Document Type

Article

Publication Date

1-1-2017

Identifier

PMCID: PMC5419064 DOI: 10.1177/2333794X17705955

Abstract

Severe hypercalcemia in infants is usually attributed to genetic etiologies and less commonly to acquired ones. An 8-week-old girl presented with failure to thrive, mild respiratory distress, and life-threatening hypercalcemia (23.5 mg/dL). Serum 1,25(OH)2-D) level was elevated and parathyroid hormone undetectable. Evaluation for genetic mutations and malignant etiologies of hypercalcemia was negative. Treatment with intravenous hydration, loop diuretic, and calcitonin failed to correct the hypercalcemia, which was subsequently controlled with bisphosphonate therapy. Due to progressive respiratory deterioration, a bronchopulmonary lavage was done on day 17 of her hospitalization disclosing Pneumocystis jiroveci infection. The subsequent immunological investigation showed no abnormalities. She was treated with trimethoprim/sulfamethoxazole resulting in gradual clearing of her lungs and normalization of serum 1,25(OH)2-D level. A year later, she remains healthy with normal biochemical parameters of mineral metabolism. We conclude that in a child with hypercalcemia with suppressed parathyroid hormone and elevated 1,25(OH)2-D, once the genetic etiology for elevated 1,25(OH)2-D and malignancy are ruled out, one should investigate closely for a chronic granulomatous disease. Among the latter Pneumocystis jiroveci pneumonia infection should be considered even in an immunocompetent child.

Journal Title

Glob Pediatr Health

Volume

4

First Page

2333794

Last Page

2333794

MeSH Keywords

Pneumonia, Pneumocystis; Pneumocystis Infections; Hypercalcemia; Infant

Keywords

Pneumocystis jiroveci pneumonia; calcitriol; hypercalcemia; zoledronic acid

Comments

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page(https://us.sagepub.com/en-us/nam/open-access-at-sage).

Publisher's Link: https://doi.org/10.1177%2F2333794X17705955

Share

COinS