Breast Changes during Pregnancy

Key points
- In experimental studies, these effects are observed when estrogen and progesterone cause a release of prolactin by reducing the hypothalamic release of prolactin-inhibiting factor (PIF).
- In the first 3 to 4 weeks of pregnancy, marked ductular sprouting occurs with some branching, and lobular formation occurs under estrogenic influence.
- At the beginning of the second trimester, the mammary alveoli, but not the milk ducts, lose the superficial layer of A cells.
- Lactation After parturition, an immediate withdrawal of placental lactogen and sex steroid hormones occurs.
During pregnancy, marked ductular, lobular, and alveolar growth occurs as a result of the influence of luteal and placental sex steroids, placental lactogen, prolactin, and chorionic gonadotropin (Fig. 1-4B). In experimental studies, these effects are observed when estrogen and progesterone cause a release of prolactin by reducing the hypothalamic release of prolactin-inhibiting factor (PIF). Prolactin in humans is also released progressively during pregnancy and probably stimulates epithelial growth and secretion. Prolactin increases slowly during the first half of pregnancy; during the second and third trimesters, blood levels of prolactin are three to five times higher than normal, and mammary epithelium initiates protein synthesis.
In the first 3 to 4 weeks of pregnancy, marked ductular sprouting occurs with some branching, and lobular formation occurs under estrogenic influence. At 5 to 8 weeks, breast enlargement is significant, with dilatation of the superficial veins, heaviness, and increasing pigmentation of the nipple–areolar complex. In the second trimester, lobular formation exceeds ductular sprouting under progestogenic influence. The alveoli contain colostrum but no fat, which is secreted under the influence of prolactin. From the second half of pregnancy onward, increasing breast size results not from mammary epithelial proliferation but from increasing dilatation of the alveoli with colostrum, as well as from hypertrophy of myoepithelial cells, connective tissue, and fat. If these processes are interrupted by early delivery, lactation may be adequate from 16 weeks of pregnancy onward.
At the beginning of the second trimester, the mammary alveoli, but not the milk ducts, lose the superficial layer of A cells. Before this, as in the nonpregnant woman, the two-layer structure is maintained. In the second and third trimesters, this monolayer differentiates into a colostrum–cell layer and accumulates eosinophilic cells, plasma cells, and leukocytes around the alveoli. As pregnancy continues, colostrum, composed of desquamated epithelial cells, accumulates. Aggregations of lymphocytes, round cells, and desquamated phagocytic alveolar cells (foam cells) may be found in colostrum; these are termed the Donne corpuscles.
Lactation
After parturition, an immediate withdrawal of placental lactogen and sex steroid hormones occurs. During pregnancy, these hormones antagonize the effect of prolactin on mammary epithelium. Concomitant to the abrupt removal of the placental hormones, luteal production of the sex steroid hormones also ceases. A nadir is reached on the fourth to fifth day postpartum; at this time, the secretion of PIF from the hypothalamus into the hypothalamoadenohypophyseal portal system decreases. This reduction in PIF secretion allows the transmembrane secretion of prolactin by pituitary lactotrophs. Sex steroid hormones are not necessary for successful lactation, and physiologic increases, such as may occur with postpartum ovulatory cycles, do not inhibit it.
Written and revised by
Andrey Nailor, M.D.
Our doctors write and review articles for accuracy and keep them up to date.
health.am provides general information, not medical advice. Always consult a qualified health professional about your own health.
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