Ludzkie koronawirusy - autor: Krzysztof Pyrć z Zakładu Mikrobiologii, Wydział Biochemii, Biofizyki i Biotechnologii, Uniwersytet Jagielloński, Kraków

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© Borgis - Nowa Medycyna 2/2020, s. 57-71 | DOI: 10.25121/NM.2020.27.2.57
*Łukasz Kozak1, Jacek Janiszewski1, 2, Joanna Woźniak1, 2, Martyna Kamrowska1, Beata Januszko-Giergielewicz3, 4
Colorectal cancer after kidney transplantation – risk factors and the need for prevention
Rak jelita grubego po zabiegu przeszczepienia nerki – czynniki ryzyka i konieczność profilaktyki
1Department of Internal Medicine and Gastroenterology, Independent Public Healthcare Centre, Ministry of the Interior and Administration with Warmia and Mazury Oncology Centre, Olsztyn
2Department of Cardiology and Internal Medicine, Collegium Medicum, University of Warmia and Mazury in Olsztyn
3Department of General, Liver and Transplant Surgery, Antoni Jurasz University Hospital No. 1 in Bydgoszcz
4Department of Family Medicine and Infectious Diseases, Collegium Medicum, University of Warmia and Mazury in Olsztyn
Streszczenie
Przeszczepienie nerki (PN) u pacjentów z przewlekłą chorobą nerek jest uznawane za metodę leczenia nerkozastępczego, która daje im najdłuższe przeżycie oraz najwyższy jego komfort. PN zmniejsza narażenie na wiele powikłań związanych z przewlekłą dializoterapią, umożliwia również pacjentom po transplantacji tego narządu pełne funkcjonowanie w środowisku rodzinnym oraz społecznym. Jak każda forma leczenia posiada ona jednak swoje ograniczenia. Spowodowane są one przede wszystkim koniecznością stosowania przewlekłego leczenia immunosupresyjnego. Udowodniono, że przewlekła immunosupresja zwiększa ryzyko występowanie nowotworów. Najczęściej występującymi nowotworami mającymi związek z immunosupresją są nowotwory skóry. Również ryzyko rozwoju raków narządów litych jest kilkakrotnie wyższe po PN w porównaniu z populacją ogólną. Choroby nowotworowe są jedną z głównych przyczyn zgonów chorych po PN. Wynika to z podstępnego i agresywnego ich przebiegu w tej populacji pacjentów oraz częstej konieczności modyfikowania stosowanej terapii onkologicznej. W przedstawionej pracy, na podstawie analizy dostępnych danych z piśmiennictwa oraz doświadczeń własnych, autorzy dyskutują fakt zwiększonej częstości występowania raka jelita grubego (RJG) u chorych po PN, odmienności jego przebiegu oraz potencjalnych możliwości jego profilaktyki w tej szczególnej grupie chorych. W oparciu o tę analizę autorzy postulują również konieczność wprowadzenia ścisłych, ujednoliconych dla wszystkich ośrodków transplantacyjnych zaleceń, dotyczących nadzoru onkologicznego w kierunku wczesnej wykrywalności RJG u pacjentów po PN.
Summary
Kidney transplantation (KT) in patients with chronic kidney disease is considered a method of renal replacement therapy offering the longest and most comfortable survival possible. Kidney transplantation reduces the risk of multiple complications associated with chronic dialysis, as well as allows patients after transplantation of this organ for full participation in family and social life. However, like any other treatment modality, kidney transplantation has its limitations. These are primarily associated with the need for chronic immunosuppressive therapy. It was shown that chronic immunosuppression increases the risk of cancer. Skin cancers are the most common immunosuppression-related neoplasms. Also, the risk of solid organ cancers is several times higher after kidney transplantation compared to the general population. Cancer is one of the leading causes of mortality in kidney graft recipients. This is due to its insidious and aggressive course in this patient population and the frequent need to modify anticancer therapy. In this paper, we discuss the increased incidence of colorectal cancer (CRC) in patients after kidney transplantation, differences in the course of the disease, as well as its potential prevention, based on the available literature and our own experience. Based on our analysis, we postulate the need for strict recommendations unified for all transplantation centres, regarding oncological surveillance for early detection of colorectal cancer in patients after kidney transplantation.
