Serum lipid levels associated with increased risk for cardiovascular disease is associated with highly active antiretroviral therapy (HAART) in HIV-1infection

The long-term effects of fat metabolism, storage and utilization in HIV-1 i nfected patients on highly active antiretroviral therapy (HAART) including a protease inhibitor are profound and cause increasing concern. The main im portance of these lipid/metabolic disorders lies in their assumed contribut ion to an increased risk of coronary heart disease (CHD). In the general po pulation increased levels of lipoprotein(a) [Lp(a)] constitute an independe nt risk factor for CHD by itself as well as in combination with increased l evels of cholesterol and low density lipoprotein (LDL)-cholesterol, respect ively. Two hundred and fifty-six patients with 27+/-7 months HAART and 84 treatmen t-naive HIV-1 positive patients were screened for cardiovascular risk facto rs. The subjective perception of fat wasting and/or accumulation in differe nt sites of the body, which was possible to evaluate in 235 patients on HAA RT and 73 treatment-naive patients, the levels of plasma triglycerides (TG) , cholesterol, LDL and high-density lipoproteins (HDL)-cholesterol, LDL/HDL ratio and Lp(a) were measured. Of the patients on HAART, 42% (98/235) reported abnormal fat distribution a s compared with 4% (3/73) of the treatment-naive patients (P < 0.0001). The levels of TG, cholesterol and LDL-cholesterol, but not HDL-cholesterol or Lp(a) were higher (P<0.0001) in the HAART group as compared with the naive group. Very high Lp(a) levels (> 700 mg/l) were more common among HAART pat ients as compared with naive, 14% (36/256) vs 2% (2/83); P=0.0022. The Lp(a ) levels correlated to the levels of LDL-cholesterol, but not to total chol esterol, HDL-cholesterol or TG, and did not differ between patients with an d without subjective perception of abnormal fat distribution. A significant number of the HAART patients had very high levels of Lp(a) an d various combinations of increased lipid values associated with considerab ly increased risk for CHD. The elevation of Lp(a) did not relate to any oth er clinical or laboratory parameter than to LDL-cholesterol.