It's not yet clear why or how lipoatrophy occurs in HIV-positive people. However, it is believed to be a side effect of anti-HIV therapy.
Nucleoside reverse transcriptase inhibitors (NRTIs) have been singled out as the most likely cause of lipoatrophy. While it is not entirely clear why these particular drugs cause this side effect, it is probably related to the ability of these drugs to damage cellular mitochondria.
Mitochondria are considered to be the "powerhouses" of cells in the body. All cells in the body, with the exception of red blood cells, contain mitochondria. They are primarily responsible for converting nutrients, such as sugar and fats, into energy that can be used by the cells. If something goes wrong with the mitochondria, the cell isn't able to get the energy it needs, which can prevent the cell from doing what it is supposed to do. If the cells in question are fat cells (adipocytes), responsible for storing and exporting fat for when it is needed, significant mitochondrial damage can cause these cells to loose both their function and shape. And if enough fat cells are affected, it can cause noticeable wasting of fat tissue in the face and other parts of the body.
Zerit® (d4T, stavudine) is the NRTI most frequently tied to lipoatrophy. In test tube studies, Zerit has been shown to cause mitochondrial damage and to alter the function of adipocytes. Clinical trials also suggest that HIV-positive people taking drug regimens that contain Zerit are more likely to experience lipoatrophy than those taking drug regimens that do not contain Zerit. However, drug regimens that contain Retrovir® (AZT; zidovudine) have also been shown to cause lipoatrophy, although not as frequently as drug regimens containing Zerit. In other words, Zerit is probably not the only NRTI associated with lipoatrophy. Experts reckon that the NRTIs Viread® (tenofovir), Epivir® (3TC; lamivudine), Emtriva® (emtricitabine), and Ziagen® (abacavir) are the least likely to cause lipoatrophy.
Protease inhibitors (PIs) may be cause lipoatrophy as well. While they do not interfere with cellular mitochondria, they can affect other components of fat cells that, researchers have found, can affect the way adipocytes work. Some data from clinical trials involving HIV-positive people taking protease inhibitors also suggest that these drugs may be partly to blame for lipoatrophy.
Other factors that may increase (or decrease) the risk of lipoatrophy include age, gender, genetic predisposition, the T-cell count at the time therapy is started (the lower the T-cell count, the more likely it is the lipoatrophy will occur), and the length of time on antiretroviral therapy (the longer the time on therapy, the more likely that lipoatrophy will occur).
It is still not clear if lipoatrophy results from the death of adipocytes or poor functioning of adipocytes. If it turns out that the death of adipocytes is the cause, it may be much more difficult to treat lipoatrophy, given that it is hard to bring dead cells back to life. However, if the cause is related to poor functioning of adipocytes, the possibility of reversing lipoatrophy is much more feasible. Considering that studies have documented that some reversal of lipoatrophy is seen in HIV-positive people who switch an offending anti-HIV drug for another medication that is less likely to cause lipoatrophy, it looks as if poor functioning of adipocytes is a likely cause.
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