Postnatal surge in serum calcitonin concentrations: no contribution to neonatal hypocalcemia in infants of diabetic mothers

It has been suggested that hypercalcitoninemia may contribute to neonatal hypocalcemia in infants of diabetic mothers (IDM). Because the role of calcitonin (CT) in Ca metabolism in humans is questionable, we hypothesized that serum CT peaks similarly after birth in IDM and controls and that serum Ca concentrations do not correlate with serum CT. Forty-seven term IDM (White classes B-RT) were compared with 31 controls. Controls were born after normal pregnancies, labors, and deliveries. Blood samples (cord and 24 h) were analyzed for Ca, Mg, parathyroid hormone (PTH), and CT. Repeated measures analysis showed increasing serum Mg, PTH, and CT, and decreasing Ca over time. The incidence of hypocalcemia was significantly higher in the diabetic group (p less than 0.01) and the incidence of hypomagnesemia was borderline significantly higher (p less than 0.06). There were no differences in cord or 24-h serum concentrations of CT between groups. In multiple regression analysis, serum Ca and PTH were correlated (p less than 0.02, R2 = 0.33), but not serum Ca and CT; the increase in serum PTH in relation to serum Ca at the nadir (24 h) correlated directly with serum Mg concentrations (R2 = 0.31, p less than 0.05). Thus, serum CT increases after birth irrespective of the rate of decrease of serum Ca in both IDM and controls; high CT concentrations observed after birth (as compared with adult norms) do not seem to play a role in the pathogenesis of neonatal hypocalcemia in IDM; and responsiveness of parathyroid gland at birth is adversely affected by hypomagnesemia, which supports the theory of functional hypoparathyroidism in Mg deficiency.     

Postnatal changes in calcium-regulating hormones in very-low-birth-weight infants. Effect of early neonatal hypocalcemia and intravenous calcium infusion on serum parathyroid hormone and calcitonin homeostasis

In very-low-birth-weight (VLBW) infants, we studied the hypotheses that in early neonatal hypocalcemia the serum parathyroid hormone (PTH) concentration would rise; the serum calcitonin (CT) concentration would decline; and, in response to intravenous (IV) calcium (Ca) infusion, the serum PTH concentration would be lowered; and the serum CT concentration would rise. Fifteen infants appropriate for gestational age (age, less than 32 weeks; birth weight, less than 1,500 g) were enrolled in the study. In eight infants in whom the serum Ca level declined to less than 6.0 mg/dL, changes in serum magnesium, phosphorus, PTH, CT, and whole blood ionized calcium (iCa) were evaluated on entry into the study, when serum Ca declined to less than 6.0 mg/dL, immediately after infusion of 18 mg/kg of elemental calcium as calcium gluconate, and at eight hours post-Ca infusion (+ 8 hr). The serum Ca concentration declined from 7.9 +/- 0.6 baseline (mean +/- SE) to 5.2 +/- 0.2 mg/dL pre-Ca infusion and rose to 9.17 +/- 0.74 mg/dL post-Ca infusion and 7.1 +/- 0.5 mg/dL at +8 hr post-Ca infusion. Whole blood iCa declined from 4.82 +/- 0.24 to 3.72 +/- 0.19 mg/dL pre-Ca infusion, rose to 6.68 +/- 0.32 mg/dL post-Ca infusion, and was 4.12 +/- 0.21 mg/dL at + 8 hr post-Ca infusion. The serum P concentration did not change significantly. The serum PTH concentration rose from 116 +/- 17 to 204 +/- 34 pmole/L pre-Ca infusion, declined to 149 +/- 22 pmole/L post-Ca infusion, and was 187 +/- 28 pmole/L at + 8 hr post-Ca infusion. The serum CT concentration was elevated and did not change significantly. Thus, in infants less than 32 weeks' gestation, the serum PTH level rises in early neonatal hypocalcemia and is suppressed by IV Ca infusion; the serum CT level is markedly elevated and is not altered in early neonatal hypocalcemia and does not rise further in response to IV Ca infusion in VLBW infants. We suggest that hypercalcitoninemia occurs in VLBW infants and that serum CT concentrations are unresponsive to changes in serum Ca.     

