Well, I have not searched about this for long, but while I wait to see if estrogen patches will be approved in europe for metastatic cancer, I am having doubts about switching from triptorelin (which did and is still doing its job) to relugolix.
I know my MO first instinct will be saying "if it's working, don't fix it".
On one side it seems that relugolix would decrease the risk of cardiovascular events (as all GnRH antagonists). I say it seems because it's not confirmed. Plus of course I can take it without having to have an injection.
On the other side I think there is still no data about combining it with darolutamide. Ok ARASENS trial did not specify which ADT was being used, so I don't even know if it's a factor! 😜
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Maxone73
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Took Orgovyxx for 4 months ONLY ..it's now over 15 months T never recovered ..had to go on trt ... many have this story...only 20-25% recover T over 60 and less older.. must have serious discussion with your MO...
This graph is taken from the PATCH phase-II study (Langley 2016), which had switched to highdoses of E2 patches (3-4 patches at a time). at the beginning, starting back in 2006, they only used low-doses (1-2 patches at a time).
You could always start on 1 patch per week, and then titrate up by adding 1 more patch at a time, until you reach whatever your desired goal(s) is/are, e.g., reducing or eliminating hot flashes, growing bone, reducing glucose, lowering bad lipid levels, or replacing Lupron ADT with E2 ADT.
Primary SEs of estradiol ? I have read somewhat scientific articles outling some concerns, but remember little re details......it was an "aha" read I do remember.
An abstract of the final results of the Phase-III PATCH trial was presented at ESMO last week. There was essentially no difference in the 14-year survival curves between Lupron ADT and transdermal (patch) estradiol ADT. In fact, the estradiol patch was a little bit better.
correct but the results presented at ESMO 2024 were referred to metastasis free survival in patients that had originally no metastasis...OS in metastatic patients is still not mature
It would be a real bet then!! I think estradiol patches will be effective also for metastatic cancer, I would do it just to stop zometa. Even if I read that (but for breast cancer bone metastasis) it makes bone metastasis progression harder, so maybe it’s not all that bad considering that it gave me no side effects
Transdermal estradiol patches cause the LH and FSH hormones to crash, which stops the signals that cause the tastes to produce testosterone. The mechanism is the same as Lupron ADT. Crashing T is what causes PSA to drop low. I don't know of any published data about T recovery after estradiol ADT. Perhaps the PATCH study will report on this later this year... They certainly have collected data about this. But, your question about T recovery is an excellent question. I'll ask Professor Wassersug about this. Stay tuned !
Is there a lack of conclusive studies proving the benefit of low dose estrdiol....is that why not just MOs but also GPs resiste low dose estradiol prescription? Is that the same or somilar to what GPs will prescribe to women for menopausal problems?
It is identical to the estrogen patches and gels used by post-menopausal women. The UK PATCH phase-III study used FEM 7 (TM) estradiol patches commercially sold for PM women.
The best review paper for using low-dose estradiol is by Nick Russell (2007):
Older MO's and GP's unfortunately remember that oral estrogen (DES) from 30 years ago caused increased risk of blood clots, due to passing through the liver first. Transdermal estradiol does not take a first pass through the liver, which eliminates any increased risk of blood clots. Younger MO's and GP's simply have not been educated about the benefits of transdermal estradiol.
well but they meant if you don't take it for a week, then you restart with 3 on the first day and then go on with one....but you would have "saved" 7 by forgetting to take them
"... I think there is still no data about combining it with darolutamide."
It was not previously tested in doublet with ADT. The ARANOTE trial has now done that, though it does not say which ADT the darolutamide was combined with.
Sep 2024. " In the Phase III ARANOTE trial, NUBEQA® (darolutamide) plus androgen deprivation therapy (ADT) demonstrated an improvement in radiological progression-free survival (rPFS) with a 46% statistically significant reduction in the risk of progression or death… NUBEQA plus ADT now has demonstrated efficacy data in metastatic hormone-sensitive prostate cancer (mHSPC) both with and without docetaxel in the pivotal Phase III ARANOTE and ARASENS trials." bayer.com/en/us/news-storie...
I had triplet with darolutamide, chemo and ADT, now going on with daro and ADT, as I said there is no precise data about which ADT they considered, I think I will have to wait! I do not have many SEs....honestly I would prefer to switch to estradiol if data is confirmed also for metastatic patients, so that I could stop zometa (for practical reasons, it never gave me any problem)
"Your understanding is correct, and it's important to clarify the potential effects of estradiol on prostate cancer.
Estrogen Receptors in Prostate Cancer:
In prostate cancer, the presence of estrogen receptors (ERs) is less common than androgen receptors (ARs). However, when cancer cells do express ERs, these receptors can potentially respond to estrogen or estrogen-like compounds.
Estradiol's Effect on Cancer with Estrogen Receptors:
1. Growth Stimulation: Traditionally, estrogen is known to promote the growth of tissues where estrogen receptors are active, such as in certain breast cancers. If prostate cancer cells have estrogen receptors, there's a concern that introducing estradiol could feed the cancer, stimulating its growth through these receptors. This is what you're referring to, and it's a valid concern.
2. Growth Inhibition (Therapeutic Use): On the flip side, estradiol has been used historically in prostate cancer treatment, particularly before the advent of more modern hormonal therapies. The reason is twofold:
Testosterone Suppression: Estradiol can suppress the hypothalamic-pituitary-gonadal axis, leading to a significant reduction in testosterone production, which is essential for prostate cancer growth.
Direct Cytotoxic Effect: In some cases, high doses of estrogen (like estradiol) have been shown to induce cell death (apoptosis) in prostate cancer cells, even those with estrogen receptors. This effect isn't fully understood but is believed to involve complex mechanisms that go beyond simply stimulating cell growth. It might involve altering the balance of pro-growth and pro-death signals within the cancer cells.
Balancing the Effects:
The key point is that while estradiol can potentially stimulate cancer growth through estrogen receptors, its overall effect depends on the balance between its testosterone-suppressing actions and any direct actions on the cancer cells. In the context of prostate cancer, estradiol has been used effectively to lower testosterone levels and sometimes to induce direct toxic effects on the cancer, particularly when traditional ADT isn’t sufficient or as part of combination therapy.
Conclusion:
The use of estradiol in prostate cancer is complex and must be carefully considered by your healthcare team. They will weigh the benefits of testosterone suppression and potential direct effects against the risk of stimulating any estrogen receptors on your cancer cells. This is why thorough monitoring and personalized treatment planning are crucial if considering estradiol therapy."
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