A significant difference was seen in the distribution of allelic frequency between patients with RHD and control patients for TGF-beta1T869C polymorphism (P =.04).
In conclusion, an ongoing inflammatory process, the expression of TGF-beta 1, and proliferation of myofibroblasts within the valves have a potential role in the valvular fibrosis, calcification, and changes in the extracellular matrix that lead to the scarring sequelae of rheumatic heart disease.
Multifactor dimensionality reduction and classification and regression tree approaches were combined with logistic regression to discover high-order gene-gene interactions in studiedgenes involved in RHD susceptibility.In univariate logistic regression analysis, we found significant association of variant-containing genotypes (CT&TT) of TGF-β1869T/C [rs1982073]; [p=0.0.004 & 0.001, OR (95% CI)=1.65 (1.2-2.3) & 2.25 (1.4-3.6) respectively], variant genotype (CC) of IL-1β -511C/T [rs2853550]; [p=0.001, OR (95% CI)=2.33 (1.4-3.8)] and IL-1 VNTR [rs2234663]; [p=0.03, OR (95% CI)=5.25 (1.2-23.4)] SNPs with RHD risk.