I have been on oestrodiol since September last year, and had been feeling great. The blood tests I'd had up to then all suggested my oestrogen was rising and testosterone falling steadily. In May of this year my oestrogen was 953 (a little on the high side but good apparently) and my testosterone was 1.2 (which is within female range and about castration level, and apparently also good according to doctor). The gender clinic doctor then put me on an anti-androgen, which I guess was to reduce possible side effects from the high oestrogen, because without fighting against the testosterone, I could have a lower dose of oestrogen.
The anti-androgen I was put on was decapeptyl, and in order to prevent the initial flare in testosterone levels from the first injection, I was put on a month's supply of cyproterone acetate. I started the cyproterone acetate a week before my decapeptyl injection to give it time to work.
The day after first taking cyproterone acetate, I started to get symptoms that to me suggested a rise in testosterone, rather than a fall. I felt more angsty, angry, and for the first time in more than 6 months, I had spontaneous night-time erections, which were painful physically as well as mentally, because the skin had not been stretched in so long. Has anyone ever heard of this happening before? I asked my doctor about it, and he just suggested I stick with it, as it hadn't been long at that point and I hadn't started the decapeptyl yet.
Then since having the decapeptyl injection, I seem to have had more of the same. My arm muscles seem to have grown, and I have had some acne on my face too. I feel like I am going insane - much the sort of feelings I had pre-transition.
The cyproterone acetate doesn't seem to be working, and quite possibly producing a rise in testosterone levels, rather than a decrease. It's also now difficult for me to know whether it's the cyproterone acetate causing this or just the fact it's not working to suppress the initial testosterone flare from the decapeptyl.
My doctor's experience with both these drugs is in treating testicular cancer, and much of the information I've been able to find online is about that. This makes me wonder whether there'd be any difference in giving thses drugs to someone with normal male testosterone levels to giving them to someone with female/castration levels like I had.
Also, does anyone have any idea of how long the flare from decapeptyl usually lasts? Most information online gives a very broad range of between 3 days and 20 days!
Quote from: charanguista on June 25, 2014, 03:57:46 PM
I have been on oestrodiol since September last year, and had been feeling great. The blood tests I'd had up to then all suggested my oestrogen was rising and testosterone falling steadily. In May of this year my oestrogen was 953 (a little on the high side but good apparently) and my testosterone was 1.2 (which is within female range and about castration level, and apparently also good according to doctor). The gender clinic doctor then put me on an anti-androgen, which I guess was to reduce possible side effects from the high oestrogen, because without fighting against the testosterone, I could have a lower dose of oestrogen.
The anti-androgen I was put on was decapeptyl, and in order to prevent the initial flare in testosterone levels from the first injection, I was put on a month's supply of cyproterone acetate. I started the cyproterone acetate a week before my decapeptyl injection to give it time to work.
The day after first taking cyproterone acetate, I started to get symptoms that to me suggested a rise in testosterone, rather than a fall. I felt more angsty, angry, and for the first time in more than 6 months, I had spontaneous night-time erections, which were painful physically as well as mentally, because the skin had not been stretched in so long. Has anyone ever heard of this happening before? I asked my doctor about it, and he just suggested I stick with it, as it hadn't been long at that point and I hadn't started the decapeptyl yet.
Then since having the decapeptyl injection, I seem to have had more of the same. My arm muscles seem to have grown, and I have had some acne on my face too. I feel like I am going insane - much the sort of feelings I had pre-transition.
The cyproterone acetate doesn't seem to be working, and quite possibly producing a rise in testosterone levels, rather than a decrease. It's also now difficult for me to know whether it's the cyproterone acetate causing this or just the fact it's not working to suppress the initial testosterone flare from the decapeptyl.
My doctor's experience with both these drugs is in treating testicular cancer, and much of the information I've been able to find online is about that. This makes me wonder whether there'd be any difference in giving thses drugs to someone with normal male testosterone levels to giving them to someone with female/castration levels like I had.
