***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: Objectives : To assess the clinical relevance ( functional outcome ) of a 3-month allopurinol regimen in patients with high serum uric acid ( SUA ) levels and acute ischemic stroke without considering the changes in SUA levels . Material s and Methods : In a r and omized , double-blind , controlled study , 70 patients ( 45 females , 25 males ) with acute ischemic stroke who had elevated levels of SUA were included . They were divided in two 35-patient groups to investigate the effect of 3 months of an allopurinol ( 200 mg/day ) regimen versus placebo on their functional outcome , which was evaluated using a modified Rankin scale . Results : The overall mean age was 68.9 ± 11.33 years ( range 27 - 89 ) . The final favorable functional status ( mRS = 0 - 2 ) was 23 ( 65.7 % ) and 14 ( 40.0 % ) in the treated and placebo groups , respectively , which was strongly associated with allopurinol consumption ( OR = 4.646 , p = 0.014 ) and age ≤70 years ( OR = 0.139 , p = 0.005 ) in patients with ischemic stroke after adjusting for confounders . There was no significant difference in death  between allopurinol-treated cases ( 3 ; 8.6 % ) and placebo-treated ones ( 6 ; 17.2 % ; p = 0.278 ) . Conclusion : Allopurinol treatment was well tolerated and improved the 3-month functional status of patients with acute ischemic stroke who had high levels of SUA without considering the decreasing effect of allopurinol on SUA Higher levels of serum uric acid are independently associated with endothelial dysfunction , a mechanism for incident hypertension . Overweight/obese individuals are more prone to endothelial dysfunction than their lean counterparts . However , the effect of lowering serum uric acid on endothelial dysfunction in these individuals has not been examined thoroughly . In this r and omized , double-blind , placebo-controlled trial of nonhypertensive , overweight , or obese individuals with higher serum uric acid ( body mass index ≥25 kg/m2 and serum uric acid ≥5.0 mg/dL ) , we assigned subjects to probenecid ( 500–1000 mg/d ) , allopurinol ( 300–600 mg/d ) , or matching placebo . The primary outcome was endothelium-dependent vasodilation measured by brachial artery ultrasound at baseline and 8 weeks . By the end of the trial , 47 , 49 , and 53 participants had been allocated to receive probenecid , allopurinol , and placebo , respectively . Mean serum uric acid levels significantly decreased in the probenecid ( from 6.1 to 3.5 mg/dL ) and allopurinol groups ( from 6.1 to 2.9 mg/dL ) but not in the placebo group ( 6.1 to 5.6 mg/dL ) . None of the interventions produced any significant change in endothelium-dependent vasodilation  ( probenecid , 7.4±5.1 % at baseline and 8.3±5.1 % at 8 weeks ; allopurinol , 7.6±6.0 % at baseline and 6.2±4.8 % at 8 weeks ; and placebo , 6.5±3.8 % at baseline and 7.1±4.9 % at 8 weeks ) . In this r and omized , double-blind , placebo-controlled trial , uric acid lowering did not affect endothelial function in overweight or obese nonhypertensive individuals . These data do not support the hypothesis that uric acid is causally related to endothelial dysfunction , a potential mechanism for development of hypertension Background Previous studies of allopurinol and stroke risk have provided contradictory findings , ranging from a protective effect to an increased risk . Our objective was to assess whether allopurinol use is associated with the risk of stroke in the elderly . Methods We used the 5 % r and om sample of Medicare beneficiaries from 2006–2012 to study the association of new allopurinol initiation and incident stroke . We used multivariable-adjusted Cox regression models adjusted for age , gender , race , Charlson index , and cardio-protective medications ( beta-blockers , ACE inhibitors , diuretics , statins ) to calculate hazards ratio ( HR ) with 95 % confidence intervals ( CI ) . Sensitivity analyses adjusted for coronary artery disease ( CAD ) risk factors including hypertension , hyperlipidemia , diabetes , and smoking instead of Charlson index . Results Among 28,488 eligible episodes of incident allopurinol , 2,177 ended in incident stroke ( 7.6 % episodes ) . In multivariable-adjusted analyses , allopurinol use was associated with 9 % lower hazard ratio for stoke , 0.91 ( 95 % CI , 0.83 to 0.99 ) . Compared to no allopurinol use , allopurinol use duration s of 181 days to 2 years , 0.88 ( 95 % CI , 0.78 to 0.99 ) and > 2 years , 0.79 ( 95 % CI , 0.65 to 0.96 ) were significantly associated with lower multivariable-adjusted hazard of stroke . Sensitivity analyses adjusted for CAD risk factors confirmed these findings . In subgroup analyses , significant associations were noted between allopurinol use and the risk of ischemic stroke , 0.89 ( 95 % CI , 0.81 to 0.98 ) ; associations were not significant for hemorrhagic stroke , 1.01 ( 95 % CI , 0.79 to 1.29 ) . Conclusions Allopurinol use is associated with lower risk of stroke overall , more specifically ischemic stroke . This association is evident after 6-months of allopurinol use , and the hazard reduction increases with longer duration of use . Future studies need to examine underlying mechanisms OBJECTIVE The aim of this study was to investigate the long-term effective control of serum uric acid by allopurinol on the carotid intima-media thickness ( IMT ) in patients with type 2 diabetes ( T2DM ) and asymptomatic hyperuricemia ( HUA ) . METHODS This was a r and omized open parallel-controlled study . In this study , 176 patients with T2DM and asymptomatic HUA were r and omly allocated to the conventional or allopurinol treatment groups on the basis of a computer-generated r and om number table . Changes in the carotid IMT , biochemical indexes , high sensitive C-reactive protein ( hs-CRP ) and the incidence of hypertension in patients before and after three years of treatment were examined and compared between the groups . RESULTS There were no statistically significant differences in the baseline characteristics of the study participants between the two treatment groups ( p>0.05 for all ) . Nevertheless , the serum uric acid , triglyceride , and hs-CRP levels and the homeostasis assessment for insulin resistance ( HOMA-IR ) , systolic blood pressure , diastolic blood pressure and the carotid IMT in the allopurinol group were significantly lower than those in the conventional group after three years of treatment ( p<0.01 for all ) . The intention-to-treat analysis indicated that the incidence of new-onset hypertension in the allopurinol group showed a declining trend compared to that in the conventional treatment group ( 6.8 % vs. 13.6 % , p>0.05 ) . CONCLUSION The long-term effective control of serum uric acid by allopurinol may improve insulin resistance , decrease the serum levels of hs-CRP , reduce the carotid IMT , and may delay the development of atherosclerosis in patients with T2DM and asymptomatic HUA Background Previous observational studies that have examined the association of allopurinol with myocardial infa rct ion ( MI ) have provided contradictory results . One study showed that allopurinol reduced the risk , while another study showed an increased risk with allopurinol . Therefore , our objective was to assess whether allopurinol use is associated with a reduction in the risk of  MI in the elderly . Method We used the 2006–2012 5 % r and om sample of Medicare beneficiaries to study the association of new allopurinol initiation and the risk of incident MI in a cohort study . Multivariable-adjusted Cox regression models adjusted for age , gender , race , and Charlson index , in addition to various cardio-protective medications ( beta-blockers , angiotensin-converting enzyme ( ACE ) inhibitors , diuretics , statins ) . We calculated hazard ratios ( HRs ) with 95 % confidence intervals ( CIs ) . Sensitivity analyses adjusted for coronary artery disease ( CAD ) risk factors , including hypertension , hyperlipidemia , diabetes , and smoking . Results Of the 29,298 episodes of incident allopurinol use , 1544 were associated with incident MI ( 5.3 % episodes ) . Allopurinol use was associated with reduced