Introduction
The shortage of organs for transplantation is a widely known problem of modern transplantation medicine, which is broadly discussed in medical societies. Combating the main causes of shorter survival in organ transplant recipients, such as cardiovascular complications and more aggressive development of malignancies compared to the general population, is no less challenging.
The kidney is the most commonly transplanted vascularised organ both in Poland and worldwide. A total of 1,473 transplantations from deceased donors, including 907 kidneys, were performed in Poland in 2019. A total of 73 organs, including 52 kidneys, were transplanted from live donors. These statistics have not changed significantly for several years, and the expected progress has not been made in this respect. A total of 1,947 patients awaited organ transplantation in Poland in 2019, including 50% of patients on the waiting list for the kidney (1). The above data illustrate the size of the described patient population. These patients require particularly increased oncological vigilance and special standards for cancer prevention.
As mentioned above, cancer is one of the leading causes of mortality in patients after kidney transplantation (KT), who are at an increased risk of malignancy compared to the general population (2, 3).
Colorectal cancer (CRC) is the third most common malignancy in men and the second most common malignancy in women. It accounts for 8% of cancer-related deaths, which makes it the fourth leading cause of cancer-related mortality globally. CRC is responsible for about 600,000 deaths annually (4). Most cases of CRC are sporadic, with only about 5-10% of cases due to genetic predisposition (4).
CRC is 2-3 times more common in patients after KT compared to the general population (5); it shows more rapid and aggressive growth pattern, the affected recipients are younger at diagnosis, and they have worse treatment outcomes (6). It should be emphasised that a kidney transplanted from a deceased and a living donor functions for an average of 7-10 and about 15 years, respectively (7). Therefore, there is a high probability of neoplastic process initiation in predisposed patients during the period of good graft function, which is often observed in everyday practice.
Risk factors for colorectal cancer
In 2013, Johnson et al. analysed the available literature and identified the following risk factors for CRC: overweight and obesity, lack of physical activity, smoking tobacco, diabetes, inflammatory bowel diseases, excess consumption of alcohol, pelvic radiotherapy, and acromegaly. The important role of genetic factors, such as family history of CRC, Lynch syndrome, type X CRC, familial adenomatous polyposis, Peutz-Jeghers syndrome and MYH-associated polyposis, was also emphasised (8).
CRC risk factors postulated by the National Cancer Registry are shown in table 1 (4).
Tab. 1. Risk factors for colorectal cancer according to the National Cancer Registry (4)
Risk factorDescription
AgeIncreased risk after the age of 50 years
Inflammatory bowel diseasesUlcerative colitis – 20-fold increase in the risk, Crohn’s disease – 3-fold increase in the risk
Metabolic syndromeHypertension, obesity, diabetes, hypertriglyceridaemia, low HDL cholesterol – increased risk, mainly in men
Smoking tobacco1/5 of CRCs are associated with tobacco smoking in the USA
LifestylePoor physical activity
RaceHigher risk among African Americans and Ashkenazi Jews
Geographical factorsMore common in Europe, North America, Australia and Japan than in Africa or Asia
Positive history of adenomas or CRC 
Genetic factorsFamilial adenomatous polyposis (FAP) is associated with a 100% lifetime risk of developing CRC
 
Hereditary non-polyposis colorectal cancer (HNPCC) – 70-80% risk of CRC
DietLow-fibre, high-fat, high-calorie diet low in calcium, alcohol abuse
Previous history of abdominal radiation therapy 
Prior cholecystectomy 
Ureterosigmoidostomy500-fold increased risk
Family history of CRC in the absence of signs of classical genetic predisposition syndrome  
It seems that diet is the most important environmental factor involved in the aetiology of CRC. The impact of diet high in red meat on the increased risk of CRC has been documented in numerous studies (9). This causal relationship may be either direct or indirect as a meat-rich diet may be deficient in other components, such as fibre and fruit/vegetable polyphenols (10). Thermal processing of meat itself can also contribute to its increased carcinogenic potential. When meats are cooked at higher temperatures, mutagenic and carcinogenic heterocyclic amines are formed as a result of interaction between muscle creatinine and amino acids (11), as well as N-nitroso compounds are formed (12). The heme contained in meat may act as a nitrosating agent, promoting formation of N-nitroso compounds. Since red meats have a higher content of heme than white meats, high consumption of red meat (beef, pork or lamb) may increase the risk of CRC (13, 14). A relationship was demonstrated between heme iron and colonic polyps, adenomas and CRC (15-18). Diet low in selenium and plant fibres also plays an important role. It has negative effects on the intestinal bacterial flora, induces synthesis of carcinogens and slows their passage through the large intestine (19).
