Comparison of High-Dose and Low-Dose Aspirin Plus Intravenous Immunoglobulin in the Treatment of Kawasaki Syndrome

2002 ◽  
Vol 41 (8) ◽  
pp. 597-601 ◽  
Author(s):  
Frank T. Saulsbury
2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yong Xie ◽  
Meng Pan ◽  
Yanpan Gao ◽  
Licheng Zhang ◽  
Wei Ge ◽  
...  

AbstractThe failure of remodeling process that constantly regenerates effete, aged bone is highly associated with bone nonunion and degenerative bone diseases. Numerous studies have demonstrated that aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) activate cytokines and mediators on osteoclasts, osteoblasts and their constituent progenitor cells located around the remodeling area. These cells contribute to a complex metabolic scenario, resulting in degradative or synthetic functions for bone mineral tissues. The spatiotemporal effects of aspirin and NSAIDs in the bone remodeling are controversial according the specific therapeutic doses used for different clinical conditions. Herein, we review in vitro, in vivo, and clinical studies on the dose-dependent roles of aspirin and NSAIDs in bone remodeling. Our results show that low-dose aspirin (< 100 μg/mL), which is widely recommended for prevention of thrombosis, is very likely to be benefit for maintaining bone mass and qualities by activation of osteoblastic bone formation and inhibition of osteoclast activities via cyclooxygenase-independent manner. While, the roles of high-dose aspirin (150–300 μg/mL) and other NSAIDs in bone self-regeneration and fracture-healing process are difficult to elucidate owing to their dual effects on osteoclast activity and bone formation of osteoblast. In conclusion, this study highlighted the potential clinical applications of low-dose aspirin in abnormal bone remodeling as well as the risks of high-dose aspirin and other NSAIDs for relieving pain and anti-inflammation in fractures and orthopedic operations.


1992 ◽  
Vol 1 (1) ◽  
pp. 80
Author(s):  
Marian E. Melish ◽  
Masato Takahashi ◽  
Stanford Shulman ◽  
Wilbert Mason ◽  
Anne Rowley ◽  
...  

Rheumatology ◽  
2020 ◽  
Vol 59 (8) ◽  
pp. 1826-1833
Author(s):  
Xinyi Jia ◽  
Xiao Du ◽  
Shuxian Bie ◽  
Xiaobing Li ◽  
Yunguang Bao ◽  
...  

Abstract Objective The use of IVIG plus high- or low-dose aspirin for the initial treatment of Kawasaki disease remains controversial. The aim of this study was to evaluate the efficacy of IVIG plus high-dose aspirin compared with IVIG plus low-dose aspirin in the treatment of Kawasaki disease. Methods Studies related to aspirin therapy for Kawasaki disease were selected by searching the databases of Medline (PubMed), Embase and the Cochrane Library before March 2019. Statistical analyses were performed by using a Review Manager Software package and STATA v.15.1. Results Eight retrospective cohort studies, characterizing 12 176 patients, were analysed. Overall, no significant difference was found in the incidence of coronary artery abnormalities between the high- and low-dose aspirin groups [relative risk (RR) 1.15; 95% CI: 0.93, 1.43; P = 0.19; random-effects model]. The patients treated with high-dose aspirin had slightly faster resolution of fever [mean difference (MD) −0.30; 95% CI: −0.58, −0.02; P = 0.04; random-effects model]. but the rates of IVIG resistance (RR, 1.26; 95% CI: 0.55, 2.92; P = 0.59; random-effects model) and days in hospital (MD, 0.22; 95% CI: −0.93, 1.37; P = 0.71; random-effects model) were similar between the two groups. Conclusion Low-dose aspirin plus IVIG might be as effective as high-dose aspirin plus IVIG for the initial treatment of Kawasaki disease. Considering that high-dose aspirin may cause more adverse reactions than low-dose aspirin, low-dose aspirin plus IVIG should be recommended as the first-line therapy in the initial treatment of Kawasaki disease.


1979 ◽  
Author(s):  
S. Moore ◽  
L.W. Belbeck ◽  
S.A. Pineau

Previous work in this laboratory has shown that an occlusive thrombus (O.T.) induced. the left anterior descending coronary artery (L.A.D.) of dogs, by the placement of a segment of magnesium-aluminum wire (M.A.W.) in the lumen of the artery, is associated with the development of full thickness infarct (F.T.I.). Incomplete (mural) thrombus is associated with focal areas of ischaemic damage, mainly sub-endocardial, in the myocardium of the antero-lateral left ventricle. A 1.0 cm. length of M.A.W., shaped in the form of a tennis racquet, was placed by cardiac catheterization in the proximal L.A.D. of 30 mongrel dogs. Ten dogs received low dose aspirin (L.D.A.); (14 or 29 mgm/Kg daily in a single dose). Ten dogs received high dose aspirin (H.D.A.); (100 mgm/Kg daily in divided doses). Treatment was begun one day before operation and continued until death or killing. Ten control dogs received no drug. All control dogs died within 3 days of operation. Five had O.T. and F.T.I. The remainder showed focal ischaemic myocardial damage. None of the L.D.A. group died. At autopsy 3 or 4 days after operation, none had O.T. or F.T.I. In the H.D.A. group 3 died; 4 had O.T. and F.T.I. Thus L.D.A. provided significant protection from death, O.T., and F.T.I. H.D.A. provided some (P <0.005) but less protection from death but did not significantly affect the incidence of O.T. or F.T.I. Supported by Ontario Heart Foundation Grant T15-7.


