Cardiovascular risk and dyslipidemia among persons living with HIV: a review.

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Term Occurence Count Dictionary
hyperlipidemia 1 endocrinologydiseases
lipodystrophy 5 endocrinologydiseases
simvastatin 5 endocrinologydiseasesdrugs
Alirocumab 2 endocrinologydiseasesdrugs
atorvastatin 1 endocrinologydiseasesdrugs
ezetimibe 10 endocrinologydiseasesdrugs
familial hypercholesterolemia 1 endocrinologydiseases
gemfibrozil 2 endocrinologydiseasesdrugs
Evolocumab 1 endocrinologydiseasesdrugs
maraviroc 1 endocrinologydiseasesdrugs
niacin 1 endocrinologydiseasesdrugs
obesity 1 endocrinologydiseases
Fluvastatin 2 endocrinologydiseasesdrugs
fenofibrate 5 endocrinologydiseasesdrugs
hypoglycemia 1 endocrinologydiseases
rosuvastatin 7 endocrinologydiseasesdrugs
pravastatin 4 endocrinologydiseasesdrugs
Insulin 2 endocrinologydiseasesdrugs
Lovastatin 1 endocrinologydiseasesdrugs
diabetes mellitus 4 endocrinologydiseases
hyperglycemia 2 endocrinologydiseases
hypertriglyceridemia 6 endocrinologydiseases

Graph of close proximity drug and disease terms (within 200 characters).

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Select Drug Character Offset Drug Term Instance
Alirocumab 42717 reduced LDL-C by −54.6% and by absolute −78.9 mg/dl versus placebo, and by −36.3% versus ezetimibe. Alirocumab lowered LDL-C by −52.6% versus placebo, by −29.9% versus ezetimibe.Alirocumab was associated withan
Alirocumab 42799 versus ezetimibe.Alirocumab lowered LDL-C by −52.6% versus placebo, by −29.9% versus ezetimibe. Alirocumab was associated withan increased rate of injection-site reactions (RR: 1.48, 95% CI: 1.05 to 2.09, P = 0.02)[[78]]ODYSSEY
Evolocumab 42576 in randomized, controlled trials (RCTs).Twenty-five RCTs encompassing 12,200 patients were included Evolocumab treatment significantly reduced LDL-C by −54.6% and by absolute −78.9 mg/dl versus placebo, and
Fluvastatin 34074 20–40 mgModerateAtorvastatin 10–20 mgRosuvastatin 5–10 mgSimvastatin 20–40 mgPravastatin 40–80 mg Fluvastatin 80 mgPitavastatin 2–4 mgLowSimvastatin 10 mgPravastatin 10–20 mgLovastatin 20 mgFluvastatin
Fluvastatin 34175 40–80 mgFluvastatin 80 mgPitavastatin 2–4 mgLowSimvastatin 10 mgPravastatin 10–20 mgLovastatin 20 mg Fluvastatin 20–40 mgPitavastatin 1 mgLDL-C, low-density lipoprotein-cholesterolOther considerations when deciding
Insulin 16600 purpose of this substudyhsCRP MCP-1 OPG IL-6 IL-10 TNF-a ICAM-1 VCAM-1 Selectin E Selectin P Adiponectin Insulin D-dimer48hsCRP (40%, P < 0.0001), MCP-1 (20%, P¼0.0003), osteoprotegerin (13%, P¼0.0024), IL-6 (46%,P < 0.0001),
Insulin 17525 intermediate, LDL phenotype B, Lp-PLA2 Total LDL-Lp-PLA2 Total HDL-Lp-PLA2 8 (4; 14.9) 8.7 (5.4; 17.2) 0.829 Insulin , C-Peptide, HOMA index48TC, LDL-c, non-HDL-c, TC/HDL, triglyceride, Apo B, Apo A-I and Lp (a) decreased
Lovastatin 34158 20–40 mgPravastatin 40–80 mgFluvastatin 80 mgPitavastatin 2–4 mgLowSimvastatin 10 mgPravastatin 10–20 mg Lovastatin 20 mgFluvastatin 20–40 mgPitavastatin 1 mgLDL-C, low-density lipoprotein-cholesterolOther considerations
atorvastatin 29280 compared with placebo [[50]]. In a trial in which PLWHIV on protease inhibitors (PIs) were randomized to atorvastatin 10 mg, rosuvastatin 10 mg, or pravastatin 20 mg, the mean reductions in the LDL-C at one year were
ezetimibe 39382 significant interaction with P-450 cytocromes [[64]].Studies on PLWHIV with dyslipidemia evaluated ezetimibe alone or in combination with statins. Ezetimibe alone showed a statistically significant reduction of
ezetimibe 39639 but no significant change in HDL-cholesterol and triglycerides [[65], [66]]. The studies that added ezetimibe to a stable statin therapy showed a significant reduction of total cholesterol (ranging from −12.9%
ezetimibe 42707 significantly reduced LDL-C by −54.6% and by absolute −78.9 mg/dl versus placebo, and by −36.3% versus ezetimibe .Alirocumab lowered LDL-C by −52.6% versus placebo, by −29.9% versus ezetimibe.Alirocumab was associated
ezetimibe 42789 by −36.3% versus ezetimibe.Alirocumab lowered LDL-C by −52.6% versus placebo, by −29.9% versus ezetimibe .Alirocumab was associated withan increased rate of injection-site reactions (RR: 1.48, 95% CI: 1.05
