Colitis and colon cancer



Ulcerative colitis

Bowel cancer

People who have ulcerative colitis have an increased risk of developing bowel cancer (cancer of the colon, rectum or bowel), especially if the condition is severe or involves most of the colon.

The longer you have ulcerative colitis, the greater the risk.

People with ulcerative colitis are often unaware they have bowel cancer as the initial symptoms of this type of cancer are similar.

These include:

  • blood in the stools
  • diarrhoea
  • abdominal pain

You’ll usually have regular check-ups to look for signs of bowel cancer from about 10 years after your symptoms first develop.

Check-ups will involve examining your bowel with a colonoscope (a long, flexible tube containing a camera) that’s inserted into your rectum – this is called a colonoscopy.

The frequency of the colonoscopy examinations will increase the longer you live with the condition, and will also depend on factors such as how severe your ulcerative colitis is and if you have a family history of bowel cancer.

This can vary between every 1 to 5 years.

To reduce the risk of bowel cancer, it’s important to:

  • eat a healthy, balanced diet including plenty of fresh fruit and vegetables
  • take regular exercise
  • maintain a healthy weight
  • avoid alcohol and smoking

Taking aminosalicylates as prescribed can also help reduce your risk of bowel cancer.

Find out more about preventing bowel cancer

I. What every physician needs to know.

Ulcerative colitis, a disease of the mucosal surface of the colon, almost always involves the rectum and may extend proximally in a continuous fashion to involve the entire colon. The extent of the disease varies and in rare cases may involve the ileum, termed “backwash ileitis.” Cases that involve the rectum only are termed “ulcerative proctitis.”

Pathogenesis is not completely understood, but pathogenesis is believed to be multifactorial, with genetic and environmental factors, immune dysregulation, and alteration in the barrier of the gastrointestinal lumen. Having a family member with inflammatory bowel disease is a risk factor. Worldwide, ulcerative colitis is the most common form of inflammatory bowel disease. It may be cured by colectomy.

II. Diagnostic Confirmation: Are you sure your patient has ulcerative colitis?

A relapsing and remitting course is typical; episodes of active disease may be followed by periods of remission. The rectum, which is almost always involved, will be uniformly inflamed. A colonoscopy or flexible sigmoidoscopy may reveal a grossly erythematous mucosa that lacks normal vascular pattern. The mucosa may appear friable and have petechiae on appearance.

Hemorrhage, continuous ulceration and exudates may be observed in more severe disease. Biopsy specimens may show gland atrophy of the mucosa, crypt abscesses, and goblet cells that do not contain mucin. With pancolitis, disease stops at the ileocecal valve, and if disease involves the terminal ileum, it may be termed “backwash ileitis.” Infiltrates in the mucosal layer consist of plasma cells, granulocytes, and lymphocytes.

A. History Part I: Pattern Recognition:

The primary symptom in ulcerative colitis is bloody diarrhea that may be accompanied by mucous. The course of the disease is usually relapsing and remitting, with periods of active disease interspersed with symptom-free periods. Mucosal inflammation usually occurs in the rectum, spreads proximally, and may involve the entire colon. The symptoms of proctitis, disease that affects primarily the rectum, include constipation, fresh blood from the rectum, and fecal urgency.

Pancolitis may cause diarrhea, abdominal pain, fever, tenesmus, weight loss, and fatigue. Extraintestinal manifestations may occur and can be multisystemic. Skin lesions may include erythema nodosum and pyoderma gangrenosum. Ocular manifestations, such as uveitis and episcleritis, may be seen. Rheumatologic symptoms, such as migratory polyarthritis, sacroiliitis, and ankylosing spondylitis, may occur, primarily involving large joints. Primary sclerosing cholangitis and venous and arterial thromboembolism may also occur.

Severity of disease based on the model by Truelove and Witts:

Mild disease may be characterized by fewer than four bloody bowel movements per day, erythrocyte sedimentation rate (ESR) less than 20 mm/h, normal c-reactive protein (CRP), heart rate less than 90 bpm, hemoglobin greater than 11.5 g/dl, and temperature less than 37.5 degrees Celsius. Hallmarks of moderate disease include an ESR of 30 mm/h or less, hemoglobin greater than or equal to 10.5 g/dL and CRP of 30 mg/L or less. Severe disease is characterized by six or more bloody bowel movements per day, hemoglobin less than 10.5 g/dL, heart rate greater than 90, ESR greater than 30 mm/h, and CRP greater than 30 mg/L.

B. History Part 2: Prevalence:

The incidence of ulcerative colitis is 1–20 per 100,000 persons per year. Prevalence is 7–246 cases per 100,000 persons per year. Ulcerative colitis has a higher incidence in European countries, Canada, Australia, New Zealand, and the United States, linking it to a Westernized lifestyle. Peak incidence occurs at three age ranges, 20–24, 40–44, and 60–64. Smoking is associated with milder disease.

C. History Part 3: Competing diagnoses that can mimic ulcerative colitis.

Ischemic colitis, radiation colitis, diverticulitis, parasitic infection, Clostridium difficile diarrhea, graft versus host disease, solitary rectal ulcer syndrome, and medication-induced colitis are competing diagnoses. Culprit medications that produce colitis that may mimic ulcerative colitis include oral contraceptives, NSAIDS, retinoic acid, ipilimumab, mycophenolate, and gold.

Infectious causes of colitis—bacterial causes such as Salmonella, Aeromonas, Shigella, Campylobacter, and especially E. coli 0157:H7—can resemble ulcerative colitis, manifested by hematochezia, abdominal pain, and diarrhea, but the course should be self-limited and not episodic in nature, as with ulcerative colitis. Travel history and food outbreaks may be historical clues that can point toward infectious colitis. Parasitic infections may cause recurrent diarrhea following travel to endemic areas.

Microscopic colitis, such as lymphocytic colitis, will present with watery diarrhea and will typically require a biopsy to diagnose. Frequent enemas may also induce colitis that may mimic ulcerative colitis.

