Tamoxifen????

[Hatemychest]

What is that, I went to the endicrinologist and he put me on that for my gyne. What will it do, will it reduce the size of the breast?

[Hypo-is-here]

Hopefully, that is the obvious intention.

Tamoxifen is a SERM, Selective Estrogen Receptor Modulator.

It blocks the Estrogen Receptors (ERs) with a weak estrogen and in doing so prevents the vastly more potent estrogen estradiol from entering the ERs and worsening your gynecomastia.

The idea is that by blocking this potent estrogen your breast tissue starved of estradiol will begin to hypertrophy, to you and me that means shrink.

In certain limited trials Tamoxifen was successful at resolving gynecomastia in upto 80% of cases.

Whether it works in your situation will depend upon a combination of varying factors, one of the most important of which is how long you have had the gynecomastia.

I say this because gynecomastia is much easier to be acted upon by hormones when it is in the proliferation phase.  After a period of around a year and a half to two years it becomes more fibrous and less likely to respond favorably to this type of intervention.

[daddynubbie]

you are probably not a doctor but
you must play one on TV.


Seriously, great info thanks!

[Hatemychest]

No He just stayed in a holiday Inn express last night . . . lol




No Thank you very much. The doctor kinda did a few test and he checked my ummm . . . testicles. I guess that was nessisary but anywho I went with my dad and he gave him the information im 18 thank you.

I would like to know how long this usually takes to redice the breast size. I developed gyne a year ago.

[Hypo-is-here]

No He just stayed in a holiday Inn express last night . . . lol

.

Is this an American reference?

I don't understand it.

[Hatemychest]

yes lol. It's from an american holdiay Inn commercial where there are people doing crazy only professionals should do stuff, and after they do heart surgery or run an entire multi-national corperation someone will ask them, did you go to doctor school, or what is your PHD, and they will say,

No but I sayed at a holiday inn express last night lol.

[Hypo-is-here]

Oh I see

However I would say take what I have written to any appointment with an endocrinologist and ask them if it is correct

[AngryPuppy]

Good to find someone with certain knowledge, and above all, a sense of humor.

I was going to ask you. What do you think of Arimidex? Many people think it is better than Tamixiofen.


Thanks for any comments you may have.

Hopefully, that is the obvious intention.

Tamoxifen is a SERM, Selective Estrogen Receptor Modulator.

It blocks the Estrogen Receptors (ERs) with a weak estrogen and in doing so prevents the vastly more potent estrogen estradiol from entering the ERs and worsening your gynecomastia.

The idea is that by blocking this potent estrogen your breast tissue starved of estradiol will begin to hypertrophy, to you and me that means shrink.

In certain limited trials Tamoxifen was successful at resolving gynecomastia in upto 80% of cases.

Whether it works in your situation will depend upon a combination of varying factors, one of the most important of which is how long you have had the gynecomastia.

I say this because gynecomastia is much easier to be acted upon by hormones when it is in the proliferation phase.  After a period of around a year and a half to two years it becomes more fibrous and less likely to respond favorably to this type of intervention.

[Hypo-is-here]

Hi Alex,

Many men who have low testosterone  (hypogonadism) have gynecomastia, 1 in 10 of all gynecomastia sufferers does in fact have hypogonadism ( statistics taken from Glen D Braunstein M.D endocrinologists 1993 white paper on "Gynecomastia" and concured with in Ismail and Barths 2002 white paper titled "The Aetiology of Gynecomastia").

Now an awful lot of these men are prescribed various medications on a permanent basis to deal with elevations in estradiol as a result of the testosterone replacement therapy they are on.

And I have spoken to simply dozens and dozens of them over the past two years.

And the feeling on the ground is this; whilst Arimidex is very successful at inhibiting production of estrogens and preventing further development of Gynecomastia, for some reason or other it does not seem to be particularly effective at reducing or resolving Gynecomastia.

This is not a scientific study of course, just an overwhelming amount of case reports I guess you would say.

In a specific case of one, namely me (I have been prescrbed Tamoxifen, Arimidex and DHT in the past), I have to say that both Tamoxifen and DHT were relatively successful in reducing my gynecomastia, but Arimidex did very little if anything at all.

Now again that is not remotely scientific, being only a case of one, but it is an observation that you may find interesting.

So I explained the situation on the ground in a given group of men/case reports, I have given you basic details of my subjective experience, so now I will refer to the scientific position in terms of the studies and anything approaching proof.