ezetimibe 45378 once monthly (QM) both with daily oral placebo or subcutaneous placebo Q2W or QM both with daily oral ezetimibe 10 mg.307 patientsAt week 12, evolocumab reduced LDL-C from baseline by 53% to 56%, corresponding to
ezetimibe 45519 evolocumab reduced LDL-C from baseline by 53% to 56%, corresponding to treatment differences versus ezetimibe of 37% to 39% (p < 0.001).Muscle adverse events occurred in 12% of evolocumab-treated patients and
ezetimibe 45637 to 39% (p < 0.001).Muscle adverse events occurred in 12% of evolocumab-treated patients and 23% of ezetimibe -treated patients. Treatment-emergent adverse events and laboratory abnormalities were comparable across
ezetimibe 50745 results in a more favorable lipid profile with a very low toxicity [[99], [100]] but the introduction of ezetimibe that shows an higher efficacy has limited the use of omega 3 only for patients with a low-moderate dyslipidemia
ezetimibe 59125 guidelines for HIV-infected persons are warranted.Another effective drug for the hypercholesterolemia is ezetimibe that markedly reduces the intestinal absorption of cholesterol. In HIV-infected subjects, ezetimibe
ezetimibe 59225 ezetimibe that markedly reduces the intestinal absorption of cholesterol. In HIV-infected subjects, ezetimibe already showed to be effective in reducing the total cholesterol and LDL-C levels when used alone or
fenofibrate 49235 with statin with a lower risk of rhabdomyolisis [[89], [90]]. Studies on HIV-population evaluating fenofibrate showed a significant reduction of triglycerides (from 18% to 58%) depending on cART regimen, study design,
fenofibrate 49469 hypertriglyceridemia [[91]]. An observational analysis including 80 patients with HIV infection on fenofibrate s with a mean baseline triglycerides value of 347 mg/dl showed a reduction of 18% of triglycerides [[91]].
fenofibrate 49642 showed a reduction of 18% of triglycerides [[91]]. A randomized trial evaluating fish-oil therapy versus fenofibrate enrolling 50 patients with HIV infection in each arm demonstrated a reduction of 58% of triglycerides
fenofibrate 49759 enrolling 50 patients with HIV infection in each arm demonstrated a reduction of 58% of triglycerides in fenofibrate arm with a median baseline of triglycerides of 694 mg/dl [[92]]. Few studies evaluated the use of fibrates
fenofibrate 52358 [HIV-infected]Randomized-Open labelStudy duration: 48 weeksMedian change: −144 mg/dl (−1492 to 927 fenofibrate ) vs −66 (−899 to 1567 prevastatin)[[89]]FO41 (HIV-infected)Randomized-Open labelStudy duration:
gemfibrozil 36647 [[59]].Combination of statins with fibrates may enhance the risk of myopathy. This risk is greater for gemfibrozil , and the association of gemfibrozil with statins should be avoided. The increased risk for myopathy,
gemfibrozil 36683 fibrates may enhance the risk of myopathy. This risk is greater for gemfibrozil, and the association of gemfibrozil with statins should be avoided. The increased risk for myopathy, when combined statins and fibrates
maraviroc 10873 little effect on lipid profile [[19]–[21]], as well as C-C chemokine receptor type 5 (CCR5) inhibitor ( maraviroc ) [[22]]. Since each cART switching has a potential virologic failure risk, it is recommended to prefer
niacin 60156 hypertrigliceridemia. Other drugs for hypertrigliceridemia are: acipimox, that showed a low efficacy; niacin that, in spite of its efficacy can induce insulin resistance and hepatotoxicity; and tesamorelin that
pravastatin 29325 PLWHIV on protease inhibitors (PIs) were randomized to atorvastatin 10 mg, rosuvastatin 10 mg, or pravastatin 20 mg, the mean reductions in the LDL-C at one year were 20%, 25%, and 18%, respectively, after one
pravastatin 37775 some antiretrovirals that may increase the risk of side effects. All current available statins, except pravastatin , rosuvastatin, and pitavastatin, undergo major hepatic metabolism through the cytochrome P (CYP) system
pravastatin 52120 duration: 18 weeksFO = 46% vs Fenofibrate (58%) vs FO + Fenofibrate (65%)[[95]]Fenofibrate vs pravastatin vs Fenofibrate + pravastatin88 vs 86, if no response at week 12 switch to combination therapy (most