D. Physical Examination Findings.

Evidence of volume depletion from diarrhea, such as orthostatic blood pressure and tachycardia, may be present. Abdominal exam will be unremarkable for peritoneal signs, such as rebound tenderness and guarding.

E. What diagnostic tests should be performed?

Colonoscopy with biopsy is the gold standard in diagnosis.

The biopsy features suggestive of ulcerative colitis include crypt abscesses, crypt branching, shortening and disarray, and crypt atrophy. Basal plasmacytosis may also be a predictor of relapse in patients with seemingly well-controlled UC with complete mucosal healing.

In acute colitis, colonoscopy should be avoided because of risk of bowel perforation. Sigmoidoscopy may be performed in an acute flare, and biopsy may be necessary to exclude CMV colitis in patients who are steroid refractory. Antibody testing not part of diagnostic evaluation of patients with suspected IBD as accuracy is uncertain including for pANCA.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

CBC, serum albumin, erythrocyte sedimentation rate, and C-reactive protein should be performed, as should evaluation of stool, such as examination for ova, parasites, and fecal leukocytes. Stool studies should look for C. difficile toxin, routine cultures (Salmonella, Shigella, Campylobacter, Yersinia), specific testing for E. coli O157:H7, Giardia stool antigen (if travel history suggests along with test for amebiasis), test for N. gonorrhoeae, HSV and Treponema pallidum if sexual history is suggestive or having severe urgency or tenesmus.

It is important to exclude infection as a cause of colitis, and a sigmoidoscopy with biopsy may be necessary if the patient fails to respond to steroids in an acute flare in order to look for CMV colitis with immunoperoxidase staining (especially if the patient is immunocompromised).

Patients with ulcerative colitis and primary sclerosing cholangitis may have an elevation in serum alkaline phosphatase.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Abdominal radiograph should be performed to evaluate for toxic megacolon. Plain abdominal radiographs should be repeated if there is clinical deterioration to determine if there is colonic dilatation >5.5 cm or toxic megacolon (diameter >6 cm or cecum >9 cm and systemic toxicity). Patient with transverse colon diameter >5.5 cm should receive decompression with a nasoenteric tube.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Fecal calprotectin, which may be an indicator of inflammation within the intestines, is nonspecific. The gold standard of diagnosis relies on an appropriate history coupled with a flexible sigmoidoscopy with biopsy. Barium enema, which is often normal in patients with mild disease severity, is not commonly used in the diagnosis of ulcerative colitis. In fulminant UC, a barium enema may lead to toxic megacolon.

III. Default Management.

Pharmacologic treatment is aimed at reducing inflammation and inducing remission of symptoms. Steroid-sparing regimens are usually preferred long-term in order to reduce systemic side effects.

For mild to moderate disease, topical (rectal) and oral aminosalicylates, such as sulfasalazine and 5-aminosalicylates, should be used first. Oral and rectal forms (suppositories and enemas), which may be used in combination, can induce remission in roughly half of patients. Sulfasalazine dosing is usually in divided doses; for example, 1g may be given orally three to four times daily. Mild to moderate proctitis should be managed topically with mesalamine suppositories (1 gram per day) or enemas (2–4 grams per day). If remission is not achieved in two weeks, 5-aminosalycilate enemas (2–4 grams per day) or hydrocortisone/budesonide enemas may be tried.

To induce remission in a first flare or a flare requiring steroids annually, patient should be given an oral prednisone equivalent of 0.75–1 mg/kg for two to four weeks and tapered. After successful tapering, maintenance therapy with 5-ASA may be used. If remission cannot be maintained, the next course of oral steroids should be combined with azathioprine at 2–2.5mg/kg or mercaptopurine at 1–1.5 mg/kg.

A. Immediate management.

For severe disease requiring hospitalization, a coagulation profile and type and screen may be indicated if blood products are required. Fulminant ulcerative colitis requires inpatient treatment. Steroids, such as methylprednisolone 60mg or hydrocortisone 400 mg intravenously daily, are the first-line therapy. If the AZA-naïve patient does not respond (sustained fever, bloody diarrhea more than four times daily or continued elevated CRP) on days 3–7, IV cyclosporine or infliximab should be started. Cyclosporine is given at a dose of 2 mg/kg after exclusion of hypomagnesemia. Cyclosporine trough levels must be checked on day 3. If there is clinical improvement, AZA at 2–2.5 mg/kg or 6-MP at 1–1.5 mg/kg should be started before discharge, and oral cyclosporin should be continued for at least three months as a bridging therapy. If no improvement is achieved within 5–7 days, infliximab may be tried, or colectomy must be considered. If there is clinical improvement, infliximab should be continued at 5 mg/kg every 8 weeks.

B. Physical Examination Tips to Guide Management.

Rectal exam is important to note presence of blood in the rectal vault. As described above, dermatologic, ocular, and rheumatologic manifestations, which can be easily identified with a visual inspection of the eyes and skin, may be associated with ulcerative colitis.

Arthritis is the most common extra intestinal manifestation and is both a nondestructive peripheral arthritis, which primarily involves large joints and ankylosing spondylitis. Eye involvement includes uveitis, episcleritis, scleritis, iritis, or conjunctivitis with presentation ranging from asymptomatic to burning, itching, or redness of eyes. Skin involvement includes erythema nodosum and pyoderma gangrenosum. Patients also are at increased risk of venous and arterial thromboembolism.

C. Laboratory Tests to Monitor Response to and Adjustments in Management.

Monitor the number of bloody bowel movements, hemoglobin, and hematocrit.

D. Long-term management.

Steroid-dependent ulcerative colitis occurs if a patient relapses within twelve weeks after corticosteroid discontinuation or if corticosteroids cannot be tapered within sixteen weeks. Compliance with 5-ASA therapy must be assessed in patients deemed steroid-refractory. Surgical treatment may be considered when the patient has failed medical therapy or cannot tolerate medical therapy, or in the presence of toxic megacolon, severe bleeding, high-grade or multifocal dysplasia, colorectal cancer, or stunted growth in children.

