Haart, Lipid metabolism and cvd risk

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In 1981, at the beginning of the HIV/AIDS epidemic, anti-viral therapies were available but they were not very effective at slowing the progression of HIV infection [11].  When HAART became available for HIV infection in 1996, patients who were hospitalized and/or bedridden, after taking the medication, were up and walking around the next day, thus making HAART seem to have a miraculous “Lazarus Effect”.  HAART successfully slowed the incidence of HIV infection and reduced deaths from AIDS over the next 10 years [12] [6]; however, metabolic co-morbidities and CVD risk were rising in the HIV infected, HAART treated, aging population.

Metabolic co-morbidities impair the ability of cells to obtain energy that is needed for them to survive.   That energy is derived from food in the form of glucose, lipids and proteins, or pulled from storage depots in the body.  Humans take excess glucose and store it as adipose tissue to use during famine.  Metabolic syndrome is a constellation of risk factors, increased blood pressure, dyslipidemia abdominal obesity and hyperglycemia) that tend to cluster together.  There is no consensus on what causes MS but many believe when  these metabolic processes do not function properly and is associated with diabetes, insulin resistance, lipodystrophy and dyslipidemia.

Patients on HAART, especially due to protease inhibitors, experience metabolic complications including dyslipidemia, high blood pressure, adipose redistribution and insulin resistance placing them at a higher risk for CVD and diabetes [6] [13].  The pathogenesis of metabolic syndrome in HIV-infected patients compared to other patients is very different.  In HIV-infected patients who are not considered obese, there is HAART-induced dyslipidemia, hypertriglyceridemia and HDL reduction where in non-HIV-infected patients hypertriglyceridemia and dyslipidemia stem from abnormal fat metabolism due to obesity.  Total cholesterol (TC), low density lipoprotein (LDL-C) and high density lipoprotein (HDL-C) levels fall after seroconversion.  Lower levels of TC and LDL-C and higher levels of HDL-C are preferable.  The lipid levels increase after HAART initiation to slightly higher levels than those seen at preseroconversion with the exception of HDL-C, which remains lower. TC, LDL-C and triglycerides (TG) remain higher than preseroconversion levels as treatment continues but HDL-C still remains lower [14].  Adipose redistribution, lipodystrophy (LD), manifests itself in peripheral fat wasting, back of neck and breast fat accumulation and increase in waist circumference [5] [15] [16].  Patients on HAART experience metabolic complications including dyslipidemia, adipose redistribution and insulin resistance which place these patients at a higher risk for cardiovascular disease and diabetes [2].  The prevalence of insulin resistance and diabetes mellitus increase the longer HIV infected men continue on HAART [17] at a higher rate than non-infected men.

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