pravastatin 52151 vs Fenofibrate (58%) vs FO + Fenofibrate (65%)[[95]]Fenofibrate vs pravastatin vs Fenofibrate + pravastatin 88 vs 86, if no response at week 12 switch to combination therapy (most patients switched) [HIV-infected]Randomized-Open
rosuvastatin 1672 warranted.Ezetimibe reduces the intestinal absorption of cholesterol. It is effective alone or in combination with rosuvastatin . It does not modify plasmatic concentrations of antiretrovirals. A number of experimental new classes
rosuvastatin 29301 [[50]]. In a trial in which PLWHIV on protease inhibitors (PIs) were randomized to atorvastatin 10 mg, rosuvastatin 10 mg, or pravastatin 20 mg, the mean reductions in the LDL-C at one year were 20%, 25%, and 18%,
rosuvastatin 30451 tomography; IMT, intima media thickness; ART, antiretroviral therapy; CCA, common carotid arteryFinally, as rosuvastatin has demonstrated to significantly reduce several markers of vascular inflammation and CD4+ and CD8+
rosuvastatin 37168 to be associated with diabetes than lower doses [[62]]. In a randomized, placebo-controlled trial of rosuvastatin versus placebo in antiretroviral treated HIV-infected patients, statin therapy showed a more than 50%
rosuvastatin 37788 antiretrovirals that may increase the risk of side effects. All current available statins, except pravastatin, rosuvastatin , and pitavastatin, undergo major hepatic metabolism through the cytochrome P (CYP) system thus, other
rosuvastatin 38559 when combined with PI-containing regimens and is contraindicated in PLWHIV on PIs. Pravastatin and rosuvastatin generally are considered the safer statins because their metabolism does not utilize CYP3A4. Pitavastatin
rosuvastatin 59356 effective in reducing the total cholesterol and LDL-C levels when used alone or in combination with rosuvastatin . PCSK9 inhibitors, MTP inhibitors, antisense oligonucleotide against apolipoprotein B, adenosine Triphosphate
simvastatin 52653 (HIV-infected)Randomized-placebo-controlledStudy duration: 8 weeksMedian decrease: −34 (−149–9.5) mg/dL[[97]]FO + simvastatin 254 (uninfected)Randomized-Open labelStudy duration: 8 weeksMean change: 29% (FO + simvastatin) vs
simvastatin 52750 mg/dL[[97]]FO + simvastatin254 (uninfected)Randomized-Open labelStudy duration: 8 weeksMean change: 29% (FO + simvastatin ) vs 6% (simvastatin)[[97]]FO + simvastatin59 with Coronary heart disease already on simvastatin (uninfected)Randomized,
simvastatin 52770 (uninfected)Randomized-Open labelStudy duration: 8 weeksMean change: 29% (FO + simvastatin) vs 6% ( simvastatin )[[97]]FO + simvastatin59 with Coronary heart disease already on simvastatin (uninfected)Randomized,
simvastatin 52795 labelStudy duration: 8 weeksMean change: 29% (FO + simvastatin) vs 6% (simvastatin)[[97]]FO + simvastatin 59 with Coronary heart disease already on simvastatin (uninfected)Randomized, Study duration: 24 weeks + 24 weeksMean
simvastatin 52848 (FO + simvastatin) vs 6% (simvastatin)[[97]]FO + simvastatin59 with Coronary heart disease already on simvastatin (uninfected)Randomized, Study duration: 24 weeks + 24 weeksMean change: 20–30%[[98]]TRG, Triglycerides;
Select Disease Character Offset Disease Term Instance
diabetes mellitus 28824 [[48], [49]]. Benefits of statin therapy were observed in nearly all subgroups, including persons with diabetes mellitus , men and women, and across age groups.The most recent clinical trials suggested that the LDL-C lowering
diabetes mellitus 32893 atherosclerotic CVD, with LDL-C level ≥ 190 mg/dl 3) Patients aged 40–75 years, with type I or II diabetes mellitus , and LDL-C level < 190 mg/dl 4) Patients without clinical atherosclerotic CVD or diabetes, aged
diabetes mellitus 34323 low-density lipoprotein-cholesterolOther considerations when deciding about statin therapy include: diabetes mellitus in individual aged less than 40 years or more than 75 years; a family history of premature CVD; elevated
diabetes mellitus 55771 [[117]]. In the general population, increased visceral adipose tissue (VAT) increases the risk of type II diabetes mellitus (T2DM), cardiovascular disease (CVD) and overall mortality. In HIV-infected subjects VAT has been also
