Colonic Polyp Najmeh Aletaha. MD
1 Polyps & classification 2 Colorectal cancer risk factors 3 Pathogenesis 4 Surveillance
polyp of the colon refers to a protuberance into the lumen above the surrounding colonic mucosa. Colonic polyp Neoplastic Serrated polyps Adenomatous polyps Non-neoplastic Inflammatory polyps Hyperplastic polyps Hamartomatous polyps
INFLAMMATORY POLYPS Non-neoplastic intraluminal projections of mucosa and inflammatory cells Inflammatory polyps include: Inflammatory pseudopolyps pedunculated or sessile Risk of malignancy: No risk but may be associated with surrounding dysplasia in patients with IBD. Prolapse type inflammatory polyps Caused by peristalsis-induced trauma
HAMARTOMATOUS POLYPS Juvenile polyps: Hamartomatous lesions that consist of a lamina propria and dilated cystic glands More common in childhood, most common in the rectosigmoid, resulting in lower gastrointestinal bleeding or prolapse through the rectum, No increased colorectal cancer risk. Juvenile polyposis syndrome (JPS) Autosomal dominant condition, multiple hamartomatous polyps throughout the gastrointestinal tract, increased risk for colorectal and gastric cancer.
HAMARTOMATOUS POLYPS Peutz-Jeghers polyps: Hamartomatous lesion of glandular epithelium supported by smooth muscle cells Peutz-Jeghers syndrome (PJS), due to STK11 mutations, undergo malignant transformation, Patients with PJS are at increased risk of both gastrointestinal (gastric, small bowel, colon, pancreas) and nongastrointestinal cancers. Cronkhite-Canada syndrome: Rare, nonfamilial disorder associated with alopecia, cutaneous hyperpigmentation, gastrointestinal polyposis, onychodystrophy, diarrhea, weight loss, and abdominal pain. polyps are hamartomas and do not appear neoplastic pathologically. Respond to immunosuppressive therapy
SERRATED POLYPS: Heterogenous group of polyps with variable malignant potential. They include Hyperplastic polyps Traditional serrated adenomas Sessile serrated polyps
Hyperplastic polyps: most common non-neoplastic polyps in the colon, typically located in the rectosigmoid and are less than 5 mm in size. Small rectosigmoid hyperplastic polyps do not appear to increase the risk of colorectal cancer. Surveillance In patients with small (<10 mm) hyperplastic polyps confined to the rectum or sigmoid colon, surveillance colonoscopy is recommended in 10 years.
Sessile serrated polyps: SSPs or sessile serrated adenoma [SSA] are more prevalent in the proximal colon. These polyps have a smooth surface, are often flat or sessile, and may be covered with mucus. Histologically, may acquire morphologic evidence of dysplasia. Traditional serrated adenomas (TSAs): More prevalent in the rectosigmoid colon and may be pedunculated or sessile. TSA have diffuse but often mild cytologic dysplasia.
Risk of cancer Risk factors for a synchronous advanced adenoma in patients with SSPs include SSP/A size 10 mm, location in the proximal colon, and the presence of dysplasia. Management TSAs and SSA/Ps are managed clinically like adenomatous polyps and complete excision is recommended.
Surveillance Individuals with SSA/P <10 mm in size with no dysplasia are managed as low risk adenomas with a first surveillance colonoscopy in five years. Individuals with SSA/P 10 mm, a SSA/P with dysplasia, or TSA are managed as high-risk adenomas with a first surveillance colonoscopy in three years. Other expert consensus recommendations have suggested earlier colonoscopic follow-up (one- to three-year interval) in individuals with two or more SSA/P larger than 10 mm and in those with any SSA/P with cytologic dysplasia (expert opinion).
Serrated polyposis syndrome (SPS) or hyperplastic polyposis syndrome (HPS): Diagnosis Based on one or more of the following World Health Organization criteria: At least five serrated polyps proximal to the sigmoid colon, of which two or more are 10 mm. Any number of serrated polyps proximal to the sigmoid colon in an individual who has a first-degree relative with SPS. >20 serrated polyps of any size, distributed throughout the colon. Surveillance one to three years based on the number and size of polyps.
ADENOMATOUS POLYPS: Approximately two-thirds of all colonic polyps Risk factor Increasing age Increased BMI (Abdominal obesity may be a better predictor). Lack of physical activity Adenomatous polyps are more common in men, and large adenomas may be more common in African- Americans.
Risk factors Risk factors for Colorectal cancer
Dietary factors implicated in colorectal carcinogenesis Diet Dietary fiber vegetables folate (B Vitamin) Decreased risk fruits calcium
Diet Alcohol Refined carbohydrates Animal and saturated fat Consumption of red meat increased risk of colorectal cancer
Endoscopic features and classification Based on their gross appearance, adenomas may be pedunculated, sessile, flat, depressed, or excavated.
