2005
DOI: 10.1093/tropej/fmh087
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High-dose Intravenous Immunoglobulin Downregulates the Activated Levels of Inflammatory Indices Except Erythrocyte Sedimentation Rate in Acute Stage of Kawasaki Disease

Abstract: We evaluated the effects of high-dose intravenous immunoglobulin (IVIG) administration on various protein parameters, including inflammatory profiles, in children with Kawasaki disease (KD). Sixty-three children with KD were treated with IVIG at 2 g/kg over 12 h. Serial examinations of laboratory indices were performed three times: before IVIG treatment, 24 h after IVIG treatment, and 7 days after IVIG treatment. The white blood cell and neutrophil counts showed significant decreases 24 h and 7 days after IVIG… Show more

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Cited by 26 publications
(28 citation statements)
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“…The mechanism of thrombosis secondary to IVIg is unknown but it is attributed to the resultant hyperviscosity of blood, as IVIg can cause remarkable biochemical and hematological changes [2,9,10]. Furthermore such changes are often confused with a serious medical problem such as disease reactivity.…”
Section: Discussionmentioning
confidence: 99%
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“…The mechanism of thrombosis secondary to IVIg is unknown but it is attributed to the resultant hyperviscosity of blood, as IVIg can cause remarkable biochemical and hematological changes [2,9,10]. Furthermore such changes are often confused with a serious medical problem such as disease reactivity.…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore such changes are often confused with a serious medical problem such as disease reactivity. ESR is elevated due to enhanced rouleaux formation, polymerisation between proteins and reduced surface area caused by the infused IVIg [10]. In addition, IVIg reportedly cause platelet activation and arterial vasospasm [2,4].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…3 A imunoglobulina intravenosa (IGIV) é o principal medicamento na doença de Kawasaki, sendo utilizada na fase aguda, preferencialmente nos primeiros sete a 10 dias da doença, a fim de diminuir a prevalên-cia de anormalidades das artérias coronárias e abreviar a duração dos sintomas clínicos. 42,[63][64][65][66] Pode ainda normalizar mais rapidamente as proteínas inflamatórias de fase aguda -mas não a velocidade de hemossedimentação (VHS) -e melhorar a função miocárdica. 4,66 Em estudo retrospectivo recente concluiu-se que o início tardio da IGIV, após o oitavo dia de doença, reduz as chances de sucesso terapêutico.…”
Section: Tratamentounclassified
“…42,[63][64][65][66] Pode ainda normalizar mais rapidamente as proteínas inflamatórias de fase aguda -mas não a velocidade de hemossedimentação (VHS) -e melhorar a função miocárdica. 4,66 Em estudo retrospectivo recente concluiu-se que o início tardio da IGIV, após o oitavo dia de doença, reduz as chances de sucesso terapêutico. 67 Os mecanismos de ação da IGIV permanecem desconhecidos; várias teorias têm sido aventadas para os possí-veis mecanismos como supressão de macrófagos e monócitos ativados, bloqueio da interação entre o endotélio e as células natural killers, estimulação de receptores inibitórios, modulação de produção de citocinas, neutralização de superantígenos bacterianos, diminuição da síntese de anticorpos e aumento da atividade de linfócitos T supressores.…”
Section: Tratamentounclassified