Lipoprotein (a) profile in HIV-1 infected patients treated with highly active antiretroviral therapy (HAART)
Abstract
Lipoprotein (a) [Lp(a)] is recognized as an independent factor of arteriosclerosis. The aim of this study
was to appreciate the profile of Lipoprotein (a) recognized as an independent factor of arteriosclerosis in the
monitoring of HIV-infected patients receiving Nevirapine (NVP) regimens, an antiretroviral known to reduce
cardiovascular disease risk. The study population (136 subjects) comprise of 106 HIV-infected subjects, and 30 HIVnegative
individuals. The 106 HIV-infected subjects were divided into groups as follows. HAART-untreated (27), HIVinfected
subjects that did not receive antiretroviral treatment; HAART-6M (36), HIV-infected subjects on antiretroviral
treatment for six months; and HAART-12M (43), HIV-infected subjects on antiretroviral treatment for twelve months.
All recruited patients had normal blood lipids values (Total cholesterol < 5.2 mmol/L, Triglycerides < 2 g/L, HDLc >
0.9 mmol/L). The Lp(a) levels were significantly higher in the HIV-infected group compared to the control (p =
0.0036). Within the HIV-infected subjects, Lp(a) level was found to be higher in HAART-treated group compared to
HAART naive group (p=0.004). Infected subjects on the antiretroviral treatment for12 months had higher Lp(a) levels
than those treated for 6 months (p=0.034). This study shows that adequate management of metabolic abnormalities
of HAART-treated HIV-infected patients must include periodic measurement of Lp(a) levels.
was to appreciate the profile of Lipoprotein (a) recognized as an independent factor of arteriosclerosis in the
monitoring of HIV-infected patients receiving Nevirapine (NVP) regimens, an antiretroviral known to reduce
cardiovascular disease risk. The study population (136 subjects) comprise of 106 HIV-infected subjects, and 30 HIVnegative
individuals. The 106 HIV-infected subjects were divided into groups as follows. HAART-untreated (27), HIVinfected
subjects that did not receive antiretroviral treatment; HAART-6M (36), HIV-infected subjects on antiretroviral
treatment for six months; and HAART-12M (43), HIV-infected subjects on antiretroviral treatment for twelve months.
All recruited patients had normal blood lipids values (Total cholesterol < 5.2 mmol/L, Triglycerides < 2 g/L, HDLc >
0.9 mmol/L). The Lp(a) levels were significantly higher in the HIV-infected group compared to the control (p =
0.0036). Within the HIV-infected subjects, Lp(a) level was found to be higher in HAART-treated group compared to
HAART naive group (p=0.004). Infected subjects on the antiretroviral treatment for12 months had higher Lp(a) levels
than those treated for 6 months (p=0.034). This study shows that adequate management of metabolic abnormalities
of HAART-treated HIV-infected patients must include periodic measurement of Lp(a) levels.
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