Studies in literature suggest that some human viruses, including JC polyomavirus (JCV), 1-3 human cytomegalovirus (HCMV), 4 human papillomaviruses (HPVs), and Epstein-Barr virus (EBV), 9,10 have a pathogenic role in starting or promoting colorectal cancer. However, a revision of the literature indi
Clinical observation on the association of gallstones and colorectal cancer
β Scribed by Tomio Narisawa; Yoshihiko Yamazaki; Hisashi Kusaka; Masahiro Takahashi; Hitoshi Kotanagi; Kenji Koyama
- Publisher
- John Wiley and Sons
- Year
- 1991
- Tongue
- English
- Weight
- 480 KB
- Volume
- 67
- Category
- Article
- ISSN
- 0008-543X
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β¦ Synopsis
A possible association between gallstones, colorectal cancer, and gastric cancer was investigated. The age distribution and mean age of the two cancer groups were identical. The incidence of gallstones in 378 colorectal cancer cases and 869 gastric cancer cases was 7.1% and 5.5%, respectively. Of colorectal cancer cases, 33 cases with multiple carcinomas had a significantly higher gallstone incidence than cases with a solitary carcinoma-24.2% and 5.5%, respectively. The mean age was 5 years older in gallstone cases than in those without gallstones in both cancer groups, and it was 4 years older in multiple-carcinoma cases than in solitarycarcinoma cases in the colorectal cancer group. These results suggest that the higher levels of same causative factors (i.e., dietary fat) are associated with a longer duration of gallstone formation and colorectal cancer development as demonstrated by multiple colorectal-carcinoma cases. Cancer 67:1696-1700,1991.
OLORECTAL CANCER A N D GALLSTONES are two C common diseases in Western countries. A positive association between colorectal cancer and gallstones was demonstrated in postmortem and clinical although one report found no obvious association between these two diseases.' Dietary factors, high-fat and low-fiber intake, have been implicated in colorectal cancer. The luminal contents of the large bowel, including high concentrations of bile acid (particularly secondary bile acids stemming from the high-fat diet), account for the effect in large bowel carcinogenesis.' Such diets also have been suggested as one of the etiologic factors in gallstone formation.' However, the presence of gallstones and the removal of the gallbladder cause an increased level of secondary bile acids in the bile and feces. Decreased pool size and increased enterohepatic recycling of bile acids lead to increased degradation of primary bile acids to secondary bile acids by intestinal microflora.'*-'' It was re-
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