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Effects of 25-hydroxyvitamin D3 therapy on bone turnover markers and PTH levels in postmenopausal osteoporotic women treated with alendronate

Abstract: Objective: Our objective was to know the extent to which a fall in bone turnover markers is influenced by serum 25-hydroxyvitamin D (25OHD) levels in patients on alendronate (ALN) treatment. Design, Participants, and Setting: A total of 140 postmenopausal osteoporotic women were randomized to receive either ALN or ALN plus 25OHD3 (ALN+VitD) over a 3-month period. Serum 25OHD, PTH, C-terminal telopeptide of type I collagen (CTX), and amino-terminal propeptide of type I collagen (P1NP) were measured at baseline and at the end of the 3 months. Results: 25OHD rose four times above baseline levels in the ALN+VitD group, whereas no changes were seen in the ALN group. Administering ALN resulted in a significant decline in both serum CTX (53 ± 24%) and P1NP (46 ± 19%). After ALN+VitD, the fall in CTX amounted to 61 ± 20% (P = 0.06 compared with ALN) and P1NP to 50 ± 23% (P = 0.35). When patients were divided into those below and above 20 ng/ml of baseline serum 25OHD, in those below, CTX decreased by 48 ± 26% in the ALN group and by 61 ± 17% in the ALN+VitD group (P = 0.015). For P1NP, the corresponding figures were 43 ± 20 and 50 ± 23% (P = 0.2). In patients above 20 ng/ml, no differences were seen regarding CTX (58 ± 21% decrease in the ALN group and 60 ± 23% in the ALN+VitD group; P = 0.7) or P1NP (49 ± 18 and 50 ± 20%; P = 0.9). Conclusions: Administration of 25OHD3 is not an indispensable requirement for bisphosphonates to develop their bone antiresorptive effect. In fact, in patients with vitamin D sufficiency, no benefit is observed when the vitamin is added. However, in patients with vitamin D deficiency, an approximately 25% greater fall in the bone resorption marker CTX is seen with its administration.

 Autoría: Olmos J.M., Hernandez J.L., Llorca J., Nan D., Valero C., González-Macias J.,

 Fuente: Journal of Clinical Endocrinology and Metabolism 2012, 97 (12): 4491-4497

Editorial: Endocrine Society

 Año de publicación: 2012

Nº de páginas: 7

Tipo de publicación: Artículo de Revista

 DOI: 10.1210/jc.2012-2999

ISSN: 0021-972X,1945-7197

Url de la publicación: https://doi.org/10.1210/jc.2012-2999