Abstract Book Vol. 2 [International Conference on AIDS (14th: 2002: Barcelona, Spain)]

XIV International AIDS Conference

Abstracts WePeB6035-WePeB6038 87

acteristics of HCC in HIV seropositives and to compare them to those observed
in HIV seronegatives.
Methods: Three HIV infection referral centers had reviewed their data base in
order to find all patients who were diagnosed as having HCC from 1987 according to European Association of the Liver guidelines. Cases of HCC found in HIV
seropositives were compared with a series of 384 consecutive HCC observed in
the same years in a single district of the same geographic area.
Results: The three centers have observed and followed up 3400 HIV+. Eleven
cases of HCC have been identified. Two out of 11 occurred in patients coming
from subsaharian Africa. The remaining 9 cases were all males infected with
HCV, 7/9 aged less than 50yrs (vs 5% in HIV-p<0.0001), 2 / 9 were multifocal
(vs. 41% in HIV-p>0.05) and larger diameter was >5 cm in 6/9 (vs. 23% in HIVp<0.01). Cirrhosis was histologically or clinically diagnosed in 9/9; Child's Pugh
class of liver function was A in 1/9 (vs 41% HIV-; p>0.05)., B in 4/9 (vs. 26% HIVp>0.05), and C in 4/9 (vs. 18% HIV-; p> 0.05). Eight out of 9 showed multiple risk
factors for liver disease (vs. 30% of HIV-; p<0.001). Survival after diagnosis was
less than 6 months in 7/9 vs 22% of HIV- (p<0.0001).
Conclusions: In HIV+ HCC seems to occurr earlier with an increased tumour
bulk and with shorter survival than in HIV-. This could be the result of HIV coinfection pro-cancerogenetic activity or alternatively of the occurrence of multiple
risk factors for liver disease in the same subjects and of a delayed diagnosis.
Presenting author: Massimo Puoti, Clinica Malattie Infettive, Rle Spedali Civili
1, 1 25123 Brescia, Italy, Tel.: [phone], Fax: [phone], E-mail: m.
puoti @ iol.it
WePeB6035 Hepatitis C RNA levels are unchanged after one
year of effective antiretroviral therapy
3 3'3
F.J. Torriani1, V. Asensi2, C. Byrnes1, J.A. Carton3, J.A. Maradona3, S. Melon3,
M. Ona3, M. Blanco3, J.M. Arribas3. 1 University of California, San Diego, ucsd
antiviral research center, 150 west washington street, suite 100, san diego, ca
92103, United States; 2University of Oviedo, Medical School, Oviedo, Spain;
3 University of Oviedo Medical School, Oviedo, Spain
Background: Although antiretroviral therapy (ARV) has no direct effect on Hepatitis C (HCV) RNA replication, it has been postulated ARV-related immune reconstitution could lead to lower levels of HCV RNA because of improved CD8 -mediated HCV-specific immunity. We characterized parameters of response to
ARV and HCV RNA levels prior to and 1 year after ARV initiation in a cohort of
HIV/HCV-infected Spanish patients.
Methods: Plasma HCV RNA levels, CD4 cell counts, and ALT levels were measured prior to and one year after starting ARV in 71 HIV/HCV infected patients
never treated for HCV. Results are in mean~SE.
Results: Pre-ARV CD4 counts, HIV RNA and HCV RNA were 287~26 cells/mm3,
4.3~10.1 log10 copies/mi 5.5~0.1 log10 IU/ml, respectively. Of the 57 patients
with matched CD4 and HIV RNA values, after 12 months of ARV, CD4 counts
had increased to 390~33 cells/mm3 (P = 0.03), HIV RNA levels had decreased
to 2.8~0.1 log10 copies/ml (P < 0.001) and HCV RNA levels were unchanged
at 5.6~0.1 Iog10 IU/ml. HIV RNA was < 400 copies in 40/57 patients. Of the 55
patients with HCV genotyping, 40 were genotype 1, 9 were genotype 3, and 6
were genotype 4. There were no differences in HCV RNA levels prior to and after
starting ARV in all genotypes.
Conclusions: In this cohort of HIV/HCV-infected patients, theabsence of change
in HCV RNA levels after one year of effective ARV suggests that neither sustained
suppression of HIV replication nor improved T cell immunity due to CD4 cell increases are associated with a better control of HCV replication.
Presenting author: francesca torriani, ucsd antiviral research center, 150 west
washington street, suite 100, san diego, ca 92103, United States, Tel.: [phone], Fax: [phone], E-mail: [email protected]
WePeB6036 Natural history of chronic hepatitis C: Unusually
rapid progression to liver fibrosis and cirrhosis in
human immunodeficiency virus co-infected
patients
C. Arizcorreta, C. Martinez, F. Diaz, R. Roldan, L. Martin-Herrera,
E. Perez-Guzman, J.A. Giron. Hospital, Servicio de Medicina Intera, Hospital
Universitario Puerta del Mar, Avda Ana de Viya 21, 11009 Cddiz, Spain
Background/Aims: To analyze the factors associated with the evolution of liver
fibrosis and cirrhosis in chronic hepatitis C, in patients with HIV coinfection.
Patients and methods: Fibrosis progression rate of (FPR) (ratio between fibrosis
stage and duration of infection) and cirrhosis were evaluated, using the Knodell
scoring system modified by Desmet, in 188 patients with chronic hepatitis C, 41 of
them coinfected with HIV. At time of diagnosis of chronic hepatitis, HIV-coinfected
patients (CD4+ cell count: 577 + 280 /mm3) had been receiving highly active antiretroviral therapy (HAART) for at least 27 months. The relationship of histological
variables with demographic parameters, HCV viral load and genotype, HIV viral

