1. Колоректальный рак

2. Толстая кишка – участок желудочно-кишечного тракта от терминального отдела подвздошной кишки до анального канала. Границей между сигмовидной и прямой кишками условно считают зону перехода лент сигмовидной кишки в круговые продольные прямокишечные мышцы. Гаустры и жировые подвески на этом уровне исчезают. Эта зона обычно располагается на расстоянии 12–15 см от зубчатой линии (на уровне мыса крестца). Длина прямой кишки примерно 12 см. Опухоли анального канала обычно рассматривают отдельно, их не относят к колоректальному раку (КРР). Саркома, лимфома, карциноиды толстой кишки и опухоли червеобразного отростка в это понятие не включены.

3. Колоректальный рак: распространенность КРР занимает 4-е место в мире в структуре онкологической заболеваемости. Более чем 2/3 новых случае выявляют в экономически развитых странах, где КРР занимает 2-е место. Из 800 тыс. больных КРР, которых регистрируют ежегодно, 440 тыс. умирают. На протяжении жизни 1 из 18 родившихся в Северной Америке жителей заболевает этой формой рака. В 2000 г. в России выявили более 47 тыс. новых случаев, что на 10,4 тыс. (23%) превысило число заболевших в 1990 г. Доля КРР в общей структуре онкозаболеваемости достигла 9,6% у мужчин и 11,4% у женщин

4. Колоректальный рак: распространенность Максимальные показатели в Австралии, Северной Америке, Западной и Северной Европе, относительно высокие в Южной и Восточной Европе, умеренные в Южной Америке. Низка заболеваемость в Африке и Азии, за исключением Японии, в которой она равна европейской

5. Колоректальный рак: распространенность Географические особенности заболеваемости раком прямой кишки соответствуют закономерностям распространения рака ободочной кишки, только при более низких уровнях показателей заболеваемости. В странах с высокими уровнями заболеваемости соотношение случаев рака ободочной кишки к прямой составляет 2:1. В регионах с низкими показателями это соотношение равно 1:1. В России рак ободочной кишки выявляют в 1,2 раза чаще, чем прямой; противоположная тенденция характерна для Индии

6. Колоректальный рак: распространенность За период с 1990 по 2000 г. в России прирост заболеваемости был выше при раке ободочной кишки (18,7% у мужчин и 18,9% у женщин). Заболеваемость раком прямой кишки выросла у мужчин с 10,5 до 12,2 на 100 000 населения, у женщин с 7,6 до 8,1 на 100 000 населения, а прирост составил 16,2 и 6,6% соответственно

7. Колоректальный рак: распространенность Показатели заболеваемости по отдельным административно-экономическим регионам России (края, области) также сильно различаются. В 2000 г. максимальные показатели заболеваемости (мировой стандарт) раком ободочной кишки зарегистрированы в Санкт-Петербурге (22,5 и 17,7 на 100 000 у мужчин и женщин соответственно), Москве (18,9 и 15,4) и Магаданской области (21,5 и 20,5); Рак прямой кишкитпреобладает у мужчин – в Карелии, Новгородской области и Санкт-Петербурге (17,3–18,0), у женщин – в Чукотском автономном округе, Сахалинской и Пермской областях, Республике Алтай (11,7–24,4)

8. Колоректальный рак: распространенность Средний возраст заболевших КРР в странах СНГ был минимальным в Туркмении, Киргизии и Азербайджане (59–62 года) и максимальным в России и Армении (65–68 лет) Около 85% случаев КРР приходилось на возраст старше 55 лет. Данная форма рака крайне редко встречается у лиц до 30 лет, заболеваемость резко возрастает с увеличением возраста, достигая максимума в 70 лет и старше. В 2000 г. в России от КРР умерли 34,8 тыс. человек. В структуресмертности от злокачественных новообразований ободочная кишка занимает 3-е место у лиц обоего пола, составляя у мужчин 4,6%, у женщин 8,2%. Динамика смертности от КРР за 1990–2000 гг. в России относительно стабильна (8–9 на 100 000 населения, 6 и 7 у мужчин и женщин соответственно)

9. Колоректальный рак: смертность Death rates from CRC have declined progressively since the mid-1980s in the United States (US cancer deaths male and US cancer deaths female) and in many other western countries [2,22,23]. This improvement in outcome can be attributed, at least in part, to detection and removal of colonic polyps, detection of CRCs at an earlier stage, and more effective treatments, particularly adjuvant therapy. However, at least in the United States, the decline in colorectal cancer mortality started well before the modern era in which any of the various screening techniques or adjuvant therapy became widely used [24]. (See "Adjuvant therapy for resected stage III (node-positive) colon cancer" and "Adjuvant therapy for resected rectal adenocarcinoma".)US cancer deaths maleUS cancer deaths female2,22,2324"Adjuvant therapy for resected stage III (node-positive) colon cancer""Adjuvant therapy for resected rectal adenocarcinoma" Globally, the United States has one of the highest survival rates from CRC. Data collected by the Surveillance, Epidemiology and End Results Reporting (SEER) Program of the United States National Cancer Institute suggest that 61 percent of all patients treated for CRC (all stages and sites combined) survive five years [25].25 In contrast to these data, mortality rates continue to increase in many countries with more limited resources and health infrastructure, particularly in Central and South America and Eastern Europe [23].23

10. Колоректальный рак: Факторы риска Все мужчины и женщины с другими факторами риска всегда имеют риск КРР в возрасте 50 лет и старше, причём он в равной степени касается мужчин и женщин. Риск КРР удваивается с каждым прожитым десятилетием.

11. Колоректальный рак: Факторы риска Риск возникновения рака толстой кишки (РТК) у лиц, не имеющих предрасполагающих факторов, составляет 1–3%; Если у родственников первой степени родства был РТК, риск повышается до 5%, среди больных язвенным колитом риск развития РТК равен 15– 30%, Среди пациентов с болезнью Крона – 15%, С неполипозным наследственным КРР – 15–20%, С наследственным семейным полипозом – 30– 100%.

