KD Patients (kd + patient)

Distribution by Scientific Domains


Selected Abstracts


Repeated systematic surveillance of Kawasaki disease in Ontario from 1995 to 2006

PEDIATRICS INTERNATIONAL, Issue 5 2010
Yahui T. Lin
Abstract Background:, Rising incidences of Kawasaki disease (KD) have been reported worldwide. Reported herein are the results of 4 triennial KD surveillances conducted in Ontario. Methods:, Between 1995 and 2006 all hospitals in Ontario were asked on 4 occasions to identify all patients with discharge diagnoses of KD and report incident cases. Results:, The latest surveillance identified 697 new KD patients (100% response rate) for a total of 2378 KD patients through all 4 surveillances. Yearly incidence was 26.2/100 000 for <5 years old, 6.7/100 000 for 5,9 years old and 0.9/100 000 for 10,14 years old. KD incidence significantly increased from 1995 to 2006, although the increase seemed to plateau between the 3rd and 4th surveillance. There was an increase in the proportion of patients diagnosed with incomplete KD and a significant reduction in the rate of coronary artery abnormalities, possibly due to better disease recognition and treatment. Hospitals reporting <20 cases per surveillance were found to be more likely to report cases with incomplete KD. These patients were also less likely to be treated with i.v. immunoglobulin and aspirin but were more likely to be treated with antibiotics, suggesting uncertainties regarding diagnosis and management of KD patients in those centers. Conclusions:, The incidence of KD in Ontario is possibly one of the highest outside of Asia and has been rising since 1995. Although the most recent surveillance demonstrated improved cardiac outcomes, treatment delays or absence thereof continue to be a problem. Effective diagnosis and prompt treatment remain critical aspects of KD management. [source]


Exercise- or dipyridamole-loaded QGS is useful to evaluate myocardial ischemia and viability in the patients with a history of Kawasaki disease

PEDIATRICS INTERNATIONAL, Issue 5 2005
Yuichi Ishikawa
AbstractBackground:,Evaluation of myocardial ischemia and viability is very important for the management of patients with a history of Kawasaki disease (KD). 99mTc-tetrofosmin myocardial perfusion scintigraphy combined with quantitative gated single photon computed emission tomography (QGS) gives us information, not only about perfusion, but also the percentage change in left ventricular wall thickness (%WT) and relative changes in left ventricular wall motion (LVM). Methods:,The subjects were 27 patients with a history of KD followed as outpatients at the National Cardiovascular Center, Osaka, Japan. Exercise-loaded QGS was performed on 21 patients, and dipyridamole- loaded QGS was performed in six patients younger than 7 years old. Results:,Perfusion defects (PD) were observed in 12 patients. Of the 12 patients, four with old myocardial infarction (OMI) had decreased %WT. All patients with OMI showed a decrease in %WT in the areas where PD was seen on the image. The other eight patients without OMI showed no decrease in %WT. In non-infarcted cases, the %WT was normal in the PD-positive area. Conclusions:,It is possible to evaluate myocardial ischemia and viability in KD patients by comparing PD on the image with %WT determined by QGS using exercise or drug-loaded myocardial scintigraphy alone. [source]


Absence of hypercoagulability in acute Kawasaki disease

PEDIATRICS INTERNATIONAL, Issue 2 2005
Ming-Tsan Lin
AbstractBackground:,Kawasaki disease (KD) is a systemic vasculitis syndrome with the striking feature of cardiovascular involvement. Endothelial cell (EC) damage has been suggested to predispose individuals to the development of coronary vascular disorders. When EC are perturbed, prethrombotic complications ensue. The purpose of this study was to examine the clinical relevance of EC activation and hypercoagulability in the pathogenesis of KD and to determine if plasma levels of these markers are correlated with the development of coronary aneurysms. Methods:,EC function and coagulation status were assessed in 52 patients with acute KD, 20 febrile control subjects, and 20 healthy control subjects. Biological markers of EC and hypercoagulability were measured and included thrombomodulin, tissue factor, tissue factor pathway inhibitor, von Willebrand factor (vWF), coagulation factor VII (FVII), activated factor VII, prothrombin fragment 1 + 2 (F1 + 2), and D-dimer. Results:,Transient dilatation of coronary arteries was the most common complication (55.8%), and coronary aneurysm was noted in five patients (9.6%). Levels of vWF, FVII, F1 + 2 and D-dimer were higher in acute KD patients compared with healthy controls but not febrile controls. Markers of EC and hypercoagulability were not different between patients with cardiac complications and those without cardiac complications. Biological and immunological assays did not demonstrate the prethrombotic state in acute KD. Conclusions:,Our results suggest that hypercoagulability does not occur during the acute stage of KD. Markers of EC damage and hypercoagulability are not predictive of coronary aneurysms in KD. [source]


Inducible and endothelial constitutive nitric oxide synthase gene polymorphisms in Kawasaki disease

PEDIATRICS INTERNATIONAL, Issue 2 2003
Vahid Khajoee
AbstractBackground: Nitric oxide (NO) is secreted by immune and vascular endothelial cells, and appears to play important roles in the pathophysiology of Kawasaki disease (KD). Thus, genetic variations in NO synthase (NOS) genes may be involved in the development of coronary artery lesions (CAL) in KD. Methods: The present study investigated the association of endothelial constitutive NOS (ecNOS) and inducible NOS (iNOS) gene polymorphisms with the development of CAL in KD in a Japanese population. Results: The genotype distributions of 27-bp tandem repeat polymorphism within intron 4 of ecNOS gene did not show any significant difference between controls and KD patients with or without CAL. In addition, there was no significant association between whole-allele distribution of iNOS gene promoter (penta-repeat CCTTT) polymorphism and KD with or without CAL. Conclusion: These results did not support any association of ecNOS and iNOS gene polymorphisms to the development of CAL in KD patients in a Japanese population. [source]


