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CRAMP, M. E. "HBV + HCV = HCC?" Gut 45, no. 2 (August 1, 1999): 168–69. http://dx.doi.org/10.1136/gut.45.2.168.
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Mujeeb, Syed Abdul, Qamar Jamal, Rafique Khanani, Nayyer Iqbal, and Shahnaz Kaher. "Prevalence of Hepatitis B Surface Antigen and HCV Antibodies in Hepatocellular Carcinoma Cases in Karachi, Pakistan." Tropical Doctor 27, no. 1 (January 1997): 45–46. http://dx.doi.org/10.1177/004947559702700117.
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Hepatocellular carcinoma (HCC) is a common cancer the world over. In Pakistan it has an incidence of 8/100 000 per annum. To assess the prevalence of Hepatitis B virus (HBV) and Hepatitis C virus (HCV) infections in biopsy proven cases of HCC a serological study was conducted at Screening Laboratory of Blood Transfusion Services, Jinnah Postgraduate Medical Centre. Of 54 sera of HCC tested for HBV and HCV infections, 67% showed HBV infection, and 33% HCV infection. Among them 24% were positive for both HBV and HCV infections. No HBV and HCV infection was found in 24% cases of HCC. Our findings suggest viral association for most of the HCC cases reported in the country. We suggest an immediate intervention strategy to prevent the spread of HBV and HCV infections by mandatory screening of blood for HBV and HCV infections, and the use of disposable/sterilized needles, instruments for all invasive procedures. For the prevention of vertical transmission of HBV infections all pregnant women should be screened and vaccinated and HBV vaccination should also be included in EPI (expanded programme for immunization).
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Stroffolini, Tommaso, and Giacomo Stroffolini. "A Historical Overview on the Role of Hepatitis B and C Viruses as Aetiological Factors for Hepatocellular Carcinoma." Cancers 15, no. 8 (April 20, 2023): 2388. http://dx.doi.org/10.3390/cancers15082388.
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Hepatitis B virus (HBV) and hepatitis C virus (HCV) are the leading cause of hepatocellular carcinoma (HCC) worldwide. Currently, HBV-related HCC predominates in Sub-Saharan Africa and South-East-Asia, while HCV-related HCC predominates in northern Africa and in the western world. Liver cirrhosis is the underlying condition in most HBV cases and in nearly all HCV cases. Several cofactors, viral and non-viral, play a role in the progression toward HCC: dual HBV/HCV infection, HDV, HIV, alcohol intake, smoking, diabetes mellitus, obesity, and NAFLD/NASH. HBV vaccine is effective in preventing both infection and HCC; antiviral drugs may suppress HBV replication and eradicate HCV infection, halting progression to HCC. Inequalities exist between high- and low-income countries with respect to vaccine availability and access to antivirals. These factors represent barriers to the control of HCC incidence. Lack of an effective vaccine against HCV is also a serious barrier to HCV elimination and HCC prevention. The most crucial steps and knowledge that have arisen over time on the association between the two major hepatotropic viruses and HCC are discussed in this historical review.
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Huang, Yen-Tsung, Chin-Lan Jen, Hwai-I. Yang, Mei-Hsuan Lee, Jun Su, Sheng-Nan Lu, Uchenna H. Iloeje, and Chien-Jen Chen. "Lifetime Risk and Sex Difference of Hepatocellular Carcinoma Among Patients With Chronic Hepatitis B and C." Journal of Clinical Oncology 29, no. 27 (September 20, 2011): 3643–50. http://dx.doi.org/10.1200/jco.2011.36.2335.
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PurposeBoth hepatitis B (HBV) and C viruses (HCV) are causes of hepatocellular carcinoma (HCC), but lifetime risk and sex difference remain unclear. This study aimed to assess the lifetime risk and sex difference of HCC among patients with chronic HBV and/or HCV.MethodsA prospective cohort of 23,820 residents of Taiwan age 30 to 65 years were enrolled from 1991 to 1992, with 477 instances of HCC occurring subsequently. Serum samples collected at enrollment were tested for seromarkers and viral load of HBV and HCV. Newly developed HCC was ascertained through computerized data linkage with national cancer registry and death certification systems.ResultsThe cumulative lifetime (age 30 to 75 years) incidences of HCC for men and women positive for both HBV surface antigen (HBsAg) and antibodies against HCV (anti-HCV) were 38.35% and 27.40%; for those positive for HBsAg only, 27.38% and 7.99%; for those positive for anti-HCV only, 23.73% and 16.71%; and for those positive for neither, 1.55% and 1.03%, respectively. There was a significant male predominance in incidence of HCC for chronic HBV carriers but not for chronic carriers of HCV or both. Multivariate adjusted hazard ratio of developing HCC decreased with age in HBsAg-seropositive men but increased with age in anti-HCV–seropositive women. Among dual-infected participants, there was an inverse association between HBV and HCV viral load. Risk of HCC increased significantly with increasing viral load of HBV and HCV.ConclusionThere exists a suppressive effect of HCV on HBV viral load. Individual and combined effects of the two viruses on HCC vary with sex and age.
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Pár, Alajos. "Prophylaxis and treatment of chronic viral hepatitis as the prevention of hepatocellular carcinoma." Orvosi Hetilap 150, no. 1 (January 1, 2009): 19–26. http://dx.doi.org/10.1556/oh.2009.28529.
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Mivel a hepatitis B- és C-vírus- (HBV-, HCV-) fertőzés döntő szerepet játszik a hepatocellularis carcinoma (HCC) keletkezésében, a HBV és HCV okozta hepatitis és cirrhosis megelőzése és kezelése egyben a HCC prevencióját is jelentheti. A HCC primer prevencióját képviseli a HBV elleni vakcináció és a donorok szűrése HBV- és HCV-markerekre. A szekunder prevencióhoz sorolható az interferonalapú és/vagy nukleozidanalóg anti-HBV- és anti-HCV-terápia, a cirrhosisos betegek HCC irányában történő alfa-foetoprotein + ultrahang szűrése, valamint a HCC kuratív reszekciója/ablatiója utáni adjuváns antivirális kezelés. Várható, hogy a HBV-vakcináció világszerte történő széles körű alkalmazása, továbbá az optimalizált individuális antivirális kezelésmódok, az új nukleozidanalógok és HCV-specifikus proteáz- és polimerázgátlók révén előrelépés történik nemcsak a vírushepatitisek megelőzésében és terápiájában, hanem a HCC prevenciójában is a nem túl távoli jövőben.
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Haberl, Elisabeth M., Thomas S. Weiss, Georg Peschel, Kilian Weigand, Nikolai Köhler, Josch K. Pauling, Jürgen J. Wenzel, et al. "Liver Lipids of Patients with Hepatitis B and C and Associated Hepatocellular Carcinoma." International Journal of Molecular Sciences 22, no. 10 (May 18, 2021): 5297. http://dx.doi.org/10.3390/ijms22105297.
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Hepatocellular carcinoma (HCC) still remains a difficult to cure malignancy. In recent years, the focus has shifted to lipid metabolism for the treatment of HCC. Very little is known about hepatitis B virus (HBV) and C virus (HCV)-related hepatic lipid disturbances in non-malignant and cancer tissues. The present study showed that triacylglycerol and cholesterol concentrations were similar in tumor adjacent HBV and HCV liver, and were not induced in the HCC tissues. Higher levels of free cholesterol, polyunsaturated phospholipids and diacylglycerol species were noted in non-tumorous HBV compared to HCV liver. Moreover, polyunsaturated phospholipids and diacylglycerols, and ceramides declined in tumors of HBV infected patients. All of these lipids remained unchanged in HCV-related HCC. In HCV tumors, polyunsaturated phosphatidylinositol levels were even induced. There were no associations of these lipid classes in non-tumor tissues with hepatic inflammation and fibrosis scores. Moreover, these lipids did not correlate with tumor grade or T-stage in HCC tissues. Lipid reprogramming of the three analysed HBV/HCV related tumors mostly resembled HBV-HCC. Indeed, lipid composition of non-tumorous HCV tissue, HCV tumors, HBV tumors and HBV/HCV tumors was highly similar. The tumor suppressor protein p53 regulates lipid metabolism. The p53 and p53S392 protein levels were induced in the tumors of HBV, HCV and double infected patients, and this was significant in HBV infection. Negative correlation of tumor p53 protein with free cholesterol indicates a role of p53 in cholesterol metabolism. In summary, the current study suggests that therapeutic strategies to target lipid metabolism in chronic viral hepatitis and associated cancers have to consider disease etiology.
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Fang, Lily, Amanda Yu, and Jane A. Buxton. "Identification of Acute Vaccine-Preventable Hepatitis in Individuals with Chronic Hepatitis in British Columbia between 1991 and 2007." Canadian Journal of Infectious Diseases and Medical Microbiology 22, no. 1 (2011): 10–14. http://dx.doi.org/10.1155/2011/564290.
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BACKGROUND: In British Columbia (BC), hepatitis A virus (HAV) and hepatitis B virus (HBV) vaccines are provincially funded for persons with chronic hepatitis infections. PURPOSE: To assess the effectiveness of BC public health follow-up of HBV and hepatitis C virus (HCV) cases and immunization policy by determining the number of vaccine-preventable acute hepatitis infections reported following a chronic HBV or HCV diagnosis, by examining demographic characteristics and by observing temporal trends.METHODS: All newly identified cases of HAV, HBV and HCV between 1991 and October 2007 were extracted from the BC integrated Public Health Information System and linked to ascertain cases of hepatitis suprainfection.RESULTS: Between 1991 and October 2007, 30 BC residents with chronic HBV and 104 with HCV were subsequently diagnosed with HAV. Acute HBV was identified in 162 persons previously diagnosed with HCV. Significantly more men than women developed hepatitis suprainfection (P<0.0001), but women were of a younger age when they were diagnosed with HAV (P=0.02) and acute HBV (P=0.0002). HAV suprainfection cases among those with HCV peaked in 1998 at 33 cases and declined to zero cases in 2007. In comparison, HBV suprainfection among individuals with chronic HCV peaked in 1996 at 26 cases and declined to two cases in 2007.DISCUSSION: Cases of HAV and acute HBV have declined among HCV-infected individuals. However, despite the availability of publicly funded vaccines for high-risk groups, a substantial number of acute HBV infections post-HCV identification are still identified, indicating that follow-up and vaccination coverage should be improved in these populations.
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Buxton, Jane A., and Jin Hee Kim. "Hepatitis A and Hepatitis B Vaccination Responses in Persons with Chronic Hepatitis C Infections: A Review of the Evidence and Current Recommendations." Canadian Journal of Infectious Diseases and Medical Microbiology 19, no. 2 (2008): 197–202. http://dx.doi.org/10.1155/2008/410362.