Type 2 diabetes is known to be associated with an increased risk of CRC. Larsson et al. demonstrated a strong correlation between type 2 diabetes and an increased incidence of CRC in their 2005 meta-analysis (20). Based on an analysis of 15 studies, the authors concluded that the risk of CRC is increased in T2D (20-22).
This hypothesis was confirmed in 2015 by Díaz-Algorri et al., who assessed a group of 451 patients. Based on the collected evidence they found that type 2 diabetes is an important risk factor for colorectal neoplasia, especially in women (23, 24).
Insulin and insulin-like growth factor (IGF-1) are known to play an important role in human metabolism, but they are also responsible for regulating cellular growth and proliferation. In addition to its role in glucose metabolism, insulin also stimulates colon epithelial growth. CRC epithelial cells have been shown to have an increased density of insulin receptors compared to normal colonic epithelium (22). It should be emphasised that the pro-proliferative effects of insulin have been shown only at its plasma levels above physiological norms (25).
Colonic and CRC epithelial cells express IGF-1 receptors. Activation of IGF-1 leads to apoptosis inhibition and cell cycle progression (26). Insulin and IGF-1 have no direct mutagenic effect. The pattern of colonic transformations follows the adenocarcinoma-cancer sequence in patients with type 2 diabetes, while insulin and IGF-1 can only accelerate this process (22).
As already mentioned above, the risk of CRC is also increased in obese individuals (27). The risk of colon cancer is significantly increased in obese men and women, with stronger carcinogenesis in obese men than women (28). It was also found that individuals with abdominal obesity have an increased risk of developing adenoma compared to those non-obese (29).
Also, it was clearly demonstrated that tobacco smokers are at an increased risk of death from CRC (30, 31). This risk is proportional to the number of cigarettes smoked per day (pack years) (32). Smoking is also associated with an increased risk of developing colorectal polyps (33).
Risk factors and the course of colorectal cancer after kidney transplantation
In addition to the above mentioned risk factors characteristic for the general population, patients after KT are exposed to additional risk factors specific for this group. Therefore, these patients are exposed both to traditional risk factors for CRC, which are proven in the literature, and risk factors resulting from chronic kidney disease (CKD) and immunosuppressive therapy. Patients with CKD are at an increased risk of cancer compared to the general population due to immune dysfunction, impaired DNA repair, higher levels of reactive oxygen species, carcinogenic effects of heterocyclic amines and nitrosodimethylamines, increased levels of parathyroid hormone, reduced levels of 1,25-dihydroxycholecalciferol, and increased inflammatory markers. Pharmacotherapy (previous immunosuppressive treatment, excess use of analgesics, the use of diuretics) and previous dialysis therapy, which is often associated with the use of iron and/or erythropoietin therapy, also play an important role in carcinogenesis. The duration of dialysis is also important – the risk of cancer increases by 10-20% per year for dialysis duration over 2-3 years (34, 35).
