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Infants with neonatal hypocalcemia often present with seizures, and neonatal hypocalcemia can be due to parathyroid (PTH) insufficiency or resistance. Causes of hypocalcemia with PTH elevation include increased phosphate load, vitamin D deficiency (VDD) or defects in metabolism, renal dysfunction, hypomagnesemia, genetic mutations resulting in end-organ resistance to PTH, or critical illness. Hypocalcemia has also been shown to be associated with Gram-negative bacteremia and sepsis in adults. We present the case of a full-term, formula-fed newborn presenting with late-onset hypocalcemic seizures and VDD in the setting of Klebsiella pneumoniae bacteremia. This case highlights that newborns presenting with hypocalcemic seizures should undergo a workup for sepsis.

Objectives: To assess the prevalence of hypocalcemia in outpatient clinic neonates and its relation to vitamin D and calcium supplementation. Methods: This cross-sectional analytical study was conducted at the University Teaching Hospital from May to October 2016. Data were collected from 100 neonates by interviewing mothers using a structured questionnaire; which included socio-demographic information, maternal and neonatal history; in addition to investigations of serum calcium total and ionized and serum vitamin D level. Results: The prevalence of hypocalcemia was 76%, late hypocalcemia represent 52% of hypocalcemic neonates. The prevalence of hypovitaminosis D was 38%. Hypocalcemia was found more prevalent among neonates with no history of vitamin D supplementation (98.7%), no history of maternal calcium supplementation (57.9%), while they had a history of neonatal jaundice on phototherapy (46.1%) which increased to 53.8% with late hypocalcemia. Conclusion: Neonatal hypocalcemia is widely prevalent in Fayoum governorate with significant association with a history of neonatal jaundice on phototherapy, not receiving maternal calcium or neonatal vitamin D supplementation. Saudi Med J 2018; Vol. 39 (3): 247-253 doi: 10.15537/smj.2018.3.21679 How to cite this article: Elsary AY, Elgameel AA, Mohammed WS, Zaki OM, Taha SA. Neonatal hypocalcemia and its relation to vitamin D and calcium supplementation. Saudi Med J . 2018 Mar;39(3):247-253. doi: 10.15537/smj.2018.3.21679.

Neonatal hypocalcemia and congenital heart defects has been known as the first clinical manifestation of the chromosome 22q11.2 deletion syndrome (22q11DS). However, because of its wide clinical spectrum, diagnosis of 22q11DS can be delayed in children without classic symptoms. We report the case of a girl with the history of imperforate anus but without neonatal hypocalcemia or major cardiac anomaly, who was diagnosed for 22q11DS at the age of 11 after the onset of overt hypocalcemia. She was born uneventfully from phenotypically normal Korean parents. Imperforate anus and partial cleft palate were found at birth, which were surgically repaired thereafter. There was no history of neonatal hypocalcemia, and karyotyping by GTG banding was normal. At the age of 11, hypocalcemia (serum calcium, 5.0 mg/dL) and decreased parathyroid hormone level (10.8 pg/mL) was noted when she visited our Emergency Department for fever and vomiting. The 22q11DS was suspected because of her mild mental retardation and velopharyngeal insufficiency, and a microdeletion on chromosome 22q11.2 was confirmed by fluorescence in situ hybridization. The 22q11DS should be considered in the differential diagnosis of hypocalcemia at any age because of its wide clinical spectrum.