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In persons with chronic hepatitis C virus (HCV) infections, superinfection by hepatitis A virus (HAV) or hepatitis B virus (HBV) can cause serious complications, including fulminating hepatitis or increased severity of hepatitis. Therefore, it is important to adequately protect persons with chronic HCV infections by immunization. Suboptimal response to vaccines has been reported in patients with chronic liver disease. The present article reviews HAV and HBV vaccine responses reported in the literature when administered to individuals with chronic HCV infection, and reviews current national and international recommendations.RESULTS: Persons with chronic HCV respond well to HAV vaccine, but studies exploring HBV vaccine efficacy in this population have equivocal results. Vaccine schedules and participant characteristics differ among studies, and most do not adjust for confounders. Some studies found no difference in HBV vaccine response between patients with chronic HCV and controls. However, HBV vaccine response was generally reduced in those with cirrhosis and HCV genotype 1. Organizations recommend HAV and HBV vaccines for persons with chronic HCV, but do not suggest alterations in schedule or dose.RECOMMENDATIONS: Because HAV vaccine response is good and routine laboratory testing may not detect lower levels of vaccine-induced anti-HAV, the standard HAV vaccine schedule is recommended without postimmunization testing. HBV vaccine should be administered early in the course of chronic HCV infection because response may be lower in patients with cirrhosis. Reflex testing of anti-HCV reactive sera for anti-HAV and hepatitis B surface antibody can facilitate appropriate follow-up and timely immunization. Determination of postimmunization hepatitis B surface antibody, especially in patients with cirrhosis or genotype 1, will allow HBV vaccine boosters to be offered.
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Shen, Yu-Chuan, Hui-Ching Hsu, Tzu-Min Lin, Yu-Sheng Chang, Li-Fang Hu, Lung-Fang Chen, Sheng-Hong Lin, et al. "H1-Antihistamines Reduce the Risk of Hepatocellular Carcinoma in Patients With Hepatitis B Virus, Hepatitis C Virus, or Dual Hepatitis B Virus-Hepatitis C Virus Infection." Journal of Clinical Oncology 40, no. 11 (April 10, 2022): 1206–19. http://dx.doi.org/10.1200/jco.21.01802.
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PURPOSE H1-antihistamines (AHs) may exert protective effects against cancer. This study investigated the association of AH use with the risk of hepatocellular carcinoma (HCC) in patients with hepatitis B virus (HBV), hepatitis C virus (HCV), or dual HBV-HCV virus infection. MATERIALS AND METHODS Patients with HBV, HCV, or dual HBV-HCV infection were enrolled from Taiwan's National Health Insurance Research Database and examined for the period from January 1, 2006, to December 31, 2015. We used the Kaplan-Meier method and Cox proportional hazards regression to evaluate the association between AH use and HCC risk. RESULTS We included patients with HBV infection (n = 521,071), HCV (n = 169,159), and dual HBV-HCV (n = 39,016). Patients with HBV, HCV, or dual virus infection who used AHs exhibited significantly lower risk of HCC relative to patients who did not use AH, with their adjusted hazard ratio being 0.489 (95% CI, 0.455 to 0.524), 0.484 (95% CI, 0.450 to 0.522), and 0.469 (95% CI, 0.416 to 0.529), respectively. Furthermore, there was a dose-response relationship between AH use and the risk of HCC in the HBV cohort. The adjusted hazard ratios were 0.597 (95% CI, 0.530 to 0.674), 0.528 (0.465 to 0.600), 0.470 (0.416 to 0.531), and 0.407 (0.362 to 0.457) for AH use of 28-42, 43-63, 64-119, and ≥ 120 cumulative defined daily doses, respectively, relative to no AH use. Additionally, there was also a dose-response relationship between AH use and the risk of HCC in the HCV and dual HBV-HCV cohorts. CONCLUSION AH use may reduce the risk for HCC among patients with HBV, HCV, or dual infection in a dose-dependent manner. Further mechanistic research is needed.
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Alhamadany, Alaa Younis Mahdy, and Wajdi Sabeeh Sadek. "Analysis of the Chromosomal Aberrations in Hepatitis B Virus (HBV), Hepatitis C Virus (HCV), and Hepatocellular Carcinoma Patients (HCC) in Mosul City, Iraq." NTU Journal of Pure Sciences 1, no. 2 (May 31, 2022): 48–53. http://dx.doi.org/10.56286/ntujps.v1i2.210.
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Abstract. Hepatocellular carcinoma (HCC) (also known as liver cancer) is one of the most frequent cancers in humans. HCC is linked to chronic hepatitis B and C virus infection, cirrhosis, and excessive alcohol consumption. The aim of this study was to use Metaphase chromosome analysis in whole blood to determine chromosomal aberrations (CA) in HBV, HCV, and HCC patients. A cohort of 145 samples have been collected from participants from the date of 5 \ 1 \ 2020 to 15\9\ 2021. Among those samples are (40 healthy controls, HBV 38, 44 HCV, and HCC 23) to make cytogenetic evaluation by observing the analysis of chromosome aberration. Our study showed that the chromosome aberration With Gap was higher in the HCC patient group followed by HBV patient group. also, the results showed that of the chromosome aberration without Gap in the HCC, and HCV patient groups were significantly higher in females than in males. the results showed that higher break, DIC was in HBV patients group followed by HCV patients group. the results showed that deletion, and ace were higher in the HCV and HCC patient group followed by HBV patient group. Finally with RO. Trans., the results showed that ace was higher in the HCV, and HBV patient groups. In conclusion, we indicate that HBV, HCV, and HCC patients have chromosomal instability because of their chromosome aberration levels.
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Kuo, Yuan-Hung, Tzu-Hsin Huang, Jing-Houng Wang, Yen-Yang Chen, Ming-Chao Tsai, Yen-Hao Chen, Sheng-Nan Lu, Tsung-Hui Hu, Chien-Hung Chen, and Chao-Hung Hung. "Well-Controlled Viremia Predicts the Outcome of Hepatocellular Carcinoma in Chronic Viral Hepatitis Patients Treated with Sorafenib." Cancers 14, no. 16 (August 17, 2022): 3971. http://dx.doi.org/10.3390/cancers14163971.
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Without analyzing the status of viremia, hepatitis C virus-related hepatocellular carcinoma (HCV-HCC) patients are proposed to have better prognosis than hepatitis B virus-related HCC (HBV-HCC) patients using sorafenib. We aimed to elucidate the efficacy of concurrent sorafenib and anti-viral treatment for HCC patients with HBV or HCV infection in real world. Between January 2018 and January 2021, 256 unresectable HCC patients receiving first-line sorafenib were evaluated. High-potency nucleoside analogs were used for HBV control, whereas direct-acting antivirals were administered for HCV eradication. Well-controlled viremia was defined as patients who had undetectable viremia, or who had been receiving antivirals at least 6 months before sorafenib. We recruited 116 (65.2%) HBV-HCC patients and 62 (34.8%) HCV-HCC patients. Using sorafenib, progression-free survival and overall survival (OS) rates between these two groups were not different. Before sorafenib, 56% of HBV-HCC patients and 54.8% of HCV-HCC patients had well-controlled viremia and their OS was superior to those who had uncontrolled viremia (15.5 vs. 11.1 months, p = 0.001). Dividing our patients into four subgroups as well-controlled HCV viremia, well-controlled HBV viremia, uncontrolled HCV viremia, and uncontrolled HBV viremia, their OS rates were distributed with a significantly decreasing trend as 21.9 months, 15.0 months, 14.2 months, and 5.7 months (p = 0.009). Furthermore, well-controlled viremia was associated with mortality in multivariate analysis (Hazard ratio: 0.63, 95% confidence interval: 0.42–0.93, p = 0.022). In real-life, HBV or HCV infection did not contribute to the prognosis of HCC patients receiving sorafenib; however, whether viremia was controlled or not did contribute.
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Alhamadany, Alaa Younis Mahdy, and Wajdi Sabeeh Sadek. "Evaluation of the genotoxicity in patients with HBV, HCV, and HCC using micronucleus and comet assay in Mosul City\Iraq." International journal of health sciences 6, S1 (March 20, 2022): 1567–79. http://dx.doi.org/10.53730/ijhs.v6ns1.4903.
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Hepatitis B virus (HBV) and hepatitis C virus (HCV) have mutagenic effects on somatic cells. HBV and HCV may be showing these mutagenic effects through its viral proteins or through integrating into host DNA. The aim of this study was to determine whether HBV and HCV have a genotoxic effect on the DNA of oral epithelial cells. A cohort of 145 samples have been collected from participants from the date of 5 \ 1 \ 2020 to 15\9\ 2021. Among those samples are (40 healthy controls, HBV 38, 44 HCV, and HCC 23) to make cytogenetic evaluation by observing the micronucleus (MNi) test and comet assay. For each individual, 100 cells were analyzed for comet assay. Around 100 cells were observed and MNi were scored for each individual. Our results showed significantly higher frequencies of MNi in HBV, HCV, and HCC patients groups than in the control group. There was no difference in MNi scores among HBV, HCV, HCC patients groups, and showed a significantly difference of study groups compared to healthy carriers. In conclusion: chronic HBV, HCV, HCC patients have genomic instability as affected as patients because of their levels of DNA damage and MNi.
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Mbaga, Donatien Serge, Sebastien Kenmoe, Cyprien Kengne-Ndé, Jean Thierry Ebogo-Belobo, Gadji Mahamat, Joseph Rodrigue Foe-Essomba, Marie Amougou-Atsama, et al. "Hepatitis B, C and D virus infections and risk of hepatocellular carcinoma in Africa: A meta-analysis including sensitivity analyses for studies comparable for confounders." PLOS ONE 17, no. 1 (January 21, 2022): e0262903. http://dx.doi.org/10.1371/journal.pone.0262903.
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Introduction Africa denotes unique facies for hepatocellular carcinoma (HCC) characterized by a conjunction of low sensitization, restricted access to diagnosis and treatment and associated with the highest incidence and mortality in the world. We investigated whether hepatitis B (HBV), C (HCV) and D (VHD) viruses were etiological agents of HCC in Africa. Methods Relevant articles were searched in PubMed, Web of Science, African Index Medicus, and African Journal Online databases, as well as manual searches in relevant reviews and included articles. Analytical studies from Africa evaluating the association between HCC development and HBV, HCV, and HDV were included. Relevant studies were selected, data extracted, and the risk of bias assessed independently by at least 2 investigators. The association was estimated using odds ratios (OR) and their 95% confidence interval (95% CI) determined by a random-effects model. Sources of heterogeneity were determined by subgroup analyses. Results A total of 36 case-control studies were included. With controls having non-hepatic disease, the overall results suggested a significantly increased risk of HCC in patients with HBV (HBeAg (OR = 19.9; 95% CI = [3.7–105.2]), HBsAg (OR = 9.9; 95%) CI = [6.2–15.6]) and DNA (OR = 8.9; 95% CI = [5.9–13.4]); HCV (Anti-HCV (OR = 9.4; 95% CI = [6.3–14.0]) and RNA (OR = 16.5; 95% CI = [7.8–34.6]); HDV (Anti-VHD, (OR = 25.8; 95% CI = [5.9–112.2]); and HBV/HCV coinfections (HBV DNA/HCV RNA (OR = 22.5; 95% CI = [1.3–387.8]). With apparently healthy controls, the overall results suggested a significantly increased risk of HCC in patients with HBV (HBsAg, (OR = 8.9; 95% CI = [6.0–13.0]); HCV (Anti-HCV, (OR = 7.7; 95% CI = [5.6–10.6]); and HBV/HCV coinfections (HBsAg/Anti-HCV (OR = 7.8; 95% CI = [4.4–13.6]) Substantial heterogeneity and the absence of publication bias were recorded for these results. Conclusions In Africa, HBV/HCV coinfections and HBV, HCV, and HDV infections are associated with an increased risk of developing HCC. The implementation of large-scale longitudinal and prospective studies including healthy participants to search for early biomarkers of the risk of progression to HCC is urgently needed.
