Search tips
Search criteria

Results 1-3 (3)

Clipboard (0)

Select a Filter Below

more »
Year of Publication
Document Types
1.  Relationship between carotid intima‐media thickness and arterial stiffness in children after Kawasaki disease 
Evidence of premature atherosclerosis and systemic arterial stiffening in patients after Kawasaki disease is accumulating.
To test the hypothesis that carotid intima‐media thickness (IMT), a surrogate marker of atherosclerosis, is associated with systemic arterial stiffness in children after Kawasaki disease.
A cohort of 72 patients was studied, comprising 26 patients with Kawasaki disease and coronary aneurysms (group I), 24 patients with Kawasaki disease and normal coronary arteries (group II) and 22 healthy age‐matched children (group III). The carotid IMT, carotid artery stiffness index, brachioradial pulse wave velocity (PWV), fasting total cholesterol, high‐density lipoprotein (HDL) cholesterol and low‐density lipoprotein (LDL) cholesterol were determined and compared among the three groups.
The carotid IMT was related to indices of arterial stiffness, and significant determinants of carotid IMT were identified by multivariate analysis. The mean (standard deviation (SD)) carotid IMT of both group I (0.41 (0.04) mm) and group II (0.39 (0.04) mm) was significantly greater than that of group III (0.36 (0.04) mm; p<0.001 and p = 0.008, respectively). For the entire cohort, carotid IMT correlated positively with LDL cholesterol (r = 0.31, p = 0.009), carotid artery stiffness index (r = 0.40, p = 0.001) and brachioradial PWV (r = 0.28, p = 0.016), but not with age, body mass index, systemic blood pressure, and HDL and total cholesterol. Multiple linear regression analysis identified carotid artery stiffness index (β = 0.25, p = 0.028) and subject grouping (β = −0.39, p = 0.001; model R2 = 0.29) as significant correlates of carotid IMT.
The increased carotid IMT in children after Kawasaki disease is associated with systemic arterial stiffening.
PMCID: PMC2083125  PMID: 16820386
2.  Association of BANK1 and TNFSF4 with systemic lupus erythematosus in Hong Kong Chinese 
Genes and Immunity  2009;10(5):414-420.
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease with complex genetic inheritance. Recently, single nucleotide polymorphisms (SNPs) in BANK1 and TNFSF4 have been shown to be associated with SLE in Caucasian populations, but it is not known whether they are also involved in the disease in other ethnic groups. Recent data from our genome-wide association study (GWAS) for 314 SLE cases and 920 controls collected in Hong Kong identified SNPs in and around BANK1 and TNFSF4 to be associated with SLE risk. On the basis of the results of the reported studies and our GWAS, SNPs were selected for further genotyping in 949 SLE patients (overlapping with the 314 cases in our GWAS) and non-overlapping 1042 healthy controls. We confirmed the associations of BANK1 and TNFSF4 with SLE in Chinese (BANK1, rs3733197, odds ratio (OR)=0.84, P=0.021; BANK1, rs17266594, OR=0.61, P=4.67 × 10−9; TNFSF4, rs844648, OR=1.22, P=2.47 × 10−3; TNFSF4, rs2205960, OR=1.30, P=2.41 × 10−4). Another SNP located in intron 1 of BANK1, rs4522865, was separately replicated by Sequenom in 360 cases and 360 controls and was also confirmed to be associated with SLE (OR=0.725, P=2.93 × 10−3). Logistic regression analysis showed that rs3733197 (A383T in ankyrin domain) and rs17266594 (a branch point-site SNP) from BANK1 had independent contributions towards the disease association (P=0.037 and 6.63 × 10−8, respectively). In TNFSF4, rs2205960 was associated with SLE independently from the effect of rs844648 (P=6.26 × 10−3), but not vice versa (P=0.55). These findings suggest that multiple independent genetic variants may be present within the gene locus, which exert their effects on SLE pathogenesis through different mechanisms.
PMCID: PMC2834352  PMID: 19357697
SLE; BANK1; TNFSF4; Chinese; genetic association
3.  Increased high sensitivity C reactive protein concentrations and increased arterial stiffness in children with a history of Kawasaki disease 
Heart  2004;90(11):1281-1285.
Objectives: To test the hypothesis that low grade inflammation persists after the acute phase and affects arterial stiffness in children with a history of Kawasaki disease.
Design and patients: A cohort of 106 children was studied, which comprised 43 patients with Kawasaki disease with coronary aneurysms (group I), 28 patients with Kawasaki disease with normal coronary arteries (group II), and 35 healthy age matched children (group III). Their systemic blood pressure, fasting cholesterol concentrations, serum high sensitivity C reactive protein (hs-CRP) concentrations, and carotid artery stiffness index were compared. Significant determinants of serum hs-CRP concentration and carotid artery stiffness were identified and the relation between hs-CRP concentration and arterial stiffness was investigated.
Setting: Tertiary paediatric cardiac centre.
Results: Serum hs-CRP concentration of group I patients (median 0.39 mg/l, interquartile range 0.28–0.65 mg/l) was significantly greater than that of group II (median 0.24 mg/l, interquartile range 0.17–0.29 mg/l, p < 0.001) and of group III patients (median 0.25 mg/l, interquartile range 0.18–0.40 mg/l, p < 0.01). Likewise, carotid artery stiffness index of group I patients (mean (SD) 5.07 (1.11)) was significantly greater than that of group II (4.27 (0.83), p  =  0.002), and of group III patients (4.24 (0.86), p  =  0.001). For the entire cohort, the carotid artery stiffness index correlated positively with log serum hs-CRP concentration (r  =  0.24, p  =  0.013). In multiple linear regression analysis, age (standardised β  =  0.22, p  =  0.02), systolic blood pressure (standardised β  =  0.28, p  =  0.01), log serum hs-CRP concentration (standardised β  =  0.21, p  =  0.017), and patient grouping (standardised β  =  −0.36, p < 0.001) were all independently associated with the carotid artery stiffness index.
Conclusions: These findings support the possibility of ongoing low grade inflammation late after the acute phase of Kawasaki disease in patients with coronary aneurysms. Furthermore, this low grade inflammation may have a role in increasing systemic arterial stiffness.
PMCID: PMC1768534  PMID: 15486121
Kawasaki disease; C reactive protein; arterial stiffness

Results 1-3 (3)