Abstract | INTRODUCTION: OBJECTIVE: METHODS: The study cohort consisted of 37 patients with Perthes disease and 50 healthy controls. Polymorphisms of well described inflammatory mediators: TLR4 (Asp299Gly, Thr39911e) and 11-6 (G-174C, G-597A) were determined by polymerase chain reaction restriction fragment length polymorphism method. Results IL-6 G-174C and G-597A polymorphisms were in complete linkage disequilibrium. A statistically significant increase of heterozygote subjects for IL-6 G-174C/G-597A was found in controls in comparison to Perthes patient group (p = 0.047, OR = 2.49, 95% CI = 1.00-6.21). Also, the patient group for IL-6 G-174C/G-597A polymorphisms was not in Hardy-Weinberg equilibrium. No statistically significant differences were found between patient and control groups for TLR4 analyzed polymorphisms. A stratified analysis by the age at disease onset also did not reveal any significant difference for all analyzed polymorphisms. Conclusion Our study revealed that heterozygote subjects for the IL-6 G-174C/G-597A polymorphisms were significantly overrepresented in the control group than in the Perthes patient group. Consequently, we concluded that children who are heterozygous for these polymorphisms have a lower chance of developing Perthes disease than carriers of both homozygote genotypes.
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Authors | Sanja Srzentić, Vesna Spasovski, Dusko Spasovski, Zorica Zivković, Dragana Matanović, Zoran Bascarević, Zorica Terzić Supić, Maja Stojiljković, Teodora Karan-Djurasević, Biljana Stanković, Sonja Pavlović, Gordana Nikcević, Zoran Vukasinović |
Journal | Srpski arhiv za celokupno lekarstvo
(Srp Arh Celok Lek)
2014 Jul-Aug
Vol. 142
Issue 7-8
Pg. 450-6
ISSN: 0370-8179 [Print] Serbia |
PMID | 25233690
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Interleukin-6
- TLR4 protein, human
- Toll-Like Receptor 4
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Topics |
- Case-Control Studies
- Child
- Child, Preschool
- Female
- Genetic Predisposition to Disease
- Humans
- Interleukin-6
(genetics)
- Legg-Calve-Perthes Disease
(genetics)
- Male
- Polymorphism, Genetic
- Toll-Like Receptor 4
(genetics)
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