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Alhamadany, Alaa Younis Mahdy, and Wajdi Sabeeh Sadek. "Evaluation of the genotoxicity and genomic instability in patients with HBV, HCV and HCC using micronucleus and comet assay." NTU Journal of Pure Sciences 1, no. 2 (May 31, 2022): 54–63. http://dx.doi.org/10.56286/ntujps.v1i2.214.
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On somatic cells, the hepatitis B virus (HBV) and the hepatitis C virus (HCV) are mutagenic. HBV and HCV may be causing these mutagenesis effects via integrating into host DNA or by viral proteins. The purpose of this research was to investigate if HBV and HCV had a genotoxic effect on renal epithelial cells' DNA. A total of 145 samples were taken from participants between the periods of 5 \1 2020 and 15\9 2021. (40 healthy controls, HBV 38, 44 HCV, and HCC 23) were used to perform cytogenetic analysis in renal epithelial cells using the micronucleus (MNi) test and comet assay. For the comet experiment, 100 cells were examined for each participant. A total of 100 cells were examined, with MNi scores assigned to each participant. The frequency of MNi was found to be considerably greater in the HBV, HCV, and HCC patient groups than in the control group. There was no significant difference in MNi scores between the HBV, HCV, and HCC patient groups, however there was a significant difference between the study groups and healthy carriers. In conclusion: due to their levels of DNA damage and MNi, chronic HBV, HCV, and HCC patients are afflicted by genomic instability much like other patients.
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Dickson-Spillmann, Maria, Severin Haug, Ambros Uchtenhagen, Philip Bruggmann, and Michael P. Schaub. "Rates of HIV and Hepatitis Infections in Clients Entering Heroin-Assisted Treatment between 2003 and 2013 and Risk Factors for Hepatitis C Infection." European Addiction Research 22, no. 4 (December 11, 2015): 181–91. http://dx.doi.org/10.1159/000441973.
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Background/Aims: We report on the rates of hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV) and human immunodeficiency virus (HIV) in 1,313 clients entering heroin-assisted treatment (HAT) in Switzerland from 2003 to 2013. We identify predictors of HCV infection. Methods: Data were collected using questionnaires within 2 weeks of clients' first entry into HAT. Prevalence of HAV, HBV, HCV and HIV was calculated using laboratory test results collected at entry or using reports of older test results. Predictors of HCV status were identified through multiple logistic regression analysis. Results: Results show stable rates of HIV-positive clients and decreasing proportions of HAV- and HBV-infected clients. In 2013, there were 12% (n = 8) HIV-, 20% (n = 12) HAV-, 20% (n = 12) HBV- and 52% HCV- (n = 34) positive clients. Vaccination against HAV and HBV had become more frequent. Predictors of positive HCV status included older age, female gender, earlier year of entry, having spent 1 month or more in detention or prison, use of injected heroin and more years of intravenous use. Conclusion: Our results highlight the fact that efforts to prevent and test for infections and to promote vaccination against HAV and HBV in heroin users need to be continued.
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Navas, Maria-Cristina, Iris Suarez, Andrea Carreño, Diego Uribe, Wilson Alfredo Rios, Fabian Cortes-Mancera, Ghyslaine Martel, et al. "Hepatitis B and Hepatitis C Infection Biomarkers and TP53 Mutations in Hepatocellular Carcinomas from Colombia." Hepatitis Research and Treatment 2011 (October 31, 2011): 1–10. http://dx.doi.org/10.1155/2011/582945.
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Hepatocellular Carcinoma (HCC) is a leading cause of cancer-related death worldwide. Globally, the most important HCC risk factors are Hepatitis B Virus (HBV) and/or Hepatitis C Virus (HCV), chronic alcoholism, and dietary exposure to aflatoxins. We have described the epidemiological pattern of 202 HCC samples obtained from Colombian patients. Additionally we investigated HBV/HCV infections and TP53 mutations in 49 of these HCC cases. HBV biomarkers were detected in 58.1% of the cases; HBV genotypes F and D were characterized in three of the samples. The HCV biomarker was detected in 37% of the samples while HBV/HCV coinfection was found in 19.2%. Among TP53 mutations, 10.5% occur at the common aflatoxin mutation hotspot, codon 249. No data regarding chronic alcoholism was available from the cases. In conclusion, in this first study of HCC and biomarkers in a Colombian population, the main HCC risk factor was HBV infection.
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Minuk, GY, M. Zhang, SGM Wong, J. Uhanova, CN Bernstein, B. Martin, MR Dawood, L. Vardy, and A. Giulvi. "Viral Hepatitis in a Canadian First Nations Community." Canadian Journal of Gastroenterology 17, no. 10 (2003): 593–96. http://dx.doi.org/10.1155/2003/978162.
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Serological markers for hepatitis A (HAV), B (HBV) and C (HCV) were documented in 315 inhabitants (27%) of a central Manitoba First Nations community. Serologic evidence of HAV infection (anti-HAV positive) was almost universal (92%) by the age of 20 years. HBV infection (antibody to hepatitis B core antigen positive) had occurred in only 2.3% of the study population and no chronic carriers were identified. Serological evidence of HCV infection (anti-HCV positive) was documented in 2.2% of the population but ongoing viremia (HCV-RNA positive by polymerase chain reaction) was absent. The results of this study highlight the importance of universal HAV vaccination; likely reflect the efficacy of existing prenatal screening and immunoprophylaxis programs for HBV; and raise the possibility that First Nations peoples have an enhanced ability to spontaneously clear HCV.
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Lu, Meng-Chuan, Ying-Hsuen Wu, Chi-Hsiang Chung, Hsuan-Hwai Lin, Tsai-Yuan Hsieh, Peng-Jen Chen, Wu-Chien Chien, and Hsuan-Wei Chen. "Association of Hepatitis B and C Virus with the Risk of Coronary Artery Disease and Cerebrovascular Disease in Patients with Hepatocellular Carcinoma." Journal of Clinical Medicine 12, no. 7 (March 30, 2023): 2602. http://dx.doi.org/10.3390/jcm12072602.
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Background: Hepatocellular carcinoma accounts for approximately 90% of primary liver cancers and hepatitis virus was believed to have the potential for altering the pathogenesis of arteriosclerosis. However, the influence of the hepatitis virus on coronary artery disease or cerebral vascular disease remains unclear. This study used the Taiwan National Health Insurance Research Database to clarify the virus-associated risk of coronary artery disease and cerebral vascular disease in patients with hepatocellular carcinoma (HCC). Methods: A total of 188,039 HCC individuals, age 20 years or older, were enrolled from the Longitudinal Health Insurance Database between 2000 and 2017 for cohort analysis. A total of 109,348 with hepatitis B virus (HBV) infection, 37,506 with hepatitis C virus (HCV) infection, 34,110 without HBV or HCV, and 7075 with both HBV and HCV were recorded. Statistically, propensity score matched by sex, age, and index year at a ratio of 15:5:5:1 and a sensitivity test using multivariable Cox regression were used. Results: The risk of coronary artery disease in the HCV-related HCC group was 1.516-fold (95% CI: 1.328–2.034, p < 0.001) higher than in the HBV-related HCC group, followed by the HBV/HCV-related HCC group and the non-B/C HCC group; the cerebral vascular disease risk in the HCV-related HCC group was 1.467-fold higher than in the HBV-related HCC group (95% CI: 1.335 to 1.786, p < 0.001), followed by the HBV/HCV-related HCC group and the non-B/C HCC group. Conclusion: Hepatitis C virus infection was found to have a higher risk of developing coronary artery disease or cerebral vascular disease in patients with hepatocellular carcinoma. For patients with hepatocellular carcinoma, our findings warrant the importance in preventing artherosclerotic disease in the setting of hepatitis C virus infection.
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Duan, Jingxian, Tianhao Mu, and Shifu Chen. "The mutation profiles of HBV or HCV infected hepatocellular carcinoma patients underlie the varied responses to second-line immunotherapy." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e16629-e16629. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e16629.
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e16629 Background: HBV and HCV infections facilitate the development of hepatocellular carcinoma (HCC) via different mechanisms, given that the DNA sequence of HBV but not HCV can integrate into the host genome. However, it remains unclear that whether the altered genomic landscape of HCC patients caused by HBV or HCV infection may result in different responses to treatments. Methods: The MSK panel sequencing results and treatment data of 127 HCC patients were downloaded from the TCGA database (MSK, Clin Cancer Res 2018). Profiles of HBV positive and HCV positive patients were extracted. Based on the treatment received, those patients were classified to sorafenib treated groups and sorafenib + immunotherapy (IT) groups. The progression-free survival (PFS, months) and overall survival (OS, months) were compared, and the mutational profiles of patients were analyzed. Results: Among patients who received sorafenib treatment alone, the mean PFS of HBV positive patients (n = 12, 4.9 ±1.1) is similar to that of the HCV positive patients (n = 21, 5.1±1.8). However, the mean OS of HBV positive patients (n = 12, 18.3 ±6.6) was longer than the mean OS of HCV positive patients (n = 21, 10.0 ±1.9). Among the patients who received immunotherapy following sorafenib treatment, the mean IT PFS of HBV positive patients was (n = 5, 4.4 ±1.8), which was longer than the mean IT PFS of HCV positive patients (n = 5, 2.5 ±0.5). Consistently, the mean IT OS of HBV positive patients (n = 5, 10.9 ±4.4) was longer than the mean IO PFS of HCV positive patients (n = 5, 4.6 ±1.0). Overall it seems that the HBV positive patients responded better to second-line immunotherapy, despite the fact that these comparisons did not reach statistical difference due to the limited sample size. By comparing the MSK panel sequencing results, mutations exclusive to the HBV or HCV infected groups were identified. Enrichment analysis showed that 7/35 mutations exclusively found in the HBV positive group are responsible for lymphocyte activation (p < 0.00001), which may underlie the better IT treatment outcome. Among the mutations restricted to the HCV infected group, 9/50 were involved in histone modification, 7/50 were involved in Hepatitis B pathways (p < 0.0001), suggesting that HCV infection may interfere with diverse molecular processes. Conclusions: HBV and HCV infected HCC patients may respond differently to second-line immunotherapy. This difference is perhaps related to the altered genetic landscape of the patients resulted from virus infections by HBV or HCV.
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Schotten, Clemens, Bastian Ostertag, Jan-Peter Sowa, Paul Manka, Lars P. Bechmann, Gudrun Hilgard, Claudio Marquardt, et al. "GALAD Score Detects Early-Stage Hepatocellular Carcinoma in a European Cohort of Chronic Hepatitis B and C Patients." Pharmaceuticals 14, no. 8 (July 27, 2021): 735. http://dx.doi.org/10.3390/ph14080735.
