Hepatitis: Vella S

Hammer SM, Saag MS, Schechter M, Montaner JS, Schooley RT, Jacobsen DM, Thompson MA, Carpenter CC, Fischl MA, Gazzard BG, Gatell JM, Hirsch MS, Katzenstein DA, Richman DD, Vella S, Yeni PG, Volberding PA, Anonymous00173. · Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA. · JAMA. · Pubmed #16905788 links to  free full text

Abstract: CONTEXT: Guidelines for antiretroviral therapy are important for clinicians worldwide given the complexity of the field and the varied clinical situations in which these agents are used. The International AIDS Society-USA panel has updated its recommendations as warranted by new developments in the field. OBJECTIVE: To provide physicians and other human immunodeficiency virus (HIV) clinicians with current recommendations for the use of antiretroviral therapy in HIV-infected adults in circumstances for which there is relatively unrestricted access to drugs and monitoring tools. The recommendations are centered on 4 key issues: when to start antiretroviral therapy; what to start; when to change; and what to change. Antiretroviral therapy in special circumstances is also described. DATA SOURCES AND STUDY SELECTION: A 16-member noncompensated panel was appointed, based on expertise in HIV research and patient care internationally. Data published or presented at selected scientific conferences from mid 2004 through May 2006 were identified and reviewed by all members of the panel. DATA EXTRACTION AND SYNTHESIS: Data that might change previous guidelines were identified and reviewed. New guidelines were drafted by a writing committee and reviewed by the entire panel. CONCLUSIONS: Antiretroviral therapy in adults continues to evolve rapidly, making delivery of state-of-the-art care challenging. Initiation of therapy continues to be recommended in all symptomatic persons and in asymptomatic persons after the CD4 cell count falls below 350/microL and before it declines to 200/microL. A nonnucleoside reverse transcriptase inhibitor or a protease inhibitor boosted with low-dose ritonavir each combined with 2 nucleoside (or nucleotide) reverse transcriptase inhibitors is recommended with choice being based on the individual patient profile. Therapy should be changed when toxicity or intolerance mandate it or when treatment failure is documented. The virologic target for patients with treatment failure is now a plasma HIV-1 RNA level below 50 copies/mL. Adherence to antiretroviral therapy in the short-term and the long-term is crucial for treatment success and must be continually reinforced.

Pirillo MF, Bassani L, Germinario EA, Mancini MG, Vyankandondera J, Okong P, Vella S, Giuliano M. · Department of Drug Research and Evaluation, Istituto Superiore di Sanità, Rome, Italy. · J Med Virol. · Pubmed #17935164 No free full text.

Abstract: A retrospective survey to estimate the prevalence of hepatitis B (HBV) and C (HCV) infections was conducted on the samples of 247 African HIV-1 positive pregnant women who had participated to a mother-to-child prevention trial carried out in urban settings in Kampala, Uganda and Kigali, Rwanda. Hepatitis B markers studied were HBs antigen (HBsAg) and, if positive after confirmatory testing, HBe antigen/anti-HBe antibodies and HBV DNA. A fourth generation HCV enzyme immunoassay (EIA) was used for primary HCV screening. Positive samples were analyzed further with a second different EIA. Both for HBV and for HCV the use of confirmatory tests allowed the removal of frequent false-positive screening results. HBsAg was found in 10/246 women (seroprevalence 4.1%, 95% confidence interval (95%CI) 1.7-6.8): 8/164 (4.9%) in Uganda and 2/82 (2.4%) in Rwanda. HBe Ag was found in 33% of HBsAg-positive patients and HBV DNA was quantifiable in 71%. Anti-HCV antibodies were found in 5/247 women (seroprevalence 2.0% 95%CI 0.3-3.9): 1/165 (0.6%) in Uganda and 4/82 (4.9%) in Rwanda. There was no interrelation between HCV and HBV markers. There was no difference between patients with and without co-infection with HBV or HCV with regards to CD4+ cell count. Overall, hepatitis B and C co-infection was relatively infrequent in this group of pregnant women. However, since approximately 6% of HIV-positive women in these countries had a co-infection with one hepatitis virus, caution should be used in the monitoring of possible hepatotoxicity related to antiretroviral drugs in these populations.