E. Common Pitfalls and Side-Effects of Management

Antibiotics have no role in the treatment of ulcerative colitis. Clinicians should avoid long-term use of corticosteroids in order to prevent systemic side effects. Common pitfalls include suboptimal dosing of medications, specifically immunosuppressants, or changing to biologic agents prematurely. Another common pitfall is the long-term use of glucocorticoids, which pose significant systemic side effects.

IV. Management with Co-Morbidities

A. Renal Insufficiency.

Mercaptopurine dosing must be adjusted for creatinine clearance less than 50 and should be dosed every 48 hours. No supplement in HD or PD is required.

Azathioprine requires a dose adjustment for renal insufficiency as well. For CrCl of 10–50, dose should be decreased by 25 percent; for CrCl less than 10, dose reduction of 50 percent is recommended. With hemodialysis, a 0.25 mg/kg supplement should be prescribed. Nephrotoxicity may occur with the use of sulfasalazine.

B. Liver Insufficiency.

Mercaptopurine may be associated with jaundice, hepatotoxicity, hepatic encephalopathy, ascites and pancreatitis. Azathioprine has also been associated with hepatotoxicity, pancreatitis, and hepatic veno-occlusive disease.

C. Systolic and Diastolic Heart Failure

If blood products are being transfused, consideration of administration of a loop diuretic may be of utility to avoid volume overload and exacerbation of heart failure symptoms.

D. Coronary Artery Disease or Peripheral Vascular Disease

If patients have severe anemia and a history of coronary artery disease, transfusion parameters may be higher (i.e., hemoglobin/hematocrit of 10 mg/dL and 30 mg/dL, respectively).

E. Diabetes or other Endocrine issues

No change in standard management.

F. Malignancy

Azathioprine carries a black box warning for risk of malignancy that is due to chronic immunosuppression, which includes post-transplant lymphoma and hepatosplenic T-cell lymphoma when used to treat inflammatory bowel disease. Infliximab treatment carries an increased risk of lymphoma and other malignancies. Cases of fatal hepatosplenic T cell lymphomas have been reported with infliximab in combination with azathioprine or 6-mercaptopurine.

Patients with UC have increased risk of colorectal cancer with the two most important risk factors being the extent of colitis and duration of the disease. The risk for colorectal cancer is highest in patients with pancolitis, and risk starts to increase 8 to 10 years following onset of symptoms.

Strictures in UC should be considered malignant until proven otherwise by endoscopic evaluation with biopsy.

G. Immunosuppression (HIV, chronic steroids, etc.)

Azathioprine acts as an immunosuppressive agent and may increase the risk of infection. Infliximab carries a black box warning for serious infection risk, including a risk of pulmonary and extrapulmonary tuberculosis, invasive fungal infections, and other opportunistic infections. Patients should be screened carefully for risk factors for tuberculosis and evidence of latent TB infection.

H. Primary Lung Disease (COPD, Asthma, ILD)

Sulfasalazine may be associated with interstitial lung disease and hypersensitivity pneumonitis.

I. Gastrointestinal or Nutrition Issues

Sulfasalazine can cause anorexia, nausea/vomiting, dyspepsia, and pancreatitis.

J. Hematologic or Coagulation Issues

Mercaptopurine may cause myelosuppression, manifested as anemia, leukopenia, or thrombocytopenia. Azathioprine can also cause myelosuppression, with side effects of anemia, thrombocytopenia, or leukopenia. Sulfasalazine may be associated with adverse reactions of hemolytic anemia, blood dyscrasias, agranulocytosis, and aplastic anemia.

Anemia can be secondary to blood loss, anemia of chronic disease, or autoimmune hemolytic anemia.

K. Dementia or Psychiatric Illness/Treatment

No change in Standard Management.

V. Transitions of Care

A. Sign-out considerations While Hospitalized.

Follow CBC.

B. Anticipated Length of Stay.

Goal length of stay should be about one week.

C. When is the Patient Ready for Discharge?

Readiness for discharge should be assessed when bloody bowel movements have resolved and the patient is afebrile and no longer requires blood product transfusion. The patient should be tolerating at least a bland diet at the time of release.

D. Arranging for Clinic Follow-up

Patients may be advised to follow up with a gastroenterologist. Patients with ulcerative colitis in whom total colectomy has not been performed, will need surveillance screening for malignant neoplasm of the colon.

1. When should clinic follow up be arranged and with whom?

Patient should follow up with a gastroenterologist within two weeks of discharge from the hospital, but sooner if symptoms of bloody diarrhea, fever, or abdominal pain return.

2. What tests should be conducted prior to discharge to enable the best clinic first visit?


3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit?


E. Placement Considerations.


F. Prognosis and Patient Counseling.

The prognosis in ulcerative colitis is good during the first decade, and only few will require colectomy. Remission is often achieved.

VI. Patient Safety and Quality Measures

A. Core Indicator Standards and Documentation.


B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

In an acute flare of ulcerative colitis, where bloody bowel movements may be present, refrain from administering pharmacologic DVT prophylaxis until symptoms have stabilized.

