Hypopituitary

[TheStrangeOne]

I have congenital hypopitruitaryism and have been on HGH since a toddler and T since a teenager.

Over the years the preparation of the T has changed either because of new technologies or because my levels have been low.

Up until recently I was on Nebido on a 12 weekly basis and everything was fine other than my haemoglobin levels had started to rise too high.

So change of Dr and some life decisions later the Dr decides to stop the T with the intention of initially putting me on LH and once T levels restored then onto FSH.

There has been a slight problem though in that 5 months after my last 12 weekly T injection my T levels are still at 14.8 but both LH and FSH could not be detected.

The Dr is at a loss and says just to keep waiting and hoping the T continues to drop as he cannot start the LH/ FSH until they are below 8.

Anyone have any ideas?

 

[Structure]

I have congenital hypopitruitaryism and have been on HGH since a toddler and T since a teenager.

Over the years the preparation of the T has changed either because of new technologies or because my levels have been low.

Up until recently I was on Nebido on a 12 weekly basis and everything was fine other than my haemoglobin levels had started to rise too high.

So change of Dr and some life decisions later the Dr decides to stop the T with the intention of initially putting me on LH and once T levels restored then onto FSH.

There has been a slight problem though in that 5 months after my last 12 weekly T injection my T levels are still at 14.8 but both LH and FSH could not be detected.

The Dr is at a loss and says just to keep waiting and hoping the T continues to drop as he cannot start the LH/ FSH until they are below 8.

Anyone have any ideas?

Wow, you've got me stumped. The only suggestions I have are rather silly, but I can't come up with a reasonable explanation for what is happening. Here are my ideas:

• You have somehow managed to keep an oil depot of T around in your body that is still supplying you with testosterone.
• You have an adrenal disorder that is blocking steroidogenesis in the adrenal pathway, which is causing a buildup of precursor hormones, which in turn are being converted into testosterone.
• You've developed a tumor that is secreting T, or a hormone that can be converted into T, or a hormone that stimulates the production of T.
• One of your other medications is causing your T to be elevated.

Five months is a long time for the occult oil depot explanation to remain plausible. However, all of the other explanation seem unlikely as well. You mention that you have congenital hypopituitarism --- I assume you don't have panhypopituitarism; which hormones are affected? Which medications are you taking? Have you checked your levels of precursor hormones? Specifically, you can narrow down whether or not the T is being generated by your body, or if it is from outside the body, by checking for precursor hormones. The only situation in which this would not be true is if you had a tumor that was secreting T that was not also secreting any of its precursors. I don't have the statistics for how often this occurs, but (shooting from the hip) I don't think it is common.

Thus, if I were you, I'd ask the doctor to test for androstenedione; this is the hormone that T is commonly made from. Less commonly, T can be made from androstenediol (you might have trouble finding that blood test --- if you can't find it, don't worry about it). If you have normal levels of androstenedione, then that means that somehow, your body is generating T without being stimulated by LH. After all, only a little bit of androstenedione will result from the adrenal pathway in men; the majority of it is created in the testes during the synthesis of testosterone. Thus, if you have normal or elevated androstenedione, but you have nonexistent LH, then something is wrong.

This can only happen as a result of a tumor, of dysfunctional adrenal steroidogenesis, or as a side effect of other hormone medication. Your doctor can do more specific tests to check adrenal function to rule out dysfunctional adrenal steroidogenesis. If adrenal function is normal, then your doctor can do some tests to look for a tumor (and locate it). I assume that your doctor is already on top of what medications you are taking, but for the sake of completeness, I thought I'd mention it here...

Hope that helps. Let us know what you find out!

 

[TheStrangeOne]

Wow, you've got me stumped. The only suggestions I have are rather silly, but I can't come up with a reasonable explanation for what is happening. Here are my ideas:

• You have somehow managed to keep an oil depot of T around in your body that is still supplying you with testosterone.
• You have an adrenal disorder that is blocking steroidogenesis in the adrenal pathway, which is causing a buildup of precursor hormones, which in turn are being converted into testosterone.
• You've developed a tumor that is secreting T, or a hormone that can be converted into T, or a hormone that stimulates the production of T.
• One of your other medications is causing your T to be elevated.