Konopnicki D, Mocroft A, de Wit S, Antunes F, Ledergerber B, Katlama C, Zilmer K, Vella S, Kirk O, Lundgren JD, Anonymous00063. · Division of Infectious Diseases, Saint-Pierre University Hospital, Brussels, Belgium. · AIDS. · Pubmed #15802978 No free full text.

Abstract: BACKGROUND: Whether hepatitis B (HBV) coinfection affects outcome in HIV-1-infected patients remains unclear. OBJECTIVE: To assess the prevalence of HBV (assessed as HBsAg) coinfection and its possible impact on progression to AIDS, all-cause deaths, liver-related deaths and response to highly active antiretroviral therapy (HAART) in the EuroSIDA cohort. METHODS: Data on 9802 patients in 72 European HIV centres were analysed. Incidence rates of AIDS, global mortality and liver-related mortality, time to 25% CD4 cell count increase and time to viral load < 400 copies/ml after starting HAART were calculated and compared between HBsAg-positive and HBsAg-negative patients. RESULTS: HBsAg was found in 498 (8.7%) patients. The incidence of new AIDS diagnosis was similar in HBsAg-positive and HBsAg-negative patients (3.3 and 3.4/100 person-years, respectively) even after adjustment for potential confounders: the incidence rate ratio (IRR) was 0.94 [95% confidence interval (CI), 0.74-1.19; P = 0.61]. The incidences of all-cause and liver-related mortalities were significantly higher in HBsAg-positive subjects (3.7 and 0.7/100 person-years, respectively) compared with HBsAg-negative subjects (2.6 and 0.2/100 person-years, respectively). The adjusted IRR values were 1.53 for global (95% CI, 1.23-1.90; P = 0.0001) and 3.58 for liver-related (95% CI, 2.09-6.16; P < 0.0001) mortality. HBsAg status did not influence viral or immunological responses among the 1679 patients starting HAART. CONCLUSIONS: The prevalence of HBV coinfection was 9% in the EuroSIDA cohort. Chronic HBV infection significantly increased liver-related mortality in HIV-1-infected patients but did not impact on progression to AIDS or on viral and immunological responses to HAART.

Dragoni F, Cafolla A, Gentile G, Mazzucconi MG, Vella S, Di Corpo U, Tosti ME, Pisani G, Donato V, Martino P. · Dipartimento di Biotecnologie Cellulari ed Ematologia, Univ. "La Sapienza", Rome, Italy. · Haematologica. · Pubmed #10366796 links to  free full text

Abstract: BACKGROUND AND OBJECTIVE: The aim of this study was to measure contemporaneously HCV-RNA load, HIV-RNA load and CD4+ lymphocyte count in HCV/HIV coinfected patients with coagulopathy and to examine the relationship between these parameters and the liver failure. DESIGN AND METHODS: A cross-sectional study was performed on 54 patients with severe coagulopathy: 39 HCV/HIV coinfected and 15 HCV+/HIV- comparable for age and HCV exposure time. HCV-RNA and HIV-RNA load, CD4+ lymphocyte count, biochemical and ultrasonographic parameters were evaluated at the time of entry to the study. RESULTS: Mean HCV-RNA load was significantly higher in coinfected patients (643,872 717,687 copies/mL) than in HCV+/HIV- (mean 161,573 276,896 copies/mL) (p = 0.01). The 39 HCV/HIV coinfected patients had a mean HIV-RNA load of 205,913 456,311 copies/mL (range 4,000-2,500,000) and a mean CD4+ lymphocyte count of 206.5171/microL (range 5-693). Five of the 39 (12.8%) coinfected patients had liver failure. In these five patients the mean HCV-RNA load (770,200 996,426 copies/mL) was high but not significantly different from that in the 34 HCV+/HIV+ patients (623,496 682,239 copies/mL) without liver failure (p = 1.0). Coinfected patients with liver failure had a significantly higher HIV-RNA load (mean 764, 599 978,542 copies/mL) and lower CD4+ lymphocyte count (mean 52.655. 6/microL) than those observed in coinfected patients without liver failure (p = 0.007 and p = 0.03, respectively). A significant inverse correlation was found between CD4+ lymphocyte count and HIV-RNA load (r = -0.37, p = 0.01). INTERPRETATION AND CONCLUSIONS: HCV-RNA load is significantly higher in HIV+ than in HIV- patients with coagulopathy. Liver failure was found only in the HCV/HIV coinfected patients with severe immunodepression, expressed either by low CD4+ lymphocyte count or by high HIV-RNA load.