# Thrombo-inflammation and Rethinking the Role of Aspirin in Kawasaki Disease

**Authors:** Begüm Kocatürk, Beyda Berberoğulları, Emil Aliyev, Erdal Sağ, Seza Özen, Moshe Arditi

PMC · DOI: 10.1007/s11926-026-01211-5 · Current Rheumatology Reports · 2026-02-06

## TL;DR

This paper reviews the role of aspirin in Kawasaki Disease, focusing on its use in managing thrombosis and inflammation in children with coronary artery aneurysms.

## Contribution

The paper re-examines aspirin dosing ambiguity and explores complementary therapies for thrombosis in Kawasaki Disease.

## Key findings

- Standard therapy with aspirin and IVIG may be sufficient for small aneurysms but insufficient for large ones.
- Low-dose aspirin shows potential superiority, though consensus remains elusive due to ethnic and individual variability.
- Thrombolytic therapy is recommended in cases of thrombosis formation.

## Abstract

Kawasaki Disease (KD) is a medium vessel vasculitis of young children that affects coronary arteries (CAs). The aim of therapy is to control inflammation and prevent coronary artery damage and alleviate thrombosis. This review aims to summarize the thrombosis-related complications and complementary therapy approaches to combat them. It also focuses on the ambiguity regarding the optimal aspirin dose in standard KD therapy.

KD patients with large or giant coronary artery aneurysms (CAAs) in particular face the risk of developing thrombosis. The standard therapy regimen during the acute phase consists of intravenous immunoglobulin (IVIG) plus aspirin. Although the dosing for IVIG is constant, the aspirin dose continues to be debated. The standard treatment with aspirin and IVIG might be adequate for individuals with small aneurysms whereas, patients suffering from large aneurysms and in a hypercoagulable state might need additional and extended therapy consisting of several antiplatelet reagents and anticoagulants. In case of thrombosis formation, thrombolytic therapy is also recommended.

Cardiac and thrombotic problems are severe outcomes of KD. Patients need to be screened on a regular basis with echocardiography. The ideal aspirin dose during acute KD treatment is still controversial and while several recent studies pinpoint the superiority of low doses, there is no universal consensus. The variation in treatment response might be due to the different ethnic composition of study groups and inter-individual differences. Overall, close monitoring of patient response and finding the optimal treatment strategy is crucial.

## Linked entities

- **Chemicals:** aspirin (PubChem CID 2244)
- **Diseases:** Kawasaki Disease (MONDO:0012727)

