Plasma Cortisol, Cortisone and Urinary Glucocorticoid Metabolites in Preterm Infants

Midgley, Paula; Holownia, Peter; Smith, John A.; Moore, M. R.; Russell, Kim; Oates, Nicola; Shaw, J.; Honour, John W.

doi:10.1159/000047071

Cited by 19 publications

(9 citation statements)

References 43 publications

(59 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cortisol levels in all three study groups showed a longitudinal pattern similar to that described by others in preterm infants (27,28). Although glucocorticoid hormones and thyroid hormones are known to influence each other's regulation in animal studies (18), we could not demonstrate any effect of T 3 and/or T 4 supplementation on cortisol levels.…”

Section: Discussionsupporting

confidence: 80%

A Randomized, Masked Study of Triiodothyronine Plus Thyroxine Administration in Preterm Infants Less Than 28 Weeks of Gestational Age: Hormonal and Clinical Effects

et al. 2004

View full text Add to dashboard Cite

A randomized, placebo-controlled, masked study was conducted of the responses of thyroid parameters, cortisol, and the cardiovascular system to a single dose of triiodothyronine (T 3 ) 24 h after birth, followed by a daily dose of thyroxine (T 4 ) during 6 wk to infants Ͻ28 wk gestational age. Thirty-one infants were assigned to three groups: 1) group A: T 3 24 h after birth plus daily T 4 during 6 wk; 2) group B: placebo T 3 and T 4 during 6 wk; and 3) group C: placebo T 3 and placebo T 4 . T 4 , free T 4 , T 3 , free T 3 , reverse T 3 , thyroid-stimulating hormone, and cortisol were measured in cord blood and on days 1, 3, 7, 14, 21, 42, and 56. Data on pulse rate, blood pressure, and cumulative dose of inotropic agents were collected. T 3 (0.5 g/kg) resulted in a plasma increase until day 3. Thereafter, plasma T 3 levels were comparable between the groups. T 4 , free T 4 , and reverse T 3 were increased in groups A and B during the period of T 4 administration. Thyroid-stimulating hormone suppression was of shorter duration in group A. T 3 and T 4 administration did not have any effect on cortisol levels. We did not find any effects of T 3 or of T 4 administration on the cardiovascular system. A single injection of T 3 (0.5 g/kg) given 22-26 h after birth only leads to a 2-d increase of T 3 levels and does not have effects on the cardiovascular system. This study does not support the use of T 3 according to our regimen in preterm infants. Thyroid hormones play an important role in normal growth and development of the CNS (1, 2). In term infants, thyroxine (T 4 ) and triiodothyronine (T 3 ) increases shortly after birth. In premature infants, transient hypothyroxinemia after birth is a common finding (3-7). This hypothyroxinemia is characterized by low levels of T 4 and T 3 , which do not cause elevations in thyroid-stimulating hormone (TSH) above 20 mU/L. The degree of hypothyroxinemia is related to gestational age (GA) and the severity of neonatal disease. Low T 3 and T 4 levels in premature infants have been found to be associated with poor neurologic and developmental outcome (8 -11).Transient hypothyroxinemia is a multicausal phenomenon in which immaturity of thyroid hormone metabolism with high activity of deiodinase type 3 together with factors such as immaturity of the hypothalamo-pituitary-thyroid axis and the sudden interruption of the maternal contribution to fetal thyroid hormone pools are involved. Thyroid hormone supplementation in preterm infants has been the subject of several clinical studies with clinical and neurodevelopmental parameters as primary outcome (12)(13)(14). To date, no clear effect of supplemental T 4 treatment on neurodevelopmental outcome has been demonstrated. In an earlier study, however, we observed that a subgroup of T 4 -treated infants of Ͻ29 wk GA tended to have a better developmental outcome than infants of similar GA in the placebo group (13,15).T 4 administration to preterm infants of Ͻ30 wk GA did not result in increased plasma T 3 levels; in fact, it resulted in de...

show abstract

Section: Discussionsupporting

confidence: 80%

A Randomized, Masked Study of Triiodothyronine Plus Thyroxine Administration in Preterm Infants Less Than 28 Weeks of Gestational Age: Hormonal and Clinical Effects

et al. 2004

View full text Add to dashboard Cite

show abstract

“…This brief spike in plasma corticosterone is enough to induce GHS to gastric distension in adult life; blocking glucocorticoid receptors by RU-486 during this period prevented the induction of GHS in FD-like rats. It is noteworthy that the timing of SHRP is species-dependent; in humans it occurs in the last trimester of pregnancy 32 .…”

