Lipodystrophy was first described in HIV-1-infected patients in 1998. The main clinical feature is subcutaneous fat loss or lipoatrophy of the face, limbs, and buttocks . Patients can also experience fat accumulation within the abdomen, neck or breasts. The pathogenesis of lipoatrophy appears to be multi-factorial. Contributing factors are CD4~+ lymphocyte cell count, HIV clinical stage, race, sex, exercise level, age at start of antiretroviral therapy , and the rapidity of its onset may depend on the individual total fat mass. The driving force behind lipoatrophy is undoubtedly the cumulative exposure to thymidine analogue drugs. These drugs, in particular stavudine and to a lesser extent zidovudine, block mitochondrial DNA poly-merase function producing apoptosis of fat cells . Earlier detection and treatment of HIV infection , as well as the use of antiretroviral drugs with less deleterious effects on body fat, make it reasonable to hypothesize a decrease in prevalence of lipodystrophy in the coming years.
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