12, 13 Both parasites increase the susceptibility of cholangiocytes
to endo- and exogenous carcinogens via chronic Mitomycin C irritation and increased cellular turnover.12 In 1994, O. viverrini was deemed by the International Agency for Research on Cancer as “carcinogenic to humans” secondary to its role in the development of CC. In 2009, the same classification was given to C. sinensis.14 Parasitic infections, particularly O. viverrini, are a major public health issue in Thailand, where the incidence of CC is still increasing in some Northeastern regions and is strongly correlated with the prevalence of parasitic infections.5 One of the early epidemiological studies (1987-1988) to show a relationship between O. viverrini and CC was a hospital-based, case-control study conducted in Thailand by Parkin et al., in which 103 patients with CC were compared with an equal number of age- and sex-matched controls. A strong association was found between elevated
O. viverrini antibody titers and increased risk of CC (odds ratio [OR] = 5.0; 95% confidence interval [CI] = 2.3-11.0).15 A more recent (1999-2001) population-based, case-control study from Thailand compared 129 cases of CC with an equal number of age- and sex-matched this website controls. Elevated O. viverrini antibody levels were, again, strongly associated with CC (OR = 27.09; 95% CI = 6.30-116.57). In endemic areas, the population-attributable risk, based on this study, was as high as 88%.16 A case-control study by Shin et al. from Korea compared 41 patients with CC with 406 controls
and reported a strong association between the presence of C. sinensis in the stool and CC (OR = 2.7; 95% CI = 1.1-6.3).17 A subsequent 2009 meta-analysis, performed by Shin et al., pooled 912 cases and 4909 controls and confirmed the strong association between C. sinensis and CC (OR = 4.7; 95% CI = 2.2-9.8). In endemic areas, the population-attributable risk, based on this study, was as high as 27.9% for men and 16.2% for MCE公司 women.14 Bile (i.e., choledochal)-duct cysts are rare congenital disorders characterized by cystic dilatation of the extra- and/or intrahepatic bile ducts. Bile-duct cysts are thought to develop from an abnormal pancreatico-biliary junction, in which the pancreatic and biliary ducts join outside the duodenum and are typically associated with a long common channel (>10 mm).18 This results in pancreatic enzymes refluxing into the biliary system with subsequent increased intraductal pressure and inflammation, leading to ductal dilatation. With regards to Caroli’s disease, the abnormality is attributed to malformation of the ductal plate.19 It has been postulated that the reflux of pancreatic enzymes, bile stasis, and increased concentration of intraductal bile acids contribute to the formation of malignant cells in patients with bile-duct cysts.20 Bile-duct cysts are an established risk factor for CC. Type I (i.e., solitary, extrahepatic) and IV (i.e.