***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: We conducted a pilot study to assess the effect of atorvastatin on HIV replication .  Patients with stable HAART-controlled infection interrupted therapy and were r and omly assigned to a control group or to start atorvastatin 40 or 80 mg/day . Statin groups showed lower serum cholesterol but similar viral loads and CD4 T-cell counts to the control group at weeks 4 and 12 . Paradoxically , baseline serum cholesterol , but not atorvastatin , influenced viral rebound at week 4 OBJECTIVES Statins and fibrates alter lipids , apolipoproteins and inflammatory markers in persons without HIV . The objective of this study was to evaluate changes in lipoproteins , apolipoproteins and other markers of inflammation with the use of pravastatin and fenofibrate . DESIGN Evaluation of participants in ACTG A5087 , a r and omized trial of pravastatin 40 mg/day or fenofibrate 200 mg/day for the treatment of dyslipidemia . Participants that failed single-agent therapy at week 12 were given the combination . METHODS Participants with available specimens were tested for apolipoproteins A1 and B , adiponectin , plasminogen-activator inhibitor type 1 ( PAI-1 ) , P-selectin , and high-sensitivity C-reactive protein ( hs-CRP ) . RESULTS 74 participants ( 37 per r and omized arm ) received either pravastatin or fenofibrate for 12 weeks with 60 receiving combination treatment from weeks 12 - 48 . There were no significant changes in hs-CRP , PAI-1 , and P-selectin . From baseline to week 12 , the median Apo B levels (-8 mg/dL , P=0.01 for fenofibrate and -27 mg/dL , P<0.01 for pravastatin ) and ApoB/A1 ratios ( -0.16 , P<0.01 for both arms ) significantly decreased . From baseline to week 48 , median adiponectin ( -1 ng/dL , P<0.01 ) , Apo B ( -22 mg/dL , P<0.01 ) and Apo B/A1 ratios ( -0.2 , P<0.01 ) all decreased in those who went on combination therapy , whereas Apo A1 ( 9.5 mg/dL , P=0.01 ) levels increased . CONCLUSION Treatment with pravastatin or fenofibrate improves the atherogenic lipid profile within the first 12 weeks and is sustained through 48 weeks with combination therapy . Adiponectin levels decrease with lipid-lowering therapy . However , markers of inflammation and platelet activation were not appreciably changed suggesting that the biologic properties of these agents differ in persons with HIV infection Recent studies have shown that rosuvastatin significantly decreases serum levels of inflammatory biomarkers and slows progression of carotid atherosclerosis in the general population . However , there are no data about its effect on progression of atherosclerosis in HIV-infected patients . Adult patients with HIV infection , on stable antiretroviral therapy , with asymptomatic carotid atherosclerosis and hypercholesterolemia , who started a rosuvastatin treatment at 10 mg daily during the period 2007 - 2009 were enrolled and followed-up for 24 months . Thirty-six patients ( 30 males ) were enrolled , with a mean age of 49 years , a mean duration of current antiretroviral therapy of 38 months , and a mean 10-year risk of myocardial infa rct ion of 18.5 % .  Rosuvastatin led to a significant decrease in mean values of intima-media thickness in all extracranial carotid arteries , with the greatest magnitude observed in carotid bifurcations ( a mean decrease of 18.7 % in the right artery and of 21.4 % in the left artery ) and in internal carotid arteries ( a mean decrease of 23.7 % in the right artery and of 25.6 % in the left artery ) . Moreover , there was a significant reduction in mean levels of total cholesterol , low-density lipoprotein ( LDL ) cholesterol , and triglycerides versus respective baseline values associated with a significantly decreased mean cardiovascular risk . The treatment with rosuvastatin was well tolerated , and serious adverse events were not reported . A 24-month treatment with rosuvastatin in HIV-infected patients on highly active antiretroviral therapy ( HAART ) with sub clinical atherosclerosis and a moderate cardiovascular risk seems to promote significantly favorable changes in carotid atherosclerosis , associated with a favorable effect on serum lipid levels and a good tolerability profile BACKGROUND Lipoatrophy can complicate thymidine analogue nucleoside reverse transcriptase inhibitor (tNRTI)-based antiretroviral therapy ( ART ) . Lipoatrophy may be less likely with ART including ritonavir-boosted lopinavir ( LPV/r ) . Small , placebo-controlled studies found that uridine ( in tNRTI recipients ) and pravastatin improved HIV lipoatrophy over 12 weeks . Today , most patients with lipoatrophy receive non-tNRTI-based ART ; the effect of uridine in such patients is unknown . METHODS We performed a prospect i ve , r and omized trial in lipoatrophic adults with plasma HIV RNA<50 HIV-1 RNA copies/mL on tNRTI-sparing ART including LPV/r . Patients received uridine [ 36 g three times a day ( tid ) on 10 consecutive days per month ; n=10 ] , pravastatin [ 40 mg every night ( nocte ) ; n=12 ] , uridine plus pravastatin ( n=11 ) or neither ( n=12 ) for 24 weeks . The primary endpoint was mean change in limb fat mass as assessed by dual-energy X-ray absorptiometry ( DEXA ) . With 20 patients per intervention , the study had 80 % power to detect a mean difference between a treatment and the control of 0.5 kg , assuming a st and ard deviation of 0.9 and an alpha threshold equal to 5 % ( two-sided ) . RESULTS Of 45 participants ( all men , with median age 49.5 years and median limb fat 2.6 kg ) , two discontinued pravastatin and one participant stopped both pravastatin and uridine . The difference between the mean changes in limb fat mass for uridine vs. no uridine was 0.03 kg [ 95 % confidence interval ( CI ) -0.35 , + 0.28 ; P=0.79 ] . The respective difference for pravastatin was -0.03 kg ( 95 % CI -0.29 , + 0.34 ; P=0.84 ) . Pravastatin slightly decreased total cholesterol ( 0.44 mmol/L ; P=0.099 ) . Visceral adipose tissue measured by computed tomography did not change significantly . CONCLUSION In this population and at the doses used , neither uridine nor pravastatin for 24 weeks significantly increased limb fat mass BACKGROUND AND OBJECTIVE We investigated atorvastatin  effectiveness and tolerance in HIV patients with hypercholesterolemia related to antiretroviral treatment . PATIENTS AND METHOD Prospect i ve study that included HIV+ patients under antiretroviral treatment who displayed secondary dyslipemia and medical treatment criteria ( according to NCEP-III ) . These patients were given 10 mg/day atorvastatin and hygienic-dietetic measures . If the therapeutic objectives were not achieved , the dose of atorvastatin was increased to 20 mg/day . Patients were followed up for 6 months . RESULTS 32 patients were included . In 5 cases it was necessary to increase the dose from 10 mg atorvastatin to 20 mg . The therapeutic objective was obtained in 62 % cases , with a good clinical tolerance . Only one adverse effect was noticed , which forced the removal of the drug . CONCLUSION In our study atorvastatin was effective for the treatment of dyslipemia in HIV patients , and it was safe and well tolerated Efavirenz  ( EFV )  is associated with hyperlipidemia when used in combination with other antiretroviral drugs . EFV is a mixed inducer/inhibitor of cytochrome P450 ( CYP ) 3A4 isozyme and may interact with hydroxymethylglutaryl coenzyme A ( HMG-CoA ) reductase inhibitors that are primarily metabolized via CYP3A4 . To assess the drug-drug interaction of EFV used in combination with simvastatin ( SIM ) , atorvastatin ( ATR ) , or pravastatin ( PRA ) , an open-label trial was conducted in 52 healthy adult HIV-seronegative subjects across AIDS Clinical Trials Group sites in the United States . Subjects received 40 mg of SIM , 10 mg of ATR , or 40 mg of PRA daily on days 0 through 3 and days 15 through 18 . EFV was administered daily at a dose of 600 mg on days 4 through 18 .  