familial hypercholesterolemia 41013 evolocumab) have been recently approved by the European Medicines Agency for the use in subjects with familial hypercholesterolemia , in patients who failed to achieve acceptable lipid control although an optimal lipid lowering therapy
hyperglycemia 25788 HIV-1 infected patients in Cabotegravir monotherapy arm. A subject with type I diabetes had grade 2 hyperglycemia at baseline and at all time points other than day 7 (hypoglycemia) and the follow-up visit (grade 3
hyperglycemia 25902 at baseline and at all time points other than day 7 (hypoglycemia) and the follow-up visit (grade 3 hyperglycemia ). The other subject, on day 7, had grade 4 TGL elevation subsequent to a very high–fat meal the previous
hyperlipidemia 48249 evaluate safety, tolerability, and efficacy on LDL-C of evolocumab in 450 subjects with HIV and with hyperlipidemia and/or mixed dyslipidemia. Start date is scheduled on May 2017.Drugs for the treatment of hypertriglyceridemiaIsolated
hypertriglyceridemia 1909 treatment of hypercholesterolemia are being studied.Fibrates represent the first choice for treatment of hypertriglyceridemia , however, the renal toxicity of fibrates and statins should be considered.Omega 3 fatty acids have a
hypertriglyceridemia 48354 hyperlipidemia and/or mixed dyslipidemia. Start date is scheduled on May 2017.Drugs for the treatment of hypertriglyceridemia Isolated hypertriglyceridemia is rare in the setting of PLWHIV on cART in the modern era, the lipid profile
hypertriglyceridemia 48383 dyslipidemia. Start date is scheduled on May 2017.Drugs for the treatment of hypertriglyceridemiaIsolated hypertriglyceridemia is rare in the setting of PLWHIV on cART in the modern era, the lipid profile usually shows a mixed
hypertriglyceridemia 48817 the risk of acute pancreatitis [[87]].FibratesFibrates represent the first choice for treatment of hypertriglyceridemia in HIV infected patients. They bind and regulate nuclear receptor peroxisome proliferator activator
hypertriglyceridemia 49370 reduction of triglycerides (from 18% to 58%) depending on cART regimen, study design, and on grade of hypertriglyceridemia [[91]]. An observational analysis including 80 patients with HIV infection on fenofibrates with a mean
hypertriglyceridemia 59662 drugs for the treatment of hypercholesterolemia.Fibrates represents the first choice for treatment of hypertriglyceridemia in HIV infected patients. Few studies evaluated the use of fibrates and statins in HIV associated dyslipidemia
hypoglycemia 25855 with type I diabetes had grade 2 hyperglycemia at baseline and at all time points other than day 7 ( hypoglycemia ) and the follow-up visit (grade 3 hyperglycemia). The other subject, on day 7, had grade 4 TGL elevation
lipodystrophy 2443 toxicities. Not all antiretrovirals have similar toxicities. Protease Inhibitors may cause dyslipidemia and lipodystrophy , while integrase inhibitors have a minimal impact on lipids profile, and no evidence of lipodystrophy.
lipodystrophy 2545 lipodystrophy, while integrase inhibitors have a minimal impact on lipids profile, and no evidence of lipodystrophy . There is still much to be written with the introduction of new drugs in clinical practice.ConclusionsCardiovascular
lipodystrophy 54876 redistribution in HIV-infected subjectsLong-term ART use has been associated with the occurrence of lipodystrophy , a medical condition characterized by an abnormal fat redistribution [[109]].Fat redistribution among
lipodystrophy 58045 that not all antiretroviral agents have similar toxicities. PI/ritonavir may cause dyslipidemia and lipodystrophy , while INI have a minimal impact on lipids profile, and not reported evidence of lipodystrophy. There
lipodystrophy 58140 and lipodystrophy, while INI have a minimal impact on lipids profile, and not reported evidence of lipodystrophy . There is still much to discover with the introduction of new drugs in clinical practice: dolutegravir,
obesity 56521 deposition is associated with inflammation and adverse metabolic impact beyond that seen with generalized obesity [[121]]. Associations between intra-abdominal VAT and increased metabolic disease risk (including CVD)

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