Abstract
Objectives
Phototherapy is demonstrated to cause hypocalcemia by decreasing melatonin levels and increasing cortisol levels. However, the relationship between parathyroid hormone (PTH) level and calcium has not been previously evaluated in patients receiving phototherapy. Our study aimed to evaluate the effect of phototherapy on ionized calcium (iCa), total calcium (tCa), corrected calcium (cCa), magnesium (Mg), phosphorus (P), 25-hydroxyvitamin D (25(OH)D), and PTH levels.
Methods
Infants who were born at term and received inpatient phototherapy for indirect hyperbilirubinemia were included in our study. The patients’ gestational age, birth weight, and phototherapy durations were recorded. Total bilirubin, albumin, iCa, tCa, cCa, Mg, 25(OH)D, and PTH levels before and after phototherapy were compared. Laboratory results were also compared between patients who received phototherapy for ≤24 h, 25–47 h, and ≥48 h.
Results
A total of 166 term infants were included in the study. The mean duration of phototherapy was 31.9 ± 9.2 h. Albumin levels before and after phototherapy were similar (p=0.246). However, there were significant decreases in iCa, tCa, cCa, Mg, 25(OH)D, and PTH levels after phototherapy (p<0.001), while P level was significantly increased after phototherapy (p<0.001). In addition, P levels increased with >24 h of phototherapy, while iCa, tCa, cCa, Mg, 25(OH)D, and PTH levels decreased significantly with ≥48 h of phototherapy (p=0.002, p=0.008, p=0.001, p=0.012, and p<0.001, respectively).
Conclusions
This study demonstrates that PTH suppression is one of the causes of phototherapy-induced hypocalcemia.
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Research funding: None declared.
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Author contributions: Concept, design and data collection or processing: Esra Beser, Nazmiye Bengu Karacaglar, and Merve Kucukoglu Keser. Data analysis and interpretation: Ufuk Cakir, Burak Ceran and Ali Ulas Tugcu. Literature search: Esra Beser, Burak Ceran, Ufuk Cakir, and Ali Ulas Tugcu. Writing: Esra Beser, Ufuk Cakir, and Cuneyt Tayman. All authors have accepted responsibility for the entire content of this manuscript and approved its submission.
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Competing interests: The authors state no conflict of interest.
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Informed consent: Informed consent was obtained from all individuals’ parents or guardians included in this study.
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Ethical approval: Ethical approval from the local Ethics Committee (date: 02.09.2020, ethic no: E1/170/2019).
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© 2022 Walter de Gruyter GmbH, Berlin/Boston
Articles in the same Issue
- Frontmatter
- Editorial
- Disorders of sex development – biologic, genetic, cultural, societal, and psychologic diversity of the human nature
- Review
- Diagnostic approach in 46, XY DSD: an endocrine society of bengal (ESB) consensus statement
- Original Articles
- Penile diameter during puberty in boys: a retrospective analysis of longitudinally obtained data
- Evaluation of bladder dysfunction in children and adolescents with type 1 diabetes mellitus by uroflowmetry
- All aspects of galactosemia: a single center experience
- The evolution of pituitary cysts in growth hormone-treated children
- Phototherapy-induced hypocalcemia and hypoparathyroidism in icteric term newborns
- Clinical and laboratory evaluation of children with congenital hyperinsulinism: a single center experience
- Does cystatin C have an immunomodulatory role in Hashimoto’s thyroiditis?
- Molecular genetic etiology by whole exome sequence analysis in cases with familial type 1 diabetes mellitus without HLA haplotype predisposition or incomplete predisposition
- Features of BSCL2 related congenital generalized lipodystrophy in China: long-term follow-up of three patients and literature review
- Case Reports
- Congenital adrenal hyperplasia with a CYP21A2 deletion overlapping the tenascin-X gene: an atypical presentation
- The smallest dislocated microduplication of Xq27.1 harboring SOX3 gene associated with XX male phenotype
- Rare PHEX intron variant causes complete and severe phenotype in a family with hypophosphatemic rickets: a case report
- Human chorionic gonadotrophin secreting adrenocortical neoplasm presenting with peripheral precocious puberty in an infant
- Atypical familial diabetes associated with a novel NEUROD1 nonsense variant
Articles in the same Issue
- Frontmatter
- Editorial
- Disorders of sex development – biologic, genetic, cultural, societal, and psychologic diversity of the human nature
- Review
- Diagnostic approach in 46, XY DSD: an endocrine society of bengal (ESB) consensus statement
- Original Articles
- Penile diameter during puberty in boys: a retrospective analysis of longitudinally obtained data
- Evaluation of bladder dysfunction in children and adolescents with type 1 diabetes mellitus by uroflowmetry
- All aspects of galactosemia: a single center experience
- The evolution of pituitary cysts in growth hormone-treated children
- Phototherapy-induced hypocalcemia and hypoparathyroidism in icteric term newborns
- Clinical and laboratory evaluation of children with congenital hyperinsulinism: a single center experience
- Does cystatin C have an immunomodulatory role in Hashimoto’s thyroiditis?
- Molecular genetic etiology by whole exome sequence analysis in cases with familial type 1 diabetes mellitus without HLA haplotype predisposition or incomplete predisposition
- Features of BSCL2 related congenital generalized lipodystrophy in China: long-term follow-up of three patients and literature review
- Case Reports
- Congenital adrenal hyperplasia with a CYP21A2 deletion overlapping the tenascin-X gene: an atypical presentation
- The smallest dislocated microduplication of Xq27.1 harboring SOX3 gene associated with XX male phenotype
- Rare PHEX intron variant causes complete and severe phenotype in a family with hypophosphatemic rickets: a case report
- Human chorionic gonadotrophin secreting adrenocortical neoplasm presenting with peripheral precocious puberty in an infant
- Atypical familial diabetes associated with a novel NEUROD1 nonsense variant