Abstract

SINCE THE FIRST description of the co-existence of Paget’s disease of bone (PDB) and hyperparathyroidism (HPT) by Albright and Reifenstein, the majority of reports appeared in the medical literature regarding the association of the two disorders have been largely limited to case reports. The only available study that extensively analyzed the topic was published in 1999 by Gutteridge et al. Therefore, even if the overproduction of PTH is reported in 12–18% of PDB, detailed studies in such patients are limited, and the differential clinical diagnosis between the more frequently PDB-associated secondary HPT and the rarely PDB-associated primary HPT can represent a difficult task for physicians lacking a training in bone and mineral metabolism. Whereas the pathophysiological relationship between PDB and secondary HPT is well established, much more debated is the etiology of the less common association of PDB and primary HPT. Secondary HPT frequently follows the treatment with antiresorptive agents and increased calcic requirements of pagetic bone. The possibility that tertiary HPT could evolve from the secondary form should be considered, particularly when calcium and vitamin D requirements cannot be chronically met by dietary sources and/or by supplements. Moreover, the knowledge accumulated on the pathogenetic bases of both PDB and HPT could make possible in the future to uncover common mechanisms that underlie the development of HPT in pagetic patients and vice versa. In view of the potential confusion arising for the general clinician between primary and secondary forms of parathyroid hyperfunction in PDB, in this report, we are presenting separately the two associations, summarizing the available data from the literature and presenting our experience from two large cohorts of PBD and of primary HPT.

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