Increased production of serum IgA-class antibody to lipid A in Kawasaki disease

PEDIATRICS INTERNATIONAL, Issue 1 2002
Seiichiro Takeshita
Abstract Background:,The etiology of Kawasaki disease (KD) remains unknown. To investigate whether a conventional bacterial antigen is involved in the pathogenesis of KD, we studied the serum response to lipopolysaccharide (LPS). Methods:,We measured the serum levels of IgG-, IgM- and IgA-class antibodies (Ab) to lipid A, a toxic site of LPS, using enzyme-linked immunosorbent assay in 20 patients with KD, 11 patients with Gram-negative bacterial infection (GNBI), 27 healthy children and 12 healthy adults. Results:,The serum levels of anti-lipid A IgG, IgM and IgA tended to increase with advancing age in healthy children older than 6 months of age. The mean level of anti-lipid A IgM in the acute phase of GNBI and the mean levels of anti-lipid A IgM and IgA in the acute phase of KD were found to increase significantly, in comparison to the age-matched controls. Furthermore, the mean level of anti-lipid A IgA also showed a significant increase from the acute to the subacute phases of KD. Regarding the IgA-subclass response, higher titers of anti-lipid A specific Ab were seen in the IgA2 subclass than in the IgA1 subclass. Conclusion:,These findings indicate that KD patients demonstrate an intense response to lipid A in the IgA, especially IgA2-subclass, thus suggesting that an unusual activation of the mucosal immune response to a ubiquitous antigen derived from Gram-negative bacteria may be involved in the pathogenesis of KD. [source]


Methylenetetrahydrofolate reductase polymorphism in Kawasaki disease

PEDIATRICS INTERNATIONAL, Issue 3 2000
Hirokazu Tsukahara
Abstract Background: A genetic aberration in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene (677 C to T substitution) has been shown to result in reduced enzyme activity. The hypothesis tested in the present study was that a higher proportion of Kawasaki disease (KD) patients with coronary artery lesions (CAL) would have the T677 allele compared with patients without CAL and healthy subjects. Methods: Genotypes for MTHFR were determined in 75 KD patients (male : female ratio 52:23) and 238 healthy subjects (male : female ratio, 110:128) by the polymerase chain reaction and restriction fragment length polymorphism method. Results: The results indicated that female KD patients had a significantly higher frequency of the TT genotype compared with female control subjects. In the female population, the frequency of the TT genotype in patients with initial coronary aneurysm was significantly lower than in patients without this manifestation. Analysis of the data for the male population showed that the frequency of the TT genotype in KD patients developing coronary stenosis, occlusion or myocardial infarction was higher than that in those without these manifestations, although the difference was statistically insignificant. Conclusions: The TT genotype may protect female KD patients against initial aneurysm formation and predispose male KD patients to severe coronary complications. Further large-scale studies may be required to confirm the contribution of homocysteine in the coronary sequelae of KD. [source]


HLA,E gene polymorphism associated with susceptibility to kawasaki disease and formation of coronary artery aneurysms

ARTHRITIS & RHEUMATISM, Issue 2 2009
Y.-J. Lin
Objective Kawasaki disease (KD) is a pediatric systemic vasculitis of unknown cause for which a genetic influence is supposed. The purpose of this study was to identify possible genetic variants in the major histocompatibility complex (MHC) region that are associated with KD and the development of coronary artery aneurysms (CAAs) in a Taiwanese population. Methods The 168 genetic variants covering the MHC locus were analyzed in an association study of a Taiwanese cohort of 93 KD patients and 680 unrelated healthy children matched for sex and age with the study patients. Results Eleven single-nucleotide polymorphisms (SNPs) were associated with the occurrence of KD. The SNP located at the 3,-untranslated region of HLA,E (rs2844724) was highly associated (P < 1 10,7). In addition, the frequency of the C allele was higher in KD patients without CAAs than in controls (P < 0.001) due to a significantly increased frequency of the CC and CT genotypes. Plasma levels of soluble HLA,E were significantly higher in KD patients than in controls regardless of the presence of CAAs. Furthermore, there was a trend toward higher plasma levels of soluble HLA,E in KD patients with the CT and TT genotypes of the HLA,E gene polymorphism. Conclusion Our results suggest that the HLA,E gene polymorphism may play a role in the pathogenesis of KD. [source]


Polymorphisms in chemokine receptor genes and susceptibility to Kawasaki disease

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2007
W. B. Breunis
Summary Kawasaki disease (KD) is an acute vasculitis occurring in young children. Its aetiology is unknown, but an infectious agent is assumed. Increased levels of proinflammatory cytokines and chemokines have been reported in KD. Genetic variation in these genes and the receptors for these genes could influence the regulation of cytokines and chemokines. In a case,control study of 170 Dutch Caucasian KD patients and 300 healthy Dutch Caucasian controls, common genetic variants in chemokine receptor genes CCR3, CCR2, CCR5, CX3CR1, CXCR1 and CXCR2 were analysed. Of the eight studied single nucleotide polymorphisms (SNPs) in the CCR3,CCR2,CCR5 gene cluster, four showed a significant association with susceptibility to KD. Moreover the CCR5 -,32 was observed with an allele frequency of 107% in the control population compared to 65% in the KD patients (P = 004). Two haplotypes of the CCR3,CCR2,CCR5 gene-cluster appear to be at risk haplotypes for KD and one a protective haplotype. No association was observed with the studied SNPs in CX3CR1, CXCR1 and CXCR2. In conclusion, in a Dutch cohort of KD patients an association of KD occurrence with common genetic variants in the chemokine receptor gene-cluster CCR3,CCR2,CCR5 was observed. [source]