12. Колоректальный рак: Факторы риска Группы риска необходимо подвергать обязательным профилактическим осмотрам, что в ряде случаев способствует раннему выявлению РТК Поскольку РТК часто возникает метахронно, больных, леченных хирургически по поводу РТК, также необходимо рассматривать как группу риска возникновения второй опухоли в кишечнике. У 50% таких больных могут возникнуть новые полипы, и в 5% случаев они малигнизируются

13. Globally, the incidence of CRC varies over 10-fold. The highest incidence rates are in Australia and New Zealand, Europe and North America, and the lowest rates are found in Africa and South-Central Asia (CRC incidence by world area) [1]. These geographic differences appear to be attributable to differences in dietary and environmental exposures that are imposed upon a background of genetically determined susceptibility.CRC incidence by world area1 Low socioeconomic status (SES) is also associated with an increased risk for the development of colorectal cancer; one study estimated the CRC risk to be about 30 percent increased in the lowest as compared to the highest SES quintile [4]. Unhealthy but potentially modifiable behaviors such as physical inactivity, unhealthy diet, smoking, and obesity are thought to account for a substantial proportion (estimates of one-third to one-half) of the socioeconomic disparity in risk of new onset colorectal cancer [4-6]. Other factors, including lower rates of CRC screening, also contribute substantively to SES differences in CRC risk [7].44-67

14. Колоректальный рак: этиология Росту заболеваемости колоректальными карциномами в развитых странах способствуют увеличение в пищевом рационе содержания мяса, особенно говядины и свинины; уменьшение клетчатки и животного жира. Природные витамины А, С и Е инактивируют канцерогены, а турнепс и цветная капуста индуцируют экспрессию бензпиренгидроксилазы, способной инактивировать поглощённые канцерогены. Отмечено резкое снижение заболеваемости среди вегетарианцев. Высока частота КРР среди работников асбестных производств, лесопилок

15. Прочие факторы риска: язвенный колит, особенно панколит и заболевание давностью более 10 лет (риск 10%); болезнь Крона, аденома толстой кишки в анамнезе; синдром полипоза – диффуз- ный семейный полипоз, одиночные и множественные полипы, вор- синчатые опухоли; рак женских половых органов или молочной железы в анамнезе; синдромы семейного рака; иммунодефицит- ные состояния В [8, 9]. Есть указания, что курение отрицательно воздействует на склон- ность к малигнизации хронических процессов слизистой оболочки толстой кишки С [26]

16. Колоректвальный рак: Скрининг American College of Physicians (ACP): Скрининг КРР следует начинать с 50 лет у лиц со средним риском (общая популяция) с 40 лет (или на 10 раньше чем был выявлен у родственников) Методы обследования - Исследование стула, сигмоскопия или колоноскопия Колоноскопия - метод выбора

17. PROTECTIVE FACTORS — A large number of factors have been reported by at least some studies to be associated with a decreased risk of CRC [147]. These include regular physical activity, a variety of dietary factors, the regular use of aspirin or nonsteroidal antiinflammatory drugs (NSAIDs), and hormone replacement therapy in postmenopausal women. None of these factors are currently used to stratify CRC screening recommendations.147aspirin

18. Колоректальный рак: протективные факторы Физическая активность Диета богатая фруктами и овощами (100 г/день) Употребление пищи богатой фолатами Витамин В6 Кальций и молочные продукты Витамин Д Чеснок Рыба Аспирин и НПВС Гормонзаместительная терапия в постменопаузе