hazards of MI , with a HR of 0.85 ( 95 % CI , 0.77 to 0.95 ) . Compared to no allopurinol use , longer duration s of allopurinol use were associated with a lower HR of MI : 1–180 days , 0.98 ( 95 % CI , 0.84 to 1.14 ) ; 181 days to 2 years , 0.83 ( 95 % CI , 0.72 to 0.95 ) ; and > 2 years , 0.70 ( 95 % CI , 0.56 to 0.88 ) . Other factors associated with a higher hazard of MI were : age 75 to < 85 years and ≥85 years , male gender , higher Charlson index score , and the use of an ACE inhibitor . Adjustment for CAD risk factors confirmed these findings . Conclusion Incident allopurinol use was associated with a reduction in the risk of incident MI in the elderly . Longer duration s of allopurinol use reduced the risk of incident MI incrementally . Future studies should assess the underlying mechanisms for MI prevention and assess the risk-benefit ratio for allopurinol use OBJECTIVE To investigate the therapeutic effect of allopurinol treatment on acute coronary syndrome and to eluci date its possible mechanism . METHODS Patients with acute coronary syndrome ( n = 100 ) were recruited as research subjects in our hospital . The patients were r and omly divided into two groups , an allopurinol group ( n = 50 ) and a control group ( n = 50 ) . These two groups were treated with conventional antiplatelet , anticoagulation and anti-ischemic therapy ; allopurinol therapy was added to the allopurinol group based on conventional treatment indications . Biochemical markers such as serum creatinine , uric acid , BNP , blood glucose and blood lipid were compared between the two groups . Indicators of oxidative stress and inflammatory response ( MDA , OX-LDL , NO , hs-CRP and TNF-α ) , as well as cardiovascular events during 2-years follow-up , were recorded . RESULTS On admission , there was no difference in serum creatinine , uric acid , BNP , blood glucose or lipid levels between the two groups ( P > 0.05 ) . However , after 1 month of treatment , these levels were improved in patients in the allopurinol group compared to the control group ( P < 0.05 ) . MDA , OX-LDL , hs-CRP and TNF-α decreased after treatment periods of 14 days and 1 month . They were also decreased at 3 month , 6 month , 1 year , and 2 year follow-up visits . However , data from the allopurinol group demonstrated significantly lower levels than in the control group ( P < 0.05 ) . Additionally , compared with the control group , allopurinol treatment significantly elevated the level of NO ( P < 0.05 ) . The total effective rates of the allopurinol group are much higher than in the control group for both angina pectoris ( 93.2 % and 76 % , respectively ) and ECG ( 96 % and 82 % , respectively ) . Most patients in the allopurinol group ( n = 40 ) and the control group ( n = 41 ) received stent implantation with no significant difference shown between them . The incidence of cardiovascular events during 2 years of follow-up in the allopurinol group was 10 % ; it was 30 % in the control group . CONCLUSION Allopurinol has a remarkable effect in the treatment of ACS and can improve the oxidative stress and inflammatory reaction indicators of patients . The protective mechanism of allopurinol might be achieved by suppressing the secretion and release of inflammatory mediators such as TNF-α , hs-CRP , OX-LDL and MDA while increasing levels of NO Allopurinol ameliorates endothelial dysfunction and arterial stiffness among patients without chronic kidney disease ( CKD ) , but it is unknown if it has similar effects among patients with CKD . Furthermore , because arterial stiffness increases left ventricular afterload , any allopurinol-induced improvement in arterial compliance might also regress left ventricular hypertrophy ( LVH ) . We conducted a r and omized , double-blind , placebo- 
    Output:
    
Accordingly , lower doses ( ≤ 300 mg/day ) of allopurinol reduced the risk of TCE , unlike higher doses .
Conclusions Purine-like XOI may reduce the incidence of adverse CV outcomes .
However , higher doses of allopurinol ( > 300 mg/day ) may be associated with loss of CV protection