Also, does anyone have any idea of how long the flare from decapeptyl usually lasts? Most information online gives a very broad range of between 3 days and 20 days!
Can i ask what you were on before and why the change?
Before starting the anti-androgens? I was only on oestrodiol.
Starting the anti-androgens was at the suggestion of the gender clinic.
Cyproterone acetate, being a progestin and having mild anti-estrogenic effects as all progestogens do, might have reduced estrogen effectiveness thereby causing these symptoms temporarily.
The testosterone flare-up on decapeptyl should last a few weeks, no more than 3-4 usually. But, if you take enough cyproterone acetate which I assume you did, this should be a non-issue and even if it is at first, don't worry. It will settle. If it doesn't, then let your doctor know but I'd be surprised.
I'm assuming (but I'm not a doctor) he prescribes this treatment to men with testicular cancer because androgens are believed to cause proliferation of the cancer (similar to prostate cancer) so in that case, it would be extremely critical to have them be as low as possible. Hence, this would be a good thing for you! No worries there.
Interestingly, there have been several studies done on men with advanced prostate cancer treated with bio-identical ESTROGEN alone non-orally where negligible health complications were found, even though levels were quite high, similar or higher than yours. You could perhaps show these to your doctor and have him change his mind. Who knows? Since you say you were doing quite well on just estrogen.
Your levels are in pmol/L. To convert pg/ml to pmol/L, multiply by 3.671.
Cancer. 2005 Feb 15;103(4):717-23.
Phase II study of transdermal estradiol in androgen-independent
prostate carcinoma.
"Patients with prostate carcinoma progressing after primary hormonal therapy received TDE (...) patches replaced every 7 days."
TDE = transdermal estradiol
"The mean (+/-95% CI) serum estradiol level increased from 17.2 pg.mL (range, 14.8-19.6 pg/mL) to 460.7 pg/mL (range, 334.6-586.7 pg/mL)."
"No change in factor VIII activity, F 1.2, or
resistance to activated protein C was observed, whereas a modest
decrease in the protein S level was observed. CONCLUSIONS: In
patients with APIC, TDE was well tolerated and produced a modest
response rate, but was not associated with thromboembolic
complications or clinically important changes in several coagulation
factors."
J Urol. 2005 Aug;174(2):527-33; discussion 532-3.
Transdermal estradiol therapy for prostate cancer reduces
thrombophilic activation and protects against thromboembolism
"These results suggest that transdermal estradiol reduces
thrombophilic activation in men with advanced prostate cancer, and
protects against the risk of thrombosis."
J Urol. 2003 May;169(5):1735-7.
Transdermal estradiol therapy for advanced prostate cancer--forward
to the past?
"PURPOSE: Current hormonal therapies for prostate cancer are
associated with significant morbidities, including symptoms of
andropause and osteoporosis. Oral estrogens prevented many of these
problems but were abandoned due to cardiovascular toxicity attributed
to hepatic effect. In contrast, parenteral estrogens prevent first
pass hepatic metabolism and substantially reduce cardiovascular risk,
and long-term transdermal estradiol therapy is believed to be
cardioprotective. We report preliminary results of a pilot study
using transdermal estradiol therapy to treat men with advanced
prostate cancer. MATERIALS AND METHODS: A total of 20 patients with
advanced prostate cancer were enrolled in a before and after study
that examined the impact of estradiol patches on hormones, disease,
thrombophilia, vascular flow, osteoporosis and quality of life.
RESULTS: Median followup is 15 months. Estradiol levels greater than
1,000 pmol./l. were achieved using (...) patches and higher levels were
obtained by increasing the number of patches. All patients achieved
castrate levels of testosterone within 3 weeks and had biochemical
evidence of disease regression. One patient died of disease at 14
months and 1 cardiovascular complication occurred. Thrombophilic
activation was avoided and vascular flow improved. Bone mineral
density was significantly increased. Mild or moderate gynecomastia
occurred in 80% of patients but no patient had hot flushes. All other
functional and symptomatic quality of life domains improved.
