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Differentiating hyperlipidaemia associated with antiretroviral therapy
 
 
  AIDS 2003; 17(2):189-194. Stefan Mauss a; Juergen Stechel b; Reinhard Willers c; Guenther Schmutz a; Florian Berger a; Werner O. Richter d
 
Background: Hyperlipidaemia associated with antiretroviral treatment has led to concerns for an increased cardiovascular risk in HIV-infected patients.
 
Objective: To assess this cardiovascular risk by comparing the lipoprotein pattern of antiretroviral-treated and untreated HIV-positive patients with patients with familial combined hyperlipidaemia (high cardiovascular risk) or familial hypertriglyceridaemia (low cardiovascular risk).
 
Methods: Fasting serum samples were drawn from consecutive patients with HIV infection or lipoprotein disorders. Total cholesterol, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, triglycerides, apolipoprotein A1 and B were determined in serum. Very low density lipoprotein (VLDL) was prepared by ultracentrifugation and analysed for cholesterol, triglycerides and apolipoprotein B.
 
Results: Lipoprotein disorders were found in 114/187 HIV-positive patients (61%). Of these, according to the Fredrickson classification, 10% were type IIa (elevated LDL-cholesterol), 14% type IIb (elevated LDL- and VLDL-cholesterol) and 76% were type IV (elevated VLDL-cholesterol). VLDL composition was analysed in 34 HIV-positive patients with type IV hyperlipidaemia. The ratio of VLDL-triglycerides to VLDL-apolipoprotein B in these patients was 16.2 6.0. This ratio was not different from 14 patients with famlial hypertriglyceridaemia (16.9 6.0; P = 0.61), but differed substantially from 10 patients with familial combined hyperlipidaemia (6.8 1.0; P < 0.0001).
 
Conclusions: In HIV-infected patients with high VLDL, large VLDL particles were found with no increase in number. This pattern resembles familial hypertriglyceridaemia. It is different from familial combined hyperlipidaemia, where an increase in number of small-sized VLDL particles occurs. Further research is needed to assess the contribution of VLDL-associated hypercholesterolaemia in those taking antiretroviral drugs to the cardiovascular risk profile of HIV-positive patients.
 
Background: Hyperlipidaemia is frequently associated with antiretroviral treatment and this has led to concerns about an increased cardiovascular risk in treated HIV-positive patients [1]. The data on cardiovascular events in HIV-positive patients are anecdotal or retrospective and do not allow firm conclusions to be drawn regarding the influence of hyperlipidaemia associated with antiretroviral therapy on cardiovascular risk [2-4]. High-resolution ultrasound studies assessing intima media thickness and the presence of atherosclerotic plaques as signs of premature atherosclerosis are conflicting [5-7]. However, despite the lack of clear evidence, most clinicians assume that hyperlipidaemia associated with antiretroviral treatment does increase the cardiovascular risk, and treatment with lipid-lowering agents is common [8].
 
It has been shown that hypercholesterolaemia found in HIV-positive patients is frequently caused by the elevation of very low density lipoprotein (VLDL) [1, 9-13]. Because of this, the proportion of hyperlipidaemia caused by VLDL in HIV-positive patients taking antiretroviral therapy is in excess of the proportion found in the general population. Two well-described genetically inherited lipid disorders that involve an increase in VLDL may serve as models to analyse further the lipoprotein pattern in HIV-positive patients with elevated VLDL and to estimate their cardiovascular risk. Familial combined hyperlipidaemia is caused by overproduction of small VLDL particles in the liver, leading to a parallel increase in apolipoprotein B and is associated with increased cardiovascular risk [14, 15]. Familial hypertriglyceridaemia is characterized by production of normal numbers of large VLDL particles containing more triglycerides than normal. This results in normal apolipoprotein B levels and no or only modestly increased cardiovascular risk [16, 17].
 
In the present study, lipoprotein patterns were analysed in HIV-positive patients with and without antiretroviral treatment, HIV-seronegative patients with familial combined hyperlipidaemia (high cardiovascular risk) or with familial hypertriglyceridaemia (low cardiovascular risk). In addition the size of VLDL particles were measured in a subgroup of HIV-positive patients who had Fredrickson type IV hyperlipidaemia and this was compared with that in those with the familial dyslipidaemias.
 
 
 
 
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