Echeverría Patricia, Guardiola Montse, González Marta, Vallvé Joan Carles, Puig Jordi, Bonjoch Anna, Clotet Bonaventura, Ribalta Josep, Negredo Eugenia
Fundació Lluita contra la Sida, Hospital Universitari Germans Trias i Pujol, Badalona Universitat Autònoma de Barcelona, HIV, Barcelona, Spain.
Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Unitat de Recerca en Lípids i Arteriosclerosi, Barcelona, Spain.
J Int AIDS Soc. 2014 Nov 2;17(4 Suppl 3):19557. doi: 10.7448/IAS.17.4.19557. eCollection 2014.
HIV-infected patients treated with Highly Active Antiretroviral Therapy (HAART) may be predisposed to hypertriglyceridemia, which gives rise to a highly atherogenic lipid profile known as atherogenic dyslipidemia (AD). We propose that genetic variability leaves some HIV-infected patients more predisposed to AD than others (1, 2).
This was a cross-sectional, observational study conducted in 468 antiretroviral-treated HIV-infected patients attending at the outpatient clinic of a tertiary hospital over a 6-month period, who were classified as normolipidemic (n=173) or presenting with AD (triglycerides: 1.7 mmol/L and HDLc < 1.02 [men] or 1.28 mmol/L [women]) (n=148). Polymorphisms were identified in the APOA5, APOC3, LPL, CETP, HL, MTP, APOE, LRP5 and VLDLR genes.
Atherogenic dyslipidemia was detected in 31% of patients, most of whom were men (77%). This group was also older and had higher levels of remnant lipoprotein cholesterol (RLPc) than normolipidemic patients. The polymorphisms rs328 in LPL, rs708272 in CETP and rs1800588 in HL were 10-40% significantly more frequent in normolipidemic patients. At least 1 of these polymorphisms was detected in 90% of normolipidemic patients; in AD patients, the percentage decreased to 75% (p=0.003). This effect was dependent on both the allele and the dose of HAART and independent of the regimen administered. The protective combination showed a trend towards higher HDLc (1.13 [0.40] vs 1.24 [0.23] mmol/L), lower triglycerides (2.23 [2.34] vs 1.89 [1.24] mmol/L) and lower RLPc (16.41 [11.42] vs 12.99 [11.69] mmol/L).
Polymorphisms in LPL, CETP and HL protect HIV-infected patients from developing AD in a dose-dependent manner (3).
接受高效抗逆转录病毒治疗（HAART）的HIV感染患者可能易患高甘油三酯血症，进而导致一种高度致动脉粥样硬化的血脂谱，即致动脉粥样硬化性血脂异常（AD）。我们提出，基因变异使一些HIV感染患者比其他患者更易患AD（1,2）。
这是一项横断面观察性研究，在一家三级医院门诊对468例接受抗逆转录病毒治疗的HIV感染患者进行了为期6个月的研究，这些患者被分为血脂正常组（n = 173）或患有AD组（甘油三酯：男性≥1.7 mmol/L且高密度脂蛋白胆固醇<1.02 mmol/L，女性≥1.7 mmol/L且高密度脂蛋白胆固醇<1.28 mmol/L）（n = 148）。对载脂蛋白A5（APOA5）、载脂蛋白C3（APOC3）、脂蛋白脂肪酶（LPL）、胆固醇酯转运蛋白（CETP）、肝脂酶（HL）、微粒体甘油三酯转运蛋白（MTP）、载脂蛋白E（APOE）、低密度脂蛋白受体相关蛋白5（LRP5）和极低密度脂蛋白受体（VLDLR）基因的多态性进行了鉴定。
31%的患者检测出有致动脉粥样硬化性血脂异常，其中大多数为男性（77%）。与血脂正常的患者相比，该组患者年龄更大，残余脂蛋白胆固醇（RLPc）水平更高。LPL基因中的rs328、CETP基因中的rs708272和HL基因中的rs1800588多态性在血脂正常患者中的频率显著高出10 - 40%。90%的血脂正常患者检测到至少一种这些多态性；在AD患者中，这一比例降至75%（p = 0.003）。这种效应既取决于等位基因，也取决于HAART的剂量，且与所采用的治疗方案无关。具有保护作用的组合显示出HDLc水平较高（1.13 [0.40] vs 1.24 [0.23] mmol/L）、甘油三酯水平较低（2.23 [2.34] vs 1.89 [1.24] mmol/L）和RLPc水平较低（16.41 [11.42] vs 12.99 [11.69] mmol/L）的趋势。
LPL、CETP和HL基因的多态性以剂量依赖的方式保护HIV感染患者不发生AD（3）。
