Ovarian failure including menopause, premature menopause, and resistant ovarian syndrome, and hormonal replacement

E. Katz, H. D. McClamrock, E. Y. Adashi

Research output: Contribution to journalReview articlepeer-review


The human female fetus is endowed with a finite number of germ cells. On arrival on the genital ridge, these cells are surrounded by a single layer of granulosa cells. The resulting structure, the primordial follicle, reaches its peak number at midgestation. For reasons not yet understood, the number of such units declines thereafter. As the ovary ages, a tendency toward less-ordered follicles, a gradual diminution of primordial follicles containing oocytes, and an increased conversion of thecal cells into stromal cells occur. Finally, the remaining follicles, unresponsive to increasing levels of gonadotropins, produce low circulating estrogen levels that are insufficient to stimulate endometrial growth. Menopause is defined as the cessation of menses associated with age. This event occurs at a remarkably consistent age, with a mean, median, and mode of 50±1.5 years. Because a total exhaustion of primordial follicles rarely is seen in natural menopause, the loss of the ovarian capacity to respond to gonadotropins appears to play an essential role in bringing about menopause. Menopause is considered 'premature' when ovarian failure occurs before the age of 40 years. This article briefly reviews the etiology of premature ovarian failure, discusses the consequences of the resultant hypoestrogenism at any age, and describes the strategies to prevent such consequences.

Original languageEnglish (US)
Pages (from-to)392-397
Number of pages6
JournalCurrent Opinion in Obstetrics and Gynecology
Issue number3
StatePublished - Jan 1 1990

ASJC Scopus subject areas

  • Obstetrics and Gynecology


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