CONCLUSIONS: Transdermal estradiol therapy produced an effective
tumor response. Cardiovascular toxicity was substantially reduced
compared with that expected of oral estrogen"
Am J Clin Oncol. 1988;11 Suppl 2:S101-3.
Single drug polyestradiol phosphate therapy in prostatic cancer.
"Serum concentrations of testosterone (T) and estradiol-17 beta (E2) were analyzed in prostatic cancer patients treated with (...) polyestradiol phosphate (PEP) i.m. every fourth week as single drug therapy during a 6 month period. (...) Accumulation of E2 occurred to mean levels 1,300-2,500 pmol/L at 6 months. At 6 months, SHBG levels had increased to 617% of pretreatment values in the oral EE2 group, to 166% in the (...) group, and were unaffected by orchidectomy. No cardiovascular side effects occurred during single-drug PEP treatment."
1,300 pmol/L = 354 pg/ml
2,500 pmol/L = 681 pg/ml
Tidsskr Nor Laegeforen 1993 Mar 10;113(7):833-5
Endocrine treatment of prostatic cancer. A renaissance for parenteral
estrogen.
"If the oestrogens are administered parenterally, changes in liver
function can be avoided and risk of side effects markedly reduced.
38 patients have been treated at Huddinge Hospital in Stockholm, and
14 patients at Aker Hospital in Oslo, with polyoestradiol phosphate
(Estradurin)(...) injected intramuscularly every 4th week (initial
dose (...)). We can sum up our own experience as follows: Plasma
testosterone is reduced to castration level after 2-3 weeks. Liver
function, evaluated by the sexual hormone binding globulin level in
plasma, remains unchanged. Morbidity and mortality from cancer are
the same as may be achieved by surgical orchidectomy. The only side
effect of significance is gynaecomastia. Follow-up of the patients
does not indicate any increased risk of thrombosis or cardiovascular
disease."
Prostate 1991;18(2):131-7
Cardiovascular and all-cause mortality in prostatic cancer patients treated
with estrogens or orchiectomy as compared to the standard population.
"Four hundred and seventy-seven prospectively randomized patients with
prostatic carcinoma were treated with a combination of intramuscular
polyestradiol phosphate (PEP) and oral ethinyl estradiol, with
intramuscular PEP alone, or with orchiectomy."
"The age-standardized rate ratios (approximately relative
risk) for cardiovascular mortality and for all-cause mortality were
1.51 and 2.31 in the combination estrogen therapy group, 0.17 and
1.50 in the PEP monotherapy group, and 0.78 and 1.78 in the
orchiectomy group, respectively. Further mortality rates by cause for
all three treatment groups were standardized for age using the
age-specific person-years at risk as standard. Age-standardized
mortality from cardiovascular diseases was very low in the PEP group,
as compared to other treatment modalities, and the mortality rates
for prostatic cancer were about equal in all three treatment groups.
It is concluded that intramuscular PEP monotherapy is associated with
low cardiovascular mortality and with an all-cause and prostatic
cancer mortality equal to orchiectomy."
Int J Technol Assess Health Care 1991;7(2):220-5
Cost comparison of parenteral estrogen and conventional hormonal treatment
in patients with prostatic cancer.
"The present study compares the cost of antitumor therapy and adverse
cardiovascular effects during the first year of treatment with oral
estrogens, nonoral estrogens, or surgical castration in patients with
prostatic cancer."
"Twenty-five percent of the patients treated with
oral estrogen suffered cardiovascular complications, compared to none
of the patients treated by orchidectomy or nonoral estrogens."
Prostate 1989;14(4):389-95
Estrogen therapy and liver function--metabolic effects of oral and parenteral
administration.
"Oral estrogen therapy for prostatic cancer is clinically effective
but also accompanied by severe cardiovascular side effects.
