Vitamin D and primary hyperparathyroidism: more insights into a complex relationship

Excerpt

In primary hyperparathyroidism (PHPT), low levels of vitamin D are found more often than in the general population [1, 2]. This well established observation is based upon measurement of the serum 25-hydroxyvitamin D level (25OHD). The operational definition of vitamin D deficiency, again based upon 25OHD levels, is viewed by The Institute of Medicine as <20 ng/mL (50 nM/l) [3]. Many experts, however, define two categories of “low” vitamin D: one in which the level is between 20 and 30 ng/mL (insufficiency) and the other in which the level is <20 ng/mL (deficiency). These cut points, while controversial, do not address the special setting of PHPT. The most recent guidelines on the management of asymptomatic PHPT, recommend maintaining or repleting 25OHD to levels >20 ng/ml [4]. The controversy was acknowledged in that publication, noting that some experts and societies favor a level >30 ng/mL. These threshold values relate to of the concentration of total 25OHD; that is, the forms that are both protein bound and free. It is the unbound or free 25OHD that is biologically active, constituting approximately only 1 % of the total concentration. Another small fraction, approximately 10 % is bound to albumin as a complex that is theoretically also biologically available since the binding partition is relatively “loose”. The vast majority of circulating 25OHD is bound to its binding protein, vitamin D binding protein (DBP) and not biologically available. In PHPT, there is limited information regarding the relative amounts of these various forms of circulating 25OHD. Whether genetic factors, such as polymorphisms in DBP, affect 25OHD levels in PHPT has not previously been investigated. …