Opisthorchis viverrini infection and cholangiocarcinoma

Kurathong, S; Lerdverasirikul, P; Wongpaitoon, Virasak; Pramoolsinsap, Chutima; Kanjanapitak, A; Varavithya, W; Phuapradit, P; Bunyaratvej, S; Upatham, E. S.; Brockelman, Warren Y.

doi:10.1016/0016-5085(85)90755-3

Cited by 96 publications

(30 citation statements)

References 15 publications

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“…It is of interest to identify CCA as the second most common type of cancer associated with PVT in our population (16 cases, 8.2%). CCA is a rare cancer in the West but its prevalence is very high in Thailand and neighboring countries, the cause of which is mainly associated with Opisthorchis viverrini infection [38,39]. …”

Section: Discussionmentioning

confidence: 99%

High Incidence of Hepatitis B Infection-Associated Cirrhosis and Hepatocellular Carcinoma in the Southeast Asian Patients with Portal Vein Thrombosis

Lertpipopmetha

Auewarakul

2011

BMC Gastroenterol

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BackgroundPortal vein thrombosis (PVT) is a rare condition associated with serious morbidity and mortality. The objective of this study was to determine the frequency, clinical presentations, and risk factors of PVT from the set of data firstly collected among the Southeast Asian population.MethodsA retrospective study was undertaken to identify patients diagnosed with thrombosis of the portal system and other abdominal veins. The hospital medical records were retrieved based on the selected ICD-10 codes. Clinical presentations were collected and risk factors determined.ResultsFrom 2000-2009, 467 hospital charts with designated ICD-10 codes of I81, I82.2, I82.3, I82.8, I82.9, or K55.0 were identified. PVT (I81) was the most common thrombosis (194 cases, 41.54%). The majority of PVT patients were males (65%), older than 40 years (75%), and presented with abdominal distension/ascites (69%), splenomegaly (54.6%), and abdominal pain (50.5%). Overall, the predominant risk factor was hepatocellular carcinoma (HCC) (52.5%), followed by liver cirrhosis without cancer (9.3%), abdominal infection/inflammation (9.3%), cholangiocarcinoma (8.2%), and abdominal intervention (7.7%). In young patients, abdominal interventions including umbilical catheterization (23.1%) and hepatectomy (7.7%) were the most frequent risks whereas in older cases, primary hepatobiliary cancer and cirrhosis (78%) were the major risks. Liver metastases from other organs were infrequently found. Chronic hepatitis B virus (HBV) infection was the main etiology associated with cirrhosis/HCC leading to PVT in this cohort. A third of the older PVT patients (age >40) had HBV and very few carried hepatitis C virus (HCV) whereas none of the young PVT patients (age <20) had HBV or HCV. A variety of abdominal infections/inflammations were also found including liver abscess, splenic abscess, cholangitis, cholecystitis, pancreatitis, omphalitis, and abdominal tuberculosis. Single cases of systemic lymphangiomatosis and Klippel-Trénaunay vascular malformation syndrome were also identified. Other thrombophilic conditions such as myeloproliferative neoplasms, paroxysmal nocturnal hemoglobinuria, protein S deficiency, and anti-phospholipid syndrome were rarely encountered.ConclusionHBV is the major risk of PVT in the Southeast Asian population. Several risk factors identified in this population have rarely been described and some are remarkably different from those reported in the West. Host and environmental factors may play a causal role in the initiation and development of PVT in various ethnicities and geographic locations.

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Section: Discussionmentioning

confidence: 99%

High Incidence of Hepatitis B Infection-Associated Cirrhosis and Hepatocellular Carcinoma in the Southeast Asian Patients with Portal Vein Thrombosis

Lertpipopmetha

Auewarakul

2011

BMC Gastroenterol

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“…36 and 37) and fluke (Opistorchis sp., Chlonorchis and Schistosoma; refs. [38][39][40][41][42] infections of the liver markedly increase the likelihood of liver cancers. Furthermore, the necroinflammatory bowel disease, ulcerative colitis, carries a high risk for development of colon cancer (43).…”

Section: Discussionmentioning

confidence: 99%

Extensive oxidative DNA damage in hepatocytes of transgenic mice with chronic active hepatitis destined to develop hepatocellular carcinoma.

