Do the epidemiology, physiological mechanisms and characteristics of hepatocellular carcinoma in HIV-infected patients justify specific screening policies?

Gelu-Simeon, Moanaa,b,l; Sobesky, Rodolphea,b,c,d; Haïm-Boukobza, Stéphanieb,c,e; Ostos, Maritaa,b; Teicher, Elinaa,b,c,f; Fontaine, Hélèneg; Salmon-Ceron, Dominiqueh; Meyer, Laurencei; Trinchet, Jean-Claudej; Paule, Bernarda,b; Samuel, Didiera,b,c,d; Lewin, Maïtéb,c,d,k; Duclos-Vallée, Jean-Charlesa,b,c,d

doi: 10.1097/QAD.0000000000000300
Editorial Review

Reducing the incidence of hepatocellular carcinoma (HCC) in HIV-infected patients has become a serious problem when managing these patients. There are many explanations for this disease evolution, which notably include their longer survival under effective antiviral therapy and also the more rapid evolution of chronic liver disease. Despite recent advances in the management of hepatitis B (HBV) and hepatitis C (HCV) viral diseases, which will probably increase the number of patients achieving a virological response, HIV-infected patients with cirrhosis are still at risk of the onset of HCC. This evolution to HCC is also correlated to other comorbidities such as excessive alcohol consumption and nonalcoholic steatohepatitis (NASH). HCC thus remains a public health issue in this population. The poor prognosis and aggressiveness of HCC have been fully demonstrated, but the mechanisms underlying this aggressiveness are not yet well defined. As well as underlying mechanisms that contribute to accelerating hepatocarcinogenesis in HIV-infected patients, there are other reasons why HIV-infected patients should be considered a higher risk population. This review discusses the principal epidemiological determinants; the mechanisms of pathogenesis; and the treatment of HCC in HIV/HBV and HIV/HCV coinfected patients. It also discusses the probable need to develop a specific screening policy for HCC in this population in order to prevent the rapid development and to make them more amenable to a curative treatment.

aAP-HP Hôpital Paul Brousse, Centre Hépato-Biliaire

bDHU Hepatinov

cInserm U785, Villejuif

dUniversité Paris-Sud, Faculté de Médecine Paris-Sud, Le Kremlin-Bicêtre

eAP-HP Hôpital Paul Brousse, Département Virologie, Villejuif

fAP-HP Hôpital Bicêtre, Service de Médecine Interne, Immunologie Clinique et Maladies Infectieuses, Le Kremlin-Bicêtre

gAP-HP Hôpital Cochin, Unité d’Hépatologie et Université Paris Descartes, Inserm U1016

hAP-HP Hôpital Cochin, Service des Maladies Infectieuses et Tropicales et Université Paris Descartes, Paris

iAP-HP Hôpital Bicêtre, Service d’Epidémiologie et de Santé Publique et Université Paris-Sud, Inserm U1018, Le Kremlin-Bicêtre

jAP-HP Hôpital Jean Verdier, Service d’Hépato-Gastro-Entérologie et Université Paris 13, Inserm UMR 1162, Bondy

kAP-HP Hôpital Paul Brousse, Service de Radiologie, Villejuif

lCHU de Pointe-à-Pitre, Service d’Hépato-Gastro-Entérologie, Pointe-à-Pitre, Guadeloupe, France.

Correspondence to Dr Moana Gelu-Simeon, Centre Hepato-Biliaire, Hôpital Paul Brousse, Assistance Publique-Hôpitaux de Paris, 12 Avenue Paul Vaillant Couturier, 94800 Villejuif, France. Tel: +33 1 45 59 67 99; fax: +33 1 45 59 67 91; e-mail: moana.simeon@gmail.com

Received 14 January, 2014

Revised 2 April, 2014

Accepted 3 April, 2014

© 2014 Lippincott Williams & Wilkins, Inc.