19. Resistant starch — Resistant starch refers to those forms of starch which escape digestion in the small bowel and pass to the colon, where they are fermented with the production of short-chain fatty acids. Butyrate, one of these fatty acids, has antineoplastic properties in the colon [175]. While this led to initial enthusiasm as to the potential of resistant starch as a chemopreventive agent, a randomized trial of resistant starch (Novelose, 30 g daily) failed to show a beneficial impact on adenoma or cancer development in individuals with hereditary non-polyposis colorectal cancer (HNPCC, Lynch syndrome) [176,177]. Additional trials of other forms of resistant starch that are capable of delivering higher levels of butyrate to the colon are in progress.175176,177 Folic acid and folate — Folate is the natural form of the vitamin occurring in food and folic acid is the synthetic form used in food fortification and supplements. Based upon biochemical pathways, the two may not be equivalent and have different in vitro effects.folic acid Data from animal and human studies have demonstrated that folate inhibits pathogenesis of cancer in a number of tissues including the colon [178]. However, whether folate and folic acid have a role in prevention of colorectal cancer is unclear. By contrast, the possibility that folic acid supplementationincreases the risk of colon cancer has also been raised. The following represents the available data on folate and colorectal cancer risk:178folic acid ●A combined analysis of data from two large cohorts from the Nurses' Health Study and the Health Professionals Follow-up Study provide observational evidence in support of a protective effect from folic acid supplementation [179]. There was an association between total folate intake 12 to 16 years before diagnosis and a lower risk of colorectal cancer (RR: 0.69; 95% CI 0.51 to 0.94 for ≥800 compared with <250 micrograms of folate per day), but no association with intake in the more recent past. In contrast, both long- and short-term intake of total folate was associated with a lower risk of colorectal adenoma, with a strong association with intake four to eight years before diagnosis (OR 0.68; 95% CI: 0.60 to 0.78 for ≥800 compared with <250 micrograms of folate per day). These observational data suggest that folic acid supplementation could be beneficial in the pre-adenoma stage but not beyond.folic acid179 ●Others have suggested that the protective effect of folates might be limited to dietary (food) rather than supplemental intake [180]. The protective effect may also depend upon an individual's particular genotype for methylenetetrahydrofolate reductase, an enzyme involved in folate metabolism [181].180181 ●In contrast to these data, at least two controlled trials involving patients with colonic adenomas found that folic acid supplementation did not reduce the risk of recurrent adenomas [182,183]. Furthermore, in one of the trials, supplementation was associated with an increased risk of having three or more adenomas and of noncolorectal cancers, raising the possibility that folic acid supplementation in adults could be detrimental rather than beneficial for adenoma formation, particularly in those who already have a propensity to form colonic neoplasms [182]. In support of this possibility are population-based studies that have correlated a small increase in the incidence of colon cancer concurrent with the fortification of the United States food supply with folic acid for prevention of neural tube defects [184]. On the other hand, a study of 99,523 US participants enrolled in the Cancer Prevention Study II Nutrition cohort that examined the association between folate intake (dietary or supplemental) and colorectal cancer risk failed to document an increased risk of colorectal cancer from high folate intake [185]. These data are consistent with the findings from the Nurses' Health Study and the Health Professionals Follow-up Study described above and should help to allay concerns about a possible strong procarcinogenic role of folate [155].folic acid182,183182184185155 Vitamin B6 (pyridoxine) — The available data suggest a modest association between higher vitamin B6 (pyridoxine) intake and decreased colorectal cancer risk. In a meta-analysis of prospective studies, the pooled relative risks (RR) of colorectal cancer for the highest versus lowest categories of vitamin B6 intake and of blood levels of pyridoxal 5'-phosphate (the active form of vitamin B6) were 0.90 (95% CI 0.75 to 1.07) and 0.52 (95% CI 0.38 to 0.71), respectively [186]. Omitting one study that contributed substantially to heterogeneity in the studies of vitamin B6 intake, the protective effect of highest versus lowest vitamin B6 intake on colorectal cancer risk was statistically significant (pooled RR 0.80, 95% CI 0.69 to 0.92).186 Calcium and dairy products — Another possible protective factor is increased intake of dietary or supplemental calcium [187-194].187-194 ●A combined analysis of the Nurses' Health Study (n = 87,998 women) and the Health Professionals' Follow-up Study (n = 47,344 men) found that higher calcium intake (>1250 mg daily versus ≤500 mg daily) was associated with a significant reduction in the risk of distal colon cancers (relative risk [RR] 0.65, 95 percent confidence interval [CI] 0.43 to 0.98) but not proximal cancers (RR 1.14, 95% C, 0.72-1.81) [191].191 ●A similar degree of benefit was noted in a pooled analysis of individual data on 534,536 individuals from 10 cohort studies that assessed dietary intake [193]. The RR for CRC in the highest as compared to the lowest quartile of calcium intake was 0.86 (95% CI 0.78-0.95). Compared to the lowest category of milk intake (<70 g/day), individuals ingesting ≥250 g/day had a comparable reduction in the risk of CRC (RR 0.85, 95% CI 0.78-0.94).193 ●The National Institutes of Health-AARP study (which included 293,907 men and 198,903 women ages 50 to 71 followed for an average of seven years) concluded that dietary calcium significantly lowered the risk of digestive cancers, particularly colorectal cancer [194]. The risk decreased up to approximately 1300 mg/day above which no further reduction was observed. Among those with the highest quintile of calcium intake, the risk of colorectal cancer was decreased by approximately 16 percent (hazard ratio [HR] 0.84, 95% CI 0.77-0.92), almost identical results to the pooled analysis described above [193].194193 At least three controlled trials have evaluated the efficacy of calcium supplementation in prevention of recurrence of colorectal adenomas. A meta-analysis of these data (including a total of 1485 subject) concluded that the risk of recurrence was significantly lower in patients randomized to calcium (RR 0.80, 95% CI 0.68-0.93) [195].195 Despite these benefits in adenoma prevention trials, whether calcium supplementation reduces the risk of colorectal cancer is unproven. The only large controlled trial to evaluate this issue included 36,282 post-menopausal women who were randomly assigned to the combination of calcium plus vitamin D or placebo [196]. No significant difference in the rate of invasive colorectal cancer was observed during a mean follow-up of seven years. Questions have been raised as to whether the doses of calcium and vitamin that were used in the trial were sufficient to prevent colon cancer. The study is continuing to determine whether a benefit might be observed with longer follow-up.196 Other data suggest that the protective effect of calcium may depend upon an individual's genotype for the vitamin D receptor [192]. A controlled trial suggested that calcium supplementation was beneficial only in patients with normal vitamin D levels [197].192197 Calcium supplementation has been recommended for the primary or secondary prevention of colonic adenomas by the American College of Gastroenterology [190]. (See "Approach to the patient with colonic polyps".)190"Approach to the patient with colonic polyps" Epidemiologic studies of dairy products and CRC risk have provided mixed results, with some studies reporting inverse associations between intake of total dairy products, milk, and/or yogurt and CRC risk, and others finding no association. Dairy products have been hypothesized to protect against CRC because of their high calcium content; however, some dairy products, such as cheese and cream, have a high fat content, which may counterbalance the protective effect, possibly by affecting the bile acid composition in the colon. (See 