Outcome of chronic hepatitis delta in Italy: A long-term cohort study

Niro, G.A.; Smedile, Antonina; Ippolito, A.; Ciancio, Alessia; Fontana, R.; Olivero, Antonella; Gioffreda, Domenica; Abate, Maria Lorena; Valvano, R.; Andriulli, Angelo; Rizzetto, M.

doi:10.1016/j.dld.2008.12.071

Cited by 10 publications

(14 citation statements)

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“…However, diagnosis of active HDV infection may be difficult, as HDV RNA assays are not standardised and HDV antigen and IgM anti-HDV assays are not widely available [174,175]. Persistent HDV replication leads to cirrhosis and HCC at annual rates of 4% and 2.8% and is the most important predictor of mortality evidencing the need of antiviral therapy [173,176,177].…”

Section: Hdv Co-infected Patientsmentioning

confidence: 99%

EASL Clinical Practice Guidelines: Management of chronic hepatitis B virus infection

2012

Journal of Hepatology

2,626

1,266

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Section: Hdv Co-infected Patientsmentioning

confidence: 99%

EASL Clinical Practice Guidelines: Management of chronic hepatitis B virus infection

2012

Journal of Hepatology

2,626

1,266

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“…Due to the seriousness of HDV‐related liver disease, accurate assessment of disease stage (fibrosis) is critical because of prognostic implications related to progressive liver disease leading to cirrhosis, portal hypertensive sequelae, mortality and HCC . Additionally, staging of liver in HDV plays an important part in determining the need for nucleos(t)ide analog therapy to treat the concomitant HBV infection, eligibility for pegylated‐interferon or an investigational therapy through a clinical trial, and the need to consider referral to a transplant center …”

Section: Introductionmentioning

confidence: 99%

Vibration‐controlled transient elastography for the detection of cirrhosis in chronic hepatitis D infection

Surana

Takyar

et al. 2019

Journal of Viral Hepatitis

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Noninvasive detection of cirrhosis via vibration‐controlled transient elastography (VCTE) has revolutionized the management of chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infection. However, VCTE has not been studied in chronic hepatitis D virus (HDV) infection and accuracy remains in question due to the significant hepatic inflammation associated with this infection. Consecutive HBV, HCV and HDV patients who underwent VCTE (2006‐2019) were evaluated. Diagnosis of cirrhosis was made via liver biopsy or clinical findings. VCTE was compared with other noninvasive serum fibrosis tests using AUROC curves. The performance of VCTE in HBV/HCV/HDV was also compared. We evaluated 319 patients (HBV‐112; HCV‐132; HDV‐75), 278(87%) patients had histology for evaluation. HDV patients had evidence of higher hepatic inflammation as evidence by aspartate aminotransferase, alanine aminotransferase and histology activity index. Cirrhotic HDV patients had higher mean liver stiffness measurements compared with noncirrhotic patients (29.0 vs 8.3 kPa, P < .0001). VCTE demonstrated excellent diagnostic accuracy for the detection of cirrhosis with an AUROC of 0.90 compared with APRI (0.83), FIB‐4 (0.88), AAR (0.73) and RPR (0.85). Performance of VCTE in HDV was comparable with HBV (0.93) and HCV (0.94). At the optimized cut‐off value of ≥14.0 kPa for determining cirrhosis in HDV, VCTE had a sensitivity of 0.78, specificity of 0.86, NPV of 0.93 and PPV of 0.64. Hence, VCTE is a useful noninvasive test in HDV for determining cirrhosis despite the presence of significant hepatic inflammation.

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“…HDV replication was also the only predictor of liver‐related mortality . In another Italian study, 9% of the patients co‐infected with HBV and HDV, and 13% of those with cirrhosis, developed HCC during a 10‐year follow‐up .…”

Section: Hepatitis Delta Virusmentioning

confidence: 93%

“…The association between HDV and HBV in humans almost always results from superinfection of individuals already infected with the latter by the former, with a small percentage only of persons resulting from simultaneous infection with the two viruses. Chronic HDV/HBV hepatitis runs a more severe course than that resulting from chronic HBV infection alone, with progression to cirrhosis being both more likely and more rapid (within two years of the onset of the co‐infection, and about 15 years earlier than those with HBV infection alone) . Although it was originally believed that the presence of HDV suppressed HBV replication, a recent study has shown a high degree of fluctuating replicative activity of either or both viruses .…”

Section: Hepatitis Delta Virusmentioning

confidence: 99%

“…The prevalence of active HBV replication is low (and that of anti‐HBe is high) in dual‐infected patients, as indicated by the detection of HBsAg and/or HBVDNA in a small proportion only (about 10%) of the patients tested . Treatment of HDV/HBV infection remains unsatisfactory, with a sustained HDV RNA clearance with pegylated interferon‐α occurring in approximately one‐quarter of patients only .…”

Section: Hepatitis Delta Virusmentioning

confidence: 99%

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Hepatitis viruses (other than hepatitis B and C viruses) as causes of hepatocellular carcinoma: an update

Kew

2012

Journal of Viral Hepatitis

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Chronic hepatitis B and C virus infections are universally accepted as causes of hepatocellular carcinoma in humans. Hepatitis A and E viruses cause only acute self-limiting infections of the liver. Of the remaining hepatitis viruses - Delta hepatitis, hepatitis G (GB-C), TT and SEN - all have at some time been incriminated as causes of hepatocellular carcinoma. Delta hepatitis virus requires helper functions from hepatitis B virus to become invasive. Chronic Delta/hepatitis B viral co-infection runs a more severe course than that resulting from chronic hepatitis B virus infection alone, with progression to cirrhosis being more likely and more rapid. A substantial majority of the early studies did not find an increased incidence of hepatocellular carcinoma in co-infected individuals. But more recently, an increased incidence of the tumour has been recorded more often than no increase. Further studies are needed to draw a firm conclusion with regard to the hepatocarcinogenic effect of dual Delta/hepatitis B virus co-infection. With one exception, no published study (of 13) has incriminated chronic infection with hepatitis G virus as a cause of hepatocellular carcinoma. The dissenting study, published in 1999, was the only one performed in the United States. Fewer studies of the hepatocarcinogenic effect of TT virus have been performed. Apart from one study, published in 1999, no convincing evidence is available that supports a causal role for TT virus in hepatocarcinogenesis. The exception was in Japanese patients with high hepatitis C viral loads but independent of chronic hepatitis C virus infection. No evidence has been produced to indicate that SEN virus causes hepatocellular carcinoma.

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Outcome of chronic hepatitis delta in Italy: A long-term cohort study

Cited by 10 publications

References 0 publications

EASL Clinical Practice Guidelines: Management of chronic hepatitis B virus infection

EASL Clinical Practice Guidelines: Management of chronic hepatitis B virus infection

Vibration‐controlled transient elastography for the detection of cirrhosis in chronic hepatitis D infection

Hepatitis viruses (other than hepatitis B and C viruses) as causes of hepatocellular carcinoma: an update

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