***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: Objective : To evaluate whether statins are associated with a protective effect on the development of rheumatoid arthritis ( RA ) .  Methods : A nested case – control study was conducted using data from the General Practice Research Data base . A study population consisting of three groups of subjects aged 40–89 years was identified : ( 1 ) patients exposed to a statin or other lipid-lowering agent ( LLA ) ; ( 2 ) patients with a diagnosis of hyperlipidaemia in the absence of lipid-lowering drug treatment and ( 3 ) a r and om sample of 25 000 individuals with no diagnosis of hyperlipidaemia nor a prescription for a LLA . From this population incident cases of RA and up to four controls for each case were identified , matched on age , sex , general practice , number of years of recorded history in the data base and index date . The independent effects of hyperlipidaemia and statins on the development of RA were evaluated using conditional logistic regression . Results : 313 cases of RA and 1252 matched controls were identified . Compared with patients with untreated hyperlipidaemia , or hyperlipidaemia treated with LLA other than statins , the adjusted odds ratio for patients with no hyperlipidaemia was 0.68 ( 95 % CI 0.50 to 0.91 ) . When those with hyperlipidaemia who received statins were compared with those with hyperlipidaemia who did not use statins ( ie , untreated hyperlipidaemia patients or those treated with non-statin LLA ) the OR was 0.59 ( 95 % CI 0.37 to 0.96 ) . Conclusion : These data provide evidence to support the hypothesis that statins may be protective against the development of RA in patients with hyperlipidaemia OBJECTIVE To investigate the longterm effects of the anti-tumor necrosis factor ( TNF ) therapy infliximab , a drug known to reduce disease activity in patients with rheumatoid arthritis ( RA ) and ankylosing spondylitis ( AS ) . METHODS Eighty-two patients ( 50 with RA , 32 with AS ) aged 17 - 77 years were enrolled . All patients were treated with intravenous infliximab .  Lipid profile was assessed at baseline and after 6 months of treatment . RESULTS Disease activity significantly decreased in patients with RA and AS at the end of infliximab therapy . Infliximab treatment significantly increased total cholesterol from 206 to 216 mg/dl ( p < 0.05 ) and triglycerides from 109 to 122 mg/dl ( p < 0.05 ) . The low density lipoprotein ( LDL ) and high density lipoprotein ( HDL ) cholesterol did not change during treatment . Furthermore , the total cholesterol/HDL cholesterol and triglycerides/HDL cholesterol ratios did not change significantly . CONCLUSION The influence of infliximab treatment on lipid profile seems to be neutral , since neither LDL cholesterol levels nor total cholesterol/HDL cholesterol and triglycerides/HDL cholesterol ratios changed significantly during the 6-month therapy . Our findings suggest that the favorable effect of infliximab treatment on cardiovascular comorbidity may not be mainly mediated by the effects on the lipid profile , but further investigations are needed in order to confirm this hypothesis OBJECTIVE Endothelial dysfunction has been found in patients with rheumatoid arthritis ( RA ) . In this study we aim ed to assess whether adalimumab , a fully human monoclonal antibody directed against TNF-alpha , was able to improve endothelial function in RA patients with long-st and ing disease refractory to infliximab . METHODS Eight RA patients ( 7 women ; range : 24- 74 years ) were studied . They had been treated with the chimeric monoclonal anti-TNF-alpha antibody-infliximab for at least 1 year and were switched to  adalimumab therapy because of loss of efficacy following periodical treatment with infliximab . Endothelial dependent ( EDV ) and independent vasodilatation ( EIV ) were measured by