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• W3087687718 abstract "The role of HDV infection in hepatocarcinogenesis remains a topic of debate and HDV is currently considered “not classifiable as to its carcinogenicity to humans” by the International Agency for Research on Cancer.[1]Hepatitis Viruses. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. 59. International Agency for Research on Cancer, Lyon (FR)1994Google Scholar Relatively few HBV carriers are coinfected with HDV,[2]Puigvehi M. Moctezuma-Velazquez C. Villanueva A. Llovet J.M. The oncogenic role of hepatitis delta virus in hepatocellular carcinoma.JHEP Rep. 2019; 1: 120-130Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar therefore, single studies on HDV and hepatocellular carcinoma (HCC) are often underpowered to assess this association.[3]Hill A.B. The environment and disease: association or causation?.Proc R Soc Med. 1965; 58: 295-300PubMed Google Scholar In such situations, a meta-analysis or pooled analysis may be useful. A meta-analysis combines weighted association estimates (e.g. odds ratios [ORs]) from different studies, while a pooled analysis combines data from individual studies and analyses them as if derived from a single sample.[4]Bravata D.M. Olkin I. Simple pooling versus combining in meta-analysis.Eval Health Prof. 2001; 24: 218-230Crossref PubMed Scopus (98) Google Scholar We, therefore, read with great interest the paper by Alfaiate et al. that pooled data from 93 studies to assess the relationship between HDV and HCC.[5]Alfaiate D. Clement S. Gomes D. Goossens N. Negro F. Chronic hepatitis D and hepatocellular carcinoma: a systematic review and meta-analysis of observational studies.J Hepatol. 2020; 73: 533-539Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar The authors report that coinfection with HDV was significantly associated with increased risk of HCC compared to infection with HBV alone, however, the OR was modest (1.28). In epidemiological studies, the effect magnitude helps one assess if a true causal association exists.[3]Hill A.B. The environment and disease: association or causation?.Proc R Soc Med. 1965; 58: 295-300PubMed Google Scholar While we commend the authors on addressing an important question, this analysis may greatly underestimate the true effect of HDV infection on HCC risk. HDV does not integrate into the human genome, therefore a direct oncogenic effect is unlikely.[2]Puigvehi M. Moctezuma-Velazquez C. Villanueva A. Llovet J.M. The oncogenic role of hepatitis delta virus in hepatocellular carcinoma.JHEP Rep. 2019; 1: 120-130Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar HBV/HDV coinfection results in greater liver inflammation than HBV monoinfection, leading to accelerated development of cirrhosis and likely to HCC.[2]Puigvehi M. Moctezuma-Velazquez C. Villanueva A. Llovet J.M. The oncogenic role of hepatitis delta virus in hepatocellular carcinoma.JHEP Rep. 2019; 1: 120-130Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar Cirrhosis and HCC are considered final stages of HDV-associated liver disease and many patients with HCC also have cirrhosis.[2]Puigvehi M. Moctezuma-Velazquez C. Villanueva A. Llovet J.M. The oncogenic role of hepatitis delta virus in hepatocellular carcinoma.JHEP Rep. 2019; 1: 120-130Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar If cirrhosis and HCC are related outcomes resulting from hepatic inflammation, patients with cirrhosis are not an appropriate comparison group for examining HDV-associated hepatocarcinogenesis. Nevertheless, in addressing whether HBV/HDV coinfection increases the risk of HCC compared to HBV infection alone, Alfaiate et al. included patients with cirrhosis amongst the controls. The analysis by Alfaiate et al. included data from our previous evaluation of the association between HBV/HDV coinfection and the risk HCC or cirrhosis among patients enrolled in The Gambia Liver Cancer Study.[6]Mahale P. Aka P. Chen X. Pfeiffer R.M. Liu P. Groover S. et al.Hepatitis D virus infection, cirrhosis and hepatocellular carcinoma in the Gambia.J Viral Hepat. 2019; 26: 738-749Crossref PubMed Scopus (10) Google Scholar There were 2 case groups in our study: individuals with HCC (with or without cirrhosis); individuals with cirrhosis alone. Controls were patients at the enrolling hospitals who had no clinical evidence of liver disease (NLD). No NLD control was infected with HDV (Table 1), therefore, although the association between HDV infection and HCC in our study was strong and statistically significant, it could not be quantified (OR = ∞; 95% CI 1.31 to ∞) and the same was true for the association between HDV and cirrhosis (OR = ∞; 95% CI 2.05 to ∞). We welcome the inclusion of these data in a larger analysis, however, in pooling our data with those from other studies Alfaiate et al. combined the 61 cirrhotic cases with the 80 NLD controls, yielding a weak, non-significant association (OR = 1.50; 95% CI 0.54–4.17; Table 1) that does not reflect the true relationship between HDV and HCC in our study. The problem with categorizing patients with cirrhosis as controls is illustrated by additional hypothetical results that we calculated, which show that the number of cirrhotic cases enrolled would determine the OR for the association between HDV and HCC (Table 1).Table 1Odds ratios and 95% confidence intervals (CI) for the association between HDV infection and hepatocellular carcinoma in The Gambia Liver Cancer Study.ExposureIndividualsOdds ratio(95% CI)HCC casesCirrhosis casesNLD controlsHCC cases vs. NLD controlsHCC cases vs. cirrhosis cases and NLD controlsMahale, et al.