Family history as a risk factor for colorectal cancer in inflammatory bowel disease

2001 ◽  
Vol 120 (6) ◽  
pp. 1356-1362 ◽  
Johan Askling ◽  
Paul W. Dickman ◽  
Anders Ekbom ◽  
Per Karlén ◽  
Olle Broström ◽  
2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 49-50
J Atin ◽  
C Hernandez-Rocha ◽  
K Borowski ◽  
J Stempak ◽  
M Smith ◽  

Abstract Background Patients with inflammatory bowel disease (IBD) are at higher risk for developing colitis-associated colorectal cancer (CAC). Clinical and endoscopic features are used to stratify the risk of CAC, but new biomarkers are necessary to improve this stratification. Recent studies have shown that loss of expression of special AT-rich sequence binding protein 2 (SATB2) is frequent in CAC compared to sporadic colorectal cancer and this SATB2 status is found in pre-cancerous dysplastic lesions as well. However, the relationship of known clinical risk factors for CAC and loss of SATB2 has not been explored. Aims To assess the association of loss of SATB2 expression in CAC with clinical characteristics of IBD. Methods Patients with a known diagnosis of ileocolonic or colonic Crohn’s disease (CD), ulcerative colitis (UC), or IBD unclassified (IBDU) who underwent colectomy between October 2010 and December 2017 for CAC were included. SATB2 expression in neoplastic tissue was evaluated using immunohistochemistry (IHC), where less than 5% of tumor cells showing staining was considered loss of SATB2. Tumor grade, P53 and mismatch repair (MMR) status were assessed as well. Available clinical data such as sex, smoking status, IBD diagnosis (CD, UC or IBDU), age at IBD diagnosis, duration of IBD, extent of colitis and previous medications were collected. We used a generalized linear model to assess the association between these biomarkers and clinical data. Results A total of 58 patients with mean age at CAC diagnosis of 50.3 ±13 years, 27 (46%) females were analyzed. Mean IBD duration was 17.6 ±10 years and 22 (37.9%), 34 (58.6%) and 2 (3.4%) were CD, UC and IBDU, respectively. Thirty-two (55.2%) CACs had loss of SATB2 expression. There was no association between age at CAC diagnosis or grade of the tumor and loss of SATB2. However, longer duration of IBD (21.2 ± 9 years vs 13.7 ± 9 years, p = 0.01) was significantly associated with loss of SATB2. There was no association between SATB2 status and other explored clinical or endoscopic variables. Tumors with P53 mutation were associated with a younger age at diagnosis of CAC (47.2 ±13 vs 55.0 ±12 years, p = 0.03), but no other associations of this marker or MMR with clinical or endoscopic variables of IBD were found. Conclusions Loss of SATB2 expression is significantly associated with IBD duration, a well-known risk factor for CAC. This association with duration of IBD could denote an effect of longer chronic inflammation on SATB2 status. Given the previously reported association of loss of expression of SATB2 with pre-cancerous lesions in IBD patients, this could be a potential biomarker for risk of CAC. Funding Agencies National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

Jayne Digby ◽  
Robert JC Steele ◽  
Judith A Strachan ◽  
Craig Mowat ◽  
Annie S Anderson ◽  

Background Faecal immunochemical tests for haemoglobin have been recommended to assist in assessment of patients presenting in primary care with lower bowel symptoms. The aim was to assess if, and which, additional variables might enhance this use of faecal immunochemical tests. Methods Faecal immunochemical test analysis has been a NHS Tayside investigation since December 2015. During the first year, 993 patients attending colonoscopy were invited to complete a detailed questionnaire on demographic background, symptoms, smoking status, alcohol use, dietary fibre, red and processed meat intake, physical activity, sitting time, dietary supplement use, family history of colorectal cancer, adenoma, inflammatory bowel disease and diabetes. Significant bowel disease was classified as colorectal cancer, advanced adenoma or inflammatory bowel disease. Results A total of 470 (47.3%) invitees agreed to complete the questionnaire and 408 (41.1%) did. Unadjusted odds ratios for the presence of significant bowel disease compared with undetectable faecal haemoglobin increased with increasing faecal haemoglobin and for faecal haemoglobin 10–49, 50–199, 200–399 and ⩾400 μg Hb/g faeces were 0.95 (95% CI: 0.16–5.63), 2.47 (0.55–1.03), 6.30 (1.08–36.65) and 18.90 (4.22–84.62), respectively. Rectal bleeding and family history of polyps were the only other variables with statistically significant ( P < 0.05) odds ratios greater than 1.00, being 1.88 (1.13–3.17) and 2.93 (1.23–6.95), respectively. Odds ratios adjusted for all other variables showed similar associations, but only faecal haemoglobin and family history of polyps had significant associations. Conclusions Faecal haemoglobin is the most important factor to be considered when deciding which patients presenting in primary care with lower bowel symptoms would benefit most from referral for colonoscopy.