## Full-text entities

- **Genes:** BLK (BLK proto-oncogene, Src family tyrosine kinase) [NCBI Gene 640] {aka MODY11}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}, COX8A (cytochrome c oxidase subunit 8A) [NCBI Gene 1351] {aka COX, COX8, COX8-2, COX8L, MC4DN15, VIII}, F8 (coagulation factor VIII) [NCBI Gene 2157] {aka AHF, DXS1253E, F8B, F8C, FVIII, HEMA}, SERPINC1 (serpin family C member 1) [NCBI Gene 462] {aka AT3, AT3D, ATIII, ATIII-R2, ATIII-T1, ATIII-T2}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, PLG (plasminogen) [NCBI Gene 5340] {aka HAE4}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, HLA-DRB1 (major histocompatibility complex, class II, DR beta 1) [NCBI Gene 3123] {aka DRB1, HLA-DR1B, HLA-DRB, SS1}, PLAT (plasminogen activator, tissue type) [NCBI Gene 5327] {aka T-PA, TPA}, CD40 (CD40 molecule) [NCBI Gene 958] {aka Bp50, CDW40, TNFRSF5, p50}, THBD (thrombomodulin) [NCBI Gene 7056] {aka AHUS6, BDCA-3, BDCA3, CD141, THPH12, THRM}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, CASP3 (caspase 3) [NCBI Gene 836] {aka CPP32, CPP32B, SCA-1}, PPBP (pro-platelet basic protein) [NCBI Gene 5473] {aka B-TG1, Beta-TG, CTAP-III, CTAP3, CTAPIII, CXCL7}, VWF (von Willebrand factor) [NCBI Gene 7450] {aka F8VWF, VWD}, HAMP (hepcidin antimicrobial peptide) [NCBI Gene 57817] {aka HEPC, HFE2B, LEAP1, PLTR}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, ITPKC (inositol-trisphosphate 3-kinase C) [NCBI Gene 80271] {aka IP3-3KC, IP3KC}, SERPINE1 (serpin family E member 1) [NCBI Gene 5054] {aka PAI, PAI-1, PAI1, PLANH1}
- **Diseases:** abdominal aorta aneurysm (MESH:D017544), atherosclerosis (MESH:D050197), pericardial tamponade (MESH:D002305), gastrointestinal irritation (MESH:D005767), hepatic toxicity (MESH:D056486), coronary complications (MESH:D003327), ischemia (MESH:D007511), Cardiovascular complications (MESH:D002318), death (MESH:D003643), coronary arteritis (MESH:D001167), Aortic root dilation (MESH:D000094628), diastolic dysfunction (MESH:D018487), giant aneurysms (MESH:D002532), coronary thrombosis (MESH:D003328), platelet aggregation (MESH:D001791), CAA (MESH:C564321), MI (MESH:D009203), febrile illnesses (MESH:D005334), unstable angina (MESH:D000789), necrosis (MESH:D009336), myocardial ischemia (MESH:D017202), CALs (MESH:D003324), ventricular dysfunction (MESH:D018754), rupture (MESH:D012421), Thrombocytosis (MESH:D013922), arrhythmia (MESH:D001145), Inflammation (MESH:D007249), coronary ectasia (MESH:D004108), hypoalbuminemia (MESH:D034141), vasculitis (MESH:D014657), lymphadenopathy (MESH:D008206), Cardiac (MESH:D006331), hyperbilirubinemia (MESH:D006932), arterial fistula (MESH:D016157), stroke (MESH:D020521), maculopapular rash (MESH:D005076), G6PD deficiency (MESH:D005955), KD (MESH:D009080), NSTEMI (MESH:D000072657), sensorineural hearing loss (MESH:D006319), CAAs (MESH:D003323), peripheral gangrene (MESH:D005734), arteriosclerosis (MESH:D001161), stenoses (MESH:D003251), aortic regurgitation (MESH:D001022), liver injury (MESH:D017093), Anemia (MESH:D000740), Sudden death (MESH:D003645), tachycardia (MESH:D013610), Thrombosis (MESH:D013927), idiopathic thrombocytopenic purpura (MESH:D016553), coagulation (MESH:D001778), disseminated intravascular coagulation (MESH:D004211), embolization (MESH:D004617), coronary artery occlusion (MESH:D054059), Thrombocytopenia (MESH:D013921), aneurysm (MESH:D000783), febrile (MESH:D000071072), hypercoagulable (MESH:D019851), enzyme (MESH:D008661)
- **Chemicals:** dipyridamole (MESH:D004176), Aspirin (MESH:D001241), LMWH (MESH:D006495), clopidogrel (MESH:D000077144), cyclic adenosine monophosphate (MESH:D000242), salicylate (MESH:D012459), abciximab (MESH:D000077284), TX (MESH:D013931), prednisone (MESH:D011241), warfarin (MESH:D014859), TXA2 (MESH:D013928), infliximab (MESH:D000069285), methylprednisolone (MESH:D008775), prostacyclin (MESH:D011464), heparin (MESH:D006493), prostaglandin (MESH:D011453), rivaroxaban (MESH:D000069552), ibuprofen (MESH:D007052), HDA (-), TXB2 (MESH:D013929), iron (MESH:D007501)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]
- **Mutations:** T > C

## Full text

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## References

3 references — full list in the complete paper: https://tomesphere.com/paper/PMC12881031/full.md

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Source: https://tomesphere.com/paper/PMC12881031