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Despite vaccination programs and direct antiviral treatments, the incidence of virus-related hepatocellular carcinoma (HCC) remains high, while ultrasound-based detection rates for early-stage HCC is continuously low. To address this insufficiency, we set out to characterize whether the GALAD score, which incorporates gender, age, and serum levels of AFP, AFP isoform L3 (AFP-L3), and des-gamma-carboxy-prothrombin (DCP), can improve early-stage HCC detection in a Caucasian HBV/HCV cohort. In a retrospective German single-center study, 182 patients with HBV, 223 with HCV and 168 with other etiology (OE) of chronic liver disease (CLD) were enrolled. HCC was confirmed in 52 HBV, 84 HCV and 60 OE CLD patients. The diagnostic performance of the single biomarkers in HCC detection was compared to the GALAD model. At initial diagnosis, most patients were at (very) early BCLC 0 (n = 14/7%) or A (n = 56/29%) or intermediate stage BCLC B (n = 93/47%) HCC in all three subgroups. In the BCLC 0/A cohort, GALAD exhibited an AUC of 0.94 discriminating HCC from non-HCC, surpassing AFP (AUC 0.86), AFP-L3 (AUC 0.83) and DCP (AUC 0.83). In the HBV population, GALAD achieved an AUC of 0.96, in HCV an AUC of 0.98 and in OE an AUC of 0.99, clearly superior to the biomarkers alone. Furthermore, in HCV patients GALAD showed a significantly higher specificity (89%) versus AFP (64%) alone. In chronic viral hepatitis, the GALAD model showed superior performance in detection of early-stage HCC, while exhibiting higher specificity in HCV patients compared to AFP alone. We conclude that the GALAD score shows potential for HCC surveillance in Caucasian HBV/HCV patients.
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Rahman, Md Tahminur, Rosy Sultana, and Sohel Reza Chowdhury. "Seropositivity and pattern of viral hepatitis in clinically suspected cases of hepatitis in Dhaka city." Bangladesh Medical Research Council Bulletin 33, no. 3 (September 15, 2010): 103–6. http://dx.doi.org/10.3329/bmrcb.v33i3.1142.
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An attempt was made to see the seropositivity and pattern of four common hepatotrophic viruses (HBV, HCV, HEV, HAV) in patients suspected to have been suffering from viral hepatitis. Blood samples from 2,995 cases of suspected HBV infection, 331 from HCV, 155 from HEV and 24 from HAV were tested for these viral markers. Of these a total of 245 (8.1%) were positive for HBsAg, 18 (5.4%) for HCV, 87 (56.1%) for HEV and 8 (33.3%) were positive for HAV infection. The predominant age group affected in HBV is 25-40 years, for HCV >61 years, HEV 26-50 years and HAV under 11 years. Seropositivity for HBsAg was statistically higher (near double) in males than females (p<0.05). HCV showed more seropositivity in males than females. HEV showed slight male preponderance and for HAV the female showed preponderance. The seropositivity rate was higher in Bangladesh in comparison to other developed and developing countries.DOI = 10.3329/bmrcb.v33i3.1142Bangladesh Med Res Counc Bull 2007; 33: 103-106
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Alqahtani, Saleh A., and Massimo Colombo. "Treatment for Viral Hepatitis as Secondary Prevention for Hepatocellular Carcinoma." Cells 10, no. 11 (November 9, 2021): 3091. http://dx.doi.org/10.3390/cells10113091.
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Chronic infections with either hepatitis B or C virus (HBV or HCV) are among the most common risk factors for developing hepatocellular carcinoma (HCC). The hepatocarcinogenic potential of these viruses is mediated through a wide range of mechanisms, including the induction of chronic inflammation and oxidative stress and the deregulation of cellular pathways by viral proteins. Over the last decade, effective anti-viral agents have made sustained viral suppression or cure a feasible treatment objective for most chronic HBV/HCV patients. Given the tumorigenic potential of HBV/HCV, it is no surprise that obtaining sustained viral suppression or eradication proves to be effective in preventing HCC. This review summarizes the mechanisms by which HCV and HBV exert their hepatocarcinogenic activity and describes in detail the efficacy of anti-HBV and anti-HCV therapies in terms of HCC prevention. Although these treatments significantly reduce the risk for HCC in patients with chronic viral hepatitis, this risk is not eliminated. Therefore, we evaluate potential strategies to improve these outcomes further and address some of the remaining controversies.
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Shao, Yu Yun, Min-Shu Hsieh, Chung-Yi Huang, Yung-Ling Chang, Chih-Hung Hsu, and Ann-Lii Cheng. "Vascular endothelial growth factor expression in hepatitis C virus (HCV)-related advanced hepatocellular carcinoma (HCC) compared with hepatitis B virus (HBV)-related advanced HCC." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 4115. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.4115.
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4115 Background: HCC with different etiologic factors may result in activation of different signaling pathways. This study aimed to clarify if HBV-related HCC (HBV-HCC) and HCV-related HCC (HCV-HCC) may have difference in the expression of key molecules that are relevant to contemporary molecular targeted therapy. Methods: We enrolled patients diagnosed with advanced HCC from 2001 to 2011 who had tumor tissues obtained upon the diagnosis of advanced HCC at our center. Tumor slides were immunohistochemically stained for phosphorylated extracellular signal-regulated kinases (p-ERK), Raf kinase inhibitory protein (RKIP), and vascular endothelial growth factor (VEGF). The expressions of p-ERK and RKIP were evaluated according to percentages of positive-staining cells and graded as: 0: 0; 1+: 1-10%; 2+: 11-50%; 3+: > 50%. Grades 0 and 1 were considered negative, and grades 2 and 3 positive. VEGF staining was evaluated as strong or weak according to staining intensity. The staining results of VEGF were further recorded as H scores, defined as intensity (0, 1, 2, or 3) × percentages of positive staining. Results: In total, 131 patients were enrolled in this study; 94 (72%) patients had HBV-HCC, and 37 (28%) patients had HCV-HCC. HBV-HCC and HCV-HCC had similar expression of p-ERK (positive: 45% vs. 51%, p = 0.491) and RKIP (positive: 83% vs. 84%, p = 0.912). HCV-HCC was more likely to have strong VEGF staining than HBV-HCC (95% vs. 72%, p = 0.005) and higher H scores for VEGF staining (289.5 vs. 248.8, p< 0.001). In multivariate analysis adjusting for age, sex, macrovascular invasion, extrahepatic metastasis, and α-fetoprotein level, HCV-HCC remained an independent factor associated with strong VEGF staining. VEGF staining intensity was not associated with age, sex, macrovascular invasion, extrahepatic metastasis, and α-fetoprotein level. Conclusions: HCV-HCC has stronger VEGF expression than HBV-HCC. (This study was supported by the grant of NSC101-2314-B-002-141, 100CAP1020-2, and NTUH.101-N1965.)
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Galy, Olivier, Isabelle Chemin, Emilie Le Roux, Stéphanie Villar, Florence Le Calvez-Kelm, Myriam Lereau, Doriane Gouas, et al. "Mutations in TP53 and CTNNB1 in Relation to Hepatitis B and C Infections in Hepatocellular Carcinomas from Thailand." Hepatitis Research and Treatment 2011 (June 30, 2011): 1–9. http://dx.doi.org/10.1155/2011/697162.
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Hepatocellular carcinoma (HCC) may develop according to two major pathways, one involving HBV infection and TP53 mutation and the other characterized by HCV infection and CTNNB1 mutation. We have investigated HBV/HCV infections and TP53/CTNNB1 mutations in 26 HCC patients from Thailand. HBV DNA (genotype B or C) was detected in 19 (73%) of the cases, including 5 occult infections and 3 coinfections with HCV. TP53 and CTNNB1 mutations were not mutually exclusive, and most of TP53 mutations were R249S, suggesting a significant impact of aflatoxin-induced mutagenesis in HCC development.
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Aimla, Kerstin, Justyna Dominika Kowalska, Raimonda Matulionyte, Velida Mulabdic, Anna Vassilenko, Natalie Bolokadze, David Jilich, et al. "Vaccination against HBV and HAV as Mode of Hepatitis Prevention among People Living with HIV—Data from ECEE Network Group." Vaccines 11, no. 5 (May 14, 2023): 980. http://dx.doi.org/10.3390/vaccines11050980.
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(1) Background: Viral hepatitis C (HCV) and viral hepatitis B (HBV) are common co-infections in people living with HIV (PLWH). All PLWH should be vaccinated against HBV and hepatitis A (HAV) and treated for HBV and HCV. We aimed to compare testing, prophylaxis and treatment of viral hepatitis in PLWH in Central and Eastern Europe (CEE) in 2019 and 2022. (2) Methods: Data was collected through two on-line surveys conducted in 2019 and 2022 among 18 countries of the Euroguidelines in CEE (ECEE) Network Group. (3) Results: In all 18 countries the standard of care was to screen all PLWH for HBV and HCV both years; screening of HAV was routine in 2019 in 54.5% and in 2022 47.4% of clinics. Vaccination of PLWH against HAV was available in 2019 in 16.7%, in 2022 in 22.2% countries. Vaccination against HBV was available routinely and free of charge in 50% of clinics both in 2019 and 2022. In HIV/HBV co-infected the choice of NRTI was tenofovir-based in 94.4% of countries in both years. All clinics that responded had access to direct-acting antivirals (DAAs) but 50% still had limitations for treatment. (4) Conclusions: Although testing for HBV and HCV was good, testing for HAV is insufficient. Vaccination against HBV and especially against HAV has room for improvement; furthermore, HCV treatment access needs to overcome restrictions.
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Hester, Caitlin A., Nicole E. Rich, Amit G. Singal, and Adam C. Yopp. "Comparative Analysis of Nonalcoholic Steatohepatitis– Versus Viral Hepatitis– and Alcohol-Related Liver Disease–Related Hepatocellular Carcinoma." Journal of the National Comprehensive Cancer Network 17, no. 4 (April 2019): 322–29. http://dx.doi.org/10.6004/jnccn.2018.7105.
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Background: Despite an increasing burden of nonalcoholic steatohepatitis (NASH), limited data are available comparing outcomes of NASH-related hepatocellular carcinoma (HCC) versus other etiologies. Methods: Patient demographic and tumor characteristics were collected for 1,051 patients diagnosed with NASH-, alcohol-related liver disease (ALD)–, hepatitis C virus (HCV)–, and hepatitis B virus (HBV)–related HCC at 2 large health systems from January 2008 through December 2016. Patient demographics, clinical characteristics, and survival were compared. Risk-adjusted treatment receipt and overall survival (OS) were examined using multivariable analysis. Results: A total of 92 patients with NASH-related HCC were compared with 153 patients with ALD-, 719 with HCV-, and 87 with HBV-related HCC. Patients with NASH were older, more likely female, and more likely Hispanic white. Patients with NASH and HBV had more compensated liver disease than those with ALD or HCV, including significantly higher proportions having noncirrhotic HCC. Despite similar surveillance receipt and Barcelona Clinic Liver Cancer (BCLC) tumor stage at diagnosis, patients with NASH had higher rates of curative-intent therapy than those with other diseases. Unadjusted median OS was 16 months for NASH, 15 months for ALD, 14 months for HCV, and 8 months for HBV. In multivariable analysis, NASH was associated with worse OS compared with ALD (hazard ratio, 1.92; 95% CI, 1.3–2.5), but there was no difference between NASH- and HCV- or HBV-related HCC. Conclusions: Patients with NASH-related HCC present with more preserved liver function, including a higher proportion having noncirrhotic HCC, than other diseases. Despite patients having similar tumor stage at diagnosis, NASH is independently associated with worse survival compared with ALD, but similar survival compared with HCV and HBV.
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Akashi, Hayato, and Masaaki Hidaka. "Comparison of the pathological features among HBV, HCV, and nonviral etiology-related hepatocellular carcinoma using explanted whole liver examinations." Journal of Clinical Oncology 35, no. 4_suppl (February 1, 2017): 245. http://dx.doi.org/10.1200/jco.2017.35.4_suppl.245.
