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Abstract

Alendronate is an antiosteoporotic drug that targets the mevalonate pathway. To investigate whether the genetic variations in this pathway affect the clinical efficacy of alendronate in postmenopausal Chinese women with osteopenia or osteoporosis, 23 single-nucleotide polymorphisms (SNPs) in 7 genes were genotyped in 500 patients treated with alendronate for 12 months. Bone mineral density (BMD) was measured at baseline and after 12 months. The rs10161126 SNP in the 3[variant prime] flanking region of MVK and the GTCCA haplotype in FDFT1 were significantly associated with therapeutic response. A 6.6% increase in BMD in the lumbar spine was observed in the GG homozygotes of rs10161126; AG heterozygotes and AA homozygotes experienced a 4.4 and 4.5% increase, respectively. The odds ratio (95% confidence interval) of G allele carriers to be responders in lumbar spine BMD was 2.06 (1.08-6.41). GTCCA haplotype in FDFT1 was more frequently detected in the group of responders than in the group of non-responders at the total hip (2.6 vs 0.5%, P=0.009). Therefore, MVK and FDFT1 polymorphisms are genetic determinants for BMD response to alendronate therapy in postmenopausal Chinese women.

Details

Title
Genetic polymorphisms in the mevalonate pathway affect the therapeutic response to alendronate treatment in postmenopausal Chinese women with low bone mineral density
Author
Wang, C; Zheng, H; He, J-w; Zhang, H; Yue, H; Hu, W-w; Gu, J-m; Shao, C; Fu, W-z; Hu, Y-q; Li, M; Liu, Y-j; Zhang, Z-l
Pages
158-164
Publication year
2015
Publication date
Apr 2015
Publisher
Nature Publishing Group
ISSN
1470269X
e-ISSN
14731150
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
1665131988
Copyright
Copyright Nature Publishing Group Apr 2015