Anti-delta antibody in primary hepatocellular carcinoma patients in the gizan area of saudi arabia

Sj, Ashraf; Sc, Arya; Cm, Parande; Sahay, Ravi; Ar, Ageel

doi:10.1007/bf01644273

Cited by 8 publications

(4 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Early reports suggested that HDV/HBV dual infection may increase the hepatocarcinogenic potential of chronic HBV infection alone . But other studies at that time failed to show an increased risk of HCC in individuals with dual infection . Moreover, in parts of sub‐Saharan Africa where high rates of HBV/DHV co‐infection were recorded in Black patients with HCC, equally high rates of dual infection were present in healthy controls .…”

Section: Hepatitis Delta Virusmentioning

confidence: 99%

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

Kew

2012

Journal of Viral Hepatitis

View full text Add to dashboard Cite

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.

show abstract

Section: Hepatitis Delta Virusmentioning

confidence: 99%

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

Kew

2012

Journal of Viral Hepatitis

View full text Add to dashboard Cite

show abstract

“…The M2 Autoantigens of Primary Biliary Cirrhosis Are Not Subunits of the Mitochondria1 which is claimed to contain the M2 antigenic proteins as the standard preparation for use in the serologic diagnosis of PBC. The M2 antigens have been suggested previously to be subunits of the mitochondrial H+-AT-Pase on the basis of the reactivity observed between an F,-ATPase (the hydrophilic catalytic sector of the enzyme complex) preparation and the anti-M2 antibodies of PBC (2)(3)(4)(5). Although more recent studies (6; Namih-isa, T., Ishii, H., Hepatology 1988; 8201, Correspondence) utilizing two-dimensional gel electrophoresis (first dimension: isoelectric focusing; second dimension: electrophoresis in sodium dodecyl sulfate-polyacrylamide gel) show clearly that the M2 antigens are neither the anor the 0-subunits of the ATPase complex, the association of the M2 antigens with the enzyme complex is still cited, thereby leading to the term "ATPase-associated antigen."…”

Section: S C Arya Mbbs Phd M-122 (Of Part 2) Greater Kailash-iimentioning

confidence: 99%

“…The significantly elevated antidelta IgG prevalence of 67% among 15 primary hepatocellular carcinoma (PHC) patients in Jordan, an area with a 10% prevalence of HBsAg (l), should not appear all that alarming, even if the earlier reports elsewhere failed to establish a definite role of delta infection in the pathogenesis of PHC. Significantly elevated antidelta prevalence in PHC was reported in 1985 and 1986 among the Bedouin and urban dwelling Saudi population domiciled in the Gizan Area of Saudi Arabia (2,3). This area, located southwest of Riyadh along the Red Sea and bordering North Yemen, had a 12.7% HBsAg prevalence in the population (2, 3).…”

mentioning

confidence: 99%

Hepatitis delta virus and primary hepatocellular carcinoma in jordan

Sc¹

1988

Hepatology

Self Cite

View full text Add to dashboard Cite

“…with chronic HDV infection [1][2][3][4][5][6][7]. The more rapid evolution of liver damage in patients infected with HOV, and hence an increased number of deaths secondary to end-stage cirrhosis rather than to HCC, may have accounted for such fmdings.…”

Section: Introductionmentioning

confidence: 99%

Relationship between hepatocyte proliferation and hepatitis delta virus replication in neoplastic and non‐neoplastic liver tissues

Negro¹,

Papotti

Taraglio

et al. 1997

Journal of Viral Hepatitis

View full text Add to dashboard Cite

We studied the relationship between hepatocyte proliferation and hepatitis delta virus (HDV) replication at the single cell level. The proliferating cell nuclear antigen (PCNA) (by immunohistochemistry) and the HDV RNA (by in situ hybridization) were stained in neoplastic and non-neoplastic liver tissues of 19 patients with chronic HDV infection, including four cases of cirrhosis with superimposed hepatocellular carcinoma (HCC). As controls, we assessed the hepatocyte proliferation of liver tissues from 16 patients with chronic hepatitis B and on three normal livers. The hepatocyte PCNA labelling index of HDV-infected tissues was comparable with that seen in chronic hepatitis B-infected livers but was significantly higher than that observed in normal livers. Although cirrhotic tissues had lower hepatocyte proliferating fractions than non-cirrhotic tissues, the difference was not statistically significant. The hepatocyte proliferation rate did not correlate with the level of intrahepatic HDV replication or with the histological activity. In double-labelling experiments, PCNA and HDV RNA staining did not co-localize, with the exception of two of three cirrhotic tissues associated with HCC, where the association between the two markers was statistically significant. This co-localization was not observed, however, in the adjacent tumorous tissues. In patients with chronic HDV infection the hepatocyte proliferation was increased with respect to normal liver tissue, but was comparable with that observed in patients with chronic hepatitis B virus infection and did not correlate with the level of HDV replication or the histological activity. In the cirrhotic tissue of patients with HCC (but not in the tumour counterpart), HDV RNA may occasionally co-localize with the marker of hepatocyte proliferation. Whether this association between viral replication and cell division is related to liver carcinogenesis remains to be established.

show abstract

Anti-delta antibody in primary hepatocellular carcinoma patients in the gizan area of saudi arabia

Cited by 8 publications

References 4 publications

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

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

Hepatitis delta virus and primary hepatocellular carcinoma in jordan

Relationship between hepatocyte proliferation and hepatitis delta virus replication in neoplastic and non‐neoplastic liver tissues

Contact Info

Product

Resources

About