Startseite Persistent hypercalcemia mimicking hypophosphatasia after discontinuation of a ketogenic diet: a case report
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Persistent hypercalcemia mimicking hypophosphatasia after discontinuation of a ketogenic diet: a case report

  • Sabitha Sasidharan Pillai ORCID logo , Renee Robilliard , Meghan E. Fredette , Monica Serrano-Gonzalez und Kevin J. Scully ORCID logo EMAIL logo
Veröffentlicht/Copyright: 5. Oktober 2023

Abstract

Objectives

Hypercalcemia has been reported as an uncommon complication of the ketogenic diet (KD). Here we present a toddler whose hypercalcemia persisted for 2 months after stopping the KD.

Case presentation

A 2 year 11-month-old child with global developmental delay, infantile spasms, neuromuscular weakness with limited mobility, tracheostomy and ventilator dependence, and oropharyngeal dysphagia with G-tube dependence presented with hypercalcemia in the setting of recurrent vomiting. At presentation, the patient was adherent to a KD and taking topiramate since infancy for intractable seizures. His laboratory parameters at presentation showed hypercalcemia (11.9 mg/dL), hypercalciuria, acute renal failure, low alkaline phosphatase (76 IU/L [110–302 IU/L]), parathyroid hormone (PTH) <6 pg/mL (18–80 pg/mL), normal thyroid function, cortisol and vitamin D level. The patient’s hypercalcemia persisted post-discontinuation of the KD and topiramate. PTH-related protein was mildly elevated at 15.3 pmol/L. Follow-up laboratory and imaging studies ruled out malignancy. He was managed with calcitonin 4 u/kg/dose Q12H × 1 day and 8 u/kg/dose Q8H × 1 day, hydration and low-calcium formula. Post-discontinuation of the KD, normalization of alkaline phosphatase levels preceded the normalization of calcium on day 55 and PTH on day 85.

Conclusions

Hypercalcemia may persist for an extended period after weaning from a KD; lab parameters may mimic that of hypophosphatasia as previously described in the literature. Normalization of alkaline phosphatase, a marker of bone turnover, indicates recovery from the adynamic state induced by the KD and typically precedes the normalization of calcium and PTH.


Corresponding author: Kevin J. Scully, MD, Assistant Professor of Pediatrics, Clinician Educator, Division of Pediatric Endocrinology, Hasbro Children’s Hospital, Rhode Island Hospital, 593 Eddy Street, Providence, RI 02903, USA; and Department of Pediatrics, The Warren Alpert Medical School of Brown University, 593 Eddy Street, Providence, RI 02903, USA, Phone: +(401) 444 5504, Fax: +(401) 793 8101, E-mail:

  1. Research ethics: Not applicable.

  2. Informed consent: Obtained written informed consent from the parent of the patient.

  3. Author contributions: SSP conceptualized the study, performed data collection and interpretation, performed literature review, and wrote the initial draft of the manuscript. KS helped to conceptualize the study, critically reviewed, and edited the manuscript. MSG, MF and RR critically reviewed and edited the manuscript. All authors have accepted responsibility for the entire content of this manuscript and approved its submission.

  4. Competing interests: None.

  5. Research funding: None.

  6. Data availability: All data generated or analyzed during this study are included in this published article or in the data repositories listed in References.

References

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Received: 2023-06-26
Accepted: 2023-09-01
Published Online: 2023-10-05
Published in Print: 2023-11-27

© 2023 Walter de Gruyter GmbH, Berlin/Boston

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