Androgen Excess Disorders in Women: Polycystic Ovary by Ricardo Azziz (auth.), Ricardo Azziz MD, MPH, MBA, John E.

By Ricardo Azziz (auth.), Ricardo Azziz MD, MPH, MBA, John E. Nestler MD, Didier Dewailly MD (eds.)

The box of androgen extra problems has complex considerably because the unique book of this ebook. The Androgen extra Society (AES) was once based to compile investigators within the box. a greater knowing of the screening, development, and molecular genetics of nonclassic adrenal hyperplasia (NCAH) has enhanced the medical care and diagnostic accuracy of those sufferers. New standards for the prognosis of the polycystic ovary syndrome (PCOS) have been proposed in Rotterdam, standards that experience ended in controversy and, confidently, initiation of latest reports. The organization of insulin resistance with PCOS has been bolstered, and the position of metformin in tre- ing the infertility of the PCOS has been tested. hazards for diabetes and, extra cont- versially, heart problems in girls with PCOS have bought mammoth research. Our realizing of the epidemiology and financial impression of those problems has accelerated, emphasizing their severe significance. those are yet a couple of highlights of ways the terrain has replaced in a comparatively short time period. in response to those advances, the identify of this e-book has been revised to mirror the growing to be value of PCOS because the so much well-known androgen extra illness in girls, and arguably, because the person who may need the main critical adversarial effects for basic healthiness. There are fewer chapters to supply a extra centred elucidation of the realm. numerous chapters have been penned via new (and younger) authors who're accomplishing state of the art examine within the field.

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The severe form of this common genetic disease can be fatal. Compromised cortisol and aldosterone synthesis can lead to hyponatremia, hyperkalemia, hypotension, and circulatory collapse, leading to death within the first month of life if not treated appropriately. Decreased cortisol production in utero results in a compensatory increase in ACTH, with consequent overstimulation of the adrenal steroid biosynthesis. 17-OHP levels rise in the face of impaired 21hydroxylation and the limited ability of P450c17 to convert 17-OHP to androstenedione.

P450scc, encoded by a single gene on chromosome 15 (14), possesses a single active site in contact with the hydrophobic lipid bilayer of the inner mitochondrial membrane. Deletion of the gene for P450scc in rabbits eliminates all steroidogenesis (15), indicating that all steroid hormone biosynthesis is initiated through the action of this one enzyme. Haploinsufficiency of P450scc as a result of de novo heterozygous mutation causes a late-onset form of congenital lipoid adrenal hyperplasia (16,17).

Germ cell differentiating factor-9, expressed by the oocyte throughout folliculogenesis, appears to promote granulosa cell differentiation, stimulate theca cells, and inhibit luteal cell formation (67). Insulin-like growth factors appear to enhance responses to FSH. Both insulin-like growth factor (IGF)-1 and IGF-2 can increase granulosa cell proliferation and estradiol secretion, but only IGF-2 mRNA is expressed in the ovary, particularly in the granulosa cells (68). Women with IGF-1 deficiency can be induced to ovulate by stimulation with gonadotropins (69), consistent with the view that IGF-1 is not required for folliculogenesis.

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