Protease Inhibitor-Associated Dyslipidemia in HIV-Infected Patients Is Strongly Influenced by the APOA5–1131T→C Gene Variation

Guardiola, Montse; Ferré, Raimón; Salazar, Juliana; Alonso-Villaverde, Carlos; Coll, Blai; Parra, Sandra; Masana, Luís; Ribalta, Josep

doi:10.1373/clinchem.2006.069583

Cited by 45 publications

(29 citation statements)

References 22 publications

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“…For instance, the most severe dyslipidemic profiles after PI therapy were obtained in those patients carrying the three APOC3 variations (i.e., at nucleotides -455, -482 and the SstI site) and a non-ε3/ε3 APOE genotype [19][20][21]. Similarly, Guardiola et al [22] indicated that in a cohort of PI treated HIV-infected patients, the -1131C carriers in APOA5 gene experienced marked increases in triglyceride levels (up to 80%) during a 3-year follow-up, while no change was recorded in patients carrying the normal -1131T allele. More recent studies [23,24] have associated nucleotide variations in resistin and β2 adrenegic receptor (ARb2) with the occurrence of lipodystrophy.…”

Section: Discussionmentioning

confidence: 99%

629 Antiretroviral Treatment-Induced Dyslipidemia in Hiv-Infected Patients Is Influenced by the Apoc3-Related Rs10892151 Polymorphism

Beltrán‐Debón¹,

Aragonès²,

Alonso-Villaverde³

et al. 2011

Atherosclerosis Supplements

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Section: Discussionmentioning

confidence: 99%

629 Antiretroviral Treatment-Induced Dyslipidemia in Hiv-Infected Patients Is Influenced by the Apoc3-Related Rs10892151 Polymorphism

Beltrán‐Debón¹,

Aragonès²,

Alonso-Villaverde³

et al. 2011

Atherosclerosis Supplements

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“…Moreover, the available evidence demonstrates that certain PIs could induce endothelial dysfunction, including a decrease of endothelium-dependent vasorelaxation, inhibition of the nitric oxide synthase system, increase of oxidative stress, and activation of mitogenactivated protein kinases [23][24][25]. Moreover, the course of atherosclerosis in patients with HIV infection seems also influenced by polymorphisms in the SDF1 and CX3C1 genes by metabolic variables and by the CD4 lymphocyte count [26,27].…”

Section: Discussionmentioning

confidence: 99%

HIV Disease, Antiretroviral Therapy Safety and the Cardiovascular System. Clinical-Instrumental Assessment of Antiretroviral-Nave Versus Subjects Already Treated with Antiretroviral Agents

Manfredi¹

2011

Open Drug Saf J

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Abstract:Background: There is controversy over whether or not HIV infection and antiretroviral therapy contribute to early atherosclerosis. Ultrasonographic evaluation of carotid intima-media thickness is considered as a reliable surrogate marker of subclinical atherosclerosis and may be employed in the setting of a cardiovascular risk assessment in HIVinfected patients. Patients and methods:A cross-sectional study evaluating classical risk factors for cardiovascular diseases, parameters of HIV infection, antiretroviral therapy and subclinical atherosclerosis in HIV-positive subjects naïve or treated with antiretroviral agents was performed. The enrolled patients underwent ultrasonography of the epi-aortic vessels using a Philips HDI 5000 power color-Doppler with 7.5-MHz probes. The 10-year risk of coronary heart disease was calculated by the Framingham equation.Results: A total of 27 patients (19 males and 8 females; mean age 44 + 13 years; range 32-59 years) was enrolled in the study: 11 subjects were naïve to all antiretroviral agents (group A) and 16 patients were treated with antiretroviral therapy for >36 months (group B). Mean duration of known HIV infection was significantly longer in group B than in group A, such as frequency of dyslipidemia and lipodystrophy syndrome. Prevalence of carotid plaques was significantly higher in group B than in group A (43.7% versus 0; p=0.012). In group B, patients with intermediate to high 10-year risk of coronary heart disease (>10%) showed a significantly higher intima-media thickness and prevalence of carotid lesions than those with low risk (<10%). Moreover, carotid plaques presented structural features comparable to those of classical atherosclerotic plaques observed in general population, with iso-hyperechonegic aspects and irregular surfaces. Conclusions:Prevalence of carotid atherosclerosis is higher in HIV-infected patients previously treated with antiretrovirals than in those naïve to antiretroviral therapy and seems mostly associated with a longer duration of HIV infection, more severe lipid metabolism alterations, presence of lipodystrophy syndrome, and a more elevated 10-year risk of cardiovascular diseases.

