Platelet Activation Dynamics Evaluated Using Platelet-Derived Microparticles in Kawasaki Disease

Yahata, Tetsutaro; Suzuki, Chinatsu; Yoshioka, Ayako; Hamaoka, Akiko; Ikeda, Kazuyuki

doi:10.1253/circj.cj-12-1037

Cited by 40 publications

(34 citation statements)

References 16 publications

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“…They suggested that platelet activation continues during the second stage (i.e., from the start of IVIG therapy to 20 days), but platelet activation is inhibited by antiplatelet agents. A recent study demonstrated that IVIG treatment significantly decreased PDMP levels in 18 patients with acute KD (17). They showed that the PDMP levels both immediately and 10–14 days after IVIG treatment were significantly lower than the pre-IVIG level.…”

Section: Discussionmentioning

confidence: 99%

The Usefulness of Platelet-derived Microparticle as Biomarker of Antiplatelet Therapy in Kawasaki Disease

et al. 2017

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Little is known about platelet dynamics and the effect of antiplatelet therapy in Kawasaki disease (KD). This study sought to define platelet activation dynamics in KD patients by assaying platelet-derived microparticles (PDMPs). We measured plasma PDMPs levels in 46 patients with KD using an enzyme-linked immunosorbent assay (ELISA). Blood samples were collected before, at 2–5 days, and 9–15 days after intravenous immunoglobulin (IVIG) infusion, 2 months and 4–5 months after the onset of KD. We measured PDMP levels in 23 febrile and 10 afebrile control patients. In the acute phase of KD patients, PDMP levels increased significantly after IVIG treatment (12.04 ± 5.58 nmol before IVIG infusion vs. 19.81 ± 13.21 nmol at 2–5 days after IVIG infusion, P = 0.006). PDMP levels were negatively correlated with age and positively correlated with procalcitonin levels in the acute phase of KD. No significant difference was found in PDMP levels between KD patients with and without coronary artery lesion (CAL). Elevated PDMP levels after IVIG therapy significantly decreased below the pre-IVIG level in subacute phase (19.81 ± 13.21 nmol at 2–5 days after IVIG infusion vs. 8.33 ± 2.02 nmol at 9–15 days after IVIG infusion, P < 0.001), and PDMP levels stayed below the pre-IVIG level in the convalescent phase, during which antiplatelet therapy was given. However, PDMP levels rebounded after discontinuing aspirin in 17 patients. In conclusion, enhanced platelet activation was noted before treatment of KD and peaked immediately after IVIG treatment. Recurrent rising of PDMP levels was observed after discontinuing aspirin, although there were no significant differences between the PDMP levels at 2 months after the onset of KD and those at 4–5 months after the onset of the disease.

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Section: Discussionmentioning

confidence: 99%

The Usefulness of Platelet-derived Microparticle as Biomarker of Antiplatelet Therapy in Kawasaki Disease

et al. 2017

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“…Platelet involvement in the pathogenesis and development of KD is not only reflected by the number of platelets, but also by the function of platelet aggregation and activation . A large number of activated platelets release blood coagulation active substance, thereby shifting the blood to a hypercoagulable state; in addition, enhanced platelets are more easily activated, which aggravates the hypercoagulable state of KD patients, thereby increasing the risk of thrombosis in patients …”

Section: Introductionmentioning

confidence: 99%

P2RY12:rs7637803 TT variant genotype increases coronary artery aneurysm risk in Kawasaki disease in a southern Chinese population

