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1.
BMJ ; 367: l6131, 2019 11 20.
Artigo em Inglês | MEDLINE | ID: mdl-31748223

RESUMO

OBJECTIVE: To evaluate if induction of labour at 41 weeks improves perinatal and maternal outcomes in women with a low risk pregnancy compared with expectant management and induction of labour at 42 weeks. DESIGN: Multicentre, open label, randomised controlled superiority trial. SETTING: 14 hospitals in Sweden, 2016-18. PARTICIPANTS: 2760 women with a low risk uncomplicated singleton pregnancy randomised (1:1) by the Swedish Pregnancy Register. 1381 women were assigned to the induction group and 1379 were assigned to the expectant management group. INTERVENTIONS: Induction of labour at 41 weeks and expectant management and induction of labour at 42 weeks. MAIN OUTCOME MEASURES: The primary outcome was a composite perinatal outcome including one or more of stillbirth, neonatal mortality, Apgar score less than 7 at five minutes, pH less than 7.00 or metabolic acidosis (pH <7.05 and base deficit >12 mmol/L) in the umbilical artery, hypoxic ischaemic encephalopathy, intracranial haemorrhage, convulsions, meconium aspiration syndrome, mechanical ventilation within 72 hours, or obstetric brachial plexus injury. Primary analysis was by intention to treat. RESULTS: The study was stopped early owing to a significantly higher rate of perinatal mortality in the expectant management group. The composite primary perinatal outcome did not differ between the groups: 2.4% (33/1381) in the induction group and 2.2% (31/1379) in the expectant management group (relative risk 1.06, 95% confidence interval 0.65 to 1.73; P=0.90). No perinatal deaths occurred in the induction group but six (five stillbirths and one early neonatal death) occurred in the expectant management group (P=0.03). The proportion of caesarean delivery, instrumental vaginal delivery, or any major maternal morbidity did not differ between the groups. CONCLUSIONS: This study comparing induction of labour at 41 weeks with expectant management and induction at 42 weeks does not show any significant difference in the primary composite adverse perinatal outcome. However, a reduction of the secondary outcome perinatal mortality is observed without increasing adverse maternal outcomes. Although these results should be interpreted cautiously, induction of labour ought to be offered to women no later than at 41 weeks and could be one (of few) interventions that reduces the rate of stillbirths. TRIAL REGISTRATION: Current Controlled Trials ISRCTN26113652.


Assuntos
Idade Gestacional , Doenças do Recém-Nascido , Trabalho de Parto Induzido , Conduta Expectante/estatística & dados numéricos , Adulto , Cesárea/estatística & dados numéricos , Feminino , Humanos , Lactente , Mortalidade Infantil , Recém-Nascido , Doenças do Recém-Nascido/epidemiologia , Doenças do Recém-Nascido/etiologia , Análise de Intenção de Tratamento , Trabalho de Parto Induzido/efeitos adversos , Trabalho de Parto Induzido/métodos , Trabalho de Parto Induzido/estatística & dados numéricos , Gravidez , Resultado da Gravidez/epidemiologia , Natimorto/epidemiologia , Suécia/epidemiologia , Nascimento a Termo
2.
Brain Behav Immun ; 37: 95-102, 2014 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-24240022

RESUMO

Preterm birth is very strongly associated with maternal/foetal inflammation and leads to permanent neurological deficits. These deficits correlate with the severity of white matter injury, including maturational arrest of oligodendrocytes and hypomyelination. Preterm birth and exposure to inflammation causes hypothyroxinemia. As such, supplementation with thyroxine (T4) seems a good candidate therapy for reducing white matter damage in preterm infants as oligodendrocyte maturation and myelination is regulated by thyroid hormones. We report on a model of preterm inflammation-induced white matter damage, in which induction of systemic inflammation by exposure from P1 to P5 to interleukin-1ß (IL-1ß) causes oligodendrocyte maturational arrest and hypomyelination. This model identified transient hypothyroidism and wide-ranging dysfunction in thyroid hormone signalling pathways. To test whether a clinically relevant dose of T4 could reduce inflammation-induced white matter damage we concurrently treated mice exposed to IL-1ß from P1 to P5 with T4 (20 µg/kg/day). At P10, we isolated O4-positive pre-oligodendrocytes and gene expression analysis revealed that T4 treatment did not recover the IL-1ß-induced blockade of oligodendrocyte maturation. Moreover, at P10 and P30 immunohistochemistry for markers of oligodendrocyte lineage (NG2, PDGFRα and APC) and myelin (MBP) similarly indicated that T4 treatment did not recover IL-1ß-induced deficits in the white matter. In summary, in this model of preterm inflammation-induced white matter injury, a clinical dose of T4 had no therapeutic efficacy. We suggest that additional pre-clinical trials with T4 covering the breadth and scope of causes and outcomes of perinatal brain injury are required before we can correctly evaluate clinical trials data and understand the potential for thyroid hormone as a widely implementable clinical therapy.


Assuntos
Encéfalo/efeitos dos fármacos , Encefalite/prevenção & controle , Fibras Nervosas Mielinizadas/efeitos dos fármacos , Oligodendroglia/efeitos dos fármacos , Tiroxina/uso terapêutico , Animais , Encéfalo/crescimento & desenvolvimento , Modelos Animais de Doenças , Expressão Gênica , Interleucina-1beta/toxicidade , Masculino , Camundongos , Fibras Nervosas Mielinizadas/metabolismo
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