Fast Liver Damage Progression in HIV/HCV Co-infected Patients

17th CROI
Conference on Retroviruses
and Opportunistic Infections
San Francisco CA
February 16-19, 2010 Back grey_arrow_rt.gif





Fast Liver Damage Progression in HIV/HCV Co-infected Patients in Spite of Effective HAART


Reported by Jules Levin
CROI 2010 Feb 16-19 SF

Juan Macias*1, M von Wichmann2, A Rivero3, F Tellez4, D Merino5, M Marquez6, A Vergara7, M Delgado8, J Iribarren2, and J Pineda1 1Hosp Univ de Valme, Seville, Spain; 2Hosp de Donostia, San Sebastian, Spain; 3Hosp Univ Reina Sofia, Cordoba, Spain; 4Hosp de la Linea, Cadiz, Spain; 5Hosp Juan Ramon Jimenez, Huelva, Spain; 6Hosp Univ Virgen de la Victoria, Malaga, Spain; 7Hosp Univ Puerto Real, Cadiz, Spain; and 8Hosp Univ Carlos Haya, Malaga, Spain

AUTHOR CONCLUSION

Achievement of HIV suppression and increase of CD4 cell counts with HAART is associated with a lower risk of worsening of liver damage. However, in spite of effective HAART, liver fibrosis progresses in a significant proportion of HIV/HCV-coinfected patients over a short period of time

ABSTRACT

Background: Elevated frequencies of fibrosis progression have been observed in studies on serial liver biopsies (LB) in HIV/HCV co-infection. However, sequential LB studies might not be representative of the co-infected population. Patients that undergo a second LB are selected. Clinicians refer them for LB because of suspicion of progression. Thus, rates of fibrosis progression may have been overestimated by these studies. Liver stiffness (LS) measurement can be repeated easily in unselected patients. LS is useful to discriminate F0 to F1 and F≥2, and can identify cirrhosis. Because of these, our aim was to analyze the frequency of changes in LS and the factors associated with them in HIV/HCV-co-infected patients without anti-HCV therapy.

Methods: Patients with HIV/HCV co-infection, without anti-HCV treatment, were prospectively included in this cohort study. LS was measured at baseline and, at least, every 12 months. Classification of fibrosis followed LS cut-offs: ≤6 KPa (F0 to F1), 6.1 to 8.9 KPa (indeterminate stage), ≥9 KPa (F≥2) and ≥14.2 KPa (F4). The outcome variable was change in this classification.

Results: In this study, 281 patients had follow-up LS values. All patients were under HAART during the follow-up. At baseline, median (Q1 to Q3) CD4 counts were 460 (331 to 695) and 225 (80%) subjects showed undetectable HIV load. Among patients without F4, 48 (20%) subjects progressed and 35 (15%) regressed at 6 to 12 months. The table summarizes changes in the classification of 137 individuals with LS at 18 to 24 months. In the multivariate analysis, male gender (adjusted OR = 3.8, 95%CI 1.03 to 13.9), P =0.05], undetectable HIV load during the follow-up (AOR = 0.34, 95%CI 0.15 to 0.77, P =0.01], and CD4 counts increase ≥20/mL (AOR = 0.15, 95%CI 0.07 to 0.35, P <0.001) were associated with change in the classification of fibrosis at 6 to 12 months.


Conclusions: Achievement of HIV suppression and increase of CD4 cell counts with HAART is associated with a lower risk of worsening of liver damage. However, in spite of effective HAART, liver fibrosis progresses in a significant proportion of HIV/HCV-co-infected patients over a short period of time.

RESULTS