Serum total magnesium and ionized calcium concentrations in asphyxiated term newborn infants with hypoxic‐ischaemic encephalopathy

Ilves, Pilvi; Kiisk, Madis; Soopõld, T; Talvik, Tiina

doi:10.1111/j.1651-2227.2000.tb00364.x

Cited by 29 publications

(26 citation statements)

References 23 publications

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“…Statistical analysis of the blood parameters showed that treatment, time, and the interaction between treatment and time undergo statistically significant variation, except for pO 2 , where interaction yielded nonsignificant results, but treatment results were significant. The large decrease in blood ionized calcium due to abrupt restoration of normocapnia, which is also seen in asphyxiated babies, 33 was suppressed by graded restoration of normocapnia (see Fig 5).…”

Section: Changes In Brain Ph Are Paralleled By Changes In Blood Parammentioning

confidence: 91%

Brain alkalosis causes birth asphyxia seizures, suggesting therapeutic strategy

Helmy

Tolner

Vanhatalo

et al. 2011

Annals of Neurology

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Section: Changes In Brain Ph Are Paralleled By Changes In Blood Parammentioning

confidence: 91%

Brain alkalosis causes birth asphyxia seizures, suggesting therapeutic strategy

Helmy

Tolner

Vanhatalo

et al. 2011

Annals of Neurology

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“…Decreased values of the postnatal arterial pH and base excess in the cases with RDS compared to the control group in our study, while there were no significant differences in the values of the umbilical cord arterial pH and base excess in the two groups, also support the presence of early acidosis resulting from RDS in the study group and the absence of pro-Sarıcı/Serdar/Erdem/Alpay/Tekinalp/ Yurdakök/Yigit/Gökcay longed or severe intrauterine hypoxia in both groups. Increases in serum total Mg concentrations have been reported in perinatal asphyxia and HIE [11,12]. Olofsson et al [14] have demonstrated higher umbilical cord arterial IMg levels (0.58 B 0.08 mmol/l) in 14 newborns with acidosis (umbilical cord arterial pH 7.0 B 0.06) when compared to 15 preterm newborns (0.51 B 0.03 mmol/l) and 19 healthy term newborns (0.49 B 0.03 mmol/l).…”

Section: Discussionmentioning

confidence: 99%

“…Serum total Mg levels have been investigated in neonatal acidosis, perinatal asphyxia and hypoxic-ischemic encephalopathy (HIE) in term newborns before [10][11][12][13]. IMg levels have been investigated in neonatal acidosis in only one study [14], and there is only a limited number of studies evaluating IMg levels in preterm and term newborns [6][7][8][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Plasma Ionized Magnesium Levelsin Neonatal Respir atory Distress Syndrome

Sarıcı

Serdar²,

Gönüllü

et al. 2004

Neonatology

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“…Accordingly, in a study performed on pediatric intensive care patients (27), hypermagnesemia has been proposed to be a poor prognostic criterion being associated with critical cellular injury. Increased levels of plasma Mg have been demonstrated in a few other situations in which generalized cellular injury occurs as a result of perinatal asphyxia and HIE (28,29) and to neonatal hypoxemia and acidosis (30,31). In the present study, the increase of IMg levels was correlated with the severity of hyperbilirubinemia, especially in the cases with serum bilirubin levels of Ն290 M, the accepted threshold level for toxic hyperbilirubinemia (25,26).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Plasma Ionized Magnesium Levels in Neonatal Hyperbilirubinemia

et al. 2004

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Plasma levels of ionized magnesium (IMg) measured by ion-selective electrode were investigated in neonatal hyperbilirubinemia by comparing the newborns with (Ն205 M) and without (Ͻ205 M) significant hyperbilirubinemia (groups of severe and moderate hyperbilirubinemia, respectively). Serum bilirubin, plasma IMg, and ionized calcium (ICa) levels were determined in 165 healthy term newborns with nonhemolytic indirect hyperbilirubinemia during the first 10 d of life. Mean serum bilirubin, plasma IMg, and ICa levels were 200.1 Ϯ 126.5 M, 0.54 Ϯ 0.12 mM, and 1.15 Ϯ 0.12 mM, respectively, in 165 newborns whose mean postnatal age was 156.1 Ϯ 46.5 h, and there was a significant positive correlation between the mean serum bilirubin and plasma IMg levels (r ϭ 0.535, p Ͻ 0.001). Serum bilirubin levels (304.4 Ϯ 83.8 M versus 94.1 Ϯ 54.7 M) and plasma IMg levels (0.6 Ϯ 0.12 mM versus 0.49 Ϯ 0.1 mM) were significantly higher and plasma ICa levels (1.13 Ϯ 0.12 mM versus 1.18 Ϯ 0.12 mM) were significantly lower in the group of severe hyperbilirubinemia (n ϭ 83) when compared with the group with moderate hyperbilirubinemia (n ϭ 82). Seventeen of the 83 cases of severe hyperbilirubinemia had IMg levels above the normal range (Ն0.69 mM), whereas none of the 82 cases of moderate hyperbilirubinemia had elevated IMg levels. Fifteen of the 17 with high IMg levels had bilirubin levels Ͼ290 M. Results of the present study suggest that increase in plasma IMg may be due to extracellular movement of Mg, a principally intracellular ion, resulting from generalized cellular injury including neurons and erythrocytes. Considering neuroprotective functions and beneficial effects of Mg ion in improving neurologic outcome, we also may speculate the possibility of a neuroprotective role or a compensatory mechanism in IMg increase against emerging toxicity risk of increasing serum bilirubin levels. Deposition of unbound bilirubin or its acid form in the neuron membrane causes permanent neuronal injury with a distinctive regional topography throughout the CNS. Considering the affinity of bilirubin molecule to phospholipids of the plasma membrane (1-4), the sequence of membrane events initiated by bilirubin molecules damages all adjacent membrane-bound enzymes and receptors. However, distant plasma membrane structures such as N-methyl-D-aspartate (NMDA) receptor/ion channel complex located within neuronal membranes on the synaptic surface of neurons are disrupted as well. Increased and prolonged activation of NMDA receptor as in perinatal asphyxia and hypoxic ischemic encephalopathy (HIE) results in brain cell injury despite its physiologic roles in brain plasticity; neuronal growth; synaptogenesis; and development of learning, memory, and vision. However, it has been shown in newborn piglets that bilirubin also increases activation of the NMDA receptor by modifying its binding characteristics, increases the receptor's affinity for NMDA receptor antagonists, and thus results in neuronal injury (5). Bilirubin-induced neurotoxicity may share common featu...

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Serum total magnesium and ionized calcium concentrations in asphyxiated term newborn infants with hypoxic‐ischaemic encephalopathy

Cited by 29 publications

References 23 publications

Brain alkalosis causes birth asphyxia seizures, suggesting therapeutic strategy

Brain alkalosis causes birth asphyxia seizures, suggesting therapeutic strategy

Plasma Ionized Magnesium Levelsin Neonatal Respir atory Distress Syndrome

Evaluation of Plasma Ionized Magnesium Levels in Neonatal Hyperbilirubinemia

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