Sessile serrated polyp mimicry in patients with solitary rectal ulcer syndrome: is there evidence of preneoplastic change?
BACKGROUND
Solitary rectal ulcer syndrome (SRUS) is associated with erythema and ulceration of the rectal wall. Serrated lesions of the colon are divided into conventional hyperplastic polyps and a new set of lesions that are variably called sessile serrated polyps (SSPs) and sessile serrated adenomas. The SSPs are epithelial proliferative lesions that appear to act as a unique pathway to colorectal carcinogenesis. No association between SRUS and SSPs has been previously reported.


OBJECTIVE
To assess a possible association between SRUS and morphologic features that mimic SSPs.


METHODS
Twenty-six patients with SRUS, who presented to our institution between January 1, 1999, and November 14, 2004, were retrospectively reviewed for SSP-type morphologic features by 3 pathologists. Ki-67 and hMLH1 immunohistochemical stains were used. Control tissues included 10 conventional left-sided hyperplastic polyps, 10 right-sided large SSPs, 7 adenocarcinomas with known loss of hMLH1 gene expression, and 4 normal human tonsil tissues.


RESULTS
Ten (38%) of 26 SRUS specimens demonstrated histologic features consistent with SSPs. These features included exaggerated serration within the lower crypt compartments, crypt branching, hypermucinous appearance of epithelium, and horizontal extension of crypt bases along the muscularis mucosa. All 10 cases of SRUS had positive basal Ki-67 staining in 10% to 20% of cells. Two (20%) of the 10 cases demonstrated focal superficial loss of hMLH1 mismatch repair gene expression within areas of serrated morphologic features. One hyperplastic polyp superimposed on SRUS showed a reduced number of surface epithelial cells that express hMLH1 protein.


CONCLUSIONS
Up to 38% of patients with SRUS have histologic changes that mimic SSPs. More importantly, 20% of these serrated lesions were found to have focal loss of hMLH1 gene expression, indicating a potential of preneoplastic change. This phenomenon may reflect an increased propensity for neoplastic progression in response to repeated trauma and repair process in certain cases of SRUS.
Ball
Chad G
CG
Department of Surgery, Foothills Medical Center, University of Calgary, Calgary, Alberta, Canada.
Dupre
Marc P
MP
Falck
Vincent
V
Hui
Susan
S
Kirkpatrick
Andrew W
AW
Gao
Zu-Hua
ZH
D048868:Adaptor Proteins, Signal Transducing; D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology; D000236:Adenoma / Q000150:complications / Q000378:metabolism / Q000473:pathology; D014408:Biomarkers, Tumor / Q000378:metabolism; D002352:Carrier Proteins; D003937:Diagnosis, Differential; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism; D000070957:MutL Protein Homolog 1; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism; D011127:Polyps / Q000378:metabolism / Q000473:pathology*; D011230:Precancerous Conditions / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D012004:Rectal Neoplasms / Q000378:metabolism / Q000473:pathology*; D012007:Rectum / Q000378:metabolism / Q000473:pathology*; D012189:Retrospective Studies; D013577:Syndrome; D014456:Ulcer / Q000150:complications / Q000378:metabolism / Q000473:pathology*
D048868:Adaptor Proteins, Signal Transducing; D014408:Biomarkers, Tumor; D002352:Carrier Proteins; D019394:Ki-67 Antigen; C501486:MLH1 protein, human; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D000070957:MutL Protein Homolog 1