SIM , ATR , and PRA concentrations were determined before and after EFV , and  EFV concentrations were determined before and after statins . EFV reduced SIM acid exposure ( area under the curve at 0 to 24 hours [ AUC0 - 24h ] ) by 58 % ( Wilcoxon signed rank test , P = 0.003 ) and active HMG-CoA reductase inhibitory activity by 60 % ( P < 0.001 ) . EFV reduced ATR exposure by 43 % ( P < 0.001 ) and the total active ATR exposure by 34 % ( P = 0.005 ) . EFV administration result ed in a 40 % decrease in PRA exposure ( P = 0.005 ) . SIM , ATR , and PRA had no effect on non-steady-state EFV concentrations . In conclusion , EFV , when administered with SIM , ATR , or PRA , can result in significant induction of statin metabolism . The reduced inhibition of HMG-CoA reductase activity during coadministration of EFV may result in diminished antilipid efficacy at usual doses of SIM , ATR , and PRA Background Treatments that reduce inflammation and cardiovascular disease ( CVD ) risk among individuals with HIV infection receiving effective antiretroviral therapy ( ART ) are needed . Design and Methods We conducted a 2 × 2 factorial feasibility study of lisinopril ( L ) ( 10 mg daily ) vs L-placebo in combination with pravastatin ( P ) ( 20 mg daily ) vs P-placebo among participants receiving ART with undetectable HIV RNA levels , a Framingham 10 year risk score ( FRS ) ≥3 % , and no indication for ACE-I or statin therapy . Tolerability and adherence were evaluated . Longitudinal mixed models assessed changes in blood pressure ( BP ) , blood lipids , and inflammatory biomarkers from baseline through months 1 and 4 . Results Thirty-seven participants were r and omized and 34  [ lisinopril/pravastatin ( n = 9 ) , lisinopril/P-placebo ( n = 8) , L-placebo/pravastatin ( n = 9 ) , L-placebo/P-placebo ( n = 8) ] attended at least one follow-up visit . Participants were 97 % male , 41 % white , 67 % were current smokers , and 65 % were taking a protease inhibitor . Median age was 48 years , CD4 count 483 cells/mm3 , FRS 7.79 % , total cholesterol 184 mg/dL , and LDL-C 95 mg/dL. There was no treatment difference for pravastatin vs P-placebo  in total cholesterol , LDL-C , or any of the inflammatory biomarkers . Participants r and omized to lisinopril vs. L-placebo had significant declines in diastolic BP ( −3.3 mmHg , p = 0.05 ) , hsCRP ( −0.61 µg/mL , p = 0.02 ) and TNF-α ( −0.17 pg/mL , p = 0.04 ) . Participants taking lisinopril vs L-placebo were more likely to report missed doses ( 88 vs 35 % ; p = 0.001 ) and have adherence < 90 % by pill count ( 42 vs. 0 % ; p = 0.02 ) . Few participants from either group reported side effects ( n = 3 vs. n = 1 ) . Conclusions The modest BP changes and decreased adherence with lisinopril and absence of lipid differences with pravastatin suggest future studies of these drug classes should consider a run-in period to assess adherence and use a different statin . Our results also indicate that ACE-I therapy may have anti-inflammatory benefits for ART-treated persons with HIV infection and this should be further evaluated . Trial Registration Clinical Trials.gov Background : Ezetimibe inhibits intestinal absorption of cholesterol . Methods : Multicentered double-blind , r 
    Output:
    
Simvastatin is contraindicated in the setting of protease inhibitor use because of toxic drug-drug interactions when the 2 drugs are taken concomitantly .
Meanwhile , atorvastatin appears to be relatively safe at submaximal doses if monitored .
Pravastatin , rosuvastatin , and  pitavastatin  appear to have the most benign safety profiles among statins when co-administered with ART and may not require dose adjustment .