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“…42,43 As described above, abnormal lipid and lipoprotein concentrations have been reported among HIVpositive patients prior to initiation of HAART, which may be exacerbated after treatment initiation. The fundamentally proatherogenic lipoprotein changes, with increased plasma TG, increased total and LDL-C, and decreased HDL-C, 26,[44][45][46][47] , can be further underscored by other potentially proatherogenic changes such as increases in the levels of small, dense LDL particles, 48 lipoprotein(a), 26,49,50 and apolipoproteins B, 51,52 , C-III, 52,53 , E, 54 and H. 55 A number of studies have addressed mechanisms for the dyslipidemic pattern in HIV/HAART.…”

Section: Pathogenesis Of Antiretroviral-induced Metabolic Disordersmentioning

confidence: 95%

“…67 Patients with the -1131T→C promoter polymorphism were shown to be predisposed to a more pronounced hyperlipidemia during PI treatment. 43 Other DNA polymorphisms have also been associated with various responses to antiretroviral treatment.…”

Section: Lipid and Bone Metabolism In Hiv/haartmentioning

confidence: 99%

Human Immunodeficiency Virus and Highly Active Antiretroviral Therapy–Associated Metabolic Disorders and Risk Factors for Cardiovascular Disease

Anuurad

Semrad

Berglund

2009

Metabolic Syndrome and Related Disorders

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The successful introduction of highly active antiretroviral therapy (HAART), a combination of potent antiretroviral agents, including protease inhibitors, nucleoside reverse transcriptase inhibitors, and nonnucleoside reverse transcriptase inhibitors, has impacted positively on morbidity and mortality among human immunodefi ciency virus (HIV)-positive patients. Over time, HAART has been associated with a number of metabolic and anthropometric abnormalities, including dyslipidemia and insulin resistance as well as subcutaneous fat loss and abdominal obesity, potentially contributing to cardiovascular risk. Recent studies have more fi rmly established that both HIV infection and HAART might increase the risk of clinical cardiovascular events. Furthermore, whereas HIV/HAART is associated with multiple aspects of endocrine dysfunction, there has been less focus on bone disease, although some studies indicate a higher prevalence of osteoporosis among HIV-positive subjects compared to HIV-negative controls. The relationship between bone and fat metabolism under HIV-positive conditions deserves further attention, and available data suggest the possibility of an intriguing connection. In the future, an increasing population of aging HIV-positive patients with a spectrum of antiretroviral therapies and accumulation of endocrine abnormalities and conventional cardiovascular risk factors will present preventive and therapeutic challenges to our health-care system.

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Protease Inhibitor-Associated Dyslipidemia in HIV-Infected Patients Is Strongly Influenced by the APOA5–1131T→C Gene Variation

Cited by 45 publications

References 22 publications

629 Antiretroviral Treatment-Induced Dyslipidemia in Hiv-Infected Patients Is Influenced by the Apoc3-Related Rs10892151 Polymorphism

629 Antiretroviral Treatment-Induced Dyslipidemia in Hiv-Infected Patients Is Influenced by the Apoc3-Related Rs10892151 Polymorphism

HIV Disease, Antiretroviral Therapy Safety and the Cardiovascular System. Clinical-Instrumental Assessment of Antiretroviral-Nave Versus Subjects Already Treated with Antiretroviral Agents

Human Immunodeficiency Virus and Highly Active Antiretroviral Therapy–Associated Metabolic Disorders and Risk Factors for Cardiovascular Disease

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