Circulation ◽  
1996 ◽  
Vol 94 (9) ◽  
pp. 2113-2116 ◽  
Author(s):  
Rau´l Altman ◽  
Jorge Rouvier ◽  
Enrique Gurfinkel ◽  
Alejandra Scazziota ◽  
Alexander G.G. Turpie

PLoS ONE ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. e0122330 ◽  
Author(s):  
Toshio Watanabe ◽  
Toshihisa Takeuchi ◽  
Osamu Handa ◽  
Yasuhisa Sakata ◽  
Tetsuya Tanigawa ◽  
...  

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2872-2872
Author(s):  
Tina Bagratuni ◽  
Efstathios Kastritis ◽  
Maria Roussou ◽  
Dimitrios Christoulas ◽  
Efthimios Kostouros ◽  
...  

Abstract Abstract 2872 The introduction of IMiDs (thalidomide, lenalidomide and recently pomalidomide) has been a major advance in the treatment of multiple myeloma. These agents have shown significant efficacy both in the relapsed/refractory setting and at the initial therapy of the disease, especially when combined with dexamethasone. However, it has been recognized that all IMiDs are associated with a significant increase in the risk of thromboembolic complications, especially when they are combined with high dose dexamethasone and chemotherapy. Genetic and environmental factors may modulate the risk for venous thromboembolism (VTE). Specific genetic polymorphisms have been associated with an increased risk of thromboembolic complications in patients treated with thalidomide-based regimens and who did not receive standard thromboprophylaxis. These single nucleotide polymorphisms (SNPs) have not been evaluated in patients treated with lenalidomide. In order to evaluate the frequency of thromboembolic complications in patients treated with lenalidomide, we analyzed 200 patients treated in a single center (Department of Clinical Therapeutics, University of Athens, Greece). All patients treated with lenalidomide-based regimens received low dose aspirin, unless there was a clear indication for other form of thromboprophylaxis (low molecular weight heparins (LMWH) or warfarin) due to: atrial fibrillation, prior thromboembolic event or immobilization (Dimopoulos et al, Leukemia 2011;25 :749–60). We also screened 6 SNPs that have been associated with increased VTE risk in patients treated with thalidomide by direct sequencing of peripheral blood derived genomic DNA. The analysis included ALDH1A1 (rs610529), CHEK1 (rs506504), CINP (rs7011), NFKB1 (rs3774968), TNFRSF17 (rs19222317), XRCC5 (rs2440) in 83 patients who received lenalidomide-based therapy. Sixty seven patients were previously untreated: 54 received first line therapy with lenalidomide plus low dose (weekly) dexamethasone (Rd) and 13 received lenalidomide with melphalan and prednisone (MPR). Among 133 previously treated patients, 84 received lenalidomide plus high dose dexamethasone (RD) and 49 received lenalidomide plus high dose dexamethasone with bortezomib (BRD). Thromboprophylaxis consisted of low dose aspirin (100 mg daily) in 165 (82.5%) patients, LMWH in 20 (10%) patients and warfarin in 15 (7.5%) patients. Eleven patients (5.5%) suffered a venous thromboembolic event (VTE), which included 8 episodes of deep vein thrombosis (DVT) while 3 patients suffered pulmonary embolism. None of the patients died because of the VTE. All VTEs occurred in patients who were receiving aspirin prophylaxis, thus, the frequency of VTE in patients receiving aspirin was 7% vs. 0% for patients receiving LMWH or warfarin. The frequency of VTEs was 9.4% for previously untreated and 5.4% for previously treated patients. Among previously treated patients, 5.6% of patient receiving RD suffered a VTE vs. 4.9% receiving BRD. We then analyzed 73 patients who received low dose aspirin, 7 of which developed VTE, for possible associations of VTE risk with specific SNPs. A trend towards increased risk for VTEs was found for 3 SNPs in genes involved in response to DNA damage and cytokine mediated apoptosis. The frequency of SNPs in patients that developed VTE vs. the ones without a thromboembolic event is the following: CHEK1_rs506504 (11% vs. 0%), XRCC5_rs2440 (15% vs. 8%) and NFKB1_rs3774968 (17% vs. 7%). For patients carrying all three SNPs, VTE rates were 50%. In conclusion, the frequency of VTE in patients treated with lenalidomide-based regimens was 5.5% but all events appeared in patients who received thromboprophylaxis with low dose aspirin. The administration of LMWH in patients at high risk for thromboembolic complications (atrial fibrillation, prior thromboembolic event or immobilization) may abrogate the risk of VTE. The identification of SNPs that confer susceptibility to thrombosis in patients treated with lenalidomide may help stratify patients according to risk for VTE and guide the choice of appropriate thromboprophylaxis. Disclosures: Dimopoulos: Celgene: Honoraria.


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