In the case of KT, the possible donor/recipient cancer transmission (0.02-0.2% of all transplantation) is an important factor contributing to cancer development in the latter (34, 36). A relatively high risk of donor-recipient transmission has been observed for renal cell carcinoma, malignant melanoma, lymphoma, lung cancer, breast cancer, choriocarcinoma, and CRC in the donor (34).
Immunosuppressants, their type and duration of their use have a significant impact on carcinogenesis. This results indirectly from the immune response as well as from the direct pro-oncogenic effects of these agents (37, 38). It was demonstrated that the risk of cancer increases with an increasing total intensity of immunosuppressive therapy (39).
Usually triple immunosuppressive regimens are used after KT due to the high immunogenicity of this organ; therefore, due to the intensity of immunosuppression, the risk of CRC after KT is higher compared to other organs, such as the liver, where mono- or dual-immunosuppression is sufficient to maintain good function of transplanted liver (40-42).
The risk of death significantly increases 10 years after transplantation. Compared to the general population, CRC is more common in younger patients after KT (58 vs 70 years) and is associated with worse prognosis (5-year survival 43.5 vs 62.3%) (43, 44). The characteristic of CRC after KT is presented in table 2.
Tab. 2. Risk factors for colorectal cancer after kidney transplantation (34, 37, 39)
Risk factorCharacteristic
Time since KTSignificantly increased risk 10 years after KT
Underlying kidney disease and its treatment prior to KTIncreased risk is associated with previous immunosuppressive therapy, steroid therapy and the length of dialysis therapy.
AgeDisease onset at a younger age than in the general population
Aggressive course of the diseaseMore rapid progression of untreated CRC than in the general population
Type of immunosuppressive therapy used after KTThe risk varies, depending on agents used and immunosuppression regimen (dual, triple)
KT – kidney transplantation; CRC – colorectal cancer
Most CRCs histologically arise from benign lesions, i.e. adenomatous polyps. Polyps and early-stage cancer are usually asymptomatic (45) until advanced stage of the disease. This is particularly dangerous in patients after KT due to therapeutic difficulties in advanced stages of the disease, which result from the possible dysfunction of the transplanted kidney and the resulting limitations and/or contraindications for chemotherapy.
Mayo Clinic researchers published an analysis of 115 patients after solid organ transplantation, of whom 63 met the inclusion criteria (the excluded patients had cancer diagnosed prior to transplantation) and developed CRC after transplantation (46). The study group included 44% of patients after kidney and 35% after liver transplantation. Mean time elapsed between transplantation and CRC diagnosis was 59 months; with stage 4 CRC in 15 patients and stage 3 CRC in 13 patients. Mean survival time was 30.8 months. The estimated 5-, 10- and 15-year survival rates were 42.5, 17.9 and 7.5%, respectively. None of patients with stage 4 CRC survived 5 years. The estimated 5-year survival rates for patients with stage 1, 2 and 3 CRC were 77, 50, and 42%, respectively (46).
In 2016, a team of Polish researchers from the Medical University of Gdańsk published a study describing their attempt to investigate a group of 950 patients under the care of a nephrological clinic (47). Of this group, only 180 patients completed a questionnaire on the alarming symptoms of CRC, and 100 of these patients had faecal occult blood test (FOBT) performed. Based on preliminary results, 45 patients were qualified for endoscopy. In this group, colonic diverticulitis was diagnosed in 18, colonic polyps in 14, inflammatory bowel disease in 7, and CRC in 3 patients (47).

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Piśmiennictwo
1. http://www.poltransplant.org.pl/statystyka_2019.html.
2. Sprangers B, Nair V, Launay-Vacher V et al.: Risk factors associated with post–kidney transplant malignancies: an article from the Cancer-Kidney International Network. Clin Kidney J 2018; 11(3): 315-329.
