Home Zoledronate-responsive calcitriol-mediated hypercalcemia in a 5-year-old case with squamous cell carcinoma on the background of xeroderma pigmentosum
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Zoledronate-responsive calcitriol-mediated hypercalcemia in a 5-year-old case with squamous cell carcinoma on the background of xeroderma pigmentosum

  • Ulkem Colak , Gul Y. Mutlu EMAIL logo , Banu O. Sozmen , Esra B. Yucel , Hulya Kayserili and Sukru Hatun
Published/Copyright: November 29, 2019

Abstract

Malignancy-induced hypercalcemia is a very rare condition in children whereas it is more common among adult patients with malignancy. The mechanisms of malignancy-induced hypercalcemia include the over-secretion of parathyroid hormone-related protein (PTHrP), osteolytic metastases and the over-production of 1,25-dihydroxyvitamin D (calcitriol). Although hypercalcemia due to PTHrP secretion has been published before, overproduction of calcitriol has not been reported yet in pediatric squamous cell skin carcinoma cases. Herein, we report calcitriol-mediated severe hypercalcemia in a 5-year-old boy with squamous cell skin carcinoma arising in the background of xeroderma pigmentosum (XP) which responded well to zoledronate treatment. To the best of our knowledge, this is the first pediatric case of malignancy-induced hypercalcemia which is mediated by calcitriol in squamous cell skin carcinoma.

Acknowledgments

We cordially thank the patient and his parents for their cooperation.

  1. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  2. Research funding: None declared.

  3. Employment or leadership: None declared.

  4. Honorarium: None declared.

  5. Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

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Received: 2019-04-26
Accepted: 2019-10-01
Published Online: 2019-11-29
Published in Print: 2019-12-18

©2019 Walter de Gruyter GmbH, Berlin/Boston

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