BENIGN COLORECTAL NEOPLASMS - ADENOMA
1. DEFINITION
Colorectal adenoma is a benign epithelial tumour in which the cells form recognisable glandular structures and which arises in the mucous membrane of the colon. It excludes benign neoplasm of the anal canal, familial adenomatous polyposis, hyperplastic polyps, inflammatory pseudopolyps and hamartomas. The ICD 10AM Code for adenomatous polyp is D12.6.
2. DESCRIPTIVE EPIDEMIOLOGY
A colorectal polyp is a mass that protrudes into the colonic lumen. There are a number of classifications. A standard one is the division:
• tubular
• villous
• tubulovillous
There are also flat (non polypoid) adenomas described as:
• tubular, villous, villomicrotubular
• serrated
• cribriform,
but the serrated and cribriform are not universally accepted.
Adenomas form up to 75% of polyps found at colonoscopy. True adenomas, as neoplasms, all show some degree of dysplasia which may be mild, moderate or severe. More than 90% of adenomas are small, less than
1cm diameter and remain static; others (<10%) progress to adenocarcinoma in a complex transformation which seems to take 10-15 years.
Although most (adenomatous) polyps protrude into the bowel lumen, some (?<10%) are flat or depressed which makes them more difficult to recognise, which is unfortunate as they may have a greater malignant potential than the exophytic type. It is possible that the flat adenoma progresses to carcinoma through a sequence that includes a protruding polypoid lesion.
Polyps are frequent; in western societies their prevalence is much greater than in the less developed societies. A more recently recognised entity is the serrated adenoma, a flat lesion with histological features combining characteristics of hyperplastic and adenomatous polyps with genetic alteration suggesting malignant potential.
3. EPIDEMIOLOGY
The autopsy prevalence in western populations is 30-40% overall in those aged 60 or more and is greater in males. It increases with age, as does the proximal prevalence. The epidemiology of adenoma resembles that of adenocarcinoma in that the prevalence of polyps in a society mirrors that of adenocarcinoma.
Adenomatous polyps arise in an area of epithelial cell hyperproliferation and crypt dysplasia consequent upon genetic alterations. The sequence to carcinoma, should it occur, takes place in multiple steps which involve alterations in tumour suppressor genes and occupies 10-15 years (1). The natural history is difficult to study but it is evident that the epidemiology of polyps differs significantly from that of adenocarcinoma with different risk factors, sex incidence and sub site distribution (2). The risk factors for small polyps are obscure and the contribution of polyps to adenocarcinoma is unclear. Whilst there is no doubt that some carcinomas arise in polyps, we lack the evidence that all arise in this way - epidemiological, histological and genetic data indicate that the vast majority do but there is also evidence against the polyp-carcinoma sequence.
•there are small carcinomas without evidence of polyps
•the size of polyps is not age dependant but adenocarcinoma is
•their topographic distribution varies
•their sex incidence varies
4. HYPERPLASTIC POLYPS
These, also known as metaplastic polyps, are frequent colorectal lesions generally found in the rectosigmoid area. They are small and histologically consist of elongated crypts showing epithelial hyperplasia and increased branching with a slowing of migration of cells up the crypt with some abnormal cellular differentiation. Until recently they were held to have no malignant potential and so were of little interest. Interest in them as a cancer precursor has arisen because of the possession of genetic changes also seen in colorectal cancer. Otherwise typical hyperplastic polyps may also show focal dysplasia - known as serrated adenomas or hyperplastic/adenomatous polyps. The follow-up studies of hyperplastic polyps are confusing - One study found that those with a hyperplastic polyp had a doubling of rate of subsequent adenocarcinoma compared with those with a clear colonoscopy at a follow up of up to 10 years (3).
There is need for further study to settle the issue.
5. RISK FACTORS FOR ADENOMATOUS POLYP 5.1 Diet
The major variation in CRC incidence between countries, the changes seen in migrant populations and within countries all suggest major environmental influences, especially diet. A similar argument applies to Adenomatous polyposis but few good data exist (4). Adenoma prevention trials have in general been consistent in showing some benefit from Vitamin C with or without vitamin E and no benefit from beta carotene, increased fibre or diminished fat intake, remembering the problems inherent in such trials.
5.2 Dietary Fat
There are no data on per capita dietary fat intake and adenoma frequency in population studies. However there is a case control study of some interest. A comparison of 516 patients with adenomatous polyps and 551 controls without polyps on sigmoidoscopy including a detailed food frequency questionnaire focussed on partially hydrogenated vegetables oils.
In the category of sweetened baked goods, a significant source of these fats, for those consuming >350kcal/day of fat the adjusted OR was 2.1 (1.3-3.5) compared with those on <50kcal/day but after adjustment for multiple
factors there was no association of total fatty acids and adenoma prevalence (5).
5.3 Dairy Products
Of more than 40 reports of colon cancer and adenoma few have found positive association with fats (6).
5.4 Meat
The role of red meat has been questioned but essentially, in spite of nearly a dozen studies the data are as soft as the conclusions. The method of cooking meat and the role of heterocyclic amines (known carcinogens) produced by meat cooked at high temperatures has received a lot of attention. A link with high temperature cooked meat has been suggested which has some laboratory support.
5.5 Fibre
Four cohort studies of bran supplementation have shown no benefit (7) as do studies including the Nurses Health Study of 88,757 women.
5.6 Fruit and Vegetables
There is evidence, regarded as not persuasive, for a protective effect of fruit and vegetables in the diet (8).
5.7 Heredity
There is a near doubling of risk in those with a family history of adenomatous polyp .
References
1. Winawer SJ. The natural history of colorectal cancer. Am. J. Med. 106(A),35-65 (1999).
2. Hill MJ, Davies DJ, Giacosa A. Should we change our dietary advice on cancer preventions?
Eur. J. Cancer Prev. 10,1-6 (2001).
3. Huang EH, Whelan RL, Gleason N R et al. Increased evidence of colorectal adenomas in follow-up evaluation of patients with newly diagnosed hyperplastic polyps. Surg. Endosc.
15,646-8 (2001).
4. Kim EC, Lance P. Colorectal polyps and their relationship to cancer. Gastroenterol. Clin.
North Am. 26,1-17 (1997).
5. McKelvey W, Greenland S, Chen MJ et al. A case control study of colorectal adenomatous polyps and consumption of foods containing partially hydrogenated oils.
Cancer Epidemiol. Biomarkers Prev. 8,519-24 (1999).
6. Giovannucci E, Goldin B. The role of fat and fatty acids, and total energy intake in colorectal cancer. Am. J. Clin. Nutr. 66,1564S-1517S (1997).
7. Sengupta S, Tjandra JJ, Gibson PD. Dietary fibre and colorectal neoplasm. Dis.Colon Rectum 44,1016-33 (2001).
8. Kim YI. Vegetables, fruits and colorectal cancer risk. Nutr. Rev. 59,394-8 (2001).