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245 Background: The aim of this study is to compare the pathological features among HBV, HCV and non-viral etiology related hepatocellular carcinoma (HCC) in the explanted cirrhotic liver using whole liver examinations. Methods: Ninety patients (HBV 23, HCV 53, HBV+HCV 3, nonBnonC 16) out of 246 recipients of liver transplantation were analyzed. All specimens were sectioned serially at 5-7 mm intervals and then were examined by an experienced pathologist. The pathological characteristics of HCC among each group were retrospectively analyzed using whole liver thin sliced histological examinations. Results: The median number and maximum size of HCC were one nodule (range 0-3 nodules), 22 mm (range 7-50 mm) by pre-operative imaging, and two nodules (range 0-37 nodules), 20 mm (range 4-50 mm) based on histological examinations. Twenty-six patients (27.4%) had more than 3 nodules measuring less than 1 cm diameter based on histological examinations. Fifteen patients (15.8%) had HCC with micro vascular invasion. Twenty-seven patients (28.4%) demonstrated findings beyond the Milan Criteria based on pathological examinations. NonBnonC related HCC tended to be within the Milan Criteria based on pathological examinations in contrast to viral related HCC (nonBnonC 12.5%, HBV 34.8% and HCV 39.6%). There were significantly more undetectable HCCs in HCV related HCC than in detectable HCCs by imaging. Conclusions: The undetectable HCCs in HCV tended to be found in the explanted liver. HCCs exceeding the rate of the Milan Criteria were less frequently found in non-viral related HCC than in viral related HCC.
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C, Nwangburuka, Ijomah M A, and Nwakuya M T. "Heteroscedasticity of unknown form: a comparison of five heteroscedasticity-consistent covariance matrix (hccm) estimators." Global Journal of Pure and Applied Sciences 29, no. 1 (May 16, 2023): 83–90. http://dx.doi.org/10.4314/gjpas.v29i1.10.
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Regression model applications frequently involve violations of the homoscedasticity assumption and the presence of high leverage points (HLPs). The Heteroscedasticity-Consistent Covariance Matrix (HCCM) estimator's impact in the presence of heteroscedasticity of an unknown form was investigated in this study. The effectiveness of five variations of HCCM namely White’s estimator (HC0), White-Hinkley (HC1), Mackinnon White (HC2), Davison –Mackinnon (HC3), and Cribari-Neto (HC4) were accessed to identify the optimal Heteroscedasticity-Consistent Covariance Matrix (HCCM) estimator. In the study a simulated dataset was analysed using the Econometric View Software Version 12. The Breush-Pagan Godfery’s test for heteroscedasticity was applied and p-value of 0.0123 was obtained indicating presence of heteroscedasticity in the model. Applying the HCCM estimators and comparing the Heteroskedasticity-consistent standard errors estimates showed that HCO had 124.104, HC1 had 1189.222, HC2 had 1175.282, HC3 had 1106.94 and HC4 had 1140.707. These results reveal that HC3 and HC4 produced smaller errors compared to HC0, HC1 and HC2. The study hence comes to the conclusion that when doing inferential tests using OLS regression, the use of HCSE estimator increases the researcher's confidence in the accuracy and potency of those tests. This study therefore suggests that to ensure that findings are not affected by heteroscedasticity; researchers should use HCCM estimator but precisely HC3 and HC4, as the presented better results in comparison to others.
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Cortes-Mancera, Fabian, Carmen Luisa Loureiro, Sergio Hoyos, Juan-Carlos Restrepo, Gonzalo Correa, Sergio Jaramillo, Helene Norder, Flor Helene Pujol, and Maria-Cristina Navas. "Etiology and Viral Genotype in Patients with End-Stage Liver Diseases admitted to a Hepatology Unit in Colombia." Hepatitis Research and Treatment 2011 (September 20, 2011): 1–10. http://dx.doi.org/10.1155/2011/363205.
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Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections are the principal risk factor associated to end-stage liver diseases in the world. A study was carried out on end-stage liver disease cases admitted to an important hepatology unit in Medellin, the second largest city in Colombia. From 131 patients recruited in this prospective study, 71% of cases were diagnosed as cirrhosis, 12.2% as HCC, and 16.8% as cirrhosis and HCC. Regarding the risk factors of these patients, alcohol consumption was the most frequent (37.4%), followed by viral etiology (17.6%). Blood and/or hepatic tissue samples from patients with serological markers for HCV or HBV infection were characterized; on the basis of the phylogenetic analysis of HCV 5′ UTR and HBV S gene, isolates belonged to HCV/1 and HBV/F3, respectively. These results confirm the presence of strains associated with poor clinical outcome, in patients with liver disease in Colombia; additionally, HBV basal core promoter double mutant was identified in HCC cases. Here we show the first study of cirrhosis and/or HCC in Colombian and HBV and HCV molecular characterization of these patients. Viral aetiology was not the main risk factor in this cohort but alcohol consumption.
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Patt, Y. Z., C. Charnsangavej, B. Yoffe, R. Smith, D. Lawrence, V. Chuang, H. Carrasco, M. Roh, J. Chase, and H. Fischer. "Hepatic arterial infusion of floxuridine, leucovorin, doxorubicin, and cisplatin for hepatocellular carcinoma: effects of hepatitis B and C viral infection on drug toxicity and patient survival." Journal of Clinical Oncology 12, no. 6 (June 1994): 1204–11. http://dx.doi.org/10.1200/jco.1994.12.6.1204.
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PURPOSE To conduct a pilot trial of hepatic arterial infusion (HAI) of floxuridine (FUDR), leucovorin, Adriamycin (doxorubicin; Adria Laboratories, Columbus, OH), and cisplatin (FLAP) in nonresectable hepatocellular cancer (HCC) confined to the liver and assess the effects of hepatitis B (HBV) and hepatitis C (HCV) viral markers on toxicity, response to treatment, and patient survival. PATIENTS AND METHODS Of 31 HCC patients, 13 were HBV- and HCV-nonreactive, and 18 had evidence of either current or prior HBV and/or HCV infection. Treatment was delivered through percutaneous hepatic arterial catheters, and Infusaid pumps (Shiley Infusaid, Norwood, MA) were placed in responding patients. Cisplatin (100 mg/m2) and Adriamycin (30 to 35 mg/m2) were administered on day 1, followed by a continuous 24-hour HAI of an admixture of floxuridine (60 mg/m2) and leucovorin (15 mg/m2) daily for 4 days. Treatment was repeated every 5 weeks. RESULTS Twelve (41%) of 29 assessable patients had a partial response (PR), with a median time to disease progression of 13 months. Six (50%) of 12 HBV-negative (HBV-)/HCV-negative (HCV-) and six of 17 (35%) HBV-positive (HCV+) and/or HCV-positive (HCV+) patients achieved a PR. Eight patients have been maintained in remission for a median duration greater than 15.5 months. The median survival duration of all 31 patients was 15 months, 7.5 months among HBV+ and/or HCV+ patients, and significantly longer among hepatitis-non-reactive patients (P = .007). (A median has not yet been reached.) Granulocylopenia (< 0.1 x 10(3)/microL), thrombocytopenia (< 25 x 10(3)/microL), and hospitalizations for infectious complications were significantly more common among HBV-HCV-reactive than -nonreactive patients: 56%, 50%, and 67% versus 15%, 15%, and 8%, respectively (P < .05 for all). CONCLUSION HAI of FLAP has induced long-term PR and has palliated extensive nonresectable HCC. Positive hepatitis serology appeared to increase bone marrow susceptibility to myelotoxic drugs. Conceivably, one or both viruses may have a direct inhibitory effect on bone marrow progenitors and thereby contribute to the observed myelotoxicity.
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Petruzziello, Arnolfo. "Epidemiology of Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) Related Hepatocellular Carcinoma." Open Virology Journal 12, no. 1 (February 28, 2018): 26–32. http://dx.doi.org/10.2174/1874357901812010026.
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Introduction:Hepatocellular carcinoma (HCC) is one of the most prevalent primary malignant tumors and accounts for about 90% of all primary liver cancers. Its distribution varies greatly according to geographic location and it is more common in middle and low- income countries than in developed ones especially in Eastern Asia and Sub Saharan Africa (70% of all new HCCs worldwide), with incidence rates of over 20 per 100,000 individuals.Explanation:The most important risk factors for HCC are Hepatitis B Virus (HBV) infection, Hepatitis C Virus (HCV) infection, excessive consumption of alcohol and exposition to aflatoxin B1. Its geographic variability and heterogeneity have been widely associated with the different distribution of HBV and HCV infections worldwide.Chronic HBV infection is one of the leading risk factors for HCC globally accounting for at least 50% cases of primary liver tumors worldwide. Generally, while HBV is the main causative agent in the high incidence HCC areas, HCV is the major etiological factor in low incidence HCC areas, like Western Europe and North America.Conclusion:HBV-induced HCC is a complex, stepwise process that includes integration of HBV DNA into host DNA at multiple or single sites. On the contrary, the cancerogenesis mechanism of HCV is not completely known and it still remains controversial as to whether HCV itself plays a direct role in the development of tumorigenic progression.
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Yen, Yi-Hao, Kwong-Ming Kee, Wei-Feng Li, Yueh-Wei Liu, Chih-Chi Wang, Tsung-Hui Hu, Ming-Chao Tsai, Yuan-Hung Kuo, and Chih-Yun Lin. "Causes of Death among Patients with Hepatocellular Carcinoma According to Chronic Liver Disease Etiology." Cancers 15, no. 6 (March 9, 2023): 1687. http://dx.doi.org/10.3390/cancers15061687.
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This study was conducted to determine whether the causes of death among patients with hepatocellular carcinoma (HCC) differ according to chronic liver disease (CLD) etiology. Between 2011 and 2020, 3977 patients who were newly diagnosed with HCC at our institution were enrolled in this study. We determined whether the cause of death was HCC-related and non-HCC-related. For patients with multiple CLD etiologies, etiology was classified using the following hierarchy: hepatitis C virus (HCV) > hepatitis B virus (HBV) > alcohol-related causes > all negative. All negative was defined as negative for HCV, HBV, and alcohol-related causes. Among 3977 patients, 1415 patients were classified as HCV-related, 1691 patients were HBV-related, 145 patients were alcohol-related, and 725 patients were all negative. HCC-related mortality was the leading cause of death, irrespective of etiology. Among patients who underwent curative treatment, HCC-related mortality was the leading cause of death for patients in the HCV, HBV, and all-negative groups, but not for patients in the alcohol-related group. Among patients 75 years and older who underwent curative treatment, HCC-related mortality was the leading cause of death in the HCV but not HBV or all-negative groups. In conclusion, although most patients with HCC die due to HCC-related causes, non-HCC-related mortality represents a competing event in certain patient subgroups. The current study results underscore the importance of assessing and managing underlying comorbidities, particularly among patients with HCC at risk of non-HCC-related mortality.
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Tong, C. Y. W., R. Khan, N. J. Beeching, W. U. Z. Tariq, C. A. Hart, N. Ahmad, and I. A. Malik. "The occurrence of hepatitis B and C viruses in Pakistani patients with chronic liver disease and hepatocellula carcinoma." Epidemiology and Infection 117, no. 2 (October 1996): 327–32. http://dx.doi.org/10.1017/s0950268800001503.
