Background:Keloid disease (KD) is common and often refractory to treatment. Definition
of the genetic mechanisms of KD can lead to a better understanding of the
disease and suggest more effective treatment strategies.Objectives:To quantitatively estimate the association between KD susceptibility and the
-509C/T polymorphism in the TGF-β1 gene.Methods:PubMed, Embase and CNKI databases were searched using a combination of the
Medical Subject Headings (MeSH) and relevant words in titles. Analyses were
performed with STATA 12.0.Results:Five case-control studies encompassing a total of 564 keloid cases and 620
healthy controls were pooled in the final meta-analysis. Among the five
studies, no significant association was detected between the TGF-β1 -509C/T
polymorphism and KD under all of the five genetic models (allele comparison,
heterozygote comparison, homozygote comparison, dominant model and recessive
model) for the overall analyses and for the subgroup analyses based on DNA
extraction method, participant ethnicity and group size. When stratified by
study quality, three high-quality studies showed significant association
under allele comparison and homozygote model (C versus T: OR = 0.80, 95%
confidence interval [CI] = 0.65–0.98, P = 0.03;
I2 = 0%, P = 0.64; CC versus TT: OR = 0.62,
95% CI = 0.41–0.94, P = 0.02; I2 = 0%,
P = 0.79); while two moderate-quality studies showed
significant association under allele comparison, homozygote model and
recessive model (C versus T: OR = 1.52, 95% CI = 1.15–2.01,
P = 0.004; I2 = 39%, P =
0.20; CC versus TT: OR = 2.14, 95% CI = 1.24–3.70, P =
0.02; I2 = 19%, P = 0.27; CC versus CT+TT: OR =
2.04, 95% CI = 1.29–3.24, P = 0.002; I2 = 0%,
P = 0.35).Conclusions:The current meta-analysis suggests that the TGF-β1 -509C/T polymorphism is
not associated with KD susceptibility. High-quality and large-scale studies
are needed to validate our findings.