
INTERLEUKIN-18 PROMOTER GENE POLYMORPHISMS
ARE NOT ASSOCIATED WITH MYOCARDIAL INFARCTION
IN TYPE 2 DIABETES IN SLOVENIA Kariž S1*, Petrovič D2 *Corresponding Author: Stojan Kariž, Department of Internal Medicine, General Hospital Izola, Polje
35, Izola 6310, Slovenia; Tel.: +386-5-660-6480; Fax: +386-660-6305; E-mail: stojan.kariz@siol.net page: 3
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RESULTS
The clinical characteristics of the subjects and
controls are listed in Table 1. The former were younger,
predominantly male and had a higher incidence
of cigarette smoking compared to the control group.
They also had higher total cholesterol and LDL cholesterol
levels, and longer duration of type 2 diabetes
than the controls. The high sensitivity CRP serum levels
were also higher in the diabetic patients with MI.
There were no significant differences in the prevalence
of hypertension, mean blood pressure, and mean BMI,
and serum HDL cholesterol, triglyceride, and Hb A1c
levels between the two groups. Therapy for diabetes
was similar in both groups.
The IL-18 genotype distributions in MI and control
groups were compatible with Hardy-Weinberg expectations
(–607: MI group χ2 = 0.40, p = 0.53; controls
χ2 = 1.65, p = 0.2; –137: MI group χ2 = 0.02, p =
0.89; controls χ2 = 1.07, p = 0.3). The distribution of genotypes in the promoter of the IL-18 gene in MI and
in control groups are shown in Table 2. There were no
differences between the two groups.
The serum IL-18 level in 70 diabetics did not differ
significantly from those of 22 controls without diabetes
(310.0 ± 234.1 ng/L vs. 250.3 ± 190.4 ng/L; p =
0.3). However, the level in 20 diabetics with MI was
statistically significantly higher than that of 50 diabetics
without CAD (534.0 ± 397.5 ng/L vs. 286.2 ± 202.4
ng/l; p <0.01). A significant difference in IL-18 serum
levels was found in diabetics with the –137 CC genotype
(10 subjects) compared to those with CG+GG
genotypes (60 subjects) (241.5 ± 132.7 ng/L vs. 340.2
± 167.4 ng/L; p <0.05). We found no significant difference
in IL-18 level in diabetics with the –607 CC genotype
(17 subjects) compared to those with CA+AA
genotypes (53 subjects) (287.3 ± 221.7 ng/L vs. 323.3
± 257.3 ng/L; p = 0.6).
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