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PURPOSE OF REVIEW: Metabolic toxicities in HIV patients are common and contribute to clinical status and long-term sequelae. Body fat mass alterations, of multifactorial causes, continue to occur, despite use of antiretroviral drugs associated with fewer metabolic side-effects. The role of HIV itself in the development of these changes is being better defined and a deeper understanding of perturbations in intermediary metabolic processes is emerging. Treatment options are also being identified. RECENT FINDINGS: HIV itself may be a direct causal factor in the accelerated atherosclerosis and decreased levels of high-density lipoprotein that occur and contribute to increased cardiovascular complications. Antiretroviral drug-related and inflammation-related effects can cause mitochondrial toxicity and are an emerging area of research. The association of increased visceral adipose tissue with both drug-related and chronic inflammation-related factors is now better understood. The role of accelerated aging as a paradigm is useful to understand long-term outcome risks for patients. The use of growth hormone-releasing factor as a viable treatment option for increased visceral abdominal tissue has recently been confirmed for selected patients. SUMMARY: Metabolic issues persist in HIV patients who are otherwise stable. Understanding the various inter-related contributing factors has allowed for rapid improvement in patients' clinical status, but long-term consequences are of concern and require ongoing investigation in order to prevent limiting the otherwise important clinical achievements that have recently occurred.
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Julian Falutz (2011) studied this question.
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