Quote from: Dani on May 15, 2018, 04:40:25 AM
The reason for stopping estrogens is the possibility of blood clots post surgery. If you do not lower your estrogen blood levels pre-surgery you increase your risk.
The risk of DVT (deep venous thrombosis) is not correlated with estrogen levels.
"This prospective study suggests that high endogenous concentrations of estradiol and testosterone in women and men in the general population are not associated with increased risk of VTE [VTE =venous thromboembolism], DVT or PE [PE =pulmonary embolism]."
Endogenous sex hormones and risk of venous thromboembolism in women and menJournal of Thrombosis and Haemostasis, 2013, 12: 297–305
Risk of thromboembolisms is correlated with Activated Protein-C (APC) resistance. APC resistance is dependent on the route of administration of estrogens, for bioidentical estrogen (estradiol) at least. For example, transdermal administration does not lead to increased risk of DVT. [This does not apply to ethinyl estradiol, and maybe not conjugated equine estrogens, either.]
"Biologic evidence supports a differential effect of oral versus transdermal estrogen on hemostasis. Randomized trials have shown that oral ERT [ERT = estrogen replacement therapy] increases plasma levels of prothrombin fragment F1+2, which is a marker for in vivo thrombin generation and which was recently related to the risk of recurrent VTE. Consistent data reported that transdermal ERT had no detrimental effect on coagulation, especially prothrombin fragment 1+2 plasma level, and our findings are in accordance with these results. Thus, oral ERT might impair the balance between procoagulant factors and antithrombotic mechanisms, whereas transdermal ERT appears to have little or no effect on hemostasis."
Differential Effects of Oral and Transdermal Estrogen/Progesterone Regimens on Sensitivity to Activated Protein C Among Postmenopausal WomenArterioscler Thromb Vasc Biol., September 2003, pp 1672-76.
Quote from: Dani on May 15, 2018, 04:40:25 AM
I have never heard of a surgeon differentiating between which route of administration for the recommended withdrawal period.
Therein lies the problem. It is oral administration of estrogens that is problematic, apparently related to first-pass liver metabolism.
"Conjugated equine extracts and 17-oestradiol are the two most widely used forms of oestrogen in postmenopausal women. Oestrogens are usually given orally, but such a delivery route has drawbacks, including intestinal and hepatic first-pass effects. Oral, but not transdermal, oestrogen administration leads to high hormone concentrations in the liver and promotes hepatic protein synthesis. Data for the pharmacokinetics of oral and transdermal oestradiol showed dose-dependent increase in serum oestradiol exposure. However, oral ERT results in a substantial increase in plasma oestrone concentration leading to non-physiological ratio of oestrone to oestradiol close to 5.18 By contrast, transdermal ERT leads to plasma oestrone to oestradiol ratios close to 1, which is similar to that in menstruating women."
Differential association of oral and transdermal oestrogen replacement therapy with venous thromboembolism riskLancet 2003 362: 428–32
Granted, these studies are on post-menopausal cis-females, but it is probably reasonable to assume liver physiology and metabolism is very similar to transgender women. It is quite likely that those patients using transdermal or parenteral (injectable) estradiol face no increased risk of blood clots. With this in mind, I switched from sublingual estradiol to transdermal estradiol before I had SRS.
And of course, I am not a doctor (of medicine, anyway) so this information is given only in the interest of being an informed patient.
With kindness,
Terri