Association of vitamin D receptor gene polymorphisms with susceptibility to childhood asthma: A meta-analysis.
Pediatr Pulmonol. 2016 Aug 23. doi: 10.1002/ppul.23548. [Epub ahead of print]
Zhao DD1, Yu DD1, Ren QQ1, Dong B1, Zhao F1, Sun YH1,2.
1Department of Epidemiology and Health Statistics, Anhui Medical University, Hefei, China.
2Centre for Evidence-Based Practice, Anhui Medical University, Hefei, China.
Overview Asthma and Vitamin D contains
- Atopies (allergy, asthma, rhinitis, etc.) variously associated with low Vitamin D and poor Vitamin D Receptor – Aug 2021
- Poor response to Asthma inhaler if poor Vitamin D Receptor – Dec 2019
- Asthma 3.7X higher risk of poor Vitamin D Receptor (teens in Taiwan in this case) – Nov 2019
- Asthma is 20 percent more likely with a poor Vitamin D Receptor gene – meta-analysis Oct 2019
- Asthmatic children 5X more likely to have a poor Vitamin D Receptor – June 2019
- Childhood asthma about 1.3 times more likely if poor Vitamin D Receptor – meta-analysis Aug 2016
- 2X higher risk of wheezing and asthma if modified receptor genes, even if vitamin D levels OK – Sept 2015
- This list is NOT automatically updated
As for the association of vitamin D receptor (VDR) gene polymorphisms with susceptibility to pediatric asthma, results of published studies yielded conflicts. A systematic review was conducted on the relationship between childhood asthma and VDR gene polymorphisms, including ApaI (rs7975232), BsmI (rs1544410), FokI (rs2228570), and TaqI (rs731236).
PubMed, Web of Science, CBM (Chinese Biomedical Database), CNKI (China National Knowledge Infrastructure), and Wanfang (Chinese) database were searched for relevant studies. Pooled odds ratios (OR) with 95% confidence interval (CI) were calculated.
Overall results suggested that there was a statistically significant association between ApaI polymorphism and childhood asthma in homozygote model (OR = 1.674, 95%CI = 1.269-2.208, P < 0.001) and allele model (OR = 1.221, 95%CI = 1.084-1.375, P = 0.001). Stratification by ethnicity revealed a statistical association in Asians (OR = 1.389, 95%CI = 1.178-1.638, P < 0.001). There was some evidence of an association between BsmI polymorphism and childhood asthma in the homozygote (OR = 1.462, 95%CI = 1.016-2.105, P = 0.041) and allele models (OR = 1.181, 95%CI = 1.006-1.386, P = 0.042). This association reached significance only in the Caucasian group (OR = 1.236, 95%CI = 1.029-1.485, P = 0.023). For FokI, a statistical association was detected in dominant model (OR = 1.281, 95%CI = 1.055-1.555, P = 0.012); this association was significant in allele model (OR = 1.591, 95%CI = 1.052-2.405, P = 0.028) in Caucasian.
ApaI polymorphism plays a particular role in childhood asthma in Asians. FokI polymorphism may be connected with pediatric asthma in Caucasian population. And BsmI polymorphism marginally contributes to childhood asthma susceptibility, while there might be no association between TaqI polymorphism and childhood asthma risk.