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SummaryTo study the occurrence of hepatitis B virus (HBV) and hepatitis C virus (HCV) in patients with chronic liver disease (CLD) and hepatocellular carcinoma (HCC) in Pakistan, blood samples from 105 sequential patients with biopsy-proven CLD (n= 82) and HCC (n= 23) were tested for HBV and HCV markers. Of the 105, 87 (83%) had evidence of hepatitis B exposure, 58 (55%) were positive for hepatitis B surface antigen (HBsAg), 23 (22%) had hepatitis C antibodies and 25 (24%) had detectable HCV RNA. Significantly more patients with HCC had evidence of HBV exposure in the absence of HCV markers (49/82vs.20/23, odds ratio 4·49,95 % CI 1·17–25·16). The proportion of patients positive for HBsAg with no HCV markers was also significantly higher in the HCC group (34/82vs.18/23, odds ratio 5·08, 95% CI 1·59—18·96). There were more patients with only HCV markers in the CLD group than the HCC group but the difference was not statistically significant (19/82vs.1/23, odds ratio 6·63, 95% CI 0·93—288·01). A modified non-isotopic restriction fragment length polymorphism study on PCR products was used to investigate the epidemiology of HCV genotypes in Pakistan. Due to depletion of the initial samples, a second series of specimens collected one year afterwards was used. Fifteen out of 40 samples had amplifiable product and all were identified as type 3. A commercial serological typing method on the same samples also confirmed that type 3 was the predominant HCV genotype in Pakistan.
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Qiu, Jinrong, Weifeng Wang, Yingmei Li, and Shifu Chen. "Comparison of mutational landscape of non-alcoholic fatty liver disease, viral hepatitis, and alcohol consumption related hepatocellular carcinoma." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e16614-e16614. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e16614.
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e16614 Background: Hepatocellular cancer (HCC) is the seventh most common cancer and the fourth leading cause of cancer-related death worldwide. The most common risk factors of HCC have traditionally included hepatitis B virus (HBV), hepatitis C virus (HCV), and alcohol-related liver disease (ALD). Recently, Non-Alcoholic Fatty Liver Disease (NAFLD) has emerged as the fastest growing risk factor for the development of HCC. This study reports the mutation landscape of NAFLD-related hepatocellular carcinoma (HCC) versus other etiologies. Methods: Mutation data of 219 HCC samples were collected from TCGA database, including 13 NAFLD, 87 HBV, 37 HCV, and 82 ALD-related samples. We analyzed mutations for different type of HCC samples using GDC level 3 mutation data. Driver mutations were called by applying software MuSig2CV. Results: In 219 samples, a total of 32189 mutations were identified, including 3163 in NAFLD, 11430 in HBV, 6390 in HCV, and 11206 in ALD-related HCC samples. Driver genes shared by viral hepatitis and ALD-related samples were TP53 (32% for ALD, 33% for HBV, 42% for HCV) and CTNNB1(32 % for HCV, 26% for HBV,29% for ALD), while TP53 was not among the highest frequency of mutations in NAFLD-related samples. As lack of NAFLD-related HCC samples (n = 13), most frequently mutated genes in NAFLD-related HCC samples were computed instead of driver genes. Top 5 mutated genes in NAFLD-related HCC samples were TTN (36%), CACNA1B (27%), DSCAM (27%), GLI2 (27%), and BEB (27%). Conclusions: From our results, TP53 has a lower mutation frequency in NAFLD-related HCC samples than in other types of HCC. To further validate this finding, a larger size of NAFLD-related HCC samples is essential.
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Pseush, S. Yu, L. V. Zozulya, and L. L. Mikhaleva. "The predictive value indicators of first trimester biochemical screening in assessing unfavorable factors of pregnancy course in women with HIV as well as hepatitis B and C." Obstetrics, Gynecology and Reproduction 15, no. 6 (January 12, 2022): 686–94. http://dx.doi.org/10.17749/2313-7347/ob.gyn.rep.2021.240.
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Aim: to find out the predictive value of blood serum biochemical parameters PAPP-A (pregnancy-associated plasma protein A) and β-hCG (beta subunit of human chorionic gonadotropin) in the assessment of unfavorable pregnancy outcomes in women infected by human immunodeficiency virus (HIV) as well as viral hepatitis B (HBV) and C (HCV).Materials and Methods. A retrospective study of the medical records from 52 women was carried out, including 19 HIV-infected women, 9 women with monoinfection HBV or HCV, 11 pregnant women who were co-infected (HIV/HBV or HIV/HCV) and 13 uninfected women. PAPP-A and β-hCG levels, expressed as MoM (multiple of median), were evaluated in all women.Results. Our study revealed that only PAPP-A was prognostically significant for developing chronic placental insufficiency in women with HIV infection and co-infection of HIV together hepatitis B and C. None of the parameters examined were significant in women with HBV or HCV monoinfection. PAPP-A and β-hCG in pregnant women without infections were effective in predicting development of chronic placental insufficiency.Conclusion. PAPP-A can be used as a diagnostic parameter of developing chronic placental insufficiency in pregnant women with monoinfection HIV and co-infection with HIV/HBV or HIV/HCV.
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Huang, Xiao-wen, Bing Liao, Yang Huang, Jin-yu Liang, Quan-yuan Shan, Shun-li Shen, Xiao-yan Xie, Ming-de Lu, Li-da Chen, and Wei Wang. "Non-Invasive Diagnostic Criteria for Hepatocellular Carcinoma in Hepatitis B Virus-Endemic Areas: Is Cirrhosis Indispensable?" Digestive Diseases 36, no. 3 (2018): 228–35. http://dx.doi.org/10.1159/000486196.
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Aim: To confirm whether cirrhosis is indispensable for the non-invasive diagnostic criteria for hepatocellular carcinoma (HCC) in hepatitis B virus (HBV)-endemic areas. Methods: Between January 2014 and December 2014, a total of 409 patients with pathologically proven focal liver lesions who underwent contrast-enhanced ultrasound (CEUS) were recruited from our institution. Clinical liver cirrhosis, HBV/HCV infection and HCC-typical vascular pattern of the targeted lesion on CEUS were evaluated. The following 3 criteria were applied to these patients to diagnose HCC: criterion 1, clinical liver cirrhosis and HCC-typical vascular pattern; criterion 2, HBV/HCV infection and HCC-typical vascular pattern; criterion 3, HBV/HCV infection or clinical liver cirrhosis and HCC-typical vascular pattern. Pathological reports were considered the gold standard. Results: A total of 311 patients had confirmed HCC by pathology. The sensitivity, specificity, accuracy, positive predictive value, negative predictive value and area under the ROC curve for criterion 1 were 29.6, 90.8, 44.3, 91.1, 28.9, and 0.60% respectively. For criterion 2, they were 83.3, 74.5, 81.2, 91.2, 58.4, and 0.79%, respectively, and for criterion 3, they were 86.2, 72.5, 82.9, 90.9, 62.3, and 0.79% respectively. Conclusions: In HBV-endemic areas, when using the HBV/HCV infection instead of cirrhosis as the precondition of the non-invasive diagnostic criteria for HCC, we should be aware of the potential false positive. Cirrhosis still plays an important role in the non-invasive diagnostic criteria for HCC because of the high specificity.
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Kishta, Sara, Ashraf Tabll, Tea Omanovic Kolaric, Robert Smolic, and Martina Smolic. "Risk Factors Contributing to the Occurrence and Recurrence of Hepatocellular Carcinoma in Hepatitis C Virus Patients Treated with Direct-Acting Antivirals." Biomedicines 8, no. 6 (June 25, 2020): 175. http://dx.doi.org/10.3390/biomedicines8060175.
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Although hepatitis C virus (HCV) RNA may be eliminated from blood circulation by direct-acting antivirals (DAA) therapy as assessed by real-time polymerase chain reaction (PCR), HCV RNA can still be present in liver tissue, and this is known as occult HCV. There has been a lot of controversy surrounding the recurrence of hepatocellular carcinoma (HCC) after DAA treatment of hepatic cells infected with chronic HCV. One of the main risk factors that leads to de novo HCC is the chronicity of HCV in hepatic cells. There are many studies regarding the progression of HCV-infected hepatic cells to HCC. However, there is a lack of research on the different molecular mechanisms that lead to the progression of chronic HCV infection to HCC, as well as on the effect of HCV on the alteration of DNA ploidy, which eventually leads to a recurrence of HCC after DAA treatment. In this review article, we will address some risk factors that could lead to the development/recurrence of HCC after treatment of HCV with DAA therapy, such as the role of liver cirrhosis, the alteration of DNA ploidy, the reactivation of hepatitis B virus (HBV), the role of cytokines and the alteration of the immune system, concomitant non- alcoholic fatty liver disease (NAFLD), obesity, alcohol consumption and also occult HCV infection/co-infection. Clinicians should be cautious considering that full eradication of hepatocarcinogenesis cannot be successfully accomplished by anti-HCV treatment alone.
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Kanda, Tatsuo, Taichiro Goto, Yosuke Hirotsu, Mitsuhiko Moriyama, and Masao Omata. "Molecular Mechanisms Driving Progression of Liver Cirrhosis towards Hepatocellular Carcinoma in Chronic Hepatitis B and C Infections: A Review." International Journal of Molecular Sciences 20, no. 6 (March 18, 2019): 1358. http://dx.doi.org/10.3390/ijms20061358.
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Almost all patients with hepatocellular carcinoma (HCC), a major type of primary liver cancer, also have liver cirrhosis, the severity of which hampers effective treatment for HCC despite recent progress in the efficacy of anticancer drugs for advanced stages of HCC. Here, we review recent knowledge concerning the molecular mechanisms of liver cirrhosis and its progression to HCC from genetic and epigenomic points of view. Because ~70% of patients with HCC have hepatitis B virus (HBV) and/or hepatitis C virus (HCV) infection, we focused on HBV- and HCV-associated HCC. The literature suggests that genetic and epigenetic factors, such as microRNAs, play a role in liver cirrhosis and its progression to HCC, and that HBV- and HCV-encoded proteins appear to be involved in hepatocarcinogenesis. Further studies are needed to elucidate the mechanisms, including immune checkpoints and molecular targets of kinase inhibitors, associated with liver cirrhosis and its progression to HCC.
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Alhaqbani, Abdulaziz H., Abdulaziz Almusalam, Abdulaziz Alnadhari, Abdulmalik Alsalem, Meshal Alrasheed, Abduljaleel Alalwan, and Bander Aldamkh. "The prevalence and associated factors of viral hepatitis and cryptogenic related hepatocellular carcinoma at King Abdulaziz Medical city-Riyadh." International Journal Of Community Medicine And Public Health 6, no. 2 (January 24, 2019): 561. http://dx.doi.org/10.18203/2394-6040.ijcmph20190060.
