Management of stage Ⅳ rectal cancer - World Journal of ...

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A Age (yr) 90 80 70 60 50 40 P < 0.05 NS P < 0.05 NS as the core protein, cause oxidative damage by exposing the endoplasmic reticulum to oxidative stress [19-21] . Hepatic oxidative stress is strongly associated with increased risk for HCC in patients with chronic HCV [22] . Because oxidative stress is also caused by various host-related factors, it is expected to be influenced more strongly by host-related factors in HCV-infected patients than in those with HCVnegative liver disease. Indeed, we have previously reported that visceral fat accumulation was associated with greater insulin resistance in chronic HCV patients than in those with non-alcoholic fatty liver disease [23] . Therefore, it is plausible that the association between earlier onset of HCC and increased BMI is due to the generation of hepatic oxidative stress. An interesting aspect of our results is that underweight patients, defined as those with a BMI of < 18.5 kg/m 2 , tended to be older at HCC onset than patients within the WJG|www.wjgnet.com P < 0.05 NS < 18.5 18.5-25 25-30 30 < BMI Figure 3 Differences in age at onset of hepatocellular carcinoma stratified by body mass index according to sex (A: Men; B: Women). Statistical analysis was performed using the Tukey-Kramer method. NS: Not significant; BMI: Body mass index. A Age (yr) 90 80 70 60 50 40 P < 0.05 P < 0.05 < 18.5 18.5-25 25-30 30 < BMI NS P < 0.05 P < 0.05 NS B Age (yr) 90 80 70 60 50 40 NS NS NS NS < 18.5 18.5-25 25-30 30 < Figure 4 Differences in age at onset of hepatocellular carcinoma stratified by body mass index according to degree of alcohol consumption (A: Non-heavy drinkers < 60 g/d; B: Heavy drinkers ≥ 60 g/d). Statistical analysis was performed using the Tukey-Kramer method. NS: Not significant; BMI: Body mass index. B Age (yr) 90 80 70 60 50 40 Akiyama T et al . BMI and age at HCC onset NS normal weight range (BMI 18.5-25 kg/m 2 ). Recently, Ohki et al [11] reported that patients with a BMI < 18.5 kg/m 2 had the lowest risk of developing HCC due to chronic HCV infection among all BMI groups. In general, the mortality rate associated with cardiovascular disease or cancer is higher in underweight patients than in normal weight patients [24,25] . Clearly, a larger cohort study is needed to investigate whether leanness confers a protective effect against hepatocarcinogenesis in HCV-infected patients. Excessive alcohol consumption is also known to exacerbate hepatic oxidative stress and evoke liver fibrosis or HCC [20,26] . In this study, there was no association between BMI and age at onset of HCC in heavy drinkers. We speculate that this group may include some patients who are malnourished and possibly losing weight. Sex modulates the natural history of chronic liver disease. Previous studies have suggested that chronic HCV 919 February 21, 2011|Volume 17|Issue 7| NS BMI NS NS NS NS NS < 18.5 18.5-25 25-30 30 < BMI NS
Akiyama T et al . BMI and age at HCC onset infection progresses more rapidly in men than women, and that cirrhosis is predominately a disease of men and postmenopausal women [27] . Shimizu et al suggested that estrogens protect against oxidative stress in liver injury and hepatic fibrosis [28] . In this study, the effect of BMI on age at onset of HCC was more remarkable in men than women. We speculate two mechanisms to account for this difference: (1) estrogens mitigate oxidative stress or insulin resistance associated with obesity; and (2) subcutaneous fat accumulation is more dominant in obese women than visceral fat, which is known to produce several adipokines that cause insulin resistance [29] . In addition, we examined factors associated with onset of HCC at an older age (≥ 80 years). In this analysis, ALT level was the only independent factor associated with hepatocarcinogenesis in HCV-infected patients at an age ≥ 80 years. It is well known that ALT levels are associated with liver inflammation and fibrosis progression, and Ishiguro et al recently reported that elevated ALT levels were strongly associated with the incidence of HCC, regardless of hepatitis virus positivity, in a large populationbased cohort study [30] . Therefore, lower ALT levels might indicate a slow course of progression of hepatic fibrosis or carcinogenesis. A limitation of this study is that it was a cross-sectional observation, rather than a cohort follow-up study. Further studies are needed to confirm our results. In conclusion, the results of the present study indicate that higher BMI, excessive alcohol consumption, and male sex are independent risk factors for onset of HCV-related HCC at an age of < 60 years. These results suggest that interventions to promote changes in the lifestyle of patients with chronic HCV may slow the progression of HCV infection to HCC. ACKNOWLEDGMENTS The authors would like to thank Yukie Watanabe and Chieko Ogawa for their assistance. COMMENTS Background The incidence and mortality associated with hepatocellular carcinoma (HCC) have been increasing worldwide, and hepatitis C virus (HCV) infection plays an important role in the pathogenesis of HCC. However, the factors that influence the development of HCC in HCV-infected patients remain largely unknown. Previous studies have suggested that host factors, such as sex, alcohol consumption, smoking, diabetes mellitus, and obesity, are important risk factors for HCC. Meanwhile, it has been reported that HCV infection causes insulin resistance and leads to oxidative stress, potentiating fibrosis and hepatic carcinogenesis. Therefore, we hypothesized that body mass index (BMI) influences the onset age of HCC related to HCV infection. Research frontiers Many studies have indicated that obesity is an independent and a significant risk factor for HCC occurrence. Recently, several metabolic markers have been implicated in the development and progression of HCC. Innovations