'Cholecystectomy' above.)'Cholecystectomy' A meta-analysis of 19 cohort studies concluded that diets with higher milk and total dairy product intake were associated with a significant, but modest, reduction in CRC risk (summary RR for milk 0.82, 95% CI 0.74-0.93) [198]. The protective effect was restricted to colon and not rectal cancer. There was no association between intake of cheese or other dairy products (including low-fat dairy products) and CRC risk.198 Vitamin D — Vitamin D and its metabolites act as inhibitors of colorectal cancer progression by effects that influence both initiation and progression [199]. Some observational studies (cross sectional studies and especially long-term prospective studies) have revealed a link between poor vitamin D status and the risk of many cancers. An analysis by the World Health Organization (WHO) identified colon cancer as the type of cancer with the greatest risk associated with poor vitamin D status [200]. This finding was supported by a meta-analysis of nine case-control studies, which showed that each 4ng/mL (10 nmol/L) increase in pre-diagnosis serum 25-hydroxyvitamin D (25-OHD) concentration was associated with a 6 percent decrease in colorectal cancer prevalence [201]. It is not clear if these observed associations are causal as the current interventional data on the protective effect of vitamin D supplementation on the development of colorectal neoplasia are conflicting and additional studies are ongoing. This subject is addressed in greater detail elsewhere. (See "Vitamin D and extraskeletal health", section on 'Cancer'.)199200201"Vitamin D and extraskeletal health", section on 'Cancer' An observational study suggests the possibility that low postoperative levels of plasma 25-OHD may be associated with significantly worse survival, especially among patients with resected stage II disease (table 3) [202]. The adjusted hazard ratios for CRC–specific and all-cause mortality were 0.68 (95% CI 0.50-0.90) and 0.70 (95% CI 0.55-0.89), respectively, for highest versus lowest 25-OHD tertiles, and for stage II disease, the HR for CRC-specific mortality was 0.44, p = 0.004. However, it isn’t certain that this association is causal, and the influence of vitamin D supplementation on CRC outcomes in patients with low 25-OHD levels has not been examined. Furthermore, there may be confounding influences relating to this observation, such as patients with more advanced disease being more likely indoors and less exposed to sunlight and thus less replete with vitamin D.table 3202 Magnesium — Animal studies suggest that dietary magnesium may influence colorectal cancer development. A population based study from Sweden found an inverse association between magnesium intake and the risk of colorectal cancer in women [203]. Compared with women in the lowest quintile of magnesium intake, the risk was reduced by approximately 40 percent (RR 0.59, 95% CI 0.40-0.87) in women with the highest quintile of intake. The inverse association was observed for both colon and rectal cancer.203 Garlic — Consumption of garlic has been associated with a reduced risk of colonic adenomas in some observational studies of patients with colorectal cancer and in laboratory studies [204,205]. Garlic has been included as a probable protective factor by the World Cancer Research Fund/American Institute of Cancer Research [205] but a review by the US Food and Drug Administration concluded that there as “very limited credible evidence for a relation between garlic consumption and reduced colon cancer risk”. Additional prospective intervention studies are needed to settle this issue.204,205205 Fish consumption — Consumption of omega 3 fatty acids (mainly as fish oil) has been associated with a reduced incidence of colorectal cancer in observational studies. A meta-analysis of 22 prospective cohort and 19 case-control studies found an overall lower incidence of colorectal cancer among individuals with the highest compared with the lowest fish consumption (summary odds ratio [OR] 0.88, 95% CI 0.80-0.95 ) [206]. Thus, the association appears to be modest and intervention trials have not yet been reported. Two grams daily of Eicosopentaenoic Acid (EPA) as its free fatty acid has been shown in a randomized controlled trial to reduce the numbers of adenomas by a net change of 22.4 percent compared with placebo, as well as to improve the global polyp burden, in familial adenomatous polyposis [207].206207 Drugs — Currently there are no generally accepted chemopreventive recommendations for patients at average risk for CRC but several agents have been shown to have modest to moderate chemopreventive effects in average and high risk populations. Aspirin and NSAIDs — A substantial body of observational and intervention trial evidence suggests that aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) protect against the development of colonic adenomas and cancer. Regular use of aspirin and other NSAIDs are associated with a 20 to 40 percent reduction in the risk of colonic adenomas and colorectal cancer in individuals at average risk. Late follow up reports of the British randomized controlled trials of aspirin primarily addressing cardiovascular endpoints are now reporting similar reductions of 50 percent in colorectal and other cancer incidences and death, after a delayed (latent) period of at least five years [208,209]. Low and high doses of aspirin were protective, and the effect was more marked for adenocarcinomas especially where proximal and with longer durations of aspirin use within the RCTs, The absolute reduction in fatal colorectal cancer was 1.76 percent (0.61-2.91; p=0.001). Definitive evidence for the protective effects of aspirin at 600 mg/day in Lynch syndrome has emerged from the CAPP2 trial, evidence which will likely be written into guidelines worldwide. With a mean of 55.7 months follow up, Poisson regression taking into account multiple primary events (as is common in Lynch syndrome) gave an incidence ratio of 0.6 (95% CI 0.32-0.99; p=0.05) with a per protocol analysis of incidence ratio of 0.37 (95% CI 0.18-0.78; p=0.008) [210]. How long-term aspirin or NSAID therapy might protect against CRC is not well understood. Proposed explanations are increased apoptosis and impairment of tumor cell growth by inhibition of cyclooxygenase-2. The minimum dose of aspirin to achieve the protective effect is still uncertain and will be the objective of a new CAPP trial in Lynch Syndrome [211].aspirin208,209210211 Sulindac and celecoxib have been shown to cause regression of adenomas in familial adenomatous polyposis (FAP), and celecoxib was approved for a time as an adjunct to surgery for the treatment of this condition. Sulindaccelecoxib These data are presented in more detail elsewhere. (See "NSAIDs (including aspirin): Role in prevention of colorectal cancer".)"NSAIDs (including aspirin): Role in prevention of colorectal cancer" DFMO plus sulindac — Chemoprevention with the combination of difluoromethylornithine (DFMO) and sulindac (a nonsteroidal antiinflammatory drug) was evaluated in a randomized controlled trial involving 375 patients with a history of a resected colonic adenoma [212]. DFMO is an enzyme-activated irreversible inhibitor of ornithine decarboxylase, the first enzyme in polyamine synthesis. It was initially developed as a chemotherapy agent because of its cytostatic effects on a variety of cell lines.sulindac212 The patients were randomly assigned to combination therapy or placebo for three years. The trial was halted after an interim analysis found marked significant reductions in the rate of recurrent adenomas (12 versus 41 percent, risk ratio 0.30), advanced adenomas (0.7 versus 8.5 percent, risk ratio 0.09), and multiple adenomas (0.7 versus 13.2 percent, risk ratio 0.06). Active therapy was associated with a higher rate of mild, subclinical changes in the audiogram (18.4 versus 9.8 percent), which improved in some patients after drug discontinuation. Large trials evaluating the efficacy and safety of this regimen have been proposed. Postmenopausal hormone therapy — Postmenopausal hormone therapy (both combined estrogen plus progestin and unopposed estrogen) has been linked to a reduced risk of colorectal cancer [213-221]. As an example, a reduction in colorectal cancer risk was noted in the Women's Health Initiative (WHI) in women taking combined estrogen plus progestin hormone therapy (hazard ratio [HR] 0.56) [222]. This protective effect remained even after women who reported