Title: Endocrinology of dysfunctional uterine bleeding: the role of endometrial prostaglandins.

POPLINE Document Number: 017108

Author(s):

Baird DT
Abel MH
Kelly RW
Smith SK

Source citation:

In: Crosignani PG, Rubin BL, ed. Endocrinology of human infertility: new aspects. London, England, Academic Press; New York, Grune and Stratton, 1981. :399-417. (Proceedings of the Serono Clinical Colloquia on Reproduction No. 2)

Abstract:

This paper reviews the hormonal requirements for normal menstruation and the endocrine background of some of the common syndromes associated with dysfunctional uterine bleeding (DUB), and reports studies of the synthesis of prostaglandins (PGs) in the uteri of women with DUB. Normal ovarian function is totally dependent on adequate gonadotropin support from the anterior pituitary. As the levels of estradiol and progesterone decline during luteal regression, the endometrium degenerates and separates and menstrual bleeding starts, but the mechanism by which their withdrawal causes menstruation is unkown. Considerable evidence, described here, has accumulated to implicate PGs in the mechanism of menstruation. According to 1 rather speculative model, as levels of progesterone fall, free arachidonic acid is liberated from phospholipids under the influence of phospholipase enzyme. The main product of arachidonic acid metabolism in late secretory endometrium is PGF2alpha, which causes vasoconstriction and is probably responsible for the intense spasm of the spinal arterioles that precedes menstruation. PGF2alpha drains back to the myometrium via the venous drainage system causing the uterine contractions of menstruation. The maintenance of patency of the arterioles and the inhibition of vascular coagulation response could be due to release of PGI2 synthesized in the intima of the vessel wall from endoperoxides carried to the myometrium from the endometrium. Women with DUB fall into 2 general classes, the anovulatory associated with an inadequate signal such as occurs in polycystic ovary syndrome or insufficient follicle development, or with impaired positive feedback; and the ovulatory, associated with an inadequate or insufficient luteal phase or with idiopathic causes. The clinical conditions and endocrine bases of these disturbances are described. It is suggested that adequate vascular control of blood loss at menstruation is dependent on a pattern of PG production which favors PGF2alpha; the optimal hormonal conditions for PGF2alpha synthesis appear to be priming of the endometrium with both estrogen and progesterone. In the absence of progesterone the markedly reduced PGF2alpha/PGE2 ratio may account for the uncontrolled bleeding and absence of uterine cramps that occur in anovulatory cycles. If the hypothesis presented above regarding PGI2 synthesis is correct, the amount of menstrual blood loss would depend on the balance between PGF2alpha on the 1 hand and PGI2 and PGE2 on the other.

Keywords:

Menstrual Cycle
Bleeding
Prostaglandins
Menstruation Disorders
Menstruation
Gonadotropins, Pituitary
Estradiol
Progesterone
Anovulation
Endometrial Effects
Reproduction
Signs and Symptoms
Diseases
Endocrine System
Physiology
Biology
Gonadotropins
Hormones
Estrogens
Progestational Hormones
Ovarian Effects
Ovary
Genitalia, Female
Genitalia
Urogenital System
Endometrium
Uterus