Maternal asthma and placental morphometry: effects of severity, treatment and fetal sex.

Asthma is the most common respiratory disease to complicate pregnancy. Although adverse effects on the fetus have been documented, there is a paucity of information regarding the effects of asthma, and its treatment, on placental morphology. The aim of this study was to test for volumetric differences in placental composition between non-asthmatic pregnancies and those associated with maternal asthma grouped according to asthma severity and glucocorticoid (GC) treatment. Each placenta was weighed and random samples of tissue were fixed in formalin-saline, embedded in wax and analysed by design-based stereology. Volume densities of parenchymal compartments (peripheral villi and maternal intervillous space) and residual non-parenchyma were estimated by test point counting and converted to absolute volumes by taking into account placental size. Relative and absolute lengths of villi and capillaries were also estimated and used to derive secondary quantities related to villous capillarization and maturation. Between-group comparisons were drawn by two-way analysis of variance with group and fetal sex as the principal factors. Compared to non-asthmatic controls, asthmatics had reduced absolute volumes of fetal capillaries which was most marked in those with moderate/severe asthma and those using low and high doses of inhaled GCs. Changes in the total length and mean cross-sectional area of capillaries and peripheral villi were also observed. Lengths were greater in mild asthmatics and lowest in those with high GC usage. Calibre areas were lower in mild asthmatics and villous calibres in the high GC group were greater than those in asthmatics not taking GCs. Those making greatest use of inhaled GCs also had villi which were hypovascularized in terms of capillary:villus length ratios. The findings suggest that the morphometric differences in fetoplacental vascularity are likely to be due to the effects of asthma and use of inhaled GCs rather than the effects of maternal or fetal hypoxic stress.