Clinical Information

Estrogens are responsible for the development and maintenance of female sex organs and female secondary sex characteristics. In conjunction with progesterone, they participate in regulation of the menstrual cycle, breast and uterine growth, and in the maintenance of pregnancy.

Estrogens affect calcium homeostasis and have a beneficial effect on bone mass. They decrease bone resorption and, in prepubertal girls, estrogen accelerates linear bone growth. Long-term estrogen depletion is associated with loss of bone mineral content, an increase in stress fractures, and postmenopausal osteoporosis.

The 3 most biologically active estrogens in order of potency are estrone (E1), estradiol (E2), and estriol (E3). Estrogens are produced primarily in the ovary (follicle, corpus luteum), but small quantities are also formed in the testes and in the adrenal cortex. During pregnancy, estrogens are mainly formed in the placenta. About 98% of estradiol is bound to transport proteins (sex hormone-binding globulin) and albumin. Estrogen secretion is biphasic during the menstrual cycle.

The determination of E2 is utilized clinically in the elucidation of fertility disorders in the hypothalamus-pituitary-gonad axis, gynecomastia, estrogen-producing ovarian and testicular tumors, and in hyperplasia of the adrenal cortex. Additional clinical indications are the monitoring of fertility therapy and determining the time of ovulation within the framework of in vitro fertilization.

The laboratory plays an important role in the process of ovulation induction. The principle involves administration of gonadotropins to stimulate follicular growth, followed by human chorionic gonadotropin (hCG) to stimulate ovulation follicular maturation. Clinical, laboratory, and ultrasound monitoring of the treatment cycle is necessary to identify the dose and length of therapy, determine when or whether to administer hCG, and obtain an adequate ovulatory response while avoiding hyperstimulation.