[6]Mahale P. Aka P. Chen X. Pfeiffer R.M. Liu P. Groover S. et al.Hepatitis D virus infection, cirrhosis and hepatocellular carcinoma in the Gambia.J Viral Hepat. 2019; 26: 738-749Crossref PubMed Scopus (10) Google ScholarAlfaiate, et al.[5]Alfaiate D. Clement S. Gomes D. Goossens N. Negro F. Chronic hepatitis D and hepatocellular carcinoma: a systematic review and meta-analysis of observational studies.J Hepatol. 2020; 73: 533-539Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar HBV+/HDV+1160∞1.50 HBV+/HDV−1726180(1.31 to ∞)(0.54–4.17)Hypothetical data with variable numbers of cirrhosis casesNumber of cirrhosis cases doubled HBV+/HDV+111201.08 HBV+/HDV−17212280Number of cirrhosis cases tripled HBV+/HDV+111800.93 HBV+/HDV−17218380Number of LC cases halved HBV+/HDV+11302.35 HBV+/HDV−1723080Based on definition of the comparison group and variable numbers of individuals with cirrhosis. HCC, hepatocellular carcinoma, NLD, no clinical evidence of liver disease. Open table in a new tab Based on definition of the comparison group and variable numbers of individuals with cirrhosis. HCC, hepatocellular carcinoma, NLD, no clinical evidence of liver disease. This issue does not appear to be limited to our data. In incorporating data from a study by Makhlouf et al.[7]Makhlouf N.A. Morsy K.H. Mahmoud A.A. Hepatitis D virus infection among hepatitis B virus surface antigen positive individuals in Upper Egypt: prevalence and clinical features.J Infect Public Health. 2019; 12: 350-356Crossref PubMed Scopus (9) Google Scholar into the pooled analysis, Alfaiate et al. included individuals with cirrhosis in the comparison group, which, by our estimate, reduces the OR for the association between HDV and HCC in that study from 3.31 to 2.16. All told, 59 of the 93 (63.4%) studies in the analysis included patients with cirrhosis in the comparison group (Table S6),[5]Alfaiate D. Clement S. Gomes D. Goossens N. Negro F. Chronic hepatitis D and hepatocellular carcinoma: a systematic review and meta-analysis of observational studies.J Hepatol. 2020; 73: 533-539Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar which may have greatly reduced the strength of the observed association between HDV infection and HCC. The magnitude of this association has important epidemiological and clinical implications. Criteria for causation posit that the strength of an association is one of the determinants to consider when assessing whether a causal relationship exists between a proposed etiological factor and an outcome.[3]Hill A.B. The environment and disease: association or causation?.Proc R Soc Med. 1965; 58: 295-300PubMed Google Scholar An OR of 1.28 provides modest support for classifying HDV as a carcinogen. This apparently attenuated OR also weakens the attributable risk of HDV infection on HCC[8]Rockhill B. Newman B. Weinberg C. Use and misuse of population attributable fractions.Am J Public Health. 1998; 88: 15-19Crossref PubMed Scopus (1245) Google Scholar and, therefore, the proportion of HCC cases that might be prevented by successful treatment of HDV infection with potentially more efficacious drugs for HDV infection on the horizon.[9]Asselah T. Loureiro D. Tout I. Castelnau C. Boyer N. Marcellin P. et al.Future treatments for hepatitis delta virus infection.Liver Int. 2020; 40: 54-60Crossref PubMed Scopus (22) Google Scholar Including patients with cirrhosis in the control group is inconsistent with the biological mechanisms through which HDV infection leads to HCC and yields an erroneously weaker estimate of the effect of HDV infection on HCC risk. We urge the investigators to re-analyze these data to generate results that more accurately reflect the true association between HDV infection and the risk of HCC. This research was supported by the Intramural Research Program of the National Institutes of Health ( National Cancer Institute , Division of Cancer Epidemiology and Genetics). I.A., P.A., J.K., and T.R.O'B. conceptualized the manuscript. I.A. and T.R.O'B. drafted the manuscript. All authors participated in the revision of the manuscript. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. The authors declare no conflicts of interest that pertain to this work. Please refer to the accompanying ICMJE disclosure forms for further details. Download .pdf (.18 MB) Help with pdf files disclosures.pdf Chronic hepatitis D and hepatocellular carcinoma: A systematic review and meta-analysis of observational studiesJournal of HepatologyVol. 73Issue 3PreviewChronic hepatitis D (CHD) is the most severe form of chronic viral hepatitis but its role in the development of hepatocellular carcinoma (HCC) remains debated. We conducted a systematic review and meta-analysis of epidemiological studies to examine whether CHD is associated with an increased risk of HCC. Full-Text PDF Reply to: “Cirrhotic controls in a pooled analysis of hepatitis D and hepatocellular carcinoma”Journal of HepatologyVol. 73Issue 6PreviewWe appreciate Argirion et al.'s interest on our paper. We agree that the overall odds ratio of 1.28 underestimates the real impact of HDV superinfection on oncogenesis. We would like to point out, however, that this figure is the consequence of including a great deal of studies of weak quality. When the data quality is assured by a robust study design – such as in prospective cohort studies – the OR is significantly increased, suggesting that HDV may indeed be a potent carcinogen. Full-Text PDF" @default.
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