Very low dose acetyl salicylic acid in the acute phase of Kawasaki disease

1992 ◽  
Vol 1 (1) ◽  
pp. 94
Author(s):  
Karen N Watanabe Duffy ◽  
Ciarán M Duffy ◽  
Julie D Paquin ◽  
Marc Paquet ◽  
Hanna Strawczynski
Keyword(s):  
Salicylic Acid ◽  
Kawasaki Disease ◽  
Acute Phase ◽  
Low Dose ◽  
Acetyl Salicylic Acid

Low-dose or no aspirin administration in acute-phase Kawasaki disease: a meta-analysis and systematic review

2020 ◽  
pp. archdischild-2019-318245
Author(s):  
Ming-Hsiu Chiang ◽  
Hsingjin Eugene Liu ◽  
Jinn-Li Wang
Keyword(s):  
Systematic Review ◽  
Kawasaki Disease ◽  
Acute Phase ◽  
Low Dose ◽  
Meta Analysis ◽  
Length Of Hospital Stay ◽  
High Dose ◽  
Cochrane Central Register ◽  
Factors Affecting ◽  
Standard Mean Difference

ObjectiveTo compare the efficacy of low-dose or no aspirin with conventional high-dose aspirin for the initial treatment in the acute-phase of Kawasaki disease (KD).DesignA meta-analysis and systematic review of randomised control trials and cohort studies.MethodsAll available articles that compared different dosage of aspirin in the acute-phase of KD published until 20 September 2019 were included from the databases of PubMed, Embase and Cochrane Central Register of Controlled Trials Central without language restrictions. Extracted data from eligible studies were reviewed by two authors independently and analysed by using RStudio software.ResultsNine cohorts with a total of 12 182 children were enrolled. We found that low-dose (3–5 mg/kg/day) or no aspirin in the acute-phase KD was associated with reducing the risk of coronary artery lesions (CALs, OR=0.81, 95% CI 0.69 to 0.95). No differences were observed in intravenous immunoglobulin resistance, length of hospital stay and fever days after admission (OR=1.35, 95% CI 0.91 to 1.98; standard mean difference (SMD)=0.17, 95% CI −1.07 to 1.4; SMD=0.3, 95% CI −1.51 to 2.11) in the low-dose/no aspirin subgroup compared with the high-dose (≥30 mg/kg/day) aspirin subgroup. We did not identify any potential factors affecting the homogeneity of CAL risk as well as clinical important effects in all included studies.ConclusionsPrescribing low-dose or no aspirin in the acute-phase of KD might be associated with a decreased incidence of CAL. However, additional well-designed prospective trials are required to support the theory.

Low dose acetyl salicylic acid in severe preeclampsia

1991 ◽  
Vol 35 (4) ◽  
pp. 311-317 ◽  
Author(s):  
M. Toppozada ◽  
E.A. Darwish ◽  
Y.F. Osman ◽  
M.S. Abd-Rabbo
Keyword(s):  
Salicylic Acid ◽  
Low Dose ◽  
Severe Preeclampsia ◽  
Acetyl Salicylic Acid

scholarly journals Efficacy of the Delayed Use of Low-dose Aspirin in Intravenous Immunoglobulin Therapy for Acute-phase Kawasaki Disease

2021 ◽  
Vol 3 (1) ◽  
pp. 121-126
Author(s):  
Toshimasa Nakada
Keyword(s):  
Coronary Artery ◽  
Kawasaki Disease ◽  
Intravenous Immunoglobulin ◽  
Acute Phase ◽  
Dose Group ◽  
Low Dose ◽  
Ivig Therapy ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Medium Dose

