Autor: |
Asensi, Víctor, Alvarez, Victoria, Valle, Eulalia, Meana, Alvaro, Fierer, Joshua, Coto, Eliecer, Carton, José Antonio, Maradona, José Antonio, Paz, José, Dieguez, Maria Angeles, Fuente, Belén de la, Moreno, Alfonso, Rubio, Silvino, Tuya, Maria José, Sarasúa, Julián, Llames, Sara, Arribas, José Manuel |
Zdroj: |
American Journal of Medical Genetics. Part A; 1 June 2003, Vol. 119 Issue: 2 p132-136, 5p |
Abstrakt: |
As osteomyelitis (OM) induces the synthesis of inflammatory cytokines and IL-1 mediates bone resorption by osteoclasts we determined if there is an association between certain common polymorphisms of the genes encoding proinflammatory cytokines (IL-1α and β, IL-6, TNF-α) and OM in adults. The IL-1α (− 889) TT genotype was significantly more frequent among 52 OM patients than in 109 healthy controls (13/52, [25.0%] vs. 9/109, [8.3%], P = 0.0081, χ2 = 7.01, OR = 3.7, 95% CI, 1.3510.34). Patients who were homozygous for the T allele were younger than the rest of the OM patients (mean age 35.7 ± 11.5 vs. 58.1 ± 18.6 years, P = 0.001). IL-1β TT (+ 3953) polymorphism was also more frequent in OM patients (P = 0.014, χ2 = 5.12, OR = 5.1, 95% CI, 1.2152.14), but IL-1β is in linkage disequilibrium with the IL-1α *T (P < 0.001). Route of infection, chronicity of the infection, type of microorganism isolated, and frequency of relapses were similar in patients with and without the IL-1α TT genotype. There were no associations between OM and polymorphisms of other cytokines genes. IL-1α serum levels were significantly increased in all the OM patients independently of their IL-1 genotype compared to the controls (P = 0.021). Although IL-1α serum levels were not significantly higher in patients with the IL-1α (− 889) polymorphism, this does not exclude a difference in production of IL-1α by osteoclasts or other inflammatory cells at the site of infection. © 2003 Wiley-Liss, Inc. |
Databáze: |
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