Elsevier

Human Pathology

Volume 46, Issue 10, October 2015, Pages 1548-1556
Human Pathology

Original contribution
Clinical, pathologic, and outcome study of hyperplastic and sessile serrated polyps in inflammatory bowel disease

https://doi.org/10.1016/j.humpath.2015.06.019Get rights and content

Summary

There is evidence that some cancers in patients with inflammatory bowel disease (IBD) develop via the serrated pathway of carcinogenesis. This study examined the clinicopathological features and outcome of 115 IBD patients (65 with ulcerative colitis, 50 with Crohn disease), all with at least 1 serrated polyp at endoscopy or colon resection, including the presence of synchronous and metachronous conventional neoplastic lesions (dysplasia or adenocarcinoma), over an average follow-up period of 56.4 months. Conventional neoplasia was categorized as flat dysplasia (low or high grade), sporadic adenoma, adenoma-like dysplasia-associated lesion or mass, or adenocarcinoma. Overall, 97% of patients had at least 1 hyperplastic polyp (HP), 6% had a sessile serrated adenoma/polyp, and none had a traditional serrated adenoma. Eight patients (7%) had a synchronous conventional neoplastic lesion; only 1 had flat dysplasia (1%) and 2 had adenocarcinoma (2%). Thirteen patients developed a metachronous conventional neoplastic lesion, with 8 developing their conventional neoplasm within an area of previous or concurrent colitis; only 1 patient developed flat dysplasia (1%), and none developed adenocarcinoma. A higher proportion of patients with both an HP and a synchronous conventional neoplastic lesion at index developed a metachronous conventional neoplastic lesion, compared with those with an index HP only (25% versus 7%). These results suggest that IBD patients (both ulcerative colitis and Crohn disease patients) with HP have a very low risk of developing a conventional neoplastic lesion (flat dysplasia or adenocarcinoma) that would warrant surgical resection.

Introduction

Patients with inflammatory bowel disease (IBD) have a well-recognized increased risk of developing colorectal cancer via an inflammation-dysplasia-carcinoma sequence [1], [2]. The goal of surveillance is to detect dysplasia, which is presently the best and most reproducible marker of malignancy risk in IBD [2]. Grossly, dysplasia is classified into 2 general categories: flat dysplasia, which is endoscopically undetectable, and elevated or raised dysplasia, referred to as dysplasia-associated lesions or masses (DALMs), which are endoscopically detectable [3]. DALMs are further subclassified into those that are adenoma-like (endoscopically resectable) and non–adenoma-like (endoscopically unresectable) [3], [4], [5]. Microscopically, dysplasia is graded as either low or high, based on a combination of architectural and cytologic features [2].

At this point in time, 3 morphologic subtypes of dysplasia in IBD have been described, all of which may exhibit flat or polypoid architecture: intestinal dysplasia, which cytologically resembles dysplasia seen in sporadic adenomas, hypermucinous/villous dysplasia, and serrated dysplasia [2], [3], [6], [7], [8]. Polypoid serrated dysplasia resembling sporadic serrated polyps has also been observed in IBD patients [6], [8], [9], [10]. The biological properties and natural history of these lesions are poorly understood. However, there is evidence that some cancers in IBD patients may develop through the serrated neoplasia pathway [8], [11], [12], [13], [14]. Most serrated pathway cancers exhibit high-level microsatellite instability and arise from malignant transformation of serrated polyps [15], [16], [17]. Serrated polyps are classified as follows: hyperplastic polyp (HP), sessile serrated adenoma/polyp (SSA/P), either with or without dysplasia, and traditional serrated adenoma (TSA) [18]. The reported prevalence of serrated polyps in the general white adult population ranges from 25% to 50% based on autopsy studies, with lower and similarly variable prevalence rates from colonoscopy-based studies [19], [20], [21]. Their prevalence in the IBD patient population is unknown. Furthermore, little is known about the clinicopathological features, and outcome, of IBD patients with serrated polyps. Therefore, the aim of the current study was to evaluate the clinical, pathologic, and outcome features of IBD patients, all of whom had at least 1 serrated polyp detected at index colonoscopy or colon resection. The principal question was to determine if these patients are at increased risk for flat dysplasia or cancer.

Section snippets

Study group

The study cohort consisted of 115 patients with IBD identified via a retrospective search of the pathology archives at 2 major hospitals (Brigham and Women's Hospital, and Boston Medical Center, Boston, MA) between the years 2002 and 2010. During this period, 1150 IBD patients were identified. Patients were included in the study if they had a clinically and pathologically established diagnosis of either ulcerative colitis (UC; 65 patients) or Crohn disease (CD; 50 patients), at least 1 serrated

Clinical features

The clinical features of the study cohort are summarized in Table 1. Of the 115 IBD patients, 65 (57%) had UC and 50 (43%) had CD. Overall, there were 62 women and 53 men, with a mean duration of IBD of 15.3 years (range, 0-48 years). Patients averaged approximately 1.4 endoscopies during the course of follow-up, with a range of 1 to 6. The overall mean follow-up time was 56.4 months (range, 2-106 months). Most patients in both IBD subgroups (UC and CD) had either subtotal (28%) or pancolitis

Discussion

We performed this study to determine the clinicopathological features and outcome of IBD patients with serrated polyps. In our cohort of IBD patients, all with at least 1 index serrated polyp, 97% had HPs, 6% had SSA/P, and 0% had TSA. Most patients presented with only 1 serrated polyp and had either subtotal or pancolitis. Endoscopically, more than half of polyps were detectable. Most polyps occurred in the left colon, and most also occurred within areas of previous or concurrent colitis. At

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    Disclosures: None declared.

    1

    Present address: Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390.

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