Background: Neonatal hypocalcemia is a metabolic abnormality commonly reported. Late onset hypocalcemia usually manifests after 7 days and requires a long-term therapy. Neonatal hypocalcemia due to hypoparathyroidism can manifest as life-threatening seizures or tetany. Initial management is important to prevent any complication due to this condition. However, the initial management to correct hypocalcemia with the administration of calcitriol, high dose intravenous and oral calcium may take longer to achieve because of hypoparathyroidism. Case summary: We report a case of late onset neonatal hypocalcemia in a nine-days-old baby. He was born on the 35-36 week of gestational age by Caesarean section, without asphyxia nor neonatal infection. The baby had a refractory seizure with low serum calcium and magnesium, high phosphate, normal alkaline phosphatase (ALP) and low calcium creatinine urine ratio. His 25-hidroxy vitamin D (25-OHD) total was as low as 12.9 ng/mL. And, he has a low level of parathyroid hormone (PTH). Adequate correction for hypocalcemia and hypomagnesemia failed to maintain calcium and magnesium to their normal value. Oral calcium gluconolactate and carbonate were added after calcitriol supplementation, but seizure still noticed. After magnesium oxide supplementation was given, another seizure had never occurred. A long-term follow-up on vitamin D and calcium level were required. Conclusion: In a hypocalcemic newborn patient, assessment of the magnesium, vitamin D, and PTH status are needed.

PubMed: 28610460 Objective: Vitamin D has many important functions in our body. Especially in intrauterine and early infancy periods, Vitamin D plays a major role in bone development, growth, and the maturation of tissues such as lung and brain. Fetus is dependent on the mother in terms of Vitamin D and maternal Vitamin D deficiency results in a Vitamin D deficient newborn. The purpose of this study was to determine the levels of Vitamin D in newborns and to investigate the association between Vitamin D status of the baby and neonatal hypocalcemia. Method: Vitamin D, calcium, and parathyroid hormone levels of 750 infants, born between 1 January 2014 and 30 June 2015 and followed in Ondokuz Mayıs University Neonatal Intensive Care Unit were analyzed retrospectively. Blood levels of Vitamin D were checked within 3 days after birth. A 25(OH)D3 level of 30 ng/ml) 25(OH)D3 levels; 68 (9%) had mild, 234 (31%) had moderate and 418 (56%) had severe vitamin D deficiency. No correlation was found between Vitamin D levels and gender, mother’s age, gestational week or birth weight. In 79 (17.2%) preterms, neonatal hypocalcemia was observed. Vitamin D levels of the premature infants who had early neonatal hypocalcemia were statistically significantly lower when compared with those who did not have early neonatal hypocalcemia (p =.02). No significant difference was found between the Vitamin D levels of the term infants who had early neonatal hypocalcemia and those who did not (p=.29). No significant difference was found between the Vitamin D levels of the infants who had late neonatal hypocalcemia and those who did not (in preterm p =.27; in term p =.29). Conclusions: Although lack of Vitamin D is preventable and curable, it is an important health problem for newborns in Turkey. In our study, 56% of the infants were found to have severe lack of Vitamin D and lack of Vitamin D was found to be associated with early neonatal hypocalcemia in preterm newborns. However, long-term effects of lack of Vitamin D in infancy are not fully known. In order to be able to prevent neonatal Vitamin D deficiency, 1200 IU/day vitamin D was supplemented to mothers from the 12th gestational week to 6th month of the birth, which was put into effect by the Ministry of Health in 2011, and should be applied by all health workers. © 2017 Informa UK Limited, trading as Taylor & Francis Group.

Background Hypocalcemia is a frequent abnormality that has been associated with disease severity and outcome in hospitalized foals. However, the pathogenesis of equine neonatal hypocalcemia is poorly understood. Hypovitaminosis D in critically ill people has been linked to hypocalcemia and mortality; however, information on vitamin D metabolites and their association with clinical findings and outcome in critically ill foals is lacking. The goal of this study was to determine the prevalence of vitamin D deficiency (hypovitaminosis D) and its association with serum calcium, phosphorus, and parathyroid hormone (PTH) concentrations, disease severity, and mortality in hospitalized newborn foals. Methods and Results One hundred newborn foals ≤72 hours old divided into hospitalized (n = 83; 59 septic, 24 sick non-septic [SNS]) and healthy (n = 17) groups were included. Blood samples were collected on admission to measure serum 25-hydroxyvitamin D3 [25(OH)D3], 1,25-dihydroxyvitamin D3 [1,25(OH) 2D3], and PTH concentrations. Data were analyzed by nonparametric methods and univariate logistic regression. The prevalence of hypovitaminosis D [defined as 25(OH)D3