Neonatal secretion of gastrin and glucagon

Plasma gastrin and glucagon levels were estimated in mothers after labour, and in their babies at birth and on the fourth day of life. The newly born baby appears to secrete gastrin independently and the plasma levels are higher on the fourth day of life. The cord gastrin level is lower when labour is induced or augmented by the intravenous infusion of oxytocin. Our results do not exclude the possibility that gastrin is transferred from mother to baby during a spontaneous labour. Such a maternal component of cord gastrin may be responsible for neonatal gastric hyperacidity.The mean cord glucagon level is higher than the maternal level at birth and the fourth day level is higher than the cord level. The C-terminal reactive glucagon-like immunoreactivity (C-GLI) in the cord blood is lower when oxytocin has been used during labour. Maternal or placental transfer of C-GLI during labour to the spontaneously born baby is one possible explanation of this finding.The raised glucagon levels on the fourth day may explain why there is low gastric acidity at this time despite the gastrin level being higher than at birth. No relation could be deduced between the C-GLI, i.e. pancreatic glucagon level, and the blood glucose level either at birth or on the fourth day of life.     

The association between neonatal polycythemia, hypocalcemia, and hypoglycemia

A study about the association between neonatal polycythemia, hypoglycemia, and hypocalcemia was carried out at the Hasan Sadikin General Hospital Bandung, Indonesia, between November 1986 and August 1987. Forty-six neonates with polycythemia were enrolled in the study and 92 neonates born during the same period formed the control subjects. The control subject neonates were sampled among those with equal birth weight and gestational age compared to the polycythemia subjects. Blood glucose levels were examined more than three hours after birth and before the first feeding by using the God-PAP method and blood calcium levels at less than 24 hours of age by using calorimetric method. The cut-off point for hypoglycemia and hypocalcemia were 30 mg% and 7 mg%, respectively. The results showed that there was a significant difference for hypoglycemia (p less than 0.01) and hypocalcemia (p less than 0.05) between the exposed subjects and the control subjects.     

Effect of calcium therapy in the sick premature infant with early neonatal hypocalcemia

Twenty-seven sick premature infants with serum calcium concentrations less than 6.0 mg/dl during the first day of age were enrolled in a prospective controlled study involving two treatment regimens--calcium given as a bolus or a drip--or no treatment. Mean total calcium concentration was 5.5 +/- 0.8 mg/dl, and ionized calcium was 3.1 +/- .3 mg/dl, with no significant difference between treatment groups. By 24 hours, in all groups total calcium had increased to greater than 6.0 mg/dl (bolus 6.5 +/- 1.1, drip 7.0 +/- 0.4, control 6.6 +/- 0.4) and ionized calcium to greater than 3.5 mg/dl (bolus 3.9 +/- 0.3, drip 3.6 +/- 0.6, control 3.6 +/- 0.3). Ionized and total calcium concentrations were significantly correlated (r = 0.562; P less than 0.001), but total calcium did not predict ionized calcium in any group. These data support the concept that, even in sick infants, early neonatal hypocalcemia is a physiologic phenomenon that may not require treatment.     

Hypercalcitoninemia and hypocalcemia in acutely ill children: studies in serum calcium, blood ionized calcium, and calcium-regulating hormones

We studied the hypotheses that serum calcium and blood ionized calcium would be low in acutely ill children and would rise with clinical improvement. In 15 children admitted to the pediatric intensive care unit, the blood ionized calcium level was 4.45 +/- 0.06 mg/dl (1.11 +/- 0.015 mmol/L) on entry versus 5.17 +/- 0.03 mg/dl (1.29 +/- 0.01 mmol/L) in control subjects (p less than 0.005), rose significantly on days 2 and 3, and was 5.12 +/- 0.04 mg/dl (1.28 +/- 0.01 mmol/L) at discharge (p less than 0.005). Changes in serum calcium level were similar, whereas serum magnesium and phosphorus levels were normal and did not change. Basal serum parathyroid hormone concentrations were elevated, rose further during the study, and were normal at discharge. Serum parathyroid hormone levels correlated inversely with blood ionized calcium levels, indicating that compensatory hyperparathyroidism occurs with low blood ionized calcium concentrations. Basal serum calcitonin values were evaluated on entry and decreased with clinical improvement. Serum calcitonin levels correlated significantly with low blood ionized calcium levels, indicating that hypercalcitoninemia may play a role in the pathogenesis of hypocalcemia in these children. Urine calcium excretion was not increased in the four children studied. We speculate that with clinical improvement, a rise in serum parathyroid hormone levels and a decline in serum calcitonin levels may help restore normocalcemia in these acutely ill children.     

Early neonatal hypocalcemia in extremely preterm infants. High incidence, early onset, and refractoriness to supraphysiologic doses of calcitriol

Nineteen preterm infants born at or before 32 weeks of gestation were studied to determine the dose of calcitriol that would be effective in the prophylaxis of early neonatal hypocalcemia (serum calcium level, less than 7.0 mg/dL [less than 1.75 mmol/L]). In these infants the course of early neonatal hypocalcemia was not modified by calcitriol administration. Serum 1,25-dihydroxyvitamin D level rose in response to intramuscular administration of calcitriol. The incidence of hypocalcemia in these infants was 37% by 12 hours, 83% by 24 hours, and 89% by 36 hours. Thus, in extremely preterm infants, the incidence of early neonatal hypocalcemia is higher and the onset earlier than in larger preterm infants; furthermore, in these infants the hypocalcemia is refractory even to high doses of calcitriol.     

Decline in serum calcium, magnesium, and phosphorus values with oral glucose in normal neonates: studies of serum parathyroid hormone and calcitonin

In 10 normal term infants aged 52 +/- 2.5 hours, serum calcium, magnesium, phosphorus, ionized calcium, parathyroid hormone, and calcitonin were studied at 0, 1/2, 1, and 2 hours after administration of 1.77 +/- 0.08 gm/kg glucose orally over 20 minutes. In response to glucose administration, serum glucose concentration rose and serum P, Ca, and Mg concentrations fell. Serum PTH concentration rose significantly, and blood ionized Ca and pH were unaltered. Serum calcitonin was elevated, as compared with adult values, and did not change. We suggest that in neonates, as in adults, oral ingestion of glucose lowers serum Ca, Mg, and P, and a compensatory rise in serum PTH concentration maintains blood ionized Ca concentration.     

Malignant infantile osteopetrosis: a rare cause of neonatal hypocalcemia

Malignant infantile osteopetrosis is a rare autosomal recessive disorder characterized by presentation in the first few months of life with manifestations relating to an underlying defect in osteoclastic bone resorption. This report describes a 10 day-old boy in whom neonatal hypocalcemia was present and whose brother had died with the diagnosis of osteopetrosis.     

Neurodevelopment of preterm infants: neonatal neurosonographic and serum bilirubin studies.

In this study of 249 preterm infants of less than 34 weeks' gestation, the relationships between maximal serum total bilirubin concentrations during the neonatal period, neonatal cranial ultrasonographic abnormalities, and severe neurodevelopmental sequelae are described. The subjects, who were selected on the basis of serial cranial ultrasonographic findings, had repeated neurologic and developmental examinations during late infancy and early childhood that established the presence (n = 45) or absence (n = 204) of spastic forms of cerebral palsy. Of the 204 subjects without cerebral palsy, 23 scored abnormally low on standardized developmental testing during early childhood. All but seven of the subjects with cerebral palsy had grade III/IV intracranial hemorrhage or moderate to severe periventricular echogenicity or both, ultrasonographic abnormalities that probably reflect a disruption in the blood-brain barrier as well as extravasation of blood into brain tissue; however, analysis of the data did not suggest that these cranial ultrasonographic abnormalities increased either the maximum serum bilirubin concentration during the neonatal period or the susceptibility of the subjects to neurologic damage from hyperbilirubinemia. Also, there was no evidence to suggest that bilirubinemia in the range studied (2.3 to 22.5 mg/100 mL total serum bilirubin) was causally related to cerebral palsy, early developmental delay, or the development of periventricular cysts in this population of preterm infants.(ABSTRACT TRUNCATED AT 250 WORDS)     

