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Endocrine Abstracts (2017) 49 EP260 | DOI: 10.1530/endoabs.49.EP260

ECE2017 Eposter Presentations: Calcium and Bone Calcium & Vitamin D metabolism (65 abstracts)

How to differentiate primary hyperparathyroidism with D hypovitaminosis from secondary hyperparathyroidism due to D hypovitaminosis?

Alina-Andreea Gatu 1 , Cristian Velicescu 1, , Cristina Preda 1, , Carmen Vulpoi 1, , Simona Mogos 1, , Voichita Mogos 1, , Valentin Zaharia 2 , Adrian Aancute 2 & Dumitru Branisteanu 1,

1Gr. T Popa University of Medicine and Pharmacy, Iasi, Romania; 2St. Spiridon Emergency Hospital, Iasi, Romania.

Background: D hypovitaminosis and primary hyperparathyroidism frequently coexist. Secondary hyperparathyroidism reactive to D hypovitaminosis is difficult to be differentiated from primary hyperparthyroidism.

Aims: To differentiate patients with D hypovitaminosis and secondary hyperparathyroidism.

Materials and methods: Prospective study involving 71 patients admitted in our department for 1 year with the initial diagnosis of primary hyperparathyroidism. Serum and urinary calcium and phosphate, PTH and 25OHD3 were evaluated at admission. Patients with vitamin D levels under 30 ng/ml were repleted with 2000 IU/day of 25OHD3 for 1 month and 1000 IU/day for other 5 months. Values between groups were compared using student’s t test. Correlations were evaluated by using Pearson correlation analysis.

Results: Forty-eight of the 71 patients had vitamin D deficiency (< 20 ng/ml) and 15 had vitamin D insufficiency (between 20 and 30 ng/ml), only eight having 25OHD3 of over 30 ng/ml. Both 25OHD3 and PTH levels normalized after 6 months of repletion with vitamin D in only 24 of the 63 patients with initial low 25OHD3 levels and they were therefore diagnosed with secondary hyperparathyroidism (group S), whereas in the other 39 patients PTH levels remained elevated despite normalization of 25OHD3 levels, setting the diagnosis of primary hyperparathyroidism associated with D hypovitaminosis (group P). Initial PTH was correlated with serum calcium in both groups, but with serum phosphate only in group P. Initial PTH and serum and urinary calcium were significantly higher, whereas serum phosphate and radius BMD were significantly lower in the patients from group P when compared with patients from the group S (P < 0.05).

Conclusions: Patients with secondary hyperparathyroidism reactive to D hypovitaminosis are frequent. Their PTH and electrolyte profile are only mildly modified, with a milder impact on bone mass than in primary hyperparathyroidism. A clear diagnosis could be, however, set only after vitamin D repletion.

Volume 49

19th European Congress of Endocrinology

Lisbon, Portugal
20 May 2017 - 23 May 2017

European Society of Endocrinology 

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