Step I Steroid synthesis

[Apoplexy__]

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I learned from BRS physio that LH upregulates cholesterol desmolase in Leydig cells just as ACTH does in the adrenals. My understanding was that Leydig cells don't have 21-hydroxylase so they can only go down the androgen pathway.

So then I just got a question wrong in UWorld saying that a kid had elevated 17-hydroxyprogesterone and testosterone. You had to know that 17-hydroxyprogesterone would only be increased in androgens of adrenal origin, not testicular origin. I figured Leydig cells would also have increased 17-hydroxyprogesterone based on my BRS Physio knowledge. Guess I'm wrong...can anyone explain? Does that apply to 17-hydroxyprenenolone too?

 

[Apoplexy__]

Actually, this answers my question (taken from BRS Physio). 17-hydroxyprogesterone is adrenal-specific, but 17-hydroxypregnenolone exists in the gonads.

I guess I'll leave the thread up in case anyone else had the same question.

 

[CherryRedDracul]

17-hydroxyprogesterone is also produced by gonads. But a massive jump in 17-hydroxyprogesterone is seen in 21-hydroxylase because the adrenals are trying to push for mineralocorticoid and glucocorticoid synthesis, revving up 17-hydroxyprogesterone production. The same thing doesn't happen in the gonads because they don't produce those other steroids hormones, hence no need to do a thang.

 

[Apoplexy__]

17-hydroxyprogesterone is also produced by gonads. But a massive jump in 17-hydroxyprogesterone is seen in 21-hydroxylase because the adrenals are trying to push for mineralocorticoid and glucocorticoid synthesis, revving up 17-hydroxyprogesterone production. The same thing doesn't happen in the gonads because they don't produce those other steroids hormones, hence no need to do a thang.

Hm...you sure? The excerpt below is from the UWorld explanation of the question, which had Leydig cell hyperplasia and LH-secreting pituitary adenoma as answer choices:

Leydig cell hyperplasia would result in masculinization due to excessive production of testosterone, androstenedione, and DHEA. However, there would be no excess of the adrenal hormone 17-hydroxyprogesterone. Pituitary adenomas producing excessive LH and FSH would result in increased testosterone levels but would not increase 17-hydroxyprogesterone levels.

 

[notbobtrustme]

LH secreting adenoma is too rare even for Step 1.

exact words from a professor.

 

[CherryRedDracul]

Hm...you sure? The excerpt below is from the UWorld explanation of the question, which had Leydig cell hyperplasia and LH-secreting pituitary adenoma as answer choices:

Leydig cell hyperplasia would result in masculinization due to excessive production of testosterone, androstenedione, and DHEA. However, there would be no excess of the adrenal hormone 17-hydroxyprogesterone. Pituitary adenomas producing excessive LH and FSH would result in increased testosterone levels but would not increase 17-hydroxyprogesterone levels.

UWorld is discussing significant and abnormal elevations of 17-hydroxyprogesterone. Our gonads naturally produce a low baseline of 17-hydroxyprogesterone because nothing's stopping 17a-hydroxylase from converting progesterone to it.

*WARNING this is ultra low-yield stuff I'm about to mention*: LH, in general, upregulates 3beta-hydroxysteroid dehydrogenase, resulting in small elevations of 17-hydroxyprogesterone, but it stills remains within normal ranges. Leydig cell tumors usually present with normal 17-hydroxyprogesterone levels, but in some cases, can be slightly elevated, but nowhere near congenital adrenal hyperplasia levels. Again, what I just mentioned is ultra low-yield. Read it once, then fuhgeddaboudit.

 

[Apoplexy__]

UWorld is discussing significant and abnormal elevations of 17-hydroxyprogesterone. Our gonads naturally produce a low baseline of 17-hydroxyprogesterone because nothing's stopping 17a-hydroxylase from converting progesterone to it.

*WARNING this is ultra low-yield stuff I'm about to mention*: LH, in general, upregulates 3beta-hydroxysteroid dehydrogenase, resulting in small elevations of 17-hydroxyprogesterone, but it stills remains within normal ranges. Leydig cell tumors usually present with normal 17-hydroxyprogesterone levels, but in some cases, can be slightly elevated, but nowhere near congenital adrenal hyperplasia levels. Again, what I just mentioned is ultra low-yield. Read it once, then fuhgeddaboudit.

Thanks for the clarification. Man you're right, I'm just going to forget about that and remember: Elevated 17-OH progesterone in the stem of a question = 21-hydroxylase/11-hydroxylase deficiency.