|LETTER TO EDITOR
|Year : 2007 | Volume
| Issue : 4 | Page : 187
Vitamin D replacement in tertiary hyperparathyroidism with vitamin D deficiency: Is there any reason for being overcautious?
J Muthukrishnan1, R Jha2, KD Modi1, JP Kumar2
1 Department of Endocrinology, Medwin Hospitals, Hyderabad - 500 001, India
2 Department of Nephrology, Medwin Hospitals, Hyderabad - 500 001, India
Department of Nephrology, Medwin Hospitals, Chirag Ali Lane, Nampally, Hyderabad - 500 001
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Muthukrishnan J, Jha R, Modi K D, Kumar J P. Vitamin D replacement in tertiary hyperparathyroidism with vitamin D deficiency: Is there any reason for being overcautious?. Indian J Nephrol 2007;17:187
|How to cite this URL:|
Muthukrishnan J, Jha R, Modi K D, Kumar J P. Vitamin D replacement in tertiary hyperparathyroidism with vitamin D deficiency: Is there any reason for being overcautious?. Indian J Nephrol [serial online] 2007 [cited 2020 Nov 30];17:187. Available from: https://www.indianjnephrol.org/text.asp?2007/17/4/187/39178
We read the case report titled " An Unusual Case of Hypercalcemic Osteomalacia: Role of a Novel Calcimimetic Agent" by Anupama et al. with great interest.  We would like to present the following comments and queries regarding this case:
- The authors have remarked that the use of vitamin D was withheld in view of hypercalcemia and instead calcimimetics were used. However, it has been shown in earlier studies that in cases of primary hyperparathyroidism with vitamin D deficiency, vitamin D replacement has improved the severity of bone disease and myopathy without worsening hypercalcemia significantly. It has also shown to lower alkaline phosphatase and PTH levels and lessen the severity of postoperative hypocalcemia and hungry bone syndrome.  Hence, the fear of using vitamin D in this case due to hypercalcemia may be unfounded.
- As the PTH levels reduced with use of vitamin D replacement, the most likely diagnosis should be secondary hyperparathyroidism with hypercalcemia contributed by prolonged immobilisation. The autonomous hypersecretion of PTH in tertiary hyperparathyroidism does not respond to the treatment of underlying vitamin D deficiency and required the surgical resection of parathyroid gland adenoma or hyperplasia.
- The urine pH and serum bicarbonate was found to be 7.2 and 19.2 mEq/L, respectively. In such a setting, renal tubular acidosis must be considered, which may contribute to osteomalacia. As severe vitamin D deficiency and PTH excess by itself may have contributed to the renal tubular acidification defect, a repeat evaluation after vitamin D replenishment must be performed. 
- Severe vitamin D deficiency in an adult male without an obvious cause requires further studies for malabsorption and liver disease.
| References|| |
|1.||Anupama YJ, Ravishankar B, Babau KS, Ballal HS. An unusual case of hypercalcaemic osteomalacia: Role of a novel calcimimetic agent. Indian J Nephrol 2007;17:17-9. |
|2.||Grey A, Lucas J, Horne A, Gamble G, Davidson JS, Reid IR. Vitamin D repletion in patients with primary hyperparathyroidism and coexistent vitamin D insufficiency. J Clin Endocrinol Metab 2005;90:2122-6. [PUBMED] [FULLTEXT]|
|3.||Taylor HC, Elbadawy EH. Renal tubular acidosis type 2 with Fanconi's syndrome, osteomalacia, osteoporosis and secondary hyperaldosteronism in an adult consequent to vitamin D and calcium deficiency: Effect of vitamin D and calcium citrate therapy. Endocr Pract 2006;12:559-67. [PUBMED] [FULLTEXT]|