VII. What’s the Evidence?

Bernstein, CN, Blanchard, JF, Houston, DS, Wajda, A. “The incidence of deep venous thrombosis and pulmonary embolism among patients with inflammatory bowel disease: a population-based cohort study”. Thromb Haemost. vol. 85. 2001. pp. 430

Irving, PM, Pasi, KJ, Rampton, DS. “Thrombosis and inflammatory bowel disease”. Clin Gastroenterol Hepatol. vol. 3. 2005. pp. 617

Bernstein, CN, Wajda, A, Blanchard, JF. “The incidence of arterial thromboembolic diseases in inflammatory bowel disease: a population-based study”. Clin Gastroenterol Hepatol. vol. 6. 2008. pp. 41

Novacek, G, Weltermann, A, Sobala, A. “Inflammatory bowel disease is a risk factor for recurrent venous thromboembolism”. Gastroenterology. vol. 139. 2010. pp. 779

Murthy, SK, Nguyen, GC. “Venous thromboembolism in inflammatory bowel disease: an epidemiological review”. Am J Gastroenterol. vol. 106. 2011. pp. 713

van Rheenen, PF, Van de Vijver, E, Fidler, V. “Faecal calprotectin for screening of patients with suspected inflammatory bowel disease: diagnostic meta-analysis”. BMJ. vol. 341. 2010. pp. c3369

Ferrante, M, Henckaerts, L, Joossens, M. “New serological markers in inflammatory bowel disease are associated with complicated disease behaviour”. Gut. vol. 56. 2007. pp. 1394

Ruemmele, FM, Targan, SR, Levy, G. “Diagnostic accuracy of serological assays in pediatric inflammatory bowel disease”. Gastroenterology. vol. 115. 1998. pp. 822

Sandborn, WJ, Loftus, EV, Colombel, JF. “Evaluation of serologic disease markers in a population-based cohort of patients with ulcerative colitis and Crohn’s disease”. Inflamm Bowel Dis. vol. 7. 2001. pp. 192

Lutgens, MW, van Oijen, MG, van der Heijden, GJ. “Declining risk of colorectal cancer in inflammatory bowel disease: an updated meta-analysis of population-based cohort studies”. Inflamm Bowel Dis. vol. 19. 2013. pp. 789

Levin, B. “Inflammatory bowel disease and colon cancer”. Cancer. vol. 70. 1992. pp. 1313

Lennard-Jones, JE. “Cancer risk in ulcerative colitis: surveillance or surgery”. Br J Surg. vol. 72. 1985. pp. S84

Rutter, MD, Saunders, BP, Wilkinson, KH. “Thirty-year analysis of a colonoscopic surveillance program for neoplasia in ulcerative colitis”. Gastroenterology. vol. 130. 2006. pp. 1030

Nugent, FW, Haggitt, RC, Gilpin, PA. “Cancer surveillance in ulcerative colitis”. Gastroenterology. vol. 100. 1991. pp. 1241

Panos, MZ, Wood, MJ, Asquith, P. “Toxic megacolon: the knee-elbow position relieves bowel distension”. Gut. vol. 34. 1993. pp. 1726

Mowat, C, Cole, A, Windsor, A. “Guidelines for the management of inflammatory bowel disease in adults”. Gut. vol. 60. 2011. pp. 571

Colon Cancer Symptoms vs. Ulcerative Colitis Differences between Symptoms Topic Guide

Colon Cancer Symptoms vs. Ulcerative Colitis Differences and Similarities:

Colon cancer or colorectal cancer is cancer that originates from the color or rectum, and is the third most common type of cancer diagnosed in the US. Ulcerative colitis or UC is not cancer, but is a disease that causes inflammation, irritation, swelling, and sores on the inner lining of the colon. Ulcerative colitis is a type of inflammatory bowel disease (IBD), which includes Crohn’s disease.

Colon cancer and ulcerative colitis have similar signs and symptoms, for example, abdominal/cramping and/or pain, fatigue, anemia due to blood loss, rectal bleeding, frequent loose bowel movements, and fatigue. Ulcerative colitis is a risk factor for getting colon cancer, however, it does not cause cancer.

Colon cancer can spread to other organs and areas of the body (metastasize) while ulcerative colitis only occurs in the large intestine. Treatment, cure, and survival rates for colon cancer depends upon the type of cancer, stage, and health of the individual. Ulcerative colitis cannot be cured; however, symptoms and recurrence of the disease can be managed with medication and lifestyle changes.

Everything You Need to Know About the Ulcerative Colitis–Colon Cancer Connection

While it’s true that people who have ulcerative colitis (UC) are at increased risk of developing colorectal (colon) cancer, having a higher risk doesn’t mean you’ll absolutely get it. Only about 5 percent of people with severe ulcerative colitis end up with colorectal cancer. Plus, there are steps you can take to reduce your risk.

When you have ulcerative colitis, your colon is essentially being attacked by your own immune system, causing inflammation. “Long-standing inflammation causes dysplasia, changes in the cells of the lining of your colon that may eventually become cancer,” says Shannon Chang, MD, assistant professor of medicine at NYU School of Medicine and a gastroenterologist at NYU Langone Medical Center in New York City. Though numbers vary, experts estimate that people with long-standing inflammatory bowel conditions have an almost two-and-a-half times greater risk of colon cancer than the regular population, according to a study published in April 2016 in the journal Digestive Endoscopy.

How Colitis May Affect Your Cancer Risk

Signs and symptoms of colon cancer can be tougher to discern in ulcerative colitis patients. Blood in the stool, for example, which is a warning sign of cancer, may also happen as a result of a flare-up of the condition. The cancer itself is different, too, says Dr. Chang. “Cancer in UC patients looks more like lesions, and less like masses or tumors,” she says. But certain factors can increase your likelihood of developing cancer, including:

  • The Severity of the Condition The longer you have uncontrolled inflammation, the more likely you are to develop dysplasia. Put another way, it’s not just having ulcerative colitis that ups your cancer risk; it’s having uncontrolled UC that puts you in the danger zone.
  • How Much of Your Colon is Affected If just the 5 to 10 centimeters (cm) of colon closest to the rectum is affected — a condition called ulcerative proctitis — your risk is similar to that of the normal population. If your entire colon is affected, your risk rises.

