1 Introduction

The secondary hyperparathyroidism is defined by an elevated parathyroid hormone (PTH) secondary to a decrease in calcemia.

2 Case Report

We report the case of a 15-year old female, followed for 3 years at the nephrology department for a nephrocalcinosis and which was addressed to us for the suspicion of a primary hyperparathyroidism. We noted in her personal history renal lithiasis and in her family history a deceased aunt following a nephropathy with repeated renal lithiasis.

The physical examination found a tooth dystrophy with decalcified teeth and diffuse bone pain.

Biology

First blood tests: calcemia: 85mg/L (80-105), phosphoremia: 55mg/L (40-70) and PTH: 147.6pg/ml high (15-65).

Second blood tests: calcemia: 90.85mg/L (81-104), phosphoremia: 40.14mg/L (25-46) and PTH: 169.4pg/ml high (15-65).

Albuminemia: 41.09g/L (35-50), magnesemia: 2.56mg/dl (1.7-2.8), urea: 0.13g/L (0.1-0.5), creatininemia: 6.02mg/L (6-12).

The blood tests were completed with a dosage of 25-hydroxy-vitamin D: 11ng/ml (deficiency), 24 hours calciuria: 198mg/24h (4.4mg/Kg/24h), high. The renal ultrasound showed a nephrocalcinosis (fig: 1).

The patient received a vitamin D treatment than the normalizing of the vitamin D was obtained (30.53ng/ml) and PTH too (56pg/ml, standards: 15-80). Because of the hypercalciuria, a gas analysis was performed by the nephrologists whom back in favor of an acidosis state: PCO_2: 29.5mmHg (38-42) low, HCO3^- : 17.6mmol/l (24-28) low, pH: 7.38 (7.38-7.42) lower limit of the normality. This biological profile eliminated a primary hyperparathyroidism masked by low vitamin D and helps to retain the diagnosis of secondary hyperparathyroidism (to vitamin D deficiency) associated with a tubular acidosis.

3 Discussion

The secondary hyperparathyroidism is due to an acceleration of the bone turnover due to a PTH hypersecretion (Tokumoto M et al., 2016).

In our patient, there was a delay of three years in the diagnosis due to a diagnostic approach that has not previously eliminated a secondary etiology before the diagnosis of a primary hyperparathyroidism. Moreover, it is well established that there is a close relationship between the levels of 25-hydroxy-vitamin D serum and those of PTH (Cormier C, 2013). When we have an elevated PTH with a normocalcemia, before the diagnosis of a primary hyperparathyroidism, it is imperative to eliminate a secondary etiology such as the vitamin D deficiency (our patient), the calcium intake, the malabsorption, the renal failure, drugs (lithium, etc.), the renal hypercalciuria (Cormier C, 2013, Souberbielle JC et al., 2015). Our patient has long been considered to have a primary hyperparathyroidism due to the presence of a complicated hypercalciuria with a nephrocalcinosis while the diagnostic process and the therapeutic test (vitamin D) revealed us a secondary hyperparathyroidism with low vitamin D which seems to be frequent since Sayed Hassan R et al. reported a vitamin D deficiency (<30 ng/mL) in all his studied population with the exception of a man (156 participants) and 89.1% had a rate below 20 ng/mL (Sayed-Hassan R et al., 2016). In our patient, the hypercalciuria was most likely secondary to a tubular acidosis.

4 Conclusion

The diagnosis of a primary hyperparathyroidism will be retained after eliminating a secondary hyperparathyroidism.

References

Cormier C., 2003, Hyperparathyroidies primitives et secondaires, EMC-Endocrinologie-Nutrition, 10 (1) :1-11 [Article 10-012-B-15].

https://doi.org/10.1016/S1155-1941(12)62375-0

Sayed-Hassan R., Abazid N., Koudsi A., and Alourfi Z., 2016, Vitamin D status and parathyroid hormone levels in relation to bone mineral density in apparently healthy Syrian adults. Arch Osteoporos, 11:18.

https://doi.org/10.1007/s11657-015-0245-0    PMid: 27126333

Souberbielle JC., Cavalier E., Cormier C., 2015, How to manage an isolated elevated PTH? Ann Endocrinol (Paris) 76: 134-141.

http://dx.doi.org/10.1016/j.ando.2015.03.005