Vitamin D threshold to prevent aromatase inhibitor-related bone loss: the B-ABLE prospective cohort study

被引:0
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作者
Daniel Prieto-Alhambra
Sonia Servitja
M. Kassim Javaid
Laia Garrigós
Nigel K. Arden
Cyrus Cooper
Joan Albanell
Ignasi Tusquets
Adolfo Diez-Perez
Xavier Nogues
机构
[1] URFOA-IMIM,Oxford NIHR Musculoskeletal Biomedical Research Unit, Nuffield Department of Orthopaedics
[2] Parc de Salut Mar,IDIAP Jordi Gol, Unitat de Suport a la Recerca Barcelona
[3] Parc de Recerca Biomèdica de Barcelona,Medicine Department
[4] Rheumatology and Musculoskeletal Sciences,RETICEF (Red Temática de Investigación Cooperativa en Envejecimiento y Fragilidad)
[5] University of Oxford,Oncology Department
[6] Institut Català de la Salut,Programa Consolider
[7] Universitat Autònoma de Barcelona Edificio W – UD de Medicina de la Vall d’Hebron Paseo Vall d’Hebron,Internal Medicine Department
[8] 119,Lifecourse Epidemiology Unit, MRC Southampton
[9] Instituto Carlos III,undefined
[10] Parc de Salut Mar,undefined
[11] Instituto de Salud Carlos III/FEDER,undefined
[12] Parc de Salut Mar,undefined
[13] Southampton General Hospital,undefined
来源
Breast Cancer Research and Treatment | 2012年 / 133卷
关键词
Epidemiology; Osteoporosis; Vitamin D; Aromatase inhibitors; Breast neoplasms;
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摘要
Aromatase inhibitor (AI)-related bone loss is associated with increased fracture rates. Vitamin D might play a role in minimising this effect. We hypothesised that 25-hydroxy-vitamin D concentrations [25(OH)D] after 3 months supplementation might relate to bone loss after 1 year on AI therapy. We conducted a prospective cohort study from January 2006 to December 2011 of a consecutive sample of women initiating AI for early breast cancer who were ineligible for bisphosphonate therapy and stayed on treatment for 1 year (N = 232). Serum 25(OH)D was measured at baseline and 3 months, and lumbar spine (LS) bone mineral density at baseline and 1 year. Subjects were supplemented with daily calcium (1 g) and vitamin D3 (800 IU) and additional oral 16,000 IU every 2 weeks if baseline 25(OH)D was <30 ng/ml. Linear regression models were fitted to adjust for potential confounders. After 1 year on AI therapy, 232 participants experienced a significant 1.68 % [95 % CI 1.15–2.20 %] bone loss at LS (0.017 g/cm2 [0.012–0.024], P < 0.0001). Higher 25(OH)D at 3 months protected against LS bone loss (−0.5 % per 10 ng/ml [95 % CI −0.7 to −0.3 %], adjusted P = 0.0001), and those who reached levels ≥40 ng/ml had reduced bone loss by 1.70 % [95 % CI 0.4–3.0 %; adjusted P = 0.005] compared to those with low 25(OH)D levels (<30 ng/ml). We conclude that improved vitamin D status using supplementation is associated with attenuation of AI-associated bone loss. For this population, the current Institute of Medicine target recommendation of 20 ng/ml might be too low to ensure good bone health.
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页码:1159 / 1167
页数:8
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