3. Wong G, Chapman JR, Craig JC: Death from cancer: a sobering truth for patients with kidney transplants. Kidney Int 2014; 85(6): 1262-1264.
4. http://onkologia.org.pl/nowotwory-zlosliwe-jelita-grubego-c18-21/.
5. Chapman JR, Webster AC, Wong G: Cancer in the Transplant Recipient. Cold Spring Harb Perspect Med 2013; 3(7). pii: a015677.
6. Collins MG, Teo E, Cole SR et al.: Screening for colorectal cancer and advanced colorectal neoplasia in kidney transplant recipients: cross sectional prevalence and diagnostic accuracy study of faecal immunochemical testing for haemoglobin and colonoscopy. BMJ 2012; 25: 345.
7. Informacja dla chorego na temat operacji przeszczepienia nerki oraz Formularz świadomej zgody chorego na operację przeszczepienia nerki; http://www.poltransplant.org.pl/form_main.html.
8. Johnson CM, Wei C, Ensor JE et al.: Meta-analyses of colorectal cancer risk factors. Cancer Causes Control 2013; 24: 1207-1222.
9. Lin OS: Acquired risk factors for colorectal cancer. Methods Mol Biol 2009; 472: 361-372.
10. Pericleous M, Mandair D, Caplin ME: Diet and supplements and their impact on colorectal cancer. J Gastrointest Oncol 2013; 4(4): 409-423.
11. Sugimura T, Wakabayashi K, Nakagama H, Nagao M: Heterocyclic amines: mutagens/carcinogens produced during cooking of meat and fish. Cancer Sci 2004; 95: 290-299.
12. Cross AJ, Sinha R: Meat-related mutagens/carcinogens in the etiology of colorectal cancer. Environ Mol Mutagen 2004; 44: 44-55.
13. Rao CV: Nitric oxide signaling in colon cancer chemoprevention. Mutat Res 2004; 555: 107-119.
14. Kuhnle GG, Bingham SA: Dietary meat, endogenous nitrosation and colorectal cancer. Biochem Soc Trans 2007; 35: 1355-1357.
15. Shaheen NJ, Silverman LM, Keku T et al.: Association between hemochromatosis (HFE) gene mutation carrier status and the risk of colon cancer. J Natl Cancer Inst 2003; 95: 154-159.
16. Bird CL, Witte JS, Swendseid ME et al.: Plasma ferritin, iron intake, and the risk of colorectal polyps. Am J Epidemiol 1996; 144: 34-41.
17. Wurzelmann JI, Silver A, Schreinemachers DM et al.: Iron intake and the risk of colorectal cancer. Cancer Epidemiol Biomarkers Prev 1996; 5: 503-507.
18. Nelson RL, Davis FG, Sutter E et al.: Body iron stores and risk of colonic neoplasia. J Natl Cancer Inst 1994; 86: 455-460.
19. Dąbrowski A: Gastroenterologia. Wyd. II. Medical Tribune Polska, Warszawa 2019; 2: 376-377.
20. Larsson SC, Orsini N, Wolk A: Diabetes mellitus and risk of colorectal cancer: a meta-analysis. J Natl Cancer Inst 2005; 97(22): 1679-1687.
21. Jarvandi S, Davidson NO, Schootman M: Increased Risk of Colorectal Cancer in Type 2 Diabetes Is Independent of Diet Quality. PLoS One 2013; 8(9): e74616.
22. Berster JM, Göke B: Type 2 diabetes mellitus as risk factor for colorectal cancer. Arch Physiol Biochem 2008; 114(1): 84-98.
23. Díaz-Algorri Y, Lozada ME, López SM: Type 2 diabetes mellitus and colorectal neoplasia risk in Hispanics: a case-control study. J Diabetes Complications 2015; 29(4): 502-507.
24. Grzeszczak W, Stepanow B, Szweda N: Jakie jest ryzyko rozwoju nowotworów u chorych na cukrzycę typu 2 – co nowego opublikowano na ten temat w 2015 roku? Chor Serca Naczyń 2016; 13(3): 203-208.
