Biomaterial Database

Prenatal thyrotropin-releasing hormone for preterm birth. 2000

C A Crowther, and Z Alfirevic, and R R Haslam

Department of Obstetrics and Gynaecology, University of Adelaide, Women's and Children's Hospital, King William Road, Adelaide, South Australia, Australia, SA 5006. ccrowthe@medicine.adelaide.edu.au

BACKGROUND Adding thyrotropin-releasing hormones (TRH) to corticosteroids has been suggested as a way of improving fetal lung development. OBJECTIVE The objective of this review was to assess the effect of giving prenatal TRH in addition to corticosteroids to women at risk of very preterm birth for the prevention of neonatal respiratory disease. METHODS We searched the Cochrane Pregnancy and Childbirth Group trials register, Cochrane Controlled Trials Register, and bibliographies. Date of last search: January 1999. METHODS Randomised controlled trials in women at sufficient risk of preterm birth to warrant the use of prenatal corticosteroids to promote lung maturity. TRH and corticosteroids were compared with corticosteroids with or without placebo. The main outcomes considered were fetal and neonatal mortality, neonatal morbidity, childhood development and maternal morbidity. METHODS All assessments of trial eligibility, quality and data extractions were done by at least two authors independently. RESULTS Over 4500 women were recruited into the 11 included trials. Five trials were rated of high quality. Overall, prenatal TRH, in addition to corticosteroids, did not reduce the risk of neonatal respiratory disease, chronic oxygen dependance, or improve fetal, neonatal or childhood outcome in any of the outcomes assessed by intention-to-treat analyses. Indeed, the data showed prenatal TRH to have adverse effects for women and their infants. All side effects monitored were more likely to occur in women receiving TRH. In the infants, prenatal TRH increased the risk of infants needing ventilation (relative risk (RR) 1.16, 95% confidence interval (CI) 1.03-1.29), having a low Apgar score at five minutes (RR 1.80, 95% CI 1.14-1.92) and, for the one trial providing data, was associated with poorer outcomes at the 12 month follow up. Sensitivity analyses by trial quality, or subgroups with differing times from entry to delivery, or different dose regimens of TRH, did not change these findings. CONCLUSIONS On the basis of currently available evidence, prenatal TRH, in addition to corticosteroids, given to women at risk of very preterm birth cannot be recommended for clinical practice.

UI	MeSH Term	Description	Entries
D007231	Infant, Newborn	An infant during the first 28 days after birth.	Neonate,Newborns,Infants, Newborn,Neonates,Newborn,Newborn Infant,Newborn Infants
D007234	Infant, Premature	A human infant born before 37 weeks of GESTATION.	Neonatal Prematurity,Premature Infants,Preterm Infants,Infant, Preterm,Infants, Premature,Infants, Preterm,Premature Infant,Prematurity, Neonatal,Preterm Infant
D007752	Obstetric Labor, Premature	Onset of OBSTETRIC LABOR before term (TERM BIRTH) but usually after the FETUS has become viable. In humans, it occurs sometime during the 29th through 38th week of PREGNANCY. TOCOLYSIS inhibits premature labor and can prevent the BIRTH of premature infants (INFANT, PREMATURE).	Preterm Labor,Labor, Premature,Premature Labor,Premature Obstetric Labor,Labor, Premature Obstetric,Labor, Preterm
D011247	Pregnancy	The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.	Gestation,Pregnancies
D012127	Respiratory Distress Syndrome, Newborn	A condition of the newborn marked by DYSPNEA with CYANOSIS, heralded by such prodromal signs as dilatation of the alae nasi, expiratory grunt, and retraction of the suprasternal notch or costal margins, mostly frequently occurring in premature infants, children of diabetic mothers, and infants delivered by cesarean section, and sometimes with no apparent predisposing cause.	Infantile Respiratory Distress Syndrome,Neonatal Respiratory Distress Syndrome,Respiratory Distress Syndrome, Infant
D005260	Female		Females
D005938	Glucocorticoids	A group of CORTICOSTEROIDS that affect carbohydrate metabolism (GLUCONEOGENESIS, liver glycogen deposition, elevation of BLOOD SUGAR), inhibit ADRENOCORTICOTROPIC HORMONE secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system.	Glucocorticoid,Glucocorticoid Effect,Glucorticoid Effects,Effect, Glucocorticoid,Effects, Glucorticoid
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D013973	Thyrotropin-Releasing Hormone	A tripeptide that stimulates the release of THYROTROPIN and PROLACTIN. It is synthesized by the neurons in the PARAVENTRICULAR NUCLEUS of the HYPOTHALAMUS. After being released into the pituitary portal circulation, TRH (was called TRF) stimulates the release of TSH and PRL from the ANTERIOR PITUITARY GLAND.	Protirelin,Thyroliberin,Abbott-38579,Antepan,Proterelin Tartrate,Proterelin Tartrate Hydrate,Protirelin Tartrate (1:1),Relefact TRH,Stimu-TSH,TRH Ferring,TRH Prem,Thypinone,Thyroliberin TRH Merck,Thyrotropin-Releasing Factor,Thyrotropin-Releasing Hormone Tartrate,Abbott 38579,Abbott38579,Hydrate, Proterelin Tartrate,Prem, TRH,Stimu TSH,StimuTSH,TRH, Relefact,Tartrate Hydrate, Proterelin,Thyrotropin Releasing Factor,Thyrotropin Releasing Hormone,Thyrotropin Releasing Hormone Tartrate