Can polycystic ovary syndrome exist without concomitant hypothalamic dysfunction?
Polycystic ovary syndrome describes a conformational ovarian state that may be the final common manifestation of several pathogenic pathways. Because the ovarian thecal and stromal hyperplasia characteristic of polycystic ovarian (PCO) morphology depends upon relative LH excess while follicular arrest requires a relative deficiency of FSH, it is likely that the PCO morphology cannot be expressed or maintained without both prior and concomitant exposure to the characteristic alterations in hypothalamic-pituitary secretion. Although increased LH and decreased FSH secretion are hypothesized to be integral to the expression of this morphological state and, in this limited sense, causal, this dependence does not necessarily mean that hypothalamic alterations are the primary etiology of this syndrome. However, recognition of the relationship between gonadotropin secretory alterations and the development of the PCO state does have treatment implications.
Berga
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SL
Department of Obstetrics, University of Pittsburgh School of Medicine, Magee-Womens Hospital, Pennsylvania 15213-3180, USA.
Daniels
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TL
D005260:Female; D005640:Follicle Stimulating Hormone / Q000502:physiology; D007987:Gonadotropin-Releasing Hormone / Q000502:physiology; D006801:Humans; D006965:Hyperplasia; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology / Q000503:physiopathology*; D007031:Hypothalamus / Q000502:physiology / Q000503:physiopathology*; D007986:Luteinizing Hormone / Q000378:metabolism; D010053:Ovary / Q000473:pathology / Q000503:physiopathology; D011085:Polycystic Ovary Syndrome / Q000503:physiopathology* / Q000628:therapy
D007987:Gonadotropin-Releasing Hormone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone