***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: BACKGROUND Evidence indicates that corticosteroid therapy might be beneficial for the primary treatment of severe Kawasaki disease . We assessed whether addition of prednisolone to intravenous immunoglobulin with aspirin would reduce the incidence of coronary artery abnormalities in patients with severe Kawasaki disease . METHODS We did a multicentre , prospect i ve , r and omised , open-label , blinded-endpoints trial at 74 hospitals in Japan between Sept 29 , 2008 , and Dec 2 , 2010 . Patients with severe Kawasaki disease were r and omly assigned by a minimisation method to receive either intravenous immunoglobulin ( 2 g/kg for 24 h and aspirin 30 mg/kg per day ) or intravenous immunoglobulin plus prednisolone ( the same intravenous immunoglobulin regimen as the intravenous immunoglobulin group plus prednisolone 2 mg/kg per day given over 15 days after concentrations of C-reactive protein normalised ) . Patients and treating physicians were unmasked to group allocation . The primary endpoint was incidence of coronary artery abnormalities during the study period . Analysis was by intention to treat . This trial is registered with the University Hospital Medical Information Network clinical trials registry , number UMIN000000940 . FINDINGS We r and omly assigned 125 patients to the intravenous immunoglobulin plus prednisolone group and 123 to the intravenous immunoglobulin  group . Incidence of coronary artery abnormalities was significantly lower in the intravenous immunoglobulin plus prednisolone group than in the intravenous immunoglobulin group during the study period ( four patients [ 3 % ] vs 28 patients [ 23 % ] ; risk difference 0·20 , 95 % CI 0·12 - 0·28 , p<0·0001 ) . Serious adverse events were similar between both groups : two patients had high total cholesterol and one neutropenia in the intravenous immunoglobulin plus prednisolone group , and one had high total cholesterol and another non-occlusive thrombus in the intravenous immunoglobulin group . INTERPRETATION Addition of prednisolone to the st and ard regimen of intravenous immunoglobulin improves coronary artery outcomes in patients with severe Kawasaki disease in Japan . Further study of intensified primary treatment for this disease in a mixed ethnic population is warranted . FUNDING Japanese Ministry of Health , Labour and Welfare Prospect i ve evaluation of  platelet activation and hypercoagulability  was performed in 31 patients with Kawasaki syndrome . Most patients had elevated  acute-phase reactants when studied during the first 3 weeks of their illness ; 17 of 25 ( 68 % ) patients had factor VIII activity greater than 150 % , 18 of 24 ( 75 % ) had fibrinogen greater than 400 mg/dl , and 17 of 31 ( 55 % ) had a platelet count greater than 450,000/mm3 . Antithrombin III was depressed initially in 17 of 25 ( 68 % ) patients . Depleted fibrinolytic activity , as measured by a euglobulin lysis time greater than 300 minutes , was documented in nine of 20 ( 45 % ) patients . Plasma beta-thromboglobulin ( BTG ) measured at 0 to 3 weeks was elevated ( greater than 43 ng/ml ) in seven of 24 ( 29 % ) patients . All patients with coronary artery aneurysms had elevated BTG values . The mean BTG in the group with aneurysms was 72.3 ng/ml when measured during the first 3 weeks after onset of fever , and 87.7 ng/ml at 4 to 7 weeks . The group without aneurysms had mean BTG values of 29.4 and 28.3 ng/ml at 0 to 3 and 4 to 7 weeks , respectively . The difference between the two groups was significant ( P less than 0.002 ) for both the initial and later values . An elevated BTG during the first 3 weeks after onset of fever was highly associated with aneurysm formation in our patients ( P less than 0.007 ) . No aneurysms occurred in patients with a normal BTG value BACKGROUND Little is known about the platelet dynamics and the effect of antiplatelet therapy  in Kawasaki disease ( KD ) . The aim of this study was to clarify platelet activation dynamics in acute-phase KD patients by assaying platelet-derived microparticles ( PDMPs ) . METHODS AND RESULTS The  PDMP level in 18 patients with acute KD was measured on ELISA . Of the 18 patients , 14 were receiving oral aspirin and i.v . immunoglobulin ( IVIG ) and 4 , oral aspirin alone .  