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Delta Infection in Hepatocellular Carcinoma Positive for Hepatitis B Surface Antigen

GIOVANNI RAIMONDO, M.D.; ANTONIO CRAXI, M.D.; GIUSEPPE LONGO, M.D.; GANDOLFO GIANNUOLI, M.D.; MARIA CALTAGIRONE, M.D.; MARCELLO ARAGONA, M.D.; GABRIELLA PECORARO, M.D.; GIUSEPPE SQUADRITO, M.D.; and LUIGI PAGLIARO, M.D.
[+] Article and Author Information

Grant support: in part by grants from Consiglio Nazionale delle Ricerche and Ministero della Pubblica Istruzione, Italy.

Presented in part in June 1983 at the International Symposium on Viral Hepatitis, Turin, Italy.

▸Requests for reprints should be addressed to Antonio Craxi, M.D.; Clinica Medica R, c/o Divisione di Medicina Interna, Ospedale V. Cervello, Via Trabucco n° 180; 90146 Palermo, Italy.


University of Messina, Messina, Italy; and the University of PalermoPalermo, Italy.


Ann Intern Med. 1984;101(3):343-344. doi:10.7326/0003-4819-101-3-343
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This excerpt has been provided in the absence of an abstract.

Chronic hepatitis B virus infection plays a major etio-logic role in hepatocellular carcinoma (1). In southern Italy, where the hepatitis B surface antigen (HBsAg) carrier status has an intermediate prevalence between high- and low-risk areas (2), hepatitis B virus has been confirmed as the main risk factor for hepatocellular carcinoma (3). In the same region superinfection of HBsAg carriers with the delta agent, a defective virus requiring helper functions of hepatitis B virus, is widespread and closely associated with chronic active liver disease (4). The prevalence of markers of delta infection in patients with HBsAg-positive hepatocellular carcinoma was compared to

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