How to Reduce Your Colon Cancer Risk

With a chronic condition like UC, you should have regular checkups with your doctor to be sure that you’re staying on top of controlling the disease, and to catch any warning signs of more serious complications, such as cancer. There are also other ways to reduce your risk, including:

  • Changing Your Medication There’s some evidence that cholesterol-lowering statin drugs can have what’s called an “immunomodulatory effect,” meaning they reduce inflammation, according to a study published in July 2016 in the journal Clinical Gastroenterology and Hepatology. Also, a study published in November 2014 in The American Journal of Gastroenterology has shown that the drug Remicade (infliximab), an anti-inflammatory usually prescribed for rheumatoid arthritis, may be effective at controlling inflammation in ulcerative colitis, which in turn may have a protective effect against cancer.
  • Eating a Healthy, Low-Fat Diet While there’s no perfect diet for reducing flare-ups of ulcerative colitis, it’s smart to reduce your intake of animal fat, which has a negative impact on the condition.
  • Scheduling Regular Cancer Screenings The current recommendation is that if you’ve had ulcerative colitis for more than eight years, you should have an annual colonoscopy. “To get the most accurate sampling of the entire colon, biopsies should be taken every 10 cm or so during the screening,” says Chang.
  • Getting More Sophisticated Testing The highest-risk patients may undergo what’s called chromoendoscopy, says Chang. In this test, the colon is sprayed with a dye that highlights areas with dysplasia more accurately.

Reducing your cancer risk when you have ulcerative colitis is all about minimizing inflammation. Talk to your doctor about the best way to manage the condition, says Chang.

“Ask whether medications are working or if you should try something different, get your cholesterol tested, and pay attention to your diet. Our aim is to try to prevent problems before they start.”


Year : 2015 | Volume : 11 | Issue : 4 | Page : 899-903

Prevalence of colorectal cancer in patients with ulcerative colitis: A retrospective, monocenter study in China
Qin Zhang, Sumei Sha, Bin Xu, Shuhui Liang, Kaichun Wu
State Key Laboratory of Cancer Biology and Xijing Hospital of Digestive Diseases, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi Province, P. R. China

Date of Web Publication 15-Feb-2016

Correspondence Address:
Kaichun Wu
17, Changle Western Road, Xi’an 710032, Shaanxi Province
P. R. China

Source of Support: This study was supported by grants from the National Healthcare Research Project (no. 201002020), National Scientific Support Project (nos. 2012BAI06B03 and BSW11J013), National Natural Science Foundation of China (Nos. 81322037, 81170360 and 81370504) and National Excellent Doctoral Dissertation of PR China (No. 201182), Conflict of Interest: None



DOI: 10.4103/0973-1482.143345

> Abstract

Background: Ulcerative colitis-associated colorectal cancer (UC-CRC) is a serious complication of UC. Data on the clinical characteristics of patients in China are scarce.
Aims: We aimed to study the incidence, characteristics, treatment, and prognosis of CRC patients with a history of UC.
Materials and Methods: We identified patients with UC and followed them until the first occurrence of cancer, death, or emigration in a single study center in China.
Results: A total of 4 UC-associated CRC patients were identified among the 642 cases recorded from January 2000 to December 2012. The overall risk of cancer was 0.64%. The overall median duration of UC was 15.5 years (range 6-21 years) in patients with UC-associated CRC. Of these patients, 75% (3/4) were at an advanced stage when they were diagnosed. Longer disease duration and extensive colitis were identified as risk factors for developing CRC, and 5-aminosalicylic acid and steroid therapies were not identified as protective factors against UC-associated CRC.
Conclusions: Patients with UC are at an increased risk for CRC. However, the prevalence of CRC in China remains lower than that in the West.

Keywords: Colorectal cancer, ulcerative colitis, ulcerative colitis-associated colorectal cancer

How to cite this article:
Zhang Q, Sha S, Xu B, Liang S, Wu K. Prevalence of colorectal cancer in patients with ulcerative colitis: A retrospective, monocenter study in China. J Can Res Ther 2015;11:899-903

> Introduction

Colorectal cancer (CRC) is the one of the leading causes of cancer-related deaths in the world. Each year more than 1.2 million cases are diagnosed with about 600,000 deaths. CRC is the third most common cancer diagnosed in both men and women in the US and the fourth most common cause of cancer mortality worldwide. CRC is also the second most common cause of cancer deaths in the United States and other developed countries, despite important advances in detection, surgery, and chemotherapy. It has been known that patients with inflammatory bowel disease (IBD) are at increased risk for cancer. Systematic review pointed out the overall risk of CRC in 181,923 ulcerative colitis (UC) patients was 1.69/1000 py, 0.91/1000 py in the first decade after the diagnosis of UC, 4.07/1000 py in the second and 4.55/1000 py in the third decade. These rates are considerably higher than the incidence of CRC reported in the general population. The incidence of CRC in the general population ranges from 0.4/1000 py in Australia, New Zealand, USA and Western Europe to 0.1/1000 py in Africa. Meta-analysis of population-based cohort studies also revealed a significant 2.4-fold increased risk of CRC among patients with UC belonging to population-based cohorts, with an average follow-up time of 14 years. Besides, UC-CRC is 15-20 years earlier at the age when diagnosed compared to sporadic CRC. Since Crohn and Rosenberg reported the first case of IBD-associated CRC, numerous studies have been conducted on the association between UC and CRC, especially in Western countries. Several decades ago, de Dombal reported that the cumulative risk of CRC in patients with extensive UC was approximately 5% after 10 years and 41.8% after 25 years in Leeds. Currently, the increased risk of CRC in UC patients is widely accepted, and there is a general consensus that longer duration and extensive UC are risk factors for developing CRC. Several papers have reported that the prevalence of CRC in IBD patients ranges from 0.6% to 17%. Although such cases account for only 1-2% of all CRC cases in the general population, CRC is considered a serious complication of IBD and accounts for approximately 10-15% of all deaths in patients with IBD.