having screening sigmoidoscopy were excluded. No significant difference in the risk of colorectal cancer compared to placebo (HR 1.08) was noted in the unopposed conjugated equine estrogen arm in the WHI [213]. An important finding was that although women receiving combined estrogen and progestin had a lower diagnosis rate of CRC than did the control group, the tumors that did occur in this group were found at a more advanced stage than those found in the control group.213-221222213 Longer term follow up of the WHI data confirmed that the CRCs diagnosed in women receiving combined hormonal therapy were more advanced at diagnosis (regional or distant metastases in 69 versus 51 percent), and were associated with a non-statistically significant higher mortality rate (37 versus 27 deaths, 0.04 versus 0.03 percent, HR for death 1.29, 95% CI 0.78-2.11) [223]. These data suggest the puzzling possibility that HRT may decrease CRC incidence but not mortality. Such a paradox could be explained by a systematic diagnostic delay in women receiving combined estrogen and progestin postmenopausal hormone therapy or could suggest that HRT actually affects the biology of CRC.223 Even before the most recent data cited above [223], postmenopausal hormone therapy was not recommended for chemoprevention of colon cancer in women because of the associated long-term risks of therapy. (See "Menopausal hormone therapy: Benefits and risks", section on 'Colorectal cancer'.)223"Menopausal hormone therapy: Benefits and risks", section on 'Colorectal cancer' Statins — Some observational data suggest that statins are associated with a protective effect against several cancers, including colon cancer, but overall, the data are conflicting. (See "Statins: Possible noncardiovascular benefits", section on 'Cancer'.)"Statins: Possible noncardiovascular benefits", section on 'Cancer' The data regarding CRC are as follows: ●A modest reduction in the incidence of colon cancer, as a secondary endpoint, was observed in two large clinical trials evaluating the benefit ofpravastatin and simvastatin for coronary artery disease [224,225].pravastatinsimvastatin224,225 ●A reduced risk of CRC was also observed in the Molecular Epidemiology of Colorectal Cancer (MECC) study, a population-based case-control study in which data regarding personal and family history of cancer, medical conditions, medication use, physical activity, and nutrition were collected from 1953 patients diagnosed with CRC and 2015 population-based controls matched for age, gender and ethnicity [226]. In this study, use of statins for at least five years was associated with a significant reduction in the risk of CRC (odds ratio [OR] 0.53, 95% CI 0.38-0.74) after adjustment for use ofaspirin and other NSAIDs, physical activity, hypercholesterolemia, vegetable consumption, and family history. A potential confounding factor is that the cancer population and the controls were drawn from two different databases.226aspirin ●Other case-control studies have failed to document a protective benefit of statin use against colon cancer [227-230].227-230 The explanation for these conflicting results is unclear. Antioxidants — Several interventional trials have evaluated the efficacy of antioxidants in the prevention of colorectal adenomas. A meta-analysis of eight controlled trials found no convincing evidence that antioxidant supplements had a significant beneficial effect on primary or secondary prevention of colorectal adenomas [231].231 Bisphosphonates — Oral bisphosphonates are commonly used for the treatment of osteoporosis. (See "The use of bisphosphonates in postmenopausal women with osteoporosis".)"The use of bisphosphonates in postmenopausal women with osteoporosis" The data linking bisphosphonate use with protection from colorectal cancer are conflicting. The possibility that long-term bisphosphonate use was associated with a reduced risk of colorectal cancer was initially suggested in two case-control studies and one cohort study [232-234], but not confirmed in a third case-control study [235] or a large prospective cohort study [236].232-234235236 A meta-analysis of three case-control studies with a total of 16,998 CRC cases and 108,197 controls, and one cohort study with 94,405 individuals exposed to bisphosphonates and 283,181 unexposed to bisphosphonates [232-235] suggested a marginally reduced risk of CRC with any exposure to oral bisphosphonates (odds ratio [OR] 0.71, 95% CI 0.78-0.97) [237]. The inverse relationship was statistically significant at a dose of 10 or more prescriptions, or one or more years of oral bisphosphonate use. However, there were two potential problems with this analysis:232-235237 ●Confounding factors may weaken the conclusions of this study. Obesity (body mass index [BMI] >30 kg/m 2 ) is a risk factor for CRC, and obese patients included in the meta-analysis might have been exposed to bisphosphonates less frequently than were non-obese patients. The risk for CRC was adjusted for BMI in only two of the four included studies [238]. (See 'Obesity' above.)238'Obesity' ●For unclear reasons, the analysis did not include a second null study of a cohort of 86,277 women enrolled onto the Nurses’ Health Study, 801 of whom developed colorectal cancer [236]. The age-adjusted hazard ratio [HR] for colorectal cancer among women who regularly used bisphosphonates was 0.92 (95% CI 0.73-1.14) and was further attenuated after adjustment for other risk factors (HR 1.14, 95% CI 0.82-1.33). Risk was not influenced by duration of therapy.236 Given the inconsistency of the data, and the apparent lack of a dose response, the issue of whether use of oral bisphosphonates protects against CRC remains unsettled. Angiotensin II inhibition — In vitro and in vivo data suggest that angiotensin II is involved in promoting cancer development and that there is a relationship between angiotensin II inhibition and reduced colon cancer cell growth. However, several observational studies and secondary analyses of data from clinical trials examining the relationship between antihypertensive therapy with an angiotensin II converting enzyme inhibitor (ACE-I) and colorectal cancer risk have yielded conflicting results [239-242]:239-242 ●A cohort study reported that long-term use of lisinopril was associated with a 41 percent reduction in the risk of advanced colorectal adenoma [239].lisinopril239 ●Another case-control study assessing ACE-I exposure among 665 patients with CRC failed to demonstrate a significant association; however, the sample size was small and the duration of exposure was short [240].240 ●A secondary analysis of data from randomized trials also did not find an association between use of an ACE-I or angiotensin receptor blocker (ARB) and colorectal cancer risk, although the follow-up durations in the included trials were relatively short [241].241 ●In contrast, a large nested case-control study among a cohort of patients with hypertension in the EPIC General Practice Research Database provides the most compelling evidence of a potential protective effect of angiotensin II inhibition on CRC risk, albeit modest [242]. Overall, 2847 case patients (diagnosed with CRC after the diagnosis of hypertension) were matched (for age, sex, calendar year, and duration of follow-up) with 28,239 controls, and the average duration of follow-up in both groups was 4.4 years. The adjusted odds ratio for CRC was 0.84 (95% CI 0.72 to 0.98) for three or more years of ACE-I/ARB therapy and 0.75 (95% CI 0.58-0.97) for five or more years of exposure. The strength of the association increased with higher dose therapy (OR 0.53, 95% CI 0.35 to 0.79 for three or more years of high-dose exposure). CRC rates were significantly lower among patients exposed to ACE-I/ARB therapy alone when compared to those exposed to other antihypertensive agents exclusive of angiotensin inhibition.242 Taken together, these observational data suggest a potential protective effect of angiotensin II inhibition on CRC risk that is more evident in those receiving long-term and high daily dose therapies, but no intervention trials have thus far shown such an effect. INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5 th to 6 th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 th to 12 th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.) ●Beyond the Basics topics (see "Patient information: Colon and rectal cancer screening (Beyond the Basics)")"Patient information: Colon and rectal cancer screening (Beyond the Basics)"