Hagen

Huang

Curnutte

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

283

190

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A transgenic mouse strain that expresses the hepatitis B virus (HBV) large envelope protein in the liver was used to determine the extent of oxidative DNA damage that occurs during chronic HBV infection. This mouse strain develops a chronic necroinflammatory liver disease that mimics the inflammation, cellular hyperplasia, and increased risk for cancer that is evident in human chronic active hepatitis. When perfused in situ with nitroblue tetrazolium, an indicator for superoxide formation, the liver of transgenic mice displayed intense formazan deposition in Kupffer cells, indicating oxygen radical production, and S-phase hepatocytes were commonly seen adjacent to the stained Kupffer cells. Similar changes were not observed in nontransgenic control livers. To determine whether these events were associated with oxidative DNA damage, genomic DNA from the livers of transgenic mice and nontransgenic controls was isolated and examined for 8-oxo-2'-deoxyguanosine, an oxidatively modified adduct of deoxyguanosine. Results showed a significant, sustained accumulation in steady-state 8-oxo-2'-deoxyguanosine that started early in life exdusively in the transgenic mice and increased progressively with advancing disease. The most pronounced increase occurred in livers exhibiting microscopic nodular hyperplasia, adenomas, and hepatocellular carcinoma. Thus, HBV transgenic mice with chronic active hepatitis display greatly increased hepatic oxidative DNA damage. Moreover, the DNA damage occurs in the presence of heightened hepatocellular proliferation, increasing the probability of fixation of the attendant genetic and chromosomal abnormalities and the development of hepatocellular carcinoma.Chronic inflammatory diseases affect millions of people world-wide and may be a primary factor in the development of up to one-third of all cancers (1). A major association between a persistent infection and cancer is evident in chronic active hepatitis B virus (HBV) infection (2). Epidemiological studies show that incidence of hepatocellular carcinoma (HCC) correlates strongly to geographical areas of endemic HBV infection (3). Furthermore, patients with chronic hepatitis have a much higher incidence of liver cirrhosis and HCC than individuals not infected with HBV (4). Also, HBV antigens in sera of patients are associated with HCC (5). Because the virus infects >300 million people throughout the world, HBV has been described as second only to tobacco as a known human carcinogen (6).Despite the apparent epidemiological association of chronic active hepatitis infection and cancer, the mechanisms involved are still not entirely understood. Research has been hampered due to the long latency period between the onset of infection and cancer development, and the lack of suitable animal models that mimic chronic active human hepatitis.HBV does not contain any known acutely transforming oncogenes, and only rarely do integrated HBV sequences activate cellular protooncogenes (7-10). In contrast, persistent inflammation associated with chro...

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“…It has been suggested that over a lifetime almost one in six of O. viverrini infected individuals will contract cholangiocarcinoma (CCA), or cancer of the bile ducts 3, 4 . CCA is a highly aggressive cancer with a very poor prognosis 5, 6 . Despite this, flukes contribute only minimally (0.12%) to world cancer rates.…”

Section: Carcinogenic Helminthsmentioning

confidence: 99%

Infection with the carcinogenic human liver fluke, Opisthorchis viverrini

et al. 2011

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Summary Throughout Southeast Asia there is a strikingly high incidence of cholangiocarcinoma (CCA - hepatic cancer of the bile duct epithelium), particularly in people from rural settings in Laos and Northeast Thailand who are infected with the liver fluke, Opisthorchis viverrini, one of only three carcinogenic eukaryotic pathogens. More ubiquitous carcinogenic microbes, such as Helicobacter pylori, induce cancer in less than 1% of infected people, while as many as one-sixth of people with opisthorchiasis will develop CCA. The mechanisms by which O. viverrini causes cancer are multi-factorial, involving mechanical irritation from the activities and movements of the flukes, immunopathology, dietary nitrosamines and the secretion of parasite proteins that promote a tumourigenic environment. Genomic and proteomic studies of the liver fluke secretome have accelerated the discovery of parasite proteins with known/potential roles in pathogenesis and tumourigenesis, establishing a framework towards understanding, and ultimately preventing, the morbidity and mortality attributed to this highly carcinogenic parasite.

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Opisthorchis viverrini infection and cholangiocarcinoma

Cited by 96 publications

References 15 publications

High Incidence of Hepatitis B Infection-Associated Cirrhosis and Hepatocellular Carcinoma in the Southeast Asian Patients with Portal Vein Thrombosis

High Incidence of Hepatitis B Infection-Associated Cirrhosis and Hepatocellular Carcinoma in the Southeast Asian Patients with Portal Vein Thrombosis

Extensive oxidative DNA damage in hepatocytes of transgenic mice with chronic active hepatitis destined to develop hepatocellular carcinoma.

Infection with the carcinogenic human liver fluke, Opisthorchis viverrini

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