International Journal of Clinical Case Reports 2016, Vol.6, No.31, 1-2
2
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.
Fig.1. Renal ultrasound highlighting a nephrocalcinosis
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].
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.
PMid: 27126333
Souberbielle JC., Cavalier E., Cormier C., 2015, How to manage an isolated elevated PTH? Ann Endocrinol (Paris) 76: 134-141.