20. Колоректальный рак: пациенты подлежащие обследованию Кровотечение из прямой кишки в сочетании с увеличением числа актов дефекации и/или ложных позывов на стул в течении 6 нед (в любом возрасте) Постоянные кровотечения из прямой кишки при отсутствии других симптомов (> 60 лет) Постоянное увеличение числа актов дефекации и/или ложных позывов на дефекацию на протяжении не менее 6 нед ( > 60 лет) Пациенты с легкопальпируемой опухолью в правой подвздошной области (в любом возрасте) Пациенты с легкопальпируемой внутрипросветной ректальной опухолью (в любом возрасте) Пациенты с необъяснимой анемией: Нb < 11 г% у мужчин (в любом возрасте) Hb < 10 г% у женщин (после менопаузы)

21. Колоректальный рак: группа низкого риска Кровотечения из прямой кишки с анальными проявлениями. Кровотечения из прямой кишки с визуально определяемой патологией (ректальная трещина, ректальный пролапс). Изменения ритма дефекации в сторону урежения или затруднение акта дефекации в течение менее 6 нед. Боль в животе, не связанная с факторами высокого риска

22. Колоректальный рак: алгоритм обследования Пальцевое исследование per rectum - позволяет диагностировать около 70% всех форм КРР и определить степень их местного распространения. Ректороманоскопия: позволяет осмотреть до 30 см дистального отдела толстой кишки с биопсией подозрительных патологических образований с последующим морфологическим исследованием. Ирригоскопия: использование бариевой клизмы с двойным контрастированием (с воздухом) позволяет исследовать рельеф слизистой оболочки толстой кишки, выявить практически все формы КРР и подавляющее число полипов размером более 1 см. Фиброколоноскопия: гибким фиброскопом с волоконной оптикой можно осмотреть все отделы толстой кишки (от ануса до баугиниевой заслонки), выявив не только опухолевое поражение, но и небольшие полипы, произвести биопсию всех подозрительных участков (более точный метод по сравнению с ирригоскопией)

23. Колоректальный рак: алгоритм обследования Всем больным раком прямой и ободочной кишок необходимо до операции определить стадию заболевания для установления распространённости опухолевого процесса и наличия отдалённых метастазов (печень, лёгкие). Необходимо выполнить трансректальное УЗИ для выявления КРР в стадии T1, когда возможно трансректальное местное удаление опухоли КТ или МРТ следует выполнить для оценки вовлечённость смежных органов в опухолевый процесс

24. Колоректальный рак: лабораторная диагностика Наиболее популярен раковоэмбриональный Аг (РЭА). Маркер неспецифичен, его концентрация повышается при раке молочной и поджелудочной желёз, лёгкого, яичников (аденокарцинома). Концентрация РЭА не всегда коррелирует с распространённостью процесса и дифференцировкой опухоли, хотя чаще повышается при распространённом раке, особенно при метастазах в печени. Пороговый уровень РЭА в сыворотке крови составляет 10 мг/мл. Снижение уровня РЭА после операции и повышение через 2–3 мес после радикального лечения может указывать на рецидив заболевания. Информативность определения других онкомаркёров (Са19–9, Sialosyl-Tn и др.) в клинических условиях находится в стадии изучения

25. Колоректальный рак: дифференциальная диагностика Воспалительные заболевания толстой кишки – неспецифический язвенный колит и болезнь Крона. Дивертикулярная болезнь Другие колоректальные опухоли: полипы, аденомы, карциноидные опухоли, лимфомы, мезенхимальные опухоли, метастатические опухоли других первичных локализаций. Геморрой. Опухоли малого таза: опухоли предстательной железы, яичников, миома матки. Синдром раздражённой толстой кишки

26. SUMMARY ●The major factors that increase the risk of colon cancer include hereditary forms of colorectal cancer, age, a personal or family history of sporadic colorectal cancer (and possibly large or advanced adenomas), and inflammatory bowel disease. Several potentially modifiable risk factors including obesity and lack of physical activity have been consistently identified in observational studies. (See 'Risk factors' above.)'Risk factors' ●A substantial body of evidence supports a protective effect of aspirin and other nonsteroidal antiinflammatory drugs on the development of colonic adenomas and cancer. Aspirin can be considered in selected patients with Lynch syndrome for chemoprevention of Lynch syndrome- associated cancers. The potential role of aspirin and other NSAIDs in colorectal cancer prevention is discussed elsewhere. (See "NSAIDs (including aspirin): Role in prevention of colorectal cancer".)aspirin"NSAIDs (including aspirin): Role in prevention of colorectal cancer" ●Other protective factors have also been identified mainly in observational studies, but the strength of these associations is uncertain. (See 'Protective factors' above.) Nevertheless, a protective diet can be defined for clinical purposes to include avoidance of processed and charred red meat, inclusion of vegetables (especially cruciferous), and unprocessed forms of wheat bran (controversial), an adequate amount of intake of folate from food, limited caloric intake, and avoidance of excessive alcohol.'Protective factors'

27. Колоректальный рак: Клинические проявления При локализации опухоли в правых отделах ободочной кишки: железодефицитная анемия проявления частичной кишечной обструкции При ректальном раке и раке сигмовидной кишки: примесь крови в кале изменение частоты дефекаций или появление ложных позывов на стул

28. Among symptomatic patients, clinical manifestations differ depending on tumor location: ●A change in bowel habits is a more common presenting symptom for left-sided than right-sided CRCs because fecal contents are liquid in the proximal colon and the lumen caliber is larger, and they are therefore less likely to be associated with obstructive symptoms. ●Hematochezia is more often caused by rectosigmoid than right-sided colon cancer. ●Iron deficiency anemia from unrecognized blood loss is more common with right-sided CRCs [10]. Cecal and ascending colon tumors have a fourfold higher mean daily blood loss (approximately 9 mL/day) than tumors at other colonic sites [11]. (See "Causes and diagnosis of iron deficiency anemia in the adult", section on 'Search for source of blood and iron loss'.)1011"Causes and diagnosis of iron deficiency anemia in the adult", section on 'Search for source of blood and iron loss' ●Abdominal pain can occur with tumors arising at all sites; it can be caused by a partial obstruction, peritoneal dissemination, or intestinal perforation leading to generalized peritonitis. ●Rectal cancer can cause tenesmus, rectal pain, and diminished caliber of stools. These concepts can be illustrated by the distribution of findings at presentation in a series of 253 CRCs that were diagnosed and treated at ateaching/national referral hospital in Kenya between 1993 and 2005, which included 140 rectal cancers, 54 right-sided colon cancers, and 59 left-sided colon cancers (table 2) [7].table 27

29. Колоректальный рак: метастазирование Пути метастазирования: Гематогенный Лимфатический Трансперитонеальный Наиболее часто: Регионарные лимфоузлы Печень Легкие Перитонеум Кости Головной мозг

30. Unusual presentations — There are a variety of atypical presentations of CRC. These include: ●Local invasion or a contained perforation causing malignant fistula formation into adjacent organs, such as bladder (resulting in pneumaturia) or small bowel. This is most common with cecal or sigmoid carcinomas; in the latter case, the condition can mimic diverticulitis. ●Fever of unknown origin, intraabdominal, retroperitoneal, abdominal wall or intrahepatic abscesses due to a localized perforated colon cancer [12,13]. Streptococcus bovis bacteremia and Clostridium septicum sepsis are associated with underlying colonic malignancies in about 10 to 25 percent of patients [14]. Rarely, other extraabdominal infections caused by colonic anaerobic organisms (eg, Bacteroides fragilis) may be associated with CRC [15]. (See "Clinical manifestations, diagnosis, and treatment of infections due to group D streptococci (Streptococcus bovis/Streptococcus equinus complex)", section on 'Association with colonic neoplasia'.)12,131415"Clinical manifestations, diagnosis, and treatment of infections due to group D streptococci (Streptococcus bovis/Streptococcus equinus complex)", section on 'Association with colonic neoplasia' ●CRC ultimately proves to be the site of origin of approximately 6 percent of adenocarcinomas of unknown primary sites [16]. (See "Adenocarcinoma of unknown primary site".)16"Adenocarcinoma of unknown primary site" ●CRC may be detected on the basis of discovery of liver metastases that are detected incidentally during studies such as gallbladder or renal ultrasound, or computed tomography (CT) scans for evaluation of other symptoms (eg, dyspnea).