2017 ◽  
Vol 19 (5) ◽  
pp. 232-236
Jana Koželuhová ◽  
Karel Balihar ◽  
Jan Kotyza ◽  
Eva Janská ◽  
Martin Matějovič

2020 ◽  
Vol 14 (8) ◽  
pp. 1172-1177 ◽  
Shailja C Shah ◽  
Steven H Itzkowitz

Abstract One of the most feared complications of inflammatory bowel disease [IBD]-associated colitis is colorectal cancer. When considering the substantial increase in the prevalence of IBD, without any anticipated decline, coupled with decreasing colectomy rates for dysplasia and expanding medical options for effectively controlling inflammation, it is predicted that the pool of people living with—and ageing with—colonic IBD, who are recommended to undergo lifelong colonoscopic surveillance for colorectal neoplasia, will strain existing resources and challenge the sustainability of current guideline-based surveillance recommendations. At the same time, we are missing the opportunity for early detection in a group that is overlooked as high-risk, as a substantial proportion of colorectal cancers are being diagnosed in individuals with colonic IBD who have disease duration shorter than when guidelines recommend surveillance initiation. Here, we reappraise: 1] inflammation as a dynamic risk factor that considers patients’ cumulative course; 2] time of screening initiation that is not based primarily on absolute disease duration; and 3] surveillance intervals as an iterative determination based on individual patient factors and consecutive colonoscopic findings. This Viewpoint supports a paradigm shift that will ideally result in a more effective and higher-value colorectal cancer prevention approach in IBD.

Chanpreet Arhi ◽  
Alan Askari ◽  
Subramanian Nachiappan ◽  
Alex Bottle ◽  
Naila Arebi ◽  

Abstract Background Inflammatory bowel disease [IBD] is a risk factor for colorectal cancer [CRC]. The aim of this study is to determine whether stage at diagnosis and survival differ between sporadic, ulcerative colitis [UC]- and Crohn’s disease [CD]-related CRC. Methods The English National Cancer Registry [NCIN], Hospital Episode Statistics [HES] and Office for National Statistics [ONS] datasets between 2000 and 2010 were linked, providing data on comorbidities, stage and date of death. A logistic regression model determined whether IBD was associated with an early [I/II] or late [III/IV] cancer. Cox regression analysis was used to examine survival differences between sporadic, UC- and CD-related cancers. Results A total of 234 009 patients with CRC were included, of whom 985 [0.4%] and 1922 [0.8%] had CD and UC, respectively. UC, but not CD, was associated with an earlier stage compared with sporadic cancers (odds ratio [OR] 0.88, 95% confidence interval [CI] 0.79 to 0.98, p = 0.02). CD had a significantly worse survival compared with sporadic patients for stage II [HR = 1.71, CI 1.26 to 2.31 p &lt;0.005] and III [1.53, CI 1.20 to 1.96, p &lt;0.005] cancer. UC patients were associated with worse survival compared with the sporadic group for both stage III [1.38, CI 1.17 to 1.63, p &lt;0.0005] and IV [1.13, CI 1.01 to 1.28, p = 0.04] cancer. After excluding sporadic patients, UC was associated with improved survival compared with CD [0.62, CI 0.43 to 0.90, p = 0.01] for stage II cancer. Conclusions Patients with IBD are diagnosed at an earlier stage but tend to have a worse survival compared with sporadic cases of CRC, in particular for nodal disease [stage III].Specifically, patients with CD-related CRC appear to fare worst in terms of survival compared with both the sporadic and UC groups.

2013 ◽  
Vol 144 (5) ◽  
pp. S-706-S-707
Lauren Kolodziej ◽  
Emanuelle Bellaguarda ◽  
Chuanhong Liao ◽  
David T. Rubin ◽  
Sonia Kupfer

2014 ◽  
Vol 33 (1) ◽  
pp. 52-57 ◽  
László Herszényi ◽  
Loránd Barabás ◽  
Pál Miheller ◽  
Zsolt Tulassay

Patients with long-standing inflammatory bowel disease (IBD) have an increased risk of colorectal cancer (CRC). The association between IBD and CRC is well supported, but reported risk estimates vary widely. Although recent evidence from population-based studies reports a decline in risk, CRC accounts for 10-15% of all deaths in IBD. The potential causes of recent epidemiological trends and the real magnitude of risk of CRC in IBD are subjects of debate. The molecular pathway leading to CRC differs from the classic adenoma-to-CRC sequence. Chronic inflammation contributes to the development of low- and high-grade dysplasia which may further convert into CRC. Patients with a young age at onset, long-standing and extensive colitis with severe inflammatory burden, a family history of sporadic CRC, and concomitant primary sclerosing cholangitis are at greatest risk. The CRC risk in patients with colonic Crohn's disease is similar to that of ulcerative colitis. IBD-associated CRC can frequently be detected at late stages and at a younger age. The long-term prognosis of CRC may be poorer in patients with IBD than in those with sporadic CRC. Regular surveillance colonoscopies may permit earlier detection of CRC, with a corresponding improved prognosis. The interval between surveillance colonoscopies is dependent on each patient's personal risk profile.

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