Primary hyperparathyroidism in prostate cancer: guilty or not guilty?
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EDITORIAL
Primary hyperparathyroidism in prostate cancer: guilty or not guilty? G. Mazziotti1 S. Frara2 A. Mosca3 ●
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Received: 9 March 2018 / Accepted: 9 May 2018 © Springer Science+Business Media, LLC, part of Springer Nature 2018
Skeletal health is a clinically relevant issue in patients with prostate cancer (PC) [1–3]. Bone is the most common site of PC cell migration with up to 90% of patients with advanced disease having bone metastases [4] with potential negative impact on quality of life and survival [5]. Since the first description of the “seed and soil” hypothesis by Stephan Paget in 1889 [6], several cellular signaling pathways, cytokines, chemokines, and adhesion molecules have been identified as players of cross-talking between PC cells and bone [7] attempting to relate them either to metastases diagnosis or to patients’ prognosis (as prognostic factors) or to response to therapy (as predictive factors) [8]. Minisola et al. [9] recently performed a systematic assessment of mineral metabolism in 69 males with PC at different stages of disease as compared to 53 patients with non-prostate tumors of various origin. The most impressive result was the occurrence of primary hyperparathyroidism (PHPT) in 13% of patients with PC, a prevalence which was much higher than that expected in the general population [10]. Interestingly, two relevant considerations emerge from the Minisola et al. [9] retrospective data. First, in PC patients, PHPT was associated with higher Gleason score (GS), which is one of the best known prognostic factors [11]. As a consequence, it could be hypothesized that, if higher GS correlates with worse PC prognosis, and PHPT is associated with higher GS, PHPT could be related to a worse PC prognosis. Second, in the paper by Minisola et al. [9], PC patients with lower GS (
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