25. Flier JS, Usher P, Moses AC: Monoclonal antibody to the type I insulin-like growth factor(IGF-I) receptor blocks IGF-I receptor-mediated DNA synthesis: clarification of the mitogenic mechanisms of IGF-I and insulin in human skin fibroblasts. Proc Natl Acad Sci USA 1986; 83: 664-668.
26. Bjork J, Nilsson J, Hultcrantz R, Johansson C: Growth regulatory effects of sensory neuropeptides epidermal growth factor insulin and somatostatin on the non-transformed intestinal epithelial cell line IEC-6 and the colon cancer cell line HT 29. Scand J Gastroenterol 1993; 28: 879-884.
27. Moghaddam AA, Woodward M, Huxley R: Obesity and risk of colorectal cancer: a meta-analysis of 31 studies with 70,000 events. Cancer Epidemiol Biomarkers Prev 2007; 16(12): 2533-2547.
28. Larsson SC, Wolk A: Obesity and colon and rectal cancer risk: a meta-analysis of prospective studies. Am J Clin Nutr 2007; 86(3): 556-565. 
29. YoungJoo K, YunJin K, Sangyeoup L: An association between colonic adenoma and abdominal obesity: a cross-sectional study. BMC Gastroenterol 2009; 9: 4.
30. Zisman AL, Nickolov A, Brand RE et al.: Associations between the age at diagnosis and location of colorectal cancer and the use of alcohol and tobacco: implications for screening. Arch Intern Med 2006; 166(6): 629-634.
31. Botteri E, Iodice S, Bagnardi et al.: Smoking and colorectal cancer: a meta-analysis. JAMA 2008; 300(23): 2765-2778.
32. Liang PS, Chen TY, Giovannucci E: Cigarette smoking and colorectal cancer incidence and mortality: systematic review and meta-analysis. Int J Cancer 2009; 124(10): 2406-2415.
33. Botteri E, Iodice S, Raimondi S et al.: Cigarette smoking and adenomatous polyps: a meta-analysis. Gastroenterology 2008; 134(2): 388-395.
34. Laudańska E, Brzósko S, Bieryłko A, Naumnik B: Czynniki ryzyka rozwoju nowotworu u chorych po przeszczepieniu nerki. Przegl Lek 2016; 73: 7.
35. Kasiske BL, Snyder JJ, Gilbertson DT, Wang C: Cancer after kidney transplantation in the United States. Am J Transplant 2004; 4: 905-913.
36. Taoil E, Mattucci DA, Palmieri S et al.: A population-based study of cancer incidence in solid organ transplants from donors at various risk of neoplasma. Transplantation 2007; 83: 13-16.
37. Geissler EK, Schlitt HJ: The relation between immunosuppressive agents and malignancy. Curr Opin Org Transplantation 2004; 9(4): 394-399.
38. Ajithkumar TV, Parkinson CA, Butler A, Hatcher HM: Management of solid tumours in organ-transplant recipients. Lancet Oncol 2007; 8(10): 921-932.
39. Lizakowski S, Imko-Walczuk B, Dębska-Ślizień A, Rutkowski B: Nowotwory u chorych po przeszczepieniu nerki. Forum Nefrol 2011; 4(3): 214-223.
40. Klimczak D: Leczenie immunosupresyjne po przeszczepieniu nerki. Prz Urol 2017; 2: 102.
41. Durlik M, Zieniewicz K: Zalecenia dotyczące leczenia immunosupresyjnego po przeszczepieniu narządów unaczynionych. Fundacja Zjednoczeni dla Transplantacji 2018; 1: 14-15.
42. Meier-Kriesche HU, Li S, Gruessner RW et al.: Immunosuppression: Evolution in practice and trends, 1994-2004. Am J Transplant 2006; 6: 1111-1131.
