title: Gonadal and adrenal androgen secretion in hirsute females.
abstract: The pathophysiology of glandular androgen hypersecretion must be regarded as a continuous process without sharp borderlines from normal to non-tumorous conditions, such as polycystic ovaries and hyperthecosis, to neoplastic disease. Hirsutism and related symptoms are most often caused by excess androgens of ovarian and/or adrenal origin, i.e. testosterone, dihydrotestosterone, delta 4-androstenedione, dehydroepiandrosterone and its sulphate. As demonstrated by selective catheterization of glandular effluents, combined hypersecretion occurs more frequently then either purely gonadal or adrenal overproduction. No correlation can be found between the type, frequency and extent of hormonal changes and the clinical, laparoscopic, angiographic, or histological findings. Dynamic function tests do not reliably discriminate between the various aetiological subgroups due to extremely variable and even non-specific individual responsiveness. Selective catheterization is presently the most sensitive method for the preoperative identification and localization of androgen-secreting neoplasms.
mesh_terms: D000310:Adrenal Gland Neoplasms / Q000378:metabolism; D000311:Adrenal Glands / Q000378:metabolism*; D000728:Androgens / Q000378:metabolism*; D000735:Androstenedione / Q000378:metabolism; D002404:Catheterization; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives / Q000378:metabolism; D019314:Dehydroepiandrosterone Sulfate; D013196:Dihydrotestosterone / Q000378:metabolism; D005260:Female; D006628:Hirsutism / Q000503:physiopathology*; D006801:Humans; D010051:Ovarian Neoplasms / Q000378:metabolism; D010053:Ovary / Q000378:metabolism*; D011085:Polycystic Ovary Syndrome / Q000503:physiopathology; D013739:Testosterone / Q000378:metabolism
chemical_list: D000728:Androgens; D013196:Dihydrotestosterone; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate