Parathyroid Disorders. Группа авторов

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      Effects of Medical Treatment

Medical treatment is recognized as an option for patients who have contraindications to surgery, or are unwilling to undergo parathyroidectomy [51]. In general, the consensus derived from the Fourth Workshop does not recommend dietary calcium restriction in patients with asymptomatic PHPT, while it expresses a favorable indication for vitamin D repletion, though suggesting monitoring of serum and urinary calcium excretion [51]. Supplemental doses of 600–1,000 IU cholecalciferol were considered a more prudent dosage regimen to follow than large doses. The goal of cautiously administered repletion regimens should be to increase the serum 25(OH)D levels to >50 and up to 75 nmol/L (20–30 ng/mL).

Just one study has investigated vitamin D repletion and alendronate treatment in NPHPT patients. In a prospective open label randomized trial, Cesareo et al. [52] investigated 15 postmenopausal women with NPHPT, treated with oral alendronate plus cholecalciferol (treated group) compared with 15 NPHPT treated only with cholecalciferol (control group). After 1 year of treatment, BMD increased significantly at the lumbar, femoral neck, and hip level in the treated group, but not in the control group. No differences were found between or within groups in serum calcium, PTH, and urinary calcium levels. The authors concluded that alendronate/cholecalciferol could increase BMD in postmenopausal women with NPHPT, while alendronate/cholecalciferol or vitamin D alone does not affect serum or urinary calcium. The administration of vitamin D was safe and it did not induce any cases of hypercalcemia or hypercalciuria and PTH was unaffected by the treatments [52]. Among antiresorptive drugs used to increase BMD, denosumab is a relatively new option. Its safe profile on kidney function makes it a good option for the treatment of osteoporosis in CKD; in patients with CKD, it should be cautiously managed as hypocalcemia may occur. There are no reports on the use of denosumab in patients with PHPT except for a recently published paper describing the occurrence of severe symptomatic hypophosphatemia 1 month after the administration of 60 mg denosumab subcutaneously in a patient with NPHPT and CKD stage IIIa [53].

      Finally, another medical option for PHPT patients is represented by cinacalcet HCl. It is a potent CASR agonist, which normalizes serum calcium levels, reducing circulating PTH levels without normalization. Cinacalcet is recommended in those PHPT patients who need to manage hypercalcemia [51]; based on this consideration, the use of cinacalcet in NPHPT patients is not reasonable. Moreover, no data are available about cinacalcet effects in NPHPT patients.

      Conclusions

      Emerging data suggest that NPHPT may not be an isolated biochemical alteration but it may affect the health of patients. It appears as a disease with some clinical features overlapping those of the HPHPT and others peculiar to NPHPT. Therefore, attention should be paid to identifying PTH-related diseases involving bone, kidney, and the cardiovascular system, and, when present, therapeutic options should be considered and discussed with the patients. Alternatively, long-term follow-up should be scheduled with the patients to detect the potential progression.

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