Endocrine Abstracts

Background: Childhood and adolescence are critical periods for the establishment of lifelong bone health. While most studies focus on vitamin-D regardless of PTH levels, Normocalcemic Primary Hyperparathyroidism (NPHPT) has been recognized more than 15 years ago as a variant of primary hyperparathyroidism (PHPT), characterized by persistently elevated PTH with normal albumin-adjusted total and ionized calcium, in the absence of secondary causes of hyperparathyroidism. PPHPT is related to an increased risk in development of osteopenia/osteoporosis, of parathyroid adenoma (15%) and hypercalcemia–hypercalciuria with renal consequences.

Aim: To redefine individual Vitamin-D sufficiency according to PTH levels, identify and treat biochemical disorders of PTH in normocalcemic children.

Methods: We performed a complete calcium metabolism evaluation (Ca, P, ALP, 25OHD, intact PTH) in all patients that visited our pediatric endocrine unit for 2 years (1 Nov 2016 until 31 Oct 2018).

Results and interventions: A total of 3060 patients – excluding those that consulted for vitamin D deficiency, Ca metabolism abnormalities or known renal pathology (i.e. Bartter syndrome). 154 patients (5.1%) had hyperparathyroidism: PTH >45 pg/ml (Horm Res Paediatr 2015;84:124–129) and normal total serum calcium levels: 51% were vitamin D replete (>30 ng/ml, group-1) and 49 % were deficient (<30 ng/ml, group-2). All received cholecalciferol (8000–16 000 IU/d) + calcium 1000 mg/day p.o. with a 3 m follow-up. In 6 patients (4 from group-1 and 2 from group-2) elevated PTH did not respond to 6 m of combined cholecalciferol/calcium therapy. These were switched to the non-calcemic synthetic 1-25(OH)2 vitamin-D analogue, paricalcitol 2 µg×1–3/day. Intact PTH (15–65 pg/ml) normalized (<35) in 5 patients by 3 m and in 1 by 10 m, with calcium in serum and urine (Ca/Cr 2-h morning sample) being normal.

Discussion: The incidence of NPHPT in childhood is high. In all normocalcemic children checked for vitamin-D, concomitant measurement of PTH is required, to individually define vitamin-D sufficiency for the given patient. Most of the cases seem to be secondary hyperparathyroidism as they are resolved with administration of cholecalciferol and calcium. Even in cases with vitamin D sufficiency, PTH fell to normal after administration of cholecalciferol and calcium.

Conclusions: Vitamin D sufficiency may not be for everybody a level >30 or 20 ng/ml, calcium intake playing also a crucial role. Subclinical Hyperparathyroidism is successfully treated with cholecalciferol (8000–16 000 IU/day) + calcium supplementation (1000 mg/day) in most cases. The non-responsive cases seem to be either primary or tertiary Hyperparathyroidism responding to Paricalcitol administration 2–6 µg/day, protecting bone and general health.