The mainstay of current standard therapy for acute-phase Kawasaki disease (KD) is intravenous immunoglobulin (IVIG) therapy at 2 g/kg. However, the efficacy of combining medium- or high-dose aspirin with IVIG therapy at 2 g/kg has not been fully investigated. Some studies suggested that aspirin may inhibit coronary artery lesion (CAL) prevention in IVIG therapy and that the delayed use of aspirin in IVIG therapy may be beneficial for the suppression of CALs and prevention of coronary artery stenosis in patients with KD. The efficacy of the delayed use of low-dose aspirin in IVIG therapy for acute-phase KD remains unclear. Therefore, this retrospective study aimed to assess the efficacy of the delayed use of low-dose aspirin, when combined with IVIG therapy for acute-phase KD. Data were obtained from 193 KD patients who underwent acute-phase treatment from January 2009 to October 2020 and IVIG therapy at 2 g/kg with the delayed use of aspirin/flurbiprofen. The patients were divided into three groups: (1) low-dose group, in which 40 patients received low-dose aspirin (5 mg/kg/day); (2) medium-dose group, in which 90 patients received medium-dose aspirin (30 mg/kg/day); and (3) flurbiprofen group, in which 63 patients received flurbiprofen (3–5 mg/kg/day). KD patients with liver damage or those present during influenza season underwent flurbiprofen therapy between January 2009 and November 2017. All patients except one received low-dose aspirin after December 2017. The serum albumin level (median 3.40 vs. 3.30 g/dL, P = 0.026) and Egami score (median 1.0 vs. 2.0, P < 0.001) before the initial treatment were significantly different between the medium-dose group and the flurbiprofen group. The rates of initial IVIG therapy resistance (25.0% vs. 18.9% vs. 25.4%, P = 0.790), rescue therapy (17.5% vs. 8.9% vs. 17.5%, P = 0.721), and CALs (5.0% vs. 0.0% vs. 4.8%, P = 0.713) were similar among the low-dose, medium-dose, and flurbiprofen groups. Overall, the efficacy of the delayed use of low-dose aspirin was similar to that of the delayed use of medium-dose aspirin/flurbiprofen in IVIG therapy for acute-phase KD.

The Combined Effect of Dipyridamole and Acetyl Salicylic Acid on Platelet Function and Bleeding Time : Evaluation of Dose for the Prophylaxis of Thrombosis

1979 ◽  
Author(s):  
A.F. Penny ◽  
M. J. Crow ◽  
S. M. Rajah ◽  
R.C. Kester
Keyword(s):  
Salicylic Acid ◽  
Platelet Function ◽  
Low Dose ◽  
Bleeding Time ◽  
Cumulative Effect ◽  
Acetyl Salicylic Acid ◽  
Additional Group ◽  
Dose Combination ◽  
Time Evaluation ◽  
Platelet Functions

The interaction of Dipyridamole (DPM) and Acetyl Salicylic Acid (ASA) on volunteers was investigated. ASA was given in single doses (multiples of 60mg) at 2 week intervals. DPM (multiples of 25 mg) was given tds for 2 days with a single dose of DPM and ASA on the morning of day 3. Bleeding time and platelet functions were performed 2 hours after each dose. ASA 300mg maximally inhibited aggregation, adhesion and PF4 release. Lower doses of ASA gave significant reductions in collagen aggregation at 120 mg, adhesion at 180mg and PF4 at 240mg. DPM 25mg tds produced reductions in collagen aggregation, adhesion and PF4. Maximal inhibition of platelet function without alteration in bleeding time was achieved by 50mg tds DPM + 180mg ASA or 75mg tds DPM + 120mg ASA. Bleeding time was normal with ASA 120mg, 180mg; prolonged at 300mg and 1000mg and tending to be normalised by 2g. Addition of DPM 75mg tds at each dose of ASA made no alteration in bleeding time. There was a cumulative effect of ASA on bleeding time. Combined DPM mg tds and low dose ASA present a balanced anti thrombotic regimen probably both inactivating thromboxane A2 production and enhancing prostacyclin activity. This dose combination is worthy of evaluation as an additional group, in trials.

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