The outcome of short-term low-dose aspirin treatment in Kawasaki disease based on inflammatory markers

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.

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Helicobacter pyloriinfection and short-term intake of low-dose aspirin have different effects on alpha-1 antitrypsin/alpha-1 peptidase inhibitor (α1-PI) levels in antral mucosa and peripheral blood

Scandinavian Journal of Gastroenterology ◽

10.1080/00365520802158598 ◽

2008 ◽

Vol 43 (10) ◽

pp. 1194-1201 ◽

Cited By ~ 5

Author(s):

Thomas Wex ◽

Doerthe Kuester ◽

Michael Vieth ◽

Gerhard Treiber ◽

Anja Krieg ◽

...

Keyword(s):

Peripheral Blood ◽

Low Dose ◽

Antral Mucosa ◽

Short Term ◽

Dose Aspirin ◽

Low Dose Aspirin ◽

Peptidase Inhibitor ◽

Alpha 1 Antitrypsin

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Abstract 5067: Responsiveness to Low Dose Aspirin Influences Levels of Inflammatory Biomarkers

Circulation ◽

10.1161/circ.118.suppl_18.s_1138-c ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Rehan Qayyum ◽

Nauder Faraday ◽

Lisa R Yanek ◽

Dhananjay Vaidya ◽

Lewis C Becker ◽

...

Keyword(s):

Inflammatory Markers ◽

Low Dose ◽

Thromboxane B2 ◽

Inflammatory Biomarkers ◽

Premature Coronary Artery Disease ◽

Dose Aspirin ◽

Low Dose Aspirin ◽

Healthy Family ◽

Hs Crp

Platelets participate in cellular and humoral immunity; however the effect of low dose aspirin (ASA) therapy on platelet-mediated inflammation is unknown. Healthy family members (N=1934) of patients with premature coronary artery disease (CAD) participated in a 14-day trial of ASA 81 mg/day. Urinary 11-dehydro thromboxane B2 (uTxM), which reflects in vivo platelet activation, was measured at baseline and after ASA. Subjects were dichotomized by post-ASA uTxM levels into ASA responsive (lower quartile) and ASA resistant (upper quartile) groups based on previous studies showing an association between the upper quartile and incident CAD events. Levels of the inflammatory biomarkers, plasma hs-CRP and IL-6, were measured at both time points and compared between the two quartile extremes using multivariable-adjusted models. The study sample had 967 participants (females, 59%; blacks, 43%, age, 43.9±13 years). At baseline, plasma hs-CRP levels were similar between the upper and the lower uTxM quartiles, but IL-6 levels were significantly higher in the upper quartile (Table ). After ASA therapy, hs-CRP and IL-6 decreased in the lowest quartile, but increased in the upper (resistant) quartile, and the between-quartile difference (post-adjusted for pre) became significant for both inflammatory markers. Compared to ASA responsive subjects, those who are ASA “resistant” have higher levels of plasma inflammatory markers after ASA therapy and demonstrate lesser reductions in inflammatory markers from baseline. These extreme quartile differences in hs-CRP and IL-6 may reflect differences in ASA’s ability to suppress platelet-mediated inflammation, and may contribute to the increased CAD risk observed in aspirin resistant persons. Table. Comparison of hs-CRP and IL-6 in the Extreme Quartiles of 11-dehydro thromboxane B2 (uTxM)

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