When it comes to controlled medical studies on differing medications that may be of use when it comes to gynecomastia, i'm afraid there has been very little interest by the pharmaceutical companies- perhaps they do not see a big enough profit margin in any end product?

In 1980 Harold Carlson wrote in his white paper "Gynecomastia current Concepts", that there were some promising moves in this area of medicine.

Yet 25 years later!!! and we are often still seeing medical trials of Tamoxifen and other drugs with very low patient numbers, sometimes less than 10 patients, sometimes no more than 30 patients, invariably less than 100.

This is obviously very disappointing as it means the information we have is very limited.

Tamoxifen has in a number of uncontrolled trials been shown to resolve gynecomastia in upto 80% of cases.

Clomiphene citrate has been shown in one controlled trial at least to have resolved gynecomastia in 74% of cases at a particular dose.

I have not seen/am not aware of any medical trials of Arimidex in this setting or in fact any aromatase inhibitor in this setting.

But I have to admit over the last eight or nine months or so I have been out of the equation and in fact have not wrote the The New England Journal of Medicine in quite some time or in fact conducted any research of late into this matter.

So perhaps trials have now taken place- maybe one of the guys on the board might wish to take a look at Medline or some such source of information and see if they can further enlighten us as to the results of any recent trials/studies?

I hope the information I have given helps a little.




 

[laurier]

Hatemychest,

What dosage are you on, how often?

Thanks.

[Hypo-is-here]

Knowing what dose someone else takes would not help you in any way as we are all different.

Our endocrine systems are like our own personal chemistry set- no two are exactly alike either in the numbers/levels or the way they respond to given endocrine affecting medication.

Which is why anyone who is interested in this treatment to reduce their gynecomastia they should make an appointment to see an endocrinologist who has an interest in reproductive endocrinology.

[dr007]

Hypo keep up giving the good advice, but just a technical note:

"The idea is that by blocking this potent estrogen your breast tissue starved of estradiol will begin to hypertrophy, to you and me that means shrink"

Hypertrophy does not mean shrink.

Hypertrophy is a general increase in bulk.

The word you should have used is atrophy.


BTW, I have just started tamoxifen for gynecomastia at 20mg o.d.   I am probaly going to aim for 3 months, since that is the duration of most of the trials.

I have previously had liposuction 6/months ago, but the glandular tissue has returned.  This is my last resort before I move towards 'breast reduction' with its associated risk of nipple inversion.

I also just graduated as a doc in aus and most GPs and physicians (endocrinologist & plastic surgeons being the exception to the rule) know very little about gynecomastia, except liver disease is the 1st differential diagnosis.  (That why the doc palpated ur testes - too rule out other causes eg Klinefelter’s syndrome & cancer) .

I am sure it has been asked a million times, but I would love to hear about personal experience with tamoxifen - how long till you can see results? how many courses for how long? and any other relvant information that other ppl thinking about tamoxifen and myself would like to know.

Thanks

[Hypo-is-here]

Quite right about the pointer, Freudian slip- I have a hypertropied left kidney and it is as you say enlarged.

One pointer if I may,

An examination of the testicles does not rule out Klinefelters Syndrome.

Depending upon the severity of the condition people with Klinefelters Syndrome can have testosterone levels up to around 15nmol/l or around 432ng/dl in US terms (I know you guys usually use the former European reference range in Australia).

A testicular examination in combination with basic bloods can point to Klinefelters, but it is not so blatantly straightforward in all cases which is why so many men with Klinefelters Syndrome are only discovered to have the condition as a result of other investigations- often when they are in their fifties or older.

1-500 men are thought to have Klinefelters from birth but this number is under-represented in all populations so there is a significant number of men that go undiagnosed, many of which are those with less blatant abnormalities.

Chromosomal testing is generally the best method of revealing the condition and that of the many other chromosomal defects that can result in gynecomastia.

But enough of that;

Can I ask what pathology investigations you had carried out?

And what were the specific results including reference ranges?

Unless you don’t want to share that of course- that would be understandable.

[dr007]

Biochem:

Prolactin

TFTs (thyroid function test – TSH, T4, T3 – free and bound to THBG) & Thyroid antibodies

Lipids (cholesterol, HDLs, LDLs, triglycerides)

FBC (Hb, MCV, WCC & differential, platelets)

ESR (erythrocyte sedimentation rate)

LFTs (ALT, AST, ALP, bilirubin, albumin, etc.)

