Result
Characteristics of the
study population
The baseline characteristics of the subjects were shown in Table A1.
There were 1993 cases in the MS group and 1079 cases in the control
group. The sex and age of the control group and the MS group could be
matched. During the 5-year follow-up, 325 subjects were lost to
follow-up, 1615 patients in the MS group and 1039 patients in the
control group were completed. (Fig. 1).
Genotype analysis was performed on
NC_000007.14:g.139985896C>T of the 3072 samples. Finally,
there were 1991 cases in the MS group and 1076 cases in the control
group completed. The frequency distribution of
NC_000007.14:g.139985896C>T genotypes and alleles in
control group and MS group was basically consistent with that in
HAPMAP-CHB, the frequency distribution of
NC_000007.14:g.139985896C>T in both groups did not deviate
from Hardy-Weinberg equilibrium.
Table A2 presents the genotype and allele frequencies of the
NC_000007.14:g.139985896C>T
in the MS group and controls,
there were no significant
difference in the NC_000007.14:g.139985896C>T genotype or
the allele distributions between MS and controls (P
> 0.05). The comparison of baseline clinical
characteristics between different genotypes in the control group and the
MS group showed that there was no significant difference in clinical
indicators between different genotypes in the MS group
(all P >
0.05). But significant difference was observed in the control group,
compared with CC genotype carriers, the CT genotype carriers had
significantly higher low-density lipoprotein cholesterol (LDL-C)
(P <0.05). (Table 1).
Relevance of SNP and
Components of MS
The components of MS include TG,
blood pressure, fasting plasma glucose (FPG), abdominal obesity, HDL-C,
the relationship between the NC_000007.14:g.139985896C>T
genotypes and the components were analyzed (Table 2).
The results showed that there was
no significant difference between the groups according to TG, blood
pressure, FPG, and abdominal obesity. (all P >
0.05). It suggested that there was no association between genotypes and
these components. But in group of HDL-C, significant differences were
observed in the distributions of the CC genotype and the C allele of
NC_000007.14:g.139985896C>T between normal HDL-C group and
abnormal HDL-C group (P = 0.023 & P = 0.018,
respectively). The HDL-C abnormality of the C allele is significantly
higher than the T allele carriers
(P < 0.05).
Relevance of SNP andendpoints
of MS
The relationship between the
NC_000007.14:g.139985896C>T
genotypes and the endpoints were analyzed of the whole population,
MS group and controls. The results
showed that there was no significant difference between all-cause death,
coronary heart disease, myocardial infarction, new-onset diabetes,
new-onset hypertension and new-onset MS in the whole population and MS
group (P > 0.05), but significant differences were
observed in ischemic stroke and the genotypes of
NC_000007.14:g.139985896C>T
(all P < 0.05), especially in the MS group (Table 3).
The incidence of ischemic stroke was significantly higher in G allele
carriers than in C allele carriers (all P <
0.05). In the control group, no
endpoint was associated with this locus (all P >
0.05).
Risk factors of the onset
of ischemic stroke
The Logistic regression analysis
was performed for screening the risk factors of the onset of ischemic
stroke (Table 4). The results showed that, in the whole population, C
allele and gender was the protective factors of the onset of ischemic
stroke, the risk of ischemic stroke was decreased when the individual
was women or with C allele. SBP was the risk factor for the onset of
ischemic stroke, the risk of ischemic stroke was increased when the SBP
was higher; in the MS population, C allele and gender was the protective
factors of the onset of ischemic stroke, the risk of ischemic stroke was
decreased when the individual was women or with C allele.
The interaction effects between C allele and the components of MS on the
onset of ischemic stroke showed that, in the whole population, there
were negative interactions between
C allele and WC, SBP, DBP, TG,
HDL-C and FPG; in the MS group,
there were also negative interactions between C allele and WC, SBP, DBP,
TG, HDL-C and FPG. In the case of same WC, SBP, DBP, TG, HDL-C and FPG,
the onset of ischemic stroke of C allele carrier were reduced (Table 5).