sodium cromoglycate. This effect was not due to a difference between the patients, since when we recalculated the results using the same 11 subjects for both placebo and sodium cromoglycate they were the same. Sodium cromoglycate has a slight phosphodiesterase inhibiting effect, which might explain the differences' 0; however, it has no effect on the histamine response of human bronchial smooth muscle.' We have also shown that sodium cromoglycate has no effect on tracheal smooth-muscle contraction induced by histamine or methacholine."1 It does, however, inhibit allergen contraction of the passively sensitised human tracheal smooth muscles.Our results of the lack of effect of sodium cromoglycate on histamine challenge are consistent with those of Pagelow.'2 He found no difference in the threshold of histamine bronchial reactivity with sodium cromoglycate or phentolamine. In contrast, Kerr et alt7 reported complete protection against histamine with both these agents. We have studied the effect of sodium cromoglycate in vitro on the alpha-receptor contraction of isolated human trachea induced by adrenaline in the presence of propranolol. In this system we are unable to show any inhibition by sodium cromoglycate of alpha-receptor contraction.13

Objective To assess the effect of maternal sildenafil therapy on fetal growth in pregnancies with early-onset fetal growth restriction.Design A randomised placebo-controlled trial.Setting Thirteen maternal-fetal medicine units across New Zealand and Australia.Population Women with singleton pregnancies affected by fetal growth restriction at 22 +0 to 29 +6 weeks.Methods Women were randomised to oral administration of 25 mg sildenafil citrate or visually matching placebo three times daily until 32 +0 weeks, birth or fetal death (whichever occurred first). Main Outcome MeasuresThe primary outcome was the proportion of pregnancies with an increase in fetal growth velocity. Secondary outcomes included live birth, survival to hospital discharge free of major neonatal morbidity and pre-eclampsia.Results Sildenafil did not affect the proportion of pregnancies with an increase in fetal growth velocity; 32/61 (52.5%) sildenafil-treated, 39/57 (68.4%) placebo-treated [adjusted odds ratio (OR) 0.49, 95% CI 0.23-1.05] and had no effect on abdominal circumference Z-scores (P = 0.61). Sildenafil use was associated with a lower mean uterine artery pulsatility index after 48 hours of treatment (1.56 versus 1.81; P = 0.02). The live birth rate was 56/63 (88.9%) for sildenafil-treated and 47/59 (79.7%) for placebo-treated (adjusted OR 2.50, 95% CI 0.80-7.79); survival to hospital discharge free of major neonatal morbidity was 42/63 (66.7%) for sildenafil-treated and 33/59 (55.9%) for placebo-treated (adjusted OR 1.93, 95% CI 0.84-4.45); and newonset pre-eclampsia was 9/51 (17.7%) for sildenafil-treated and 14/55 (25.5%) for placebo-treated (OR 0.67, 95% CI 0.26-1.75).Conclusions Maternal sildenafil use had no effect on fetal growth velocity. Prospectively planned meta-analyses will determine whether sildenafil exerts other effects on maternal and fetal/neonatal wellbeing.Keywords Fetal growth restriction, intrauterine growth restriction, pre-eclampsia, sildenafil, small for gestational age, uterine artery Doppler.Tweetable abstract Maternal sildenafil use has no beneficial effect on growth in early-onset FGR, but also no evidence of harm.

A PPC has a low diagnostic yield and is associated with a significant complication rate. While the therapeutic benefit of this procedure is unclear, expectant management is appropriate especially in the presence of pelvic sepsis.

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