7Epidemiology and risk factors of colorectal polyps
Introduction
In the Western world, the lifetime risk of colorectal cancer (CRC) is around 5% [1]. Certain high-risk groups such as strong family history of CRC and rare genetic syndromes exist, but 85% of CRC occur in individuals without known risk factors [2].
There are different biological pathways leading from normal mucosa to CRC, but they all encompass precursor lesions termed polyps [3]. Polyps are caused by proliferation of the colonic mucosa, creating pedunculated or sessile outgrowths. Modern histology classifies these lesions as serrated or adenomatous polyps (adenomas) according to growth pattern, further subdividing adenomas into villous, tubulovillous or tubuluar, and serrated polyps into hyperplastic polyps, sessile serrated polyps or traditional serrated adenomas [3].
Despite the well-known connection between polyps and cancer (the vast majority of CRCs develop from polyps), it is important to highlight that most polyps will never develop into CRC [4]. Fig. 1 shows the long-term colorectal cancer mortality after adenoma removal [5].
The most common pathway from precursor lesion to cancer is the adenoma-carcinoma-sequence, which accounts for approximately 75% of all CRC cases [6]. Another pathway, called the serrated pathway, has been recognized over the last two decades. Clinical trials have shown that individuals with large serrated polyps have a risk of CRC comparable to that of individuals with advanced adenomas (defined as ≥1 cm in size, tubulovillous or villous growth or high grade dysplasia) [7]. The cancers developing trough the serrated pathway may be genetically different from those developing through the adenoma-carcinoma pathway [8]. The serrated pathway includes what was previously called hyperplastic polyps, earlier considered not to have any malignant potential. However, a subset of the hyperplastic polyps has now been reclassified as sessile serrated polyps, and are thought of progressing through the serrated pathway [9], [10]. The sessile serrated polyps account for about 10–25% of serrated polyps [11]. The traditional serrated adenomas have been identified as precursors of CRC for a long time, but they account for only about 1% of the serrated polyps [11].
It is estimated that it takes at least 10 years for a polyp to grow to cancer [4], and hence there is opportunity for interventional strategies for cancer prevention. Modifiable life-style factors could possibly have an impact on reducing the burden of CRC. These type of interventions are unfortunately difficult to study. Although robust evidence is often difficult to find - modifiable risk factors for CRC should not be underemphasized in the clinical care for patients with CRC precursors.
Serrated and adenomatous polyps share many of the same risk factors, but certain risk factors differ or have a stronger or weaker association with one group than the other [12]. This article provides an overview of the epidemiology and risk factors for the different types of colorectal polyps in the average risk population.
Different studies report different prevalence of polyps, often varying between 30 and 50% [13], [14], [15], [16], [17]. The reported prevalence of polyps is closely related to adenoma detection rates, and a significant part of the variation in prevalence is thus due to technological differences and the individual clinician's performance.
The NordICC-study is a European population based randomized trial examining the effect of colonoscopy screening on CRC incidence and mortality in average-risk individuals age 55–64 years [15]. Of the 12 000 individuals who underwent colonoscopy in the trial, polyp(s) were found in 48%. The overall adenoma detection rate was 31%, but varied substantially between and within the different participating countries [15]. In a Dutch colonoscopy study the median adenoma detection rate was 39% [16], whereas the highest reported prevalence of polyps that we know of in a screening population is 58% [17].
The reported prevalence of serrated polyps also varies greatly, from 13-52% in autopsy studies [7] to 6–29% in meta-analyses of endoscopy trials [18]. The distinctive division of serrated polyps into three subgroups (hyperplastic polyps, sessile serrated polyps and traditional serrated adenomas) is of quite recent origin, and thus most studies have investigated the prevalence of serrated polyps without applying this subdivision.
The distribution of different polyp types within the colon is illustrated in Fig. 2 [19]. Adenomas and hyperplastic polyps are most often found in the distal colon, and the sessile serrated polyps are more commonly found in the proximal colon, although all of polyp types can be found anywhere in the large bowel [15], [19], [20], [21], [22].
As with CRC, adenomas are more common in men than in women. Most studies report almost twice as high prevalence in men compared to women [13], [23], and the prevalence of colorectal polyps in general increases with age, as illustrated in Fig. 3 [24]. For serrated polyps, the age and gender pattern is more uncertain, with some studies indicating that the prevalence increases only slightly with age [22], [25], [26], [27], and that sessile serrated polyps are more prevalent in females as compared to males [21], [28], [29].
The distribution of adenomas within the bowel also differ between genders, with a more proximal pattern in women [30]. These gender differences may have implications for the choice of CRC screening modality, a point that is emphasized by the fact that sigmoidoscopy screening has been shown to be less effective in women than in men [30], [31].
The highest incidence rates of CRC are found in the Western countries (Australia, New Zealand, Europe and North America). The lowest rates are found in Africa and South-Central Asia [1]. However, it is important to keep in mind that endoscopy is much more accessible in Western countries. Thus, the true prevalence of colorectal polyps are not known for many countries in the developing world. The differences in rates by country, and elevated risk among immigrants from a low- to high-risk country, supports that environmental factors play an important role in CRC risk [32]. The introduction of widespread screening may also change the incidence and mortality of CRC in many countries [33].
Race and ethnicity is strongly associated with the risk for developing polyps. African Americans are more likely to be diagnosed with and die from CRC than white Americans [34]. In a comparison of individuals participating in colorectal screening, multivariate analysis showed that blacks had a 76% and Hispanics a 37% increased relative risk of adenomas compared to whites, and the risk of advanced adenomas were doubled in both Hispanics and blacks compared to whites [35]. Contrary to the risk of adenomas and CRC, African Americans and Hispanics seems to have a lower risk of serrated polyps than whites, with a relative reduction of 35% and 67% respectively [25].
Section snippets
Smoking
Smoking is the most well-known and well-documented modifiable risk factor for colorectal polyps and CRC [36], [37], [38]. Tobacco contains carcinogens that are thought to create irreversible genetic damage to the colorectal mucosa, initiating the formation of colorectal polyps [36], [39]. The association of cigarette smoking and risk of polyps is prominent, regardless of sex, polyp subtype, location and severity, and most studies show at least a 2–3-fold increased risk of polyps in smokers [38]
Summary
This overview presents the epidemiology of and the most common risk factors for colorectal polyps. Age and gender are important predictors for colorectal polyps, as they are for colorectal cancer. Furthermore there are differences in incidence according to geography, but this might be affected by adenoma detection rates (or endoscopy rates), and effects of modifiable risk factors specific for that country or region. It is important that clinicians are aware of epidemiological differences in
Conflicts of interest
None.
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MØ and LMH contributed equally to this paper.