Polycystic ovarian disease as a neuroendocrine disorder of the female reproductive axis.
Despite many years of investigation, the benign syndrome(s) of hyperandrogenic amenorrhea, commonly known as PCOD, remains an enigma. Although hyperinsulinemia and hyperandrogenemia from any cause may produce many of the signs and symptoms common to PCOD secondarily, there exists a subset of patients in whom the major abnormality is neuroendocrine. These patients have a gonadotropin profile characterized by an elevated amplitude of LH pulsations in association with normal to low levels of FSH and a fast frequency of pulsatile LH secretion. A major question still remaining is whether the neuroendocrine abnormality is primary or secondary to abnormal ovarian feedback by androgens, or more likely, estrogens. Some evidence suggests that the pattern of secretion of LH and FSH from the pituitary may be owing solely to an increased frequency of GnRH stimulation, but there is little evidence of a specific primary abnormality of neurotransmitters. Subsequent studies in which the various subgroups of PCOD are carefully delineated will be required to clarify these relationships and in so doing provide patients with optimal therapeutic choices.
Hall
J E
JE
Department of Medicine, Harvard Medical School, Boston, Massachusetts.
D004702:Endocrine Glands / Q000503:physiopathology*; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology; D006065:Gonadotropins, Pituitary / Q000502:physiology; D006801:Humans; D009420:Nervous System / Q000503:physiopathology*; D018377:Neurotransmitter Agents / Q000502:physiology; D010053:Ovary / Q000503:physiopathology; D011085:Polycystic Ovary Syndrome / Q000503:physiopathology*
D012739:Gonadal Steroid Hormones; D006065:Gonadotropins, Pituitary; D018377:Neurotransmitter Agents