et al. 2019

The Journal of Gene Medicine

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Background Activated‐platelet increases the risk of thrombosis in Kawasaki disease (KD) patients with a coronary artery aneurysm (CAA). The ADP pathway is one of the platelet activation and aggregation pathways. The P2RY12 gene encodes the ADP receptor that is highly concentrated on platelets. However, few studies have reported on P2RY12 in relation to KD susceptibility with or without CAA. Methods We recruited 1335 healthy controls and 776 KD patients, including 103 with CAA, and selected five P2RY12 polymorphisms: rs9859538, rs1491974, rs7637803, rs6809699 and rs2046934. The present study focused on the relationship between the P2RY12 polymorphisms and KD with or without CAA. Results Among all of the selected polymorphisms, single‐locus analysis showed no significant association between the P2RY12 polymorphism and KD susceptibility. However, we found a significant relationship between rs7637803 and CAA risk in KD patients [CT versus CC: odds ratio (OR) = 0.41, 95% confidence interval (CI) = 0.22–0.75; p = 0.0041; TT versus CC: OR = 2.90, 95% CI = 1.12–7.46; p = 0.0276]. Stratification analysis by age in KD patients indicated that the rs7637803 TT genotype increased CAA formation risk among children aged (OR = 3.90, 95% CI = 1.42–10.69; p = 0.0081) and increased the onset risk of CAA in males (OR = 6.28, 95% CI = 2.01–19.65; p = 0.0016). The combined effect of the five selected P2RY12 risk genotypes with the KD patients compared to non‐mutated P2RY12 genotypes (score: 0) showed that patients with P2RY12 genotype polymorphisms (score: 1–5) had a significantly increased CAA risk (p = 0.0086). Stratification analysis for the severity of CAA found that the rs7637803 TT genotype reduced giant CAA (GCAA) risk (OR = 4.60, 95% CI = 1.70–12.41; p = 0.0026). Conclusions The results of the present study indicate that the P2RY12 rs7637803 genotype might be used as a biomarker to predict the occurrence of GCAA.

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“…In the field of autoimmune diseases, increased levels of circulating MP have been described in patients with SLE [20], Sjögren's syndrome and rheumatoid arthritis [21], antiphospholipid syndrome [22], systemic sclerosis [23], inflammatory myopathies [24], and vasculitis [25,26]. Pisetsky et al [27] have recently reviewed the different functions of circulating MP in these conditions, including modulation of inflammation, endothelial cell activation, and immune complex formation.…”

Section: Discussionmentioning

confidence: 99%

Procoagulant microparticles are increased in patients with Behçet’s disease but do not define a specific subset of clinical manifestations

et al. 2015

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Microparticles (MP) are considered a key component in the haemostatic response. Beyond their in vitro procoagulant properties, a number of pieces of evidence points to procoagulant MP as efficient effectors in the haemostatic response and as pathogenic markers of thrombotic disorders and vascular damage. The aim of the present study was to analyze the procoagulant activity of MP and its correlation with clinical manifestations focusing on vascular involvement in patients with Behçet's disease (BD). We analyzed 55 BD patients in inactive phase of the disease (26 men; mean age, 35 ± 15 years) of which 19 had previously suffered from thrombosis (deep venous thrombosis in 17 and ischemic stroke in 2), and 73 healthy controls matched for age and sex. Procoagulant MP were assessed by a functional assay. BD patients showed higher procoagulant MP values than controls (22.89 ± 15.74 nM versus 14.47 ± 7.34 nM; p < 0.0001). Conversely, we did not find differences in the levels of procoagulant MP according to the gender of patients (22.22 ± 16.23 nM for men versus 21.46 ± 16.47 for women; p = 0.846) or to previous and current treatments. Moreover, the plasmatic concentration of MP does not define any clinical phenotype and it was not related to the time of evolution of the disease. Although inactive BD patients had high values of procoagulant MP, they did not differentiate between BD patients with or without thrombosis.

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Platelet Activation Dynamics Evaluated Using Platelet-Derived Microparticles in Kawasaki Disease

Cited by 40 publications

References 16 publications

The Usefulness of Platelet-derived Microparticle as Biomarker of Antiplatelet Therapy in Kawasaki Disease

The Usefulness of Platelet-derived Microparticle as Biomarker of Antiplatelet Therapy in Kawasaki Disease

P2RY12:rs7637803 TT variant genotype increases coronary artery aneurysm risk in Kawasaki disease in a southern Chinese population

Procoagulant microparticles are increased in patients with Behçet’s disease but do not define a specific subset of clinical manifestations

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