43. Papaconstantinou HT, Sklow B, Hanaway MJ et al.: Characteristics and survival patterns of solid organ transplant patients developing de novo colon and rectal cancer. Dis Colon Rectum 2004; 47: 1898-1903.
44. Renke M, Lizakowski S, Palenicek Ł et al.: Znaczenie wykonywania badań kolonoskopowych u pacjentów przed przeszczepieniem i po przeszczepieniu nerki. Forum Nefrol 2015; 8: 163-167.
45. Bianchi-Porro G: Gastroenterologia i hepatologia. Wyd. I. Czelej, Lublin 2003: 398-399.
46. Merchea A, Shahjehan F, Croome KP et al.: Colorectal Cancer Characteristics and Outcomes after Solid Organ Transplantation. J Oncol 2019; 2019: 5796108.
47. Dobies A, Renke M, Wołyniec W et al.: Gastrointestinal pathologies in patients after successful renal transplantation – a pilot study. Transplant Proc 2016; 48: 1566-1569.
48. Januszko-Giergielewicz B, Kozak Ł, Janiszewski J et al.: Colorectal cancer secondary to kidney transplantation: a need for prophylaxis. Pol Arch Med Wew 2019; 129: 52-54.
49. Niedzielska I, Orawczyk T, Szaniewski K, Ziaja K: Polip a rak jelita grubego. Chir Pol 2008; 10(1): 30-34.
50. Lin JS, Piper MA, Perdue LA et al.: Screening for Colorectal Cancer: A systematic review for the U.S. Preventive Services Task Force. Evidence Syntheses, No. 135.
51. Leontiadis GI: Fecal Immunochemical Tests in Patients at Increased Risk for Colorectal Cancer-Is It Prime Time Yet? JAMA Intern Med 2017; 177(8): 1119-1120.
52. Ostrow JD: Tests for Fecal Occult Blood. [In:] Walker HK, Hall WD, Hurst JW (eds.): Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd ed. Butterworths, Boston 1990: 1: 98.
53. Martínez-Ares D, Barrenechea IMG, Souto-Ruzo J et al.: The value of abdominal ultrasound in the diagnosis of colon cancer. Rev Esp Enferm Dig 2005; 97: 877-886.
54. Musińska M, Minkiewicz M, Wasielica-Berger J et al.: Badania przesiewowe w profilaktyce raka jelita grubego. Med Rodz 2018; 21(3): 232-244.
55. Lebda-Wyborny T, Barczyk A, Pilch-Kowalczyk J: Wirtualna kolonoskopia CT – nowa metoda oceny patologii jelita grubego. Chir Pol 2008; 10(2): 88-100.
56. Pickhardt PJ, Choi JR, Hwang I et al.: Computed tomographic virtual colonoscopy to screen for colorectal neoplasia in asymptomatic adults. N Engl J Med 2003; 349(23): 2191-2200.
57. Johnson CD, Chen MH, Toledano AY et al.: Accuracy of CT colonography for detection of large adenomas and cancers. N Engl J Med 2008; 359(12): 1207-1217.
58. Levin B, Lieberman DA, McFarland B et al.: Screening and surveillance for the early detection of colorectal cancer and adenomatous polyps, 2008: a joint guideline from the American Cancer Society, the US Multi-society Task Force on Colorectal Cancer, and the American College of Radiology. CA Cancer J Clin 2008; 58: 130-160.
59. http://pbp.org.pl/program/.
otrzymano: 2020-03-13
zaakceptowano do druku: 2020-04-03

Adres do korespondencji:
*Łukasz Kozak
Samodzielny Publiczny Zakład Opieki Zdrowotnej MSWiA z Warmińsko-Mazurskim Centrum Onkologii Oddział Chorób Wewnętrznych i Gastroenterologii
Al. Wojska Polskiego 37, 10-228 Olsztyn
tel.: +48 (89) 539-85-35
lukaszko1@o2.pl

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