Distinct hepatitis C virus kinetics in HIV-infected patients treated with ribavirin plus either pegylated interferon alpha2a or alpha2b.

Background: Pegylated interferon (PEG-IFN) alpha2a and alpha2b differ in their pharmacokinetic properties, which might have an effect on their antiviral effects against hepatitis C virus (HCV). Differences between PEG-IFN-alpha molecules could be more pronounced in HIV-coinfected individuals, in whom response to HCV treatment is impaired.

Methods: All HCV-HIV-coinfected patients included in PRESCO and EXTENT trials recruited at one referral centre were retrospectively analysed.

Switch from ritonavir-boosted to unboosted atazanavir guided by therapeutic drug monitoring.

Plasma concentration of atazanavir (ATV) may be reduced when coadministered with tenofovir (TDF) or proton pump inhibitors. Boosting ATV exposure with ritonavir (r) may make it possible to overcome these drug interactions. However, jaundice and loss of the metabolic advantages of ATV are more frequent using ATV/r than ATV alone.

Antiretroviral-associated portal hypertension: a new clinical condition? Prevalence, predictors and outcome.

Background: Cases of severe unexplained liver disease in HIV-infected individuals have recently been reported and are often associated with exposure to didanosine (ddl) and nodular regenerative hyperplasia. Herein, we examine the clinical outcome following ddl removal.

Methods: From 3,300 HIV-infected patients attending three clinics since 2004, all who exhibited persistently elevated aminotransferases and/or significant liver fibrosis in the absence of any known cause of liver damage were identified.

Association between tipranavir plasma levels and virological response in HIV-infected patients.

The impact of tipranavir plasma levels (TPV C(min)) on virological response was examined in 36 antiretroviral-experienced HIV-infected individuals. Although TPV C(min) did not predict outcome in patients with less than five or more than eight baseline TPV-associated resistance mutations, TPV C(min) values were greater in responders than in nonresponders with five to seven baseline TPV-associated resistance mutations (38.8 vs.

Evidence for different susceptibility to tipranavir and darunavir in patients infected with distinct HIV-1 subtypes.

Background: Tipranavir (TPV) and darunavir (DRV) are potent against protease inhibitor (PI)-resistant viruses. Efficacy of these compounds when confronting distinct HIV subtypes is not known.

Methods: All clinical specimens from HIV-positive patients sent to our institution for drug resistance testing between 1999 and 2006 were analysed.

Episodes of low-level viral rebound in HIV-infected patients on antiretroviral therapy: frequency, predictors and outcome.

Background: The rate, predictors and outcome following episodes of low-level viral rebound (LLVR) in HIV patients on highly active antiretroviral therapy (HAART) are unknown.

Methods: Retrospective assessment of all HIV patients who experienced LLVR episodes on HAART at one institution from January 1999 to December 2006. LLVR was defined as plasma HIV-RNA between 51 and 500 copies/mL after at least two consecutive undetectable plasma viral load measurements made during the last 6 months.

Value of the HLA-B*5701 allele to predict abacavir hypersensitivity in Spaniards.

The use of abacavir (ABC) may be associated with a hypersensitivity reaction (HSR) that requires discontinuation of the drug. The HLA-B*5701 allele has been linked to this HSR. Information on the strength of this association across distinct geographic regions and ethnicities is scarce.

Efficacy and safety of replacing lopinavir with atazanavir in HIV-infected patients with undetectable plasma viraemia: final results of the SLOAT trial.

Background: Atazanavir seems to be a protease inhibitor (PI) with a more favourable metabolic profile. Information regarding the potential benefit of replacing lopinavir/ritonavir by atazanavir in HIV-infected patients with prolonged viral suppression is scarce. If proved, this strategy could be particularly attractive for the subset of patients with greater cardiovascular risk.

Human T lymphotropic virus type 1-associated myelopathy/tropical spastic paraparesis in an HIV-positive patient coinfected with human T lymphotropic virus type 2 following initiation of antiretroviral therapy.

We describe a patient coinfected with human immunodeficiency virus (HIV) and human T lymphotropic virus type 2 in Spain who developed paraparesis resembling human T lymphotropic virus type 1-associated myelopathy/tropical spastic paraparesis shortly after initiation of highly active antiretroviral therapy, hypothetically as the result of an immune reconstitution inflammatory syndrome.

Hepatotoxicity of antiretroviral drugs is reduced after successful treatment of chronic hepatitis C in HIV-infected patients.

Background: The risk of liver toxicity during antiretroviral drug use in human immunodeficiency virus (HIV)-positive patients increases in the presence of chronic hepatitis C virus (HCV) infection. It is unknown whether sustained HCV clearance after interferon (IFN)-based therapy might reduce this complication.

Methods: The incidence of severe elevations in liver enzyme levels during antiretroviral therapy was retrospectively analyzed in a group of HIV/HCV-coinfected patients after completion of a full course of IFN-based therapy.

Tipranavir: a new protease inhibitor for the treatment of antiretroviral-experienced HIV-infected patients.

Tipranavir (TPV) is a novel non-peptidic protease inhibitor (PI). It binds strongly and selectively to the HIV-1 protease, is orally administered twice daily, boosted with low doses of ritonavir, and shows a favourable resistance profile. In the two registrational trials, named RESIST 1 and 2, TPV/ritonavir 500/200 mg b.

Successful rescue therapy with darunabir (TMC114) in HIV-infected patients who have failed several ritonavir-boosted protease inhibitors.

Darunabir, formerly TMC114, is a new protease inhibitor (PI) under clinical development designed to be active against HIV strains resistant to currently available PI. The virological and immunological response to ritonavir-boosted darunabir was assessed in four heavily antiretroviral-experienced patients who had failed enfuvirtide and two or more previous ritonavir-boosted PI regimens, including tipranavir in one instance. All four patients reached undetectable plasma HIV-RNA levels within 8 weeks of therapy and experienced significant CD4 cell count gains.