Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

9026 Background: Aromatase inhibitor (AI)-associated bone loss increases fracture rates. Vitamin D might play a role in minimizing this fracture risk. We sought to assess the association between 25-hydroxy-Vitamin D concentrations ([25(OH)D]) at baseline, after 3-months of supplementation, and bone loss after 1 year on AI therapy. Additionally, we investigated the relationship between [25(OH)D] increments ([25(OH)D] at 3 months minus baseline) and AI-associated bone loss. METHODS: Prospective cohort study including a consecutive women initiating AIs for early breast cancer from January/2006 to June/2009 (N=230). Serum [25(OH)D] was measured at baseline and at 3 months, and bone loss was defined as: lumbar spine (LS) absolute loss (baseline minus 1-year BMD) and bone loss rate (absolute loss over baseline BMD). Participants were supplemented with daily oral calcium (1g) and vitamin D3 (800 IU) and, in those with baseline [25(OH)D] was <30 ng/ml,with additional oral 16,000 IU every 2 weeks if. Linear regression models were fitted to adjust for potential confounders. For the current analyses, we included those whithout basal osteoporosis and, hence, not eligible for bisphosphonate therapy. RESULTS: In the overall population (N=156), increasing levels of [25(OH)D] at 3 months were inversely correlated to LS bone loss rates (adjusted beta for each 10ng/ml -0.41 [95%CI - 0.68 to -0.13], p=0.005) and to absolute bone loss (-0.004 g/cm2, [-0.007 to -0.004], p=0.003) at 1 year. [25(OH)D] increments at 3 months were also protective (adjusted beta for each 10 ng/ml for bone loss rates: -0.46 [-0.71 to -0.21], p<0.001; for absolute bone loss: -0.004 [-0.007 to -0.002], p<0.001). Of note, in the subset with baseline deficiency, baseline [25(OH)D] appeared directly related with BMD loss, although this was of borderline significance (adjusted beta for each 10 ng/ml 1.1, 95%CI -0.008 to 2.25, p-val 0.07). CONCLUSIONS: [25(OH)D] increments due to supplementation prevents AI-associated bone loss, independently of baseline [25(OH)D]. Hence, vitamin D supplements, with higher dosage than the standard 400 to 800 IU/day, might be useful to minimize bone loss in low risk women starting on AIs.

Type

Journal article

Journal

J Clin Oncol

Publication Date

20/05/2011

Volume

29