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H Devlieger

Publications and source records attributed to H Devlieger.

At least 91 records · Page 5Linked to original sources
PubMed1994

Properties of thyroid-stimulating hormone and cortisol secretion by the human newborn on the day of birth.

Secretory activation of the thyroid and adrenal glands is a hallmark of the neonatal adaptation to extrauterine life. TSH and cortisol play key roles in these axes. The highest serum concentrations of TSH attained over the full span of human life are normally found shortly after birth. Serum cortisol is also known to be elevated in the immediate postnatal period. However, the dynamics of TSH and cortisol secretion have hitherto not been documented on the day of birth. To study the properties of neonatal TSH and cortisol secretion, we obtained arterial blood at regular intervals (every 20 min for 6 h) from nine polycythemic newborns (gestational age, 34-41 weeks) on the first and/or fourth days after birth during a therapeutic, standardized, isovolumetric, partial exchange transfusion. One premature infant had received betamethasone antenatally. The serum TSH level of an infant with congenital hyperthyroidism of transplacental origin was also measured at the postnatal age of 1 h. Deconvolution analysis of the profiles revealed that all infants displayed a combination of basal and pulsatile TSH release. Bursts of TSH secretion occurred at a median interval of 133 min. The median serum TSH half-life was 75 min. On the day of birth, basal TSH secretion and the amplitude of pulsatile TSH secretion were higher than 3 days later. Cortisol was secreted exclusively in a pulsatile fashion. Bursts of cortisol release occurred at a median interval of 69 min. The median serum cortisol half-life was 60 min. Cortisol secretion appeared to shift gradually from a high frequency, low amplitude pattern early on the first day toward a lower frequency, higher amplitude pattern 3 days later. TSH and cortisol secretion were low in the infant who received betamethasone prenatally. Serum TSH was undetectable in the infant with congenital hyperthyroidism. In conclusion, serum TSH concentrations in the human newborn appear to be elevated on the day of birth as a result of amplified basal and pulsatile TSH release, then fall rapidly through a mechanism that decreases the amplitude of TSH secretion and are affected by modulation of the fetal thyroid axis. From the day of birth onward, cortisol was found to be released in an exclusively pulsatile mode, with characteristics that appear to depend on postnatal age and prenatal glucocorticoid exposure.

Aging↗
PubMed1993

Congenital pulmonary lymphangiectasis with chylothorax: a heterogeneous lymphatic vessel abnormality.

We report on 7 perinatal autopsy cases of primary congenital pulmonary lymphangiectasis (CPL) with bilateral chylothorax. This study demonstrates that primary CPL is often complicated by chylous pleural effusions with ensuing pulmonary hypoplasia. Conversely, CPL appears to be a constant pathological finding in spontaneous congenital chylothorax. These observations indicate a common pathogenesis for both disorders. The basic defect is not an intrinsic lung abnormality, but a developmental error of the lymphatic system resulting in a pulmonary lymphatic obstruction sequence. The cause of CPL is heterogeneous. Apparently, most cases are sporadic occurrences. We report the second instance of CPL in sibs. This indicates that some cases are genetically determined with autosomal recessive inheritance. CPL may also be part of a multiple congenital anomalies (MCA) syndrome such as Noonan, Ullrich-Turner, and Down syndrome.

Abnormalities, Multiple↗
PubMed1993

Calcium and phosphorus retention in the preterm infant during total parenteral nutrition. A comparative randomised study between organic and inorganic phosphate as a source of phosphorus.

The preterm infant fed parenterally is prone to some demineralisation due in part to insufficient Calcium (Ca) and Phosphorus (P) retention. In an attempt to augment Ca and P retention, we prepared a standardised parenteral solution containing calcium gluconate and glucose-1-phosphate (Phocytan) as source of phosphorus, yielding a daily supply of 75 mg/kg Ca and 45 mg/kg P. 28 very low birthweight infants were randomly assigned to receive either this solution (high Ca P ; n = 15) or a conventional formulation containing calcium gluconate and potassium mono- and dibasic phosphate delivering 42 mg/kg Ca and 36 mg/kg P daily (low Ca P ; n = 13). In the high Ca P daily retention was respectively 80% and 99% for Ca and P whereas in the low Ca P group, retention was 70% and 82%. Serum parathormone levels were significantly lower in the high Ca P group. We conclude that parenteral nutrition with a new high Ca P supplement results in an augmented Ca and P retention in very low birthweight infants. This may help to prevent neonatal bone demineralization.

Journal Article↗
PubMed1993

Standard two-compartment formulation for total parenteral nutrition in the neonatal intensive care unit: A fluid tolerance based system.