load, CD4 cell count, and response to HAART was evaluated.
Results: HIV-infected patients (HCV+HIV+) showed significantly higher HCV load
(5,70 x 10 (range: 1,1 - 8,1) vs 2,33 x 10 (1,4 - 3,1) millions of copies/ml, p <
0,005), more advanced fibrosis (1,80 (range: 0,4-3) vs 1,18 (0,9-2,4), p < 0,04)
and higher FPR (0,144 (0,11 -0,17) vs 0,106 (0,08-0,01), peryear, p < 0,04), in
comparison with HCV+HIV-patients. HCV viral load and immunodepressed state
were the parameters associated with a higher FPR in the HIV+HCV+ group. Im
mune reconstitution induced by HAART did not influence this progression. Cirrhosis developed more precociously in HIV-coinfected patients: at 16, 20 and 25
years after HCV infection, HIV-coinfected patients showed cirrhosis in 19%, 35%
and 65% of the cases, whereas the corresponding percentages were 2%, 3%
and 6% in HCV+HIV- patients. In the multivariate analysis, only HIV infection was
associated with the early development of cirrhosis.
Conclusions: In patients with chronic hepatitis C, a higher FPR should be expected in those HIV-coinfected individuals, mainly in those with a high HCV viral
load and a low CD4 cell count. HIV infection is the most important risk factor for
accelerated cirrhosis development.
Presenting author: Ana Arizcorreta, Servicio de Medicina Interna, Hospital Universitario Puerta del Mar, Avda Ana de Viya 21, 11009 Cadiz, Spain, Tel.: +34
956002879, E-mail: medinternal @hpm.sas.junta-andalucia.es
WePeB6037I Interferon alfa-2a and ribavirin "low dose" for the
treatment of HCV infection in HIV co-infected
patients. An open-label, pilot study
E. Bernasconi1, L. Magenta', P Vernazza2, C. Bellinil, P. Schmid2, B. Miazza1,
J.C. Piffaretti3, A. Cerny'. 1Dept of medicine/Regional Hospital, Ospedale
Civico, v. Tesserete 46, CH-6903 Lugano, Switzerland; 2Div of infectious
diseases/Cantonal Hospital, St. Gallen, Switzerland; 3Institute of clinical
microbiology Lugano, Switzerland
Background: To assess efficacy and tolerance of a combination therapy of interferon alpha-2a with ribavirin in interferon-naive patients infected with chronic
hepatitis C and co-infected with HIV.
Methods: Open-label study with selection of interferon-naive patients. Rx: Interferon 6 MIU qd for 14 days, followed by 6 MIU tiw, in combination with ribavirin 600 mg qd. Determination of primary response (clearance of HCV-RNA in
plasma, serum-ALT normalization) at week 28; stop of treatment in primary nonresponders genotype 1,4,5,6 and in genotypes 2,3; continuation of treatment in
primary responders in genotypes 1,4,5,6 for a total of 12 months.
Results: Up to now 11 patients (mean age 37.9~4.9 years, 8 men) were included
in the study (6 genotypes 3; 5 genotypes 1; median baseline HCV RNA 6.04~6.97
log10 copies/mL). Nine out of 11 patients were on highly active antiretroviral therapy (HAART). End of therapy response was obtained in 3/5 patients with genotype 3, and in 0/4 patients with genotype 1. Only one patient withdrew from the
