Introduction

Abstract

Pregnancy is a time of marked hormonal and immunological changes. Not only is there a disruption of the monthly alterations of FSH, LH, estrogen, and progesterone that accompany the menstrual cycle, but new hormonal and immune homeostasis is achieved. Simultaneously, new hormones are produced which have important metabolic impacts. Specifically, the placenta produces human chorionic gonadotropin (hCG) and human placental lactogen (HPL), both of which are critical to the progression of a normal pregnancy. However, both have unintended metabolic consequences. Human chorionic gonadotropin and thyrotropin-stimulating hormone (TSH) are composed of an alpha and beta subunit. The alpha subunit is identical in hCG and TSH, while the beta subunit in the two hormones shares approximately 85 % homology. Consequently, as hCG rises in the first trimester, it crossreacts with the TSH receptor resulting in a decrease in TSH levels and a constriction of the normal TSH range to 0.1–2.5 mIU/ml. Human placental lactogen peaks later in pregnancy and has the unintended impact of increasing insulin resistance. The selective immunosuppression which accompanie s pregnancy has a direct impact on autoimmune diseases by impacting the titer of the etiological antibody. The present chapter discusses three common endocrinological abnormalities that are related to the hormonal and immunological perturbations of pregnancy. Specifically, this chapter will focus on a metabolic disorder which impedes a woman’s ability to become pregnant (polycystic ovarian syndrome), impacts the natural course of the disease (Graves’ disease), or results in the new onset of a disease state (gestational diabetes mellitus).