Document Type


Publication Date



Maine Medical Center, Medical Education, Maine Medical Center Research Institute

MeSH Headings

Humans, Testosterone, Transgender Persons, Estradiol, Gonads, Transsexualism, Testosterone Congeners


Suppression of endogenous gonadal function is an important goal of transgender hormone therapy in both female-to-male (FTM) and male-to-female (MTF) patients. Current recommendations include exogenous hormone therapy in the form of testosterone (T) for FTM or estradiol (E2) for MTF, in addition to a GnRH agonist or progestin to effectively suppress endogenous gonadal activity. It has been claimed, however, that routine use of a GnRH agonist is not justified in terms of a cost-benefit analysis and there is no clear evidence that progestins add to the feminization of MTF patients. To determine how often T or E2 therapy alone is effective for gonadal suppression we performed a retrospective evaluation of adult transgender patients. Inclusion criteria were: 1) age 18-40 years for FTM and 18-50 years for MTF; 2) normal reproductive/endocrine function prior to therapy; 3) intact gonads; 4) serum levels of the administered hormone (E2 or T) within the therapeutic target range while on hormone therapy; 5) no concurrent therapy with a GnRHa or progestin at the time of reported laboratory measurements; and, 6) all T and E2 measurements performed at a specified reference laboratory (LabCorp). Sex hormone binding globulin (SHBG) and body mass index (BMI) were also measured. Consistent with Endocrine Society guidelines, effective suppression of ovarian function in FTM patients was assessed by cessation of menses and a serum E2 of/mL. In MTF patients, testicular suppression was assessed by a total T within the premenopausal adult female normal range (10-55 pg/mL). Mean age was(25.5 years) and MTF (29.2 years). FTM patients (n=65) received T through subcutaneous (SC, n=60), intramuscular (IM, n=4), or gel (n=1). MTF patients (n=33) received oral (n=27) or SC (n=6) as well as spironolactone. The median serum total T level for FTM patients was 712 ng/dL (range, 370-1164 ng/dL). On T therapy alone, 90.8% of FTM patients achieved amenorrhea and 73.8% achieved serum E2 level/mL. For MTF patients, the median serum E2 level was 129.2 pg/mL (range, 75-197 pg/mL). On E2 therapy alone, 84.8% of MTF patients had adequate suppression of testicular function (T/dl). Our results indicate that most transgender patients do not need GnRH agonists or progestin treatment in addition to T or E2 therapy to suppress endogenous gonadal activity. This suggests that it is reasonable to add GnRHa or progestin therapy only to those patients in whom testicular or ovarian function is not suppressed by estrogen or testosterone therapy alone. Additional unnecessary endocrine therapies to suppress ovarian or testicular function incur a significant expense without providing a clear change in clinical outcome.


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