Abstract
data that hypovitaminosis D is a reliable prognostic parameter or that the outcome of patients with PC might be improved by vitamin D supplementation. Several drawbacks hamper the clinical interpretation of serum vitamin D levels in cancer: the hormonal activity of vitamin D is mediated by its binding to vitamin D receptor (VDR) within the cell nuclei, and both VDR expression and VDR polymorphisms reflect the individual susceptibility to vitamin D action 3 ; and hypovitaminosis D is associated with secondary hyperparathyroidism, which could have contributed tothe negative prognostic features observed. Parathyroid hormone (PTH), in fact, is similar to PT-related peptide, which is a potent growth factor, and both PTH and PT-related peptide interact with the same receptor that is expressed by PC cells. 4 In the study by Nyame et al, 1 neither tissue VDR and its relevant polymorphisms nor serum PTH were measured; therefore, information on the interaction between vitamin D status and these important biologic parameters is lacking. Moreover, the assays to determine serum vitamin D levels are not standardized, and a significant variability among methods and laboratories was reported. 5 This further complicates the application of the results of the Nyame et al 1 study to clinical practice. In their discussion, Nyame et al 1 stated that patients with PC with intermediate risk may benefit, in terms of disease outcome, from the normalization of vitamin D levels. In principle, we agree with the authors that future studies are warranted to assess the efficacyofvitaminD supplementationin terms ofPC aggressiveness. However, caution should be taken in administering vitamin D to patients with PC outside a clinical trial. In fact, the results of a prospective phase III clinical trial testing the efficacy of high-dose calcitriol plus docetaxel versus single-agent docetaxel in men with castrate-resistant metastatic PC showed a shorter survival in the vitamin D arm compared with the control arm. 6
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