Vitamin D via its receptor has essential actions on parathyroid cells, inhibiting PTH secretion, and parathyroid cell proliferation. While the effects of vitamin D depletion in the pathogenesis of secondary hyperparathyroidism in elderly individuals or in the occurrence of parathyroid hyperplasia in patients with renal insufficiency are well established, the association between hypovitaminosis D and primary hyperparathyroidism (P-HPT) has only recently become appreciated. In different cohorts of patients with P-HPT, vitamin D deficiency has been recently associated with higher PTH levels, larger adenomas, and a more severe phenotype (including osteitis fibrosa cystica) as well as negative post-operative outcomes following parathyroidectomy. Despite current guidelines recommend measurement of serum 25OHD (25-hydroxy-cholecalciferol) in P-HPT and their repletion if the levels are <20 ng/ml, future well-designed trials of vitamin D supplementation in P-HPT patients with coexisting vitamin D deficiency are needed to evaluate the risk/benefit profile of this treatment.