Clinical and Endoscopic Features in Patients with Inflammatory Bowel Disease and Serrated Epithelial Change

Abstract

Background and Objectives

Serrated epithelial change (SEC) is an increasingly recognized histologic finding in patients with inflammatory bowel disease (IBD) and may be associated with an increased risk of colorectal dysplasia. SEC is defined as colonic mucosa with goblet cell–rich epithelium and serrated crypt architecture without basal crypt distortion or dysplasia. This study aimed to characterize the clinical, endoscopic, and histologic features of SEC in IBD patients and determine the incidence of associated dysplasia.

Materials and Methods

A retrospective single-center study was conducted at a tertiary referral hospital. IBD patients with histologically confirmed SEC from colonic biopsies between January 1, 2015 and December 31, 2024 were identified via pathology database searches. Patients without follow-up colonoscopy or flexible sigmoidoscopy were excluded. Clinical, endoscopic, and histologic data were extracted from electronic records. Descriptive statistics were used to summarize demographics, endoscopic findings, and histologic data. Median values were reported for age and follow-up time; mean values described disease duration.

Results

Twenty-six IBD patients (16 Crohn's disease, 10 ulcerative colitis) with SEC were analyzed (14 males; median age 58 years). Mean disease duration was 15 years, with a median follow-up of 24.5 months. The estimated prevalence of SEC was . A total of 30 SEC specimens were identified, most commonly located in the cecum (30%), rectum (23.3%), and transverse colon (16.7%). SEC presented as nodular or polypoid lesions in 60% of cases and was detected by high-definition white light endoscopy in 61.5% of patients. Multifocal SEC occurred in 19.2% of patients. Endoscopic and histologic inflammations were present in approximately half of the cases. Only one patient (3.8%) developed low-grade dysplasia adjacent to SEC.

Conclusion

SEC was predominantly observed in patients with long-standing IBD as polypoid or nodular lesions proximal to the splenic flexure and associated with mucosal inflammation. A solitary case of colorectal dysplasia was observed. Larger prospective studies are needed to clarify SEC's role in colorectal carcinogenesis and to guide dysplasia surveillance strategies in IBD.

 

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Keywords

serrated epithelial change - inflammatory bowel disease - dysplasia - endoscopy

Introduction

Patients with inflammatory bowel disease (IBD) have an increased risk of developing colorectal cancer (CRC), which rises further with longer disease duration, greater inflammatory activity, and more extensive colonic involvement.[1] [2] The relative risk is at least twofold higher in patients with colonic Crohn's disease or ulcerative colitis compared to the general population.[3] [4]

Serrated epithelial change (SEC) in colonic biopsies is an increasingly recognized histopathological finding in patients with IBD. However, there is a lack of robust data on its prognostic significance. Several studies have suggested an association between SEC and an increased risk of colorectal dysplasia.[5] [6] [7] Consequently, the identification of SEC may have implications for dysplasia surveillance intervals in this population. Nonetheless, the clinical significance of SEC remains uncertain.

SEC is histologically distinct from hyperplastic polyps, which exhibit evenly spaced, straight funnel-shaped crypts with a basally located proliferation zone, and from sessile-serrated lesions, which are characterized by serrated architecture extending to the base of irregularly distorted crypts. While hyperplastic polyps and sessile-serrated lesions are typically visible endoscopically, SEC may appear as polypoid or nodular lesions but can also be invisible and only detectable through random biopsies of flat mucosa. Currently, No widely accepted histopathological criteria exist for diagnosing SEC. However, it has been described as colonic mucosa with goblet cell–rich epithelium and serrated crypt architecture without basal crypt distortion or dysplasia.[6] [8] [9]

Dysplasia detection in IBD has traditionally relied on mucosal inspection with targeted and random biopsies to identify both visible and invisible lesions.[10] In the past decade, advances such as chromoendoscopy and high-definition imaging, endorsed by the 2015 SCENIC international consensus[11] and the 2021 American Gastroenterology Association update,[12] have significantly improved dysplasia detection rates.[13] [14] Dye-based and virtual chromoendoscopy may also contribute to the declining incidence of IBD-related CRC.[14] [15] However, invisible dysplasia, which may include SEC, remains a concern due to inherent limitations of random biopsies, complicating surveillance strategies in affected patients. The potential association between SEC and dysplasia presents a challenge for safe and effective dysplasia surveillance for IBD patients.

