***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: CONTEXT Cardiovascular disease is increased in patients with human immunodeficiency virus ( HIV ) , but the specific mechanisms are unknown . OBJECTIVE To assess arterial wall inflammation in HIV , using 18fluorine-2-deoxy-D-glucose positron emission tomography ( 18F-FDG-PET ) , in relationship to traditional and nontraditional risk markers , including soluble CD163 ( sCD163 ) , a marker of monocyte and macrophage activation . DESIGN , SETTING , AND PARTICIPANTS A cross-sectional study of 81 participants investigated between November 2009 and July 2011 at the Massachusetts General Hospital . Twenty-seven participants with HIV without known cardiac disease underwent cardiac 18F-FDG-PET for assessment of arterial wall inflammation and coronary computed tomography scanning for coronary artery calcium . The HIV group was compared with 2 separate non-HIV control groups . One control group ( n = 27 ) was matched to the HIV group for age , sex , and Framingham risk score ( FRS ) and had no known atherosclerotic disease ( non-HIV FRS-matched controls ) . The second control group ( n = 27 ) was matched on sex and selected based on the presence of known atherosclerotic disease ( non-HIV atherosclerotic controls ) . MAIN OUTCOME MEASURE Arterial inflammation was prospect ively determined as the ratio of FDG uptake in the arterial wall of the ascending aorta to venous background as the target-to- background ratio ( TBR ) . RESULTS Participants with HIV demonstrated well-controlled HIV disease ( mean [ SD ] CD4 cell count , 641 [ 288 ] cells/μL ; median [ interquartile range ] HIV-RNA level , < 48 [ < 48 to < 48 ] copies/mL ) . All were receiving antiretroviral therapy ( mean [ SD ] duration , 12.3 [ 4.3 ] years ) . The mean FRS was low in both HIV and non-HIV FRS-matched control participants ( 6.4 ; 95 % CI , 4.8 - 8.0 vs 6.6 ; 95 % CI , 4.9 - 8.2 ; P = .87 ) . Arterial inflammation in the aorta ( aortic TBR ) was higher in the HIV group vs the non-HIV FRS-matched control group ( 2.23 ; 95 % CI , 2.07 - 2.40 vs 1.89 ; 95 % CI , 1.80 - 1.97 ; P < .001 ) , but was similar compared with the non-HIV atherosclerotic control group ( 2.23 ; 95 % CI , 2.07 - 2.40 vs 2.13 ; 95 % CI , 2.03 - 2.23 ; P = .29 ) . Aortic TBR remained significantly higher in the HIV group vs the non-HIV FRS-matched control group after adjusting for traditional cardiovascular risk factors ( P = .002 ) and in stratified analyses among participants with undetectable viral load , zero calcium , FRS of less than 10 , a low-density lipoprotein cholesterol level of less than 100 mg/dL ( < 2.59 mmol/L ) , no statin use , and no smoking ( all P ≤ .01 ) . Aortic TBR was associated with sCD163 level ( P = .04 ) but not with C-reactive protein ( P = .65 ) or D-dimer ( P = .08 ) among patients with HIV . CONCLUSION Participants infected with HIV vs noninfected control participants with similar cardiac risk factors had signs of increased arterial inflammation , which was associated with a circulating marker of monocyte and macrophage activation BACKGROUND The objective of this study was to examine the association of Joint National Committee ( JNC-V ) blood pressure and National Cholesterol Education Program ( NCEP ) cholesterol categories with coronary heart disease ( CHD ) risk , to incorporate them into coronary prediction algorithms , and to compare the discrimination properties of this approach with other noncategorical prediction functions . METHODS AND RESULTS This work was design ed as a prospect i ve , single-center study in the setting of a community-based cohort . The patients were 2489 men and 2856 women 30 to 74 years old at baseline with 12 years of follow-up . During the 12 years of follow-up , a total of 383 men and 227 women developed  CHD , which was significantly associated with categories of blood pressure , total cholesterol , LDL cholesterol , and HDL cholesterol ( all P<.001 ) . Sex-specific prediction equations were formulated to predict CHD risk according to age , diabetes , smoking , JNC-V blood pressure categories , and NCEP total cholesterol and LDL cholesterol categories . The accuracy of this categorical