After being diagnosed with anemia, Mr. A, a 67-year-old African American, was referred to our gastroenterology clinic by his primary-care provider. He reported no recent melena, rectal bleeding, diarrhea, constipation, unintentional weight loss, or changes in bowel habits. His past medical history was significant for hypertension and a remote appendectomy. He was not overweight and had no history of alcohol or tobacco use. The patient reported no history or present use of nonsteroidal anti-inflammatory drugs (NSAIDs). Family history was unremarkable for colorectal cancer or polyps. The patient had never undergone any form of colorectal cancer (CRC) screening.
Mr. A was well developed with vital signs as follows: BP 140/85 mm Hg; pulse 88 beats per minute; respirations 24 breaths per minute; temperature 98.8°F. His physical exam was unremarkable. A rectal exam demonstrated no masses, hemorrhoids, or fissure. A fecal occult blood test was negative.
Laboratory findings provided by the patient’s primary-care provider at the time of his evaluation demonstrated hemoglobin 10.4 g/dL, WBCs 4,500/µL, hematocrit 35%, mean corpuscular volume 68.9 fL, and platelet count 223,000/µL. Iron studies drawn during the patient’s initial evaluation with our office confirmed iron deficiency anemia. The differential diagnosis under consideration was likely a colorectal source contributing to occult GI bleeding. The absence of dyspeptic symptoms and the patient’s lack of NSAID use made an upper GI source less likely.
Based on Mr. A’s history, physical exam, and lab results, he was scheduled for colonoscopy. The examination was significant for sigmoid diverticulosis; a 1-cm polyp at 50 cm; a 1-cm polyp at the splenic flexure; and a large, circumferential, friable, partially obstructing mass at the hepatic flexure (Figure 1). The remainder of the colon beyond the mass demonstrated no abnormalities. Biopsy of the friable mass confirmed our suspicions—moderately differentiated adenocarcinoma. The polyps at 50 cm and the splenic flexure were a tubular adenoma and hyperplastic polyp, respectively. Mr. A was subsequently referred for surgical resection.
Colonoscopy is the gold standard for CRC screening. A colonoscopy visualizes the entire colon, enhancing the detection rate for polyps and cancer. If Mr. A had undergone a sigmoidoscopy, his cancer would not have been detected. Twenty percent of CRCs occur in the rectum, with the rest being distributed throughout the colon as follows: sigmoid 25%, descending 5%, transverse 15%, rectosigmoid 10%, ascending/cecum 25%.
CRC continues to be the No. 1 cause of GI-related mortality and is the second-leading cause of cancer-related deaths. The lifetime risk for the development of CRC is approximately 6%; most cases (98%) are adenocarcinoma. The incidence is similar in both sexes. African Americans have higher incidence and mortality rates for CRC. A first-degree relative with the same condition can double or triple an individual’s risk. Risk factors include age (incidence of cancer doubles during each successive decade from age 40-80 years), history of adenomatous colorectal polyps or cancer, family history of CRC, and a personal history of inflammatory bowel disease.
Mr. A’s case also highlights the importance of CRC screening, which is recommended for average-risk individuals at age 50. Given the higher incidence of CRC in African Americans, the Committee of Minority Affairs and Cultural Diversity and the American College of Gastroenterology recommends starting screening at age 45 with the colonoscopy as the first-line screening test. Determine an individual patient’s risk status before the initiation of screening. This, in turn, determines when a colonoscopy should be performed and how frequently. Currently accepted CRC screening guidelines can be reviewed on the Web sites of the U.S. Preventive Services Task Force (www.ahrq.gov/clinic /uspstf/uspscolo.htm, accessed June 8, 2008) or the American College of Gastroenterology (www.acg.gi.org/patients/ccrk, accessed June 8, 2008).