Osteopetrosis is a rare genetic condition of reduced osteoclastic bone resorption which causes defective bone remodeling and skeletal sclerosis during growth, having effects on many organs and tissues. Mutation of T-cell immune regulator 1 (TCRG1) gene is the most common genetic defect leading to osteopetrosis, with poor prognosis. The autosomal recessive form presents in the infantile period (also known as malignant infantile osteopetrosis - MIOP), and is characterized by fractures, short stature, hepatosplenomegaly, compressive neuropathies, hypocalcemia and pancytopenia. Being a rare disease with non-specific clinical manifestations, the diagnosis is difficult and usually delayed. Rickets is a characteristic feature of MIOP which results from the defect in osteoclasts to provide a normal Ca/P balance resulting in the poor mineralization of the osteoid. Various treatment options have been suggested for osteopetrosis, but hematopoietic stem cell transplantation still remains the only curative treatment option presently. The authors report the case of a 46-day-old girl with late-onset neonatal hypocalcemia and rickets that was later diagnosed as osteopetrosis. This case report emphasizes that infantile osteopetrosis is an important cause of neonatal hypocalcemia. As irreversible complications develop within the first months of life, immediate diagnosis and early intervention are crucial and may be life-saving.

Objective To investigate the clinical manifestations at diagnosis and during follow-up in patients with 22q11.2 deletion syndrome to better define the natural history of the disease. Study design A retrospective and prospective multicenter study was conducted with 228 patients in the context of the Italian Network for Primary Immunodeficiencies. Clinical diagnosis was confirmed by cytogenetic or molecular analysis. Results The cohort consisted of 112 males and 116 females; median age at diagnosis was 4 months (range 0 to 36 years 10 months). The diagnosis was made before 2 years of age in 71% of patients, predominantly related to the presence of heart anomalies and neonatal hypocalcemia. In patients diagnosed after 2 years of age, clinical features such as speech and language impairment, developmental delay, minor cardiac defects, recurrent infections, and facial features were the main elements leading to diagnosis. During follow-up (available for 172 patients), the frequency of autoimmune manifestations ( P = .015) and speech disorders ( P = .002) increased. After a median follow-up of 43 months, the survival probability was 0.92 at 15 years from diagnosis. Conclusions Our data show a delay in the diagnosis of 22q11.2 deletion syndrome with noncardiac symptoms. This study provides guidelines for pediatricians and specialists for early identification of cases that can be confirmed by genetic testing, which would permit the provision of appropriate clinical management.

Background. Late transient neonatal hypocalcemia with hyperphosphatemia is potentially life-threatening. The use of dihydroxycholecalciferol in the management of neonatal hypocalcemia is unexplored. Objective. We hypothesized adding dihydroxycholecalciferol to intravenous continuous calcium infusion (CaI) will achieve accelerated correction of hypocalcemia. Design/Methods. A controlled double-blind randomized placebo group was organized to compare the addition of dihydroxycholecalciferol to CaI in 3–14 day old neonates presenting with hypocalcemia, hyperphosphatemia and seizures. Ionized calcium and phosphorus were measured to adjust CaI and maintain eucalcemia. Time to resolution of hypocalcemia was defined as time from starting CaI to the first ionized calcium of mmol/L. CaI was discontinued when ionized calcium levels were mmol/L on two measurements and the infant tolerated feeds. Results. Fourteen neonates were studied without statistical difference between groups. Time to correction of hypocalcemia for 1,25 dihydroxycholecalciferol versus placebo was versus hours respectively ( ). The duration of CaI was versus hours respectively ( ). Conclusions. The addition of dihydroxycholecalciferol to standard CaI therapy reduced the duration of CaI, but did not reduce the time to correct hypocalcemia in neonates with late transient hypocalcemia.

Serum immunoreactive parathyroid hormone (iPTH) and plasma total calcium, ionized calcium, magnesium, and phosphorus levels were determined during the first 9 days of life in 137 normal term infants, 55 "sick" infants, and 43 hypocalcemic (Ca