31. Impact of symptoms on prognosis — The presence of symptoms and their particular type provide some prognostic importance: ●Patients who are symptomatic at diagnosis typically have more advanced disease and a worse prognosis. In one study of 1071 patients with newly-diagnosed colon cancer, 217 of whom were diagnosed through screening, the patients not diagnosed through screening were at significantly higher risk for a more invasive tumor (≥T3: relative risk [RR] 1.96), nodal involvement (RR 1.92), and metastatic disease on presentation (RR 3.37). In addition, patients not diagnosed through screening had significantly higher death rates (RR 3.02) and recurrence rates (RR 2.19) as well as shorter survival and disease-free intervals [17]. (See "Tests for screening for colorectal cancer: Stool tests, radiologic imaging and endoscopy".)17"Tests for screening for colorectal cancer: Stool tests, radiologic imaging and endoscopy" ●The total number of symptoms may be inversely related to survival for colon but not for rectal cancer [18]. Whether the duration of symptoms influences prognosis is unclear; the available data are mixed [19-21].1819-21 ●Obstruction and/or perforation, although uncommon, carry a poor prognosis, independent of stage [4,22-25]. Among patients with node-negative colon cancer, obstruction or perforation are poor prognostic factors that may influence the decision to pursue adjuvant chemotherapy. (See "Adjuvant chemotherapy for resected stage II colon cancer", section on 'Clinicopathologic variables'.)4,22-25"Adjuvant chemotherapy for resected stage II colon cancer", section on 'Clinicopathologic variables' ●Tumors presenting with rectal bleeding (typically those involving the distal colon and rectum) have been thought to have a better prognosis because of their tendency to be diagnosed at an earlier stage [26,27]; however, bleeding is not an independent predictor of outcome [23,28]. Rectal bleeding is more commonly seen with distal tumors, and a larger proportion of distal colon cancers present as early-stage tumors as compared with proximal tumors [27].26,2723,2827 Other determinants of prognosis, including clinicopathologic and molecular features, are discussed elsewhere. (See "Pathology and prognostic determinants of colorectal cancer".)"Pathology and prognostic determinants of colorectal cancer"

32. DIAGNOSIS — Colorectal cancer (CRC) may be suspected from one or more of the symptoms and signs described above or may be asymptomatic and discovered by routine screening of average- and high-risk subjects. Once a CRC is suspected, the next test can be a colonoscopy, barium enema, or computed tomography colonography. However, examination of tissue is required to establish the diagnosis; this is usually accomplished by colonoscopy. (See "Screening for colorectal cancer: Strategies in patients at average risk" and "Screening for colorectal cancer in patients with a family history of colorectal cancer" and "Lynch syndrome (hereditary nonpolyposis colorectal cancer): Screening and management" and "Familial adenomatous polyposis: Screening and management of patients and families" and "Peutz-Jeghers syndrome and juvenile polyposis: Screening and management of patients and families".)barium"Screening for colorectal cancer: Strategies in patients at average risk""Screening for colorectal cancer in patients with a family history of colorectal cancer""Lynch syndrome (hereditary nonpolyposis colorectal cancer): Screening and management""Familial adenomatous polyposis: Screening and management of patients and families""Peutz-Jeghers syndrome and juvenile polyposis: Screening and management of patients and families" Histopathologically, the majority of cancers arising in the colon and rectum are adenocarcinomas. The histologic diagnosis of CRC is discussed in detail elsewhere. (See "Pathology and prognostic determinants of colorectal cancer", section on 'Histologic type'.)"Pathology and prognostic determinants of colorectal cancer", section on 'Histologic type'

33. Colonoscopy — Colonoscopy is the most accurate and versatile diagnostic test for CRC, since it can localize and biopsy lesions throughout the large bowel, detect synchronous neoplasms, and remove polyps. Synchronous CRCs, defined as two or more distinct primary tumors diagnosed within six months of an initial CRC, separated by normal bowel, and not due to direct extension or metastasis, occur in 3 to 5 percent of patients [29-31]. The incidence is somewhat lower (about 2.5 percent) when patients with Lynch syndrome (see below) are excluded; the presence of synchronous cancers should raise the clinical suspicion for Lynch Syndrome [32]. (See "Lynch syndrome (hereditary nonpolyposis colorectal cancer): Clinical manifestations and diagnosis", section on 'Colonic manifestations'.)29-3132"Lynch syndrome (hereditary nonpolyposis colorectal cancer): Clinical manifestations and diagnosis", section on 'Colonic manifestations'

34. Flexible sigmoidoscopy — Over the last 50 years, a gradual shift toward right-sided or proximal colon cancers has been observed both in the United States and internationally, with the greatest increase in incidence is in cecal primaries (picture 2). Because of this, and because of the high frequency of synchronous CRCs, flexible sigmoidoscopy is generally not considered to be an adequate diagnostic study for a patient suspected of having a CRC, unless a palpable mass is felt in the rectum. In such cases, a full colonoscopy will still be needed to evaluate the remainder of the colon for synchronous polyps and cancers. (See "Colorectal cancer: Epidemiology, risk factors, and protective factors", section on 'Incidence'.)picture 2"Colorectal cancer: Epidemiology, risk factors, and protective factors", section on 'Incidence'

35. Barium enema — Barium enema is widely available and may be used to investigate patients with symptoms suggesting of CRC (image 1A-B) [44,45]. However, the diagnostic yield of both double-contrast barium enema (DCBE) alone and the combination of DCBE plus flexible sigmoidoscopy is less than that of colonoscopy or CT colonography for the evaluation of lower tract symptoms [45,46].Bariumimage 1A-B44,4545,46 The yield of DCBE alone was addressed in a randomized trial comparing DCBE versus CT colonography in 3838 patients with symptoms suggestive of CRC [45]. Of the 2527 patients assigned to DCBE, the detection rate for CRC or large polyps was significantly lower (5.6 versus 7.3 percent with CT colonography). Rates of additional studies after the initial procedure were significantly lower after DCBE than CT colonography (18 versus 24 percent) with three years of follow-up. The need for additional studies following CT colonography was due mostly to the higher polyp detection rate; CRC was subsequently diagnosed in more patients who had initially undergone DCBE (miss rate 14 versus 7 percent).45 If a polyp or mass is detected by barium enema, colonoscopy is recommended to establish the histology, remove the polyp, and search for synchronous lesions.barium

36. CT colonography — CT colonography (also called virtual colonoscopy or CT colography) provides a computer-simulated endoluminal perspective of the air-filled distended colon. The technique uses conventional spiral or helical CT scan or magnetic resonance images acquired as an uninterrupted volume of data, and employs sophisticated postprocessing software to generate images that allow the operator to fly-through and navigate a cleansed colon in any chosen direction. CT colonography requires a mechanical bowel prep that is similar to that needed for barium enema, since stool can simulate polyps. (See"Computed tomographic colonography".)barium"Computed tomographic colonography" CT colonography has been evaluated in patients with incomplete colonoscopy and as an initial diagnostic test in patients with symptoms suggestive of CRC.

