World J Surg DOI 10.1007/s00268-014-2836-0

LETTER TO THE EDITOR

Effect of Parathyroidectomy on Vitamin D Levels Caroline Lamarche • Franc¸ois Leblond Denis Ouimet • Vincent Pichette

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Ó Socie´te´ Internationale de Chirurgie 2014

To the Editor, It is with great interest that we read the manuscript entitled ‘‘Predictors of Bone Mineral Density Improvement in Patients Undergoing Parathyroidectomy for Primary Hyperparathyroidism’’ [1]. In that study, several factors have been identified as predictors of bone mineral density (BMD) improvement following parathyroidectomy (PTX) in primary hyperparathyroidism (PHPT). Unfortunately, no firm conclusion could be drawn about vitamin D levels mainly because no follow-up vitamin D levels were available [1]. However, vitamin D status probably plays an important role in the improvement of BMD in these patients.

C. Lamarche
D. Ouimet
V. Pichette Department of Nephrology, Maisonneuve-Rosemont Hospital, Montreal, Canada e-mail: [email protected] F. Leblond
V. Pichette (&) Maisonneuve-Rosemont Hospital Research Center, Montreal, Canada e-mail: [email protected]

Table 1 Parathyroidectomy effect on calcium, PTH, and vitamin D levels Before PTX Calcium (mmol/L)

After PTX

p value \0.001

2.9 ± 0.2

2.4 ± 0.1

Intact PTH (pmol/L)

44.3 ± 54.3

6.6 ± 4.3

0.054

25(OH)D (nmol/L)

44.5 ± 16.5

68.6 ± 28.6

0.044

224.5 ± 79.5

117.0 ± 69.7

0.017

1.25(OH)D (pmol/L)

It has been known for several years that PHPT is associated with vitamin D deficiency (25OHD) [2]. Although the mechanism is still poorly understood, several mechanisms have been proposed: increased conversion of 25OHD to 1.25OHD or inactivation of 25OHD [2]. However, recent data suggest that PTH itself could inhibit liver hydroxylation of vitamin D2 or D3 by decreasing key cytochrome P450 isoforms [3]. Moreover, PTX done in the setting of secondary HPT (SHPT) (as seen in renal failure) restores the ability of the liver to hydroxylate vitamin D [3]. In PHPT, very few studies have evaluated the effect of PTX on 25OHD levels [4]. We reviewed nine cases of PHPT where vitamin D measurements were available preand post-PTX and in whom no vitamin D supplementation was administered. As shown in Table 1, following PTX, there was an increase in 25OHD and a decrease in 1.25OHD. Thus, PTX in PHPT could restore vitamin D by a mechanism probably similar to SHPT. Although the impact of restoring vitamin D levels in PHPT by PTX on BMD has not been studied directly, recent data clearly suggest that the administration of cholecalciferol in PHPT is accompanied by an improvement of BMD [5].

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References 1. Sharma J, Itum DS, Moss L et al (2014) Predictors of bone mineral density improvement in patients undergoing parathyroidectomy for primary hyperparathyroidism. World J Surg 38:1268–1273. doi:10. 1007/s00268-014-2555-6 2. Rathi MS, Gonzalez S, Wright D et al. (2014) Management of hypovitaminosis D in patients with primary hyperparathyroidism. J Endocrinol Invest 37(5):467–471

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3. Michaud J, Naud J, Ouimet D et al (2010) Reduced hepatic synthesis of calcidiol in uremia. J Am Soc Nephrol 21:1488–1497 4. Clements MR, Davies M, Fraser DR et al (1979) Metabolic inactivation of vitamin D is enhanced in primary hyperparathyroidism clinical science. Clin Sci (Lond) 1987(73):659–664 5. Rolighed L, Rejnmark L, Sikjaer T et al (2014) Vitamin D treatment in primary hyperparathyroidism: a randomized placebo controlled trial. J Clin Endocrinol metab 99:1072–1080