Other neonatal outcomes
Table 1 presents the results for other neonatal outcomes. Six studies
evaluated the rate of low birth weight, and we found a reduced risk of
low birth weight involving neuraminidase-inhibitor exposure (OR 0.79,
95% CI 0.68–0.92, P = 0.002; I2 = 0%) (Figure 3A).
Also, oseltamivir exposure during pregnancy was associated with a
reduced risk of low birth weight (OR 0.84, 95% CI 0.71–0.99, P =
0.039; I2 = 0%) (Figure S4A).
We identified five studies reporting low Apgar scores that were eligible
for inclusion. No significant association was detected between
neuraminidase-inhibitor use and a low Apgar score in comparison with
mothers who were not exposed to a neuraminidase inhibitor (OR 0.96, 95%
CI 0.77–1.2, P = 0.733; I2 = 0%) (Figure 3B). When
our analysis was limited to oseltamivir exposure, we observed no
significant association between oseltamivir exposure and a low Apgar
score (OR 0.96, 95% CI 0.74–1.25, P = 0.785; I2 =
0%) (Figure S4B).
Four studies reported the risk of an SGA outcome in relation to
neuraminidase-inhibitor exposure during pregnancy; the combined OR of an
SGA outcome was 0.78 (95% CI 0.69–0.88, P < 0.001;
I2 = 0%) (Figure 3C). Oseltamivir exposure during
pregnancy was associated with a lower risk of an SGA outcome (OR 0.77,
95% CI 0.68–0.88, P < 0.001; I2 = 0%)
(Figure S4C).
We also analyzed the association between neuraminidase-inhibitor
exposure and the preterm birth rate (OR 0.99, 95% CI 0.89–1.09, P =
0.771; I2 = 0%) (Figure 3D). When our analysis was
limited to oseltamivir exposure, we observed no significant association
between oseltamivir exposure and preterm birth (OR 1.03, 95% CI
0.93–1.15, P = 0.542; I2 = 0%) (Figure
S4D).