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Background: Worldwide, viral hepatitis is the major risk factor for HCC with hepatitis B (HBV) being more than hepatitis C (HCV). Saudi Arabia is one of the endemic areas of viral hepatitis. Cryptogenic HCC is thought to arias from unknown causes of liver cancers. Thus, the purpose of this study was to find the prevalence of viral and cryptogenic HCC in King Abdulaziz Medical City-Riyadh (KAMC-R).Methods: A retrospective chart review was performed for all HCC patients diagnosed between 2010 to 2017 at KAMC-R. Information regarding age, gender, comorbidity, alcohol consumption, serology tests, liver enzymes, body mass index, model for end-stage liver disease score, alpha-fetoprotein and Child-Turcotte-Pugh score were included. The Chi-square test was used to determine the differences between categorical data. A p<0.05 was considered statistically significant.Results: Total of 294 patients with HCC charts were reviewed. HCV and HBV were found in 42.85% and 20.74% of the patients, respectively. Co-infection with HBV and HCV were reported in 1.7% whereas cryptogenic HCC was found in 32.65% of the patients. High BMI and DLP were noticeably higher in cryptogenic group (p=0.045 and p=0.022 respectively). Multiple lesions were noticed more in HCV group whereas single lesion was more in the cryptogenic group (p=0.0343). Also, large lesions (>5 cm) were remarkably found more in cryptogenic HCC whereas small lesions were more in HCV group (p=0.006).Conclusions: Hepatitis C was the major risk factor associated with HCC, followed by Cryptogenic HCC. High BMI and DLP were common features of cryptogenic HCC.
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Higgs, Martin R., Philippe Chouteau, and Hervé Lerat. "‘Liver let die’: oxidative DNA damage and hepatotropic viruses." Journal of General Virology 95, no. 5 (May 1, 2014): 991–1004. http://dx.doi.org/10.1099/vir.0.059485-0.
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Chronic infections by the hepatotropic viruses hepatitis B virus (HBV) and hepatitis C virus (HCV) are major risk factors for the development of hepatocellular carcinoma (HCC). It is estimated that more than 700 000 individuals per year die from HCC, and around 80 % of HCC is attributable to HBV or HCV infection. Despite the clear clinical importance of virus-associated HCC, the underlying molecular mechanisms remain largely elusive. Oxidative stress, in particular DNA lesions associated with oxidative damage, play a major contributory role in carcinogenesis, and are strongly linked to the development of many cancers, including HCC. A large body of evidence demonstrates that both HBV and HCV induce hepatic oxidative stress, with increased oxidative DNA damage being observed both in infected individuals and in murine models of infection. Here, we review the impact of HBV and HCV on the incidence and repair of oxidative DNA damage. We begin by giving a brief overview of oxidative stress and the repair of DNA lesions induced by oxidative stress. We then review in detail the evidence surrounding the mechanisms by which both viruses stimulate oxidative stress, before focusing on how the viral proteins themselves may perturb the cellular response to oxidative DNA damage, impacting upon genome stability and thus hepatocarcinogenesis.
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Hsiao, Yi-Wen, Lu-Ting Chiu, Ching-Hsuan Chen, Wei-Liang Shih, and Tzu-Pin Lu. "Tumor-Infiltrating Leukocyte Composition and Prognostic Power in Hepatitis B- and Hepatitis C-Related Hepatocellular Carcinomas." Genes 10, no. 8 (August 20, 2019): 630. http://dx.doi.org/10.3390/genes10080630.
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Background: Tumor-infiltrating leukocytes (TILs) are immune cells surrounding tumor cells, and several studies have shown that TILs are potential survival predictors in different cancers. However, few studies have dissected the differences between hepatitis B- and hepatitis C-related hepatocellular carcinoma (HBV−HCC and HCV−HCC). Therefore, we aimed to determine whether the abundance and composition of TILs are potential predictors for survival outcomes in HCC and which TILs are the most significant predictors. Methods: Two bioinformatics algorithms, ESTIMATE and CIBERSORT, were utilized to analyze the gene expression profiles from 6 datasets, from which the abundance of corresponding TILs was inferred. The ESTIMATE algorithm examined the overall abundance of TILs, whereas the CIBERSORT algorithm reported the relative abundance of 22 different TILs. Both HBV−HCC and HCV−HCC were analyzed. Results: The results indicated that the total abundance of TILs was higher in non-tumor tissue regardless of the HCC type. Alternatively, the specific TILs associated with overall survival (OS) and recurrence-free survival (RFS) varied between subtypes. For example, in HBV−HCC, plasma cells (hazard ratio [HR] = 1.05; 95% CI 1.00–1.10; p = 0.034) and activated dendritic cells (HR = 1.08; 95% CI 1.01–1.17; p = 0.03) were significantly associated with OS, whereas in HCV−HCC, monocytes (HR = 1.21) were significantly associated with OS. Furthermore, for RFS, CD8+ T cells (HR = 0.98) and M0 macrophages (HR = 1.02) were potential biomarkers in HBV−HCC, whereas neutrophils (HR = 1.01) were an independent predictor in HCV−HCC. Lastly, in both HBV−HCC and HCV−HCC, CD8+ T cells (HR = 0.97) and activated dendritic cells (HR = 1.09) had a significant association with OS, while γ delta T cells (HR = 1.04), monocytes (HR = 1.05), M0 macrophages (HR = 1.04), M1 macrophages (HR = 1.02), and activated dendritic cells (HR = 1.15) were highly associated with RFS. Conclusions: These findings demonstrated that TILs are potential survival predictors in HCC and different kinds of TILs are observed according to the virus type. Therefore, further investigations are warranted to elucidate the role of TILs in HCC, which may improve immunotherapy outcomes.
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Glitscher, Mirco, Eberhard Hildt, and Daniela Bender. "Hepatitis B und C: Mechanismen der virusinduzierten Leberpathogenese und Tumorentstehung." Bundesgesundheitsblatt - Gesundheitsforschung - Gesundheitsschutz 65, no. 2 (January 11, 2022): 228–37. http://dx.doi.org/10.1007/s00103-021-03482-y.
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ZusammenfassungDie Hepatitisviren B und C (HBV, HCV) sind weltweit die relevantesten viralen Auslöser einer chronischen Hepatitis (Leberentzündung). Derzeit leiden weltweit mehr als 250 Mio. Menschen an einer chronischen HBV-Infektion, jährlich versterben 0,8 Mio. an den Folgen. Von einer chronischen HCV-Infektion sind ca. 70 Mio. Menschen betroffen, es versterben ca. 1 Mio. im Jahr. Bisher steht nur für HBV eine zugelassene Impfung zur Verfügung. Chronische Infektionen mit HBV und HCV gehen mit einem erhöhten Risiko für die Entwicklung einer Leberfibrose, einer Leberzirrhose und eines hepatozellulären Karzinoms (HCC) einher.Diese Übersichtsarbeit beschreibt Mechanismen der HBV- und HCV-assoziierten Pathogenese. Im Vordergrund stehen dabei die Wechselwirkung der chronischen Infektion mit intrazellulären Signaltransduktionswegen, mit einzelnen Stoffwechselwegen, insbesondere dem Lipidmetabolismus, die Fibrose- und Zirrhoseentstehung im Laufe der chronischen Infektion sowie Mechanismen der virusinduzierten HCC-Entstehung.Trotz großer Fortschritte in der Charakterisierung der viralen Lebenszyklen und der Entwicklung robuster antiviraler Strategien bleiben Herausforderungen bestehen: u. a. die Gewinnung eines noch besseren Verständnisses der Mechanismen, die zur Entwicklung der virusassoziierten Pathogenese beitragen, sowie die Erforschung der Relevanz verschiedener Genotypen für Unterschiede in der Pathogenese.
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Minuk, Gerald Y., and J. Uhanova. "Viral Hepatitis in the Canadian Inuit and First Nations Populations." Canadian Journal of Gastroenterology 17, no. 12 (2003): 707–12. http://dx.doi.org/10.1155/2003/350175.
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OBJECTIVE: To review published prevalence data regarding hepatitis A (HAV), B (HBV) and C (HCV) in Canadian Inuit and First Nations populations.METHODS: PubMed database search and review of all papers describing data derived from seroepidemiological surveys.RESULTS: The prevalence of anti-HAV positivity in Canadian Inuit and First Nations populations reported to date is high (range 75% to 95%) and approximately three times that of non-Aboriginal Canadians residing in the same communities. Among the Canadian Inuit, the prevalence of HBV infection is approximately 5%, or 20 times that of non-Aboriginal Canadians, while the risk of exposure to HBV is 25%, or five times higher. Regarding the First Nations population, preliminary data suggest the prevalences of HBV infection (0.3% to 3%) and exposure (10% to 22%) are similar to rates in non-Aboriginals residing in the same regions and participating in similar high risk activities. Serological evidence of HCV infection (anti-HCV) is more common in the Canadian Inuit and First Nations (1% to 18%) than the remainder of the Canadian population (0.5% to 2%); however, viremia (HCV-RNA positivity) is less common (less than 5% versus 75% of anti-HCV positive individuals, respectively).CONCLUSIONS: Viral hepatitis is common in the Canadian Inuit and First Nations populations. In the absence of coexisting human immunodeficiency virus infection and alcohol abuse, the outcomes of HBV and HCV appear to be more benign than in non-Aboriginal Canadians.
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Schaer, Robert, Fernanda Anjos Bastos, Juçara Magalhães Simões, Juvenal Encarnação Silva, Soraya Castro Trindade, Roberto José Meyer Nascimento, Songeli Menezes Freire, and Maria Isabel Schinoni. "Seroprevalence of viral Hepatitis of enteric (A and E) and parenteral / sexual (B and C) transmission of individuals aged 30 to 70 residents in Salvador-Brazil." STUDIES IN HEALTH SCIENCES 3, no. 2 (May 19, 2022): 1095–111. http://dx.doi.org/10.54022/shsv3n2-037.
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Viral hepatitis are still considered as public health problems. Hepatitis caused by HAV and HEV, spread by enteric transmission are, acute infections associated with precarious basic sanitation, inappropriate hygiene and consumption of contaminated food. Hepatitis caused by HBV and HCV viruses transmitted by parenteral /sexual route are associated with chronic diseases and progression to cirrhosis and hepatocarcinoma OBJECTIVES: to estimate the seroprevalence of serological markers of hepatitis A, B, C and E hepatitis, the concomitance of enteric and parenteral / sexual transmission hepatitis in a population aged between 30-70 years and to observe possible relationships with sociodemographic data. METHODS: A cross-sectional study with 650 individuals born between 1945 and 1985 attended at a laboratory in the public health network of Salvador-Brazil. Serological tests included IgG anti-HAV, IgG anti-HEV, IgG anti-HBc, IgG anti-HCV. The volunteers answered a questionnaire containing questions about habits, conducts, previous medical procedures and sociodemographic data. RESULTS: 208 of the participants were men (32.00%) and 442 were women (68.0%) and in the groups younger than 31-50 years (301) and older individuals from 51 to 70 years (349). Seroprevalence of HVA (92.46%), HEV(2.15%), HBV (17.76%) and HCV (3.69%). Of the total population, the concomitant seroprevalence of Ig G anti-HAV and IgG anti-HEV (1.85%) and IgG anti-HBc and IgG anti-HCV (1.38%). With the epidemiological and sociodemographic data it is not possible to associate common risk factors for HAV and / or HEV contact in the study population, however, the association of HEV with the proximity of contact / management with swine reported by some participants can not be excluded. Seroprevalence of HBV and HCV was associated with unprotected sex, sharing of needles and syringes in the older group, and injecting drug use. The group of older and males had a higher prevalence of contact with B and C viruses. CONCLUSION: The contact markers that presented the highest seroprevalence were anti-HAV IgG, followed by the markers for HBV, HCV and HEV. The anti-HCV IgG marker presented a higher prevalence than in the general population and the HEV presented a low prevalence. The group of older individuals and male gender presented a higher seroprevalence of contact with HBV and HCV. Concomitant seroprevalence was low in both enteric and parenteral / sexual transmission hepatitis.