UEC (urea, electrolytes & creatinine)

All these where normal except cholesterol which was low and urea which was mildly elevated (breakdown product from the protein shakes I drink – therefore of no significance)

Sorry but I won’t supply values and reference ranges, because they vary greatly between labs and countries – so this makes this info useless to you anyway, the major concern is whether the value is within the reference range – 95% of the population

I didn’t bother with testosterone or estradiol (or ratio)for several reasons:
1.  Regardless of the result it would not change my management (ie tamoxifen) – if I normal estradiol/testosterone ratio, it could just be my extreme sensitivity that is causing the gynecomastia
2.  It is not excluding/confirming any other diagnoses
3.  Besides gynecomastia, I have no symptoms/signs of low/high testosterone/estradiol

There is not heaps of info or standard tests for gynecomastia - so i just did a mix to test other diagnoses and check liver and renal function.

[Hypo-is-here]

Biochem:

Prolactin

TFTs (thyroid function test – TSH, T4, T3 – free and bound to THBG) & Thyroid antibodies

Lipids (cholesterol, HDLs, LDLs, triglycerides)

FBC (Hb, MCV, WCC & differential, platelets)

ESR (erythrocyte sedimentation rate)

LFTs (ALT, AST, ALP, bilirubin, albumin, etc.)

UEC (urea, electrolytes & creatinine)

All these where normal except cholesterol which was low and urea which was mildly elevated (breakdown product from the protein shakes I drink – therefore of no significance)

Sorry but I won’t supply values and reference ranges, because they vary greatly between labs and countries – so this makes this info useless to you anyway, the major concern is whether the value is within the reference range – 95% of the population

First of all I would have only considered the figures in relation to the reference ranges that you would have provided me with as I am well aware of what you have stated regarding differing labs and countries.  

Second of all, what are termed normal reference ranges are sometimes anything but I’m afraid.

None of the top reproductive Andrologists/endocrinologists (Dr Malcolm Carruthers, Dr Eugene Shippen, the andropause society etc) in the world go off what are termed normal reference ranges alone.  I can and will explain why should you wish to know the reasons for this.

I am not coming out with incorrect information here either;

I suffer from hypogonadism, have seen some of the top anthologists and endocrinologists in the world, have read all the books of the leading doctors in this field that have been published for the last five years.  And have been part of support groups for men with hypogonadism in both the US and the UK for the last two years.

I didn’t bother with testosterone or estradiol (or ratio)for several reasons:
1.  Regardless of the result it would not change my management (ie tamoxifen) – if I normal estradiol/testosterone ratio, it could just be my extreme sensitivity that is causing the gynecomastia
2.  It is not excluding/confirming any other diagnoses
3.  Besides gynecomastia, I have no symptoms/signs of low/high testosterone/estradiol

There is not heaps of info or standard tests for gynecomastia - so i just did a mix to test other diagnoses and check liver and renal function.

Sorry but that doesn’t make much sense to me.

The protocol for management of gynecomastia is to exclude a definable aetiology first and then treat as idiopathic if a cause is not found.

I think you are simplifying what should be tested for and missing out some vital tests IMHO.

If you use Tamoxifen without having had at the very least a baseline test for your estradiol level, you will not have any idea whatsoever if in fact your estradiol is high to start with.

Therefore you will not know how to dose appropriately.

If your estradiol level is not high, something that can often be the case in men with gynecomastia for a whole variety of reasons, then you could easily take too high a dose.  This would result in severe fatigue, erection problems, lowered libido and maybe throw your thyroid function out.

Also with Tamoxifen you have no way of measuring what is going on in the blood whilst on treatment.

If you do not test for Testosterone, then you have no way of knowing if that is the culprit and not the estradiol.  I say this because gynecomastia can occur with normal levels of estradiol and low testosterone as this can allow for a poor androgen to estrogen balance and the resulting problem.

So you could be looking to treat something (estradiol) that isn’t a problem whilst not treating something that is a problem (low testosterone).

There is also the possibility that you could have gynecomastia as a result of elevated SHBG, which lowers free testosterone, again this would require a different approach in terms of medication.

If you have LH tested you would be given an indication as to possible issues with the testicles or pituitary as well.

I hope you understand I am only trying to help.

If you want to ask me anything privately then please feel free and I will try and provide as many answers on these topics as sufficiently answers any question you may have.

P.S

I also speak from the experience of having been on many treatments for my hypogonadism, including SERMs and Aromatase Inhibitors and I have not only seen my blood work on these meds, I have seen hormonal work-ups works for literally dozens and dozens of men over the last few years.