approach was found to be comparable to CHD prediction when the continuous variables themselves were used . After adjustment for other factors , approximately 28 % of CHD events in men and 29 % in women were attributable to blood pressure levels that exceeded high normal ( > or = 130/85 ) . The corresponding multivariable-adjusted attributable risk percent associated with elevated total cholesterol ( > or = 200 mg/dL ) was 27 % in men and 34 % in women . CONCLUSIONS Recommended guidelines of blood pressure , total cholesterol , and LDL cholesterol effectively predict CHD risk in a middle-aged white population sample . A simple coronary disease prediction algorithm was developed using categorical variables , which allows physicians to predict multivariate CHD risk in patients without overt CHD Background Therapy with a HIV protease inhibitor is associated with elevations in cholesterol and triglycerides . HMG-CoA reductase inhibitors ( ` statins ' ) are the established therapy for persons with primary hypercholesterolaemia . Because of drug interactions , pravastatin may represent the preferred choice in those taking HIV protease inhibitors . Design A r and omized , open-label comparative 24 week trial of dietary advice alone or with pravastatin in 31 male patients established on protease inhibitor-based regimens for greater than 12 weeks with viral load < 500 copies/ml and cholesterol > 6.5 mmol/l . Results There were no significant clinical or laboratory events and no patient discontinuation secondary to adverse effects . Viral rebound did not occur . Relative to baseline , total cholesterol at week 24 fell significantly in the pravastatin ( 1.2 mmol/l ; 17.3 % ) ( P < 0.05 ) but not in the dietary advice ( 0.3 mmol/l ; 4 % ) group . The difference between the two groups approached significance at week 24 ( P = 0.051 ) . This fall was accounted for entirely by a reduction in low density lipoprotein [ calculated change 1.24 mmol/l ( 19 % ) and 0.07 mmol ( 5.5 % ) in pravastatin and dietary advice groups , respectively ] as high density lipoprotein rose non-significantly by 0.6 mmol/l in both groups . Weight , basal metabolic rate , fasting glucose and triglycerides did not change significantly in either group . Conclusions Dietary advice plus pravastatin significantly reduced total cholesterol in HIV-positive individuals taking protease inhibitors , without significant adverse effects . The inclusion of pravastatin substantially increases the magnitude of the change , which is comparable with changes achieved in endogenous hyperlipidaemia Background : The effect of specific antiretrovirals on inflammation is unclear . Methods : A5224s was a sub study of A5202 , which r and omized HIV-infected treatment-naïve patients to blinded abacavir/lamivudine ( ABC/3TC ) or tenofovir/emtricitabine ( TDF/FTC ) with open-label efavirenz ( EFV ) or atazanavir/ritonavir ( ATV/r ) in a factorial design . Our analysis compared changes in inflammation markers from baseline to week 24 between ABC/3TC and TDF/FTC . Secondary analyses included changes at week 96 and comparisons of EFV vs. ATV/r . Results : Analyses included 244 patients ( 85 % male , 48 % white non-Hispanic ) , median age 39 years , HIV-1 RNA 4.6 log10 copies/ml , CD4 240 cells/&mgr;l . TNF-&agr ; , soluble receptors of TNF-&agr ; (sTNFR)-I and II , soluble vascular cellular adhesion molecule (sVCAM)-1 and soluble intercellular adhesion molecule (sICAM)-1 decreased significantly at weeks 24 and 96 , without significant differences between components ( P ≥ 0.44 ) . At week 24 , ABC/3TC had a greater high-sensitivity C-reactive protein ( hsCRP ) mean fold change than TDF/FTC { 1.43 vs. 0.88 , estimated mean fold change percentage difference [ & Dgr ; ] 61.5 % [ 95 % confidence interval ( CI ) 13.6 % , 129.5 % ] ; P = 0.008}. Similar results were seen at week 96 ( P = 0.021 ) . At week 24 ( but not 96 ) , EFV had a greater hsCRP mean fold change than ATV/r [ 1.41 vs. 0.88 ; & Dgr ; = 60.2 % ( 12.6 % , 127.7 % ) ; P = 0.009 ] . IL-6 decreased significantly at week 24 with TDF/FTC but not with ABC/3TC ( between-components P = 0.019 ) . At week 96 , IL-6 decreased significantly in both