A meta-analysis of studies in Western countries estimated that the risk of CRC in UC (cumulative incidence) is 1.6% after 10 years, 8.3% after 20 years, and 18.4% after 30 years of the disease, with overall prevalence of 3.7%. Studies with patients in tertiary care centers or hospitals have demonstrated a higher cancer risk and worse prognosis. One study also suggested that CRC incidence rates in UC patients varied geographically, with higher risk among the residents of the USA and the UK than among Scandinavians and residents of other countries. The limited data available from other countries such as India, South Korea, and Hungary show a lower risk than that reported in the West. Retrospective studies have shown UC cancer rates of 0.87% and 1.5% in Mainland China and Taiwan, respectively. , However, the number of patients with UC has increased three-fold in the past 10 years in China. There is limited knowledge about the possible relationship between clinical parameters and the incidence rate of cancer in UC. The risk factors and clinical features of UC-CRC patients are not well understood.
In the current study, we retrospectively observed the malignant transformation of UC patients who had been diagnosed with CRC from January 2000 to December 2012 in a single center. The purpose of this study was to determine the variability of the incidence of UC-CRC in a relatively large cohort of patients. We also analyzed whether demographic and clinical factors had an effect on the incidence of CRC in UC.

> Materials and methods

Patient selection
This study was a retrospective cohort analysis of all patients with a confirmed diagnosis of UC. The diagnosis was confirmed using clinical, endoscopic, histopathological, and radiologic findings according to the internationally accepted Lennard-Jones criteria. The majority of patients were advised to undergo a mapping colonoscopy during their first visit and yearly follow-up colonoscopies after 7 years of disease. Therefore, patients were included in the study only if they had undergone colonoscopy. Cancers diagnosed within 1 year of the UC diagnosis were excluded. From January 2000 to December 2012, 624 patients were reviewed. CRC was diagnosed by one experienced gastrointestinal pathologist and confirmed by another. The current study was performed with the approval of the local ethics committee, and informed consent was obtained from the patients.
Data extraction
During colonoscopy, biopsies were taken when there was an abnormal pit pattern according to Kudo’s classification. The patients’ complete medical history was assessed, including prior colonoscopies and pathology reports. Patient records were reviewed for demographic features, endoscopic characteristics, operative approaches, and vital status at last follow-up. Data on gender, age, disease location, disease duration, colonoscopic follow-up, 5-aminosalicylic acid (5-ASA), and steroid therapy were collected from all of patients for analysis. The extent of inflammation was retrieved from histology and colonoscopy reports or barium enema X-ray reports, as recorded in medical records at the time of the UC diagnosis. The prevalence of UC-CRC was estimated, and the clinical characteristics of these patients were observed. The localization of CRC was described in terms of the eight segments of the colorectum, as follows: The cecum, the ascending colon, hepatic flexure, the transverse colon, splenic flexure, the descending colon, the sigmoid colon, and rectum. For the statistical analyses, the localization was re-coded as the right colon (cecum, ascending or transverse colon), the left colon (splenic flexure and descending and sigmoid colon), or rectum. The cancer site was classified according to the International Classification of Diseases for Oncology. The extent of cancer at the time of diagnosis was classified according to the TNM classification. The follow-up time was defined as the time in years from the diagnosis of UC to the diagnosis of CRC.
Statistical analysis
The associations between categorical variables were analyzed using the χ2 test. Mean age was compared using the two-tailed Student’s t-test. Cox’s proportional hazards regression was used to estimate univariable and multivariable hazard ratios to analyze the effect of several risk factors on the development of UC-CRC. Odds ratios and 95% confidence interval were calculated. All the data analyses were performed using SPSS 19.0 software (SPSS, Inc., Chicago, IL, USA). P < 0.05 were considered as statistically significant.

> Results

Clinical characteristics and incidence of ulcerative colitis in ulcerative colitis patients
A total of 624 patients with UC were enrolled. Altogether, excluding the cancers diagnosed within 1 year of the UC diagnosis, four of the 624 patients were diagnosed with UC-CRC by both colonoscopy and biopsy pathology. The overall risk of cancer was 0.64%. All of patients with UC-CRC had received regular colonoscopy examinations. The clinical features of the UC group and the UC-CRC group are shown in. Of the UC-CRC patients, 50% (2/4) were male. The median age at the time of the CRC diagnosis was 54.5 years (range 48-63 years), compared with 39.0 years (10-86 years) for the UC patients (P < 0.01). The overall median duration of UC was 15.5 years (range 6-21 years) in patients with UC-associated CRC and 1 year (range 0.1-40 years) in the UC patients without CRC. 75% (3/4) of the UC-CRC patients and 11.8% (112/620) of the UC patients were the severity disease according to the Truelove-Witts index scoring system. Of the UC-CRC patients, 75% (3/4) were at an advanced stage when diagnosed. All four patients had extensive colitis.

Table 1: The clinical characteristics between UC-CRC and UC patients
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Tumor characteristics of ulcerative colitis in ulcerative colitis patients
By the time they were diagnosed with CRC, all of the patients had progressed to total colitis. Of the four tumors, 25% (n = 1) were located in the rectum, 25% (n = 1) in the sigmoid colon, and 50% (n = 2) in the transverse and right colon. The distribution of the CRC stages at diagnosis in patients with UC was as follows: 50% (n = 2) in situ and 50% (n = 2) in Stage I. The histological type was available for all cases of CRC, and the distribution was as follows: 50% (n = 2) severe a typical hyperplasia and 50% (n = 2) well-differentiated adenocarcinoma. With regard to the treatment, a total proctocolectomy with end ileostomy (EI) was performed on two patients (50%) and a subtotal colectomy with EI was performed on two patients (50%). One of the 4 UC-CRC patients was treated with chemotherapy after surgery.
Risk factors for ulcerative colitis in ulcerative colitis patients
As shown in, there were statistically significant differences between the UC and the UC-CRC patients in terms of gender, age, the duration of UC, the degree of pathological changes, the extent of disease, and whether corticosteroids or 5-ASA medications were used. We further analyzed these factors using logistic regression. As shown in

, disease duration and extensive colitis were identified as risk factors of UC-CRC. Symptom activity was also significantly related to colitis-CRC. The results also showed that UC duration >10 years, entire colon lesions, and severe inflammatory lesions were risk factors for UC-CRC. However, gender and the use of 5-ASA/sulfasalazine or corticosteroids were not identified as protective factors or risk factors for UC-CRC; the difference did not reach significance.