study because of severe depression. One patient interrupted the treatment for 4
weeks because of thrombocytopenia with gastric hemorrhage (preexisting esophagus varices), but could resume the treatment at a lower interferon dose. In no
case hemoglobin dropped below 10 g/dl. HIV viral load remained below the limit
of detection in the 6 patients who reached week 28 and were on HAART.
Conclusions: In our population of HCV-HIV co-infected patients, the combination of interferon alpha-2a with ribavirin was better tolerated than previously reported. However, a satisfactory virologic response was achieved only in patients
with genotype 3. maximum
Presenting author: Enos Bernasconi, Ospedale Civico, v. Tesserete 46, CH6903 Lugano, Switzerland, Tel.: [phone], Fax: [phone], E-mail: [email protected]
WePeB6038 Analysis of Liver Fibrosis progression markers in
a cohort of 70 Hiv/Hcv coinfected patients
J. Murillas1, J. Mallolas1, J. Sanchez-Tapias', R. Miquell, M. Garcia-Gasalla1,
L. Bianchi1, E. Lazzari2, J.L. Blanco2, A. Milinkovic2, E. Martinez2, M. Lonca2,
J.M. Gatell2. I Hospital Clinic, Hospital Clinic, Calle Villaroel170, Barcelona,
Spain; 2Hospital Clinic-IDIBAPS, Barcelona, Spain
Objective: To identify liver fibrosis progression markers in a selected population of HCV-HIV coinfected patients that meets some requirements needed to be
treated with interferon plus ribavirin.
Methods: Analysis of Liver biopsies of 70 HCV-HIV coinfected patients with CD4
cell count higher than 250 cel/ il and viral load less than 10.000 copies/ml, excluded any other cause of liver disease including alcohol consumption and positive HbsAg, with ALT higher than 1,5 fold Upper Normal Limit and HCV RNA
detectable. A logistic regression analysis was performed to asses the association of prebiopsy clinical and laboratory data including gender, age, estimated
HCV infection duration, antiretroviral treatment, AST, ALT and a-GT determinations AST/ALT ratio, liver ultrasound assesment, antiHBc, HCV genotype and
RNA (RIBA), CD4 cell count and HIV viral load to the presence of significant
liver fibrosis (at least, METAVIR scale 2 or higher).
Results: Liver biopsy with fibrosis 0 or 1 was shown in 27 patients (38,6%), fibrosis 2 and 3 in 34 patients (48,5%) and cirrhosis in 8 (11,4%). Univariate regression analysis showed that ALT increments, AST higher than 67,5 UI/L(median
value), positive anti smooth muscle antibodies and any abnormality in the liver
ultrasound (hepatomegaly, echostructure alteration, nodular borders) were associated to significant liver fibrosis. When multivariate logistic regression was done,

only AST higher than 67,5 UI/L remained associated to liver fibrosis.
Conclusions: The AST higher than 67,5 UI/L was the only clinical or laboratory
marker that could help to predict the presence of significant liver fibrosis in these
selected HCV-HIV coinfected patients with similar HIV and HCV infection status.
The liver ultrasound could also have a role to predict advanced liver fibrosis that
needs further clarification.