Five months is a long time for the occult oil depot explanation to remain plausible. However, all of the other explanation seem unlikely as well. You mention that you have congenital hypopituitarism --- I assume you don't have panhypopituitarism; which hormones are affected? Which medications are you taking? Have you checked your levels of precursor hormones? Specifically, you can narrow down whether or not the T is being generated by your body, or if it is from outside the body, by checking for precursor hormones. The only situation in which this would not be true is if you had a tumor that was secreting T that was not also secreting any of its precursors. I don't have the statistics for how often this occurs, but (shooting from the hip) I don't think it is common.

Thus, if I were you, I'd ask the doctor to test for androstenedione; this is the hormone that T is commonly made from. Less commonly, T can be made from androstenediol (you might have trouble finding that blood test --- if you can't find it, don't worry about it). If you have normal levels of androstenedione, then that means that somehow, your body is generating T without being stimulated by LH. After all, only a little bit of androstenedione will result from the adrenal pathway in men; the majority of it is created in the testes during the synthesis of testosterone. Thus, if you have normal or elevated androstenedione, but you have nonexistent LH, then something is wrong.

This can only happen as a result of a tumor, of dysfunctional adrenal steroidogenesis, or as a side effect of other hormone medication. Your doctor can do more specific tests to check adrenal function to rule out dysfunctional adrenal steroidogenesis. If adrenal function is normal, then your doctor can do some tests to look for a tumor (and locate it). I assume that your doctor is already on top of what medications you are taking, but for the sake of completeness, I thought I'd mention it here...

Hope that helps. Let us know what you find out!

It is not panhypopituitaryism, though the Drs have always wondered why not. MRI scans puts my pituitary at less than 3% normal volume - reason unknown.

The only medication I am on is HGH at 0.6 per day by injection.

They did to tests for other elements at the same time as the LH/ FSH/ T but the results of the other tests hadnt come back by the time of seeing the Dr. He was very uncertain what was occurring as he had never heard of anyone with such levels after 5 months and 0 LH, he did mention the possibility of some coming from the adrenals but had never known such levels being achieved.

 

[Michael Scally MD]

I have congenital hypopitruitaryism and have been on HGH since a toddler and T since a teenager.

Over the years the preparation of the T has changed either because of new technologies or because my levels have been low.

Up until recently I was on Nebido on a 12 weekly basis and everything was fine other than my haemoglobin levels had started to rise too high.

So change of Dr and some life decisions later the Dr decides to stop the T with the intention of initially putting me on LH and once T levels restored then onto FSH.

There has been a slight problem though in that 5 months after my last 12 weekly T injection my T levels are still at 14.8 but both LH and FSH could not be detected.

The Dr is at a loss and says just to keep waiting and hoping the T continues to drop as he cannot start the LH/ FSH until they are below 8.

Anyone have any ideas?

It is very likely due to the TU. There is NO need for additional testing or workup at this time. The important consideration is the TU dose administered and how long you have been on TU. Is it 1000 mg? Have you been on TU for many years? These will provide information on the steady state T levels. Also, labs while being under TU will help. At this time, do NOT do any other testing. What is the reason for the change to LH/FSH? Is infertility an issue?

 

[TheStrangeOne]

Even after 5 full months?

I had been in nebido for 2 years (1 ampule). Prior to that about 2 years on the gel (1 sachet) about 3 years on the patches before that (1 small one large) and before that 10 years or so on 3 weekly injections.

Whilst using the gel the T was at 7, LH/FSH undetectable hence switching to the quarterly injections. Post switching T level went up, all the letters simply say normal but from memory T was 20.

The reason for switching to LH/ FSH is fertility. Count just after switching to Nebido was 9m with all other factors being average to good. 18 months after switching count down to <2 million all other factors good. Prestopping nebido count 0.

Endocrinologist uncertain of cause but suggested switching to LH/FSH but deferred treatment to andrologist. Andrologist believes nebido is the cause and agrees on LH/FSH treatment but says it can't start until T is down but doesn't know why T hasn't come down

 

[Michael Scally MD]

Even after 5 full months?

I had been in nebido for 2 years (1 ampule). Prior to that about 2 years on the gel (1 sachet) about 3 years on the patches before that (1 small one large) and before that 10 years or so on 3 weekly injections.

