Increased incidence of hepatocellular carcinoma (HCC) in HIV-1 infected patients

Murillas, Javier; Rio, Manuel Del; Riera, Melchor; Vaquer, P; Salas, Ana; Leyes, María; Ribas, Montse; Vera, María Peñaranda; Villalonga, C

doi:10.1016/j.ejim.2004.09.011

Cited by 32 publications

(27 citation statements)

References 13 publications

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“…Although clearly linked to chronic HBV and HCV infection in other populations, hepatocellular carcinoma (HCC) was simply not frequently observed in early HIV cohort studies, many of which were conducted prior to the introduction of potent ART. In the second decade of highly effective ART, several studies suggest that HCC may be increasing in HIV-infected persons, particularly in those co-infected with hepatitis C [11][12][13][14][15][16]. In this issue of the Journal, the study by Salmon et al, [17] reports that in France, the proportion of liver-related deaths due to hepatocellular carcinoma increased from 15% in 2000 to 25% in 2005 with underlying HCV infection in the majority (HCV/HIV, 69% and HCV/HBV/HIV, 11%) of deaths due to HCC whereas HBV was the sole risk factor in only 17% of cases.…”

mentioning

confidence: 99%

Hepatocellular carcinoma in HIV-infected patients comes of age: The convergence of epidemiology and treatment effectiveness

Sulkowski

2009

Journal of Hepatology

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confidence: 99%

Hepatocellular carcinoma in HIV-infected patients comes of age: The convergence of epidemiology and treatment effectiveness

Sulkowski

2009

Journal of Hepatology

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“…The prevalence of HCV infection among HIVpositive patients averages about 35% in the United States and Europe, but in clinical populations where there is a great prevalence of i.v. drug use as a risk factor for acquiring HIV, this value may be as high as 80% to 90% (18). HIV/HCVcoinfected patients with ongoing HIV viremia have a faster rate of HCV-related liver fibrosis progression and a more rapid progression to liver failure or hepatocellular carcinoma than HCV-monoinfected persons.…”

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confidence: 99%

Evaluation of Antitumoral Properties of the Protease Inhibitor Indinavir in a Murine Model of Hepatocarcinoma

Esposito

Palescandolo

Spugnini³

et al. 2006

Clinical Cancer Research

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Purpose: Accumulating evidences show a higher incidence of hepatic neoplasm in HIV/ hepatitis C virus (HCV)^coinfected individuals compared with HCV-monoinfected patients. Treatment with HIV-1 protease inhibitors inhibited cancer-promoted angiogenesis in HIVinfected patients affected by Kaposi sarcoma. We aimed to evaluate the antineoplastic potential activities of the protease inhibitor indinavir (Crixivan) in in vitro and in vivo hepatocarcinoma models. Experimental Design:We analyzed effects of indinavir on cell growth and invasiveness in Huh7 and SK-HEP-1hepatocarcinoma cell lines and on in vivo tumor growth of the same cells in nude mice. Morphologic and molecular analyses on explanted tumors were carried out to evaluate vascularization and apoptosis. Results: We observed a reduced ability to invade an in vitro extracellular matrix for both cell lines treated with indinavir compared with controls (P = 0,001). Moreover, indinavir treatment was able to inhibit matrix metalloproteinase-2 proteolytic activation, whereas there was no effect on cell proliferation.The drug was also able to delay in vivo tumor growth.The inhibition of tumor growth was statistically significant from days 6 to 21 (P = 0.004 and P = 0.003, respectively). Moreover, the drug showed antiangiogenic and proapoptotic actions, as revealed by vessel count and apoptotic index by terminal deoxynucleotide transferase^mediated nick end labeling in explanted tumors. Finally, treatment with indinavir did not block the production of vascular endothelial growth factor in the tumors. Conclusion: Indinavir could be helpful to prevent the development of hepatocarcinomas in HIV/HCV^coinfected individuals. In view of the current trend to substitute protease inhibitors with other antiretroviral agents, this information may have clinical implications.

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“…The reduction in AIDS-defining malignancies such as Kaposi's sarcoma and non-Hodgkin's lymphomas has been accompanied by an increase in non-AIDS-defining malignancies [6], and HCC secondary to viral hepatitis has emerged as a major source of morbidity and mortality in HIV-infected people [7][8][9][10][11]. The prevalence of chronic HCV in HIV-infected patients is about 33%, but this varies geographically and, because of the shared mode of transmission, is much higher in certain populations, such as injection drug users and hemophiliacs.…”

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confidence: 99%

Sorafenib Therapy for Hepatocellular Carcinoma in an HIV–HCV Coinfected Patient: A Case Report

et al. 2010

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Background/Aims. HIV and hepatitis C virus (HCV) share common modes of transmission, resulting in about 33% incidence of coinfection among people infected with HIV. The survival benefit from highly effective antiretroviral therapy (HAART) for HIV infection is resulting in an increased incidence of hepatocellular carcinoma (HCC) in this population. There are no reports to date regarding the coadministration of HAART and sorafenib for hepatocellular carcinoma.Methods. We report the case of a 42-year-old male patient coinfected with HIV and HCV who developed advanced HCC not amenable to curative therapy. The patient was treated with sorafenib, an oral multikinase inhibitor shown to lead to a longer median survival time and time to progression in patients with advanced HCC.

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Increased incidence of hepatocellular carcinoma (HCC) in HIV-1 infected patients

Cited by 32 publications

References 13 publications

Hepatocellular carcinoma in HIV-infected patients comes of age: The convergence of epidemiology and treatment effectiveness

Hepatocellular carcinoma in HIV-infected patients comes of age: The convergence of epidemiology and treatment effectiveness

Evaluation of Antitumoral Properties of the Protease Inhibitor Indinavir in a Murine Model of Hepatocarcinoma

Sorafenib Therapy for Hepatocellular Carcinoma in an HIV–HCV Coinfected Patient: A Case Report

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