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CASE STUDY

CASE STUDY

A 25-year-old woman with menarche at 13 years and menstrual periods until about 1 year ago complains of hot flushes, skin and vaginal dryness, weakness, poor sleep, and scanty and infrequent menstrual periods of a year’s duration. She visits her gynecologist, who obtains plasma levels of follicle-stimulating hormone and luteinizing hormone, both of which are moderately elevated. She is diagnosed with premature ovarian failure, and estrogen and progesterone replacement therapy is recommended. A dual-energy absorptiometry scan (DEXA) reveals a bone density t-score of <2.5 SD, ie, frank osteoporosis. How should the ovarian hormones she lacks be replaced? What extra measures should she take for her osteoporosis while receiving treatment?

THE OVARY (ESTROGENS, PROGESTINS, OTHER OVARIAN HORMONES, ORAL CONTRACEPTIVES, INHIBITORS & ANTAGONISTS, & OVULATION-INDUCING AGENTS)

The ovary has important gametogenic functions that are integrated with its hormonal activity. In the human female, the gonad is relatively quiescent during childhood, the period of rapid growth and maturation. At puberty, the ovary begins a 30- to 40-year period of cyclic function called the menstrual cycle because of the regular episodes of bleeding that are its most obvious manifestation. It then fails to respond to gonadotropins secreted by the anterior pituitary gland, and the cessation of cyclic bleeding that occurs is called menopause.

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ACRONYMS

CBG

Corticosteroid-binding globulin (transcortin)

DHEA

Dehydroepiandrosterone

DHEAS

Dehydroepiandrosterone sulfate

ERE

Estrogen response element

FSH

Follicle-stimulating hormone

GnRH

Gonadotropin-releasing hormone

HDL

High-density lipoprotein

HRT

Hormone replacement therapy (also called HT)

LDL

Low-density lipoprotein

LH

Luteinizing hormone

PRE

Progesterone response element

SERM

Selective estrogen receptor modulator

SHBG

Sex hormone-binding globulin

TBG

Thyroxine-binding globulin

The mechanism responsible for the onset of ovarian function at the time of puberty is thought to be neural in origin, because the immature gonad can be stimulated by gonadotropins already present in the pituitary and because the pituitary is responsive to exogenous hypothalamic gonadotropin-releasing hormone (GnRH). Despite extensive research in the field, the mechanism of puberty initiation still remains an enigma. Pulsatile pituitary gonadotropin secretion under the guidance of GnRH definitely constitutes a sine qua non for pubertal onset. However, the secretion of GnRH in the human hypothalamus is regulated by kisspeptin and its receptor, as well as by permissive or opposing signals mediated by neurokinin B and dynorphin acting on their respective receptors. These three supra-GnRH regulators compose the Kisspeptin, Neurokinin B, and Dynorphin neuron (KNDy) system, a key player in pubertal onset and progression. Recently, makorin ring finger protein 3 (MKRN3) was also implicated in pubertal onset by contributing to the regulation of the KNDy system. However, the inhibitory (gamma-amino butyric acid, neuropeptide Y, and RFamide-related peptide-3) and stimulatory (glutamate) signals acting upstream of KNDy call into question the primary role of MKRN3 as the gatekeeper of puberty. Recently, epigenetic mechanisms involving derepression of genes, such as that of kisspeptin, have ...

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