The nutrient requirements of most (pre) term newborns receiving intensive care appear to be relatively fixed. The range of optimal fluid load however, is perceived as being quite narrow and highly variable in time. We designed four amino acid-dextrose mixtures for a standardized neonatal parenteral nutrition, delivering a fixed amount of nutrients in four dilutions with water and corresponding to a fluid load of 90, 110, 130 or 170 ml/kg per day. The addition of a lipid emulsion completes the TPN. In a pilot study, we followed the weight of 30 very low birthweight infants on this parenteral nutrition. After a stabilisation period, the weight gain was found to be similar to the normal fetal weight accretion in utero. We have now infused these solutions in to more than 1000 infants, without significant complications. These formulations proved to have substantial advantages compared to the individualized prescription in terms of availability, safety and time- and cost-effectiveness.

Journal Article↗
PubMed1993

Child morbidity patterns in two tropical seasons and associated mortality rates.

Cross-sectional morbidity recorded during two successive quarterly survey rounds and subsequent 27-months mortality were studied in a random sample of 4238 preschool children in a rural Zairian area. Analysis focuses on morbid patterns, i.e. any combination of the principal signs and symptoms encountered in tropical areas (oedema, marasmus, cough, fever, diarrhoea and tachypnoea). Almost half the children (45-48%) had signs of morbidity, a very high rate. The 3-6 month age group emerged as particularly vulnerable with the highest prevalences of all morbid patterns except for isolated fever. Isolated cough was more prevalent in the dry season probably as an effect of nightly indoor woodburning. All other morbid patterns were significantly more prevalent in the rainy season. Diarrhoea with cough was found to constitute half of all cases of diarrhoea. The results show that with a few simple questions on major symptoms and a brief examination by paramedical health workers, children with an increased risk of death can be identified. The method can be applied at under-5 clinics. Prognosis is particularly bad in severe malnutrition, especially when associated with diarrhoea, in diarrhoea with cough, cough with fever/tachypnoea and for children who are found sick both in the rainy and the subsequent dry season.

Child, Preschool↗
PubMed1993

Dopamine inhibits growth hormone and prolactin secretion in the human newborn.

Dopamine is frequently used in neonatal intensive care for its vasopressor, renal vasodilating, and cardiac inotropic properties. The effect of i.v. dopamine infusion on neonatal pituitary hormone secretion is currently unknown. We observed strikingly low serum concentrations of growth hormone (GH) and prolactin (PRL) during a therapeutic, standardized, isovolumetric, partial exchange transfusion (blood sampling every 20 min for 6 h) in two polycythemic neonates requiring intensive therapy, including continuous dopamine infusion. In addition, the secretion of GH and PRL was studied in three neonates with symptomatic polycythemia (gestational age 34-38 wk; birth weight 2110-2530 g; postnatal age 10-30 h) during a partial exchange transfusion, including an intervening dopamine infusion (8 micrograms/kg/min i.v. for 2 h). The GH and PRL profiles were evaluated by deconvolution analysis. Initially, the three newborns exhibited high-amplitude, pulsatile GH secretion and continuously elevated PRL release. During the dopamine infusion, GH secretion was virtually abolished and PRL release was reduced by at least 50%. Dopamine withdrawal was associated with a rebound release of GH and PRL. Finally, serum GH and PRL concentrations were studied in nine nonpolycythemic newborns (gestational age 31-40 wk; birth weight 1680-4000 g; postnatal age 2-28 d) at the end of a prolonged dopamine infusion (3-5 micrograms/kg/min i.v. for 2-27 d). Within 2 h after dopamine withdrawal, GH and PRL levels increased a median 3-fold and 10-fold respectively. These data concord to indicate that dopamine is a potent inhibitor of GH and PRL secretion in the human newborn.

Dopamine↗
PubMed1993

Properties of growth hormone and prolactin hypersecretion by the human infant on the day of birth.

The neonatal period is the only interval in postnatal life characterized by physiologically elevated plasma concentrations of GH and PRL, two hormones of common origin. To study the secretion of GH and PRL on the day of birth, we obtained at regular intervals (every 20 min for 6 h) blood from seven polycythemic newborns (gestational age 34-41 weeks; birthweight 1600-3960 g; postnatal age 6-23 h) during a therapeutic, standardized, isovolumetric, partial exchange transfusion. Serum GH concentrations were measured by RIA and PRL levels by immunoradiometric assay. Deconvolution analysis of the profiles revealed that all infants displayed a pulsatile pattern of amplified GH release (range 9-191 micrograms/L). Bursts of GH secretion occurred at a median interval of 73 min. The median serum GH half-life was 18 min. All infants had continuously elevated serum PRL concentrations (range 86-191 micrograms/L) and none appeared to release PRL episodically. There was no significant cross-correlation between the secretion of GH and PRL. Mean serum GH concentrations during the 6-h study were higher than in cord serum at birth, whereas PRL and insulin-like growth factor-1 levels were lower than at birth. In conclusion, the neonatal hypersomatotropism appears to be characterized by high-amplitude, high-frequency, pulsatile secretion of GH without a prolonged GH half-life, whereas hyperprolactinemia seems to result from GH-independent, continuous PRL release. The immediate postnatal rise of GH secretion in the human newborn may be related to decreased inhibition by circulating insulin-like growth factor-1.

