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The management and treatment of HIV and hepatitis B virus (HBV)-coinfected patients present specific challenges for clinicians. The morbidity and mortality related to these concomitant infections are growing concerns, while the use of antiviral drugs effective against both viruses complicates therapeutic decision making. The present document provides guidelines for physicians regarding care and treatment of patients coinfected with HIV and HBV. Primary prevention of HBV in HIV-positive patients is achieved through appropriate vaccination schedules. Follow-up before treatment of HBV may include liver biopsy, screening for hepatocellular carcinoma and testing for esophageal varicies in cases of cirrhosis. In HBV-infected patients requiring treatment, recommendations regarding initiation, duration and choice of first-line drugs are made. Finally, in the case of resistance, appropriate alternative therapies are necessary.

Concomitant HIV and hepatitis C virus (HCV) is a common yet complex coinfection. The present document is a practical guide for treating HCV infection in people coinfected with HIV. Effective antiretroviral therapies have prolonged survival rates for HIV-infected people over the past decade, which have made latent complications of HCV major causes of morbidity and mortality in these patients. Advances in the treatment of HCV (eg, combined pegylated interferon and ribavirin) offer the possibility of eradicating HCV infection in coinfected persons. The treatment of HCV must be considered in all cases. Intensive management of the adverse effects of HCV treatment is one of the factors for the success of these therapies. HCV eradication is predicted to decrease the mortality associated with coinfection and reduce the toxicity of HIV treatment.

Approximately two years after the introduction of highly active antiretroviral therapy for the treatment of HIV infection, body shape changes and metabolic abnormalities were increasingly observed. Initially, these were ascribed to protease inhibitors, but it is now clear that nucleoside reverse transcriptase inhibitors also contribute to lipodystrophy syndrome. The syndrome groups together clinical conditions describing changes in body fat distribution that include lipoatrophy, lipoaccumulation or both. However, there does not appear to be a direct link between lipoatrophy and lipoaccumulation that would support a single mechanism for the redistribution of body fat. Currently, there is no clear definition of lipodystrophy, which explains the difficulty in determining its prevalence and etiology. There are no current guidelines for the treatment of fat distribution abnormalities that occur in the absence of other metabolic complications. The present article reviews the current state of knowledge of the definition, symptoms, risk factors, pathogenesis, diagnosis and treatment of the morphological changes associated with lipodystrophy syndrome.

BACKGROUND AND OBJECTIVES: A meeting of a Canadian group with significant experience and knowledge in HIV management, consisting of five physicians, a pharmacist and an AIDS researcher, was convened. Their goal was to develop guidance for Canadian HIV-treating physicians on the appropriate use of raltegravir (MK-0518, Isentress®, Merck Frosst Canada Inc) in HIV-infected adults.

Efavirenz is in the non-nucleoside reverse transcriptase inhibitor category of HIV antiretroviral medicines. It is an in vivo inducer of the CYP3A4 isoenzyme within the cytochrome P450 (CYP450) system, and an in vitro inhibitor of the system’s CYP2C9/2C19, 3A4 and 2B6 isoenzymes; as a result, concentrations of psychotropic drugs can be increased or decreased depending on the specific enzyme pathway involved in their metabolism. CYP3A4 is responsible for metabolizing many benzodiazepines and other psychotropics, as well as selective serotonin reuptake inhibitors and tricyclic antidepressants. As an inducer of CYP3A4, efavirenz can increase the rate at which these agents are metabolized, resulting in administered psychotropic drug levels that are below their therapeutic thresholds. Conversely, efavirenz is an inhibitor of CYP2B6, which metabolizes agents such as bupropion; consequently, bupropion levels in the blood can increase. Given the existing conflicting data, the clinician may find it impractical to use an evidence-based approach when concomitantly prescribing efavirenz and psychotropic drugs to their HIV patients. Instead, it may be preferable to use a more pragmatic approach that applies knowledge of the most current pharmacological and pharmacokinetic data for psychotropics and non-nucleoside reverse transcriptase inhibitors, which may help better predict their potential interactions.