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Kee, Kwong-Ming, Chien-Hung Chen, Jui-Ting Hu, Yi-Hsiang Huang, Tsang-En Wang, Gar-Yang Chau, Kuo-Hsin Chen, et al. "Secular Trends of Clinical Characteristics and Survival of Hepatocellular Carcinoma in Taiwan from 2011 to 2019." Viruses 15, no. 1 (December 31, 2022): 126. http://dx.doi.org/10.3390/v15010126.
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Hepatocellular carcinoma (HCC) is a major cause of cancer death in Taiwan, and in the past 30–40 years, Taiwan has been committed to its prevention and treatment. We aimed to investigate the secular trends of characteristics and the survival of HCC in recent decades after making increased efforts. Between 2011 and 2019, a total of 73,817 cases were enrolled from the TCR database. The overall male-to-female ratio was 7/3. The overall, male and female mean ages increased from 63.8 to 66.1 years, 62.0 to 64.3 years and 68.3 to 70.4 years, respectively. After dividing by viral etiologies and gender, the mean age showed increasing trends in all subgroups. The proportions of HBV-HCC, HCV-HCC, HBV+HCV-HCC and Non-HBV+non-HCV-HCC were 48.3%, 25.2%, 5.3% and 21.3% in males, compared with 25.5%, 48.6%, 5.3% and 20.5% in females, respectively. The 5-year survival rates of BCLC stages 0, A, B, C and D were 70%, 58%, 34%, 11% and 4%, respectively. The proportion of BCLC stage 0 increased from 6.2% to 11.3%. Multivariate analysis showed that being female, older age, diagnostic year, BCLC stages, hospital level, body mass index, smoking, alcohol consumption, AFP, Child–Pugh classification and HBV/HCV status were independent predictors for survival. In recent decades, the overall survival of HCC in Taiwan has been improving and might be partly associated with increased BCLC 0 and Child–Pugh A patients, while with the consequent age of patients increasing over time. The proportion of viral-related HCC is decreasing, while nonviral-related HCC is increasing.
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Russo, Francesco Paolo, Alberto Zanetto, Elisa Pinto, Sara Battistella, Barbara Penzo, Patrizia Burra, and Fabio Farinati. "Hepatocellular Carcinoma in Chronic Viral Hepatitis: Where Do We Stand?" International Journal of Molecular Sciences 23, no. 1 (January 2, 2022): 500. http://dx.doi.org/10.3390/ijms23010500.
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Hepatocellular carcinoma (HCC) is one of the major causes of cancer-related death. Although the burden of alcohol- and NASH-related HCC is growing, chronic viral hepatitis (HBV and HCV) remains a major cause of HCC development worldwide. The pathophysiology of viral-related HCC includes liver inflammation, oxidative stress, and deregulation of cell signaling pathways. HBV is particularly oncogenic because, contrary to HCV, integrates in the cell DNA and persists despite virological suppression by nucleotide analogues. Surveillance by six-month ultrasound is recommended in patients with cirrhosis and in “high-risk” patients with chronic HBV infection. Antiviral therapy reduces the risks of development and recurrence of HCC; however, patients with advanced chronic liver disease remain at risk of HCC despite virological suppression/cure and should therefore continue surveillance. Multiple scores have been developed in patients with chronic hepatitis B to predict the risk of HCC development and may be used to stratify individual patient’s risk. In patients with HCV-related liver disease who achieve sustained virological response by direct acting antivirals, there is a strong need for markers/scores to predict long-term risk of HCC. In this review, we discuss the most recent advances regarding viral-related HCC.
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Zaki, Marco Y. W., Ahmed M. Fathi, Samara Samir, Nardeen Eldafashi, Kerolis Y. William, Maiiada Hassan Nazmy, Moustafa Fathy, Upkar S. Gill, and Shishir Shetty. "Innate and Adaptive Immunopathogeneses in Viral Hepatitis; Crucial Determinants of Hepatocellular Carcinoma." Cancers 14, no. 5 (February 28, 2022): 1255. http://dx.doi.org/10.3390/cancers14051255.
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Viral hepatitis B (HBV) and hepatitis C (HCV) infections remain the most common risk factors for the development of hepatocellular carcinoma (HCC), and their heterogeneous distribution influences the global prevalence of this common type of liver cancer. Typical hepatitis infection elicits various immune responses within the liver microenvironment, and viral persistence induces chronic liver inflammation and carcinogenesis. HBV is directly mutagenic but can also cause low-grade liver inflammation characterized by episodes of intermittent high-grade liver inflammation, liver fibrosis, and cirrhosis, which can progress to decompensated liver disease and HCC. Equally, the absence of key innate and adaptive immune responses in chronic HCV infection dampens viral eradication and induces an exhausted and immunosuppressive liver niche that favors HCC development and progression. The objectives of this review are to (i) discuss the epidemiological pattern of HBV and HCV infections, (ii) understand the host immune response to acute and chronic viral hepatitis, and (iii) explore the link between this diseased immune environment and the development and progression of HCC in preclinical models and HCC patients.
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Wang, Ling, Jiabao Geng, Jie Li, Tong Li, Akira Matsumori, Yibin Chang, Fengmin Lu, and Hui Zhuang. "The biomarker N-terminal pro-brain natriuretic peptide and liver diseases." Clinical & Investigative Medicine 34, no. 1 (February 1, 2011): 30. http://dx.doi.org/10.25011/cim.v34i1.14910.
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Purpose: NT-proBNP has emerged as a powerful diagnostic and prognostic biomarker in heart disease. Studies showed that NT-proBNP is a sensitive biomarker for identifying patients with heart failure caused by hepatitis C virus (HCV) related myocarditis. The purpose of this study was to evaluate the correlation between the serum concentration of NT-proBNP and hepatitis virus infection/liver disease. Methods: 223 serum samples from blood donors (aged 19~50 years old) were collected as a control group, and 644 samples were obtained from patients infected by hepatitis viruses including 493 HBV: 364 chronic hepatitis (CH), 86 hepatocellular carcinoma (HCC) and 43 liver cirrhosis (LC) and 151 HCV (85 CH, 14 HCC, 52 LC). All samples were assayed with an Elecsys immunoassay analyzer for NT-proBNP concentration. Results: The mean concentration of NT-proBNP in the control group was 21.77 pg/ml and showed no significant variation with either age or gender. Both the mean value and the rate of abnormality of NT-proBNP were significantly higher for the HBV- and HCV-infected groups in comparison with the control group. The mean NT-proBNP value (380.24 pg/ml) and abnormality rate (38.41%) in the HCV group were higher than that of the HBV group. For samples from patients with HBV/HCV-related hepatic disease/pathology, the mean NT-proBNP value (517.19 pg/ml/597.18 pg/ml) were the highest in the liver cirrhosis group. Conclusions: Hepatic pathologic lesions, particularly cirrhosis, may contribute to the elevation of NT-proBNP in subjects with HBV/HCV infection.
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Samson, Adel, Matthew J. Bentham, Karen Scott, Gerard Nuovo, Abigail Bloy, Elizabeth Appleton, Robert A. Adair, et al. "Oncolytic reovirus as a combined antiviral and anti-tumour agent for the treatment of liver cancer." Gut 67, no. 3 (November 15, 2016): 562–73. http://dx.doi.org/10.1136/gutjnl-2016-312009.
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ObjectiveOncolytic viruses (OVs) represent promising, proinflammatory cancer treatments. Here, we explored whether OV-induced innate immune responses could simultaneously inhibit HCV while suppressing hepatocellular carcinoma (HCC). Furthermore, we extended this exemplar to other models of virus-associated cancer.Design and resultsClinical grade oncolytic orthoreovirus (Reo) elicited innate immune activation within primary human liver tissue in the absence of cytotoxicity and independently of viral genome replication. As well as achieving therapy in preclinical models of HCC through the activation of innate degranulating immune cells, Reo-induced cytokine responses efficiently suppressed HCV replication both in vitro and in vivo. Furthermore, Reo-induced innate responses were also effective against models of HBV-associated HCC, as well as an alternative endogenous model of Epstein–Barr virus-associated lymphoma. Interestingly, Reo appeared superior to the majority of OVs in its ability to elicit innate inflammatory responses from primary liver tissue.ConclusionsWe propose that Reo and other select proinflammatory OV may be used in the treatment of multiple cancers associated with oncogenic virus infections, simultaneously reducing both virus-associated oncogenic drive and tumour burden. In the case of HCV-associated HCC (HCV-HCC), Reo should be considered as an alternative agent to supplement and support current HCV-HCC therapies, particularly in those countries where access to new HCV antiviral treatments may be limited.
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Brogden, Ruth, Su Wang, and Binghong Xu. "Finding the missing millions: Integrating automated viral hepatitis screening in a hospital with care and treatment in a primary care setting." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 108. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.108.
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108 Background: Rates of hepatocellular carcinoma (HCC) are rising in the US. Patients at Saint Barnabas Medical Cancer Center (SBMC) present with late-stage HCC at higher rates (29%) compared to the national (16%). Chronic Hepatitis C (HCV) and Hepatitis B (HBV) are major drivers of liver cancer, yet screening rates are low. Finding these missing millions is important to reducing rates of HCC. An automated emergency department (ED) viral hepatitis (VH) screening program was initiated in 2018 at SBMC. In January 2020, it was expanded to the inpatient setting and HCV screening was modified from cohort screening (those born in 1945-65) to a one time test for anybody 18 years or over, per updated Centers for Disease Control (CDC) and USPSTF (US Preventive Services Taskforce) recommendations. Methods: The electronic medical record (EMR) was modified to automate screening. HBV testing is triggered by a patient’s country of birth or race, and HCV testing is triggered by age over 18 and no previous testing. The automated HCV (HCV Ab with reflex to HCV RNA) or HBV (HBsAg) lab orders lead to an EMR notification to the nurses of patient eligibility and education is provided to patients. Alerts of positive results are sent to nursing staff, physicians, and the patient navigator (PN). The PN is sent a real-time secure text message and works individually with patients to arrange linkage-to-care (LTC) for evaluation and treatment. Results: From March 2018 - December 2020, 44,002 patients were screened for HCV and 884 (2.0%) were HCVAb+ and 242 (0.55%) HCV RNA+. For HBV, 21,328 patients were screened and 212 (0.99%) were HBsAg+. The expanded screenings accounted for 8,716 (19.8%) of the total HCV screenings. Individuals born outside the 1945-65 birth cohort (younger and older) made up 76.2% of those screened and 41% of the infected. The top 3 countries for HBV screenings were Haiti, Jamaica, and Ecuador. LTC rates, defined as attending first medical appointment or already in care, were 86.8% for HCV and 85.4% for HBV. Of those linked to care, 43 HCV+ patients were seen at a outpatient primary care practice part of SBMC, and of those, 39 initiated HCV cure therapy and 33 were cured (confirmed sustained virologic response at 12 weeks), and 35 HBV+ patients were seen and 6 initiated treatment. Conclusions: This automated program for VH has led to a significant scale up of screening with successful LTC and treatment of patients. Expansion to universal screening of all adults and to the inpatient setting found additional viral hepatitis patients who would have otherwise been missed. In addition to the automated screening, a multidisciplinary team including internists, pharmacists, and patient navigators were part of creating a primary care based program. Integration of viral hepatitis screening and care in a hospital system can be initial steps towards establishing liver cancer prevention program.