Adenomatous Polyp Occur mainly in large bowel. Spordic and familial Vary from small pedunculated to large sessile Epithelium proliferation and dysplysia Histologic features 1. Tubular adenoma: tubular component of at least 75 percent. (more than 80 percent of colonic adenomas) 2. Villous adenoma: >75 percent villous features (5 to 15 percent of adenomas) 3. Tubulovillous adenoma: 25 to 75 percent villous features. (5 to 15 percent of colonic adenomas)
Neoplastic Polyps 1] Tubular adenoma Represents 75% of all neoplastic polyps. 75 % occur in the distal colon and rectum.
Neoplastic Polyps 2] Villous Adenoma The least common, largest and most ominous of epithelial polyps. Age: 60 to 65 years, Present with rectal bleeding or anemia, large ones may secrete copious amounts of mucoid material rich in protein. 75% located in rectosigmoid area.
3] Tubulovillous adenoma Intermmediate in size, degree of dysplasia and malignant potential between tubular and villous adenomas.
ADENOMATOUS POLYPS: 5 percent or less of adenomas progress to cancer over 7 to 10 years. The risk of progression is higher for advanced adenomas (adenoma with high-grade dysplasia, >10 mm in size, or a villous component).
Management: Polypectomy Adenomas should be resected completely. Small adenomas may be completely removed using biopsy forceps larger adenomas require snare resection, with or without electrocautery or advanced endoscopic resection techniques (eg, EMR or ESD). Large sessile adenomas often require piecemeal resection. (& repeat colonoscopy to evaluate the site of excision within six months) In cases where endoscopic resection is not possible, surgical resection is required.
Management: Management of a polyp containing invasive carcinoma must be individualized. In early-stage (T1) colon cancers, polypectomy alone is usually adequate if the following risk factors for residual cancer and/or nodal metastases are absent: Poorly-differentiated histology. Lymphovascular invasion. Cancer at the resection margin. Invasion of the stalk of pedunculated polyp, by itself, is not an unfavorable prognostic finding, as long as the cancer does not extend to the margin of stalk resection. A 2 mm resection margin is regarded as adequate.
Invasion into the muscularis propria of the bowel wall (T2 lesion). Invasive carcinoma arising in a sessile (flat) polyp with unfavorable features (eg, lower third submucosal penetration, lymphovascular invasion, poorly differentiated). After complete resection of a polyp with cancer, we perform follow-up colonoscopy in three months to check for residual abnormal tissue at the polypectomy site if the polyp was sessile. The presence of any one of the risk factors for residual cancer and/or nodal metastases should prompt consideration of radical surgery.
Adenoma-carcinoma sequence Most colorectal cancers (CRCs) arise from adenomas, many of which are polyps that progress from small (<8 mm) to large ( 8 mm) polyps, and then to dysplasia and cancer. Neoplastic changes result from both inherited and acquired genetic defects.
Adenoma to Carcinoma Pathway Normal Adenoma Cancer APC loss K-ras mutation Chrom 18 loss p53 loss Normal Hyperproliferation pithelium Early Adenoma Intermediate Adenoma Late Adenoma Cancer
Familial Polyposis Syndrome Patients have genetic tendencies to develop neoplastic polyps. Familial polyposis coli (FPC) Genetic defect of Adenomatous polyposis coli (APC). APC gene located on the long arm of chromosome 5 (5q21). APC gene is a tumor suppressor gene Innumerable neoplastic polyps in the colon (500 to 2500) Polyps are also found elsewhere in alimentary tract Most polyps are tubular adenomas The risk of colorectal cancer is 100% by midlife. Gardener s syndrome Polyposis coli, multiple osteomas, epidermal cysts, and fibromatosis. Turcot syndrome Polyposis coli, glioma and fibromatosis
Familial polyposis coli (FPC)
Adenocarcinoma of Large Intestine Carcinogenesis Two pathogenetically distinct pathways for the development of colon cancer, both seem to result from accumulation of multiple mutations: 1- The APC/B-catenin pathway ( 85 % ) chromosomal instability that results in stepwise accumulation of mutations in a series of oncogenes and tumor suppressor genes. adenoma-carcinoma sequence
Malignant Tumors of Large Intestine Adenocarcinoma Carcinogenesis 2- The DNA mismatch repair genes pathway: 10% to 15% of sporadic cases. There is accumulation of mutations (as in the APC/B-catenin schema) Five DNA mismatch repair genes (MSH2, MSH6, MLH1, PMS1, AND PMS2) Give rise to the hereditary non polyposis colon carcinoma (HNPCC) MLH1 gene is the one most commonly involved in sporadic colon carcinomas