Most maternal diseases that affect fetal development probably do so by multiple mechanisms. However, for the purpose of study, it is useful to categorize diseases by mechanism of teratogenesis. Maternal disease can effect fetal development in the following ways: (1) specific effects of metabolic end products or antibodies, (2) placental insufficiency, (3) maternal medications or toxic exposures, (4) infection, and (5) genetic disease. The main focus of this chapter is to discuss maternal disease that has primary effects on fetal development. Placental insufficiency, medication/toxic exposures, infection, and genetic disease are mentioned for the sake of completeness and will be discussed briefly. All maternal illnesses, whether they directly affect the fetus or not, can cause iatrogenic premature delivery in the case of an unstable mother.
Specific fetal effects of over- or underproduced metabolic end products or antibodies
Maternal diseases that cause specific fetal disease can do so by transplacental passage of a toxic maternal metabolic end product (e.g., high glucose or high androgen), by lack of transplacental passage of an essential maternal metabolic end product (e.g., thyroxine), or by transplacental passage of a maternal antibody. Well-studied maternal diseases that are prototypes for the above-described mechanisms of fetal disease include (1) diabetes mellitus, congenital adrenal hyperplasia, and phenylketonuria (toxic metabolic end product), (2) hypothyroidism (maternal underproduction of an essential metabolic end product), and (3) Grave's disease, systemic lupus erythematosus, and rhesus alloimmunization (maternal antibody transfer). There are many other examples of maternal diseases which affect fetal development. However, the above-mentioned prototypic diseases will be discussed below.