37. PILLCAM 2 — A colon capsule for CRC screening has been approved by the EMA in Europe and by the US Food and Drug Administration. In the United States, it is approved for use in patients who have had an incomplete colonoscopy. While its role in screening for CRC is still uncertain, it could be considered in a patient with an incomplete colonoscopy who lacks obstruction.

38. Laboratory tests — Although CRC is often associated with iron deficiency anemia, its absence does not reliably exclude the disease. There is no diagnostic role for other routine laboratory test, including liver function tests, which lack sensitivity for detection of liver metastases.

39. Tumor markers — A variety of serum markers have been associated with CRC, particularly carcinoembryonic antigen (CEA). However, all these markers, including CEA, have a low diagnostic ability to detect primary CRC due to significant overlap with benign disease and low sensitivity for early-stage disease [54-57]. A meta-analysis concluded that the pooled sensitivity of CEA for diagnosis of colorectal cancer was only 46 percent (95% CI 0.45-0.47) [58]. No other conventional tumor marker had a higher diagnostic sensitivity, including carbohydrate antigen 19-9 (CA 19-9, pooled sensitivity 0.30, 95% CI 0.28-0.32).54-5758 Furthermore, specificity of CEA is also limited. In the previously mentioned meta-analysis, the specificity of CEA for diagnosis of CRC was 89 percent (95% CI 0.88-0.92). Non-cancer-related causes of an elevated CEA include gastritis, peptic ulcer disease, diverticulitis, liver disease, chronic obstructive pulmonary disease, diabetes, and any acute or chronic inflammatory state. In addition, CEA levels are significantly higher in cigarette smokers than in non-smokers [59,60].59,60 An expert panel on tumor markers in breast and colorectal cancer convened by the American Society of Clinical Oncology (ASCO) recommended that neither serum CEA nor any other marker, including CA 19-9, should be used as a screening or diagnostic test for colorectal cancer [55]. A similar recommendation has been made by the European Group on Tumor Markers [61].5561 However, CEA levels do have value in the follow-up of patients with diagnosed CRC. ASCO guidelines recommend that serum CEA levels be obtained preoperatively in most patients with demonstrated CRC to aid in surgical treatment planning, posttreatment follow-up, and in the assessment of prognosis [55]:55 ●Serum levels of CEA have prognostic utility in patients with newly-diagnosed CRC. Patients with preoperative serum CEA >5 ng/mL have a worse prognosis, stage for stage, than those with lower levels. (See "Pathology and prognostic determinants of colorectal cancer", section on 'Category I factors'.)"Pathology and prognostic determinants of colorectal cancer", section on 'Category I factors' ●Elevated preoperative CEA levels that do not normalize following surgical resection imply the presence of persistent disease and the need for further evaluation. (See "Surveillance after colorectal cancer resection", section on 'Carcinoembryonic antigen'.)"Surveillance after colorectal cancer resection", section on 'Carcinoembryonic antigen' Furthermore serial assay of postoperative CEA levels should be performed for five years for patients with stage II and III disease if they may be a potential candidate for surgery or chemotherapy if metastatic disease is discovered. A rising CEA level after surgical resection implies recurrent disease and should prompt follow-up radiologic imaging. (See "Surveillance after colorectal cancer resection".)"Surveillance after colorectal cancer resection"

40. ] PET scans — Positron emission tomography (PET) scans do not appear to add significant information to CT scans for routine preoperative staging of CRC [90,91]. The established role of PET scanning in patients with CRC as an adjunct to other imaging modalities is described in the following settings:90,91 ●Localizing site(s) of disease recurrence in patients who have a rising serum carcinoembryonic antigen (CEA) level and nondiagnostic conventional imaging evaluation following primary treatment. In this setting, PET scanning can potentially localize occult disease, permitting the selection of patients who may benefit from exploratory laparotomy [92-95]. (See "Surveillance after colorectal cancer resection".) In an illustrative series, 105 such patients underwent PET scanning and subsequent abdominopelvic CT scans [92]. Compared to CT and other conventional diagnostic studies, PET scanning had a higher sensitivity (87 versus 66 percent) and specificity (68 versus 59 percent) for the detection of clinically relevant tumor. In a second report, PET scan findings led to a potentially curative resection in 14 of 50 patients (28 percent) with elevated serum CEA levels and a completely normal or equivocal conventional diagnostic work-up [93].92-95"Surveillance after colorectal cancer resection"9293 ●Evaluation of patients who are thought to be present or future candidates for resection of isolated colorectal cancer liver metastases. The routine use of PET prior to attempted resection reduces the number of nontherapeutic laparotomies. (See "Management of potentially resectable colorectal cancer liver metastases", section on 'PET scans'.)"Management of potentially resectable colorectal cancer liver metastases", section on 'PET scans' Recent chemotherapy may alter the sensitivity of PET for the detection of colorectal liver metastases, an effect thought related to decreased cellular metabolic activity of the tumor. However, generally, the benefit of a PET scan is to detect extrahepatic metastases in patients considered liver resection candidates, and in this situation, it is appropriate to obtain a PET prior to initiation of chemotherapy. This subject is addressed in detail elsewhere. (See"Management of potentially resectable colorectal cancer liver metastases", section on 'PET scans'.)"Management of potentially resectable colorectal cancer liver metastases", section on 'PET scans'

41. Колоректальный рак: резюме Варианты проявлений у пациентов: Асимптомное Симптомы подозрительные на КРР Экстренная госпитализация (ЖКК, перитонит) Примерно у каждого 5-й пациента обнаруживаются метастазы: Наиболее часто регионарные лимфоузлы Печень, легкие и брюшина Положительный тест на скрытую кровь имеет большее предиктивное значение чем, любой другой в отдельности взятый симптом. Колоноскопия наиболее оптимальный метод исследования Не существует точного лабораторного маркера КРР, однако исследование СЭА полезно для определения пре- и постоперативной тактики лечения

42. Спасибо за внимание