Section: Discussionmentioning

confidence: 99%

Developmental Origins of Functional Dyspepsia-Like Gastric Hypersensitivity in Rats

Winston

Sarna

2013

Gastroenterology

View full text Add to dashboard Cite

Background & Aims Gastric hypersensitivity (GHS) contributes to epigastric pain in patients with functional dyspepsia (FD); the etiology and cellular mechanisms of this dysfunction remain unknown. We investigated whether inflammatory insult to the colons of neonatal rats induced GHS in adult life. Methods We used cellular, molecular, and in vivo approaches to investigate the mechanisms of GHS in adult rats subjected to neonatal colonic insult by intraluminal administration of trinitrobenzene sulfonic acid (TNBS); controls received saline. Six to 8 weeks later, rats were evaluated for GHS and tissue was collected for molecular experiments.’ Results Inflammatory insult to the colon on post-natal day (PND) 10 caused an aberrant increase of corticosterone on PND 15 and induced GHS in adult life. We called these FD-like rats. Inhibition of glucocorticoid receptors following neonatal insult blocked the induction of GHS in adult rats. The aberrant increase of plasma corticosterone in neonates elevated the plasma concentration of norepinephrine, nerve growth factor (NGF) in the gastric fundus muscularis externae, brain-derived neurotrophic factor (BDNF) in the thoracic dorsal root ganglia (DRG) and spinal cord, and downregulated Kv1.1 mRNA in thoracic DRG without affecting the expression of Kv1.4, Nav1.8, TrpA1, TrpV1, or P2X3 in FD-like rats. Inhibition of glucocorticoid receptors during neonatal insult or the inhibition of adrenergic receptors, NGF or BDNF in FD-like rats suppressed GHS. The intrathecal administration of small interfering RNAs against Kv1.1 increased GHS in naïve rats. Conclusion Inflammatory insult to the colons of rat pups leads to GHS in adult life. GHS is caused by altered expression of genes encoding neurotrophins and ion channels, and altered activity of the sympathetic nervous system.

show abstract

“…The larger (compared to fetal) placental contribution to F inactivation, however, is removed at birth. While plasma E levels do remain higher than at other times in life in both preterm and term infants [32,33,34], functional deactivation of F does not appear to occur after birth in infants born <30 weeks’ gestation, resulting in F levels higher than E [35, 36]. …”

Section: Discussionmentioning

confidence: 99%

Lack of Adult-Type Salivary Cortisol Circadian Rhythm in Hospitalized Preterm Infants

et al. 2005

View full text Add to dashboard Cite

Background/Aims: Knowledge of the presence or absence of cortisol (F) circadian rhythm in preterm infants is important for the interpretation of F measurements made in samples taken for both clinical and research purposes. Little is known about its emergence in very preterm infants. This study examines circadian rhythm in F secretion in hospitalized infants born before 30 weeks’ gestation. Methods: Design: Prospective longitudinal observational study. Subjects: 11 infants admitted consecutively and born before 30 completed weeks of gestation. Measurements: F was measured by highly specific radioimmunoassay on morning and evening saliva samples gathered at weekly intervals until discharged home. Circadian rhythm was defined as ≧40% reduction from morning to evening level. Results: For all data, the median salivary F was 10.3 nmol/l (range <0.5–372.8). F levels were highest in the first 3 weeks of life. No infants displayed classical circadian rhythm for 4 weeks or more prior to being discharged from hospital. The other infants showed randomly distributed morning and evening F values with a trend in 4 infants towards periods of consistently higher evening than morning values. Conclusion: Adult-type F circadian rhythm is rarely evident in hospitalized preterm infants born before 30 weeks’ gestation.

show abstract

Plasma Cortisol, Cortisone and Urinary Glucocorticoid Metabolites in Preterm Infants

Cited by 19 publications

References 43 publications

A Randomized, Masked Study of Triiodothyronine Plus Thyroxine Administration in Preterm Infants Less Than 28 Weeks of Gestational Age: Hormonal and Clinical Effects

A Randomized, Masked Study of Triiodothyronine Plus Thyroxine Administration in Preterm Infants Less Than 28 Weeks of Gestational Age: Hormonal and Clinical Effects

Developmental Origins of Functional Dyspepsia-Like Gastric Hypersensitivity in Rats

Lack of Adult-Type Salivary Cortisol Circadian Rhythm in Hospitalized Preterm Infants

Contact Info

Product

Resources

About