brachial ultrasonography . Patients were assessed prior to ( day 0 ) and at day 2 , and weeks 2 and 12 after the onset of adalimumab therapy . RESULTS Following adalimumab administration a rapid increase in the percentage ( % ) of EDV was found in all patients ( mean + /- SD : 10.1 + /- 5.1 % at day 2 compared to 5.8 + /- 4.1 % at day 0 ) . At weeks 2 and 12 the % EDV was also significantly increased compared to day 0 . All patients showed decrease in the disease activity score 28 and C-reactive protein levels ( P = 0.012 ) . Moreover , at week 12 the atherogenic index was reduced in all patients ( P = 0.012 ) . CONCLUSION Our study confirms that short-term adalimumab therapy yields an active and positive effect on endothelial function in long-st and ing RA patients with severe disease . This observation emphasizes the potential role of the TNF-alpha blockade in the mechanisms implicated in the development of atherogenesis in RA OBJECTIVE Tumor necrosis factor-a ( TNF-a ) is a key cytokine in the pathogenesis of chronic inflammatory arthritides , has proatherogenic effects , and may be positively correlated with impairment of the action of insulin . Patients with chronic inflammatory arthritides have an increased risk for cardiovascular diseases . We assessed whether anti-TNF-a treatment modifies the unfavorable lipid profile induced by chronic inflammatory arthritides . METHODS Sixty patients ( 24 with rheumatoid arthritis , 26 ankylosing spondylitis , and 10 psoriatic arthritis ) receiving infliximab because of ongoing disease activity despite disease modifying drugs ( DMARD ) were prospect ively studied for 6 months . Lipid profile , total cholesterol/high density lipoprotein cholesterol ( TC/HDL-C ) , and low density lipoprotein cholesterol (LDL-C)/HDL-C ratios , as well as disease activity indices ( DAS28 and BASDAI ) , were assessed . RESULTS A sustained increase of serum HDL-C was observed [ mean increase ( 95 % CI ) ] 5 ( 3 - 7 ) mg/dl , 3.5 ( 1 - 6 ) mg/dl , and 3 ( 1 - 5 ) mg/dl at 1 , 3 , and 6 months , respectively ( p < 0.01 ) . Compared to nonresponders , HDL-C increased significantly more in EULAR or BASDAI responders ( 0.8 vs 5.8 mg/dl ; p = 0.05 ) . Serum TC was significantly increased [ 11 ( 4 - 8 ) mg/dl ; p = 0.001 ] only after the first month of treatment . TC/HDL-C and LDL-C/HDL-C decreased only after the first month [ 0.3 ( 0.1 - 0.4 ) , p < 0.01 , and 0.2 ( 0.1 - 0.4 ) , p < 0.01 , respectively ] . For patients with baseline LDL-C > 130 mg/dl , LDL-C/HDL-C decreased ( p < 0.05 ) during the whole study period and TC/HDL-C decreased ( p < 0.05 ) at 1 and 3 months . CONCLUSION Anti-TNF-a treatment in patients with chronic inflammatory arthritides induces a modest , but sustained , increase in serum HDL-C levels , which may have a favorable effect in reducing the cardiovascular risk in these patients BACKGROUND Adipose tissue contains a large amount of cholesterol and performs a buffer function for circulating cholesterol . Liver X receptors ( LXR ) alpha and peroxisome proliferator-activated receptor gamma ( PPARgamma ) might play a significant role in adipocyte cholesterol metabolism through mediation of cholesterol efflux . The aim of this study was to evaluate the effect of niacin on LXRalpha and PPARgamma expression and HDL-induced cholesterol efflux in adipocytes from hypercholesterolemic rabbits . METHODS Twelve rabbits fed with high-cholesterol diet for 8 weeks were r and omly divided into two groups : ( 1 ) high cholesterol group ( n=6 ) : maintained high cholesterol diet for 6 weeks ; ( 2 ) niacin group ( n=6 ) : the same cholesterol diet plus niacin ( 200 mg/kg/d ) for 6 weeks . Control group ( n=6 ) was fed with normal diet for 14 weeks . Subcutaneous adipose was collected for adipocyte culture . Reverse transcription polymerase chain reaction ( RT-PCR ) was used to evaluate adipocytes