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Review
. 2018 May 15;12(3):236-245.
doi: 10.5009/gnl17102.

Liver Fluke-Associated Biliary Tract Cancer

Piyapan Prueksapanich  1 , Panida Piyachaturawat  1 , Prapimphan Aumpansub  1 , Wiriyaporn Ridtitid  1 , Roongruedee Chaiteerakij  1 , Rungsun Rerknimitr  1
Affiliations
Review

Liver Fluke-Associated Biliary Tract Cancer

Piyapan Prueksapanich et al. Gut Liver. .

Abstract

Cholangiocarcinoma (CCA) is an aggressive cancer arising from epithelial cells of the bile duct. Most patients with CCA have an unresectable tumor at the time of diagnosis. In Western countries, the risk of CCA increases in patients with primary sclerosing cholangitis, whereas liver fluke infection appears to be the major risk factor for CCA in Asian countries. A diagnosis of liver fluke infection often relies on stool samples, including microscopic examination, polymerase chain reaction-based assays, and fluke antigen detection. Tests of serum, saliva and urine samples are also potentially diagnostic. The presence of liver fluke along with exogenous carcinogens magnifies the risk of CCA in people living in endemic areas. The "liver fluke-cholangiocarcinoma" carcinogenesis pathways consist of mechanical damage to the bile duct epithelium, immunopathologic and cellular reactions to the liver fluke's antigens and excretory/secretory products, liver fluke-induced changes in the biliary tract microbiome and the effects of repeated treatment for liver fluke. A vaccine and novel biomarkers are needed for the primary and secondary prevention of CCA in endemic areas. Importantly, climate change exerts an effect on vector-borne parasitic diseases, and awareness of liver fluke should be enhanced in potentially migrated habitat areas.

Keywords: Cholangiocarcinoma; Clonorchiasis; Opisthorchiasis.

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Conflict of interest statement

CONFLICTS OF INTEREST

No potential conflict of interest relevant to this article was reported.

Figures

Fig. 1
Fig. 1
Mechanical damage to the bile duct epithelium caused by liver fluke.
Fig. 2
Fig. 2
Immunopathologic reactions of human cells to liver fluke infection. ESP, excretory/secretory products; OvGST, Opisthorchis viverrini glutathione S-transferase; Ov-GRN-1, O. viverrini granulin; Ov-Trx-1, O. viverrini thioredoxin; TLR, Toll-like receptors; NF-κB, nuclear factor-κB; IL, interleukin; TNF, tumor necrosis factor; IFN, interferon; iNOS, inducible nitric oxide synthase; COX-2, cyclooxygenase-2; miRNA, microribonucleic acid; ER, endoplasmic reticulum.
Fig. 3
Fig. 3
Cellular reactions to liver fluke antigens, excretory/secretory products and changes in the biliary tract microbiome. H. pylori, Helicobacter pylori.
Fig. 4
Fig. 4
The cooperation of liver fluke infection, liver fluke treatment, and exogenous carcinogens in the carcinogenesis of cholangiocarcinoma.
See this image and copyright information in PMC

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