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Polycystic Ovarian Disease — Current Concepts
Author(s) -
Biggs J. S. G.
Publication year - 1981
Publication title -
australian and new zealand journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.734
H-Index - 65
eISSN - 1479-828X
pISSN - 0004-8666
DOI - 10.1111/j.1479-828x.1981.tb00120.x
Subject(s) - polycystic ovarian disease , infertility , polycystic ovary , medicine , endocrinology , follicular phase , luteinizing hormone , hirsutism , androgen , congenital adrenal hyperplasia , endocrine system , hormone , biology , insulin , pregnancy , insulin resistance , genetics
Summary: The Stein Leventhal syndrome, now commonly referred to as polycystic ovarian disease (PCOD) has provided a focus for application of new methods of investigation of the ovary. The first description of the condition referred to 7 women; subsequent large‐scale studies have confirmed menstrual irregularity, hirsutism and infertility as the principal symptoms. PCOD has been shown to be associated with certain histopathological changes in the ovaries, notably capsular thickening, subcapsular follicular cysts and hyperplasia of the theca interna, with or without follicular atresia. The development of urine hormone assays allowed the endocrine basis of PCOD to be described. Urine determinations have now been largely replaced by assays in blood and profiles of hormone changes in PCOD have been proposed. The significant changes are high, fluctuating levels of luteinizing hormone, raised oestrone and androgen concentrations. Oestradiol and follicle stimulating hormone levels are often reduced. Other abnormalities underlying PCOD include defects in steroidogenic enzymes, especially aromatase, this leading to blocked conversion of oestrogen precursors and a resulting accumulation of androgenic steroids. The origin of the disease is unknown. The abnormal gonadotrophin release which is found, however, leads to deficient follicular development and androgen excess at the expense of oestradiol production. The disordered gonadal steroid secretion results in altered pituitary sensitivity to gonadotrophin releasing hormone and abnormal gonadotrophin production. Once established, the disease is self‐perpetuating. Current management problems include the uncertain value of ovarian resection, the best method of treatment where infertility is no longer a problem, and the risks of endometrial cancer in the presence of chronically‐raised endogenous oestrogen levels. The inadequacy of treatment of hirsutism in these women is a particular problem. More work is needed to establish the factors which initiate PCOD and to resolve the problems in its management.