With the clinical significance of SEC remaining unclear, our aims were to expand the understanding of the clinical, endoscopic, and histological features of IBD patients with SEC and determine the overall rate and incidence of dysplasia.

 

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Materials and Methods

We performed a single-center, retrospective study at the Gold Coast University Hospital, a large tertiary referral center in Queensland, Australia.

Study Population

Patients with a confirmed diagnosis of IBD (Crohn's disease or ulcerative colitis) with SEC were identified by searching the Gold Coast University Hospital pathology database for the terms “serrated,” “epithelial,” and “change” in pathology reports. The first colonic biopsy demonstrating SEC between January 1, 2017 and December 31, 2024 was designated as the index SEC. Colonic biopsies obtained from colonoscopy or flexible sigmoidoscopy were included and classified as targeted or nontargeted based on the presence of a visible lesion. Patients were included if they (1) were aged 18 years or older and (2) had a confirmed diagnosis of IBD. Patients were excluded if (1) there was no follow-up colonoscopy or flexible sigmoidoscopy, (2) SEC was identified in a surgical specimen, or (3) the diagnosis was IBD-unidentified. Two expert gastrointestinal pathologists reviewed relevant pathology slides to confirm the diagnosis of SEC.

 

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Patient and Endoscopic Data

Clinical, endoscopic, and histological data were extracted from electronic medical records and endoscopy reports. Clinical data included year of IBD diagnosis, patient age, IBD treatment at the time of index SEC diagnosis, disease duration, smoking status, co-existence of primary sclerosing cholangitis, prior history of conventional colonic dysplasia, and family history of CRC. Endoscopic data included the method of SEC detection, use of high-definition white light endoscopy or chromoendoscopy, SEC morphology, SEC location, presence of multifocal SEC, pseudopolyps, endoscopic inflammation, and histological inflammation. Colonic segment concordance between SEC and dysplasia was also recorded. Follow-up time was defined as the interval from the index SEC diagnosis to the most recent repeat endoscopic assessment.

 

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IBD Characteristics

The Montreal classification system was used to define disease extent and location for UC (E1: proctitis, E2: left-sided colitis, E3: pancolitis) and CD (L1: ileal, L2: colonic, L3: ileocolonic; B1: non-stricturing and nonpenetrating, B2: stricturing, B3: penetrating). Endoscopy reports and photo-documentation were reviewed to identify the presence of endoscopic inflammation. Previous biologic treatment exposure and disease treatment at the time of index SEC diagnosis were captured. Treatment categories included 5-aminosalicylates, immunomodulators (thiopurine, methotrexate), small molecules (tofacitinib, upadacitinib), biologic therapy (infliximab, adalimumab, golimumab, vedolizumab, ustekinumab), corticosteroids and combination therapy (immunomodulator with a biologic).

 

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Histology

In this study, SEC was defined as nondysplastic colonic mucosa with goblet cell–rich epithelium and distorted serrated architecture involving the upper crypts, without distortion of the basal crypt architecture (see [Fig. 1]).

Fig. 1 Serrated epithelial change. Nondysplastic colonic mucosa with goblet cell-rich epithelium and distorted, serrated architecture involving the upper crypts, without distortion of the basal crypt architecture.

 

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Serrated Epithelial Change Characteristics

The location of SEC was defined by the colonic segment in which it was identified. Endoscopy and pathology reports were used to determine whether SEC was detected on random biopsies of flat mucosa or on targeted biopsies of nodular or polypoid mucosa. Multifocal SEC was defined as SEC identified in multiple colonic segments during the same endoscopic assessment. Consecutive SEC was defined as SEC identified in a different colonic segment from the previous endoscopic assessment. The locations of SEC and dysplasia were also reviewed.

 

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Statistical Analysis

Descriptive statistics were used to summarize key data pertaining to patient demographics, endoscopy, and histology. To account for the small sample size and minimize the influence of outliers in the data distributions, median values with interquartile range (IQR) were used to report the patient age (years) and endoscopic follow-up time (months). Mean values with standard deviation (SD) were used to report disease duration (years), consistent with methodologies used in comparable studies. The estimated prevalence of SEC and the overall rate and incidence of dysplasia are also calculated.