and breakthroughs This study indicated that higher BMI, heavy alcohol consumption, male sex, and high γ-glutamyl transpeptidase levels are independent risk factors for younger age at onset of HCV-related HCC. Interestingly, the underweight patients (BMI WJG|www.wjgnet.com < 18.5 kg/m 2 ), tended to be older at HCC onset than patients within the normal weight range (BMI 18.5-25 kg/m 2 ). Applications The results of this study suggest that achieving an adequate body weight along with a reduction of alcohol intake in patients with chronic hepatitis C could help prevent hepatic carcinogenesis. Peer review The study was reasonably designed and well conducted, and the data support their conclusions. REFERENCES 1 El-Serag HB. Epidemiology of hepatocellular carcinoma in USA. Hepatol Res 2007; 37 Suppl 2: S88-S94 2 El-Serag HB, Rudolph KL. Hepatocellular carcinoma: epidemiology and molecular carcinogenesis. Gastroenterology 2007; 132: 2557-2576 3 Umemura T, Ichijo T, Yoshizawa K, Tanaka E, Kiyosawa K. Epidemiology of hepatocellular carcinoma in Japan. J Gastroenterol 2009; 44 Suppl 19: 102-107 4 El-Serag HB. Hepatocellular carcinoma and hepatitis C in the United States. Hepatology 2002; 36: S74-S83 5 Fattovich G, Stroffolini T, Zagni I, Donato F. Hepatocellular carcinoma in cirrhosis: incidence and risk factors. Gastroenterology 2004; 127: S35-S50 6 Sinn DH, Paik SW, Kang P, Kil JS, Park SU, Lee SY, Song SM, Gwak GY, Choi MS, Lee JH, Koh KC, Yoo BC. Disease progression and the risk factor analysis for chronic hepatitis C. Liver Int 2008; 28: 1363-1369 7 Marrero JA, Fontana RJ, Fu S, Conjeevaram HS, Su GL, Lok AS. Alcohol, tobacco and obesity are synergistic risk factors for hepatocellular carcinoma. J Hepatol 2005; 42: 218-224 8 Hara M, Tanaka K, Sakamoto T, Higaki Y, Mizuta T, Eguchi Y, Yasutake T, Ozaki I, Yamamoto K, Onohara S, Kawazoe S, Shigematsu H, Koizumi S. Case-control study on cigarette smoking and the risk of hepatocellular carcinoma among Japanese. Cancer Sci 2008; 99: 93-97 9 Polesel J, Zucchetto A, Montella M, Dal Maso L, Crispo A, La Vecchia C, Serraino D, Franceschi S, Talamini R. The impact of obesity and diabetes mellitus on the risk of hepatocellular carcinoma. Ann Oncol 2009; 20: 353-357 10 Aizawa Y, Shibamoto Y, Takagi I, Zeniya M, Toda G. Analysis of factors affecting the appearance of hepatocellular carcinoma in patients with chronic hepatitis C. A long term followup study after histologic diagnosis. Cancer 2000; 89: 53-59 11 Ohki T, Tateishi R, Sato T, Masuzaki R, Imamura J, Goto T, Yamashiki N, Yoshida H, Kanai F, Kato N, Shiina S, Yoshida H, Kawabe T, Omata M. Obesity is an independent risk factor for hepatocellular carcinoma development in chronic hepatitis C patients. Clin Gastroenterol Hepatol 2008; 6: 459-464 12 Vidali M, Tripodi MF, Ivaldi A, Zampino R, Occhino G, Restivo L, Sutti S, Marrone A, Ruggiero G, Albano E, Adinolfi LE. Interplay between oxidative stress and hepatic steatosis in the progression of chronic hepatitis C. J Hepatol 2008; 48: 399-406 13 Koike K. Steatosis, liver injury, and hepatocarcinogenesis in hepatitis C viral infection. J Gastroenterol 2009; 44 Suppl 19: 82-88 14 Sheikh MY, Choi J, Qadri I, Friedman JE, Sanyal AJ. Hepatitis C virus infection: molecular pathways to metabolic syndrome. Hepatology 2008; 47: 2127-2133 15 Liver Cancer Study Group. The General Rules for the Clinical and Pathological Study of Primary Liver Cancer. 5th ed. Japan, 2008: 24-28 16 World Health Organization. Obesity: Preventing and managing the global epidemic; Report of a WHO Consultation on Obesity, Geneva, 3-5, June 1997. Geneva: WHO, 1998 17 Report of a WHO Consultation. Definition, diagnosis and classification of diabetes mellitus and its complication: 920 February 21, 2011|Volume 17|Issue 7|
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World Journal of Gastroenterology W
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Robert JL Fraser, Daw Park Jacob Ge
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Italy Donato F Altomare, Bari Piero
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Fernando Azpiroz, Barcelona Ramon B
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Contents BRIEF ARTICLE WJG|www.wjgn
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Online Submissions: http://www.wjgn
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expressed miRNAs including known on
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Oh et al [73] have shown that upreg
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5 Bardeesy N, DePinho RA. Pancreati
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Fazli L, Motoo Y, Wang Q, Rocchi P,
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standard investigation to confirm t
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proximity to a T3 tumor or nodules
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CONCLUSION Imaging in rectal cancer
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Ronnekleiv-Kelly SM et al . Palliat
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Popek S et al . Neoadjuvant vs adju
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esection [19] . Conversely, approxi
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that option again, than patients wh
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Mulsow J et al . Treatment options
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most significant is ensuring oncolo
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tive times and concerns over both l
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Page 67 and 68: Sharma C et al . Clinical advances
Page 76: Table 10 Published results on lapar
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Page 116 and 117: Part1. Diagnosis and classification
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Page 142 and 143: INTRODUCTION Hepatocellular carcino
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