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    • Antenatal corticosteroids induce fetal lung maturation throu

    2019-04-24

    Antenatal corticosteroids induce fetal lung maturation through the same biological mechanism in low-income settings as in high-income settings and reduce the need for neonatal mechanical ventilation. Although antenatal corticosteroids might not be a so-called magic bullet as a standalone vertical intervention, no biological basis exists to presume that babies born preterm in resource-poor settings will succumb to respiratory distress syndrome any more than do those in resource-rich countries. I support the existing recommendation of a single-course of antenatal corticosteroids to mothers at high risk of preterm birth between 24 weeks and 33 weeks\' gestation, but question Azad and Costello\'s unrealistic prerequisite for round-the-clock access to level 2 care in a low-income setting. Low-income settings, which have the highest burden of preterm neonatal deaths, urgently need proven beneficial interventions, not the assessment of therapeutic efficacy on the basis of resource profiling that could delay treatment. Contrary to Azad and Costello\'s speculation, antenatal corticosteroids are likely to have a greater effect in the absence of level 2 care, not a lesser effect. The difference between low-income and high-income settings is not biology, but an increased burden of disease and reduced access to even basic health care. Our experience in Malawi offers a powerful example for generalising this standard of care to the regions where it nk1 receptor antagonist will save the most lives and also reduce neonatal disability.
    Kishwar Azad and Anthony Costello suggest the use of extreme caution in scaling up of antenatal corticosteroid treatment in low-income settings. They raise three important questions with respect to the efficacy, safety, and the appropriate gestational age at which to give corticosteroids to patients in low-income countries. Firstly, in terms of efficacy, there is high-quality evidence on the benefits of antenatal corticosteroids for lung maturation in utero. A large decrease in neonatal mortality was reported in trials in four middle-income countries, including those in Africa and the Middle East (relative risk [RR] 0·47, 95% CI 0·35–0·64), compared with 14 studies in high-income countries (0·79, 0·65–0·96). Antenatal corticosteroids actually reduced the need for level 2 care, including mechanical ventilation or continuous positive airway pressure in four studies (0·69, 0·53–0·90) and intensive care in two studies (0·80, 0·65–0·99) suggesting that, in regions where mechanical ventilation is not available, substantial benefits could be expected. We agree that more research is needed but in view of the biological basis for the effect of antenatal corticosteroids on infant mortality, G banding is extremely unlikely, statistically, that antenatal corticosteroids would be shown not to work in African or Asian babies. Secondly, we agree with Azad and Costello that potential harm to the patient is always a critical issue. However, a one-off course of antenatal corticosteroids (<48 h) poses a very low risk of adverse effects. The Cochrane systematic review discussed by Azad and Costello shows antenatal corticosteroids are associated with major reductions in, death, severe disability and lower rates of retinopathy of prematurity so their concerns with respect to perinatal death or disability are hard to justify. Repeat antenatal corticosteroids have been linked to learning disabilities compared with a single dose, and late-onset metabolic syndrome might also be a risk. With respect to maternal outcomes there is no robust evidence of increased infections. Because preterm deaths are now the leading cause of child deaths at 1 million per year, the balance lies in the direction of reducing mortality rather than the unknown risks of less severe outcomes. Thirdly, although the proven benefit of antenatal corticosteroids is when they are administered to patients at 28–33 weeks\' gestation, this gestational age band is partly due to enrolment criteria in the original trials. The gestational-age limit for antenatal corticosteroids in high-income countries has been extended with guidelines supporting use at less than 26 weeks\' gestation. More than 85% of preterm infants are born at least 32 weeks\' gestation, and although few have major preterm birth complications, this amounts to a large proportion of infants potentially at risk. The upper gestational-age limit for corticosteroid use is a critical question yet to be answered, especially in health-care settings where mechanical ventilators are not widely available and antenatal corticosteroids are more likely to be life-saving. WHO is presently reviewing the recommended upper and lower gestational-age cutoffs for antenatal corticosteroid treatment. When gestational-age of an infant is unknown or is imprecisely known, the balance of risks needs to be considered and in high mortality settings the balance will be in favour of treatment.