Whilst using the gel the T was at 7, LH/FSH undetectable hence switching to the quarterly injections. Post switching T level went up, all the letters simply say normal but from memory T was 20.

The reason for switching to LH/ FSH is fertility. Count just after switching to Nebido was 9m with all other factors being average to good. 18 months after switching count down to <2 million all other factors good. Prestopping nebido count 0.

Endocrinologist uncertain of cause but suggested switching to LH/FSH but deferred treatment to andrologist. Andrologist believes nebido is the cause and agrees on LH/FSH treatment but says it can't start until T is down but doesn't know why T hasn't come down

Absolutely!!! TU is a very long acting ester. The very reason I asked about the duration and dose was to provide some context for its ability to still be detected this far out. The following figures is from the article below (full-text is available at the link). From your stated level of 20, you can see that it is easy to go another 8 weeks or even more and have normal T levels. Note: This study is for a single injection, which makes your situation even more reasonable. I would imagine that your high levels are higher than that pictured below. The typical Nebido dose is 1000 mg. [As far as fertility, I would go a slightly different route for starters, but the combined LH/FSH is acceptable. And there is NO need or indication for additional testing.]



Zhang GY, Gu YQ, Wang XH, Cui YG, Bremner WJ. A pharmacokinetic study of injectable testosterone undecanoate in hypogonadal men. J Androl 1998;19(6):761-8. A pharmacokinetic study of injectable testosterone undecanoate in hypogonadal men -- Zhang et al. 19 (6): 761 -- Journal of Andrology

Testosterone undecanoate (TU) provides testosterone (T) replacement for hypogonadal men when administered orally but requires multiple doses per day and produces widely variable serum T levels. We investigated the pharmacokinetics of a newly available TU preparation administered by intramuscular injection to hypogonadal men. Eight patients with Klinefelter's syndrome received either 500 mg or 1,000 mg of TU by intramuscular injection; 3 months later, the other dose was given to each man (except to one, who did not receive the 1,000-mg dose). Serum levels of reproductive hormones were measured at regular intervals before and after the injections. Mean serum T levels increased significantly at the end of the first week, from less than 10 nmol/L to 47.8+/-10.1 and 54.2+/-4.8 nmol/ L for the lower and higher doses, respectively. Thereafter, serum T levels decreased progressively and reached the lower-normal limit for adult men by day 50 to 60. Pharmacokinetic analysis showed a terminal elimination half-life of 18.3+/-2.3 and 23.7+/-2.7 days and showed a mean residence time of 21.7+/-1.1 and 23.0+/-0.8 days for the lower and higher doses, respectively. The area under the serum T concentration-time curve and the T-distribution value related to serum T concentration were significantly higher following the 1,000-mg dose than following the 500-mg dose. The 500-mg dose, when given as the second injection, yielded optimal pharmacokinetics (defined as mean peak T values not exceeding the normal range and persistence of normal levels for at least 7 weeks), suggesting that repeated injections of 500 mg at 6-8-week intervals may provide optimal T replacement. The mean serum levels of estradiol were normalized following the injections, and prolactin levels were normal throughout the study. Significant decrease of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels was observed, with the decrease in LH levels being more pronounced. There were no significant differences in serum LH and FSH levels between the two doses. Sex hormone-binding globulin (SHBG) levels before any T therapy were near the upper limit of normal for adult men and were reduced by approximately 50% just prior to the second dose of TU. The decreased SHBG levels produced by the first TU injection could have led to lower peak total T levels and to a more rapid clearance of T following the second TU injection. We conclude that single-dose injections of TU to hypogonadal men can maintain serum T concentration within the normal range for at least 7 weeks without immediately apparent side effects. It is likely that this form of T would require injections only at 6-8-week or longer intervals, not at the 2-week intervals necessary with currently used T esters (enanthate and cypionate). This injectable TU preparation may provide improved substitution therapy for male hypogonadism and, in addition, may be developed as an androgen component of male contraceptives.

 

[TheStrangeOne]

What route would you go given the congenital nature of my issues combined with the apparent recent aspect to the issue ( though the endocrinologist was surprised at the original results and the androcrinologist suggested they may be wrong (he is based a different hospital))