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More than 15 years after the introduction of highly active antiretroviral therapy, HIV/HAART-associated lipodystrophy syndrome still shadows the indisputable efficacy of antiretroviral therapy. Several issues related to this complication (prevalence, diagnosis, pathogenesis, prevention, or clinical management) have not been completely clarified. However, in the last years, substantial progress has been made in elucidating some of these basic aspects. This includes a better knowledge of the pathogenic mechanisms underlying HIV/HAART-associated lipodystrophy syndrome such as genetic host determinants, the impact of HIV infection per se, as well as the contribution of antiretroviral therapy. In regard to treatment, we have learned that certain drugs are especially prone to cause HIV/HAART-associated lipodystrophy syndrome (i.e. thymidine analogues). Pharmacological interventions to treat this condition have yielded mostly disappointing results, and the only intervention which offers an immediate aesthetical improvement for patients with HIV/HAART-associated lipodystrophy syndrome is plastic surgery. Even under the most favorable conditions (ideal host genetic make-up, and the timely initiation of HIV therapy with less toxic drugs), current data show that HIV/HAART-associated lipodystrophy syndrome is a complication of HIV infection and/or antiretroviral treatment that we are unable to avoid. In the context of HIV-1-infected patients under long-term antiretroviral therapy, fat toxicity is still the dark side of the rainbow.

Dyslipidemia is frequently observed in HIV-infected patients. Its pathogenesis is complex and includes factors related to the virus, the host, and antiretroviral treatment. Dyslipidemia is a main cardiovascular risk factor and it is partially modifiable. Whereas HIV infection and its treatment are associated with a state of accelerated atherosclerosis and an increase in the number of cases of myocardial infarction, dyslipidemia management must be a priority in the clinical care of patients with HIV infection. In this review, we discuss the major pathogenic mechanisms of dyslipidemia associated with antiretroviral therapy and the effect of the currently used drugs on the lipid profile. The current recommendations for dyslipidemia management include the control of other cardiovascular risk factors, the choice of antiretroviral drugs with a better lipid profile, and lipid-lowering drug use when clinically indicated.

Body fat disorders are a common and relevant problem in HIV-1-infected patients that can be associated with metabolic alterations. Many controversies in their definition, pathogenesis, measurement, and management remain unclear. Several factors including HIV-1 infection itself and antiretroviral therapy have been associated with the development of these alterations. Most studies show that the action of drugs on the pathogenesis of lipoatrophy is undeniable. However, they also show that there are considerable differences not only between the different families of antiretroviral drugs, but also between the individual members of these families. The diagnosis of lipodystrophy is limited by the absence of an agreed definition and a reference for normality. Accurate diagnosis, especially in mild-moderate cases, is difficult, almost always subjective, not standardized, and cannot be carried out by a single method. In general, subjective evaluation by the physician and patient, together with simple techniques such as anthropometry, can provide highly valuable information, especially when used over time. Although there is no known therapy to completely reverse lipodystrophy once it becomes established, there is evidence that lipoatrophy can be partially improved by replacing thymidine analogs in certain cases. In addition, reparative surgery may prove useful in moderate or severe cases. Neither the interruption of antiretroviral therapy nor the use of metformin, glitazones or growth hormone analogs can be recommended due to their limited efficacy or associated complications.