新生儿气管软化症发病机制和对策

正新生儿的气管软化症(tracheomalacia,TM)中仅约41. 1%得到耳鼻喉科评估,其病因、发病机制、气道狭窄的程度以及临床表现的严重程度影响临床治疗决策的制定。因此深入认识气道病变,早期发现和个体化的对症治疗对改善病情及减少并发症将大有裨益。本文对新生儿TM的发病机制、临床表现及诊断和治疗的进展作一介绍。     

危重症患儿血中胃泌素、胃动素水平的变化及临床意义

目的 研究血中胃泌素(GAS)、胃动素(MTL)水平在危重症及并发胃肠功能障碍患儿中的变化及意义.方法 将75例患儿分为极危重组、危重组、非危重组,检测其急性期、恢复期及25例对照组血中GAS、MTL水平,分析GAS和MTL水平与病情危重程度、胃肠功能障碍的关系.结果 极危重组、危重组、非危重组GAS分别为(227.41±62.80)、(154.25±38.84)、(84.01±17.10)ng/L,差异有非常显著性(P＜0.01);MTL分别为(413.53±59.80)、(368.36±43.64)、(279.97±33.51)ng/L,差异有非常显著性(P＜0.01).有胃肠功能障碍组血清GAS、血浆MTL水平明显高于无胃肠功能障碍组(P＜0.01).极危重组、危重组患儿恢复期GAS、MTL水平低于急性期,差异有显著性(P＜0.01).非危重组恢复期GAS、MTL水平与急性期比较,差异无显著性(P＞0.05).结论 血液GAS和MTL水平可作为检测胃肠功能障碍的实验室指标.     

胃动素、胃泌素水平及胃黏膜pH值的变化与新生儿胃肠功能障碍的关系

目的 探讨新生儿胃肠功能障碍时胃动素(MTL)、胃泌素(GAS)和胃黏膜pH值(胃pHi)的变化及意义.方法 分别测定72例胃肠功能障碍新生儿和60例无胃肠功能障碍新生儿(对照组)的MTL、GAS和胃pHi,比较两组患儿检测值的差别.血浆MTL和血清GAS用放射免疫方法测定,根据Henderson-Hasselbach公式计算出胃pHi,同时做胃液潜血检查.结果 胃肠功能障碍组MTL(158.6±21.7)ng/L、胃pHi(7.280±0.045)均较对照组(198.2±19.5)ng/L、(7.410±0.037)低,差异有非常显著性(P＜0.01);而GAS(171.9±19.1)ng/L较对照组(110.4±16.3)ng/L高,差异有非常显著性(P＜0.01).胃液潜血检测:胃肠功能障碍组阳性61例,对照组仅2例阳性.结论 MTL、GAS及胃pHi与新生儿胃肠功能障碍密切相关,当MTL、胃pHi降低,GAS升高时,则提示可能存在胃肠功能障碍.     

Permanent neonatal diabetes mellitus: A case report with plasma insulin studies

The 11th case of permanent neonatal diabetes mellitus appearing during the first month of life is reported. A critical review of the literature is also presented. The permanence of diabetes is demonstrated by the duration of insulin therapy still necessary after 30 months. Insulin-stimulation tests have been performed some for the first time in such a young diabetic. They have shown a nearly total failure in β-cell response, only very high doses of glucagon provoking a moderate insulin secretion. The absence of acetonuria is discussed. It can perhaps be explained by the hyperglycemia which, by a mass effect, brings about cellular glucose penetration and this stops liberation of Nefa's from adipose tissue.     

Age-related decrease in plasma levels of gastrin, cholecystokinin and somatostatin

Newborn babies have higher concentrations of gastrointestinal hormones than adults. The aim of the present study was to investigate the relationship between age and plasma levels of the three peptides gastrin, cholecystokinin and somatostatin in healthy children aged 1–15 years. Gastrin, cholecystokinin and somatostatin concentrations were twice as high at 1–2 years of age compared with children older than 10 years. Significant negative correlations between age and hormone concentrations were established. It is suggested that these age-dependent differences are related to the growth rate and relative energy consumption during the early years of life.