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Old 08-23-2014
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Default Plz Help Superconfused with Klinefelter's Syndrome

Hello everybody
Hope all r doing good with their studyings
I wanna ask ..
How Estrogen is increased in Klinefelter's Syndrome ?
In First Aid It says that Increased LH leads to increased Estrogen .. and Leydig cells have Aromatase
In Kaplan Qbank It's written Increased LH stimulates Leydig cells to Increase Estrogen ..
The thing is inKaplan Physiology It's the Sertoli cells who have the Aromatase and Leydig cells doesn't produce Estrogen ..
And I wanna know if the Leydig cells r defective in Testosterone production ,,how it will produce increased Estrogen , which comes from testosterone !
Did peripheral aromatization has anything to do with it ?
Plz Help
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Old 08-23-2014
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hey was87

it was really concept oriented topic regarding testeosterone and LH, esterogen levels in Klinfelter syndrome.

pathophysio: fibrosis of seminiferous tubules: loss of spermatogenesis, loss of sertoli cells.

loss of serto cells: decreased INHIBIN so as increased FSH.(loss of negative feed back with inhibin)

increased FSH increases synthesis of AROMATASE from LEYDIG cells. so causing more ESTRADIOL formation.

LEYDI cells are prominent in klinfelter synd.


but the main reason underneath increased aromatase and cause of hypogonadism and feminization in Klinfelter is

X-chromosome has genes responsible for ANDROGEN RECEPTOR SYNTHESIS, TESTIS FUNCTION,GROWTH,BRAIN DEVELOPEMNT,

X-chrom has genes with CAG repeats for ANDROGEN RECEP SYNT.

SHORTEST CAG repeats for androgen receptors- TESTOSTERONE binds to ANDROG RECEPT well and hormone functions normally

LONGEST CHAIN OF CAG repeats- TESTO. cant bind to ANDR. so no hormone function. As this will happen in 47XXY Klinfelter synd as SHORTEST CAG repeats gene is inactivated and only longest CAG one is left.

so defective gene for androgen receptor synt. leads to no testosterone binding n no hormone functioning. This will lead to more ESTRADIOL conversion from AROMATASE leading to HYPOGONADISM and feminisation in klinfelter synd.

labs: decreased TESTOSTERONE, increased LH
decreased INHIBIN, increased FSH, increased ESTRADIOL
NO SPERM- AZOO SPERMIA.


hope u understood wt i mean.

Last edited by drneelema; 08-23-2014 at 09:28 PM.
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The above post was thanked by:
DrNewB (08-24-2014), wa87el (08-24-2014)
  #3  
Old 08-24-2014
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Quote:
Originally Posted by drneelema View Post
hey was87

it was really concept oriented topic regarding testeosterone and LH, esterogen levels in Klinfelter syndrome.

pathophysio: fibrosis of seminiferous tubules: loss of spermatogenesis, loss of sertoli cells.

loss of serto cells: decreased INHIBIN so as increased FSH.(loss of negative feed back with inhibin)

increased FSH increases synthesis of AROMATASE from LEYDIG cells. so causing more ESTRADIOL formation.

LEYDI cells are prominent in klinfelter synd.


but the main reason underneath increased aromatase and cause of hypogonadism and feminization in Klinfelter is

X-chromosome has genes responsible for ANDROGEN RECEPTOR SYNTHESIS, TESTIS FUNCTION,GROWTH,BRAIN DEVELOPEMNT,

X-chrom has genes with CAG repeats for ANDROGEN RECEP SYNT.

SHORTEST CAG repeats for androgen receptors- TESTOSTERONE binds to ANDROG RECEPT well and hormone functions normally

LONGEST CHAIN OF CAG repeats- TESTO. cant bind to ANDR. so no hormone function. As this will happen in 47XXY Klinfelter synd as SHORTEST CAG repeats gene is inactivated and only longest CAG one is left.

so defective gene for androgen receptor synt. leads to no testosterone binding n no hormone functioning. This will lead to more ESTRADIOL conversion from AROMATASE leading to HYPOGONADISM and feminisation in klinfelter synd.

labs: decreased TESTOSTERONE, increased LH
decreased INHIBIN, increased FSH, increased ESTRADIOL
NO SPERM- AZOO SPERMIA.


hope u understood wt i mean.
THANK YOU VERY MUCH I REALLY APPRECIATE YOUR HELP
I will write every single word in my First Aid
thank you very much
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