 

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Results

Population

The Gold Coast University Hospital pathology database was used to identify 113 patients with endoscopic histopathology reports containing the words “serrated”, “epithelial” and “change”. Of these, 78 had no IBD diagnosis and were excluded. The remaining 35 reports, each corresponding to a unique patient with confirmed IBD and SEC, were included for further review. Histopathology slides were re-examined by two gastrointestinal pathologists to confirm the diagnosis of SEC. Nine patients had no follow-up endoscopic assessment, leaving a total of 26 patients for the final analysis (see [Fig. 2]). Over the study period, 1,621 colonoscopies were performed on individual patients with IBD.

Fig. 2 Flowchart of patient inclusion. A total of 113 histopathology reports from colonic biopsies containing the terms “serrated,” “epithelial,” and “change.” Of these, 35 corresponded to a patient with confirmed IBD and their pathology slides were reviewed by two gastrointestinal pathologists to confirm SEC. Twenty-six patients had at least one follow-up endoscopic assessment and were included in the final analysis. IBD, inflammatory bowel disease; SEC, serrated epithelial change.

 

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Patient Characteristics

Key patient demographics and relevant endoscopic and histological data are presented in [Table 1]. The cohort included a total of 26 patients, 14 (53.8%) of whom were males. The median age at the time of the index diagnosis of SEC was 58 years (IQR: 51–68). There were 16 (61.5%) patients with either colonic or ileocolonic Crohn's disease, and 14 (87.5%) had an inflammatory phenotype of disease. There were 10 (38.5%) patients with ulcerative colitis, and 6 (60%) had a pan-colonic phenotype. The mean disease duration was 15 years (SD: 10), and the median follow-up time was 24.5 months (range: 5–60).

Table 1 Patient characteristics and key clinical, histological, and endoscopic data

KEY DATA	VALUE
Number of patients	26
Number of SEC specimens	30
Median age (IQR), y	58 (51–68)
Male gender	14 (53.8%)
Diagnosis
Crohn's disease	16 (61.5%)
L1	0 (0%)
L2	11 (68.8%)
L3	4 (31.2%)
L4	0 (0%)
B1	14 (87.5%)
B2	1 (6.25%)
B3	1 (6.25%)
Ulcerative colitis	10 (38.5%)
E1	1 (10%)
E2	3 (30%)
E3	6 (60%)
Mean duration of IBD, y (SD)	15 (10)
Median follow-up, mo (range)	24.5 (5–60)
Endoscopic method of SEC diagnosis
Colonoscopy	24 (92.3%)
Flexible sigmoidoscopy	2 (7.7%)
HDWL endoscopy	16 (61.5%)
Chromoendoscopy (dye-based or virtual)	10 (38.5%)
SEC morphology
Nodular/polypoid mucosa	18 (60%)
Size of lesion ≥10 mm	12 (66.7%)
Size of lesion <10 mm	6 (33.3%)
On flat mucosa	12 (40%)
SEC location
Cecum	9 (30%)
Ascending colon	3 (10%)
Transverse colon	5 (16.7%)
Descending colon	3 (10%)
Sigmoid colon	3 (10%)
Rectum	7 (23.3%)
Multifocal SEC	5 (19.2%)
SEC on consecutive endoscopy (different colonic segment)	7 (26.9%)
Active medications for IBD
Oral/rectal 5-ASA	9 (34.6%)
Immunomodulators	2 (7.7%)
Small molecules	2 (7.7%)
Biologics	6 (23.1%)
Combination therapy (biologic and immunomodulator)	4 (15.4%)
None	3 (11.5%)
Previous biologic exposure
Yes	12 (46.2%)
No	14 (53.8%)
Patient factors
PSC	3 (11.5%)
Smoker	3 (11.5%)
Family history of CRC	4 (15.4%)
Previous adenomas with dysplasia	6 (23.1%)
Endoscopic and histologic factors
Colonic strictures	0 (0%)
Tubular colon	3 (11.5%)
Post-inflammatory polyps	5 (19.2%)
Histologic inflammation	12 (46.2%)
Endoscopic inflammation	13 (50%)
Overall rate of dysplasia	1/26 (3.8%)
Incidence rate of dysplasia	1.65/100 person-years

Abbreviations: 5-ASA, 5-aminosalicylic acid; CRC, colorectal cancer; HDWL, high-definition white light; IBD, inflammatory bowel disease; IQR, interquartile range; PSC, primary sclerosing cholangitis; SD, standard deviation; SEC, serrated epithelial change.

 

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Serrated Epithelial Change Characteristics

A total of 30 specimens with SEC were identified. Of these, 18 (60%) were visible endoscopically as polypoid or nodular mucosa, with 12 (66.7%) measuring ≥10 mm. Colonoscopy was the primary endoscopic method of diagnosis in most cases (92.3%). High-definition white light endoscopy and chromoendoscopy were used in 16 (61.5%) and 10 (38.5%) cases, respectively. SEC was primarily located in the caecum (30%), rectum (23.3%), and transverse colon (16.7%), and exhibited multifocal distribution in 5 (19.2%) patients. Endoscopic and histological inflammation were demonstrated in 50 and 46.2% of cases, respectively.

 

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Dysplasia

The overall dysplasia rate in this cohort was 3.8%, represented by one case detected among 26 patients. The incidence rate of dysplasia was 1.65 cases per 100 person-years, calculated by dividing this single dysplasia event by the total person-years of follow-up.

 

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Discussion

This study describes a cohort of IBD patients with SEC consisting of an almost equal male-to-female distribution, with a median age of 58 years (IQR: 51–68) and a mean disease duration of 15 years (SD: 10). Gender distribution, age at index diagnosis of SEC, and disease duration were all comparable to those reported in previous studies.[5] [6] [7] Approximately half of the patients in this study were being treated with advanced therapies, including biologics and small molecules, which were not widely available at the time of earlier studies.[5] [6] [7] Additionally, nearly half of the patients had evidence of endoscopic and histological inflammation at the time of SEC diagnosis. These data reflect a population with long-standing active disease and treatment complexity, both of which may contribute to the development of colorectal dysplasia.[5] [6] [7]

Our findings indicate that the highest occurrence of SEC was observed proximal to the splenic flexure (56.7%) and in the rectum (23.3%). This pattern contrasts with previous studies by Parian and colleagues, where SEC predominantly occurred in the left colon and rectum in approximately 75% of cases. This difference may be attributed to the small sample size of our analysis. However, multifocal SEC was observed in 19.2% of patients, which is a proportion closely aligning with the 22.4% previously reported. We observed that about one-quarter of patients had SEC detected in a different colonic segment on successive endoscopic assessments, a phenotype associated with an increased risk of dysplasia.[6] [7]

Notably, we observed 40% of SEC was not endoscopically visible and detected only through random biopsies of flat mucosa, despite chromoendoscopy being employed in 38.5% of cases. Prior studies indicate that rates of invisible SEC are as high as 66.3 to 73.4%,[6] [7] although the use of chromoendoscopy was not specified. Johnson and colleagues reported a lower rate of 62%, where chromoendoscopy was used in 20% of cases.[5] These differences may be explained by the application of high-definition endoscopy and higher rates of chromoendoscopy within our cohort. These findings raise concerns regarding the effectiveness of white-light colonoscopy in detecting SEC and underscore the limitations of random biopsies. It is plausible that the actual prevalence of SEC is underestimated.[5] [6] [7]

In our study, endoscopic and histological inflammations were frequently associated with SEC, occurring in 50 and 46.2% of cases, respectively. Previous studies reported similar figures, with moderate to severe endoscopic inflammation observed in 56.1% and histological inflammation in 49.2% of cases.[6] A subsequent study reported rates of 41.8 and 57.1%, respectively.[7] These data suggest that inflammation and ongoing disease activity may drive specific molecular alterations resulting in SEC. Moreover, given the known correlation between disease activity and CRC, the development of SEC may potentially represent a morphological indicator or precursor of dysplasia.

In our cohort, we observed a dysplasia rate of 3.8%, represented by a single case of nonconventional low-grade dysplasia associated with SEC. This rate is considerably lower than the reported 11.2 to 21%,[5] [6] [7] [16] likely due to variable study designs and heterogenous populations. When adjusting for the differences in follow-up time, the incidence rate of dysplasia was 1.65 cases per 100 person-years, which closely aligns with the findings reported by Parian and colleagues.[6] Interpretation of this data, however, is challenging given the small sample size and presence of several potential confounders in the affected patient, including previous conventional dysplasia, a family history of CRC, and a tubular colon. Notably, all procedures in our analysis were performed using high-definition endoscopes, with chromoendoscopy employed at a relatively high frequency of 38.5%. Consistent with the SCENIC consensus recommendations, these methods are known to improve dysplasia detection in this population,[11] but their utility in detecting SEC specifically remains unclear and warrants further investigation.

Several studies have reviewed SEC and colorectal dysplasia, but current data are inconsistent. SEC was first described by Kilgore and colleagues in 2000, who identified “hyperplastic-like mucosal change” in surgical specimens of adenocarcinoma from patients with Crohn's disease. They suggested a potential link between this histological finding and colorectal adenocarcinoma,[17] but the study was likely underpowered. Parian and colleagues published a large case series of 187 IBD patients, reporting that 21% of patients with SEC had synchronous or metachronous colorectal dysplasia after adjusting for prior dysplasia. Longer disease duration increased the likelihood of dysplasia,[6] a factor also validated in our cohort. The study was possibly subject to detection and selection bias, as patients with SEC underwent more endoscopic assessments and had longer follow-up times. In contrast, other studies have demonstrated no significant associations between SEC and colorectal dysplasia after adjusting for confounding factors.[5] [16] The variability in findings stresses the need for high-quality research, as compelling evidence of a causal relationship between SEC and dysplasia in the IBD cohort remains elusive.

Overall, SEC emerges as a histopathological diagnosis of increasing interest within the IBD population, though its clinical significance remains to be fully elucidated. The current literature on its association with colorectal dysplasia lacks consensus and is primarily constrained to low-quality analyses. Considering the growing attention on SEC, we propose that this unique descriptive analysis, set within the era of advanced endoscopic imaging and techniques, can stimulate further much-needed research in this area.

Strengths

This study represents the largest Australian cohort of IBD patients with SEC. The integrity of histological data is supported by the expertise of gastrointestinal histopathologists at the Gold Coast University Hospital. Additionally, this study included only patients with follow-up endoscopic assessment using high-definition endoscopes and chromoendoscopy, both of which have been demonstrated to enhance dysplasia detection.

 

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Limitations

The retrospective design inherently limits control over data collection and may introduce bias through incomplete or inaccurate documentation in electronic records. The small sample size, which resulted from a stringent patient selection process, may limit data acquisition and the generalizability of our findings. The absence of a control group precludes comparison of dysplasia rates between patients with and without SEC, which is necessary to more definitively ascertain the risk SEC confers for colorectal dysplasia. While this was not a primary aim, it limits the ability to fully contextualize the clinical significance of SEC. Lastly, the indications for endoscopic assessment were not provided, which may introduce a recall and detection bias, as the frequency of procedures varies significantly depending on disease severity, as does the need to perform segmental colonic biopsies. This also appeared to be a common challenge in related studies. These factors emphasize the need for larger, prospective studies to overcome these limitations and to validate our findings.

 

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Conclusion

In this uncontrolled study, SEC was predominantly found in patients with long-standing colitis as polypoid or nodular lesions situated proximal to the splenic flexure and associated with both endoscopic and histological inflammation. We observed a solitary case of nonconventional dysplasia, occurring in a patient with several other risk factors for dysplasia, which confounds interpretation. Given the small sample size, robust conclusions about the role of SEC in dysplasia development cannot be drawn. Overall, SEC remains an understudied entity, necessitating further research into any potential association with dysplasia, particularly in the context of advanced endoscopic imaging techniques such as chromoendoscopy.

 

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Conflicts of Interest

None declared.

Authors' Contributions

L.V.: Study design, methodology, data collection, formal analysis, original draft preparation, and final approval of the manuscript.

P.K.R.: Study design, methodology, formal analysis, review and editing, and final approval of the manuscript.

S.P.: Formal analysis, review and editing, and final approval of the manuscript.

T.W.: Formal analysis and final approval of the manuscript.

W.M.: Study design, methodology, formal analysis, data curation, review and editing, and final approval of the manuscript.

Ethical Approval

The Gold Coast Hospital and Health Service Human Research Ethics Committee has reviewed this study and granted ethical approval on 08/05/2024. HREC reference: HREC/2024/QGC/106193.

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Publikationsverlauf

Artikel online veröffentlicht:
25. September 2025