Blood sample s were drawn before , immediately after , and 10 - 14 days after IVIG infusion ; thereafter , at 1 , 2 , and 3 months after the onset of disease . PDMP level before aspirin treatment was significantly higher in acute-phase KD patients than in the control subjects with common febrile diseases ( P<0.01 ) . In the acute-phase KD patients , IVIG significantly decreased PDMP level ; the PDMP level was not lower on the similar day of KD in the patients who did not receive IVIG . Eight patients ' PDMP level rebounded after aspirin was discontinued . CONCLUSIONS Platelets are activated during acute-phase KD , which confirms the importance of antiplatelet therapy . In addition , platelet activation continues as long as 2 or 3 months after the acute phase , the time at which aspirin is commonly discontinued , and the timing of aspirin discontinuation should therefore be evaluated in each individual patient The comparative effectiveness of small-dose ( 30 mg/kg ) aspirin and highdose ( 150 mg/kg ) in Kawasaki disease was evaluated in clinical symptoms and platelet aggregation . Twenty-three patients with Kawasaki disease were entered in the r and omized study and devided into three groups . The duration s of fever were 14.8± 3.5 days in the control group , 11.3 ± 2.1 d. in the small-dose group and 8.7 ± 2.3 d. in the high-dose group . The high-dose group showed a significantly shorter duration of fever (P<.01).The platelet aggregation induced by ADP in the second week of illness were 82.4 ± 11.6 % in the control group , 66.8 ± 9.6 % in the small-dose group and 88.0 ± 10.7 % in the high-dose group ( 69.0 ± 5.0 % in healthy children ) . The control group and high-dose group showed significantly increased aggregation as compared with healthy  children . The platelet aggregation in small-dose group was significantly lower than that in the control group ( P<.01 ) . SGOT and SGPT elevated in half of the patients treated with high dose of aspirin . In Kawasaki disease , 30 mg/kg/day of aspirin is recommended to prevent arterial thrombi Once-daily ( od ) , low-dose aspirin ( 75–100 mg ) is recommended to reduce the thrombotic risk of patients with essential thrombocytemia ( ET ) . This practice is based on data extrapolated from other high-risk patients and an aspirin trial in polycythemia vera , with the assumption of similar aspirin pharmacodynamics in the two setting s. However , the pharmacodynamics of low-dose aspirin is impaired in ET , reflecting accelerated renewal of platelet cyclooxygenase (COX)-1 . ARES is a parallel-arm , placebo-controlled , r and omized , dose-finding , phase II trial enrolling 300 ET patients to address two main questions . First , whether twice or three times 100 mg aspirin daily dosing is superior to the st and ard od regimen in inhibiting platelet thromboxane (TX)A2 production , without inhibiting vascular prostacyclin bio synthesis . Second , whether long-term persistence of superior biochemical efficacy can be safely maintained with multiple vs. single dosing aspirin regimen . Considering that the primary study end point is serum TXB2 , a surrogate biomarker of clinical efficacy , a preliminary exercise of reproducibility and validation of this biomarker across all the 11 participating centers was implemented . The results of this preliminary phase demonstrate the importance of controlling reproducibility of biomarkers in multicenter trials and the feasibility of using serum TXB2 as a reliable end point for dose-finding studies of novel aspirin regimens 
    Output:
    
The groups with antiplatelet treatment tended to have a decreased platelet aggregation function .
What is New:• This systematic review showed that the groups with antiplatelet treatment tended to have a decreased platelet aggregation function.• There is insufficient evidence for the effectiveness of antiplatelet therapy for Kawasaki disease