Table 2: UC cancerous risk factor analysis
Click here to view

> Discussion

Ulcerative colitis is associated with a marked increased risk of colonic dysplasia and CRC. Specifically, the risk is estimated to be 1.5-5 times higher than that of non-UC controls. After 8-10 years, since the diagnosis of UC, the cancer risk increases annually by a proportion of 0.5 ~ 1%. Although it only accounts for 1 ~ 2% of all CRC cases, 15% of the UC-related deaths were due to CRC. Numerous studies have been carried out in Western countries, and the risk of CRC in UC varied substantially across studies. This variation can be attributed to many factors, including the study design. Moreover, studies have suggested that CRC incidence rates in UC patients vary geographically, with a higher risk among the residents of the USA and the UK than among Scandinavians and the residents of other countries. Data from Asian countries were limited, potentially due to the lower UC incidence. A national population survey in South Korea showed that the prevalence of CRC in patients with UC was 0.37%, whereas the prevalence was 0.94% in India. The number of UC patients in China has increased in the past decade. It is anticipated that the incidence of UC-CRC will increase simultaneously. Meta-analysis recently revealed the risk of patients with UC developing CRC has decreased over the last six decades, the risk of CRC in UC are lower than those reported by Eaden et al. in 2001. With a tighter control of the inflammation, higher colectomy rates, the use of drugs with chemopreventive effects and a better adherence to endoscopic surveillance programs in high-risk patients, the incidence of CRC in UC patients seems to have decreased during the last few decades. Moreover, Jess and co-investigators published a meta-analysis of population-based cohort studies to determine the risk of CRC in patients with UC. In these population-based cohorts, the authors also suggested that the long-term risk of CRC among patients with UC was overestimated in the previous meta-analysis performed by Eaden et al. However, data on the incidence, characteristics, treatment modalities, and prognosis of UC-CRC in China are scarce. The present study reports the frequency of UC-CRC and the survival rates in China over a period of 12 years. In this single-center retrospective study, the data showed that the prevalence of CRC in Chinese UC patients was 0.64%. In accordance with previous reports in other Asian countries, the prevalence of UC-CRC observed in this study was lower than that in the global meta-analysis. In a multi-center retrospective study, data showed that the period prevalence of CRC in Chinese UC patients was 0.87%, which was similar to our results, indicated that while there is a trend of declining risk of developing CRC in UC patients, this trend is also confirmed by our study.
Several factors may contribute to the low incidence. First, although the incidence of UC in China increased in recent years, it was lower than that in Western countries. Second, the severity of inflammation is a risk factor for CRC in UC. However, most UC patients in China have mild inflammation and can maintain remission with proper treatment. Third, this study was retrospective and some of the patients did not complete follow-up visits regularly. Even among patients who completed regular follow-up visits, fewer specimens from fewer parts were taken. As a result, certain findings may have been missed.
In chronic UC, risk largely depends on the duration and extent of the disease. Research studies have shown that a variety of inflammatory factors, such as tumor necrosis factor alpha, interleukin (IL-31), IL-6, IL-23, and the nuclear factor-κB, predominate the related network signaling pathways in the inflammation of UC and play an important role in the process of cancer. In accordance with previous studies, of the 4 UC-CRC patients in the current cohort, three had the disease for more than 10 years and all had extensive colitis or pancolitis. The statistical analyses also revealed that disease duration longer than 10 years and extensive colitis were risk factors for CRC in UC patients.
Given the theory that chronic inflammation plays the most important role in malignant transformation, it can be reasonably concluded that anti-inflammatory therapy, such as 5-ASA or steroid use, may serve as a protective factor against malignant transformation in UC patients. In particular, 5-ASA and thiopurines are thought to decrease or increase the risk of cancer development in IBD patients. However, there is a debate concerning whether they can prevent CRC progression in UC patients. Eaden et al. had reported that the use of sulfasalazine can reduce the risk of colon cancer by 75%, but it does not affect the risk. Bernstein indicated that 5-ASA medications did not have a protective function in patients with UC. The current study found no association between 5-ASA or corticosteroid use and UC-CRC. The risk of CRC was similar between users and non-users of 5-ASA and thiopurines, suggesting that these treatments may not be protective against UC-CRC.
Gyde et al. investigated 35 patients with CRC in a retrospective cohort of 823 patients with UC onset between 1945 and 1965 and showed that age at the onset of IBD symptoms was associated with the colitis-CRC interval. The risk of CRC was higher in patients who were diagnosed with UC at a young age. The UC patients who were smokers tended to have a lower risk of CRC than nonsmokers. With regard to gender, studies in the United States and Canada , reported that two-thirds of UC-CRC patients were male. In addition, the literature indicates that primary sclerosing cholangitis, diabetes, and appendix resections for cancer are risk factors for UC; however, we did not analyze these factors in the present retrospective study. Endoscopic surveillance remains an important method for detecting UC-CRC. Regular colonoscopy examinations could help to identify a typical hyperplasia or CRC at an early stage and administer the proper treatment quickly, reducing the incidence of UC-CRC and mortality.

Studies on the outcomes and prognosis of UC-CRC have reached conflicting results. , Some of these studies have suggested that survival is similar between sporadic CRC and IBD-associated CRC. In fact, IBD-related CRC is generally more poorly differentiated and exhibits differing frequencies of genetic alterations (p53 and K-ras mutations) in comparison with sporadic CRC. , In the current study, the 4 patients with UC-CRC were treated with either chemotherapy or surgery, and all of them were alive when the study concluded.

> Conclusion

We identified patients with a diagnosis of UC recorded from January 2000 to December 2012 and followed them until the first occurrence of cancer, death, or emigration. We found that the cumulative risk of CRC was high in patients with UC; however, it was lower than that in Western countries. While there is a trend of declining risk of developing CRC in UC patients, this trend is also confirmed by our study. Disease duration >10 years and extensive colitis were identified as important risk factors for developing CRC. Symptoms, but not gender or the use of 5-ASA/sulfasalazine or corticosteroids, had an effect on the UC-CRC interval.

