and Shiming Zhou.

Data analysis: Ting Yi, Zejun Song, Hongliang Zhao, Ruifeng Wang, and Yutang Ren.

Statistical analysis: Ting Yi, Zejun Song, Hongliang Zhao, Ruifeng Wang, and Yutang Ren.

Manuscript preparation: Ting Yi, Ruifeng Wang, and Yutang Ren.

Manuscript editing: Ting Yi, Zejun Song, Hongliang Zhao, Xiaojuan Guo, Ruifeng Wang, and Yutang Ren.

Manuscript review: Ting Yi, Zejun Song, Hongliang Zhao, Bo Jiang, Ruifeng Wang, and Yutang Ren.

All authors approved the final version of the manuscript.

Consent to participate

Not applicable.

Consent for publication

Not applicable.

Data availability

Data are stored in an Excel spreadsheet and are available at .

Declaration of conflicting interest

All authors declare no conflict of interest.

Ethical considerations

This study was approved by the Ethics Committee of Beijing Tsinghua Changgung Hospital (No. 23380-6-01).

Funding

The authors did not receive any financial support for the research, authorship, or publication of this article.

ORCID iDs

Ting Yi

Ruifeng Wang

Yutang Ren

References

Rogler

Singh

Kavanaugh

, et al. Extraintestinal manifestations of inflammatory bowel disease: current concepts, treatment, and implications for disease management. Gastroenterology 2021; 161: 1118–1132.

Sahami

Kooij

Meijer

, et al. The link between the appendix and ulcerative colitis: clinical relevance and potential immunological mechanisms. Am J Gastroenterol 2016; 111: 163–169.

Park

Loftus

Jr Yang

SK.

Appendiceal skip inflammation and ulcerative colitis. Dig Dis Sci 2014; 59: 2050–2057.

Takizawa

Yamaguchi

Kaizu

, et al. [A case of appendiceal lesion prior to the manifestation of ulcerative colitis: so-called “ulcerative appendicitis” as an antecedent lesion]. Nihon Shokakibyo Gakkai Zasshi 1996; 93: 109–113.

Anzai

Hata

Kishikawa

, et al. Appendiceal orifice inflammation is associated with proximal extension of disease in patients with ulcerative colitis. Colorectal Dis 2016; 18: O278–O282.

Kuk

Gwon

Soh

, et al. Clinical significance and long-term prognosis of ulcerative colitis patients with appendiceal orifice inflammation. BMC Gastroenterol 2022; 22: 532.

Ladefoged

Munck

Jorgensen

, et al. Skip inflammation of the appendiceal orifice: a prospective endoscopic study. Scand J Gastroenterol 2005; 40: 1192–1196.

Arjomand Fard

Armstrong

Perry

, et al. Appendix and ulcerative colitis: a key to explaining the pathogenesis and directing novel therapies? Inflamm Bowel Dis 2023; 29: 151–160.

Reijntjes

Heuthorst

Gecse

, et al. Clinical relevance of endoscopic peri-appendiceal red patch in ulcerative colitis patients. Therap Adv Gastroenterol 2022; 15: 17562848221098849.

10.

Park

Yang

Park

, et al. Atypical distribution of inflammation in newly diagnosed ulcerative colitis is not rare. Can J Gastroenterol Hepatol 2014; 28: 125–130.

11.

Heuthorst

Mookhoek

Wildenberg

, et al. High prevalence of ulcerative appendicitis in patients with ulcerative colitis. United European Gastroenterol J 2021; 9: 1148–1156.

12.

Kooij

Sahami

Meijer

, et al. The immunology of the vermiform appendix: a review of the literature. Clin Exp Immunol 2016; 186: 1–9.

13.

Sahami

Wildenberg

Koens

, et al. Appendectomy for therapy-refractory ulcerative colitis results in pathological improvement of colonic inflammation: short-term results of the PASSION study. J Crohns Colitis 2019; 13: 165–171.

14.

Von Elm

Altman

Egger

; STROBE Initiativeet al. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement: guidelines for reporting observational studies. Ann Intern Med 2007; 147: 573–577.

15.

Silverberg

Satsangi

Ahmad

, et al. Toward an integrated clinical, molecular and serological classification of inflammatory bowel disease: report of a Working Party of the 2005 Montreal World Congress of Gastroenterology. Can J Gastroenterol 2005; 19: 5A–36A.

16.

Schroeder

Tremaine

Ilstrup

DM.

Coated oral 5-aminosalicylic acid therapy for mildly to moderately active ulcerative colitis. A randomized study. N Engl J Med 1987; 317: 1625–1629.

17.

Girard-Madoux

MJH

Gomez de Agüero

Ganal-Vonarburg

, et al. The immunological functions of the appendix: an example of redundancy? Semin Immunol 2018; 36: 31–44.

18.

Vitetta

Chen

Clarke

The vermiform appendix: an immunological organ sustaining a microbiome inoculum. Clin Sci (Lond) 2019; 133: 1–8.

19.

Reijntjes

De Voogd

FAE

Bemelman

, et al. Intestinal ultrasound detects an increased diameter and submucosal layer thickness in the appendix of patients with ulcerative colitis compared to healthy controls - a prospective cohort study. Aliment Pharmacol Ther 2023; 57: 127–135.

20.

Andreou

Blain

Du Boulay

CE.

A histopathological study of the appendix at autopsy and after surgical resection. Histopathology 1990; 17: 427–431.

Peri-appendiceal inflammation is associated with appendiceal orifice stenosis and appendiceal body thickening in ulcerative colitis: A case–control study

Abstract

Objective

Methods

Results

Conclusions

Keywords

Introduction

Methods

Case selection

Information and data extraction

Definition of appendiceal internal orifice stenosis

Definition of ABT

Statistical analysis

Results

Demographic information of the included UC patients

Appendiceal internal orifice stenosis in UC patients

ABT in UC patients

Discussion

Footnotes

Acknowledgments

Author contributions

Consent to participate

Consent for publication

Data availability

Declaration of conflicting interest

Ethical considerations

Funding

ORCID iDs

References