Hypertension, venous thromboembolism, and other cardiovascular
disorders are associated with alterations in liver metabolism. The
impact of exogenous estrogens on the liver is dependent on the route
of administration and the type and dose of estrogen. Oral
administration of synthetic estrogens has profound effects on
liver-derived plasma proteins, coagulation factors, lipoproteins, and
triglycerides, whereas parenteral administration of native estradiol
has very little influence on these aspects of liver function."
Prostate 1988;13(3):257-61
Cardiovascular follow-up of patients with prostatic cancer treated with
single-drug polyestradiol phosphate.
"Thirty-eight patients with cancer of the prostate were treated with
strict parenteral estrogen in the form of monthly polyestradiol
phosphate injections"
"In contrast to studies with oral estrogens,
there have been no cardiovascular complications at a mean follow-up
of 12.9 +/- 0.7 months (SEM)."
During pregnancy, women also have levels that range from 1,000-40,000, up to 75,000 pg/ml. Even during every menstrual cycle, levels can reach 600 pg/ml +.
http://cebp.aacrjournals.org/cgi/conten ... 2/5/452/T1 (http://cebp.aacrjournals.org/cgi/conten%20...%202/5/452/T1)
http://www.ilexmedical.com/files/PDF/Estradiol_ARC.pdf (http://www.ilexmedical.com/files/PDF/Estradiol_ARC.pdf)
"Normal estradiol levels are lowest at menses and into the early follicular
phase (25-75 pg/mL) and then rise in the late follicular phase to a peak
of 200-600 pg/mL just before the LH surge, which is normally followed
immediately by ovulation. As LH peaks, estradiol begins to decrease
before rising again during the luteal phase (100-300 pg/mL). If conception
does not take place, estradiol falls further to its lowest levels, and menses
begins shortly thereafter. 2-5 If conception occurs, estradiol levels continue
to rise, reaching levels of 1,000-5,000 pg/mL during the first trimester,
5,000-15,000 pg/mL during second trimester, and 10,000-40,000 pg/mL
during third trimester. 6-8"
http://www.specialtylabs.com/clients/ou ... 1&keyword= (http://www.specialtylabs.com/clients/ou%20...%201&keyword=)
And finally this...
Am J Obstet Gynecol. 1993 Dec;169(6):1549-53.
Fibrinolytic parameters in women undergoing ovulation induction.
"As serum estradiol levels increased throughout each phase (maximum mean estradiol 739.8 pg/ml)"
"Down-regulation of the fibrinolytic system was observed as estradiol levels increased. However, thrombin formation did not change, thus suggesting that elevated circulating estradiol alone does not predispose to a thromboembolic event."
Pharmacology of estrogens and progestogens: influence of different routes of administration, CLIMACTERIC 2005;8(Suppl 1):3–63
"In women with supraphysiological estradiol levels during treatment with implants, no adverse effects on lipid metabolism, but a reduction in LDL cholesterol and fasting insulin were observed150."
Aust N Z J Obstet Gynaecol. 1978 Aug;18(3):198-201.
The effect of oestradiol valerate therapy on coagulation factors and lipid and oestrogen levels in oöphorectomised women.
"The effect of oestradiol valerate on levels of blood cholesterol, triglycerides, free oestradiol and coagulation factors, as well as on urinary oestrogens and free cortisol was measured in 10 oöphorectomised women. Despite the very high urinary oestrogen levles obtained, there was no significant change found in the other parameters during and after treatment."
You was with the GIC for a year before they put you on the decapeptyl? Was you seeing someone else privately before switching over to the GIC?
Sorry for all the questions. i have no idea why they would alter your meds if everything was fine on oestradiol alone.
Quote from: jname on June 26, 2014, 05:36:11 AM
You was with the GIC for a year before they put you on the decapeptyl? Was you seeing someone else privately before switching over to the GIC?
Sorry for all the questions. i have no idea why they would alter your meds if everything was fine on oestradiol alone.
Yes, I was seeing someone privately prior to getting HRT from the GIC. However the GIC did put me on oestradiol 3 months before putting me on decapeptyl.