bluestar
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characteristic: amenorrhea, infertility, obesity and hirsutism.
endocrine change: insulin resistance--> increased androgen production--> excess LH. anybody can explain the underlying mechanism of all these endocrine changes? also, is there also a hyperestrogenism as well?
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| Sakaki-
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Yes, there is a hyperestrogenism as well. As for the mechanism, I'm not too sure.
(As for hyperestrogenism, only estrone is elevated; 17-beta-estradiol is usually normal).
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| Gul
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Inc LH :arrow: Inc Testosterone
Obesity(adipose) :arrow: androgen aromatisation :arrow: estrogen
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| bluestar
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Gul, which do you think gets increased first? LH or androgen? according to the textbook, it seems increased androgen causes burst of LH?
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| mani
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would inc testosterone lead to inc LH??
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| Gul
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well, yes .
But about which getting increased 1st, i am getting confused too coz BRS and Goljan are stating the opposite.
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| bluestar
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anyone else knows this better? also who can explain why "insulin resistance--> increased androgen production"?
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| Gul
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THATS FOR YOU BLUESTAR 
Women with PCOS have abnormalities in the metabolism of androgens and estrogen and in the control of androgen production. High serum concentrations of androgenic hormones, such as testosterone, androstenedione, and dehydroepiandrosterone sulfate, may be encountered in these patients. However, significant individual variation exists, and a particular patient might have normal androgen levels. PCOS also is associated with peripheral insulin resistance and hyperinsulinemia, and the degree of both abnormalities is amplified by the presence of obesity. Insulin resistance is not due to defects in insulin binding to the insulin receptors; rather, it involves postbinding signaling pathways. The elevated insulin levels may have gonadotropin-augmenting effects on ovarian function.
A proposed mechanism for anovulation and elevated androgen levels suggests that under the increased stimulatory effect of luteinizing hormone (LH) secreted by the anterior pituitary, stimulation of the ovarian theca cells is increased. In turn, these cells increase the production of androgens (eg, testosterone, androstenedione). Because of a decreased level of follicle-stimulating hormone (FSH), the ovarian granulosa cells are not able to aromatize the androgens to estrogens, leading to decreased estrogen levels and consequent anovulation. Growth hormone (GH) and insulinlike growth factor-1 (IGF-1) also may have an augmenting effect on ovarian function.
Hyperinsulinemia also is responsible for dyslipidemia and elevated levels of plasminogen activator inhibitor 1 (PAI-1) in patients with PCOS. Elevated PAI-1 levels constitute a risk factor for intravascular thrombosis. Polycystic ovaries are enlarged bilaterally and have a smooth thickened capsule that is avascular. On cut section, subcapsular follicles in various stages of atresia are seen in the peripheral part of the ovary. The most striking ovarian feature of PCOS is hyperplasia of the theca stromal cells surrounding arrested follicles. Upon microscopic examination, luteinized theca cells are seen.
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| Sakaki-
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But that mechanism proposes "decreased estrogen levels", which is incorrect.
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| Gul
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So we have to solve this puzzle but thats a fact that there is inc LH and dec FSH.. :? so help us Anyone wiser?
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| suvi21
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Pathogenesis: thought to be increased pit synthesis of LH --inc testosterone from stromal cell---aromatized into estrogen in adipose---hyperestronism--positive feedback on LH and negative feedback on FSH--follicle degeneration and cyst dev
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| Gul
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Thank u soo much for summarizing ... I hope no more complication arises
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| mani
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justa comment, ,even if estrogen wouldnt cause +ve feedback on the LH, even then Lh will be elevated as its excess production is pri factor
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| Sakaki-
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From what I've read, it appears to be quite unclear what the primary factor in PCOS is. That pathogenesis is more of a "vicious cycle" present in PCOS.
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| bluestar
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this is really a complicated problem and seems that no single explanation satifies us all. In summary, the endocrine changes in PCOS is,
:arrow: increase LH--> increase testosterone --> increase estrogen --> decrease FSH and increase LH
:arrow: insulin resistance and hyperinsulinemia
Thank you guys all for participation in discussion!
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| mani
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just 1 more point , perhaps it would add to the controvery. FA says that primary disturbance is increased estrogen production!!
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| bluestar
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ah! well... sometimes I really don't know if we should believe in FA or not. FA makes mistakes yet it's still the Bible we need to obey, isn't it? If FA says increase of estrogen is the primary change then we'll have to go with it. but I still doubt about how FA put it: peripheral estrogen production --> LH increase--> anovulation. how come estrogen increase causes LH increase? I think it would actually "decrease". also, increase of LH should promote ovulation. :roll:
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| Sakaki-
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I'm pretty sure that the increased androgens (ex. androstenedione) are responsible for the decrease in follicular maturation and atresia. Moreover, the ovaries are deficient in aromatase in such an instance.
As for estrogen increasing LH production, I was curious about that as well. I'm supposing that it might have something to do with the tonically high levels of estrogen. I'm aware that estradiol isn't elevated, but apparently, the biologically active fraction is (due to decreased SHBG); this may stimulate GnRH pulsatility and produce tonically elevated LH levels.
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| syedaAsma
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could u please give reference
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| Sakaki-
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I'm pretty sure that you can find PCOS in any gynecology textbook. Comprehensive gynecology (the big one - I don't remember the authors) has a good section on it; I found the diagram of the "vicious cycle" in there.
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