Placentas in pregnancies complicated by maternal diabetes

PDMs tend to be large and the size is generally in proportion to fetal size. Infarcts are both more numerous and more common in PDMs than in normal placentas. These reflect the in utero hypoxia found in IDMs. Placental infarcts are increased not only in cases of severe DM (classes D, F-R) but also mild and early DM (class A). We infer from this that maternal vascular disease may be present functionally long before pathologic changes can be detected by direct examination of vessels. More subtle evidence of hypoxia in PDMs, such as an increased number of syncytial knots, has been suggested by qualitative data but has not been confirmed by morphometric analysis. Other qualitative observations in PDMs include thickened basement membranes, flattened microvilli on trophoblasts, ectasia of capillaries and villous stromal edema; changes in intracellular organelles and structures include enlarged mitochondria, increased pinocytotic vesicles, and dilated profiles of endoplasmic reticulum. Quantitative morphometric analysis shows no differences between normal placentas and PDMs with regard to these changes. The transport and secretory functions of the placenta, especially important in pregnancy complicated by DM, are not addressed here. As our understanding of placental physiology enlarges, it will be useful to relate each function with its structural counterpart. Perhaps this review will in part provide rational data from which to proceed with the task.