> References

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The Risk of Colorectal Cancer in Crohn’s Disease and Ulcerative Colitis Patients

Patients with ulcerative colitis and Crohn’s disease involving the colon need to be especially vigilant about screenings for colorectal cancer. These patients are at higher risk for developing colorectal cancer than the general population.

Inflammation of the colon can cause continuous turnover of cells in the intestinal lining, which increases the chance of irregularities that may lead to cancer. Though the vast majority of patients with Crohn’s disease and ulcerative colitis will never develop colorectal cancer, it is important to discuss the risk with your doctor. Colorectal cancer is a highly treatable disease when it’s found early.

Minimizing your Colorectal Cancer Risk

Video Length 3:00

Minimizing your Colorectal Cancer Risk IBD patients can minimize their colorectal cancer risk. Listen to learn more!


after spending eight years with an

inflammatory bowel disease you learn to

live with it but then at that eight year

mark another wrinkle gets thrown in

you’re an increased risk of developing

colorectal cancer I can’t say that I’m

not nervous about it that’s Jonathan

Miller a 28 year old salesman in Chicago

he was diagnosed eight years ago so he’s

just entering that era of heightened

risk whatever happens is gonna happen

when I get there I’m gonna deal with it

trying to eat right trying to work out

it’s all about keeping my IBD under

control if I’m experiencing something

like the T nausea diarrhea I’m gonna

talk to my doctor because that could be

a normal flare-up or it could be

something more he’s got the right idea

because the formula for minimizing your

colorectal cancer risk is first to

control your IBD and then to make sure

you and your doctor are vigilant about

monitoring for cancer and that’s a

challenge when things are going well

here’s dr. Jeannie Ashburn from the

Cleveland Clinic it’s very easy to look

at that patient and say we’re doing a

great job at controlling their symptoms

and their flares but what goes

hand-in-hand with that is these patients

have an increased risk for developing a

cancer down the road or even in the

short term and we need to survey them

and make sure we’re staying on top of

that the key risk factors of the

duration and severity of the disease and

also genetics it’s important to stick to

your meds control flare-ups and have

regular checkups that focus on cancer

surveillance as well as a colonoscopy

every 1 to 2 years the benefit of doing

this routinely is that we can pick up on

surveillance abnormal cells that may

alert us to either a precancerous lesion

or a cancer itself diagnostic technology

is improving helping doctors catch

problems early last week for example

doctors discovered a polyp on the colon

of missio Doherty a senior at the

University of Denver I ended up going to

the hospital because I was just having

IBD symptoms it was so severe something

I never felt before and there was the

polyp her doctors don’t yet know if it’s

precancerous but still it was unwelcome


I had a breakdown and was pretty upset I

was falling and just saying why like

this is not fair like why does this have

to happen to me but the good news is

that it was caught early and now Missy

and her doctor have time to make the

best choice I don’t want to get to a

point where we’ve waited too long and

then we go in and see that it’s really

severely I’d rather have my colon

removed and have really severe cancer

Missy was back at the gym this morning

working out and by afternoon was helping

her sorority recruit new members she’s

managing cancer risk just like her IBD

with determination that discipline and

practicality I think it’s only gonna

slow me down as much as I let it just

like I’m Edie

Colorectal Cancer Risk Factors

  • A diagnosis of ulcerative colitis or a type of Crohn’s disease that only affects the colon, called Crohn’s colitis

  • Eight to 10-year history of Crohn’s disease or ulcerative colitis

  • Severe and/or extensive colon inflammation

  • Primary sclerosing cholangitis, a rare condition that causes bile duct inflammation and scarring

  • Dysplasia, or changes in cells that are precursors of cancer, of the colon or rectum

  • Family history of colorectal cancer

Thinking About Colorectal Cancer

Video Length 00:01:56

Thinking About Colorectal Cancer

Early Detection is Key

Screening for colorectal cancer should be a regular and ongoing conversation between you and your doctors. There are things you can do to reduce your risk of developing colorectal cancer.

Screening Recommendations

  • Patients who have had symptoms for eight years or longer should get a colonoscopy every one to two years..

  • Regular colonoscopies can find precancerous tissue and early cancers, making it easier to treat.

  • Work with your healthcare team to get your Crohn’s disease or ulcerative colitis inflammation under control. This will make finding colorectal cancer easier.

  • Make sure to follow all instructions from your doctor on preparing your bowel before a colonoscopy.

Reduce Your Risk

  • See your gastroenterologist at least once a year.

  • Keep a list of symptoms or concerns, and discuss these with your doctor at clinic visits.

  • Take your prescribed medications to keep your colon inflammation well-controlled.

  • Continue your medications, even when you are feeling healthy.

  • Notify your doctor if a family member develops colorectal cancer.

  • Exercise regularly and eat a healthy diet.

Advances in Cancer Screening

There have been several advances in technology that can be used during a colonoscopy to improve the quality of surveillance and help identify cancer or precancerous lesions in the colon.

These tools include high-definition colonoscopy, scopes, processors, and screens, which can help increase the resolution of the images your doctor takes during during a colonoscopy.

A chromoendoscopy may be done to help your doctor find polyps or precancerous changes during a colonoscopy. During a chromoendoscopy, a blue liquid dye is sprayed into the colon to highlight and detect slight changes in the lining of your intestine. You may have blue bowel movements after this procedure.

To read more about colorectal cancer screening and chromoendoscopy, visit the American Society for Gastrointestinal Endoscopy.

This educational material is supported by the Maxine and Jack Zarrow Family Foundation. Additional support is provided through the Crohn’s & Colitis Foundation’s annual giving programs and donors.

A special thank you to the patients, caregivers, and medical professionals on our Patient and Professional Educational Advisory Committee for their contributions to this resource.

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