LXRalpha mRNA expressions . Cholesterol efflux rate was determined through measuring release of radioactivity from (3)H-cholesterol prelabeled cells into medium containing high-density lipoprotein ( HDL ) . The direct effect of niacin on LXRalpha and PPARgamma mRNA expression in primary rabbit adipocytes was assayed . RESULTS High cholesterol diet result ed in decreased LXRalpha mRNA expressions and reduced HDL-induced cholesterol efflux rate in adipocytes . Six weeks of niacin treatment significantly enhanced the cholesterol efflux from adipocytes , which was related to the increased mRNA expressions of LXRalpha ( r=0.71 , P<0.05 ) . In in vitro study , niacin dose-dependently stimulated LXRalpha and PPARgamma mRNA expression in cultured adipocytes . And various doses of niacin-induced cholesterol efflux was positive correlation with LXRalpha and PPARgamma mRNA expression ( r=0.83 P<0.01 ; r=0.76 P<0.05 ; respectively ) . CONCLUSION Niacin can up-regulate LXRalpha and PPARgamma mRNA expression and promote the HDL-induced cholesterol efflux in adipocytes from hypercholesterolemic rabbits BACKGROUND Patients with rheumatoid arthritis ( RA ) frequently display an atherogenic lipid profile which has been linked with inflammation . Tumor necrosis factor-alpha ( TNF-alpha ) , a pivotal pro-inflammatory cytokine in RA may be involved in the development of the disturbed lipid metabolism . We investigated whether infliximab , an anti-TNF-alpha therapy , may modify the lipid profile . METHODS 56 consecutive RA patients were treated with infliximab ( 3 mg/kg at weeks 0 , 2 , 6 , 14 , 22 , 30 ) .  Lipid profile and CRP  were assayed at baseline and before infusion at weeks 6 and 30 . Baseline values were compared with those in 56 healthy volunteers . RESULTS At baseline , the concentrations of HDL-cholesterol were lower in RA patients than in the controls ( 1.3+/-0.4 vs. 1.5+/-0.2 mmol/L ; p<0.01 ) . The triglyceride concentrations ( 1.6+/-0.8 vs. 1.3+/-0.4 mmol/L , p<0.01 ) , the ratio of total cholesterol/HDL-cholesterol ( 4.3+/-1.6 vs. 3.2+/-0.5 , p<0.001 ) and LDL-cholesterol/HDL-cholesterol ( 2.6+/-1.2 vs. 1.7+/-0.5 , p<0.001 ) were significantly higher in RA patients than in controls . After 6 weeks of infliximab therapy , the mean total cholesterol concentration increased by 25 % ( p<0.001 ) , LDL-cholesterol by 24 % ( p<0.001 ) and HDL-cholesterol by 30 % ( p<0.001 ) . The decrease in CRP levels to 30 week inversely correlated with the increase in HDL-cholesterol ( r=-0.47 , p=0.005 ) . CONCLUSIONS Infliximab administration is associated with important increases in cholesterol levels in all its forms but as no significant beneficial effect on the atherogenic ratio Patients with rheumatoid arthritis ( RA ) have increased cardiovascular mortality . TNF-α is a critical mediator of inflammation and metabolic response in patients with RA . Increased insulin resistance and dyslipidemia were known risk factors in patients with active RA , however , the regulation of these metabolic parameters by TNF-α is poorly understood . Neutralization of TNF-α with infliximab offers a unique opportunity to study TNF-α-mediated regulation of these metabolic parameters in RA . The aim of the study was to assess the in vivo TNF-α-mediated regulation of insulin resistance and lipids levels in RA . Nineteen patients with active RA treated with infliximab were prospect ively followed for 14 weeks . Plasma lipids levels and insulin resistance were measured at baseline , 6 and 14 weeks after infliximab treatment . At week 14 , the disease activity ( DAS-28 score ) improved significantly ( p < 0.000 ) , with a significant reduction in both C-reactive protein ( p = 0.007 ) and erythrocyte sedimentation rate ( p = 0.006 ) levels . The body weight did 
    Output:
    
There was a small trend to increased TG , and no changes in ApoB/ApoA1 ratio .