Delivery, Obstetric↗
PubMed1993

[Familial occurrence of esophageal atresia].

Two siblings with esophageal atresia are reported, and literature data as to familial occurrence and heredity have been reviewed. Until now, only statistical data can be given: the recurrence risk for sibs after one affected child is around 0.5-2% and after two affected children around 20%. The risk for the children of a parent affected by congenital esophageal atresia is estimated at around 3-4%. This is compatible with the recurrence risk of a multifactorial condition in first degree relatives. However, two patients have been described in which the possibility of autosomal dominant transmission has been raised.

Chromosome Aberrations↗
PubMed1992

Unilateral thalamic haemorrhage in the pre-term and full-term newborn.

One full-term and three premature newborns with a unilateral thalamic haemorrhage are reported. The lesion was diagnosed using cranial ultrasonography and confirmed in three using magnetic resonance imaging. Severe perinatal asphyxia occurred in all infants. The neonatal clinical history, subsequent neuro-developmental outcome and neuroimaging findings are discussed. As the prognosis appears to be much better than for infants with bilateral thalamic densities, it is important that this type of lesion is recognised as a separate entity.

Cerebral Hemorrhage↗
PubMed1992

Pathogenesis of congenital cystic adenomatoid malformation of the lung.

Congenital cystic adenomatoid malformation is a rare developmental abnormality of the lung. In most earlier reported cases, the anatomy of the bronchial tree was poorly documented. We describe four cases studied following autopsy. Post-mortem bronchography or serial microscopical examination showed segmental bronchial absence or atresia in each of them. Our observations provide further evidence pointing to bronchial atresia as being the primary defect leading to the development of congenital cystic adenomatoid malformation. The morphology of the lesion, i.e. the type of malformation, is determined by the extent of dysplastic lung growth beyond the atretic segment. The aetiology of the bronchial atresia is probably heterogeneous and may either represent a primary malformation, or be the result of vascular disruption.

Autopsy↗
PubMed1992

Effect of prenatal betamethasone/thyrotropin releasing hormone treatment on somatosensory evoked potentials in preterm newborns.

The maternal administration of betamethasone and thyrotropin releasing hormone (TRH) to accelerate the maturation of the fetus is an increasingly adopted strategy to prevent neonatal morbidity in preterm infants. The effect of this prenatal treatment on the neural maturation of the infant was assessed by measuring somatosensory evoked potentials (SEP) in preterm infants (gestational age 29-36 wk) on the 1st postnatal day, at the age of 1 wk, and before discharge. The N1 latency values of the SEP obtained in 14 infants who were exposed prenatally to betamethasone/TRH were compared with the N1 latencies measured in 12 control infants. On the 1st postnatal day, the N1 latencies in the betamethasone/TRH-treated infants were strikingly shorter (p less than 0.01) than in the controls. However, at the age of 1 wk and at discharge, the N1 latency values of both groups were similar. In conclusion, the present study provides the first solid evidence for the concept that the prenatal exposure to betamethasone/TRH accelerates the SEP-assessed neural maturation of the human fetus, that this prenatal acceleration is followed by a compensatory relative deceleration during the early neonatal period, and that the subsequent SEP-assessed neural maturation proceeds at a normal velocity.

Betamethasone↗
PubMed1992

Pulsatile and sexually dimorphic secretion of luteinizing hormone in the human infant on the day of birth.

Experimental evidence indicates that the hypothalamic-pituitary-gonadal axis is operational and sexually dimorphic in the mammalian fetus and newborn. We examined the dynamics of human luteinizing hormone (LH) secretion in five male and three female infants on the day of birth, after 34-41 wk of gestation. The infants were polycythemic, and blood samples were obtained every 20 min for 160 to 360 min during a therapeutic, standardized, isovolumetric, partial exchange transfusion. Serum LH was measured by an immunoradiometric assay that does not cross-react with human chorionic gonadotropin. The serum profiles of LH presented a striking sex dimorphism with elevated LH levels in male compared with female newborns. Deconvolution analysis of all male LH profiles was consistent with a high-frequency, pulsatile secretory pattern. Testosterone, measured in a pooled serum sample of each infant, was 10-fold higher in male than in female newborns. These results document pulsatile and sexually dimorphic secretion of LH in the human infant as early as the first day of postnatal life. It is possible that the augmented LH secretion in the male newborn participates in the neonatal rise of the serum testosterone concentration.

Estradiol↗
PubMed1992

Laryngeal atresia sequence as part of the DiGeorge developmental field defect.

The subject of the present report is a male newborn with laryngeal atresia (LA) type I, giving rise to a malformation sequence consisting of overdistended polyalveolar lungs and nonimmune fetal hydrops with massive ascites. The infant was chromosomally normal and the first child of consanguineous parents. Retention of liquid secreted by the fetal lungs in utero was the pathogenetic mechanism, responsible for the LA sequence. The LA was part of a complex constellation of anomalies, compatible with the DiGeorge developmental field defect.

Asphyxia Neonatorum↗