Quote from: anamarisol24 on April 27, 2016, 07:45:50 PM
Hi I have recently switched to IV/Injectable E and am a bit worried about my blood E levels. My Dr checked my labs and said it might be too high and may have to switch me back to the pills. I am not a great pill taker as I then to forget any kind of pills, so I loved the idea of starting on self injections of Estradiol Valerate. I didnt get to see the lab values of the E when we had them drawn back in Feb/Mar but she said it may be a bit too high. I had my blood redrawn on Monday (4/25/16) and got the results back yesterday and it read that my estradiol levels is: 471 ng/ml
Are you sure the units are ng/ml? More likely, they are pg/ml. If so, I personally see no reason to be concerned especially considering you are taking bio-estradiol non-orally. I am not a doctor though. Perhaps, you can share the following with your doctor.
Levels in ciswomen can reach 650 pg/ml during a menstrual cycle (
http://www.specialtylabs.com/clients/outreach/web/site/details.asp?tid=44312&cid=301&keyword=), 75,000 pg/ml during pregnancy. Women aren't dying left and right, embolism risk remains very low during pregnancy, at less than 0.02%.
A study in men with prostate cancer aged 49-91, found that parenteral estradiol with levels going as high as 700 pg/ml, did not increase health risks.
Am J Obstet Gynecol. 1993 Dec;169(6):1549-53."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."
Br J Obstet Gynaecol. 1990 Oct;97(10):917-21."There is some anxiety about the possible harmful sequelae of supraphysiological estradiol levels but no data are currently available to show any deleterious effects of these levels on coagulation factors, blood pressure, glucose tolerance or the occurrences of endometrial or breast cancer (Hammond et al. 1974; Thom et id. 1978; Studd B Thom 1981; Armstrong 1988)."
Interestingly, an inverse association has been found between breast cancer and pregnancy.
Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):452-6.http://cebp.aacrjournals.org/cgi/content-nw/full/12/5/452/T1 These levels were obtained just before labor/delivery, at the end of pregnancy which lasted on average, 38 weeks.
Mean estradiol levels (E2): 24,000 pg/ml, Range: from 800-75,000 pg/ml
http://www.ilexmedical.com/files/PDF/Estradiol_ARC.pdf "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"
Curr Opin Obstet Gynecol. 2014 Dec;26(6):469-75.« Venous thromboembolism is, in the developed world, a major cause of maternal morbidity and mortality during pregnancy or early after delivery, with a reported incidence ranging from 0.49 to 2.0 events per 1000 deliveries."
Ann Intern Med. 2005 Nov 15;143(10):697-706."Women with deep venous thrombosis or pulmonary embolism first diagnosed between 1966 and 1995, including women with venous thromboembolism during pregnancy or the postpartum period (defined as delivery of a newborn no more than 3 months before the deep venous thrombosis or pulmonary embolism event date, including delivery of a stillborn infant after the first trimester)."
« The relative risk (standardized incidence ratio) for venous thromboembolism among pregnant or postpartum women was 4.29 (95% CI, 3.49 to 5.22;P < 0.001), and the overall incidence of venous thromboembolism (absolute risk) was 199.7 per 100,000 woman-years. The annual incidence was 5 times higher among postpartum women than pregnant women (511.2 vs. 95.8 per 100,000), and the incidence of deep venous thrombosis was 3 times higher than that of pulmonary embolism (151.8 vs. 47.9 per 100,000). Pulmonary embolism was relatively uncommon during pregnancy versus the postpartum period (10.6 vs. 159.7 per 100,000). "
"Among pregnant women, the highest risk period for venous thromboembolism and pulmonary embolism in particular is during
the postpartum period." (When estrogen levels drop and are low)
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"
"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."
Median age of patients was 75 (49-91).
Am J Clin Oncol. 1988;11 Suppl 2:S101-3."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"
"No cardiovascular side effects occurred during single-drug PEP treatment."
Tidsskr Nor Laegeforen 1993 Mar 10;113(7):833-5
Endocrine treatment of prostatic cancer. A renaissance for parenteral
estrogen."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"
"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 1989;14(4):389-95"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."
My own levels range from 1,000-4,000 pg/ml. Clotting times are normal, everything else is normal. My doctors see no reason to lower my dose.
Also this study in transsexual women, where high dose intramuscular estradiol valerate (and medium to high dose oral E2) was given and yet, there were no incidences of thrombosis.
Archives of Sexual Behavior, Vol. 27, No. 5, 1998"The incidence of thromboembolic events during cross-
gender hormone treatment in our patients was zero."
Quoteit does not give ranges for whats normal but says needs interpretation. I do not want to switch back to the pill. Is there another alternative or possibility of lowering a dosage of the injectable? I am currently on 1ml IM every 2 weeks.
Anyone have any suggestions or comments on if this is normal range or not? 
Show this to your doctor. Ask what they base themselves on, what studies exactly they have in mind for them to decide to lower your dose. Have they measured clotting times? Are all other results (liver enzymes, etc.) normal?
Quote from: Laura_7 on April 28, 2016, 05:02:24 AM
Studies showing adverse efects of high e levels usually are based on oral intake, which can raise blood clotting because the liver presumes a leak if it encounters estrogen in the digestive tract, and studies done with non bioidentical forms of estrogen.
No such studies. The studies in transsexual and ciswomen (and men with prostate cancer) showing an increase in health risks comprised of oral non bio-identical estrogen such as conjugated equine estrogens or ethinyl estradiol. Nothing to do with levels, more to do with the type of estrogen used because it is difficult to metabolize by the body, remains longer in the body, circulates through portal vein many more times where it triggers estrogen receptors and causes changes in coagulation (an evolutionary mechanism to stop bleeding after pregnancy because animal eats placenta).