nucleoside reverse transcriptase inhibitor components ( between-components P = 0.11 ) . IL-6 changes were not significantly different between ATV/r and EFV at either time point ( P ≥ 0.89 ) . Conclusions : Soluble TNF-receptors and adhesion molecules decreased following treatment initiation and did not differ by regimens . Differences were seen on hsCRP and IL-6 changes with ABC/3TC vs. TDF/FTC and on hsCRP with EFV vs. ATV/r Objectives : To evaluate simplified protease inhibitor (PI)-sparing antiretroviral treatment versus lipid-lowering therapy for the management of  highly active antiretroviral therapy (HAART)-induced hyperlipidaemia .  Design : R and omized , open-label clinical trial assessing the efficacy on hyperlipidaemia of a switching therapy from PI to non-nucleoside reverse transcriptase inhibitor ( NNRTI ) nevirapine or efavirenz versus a hypolipidaemic treatment ( with pravastatin or bezafibrate ) added to current , unchanged antiretroviral combination . Methods : All HIV-infected patients on their first HAART regimen , with stable immuno-virological features , naive to all NNRTIs , and with mixed hyperlipidaemia , were r and omized to replace PI with nevirapine ( arm A ) or efavirenz ( arm B ) , or to receive pravastatin ( arm C ) or bezafibrate ( arm D ) with unchanged HAART regimen , and were followed-up for 12 months . Results : One hundred and thirty patients were evaluated : 29 patients were r and omized to arm A , 34 to arm B , 36 to arm C , and 31 to arm D. At the end of the 12-month follow-up , a reduction of 25.2 , 9.4 , 41.2 and 46.6 % in mean triglyceridaemia versus respective baseline values was reported in groups A , B , C and D , respectively , with statistically significant difference between arms A – B and C – D ( P < 0.01 ) . Similar results were reported for total and low-density lipoprotein cholesterol levels . Viro-immunological efficacy and tolerability profile were comparable in all considered arms . Conclusion : Pravastatin and bezafibrate proved significantly more effective in the management of HAART-related hyperlipidaemia than the switching therapy from PI to nevirapine or efavirenz CONTEXT A syndrome of lipodystrophy , characterized by fat redistribution and insulin resistance , has been estimated to affect the majority of human immunodeficiency virus (HIV)-infected individuals who are treated with combination antiretroviral therapy .  There are no proven therapies for the metabolic disturbances associated with HIV lipodystrophy syndrome . OBJECTIVE To determine the safety and efficacy of metformin therapy in HIV-infected patients with fat redistribution and abnormal glucose homeostasis . DESIGN AND SETTING R and omized , double-blind , placebo-controlled pilot study conducted in a university hospital between December 1998 and January 2000 . PATIENTS Twenty-six HIV-infected , nondiabetic patients with fat redistribution and abnormal oral glucose tolerance test ( OGTT ) results , hyperinsulinemia , or both . INTERVENTIONS Patients were r and omly assigned to receive metformin , 500 mg twice daily ( n = 14 ) , or identical placebo ( n = 12 ) , for 3 months . MAIN OUTCOME MEASURES Insulin area under the curve ( AUC ) , calculated 12 
    Output:
    
Among HIV-infected individuals , the prevalence of CVD risk factors and the risk for CVD is higher compared with HIV negatives .
Antiretroviral drugs may induce dyslipidaemia , reduce insulin sensitivity , and promote body fat redistribution that additionally contributes to CVD risk .
Some antiretroviral drugs may increase risk for CVD events , but the absolute risk increase is moderate and has to be put into perspective with the massive HIV-related benefits .
Sustained HIV suppression reduces systemic inflammatory markers and is associated with a moderate reduction in CVD events .
Statins are effective for the treatment of dyslipidaemia in HIV infection , but drug interactions with ART need to be considered .
Human immunodeficiency virus-infected individuals are at increased risk for CVD .
Timely initiation of ART with consequent viral suppression is likely to reduce CVD events and to offset potential side effects from ART-induced metabolic changes .