Our observations indicate that SC T injections are an effective, safe, and well-accepted alternative to IM T injections.
Context Testosterone (T) or estradiol (E2) are administered to suppress gonadal function in female-to-male (FTM) and male-to-female (MTF) transgender patients. How often sex steroid cause adequate suppression without GnRH agonist (GnRHa) or progestin therapy has not been reported. Objectives 1) To determine how often T and E2 therapy alone can effectively suppress gonadal function in MTF and FTM transgender patients. 2) To determine the frequency and range of serum E2 levels above the normal male range in FTM patients receiving T therapy. Design Retrospective cohort study. Setting Outpatient reproductive endocrinology clinic at an academic medical center. Patients 65 FTM and 33 MTF patients were included who were > 18 years old and not receiving a progestin or GnRHa. Intervention FTM patients were receiving T through injections or gel. MTF patients were receiving oral or subcutaneous E2. Main Outcome Measurements In FTM patients the indicator of ovary suppression was amenorrhea. In MTF patients the indicator of testes suppression was T levels <50 ng/dL. Results Median serum total T level for FTM patients was 712 ng/dL (range, 370-1164 ng/dL). On T therapy alone, 90.8% of patients achieved amenorrhea. 49.2% of patients had serum E2 levels above the normal range for women. 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. Conclusions T and E2 therapy are usually effective without progestin or GnRHa therapy to suppress gonadal function in transgender patients. Progestin and/or GnRHa therapy should only be initiated in those patients who do not have adequate gonadal suppression on optimized doses of T or E2 alone.
OBJECTIVE: To determine the efficacy of testosterone (T) or estradiol (E2) therapy alone, without a GnRH agonist or progestin, to suppress endogenous gonadal activity in female-to-male (FTM) or male-to-female (MTF) transgender patients. DESIGN: A retrospective cohort study of transgender patients undergoing routine therapy in the Reproductive Endocrinology Clinic at Maine Medical Center. MATERIALS AND METHODS: Data were collected from all transgender patients seen in the outpatient clinic between 03/2013 and 01/2018 who met inclusion criteria: 1) age 18-40 years for FTM and 18-50 years for MTF; 2) normal reproductive function prior to therapy; 3) total T within the normal adult male range (348-1197 ng/dL) in FTM patients while on T therapy; 4) serum E2 greater than 100 pg/mL in MTF patients while on E2 therapy unless T was adequately suppressed at lower serum E2 concentrations; 5) no concurrent therapy with a progestin or GnRH agonist; and 6) no history of oophorectomy or orchiectomy. Consistent with Endocrine Society guidelines, effective suppression of ovarian function in FTM patients was assessed by cessation of menses and a serum E2 of (<50 pg/mL). In MTF patients, testicular suppression was assessed by total serum T concentrations below the upper limit of the premenopausal adult female normal range (<55 ng/mL) 1. RESULTS: FTM patients (n¼50) were aged 26.2AE5.9 years and received T through subcutaneous (SC, n¼58) or intramuscular (IM, n¼2) injections. T doses ranged from 40-100 mg per week. All FTM patients were amenorrheic on T therapy alone. The mean serum E2 concentration was 39.8AE21.4 pg/ mL. Among these 50 patients, 36 (72%) had serum E2 <50 pg/mL. The median serum E2 value for the 14 patients with E2 R50 pg/mL was 55 pg/mL (range, 55-130). Thus, 36 out of 50 (72%) FTM patients had effective biochemical suppression of ovarian function without a GnRH agonist or progestin therapy and all FTM patients had clinical suppression of ovarian function (amenorrhea). MTF patients (n¼24) were aged 29.7AE9.0 years and received oral (n¼25), SC (n¼1), or IM (n¼1) E2 as well as spironolactone. Oral E2 doses ranged from 3-12 mg per day. Serum total T values for the 24 MTF patients were all within the target range (median 8.2, range 2.7-36 ng/ dL). Thus, all MTF patients had effective biochemical suppression of testicular function without GnRH agonist or progestin therapy. CONCLUSIONS: Our results indicate that most transgender patients do not need GnRH agonist or progestin treatment in addition to T or E2 therapy to suppress endogenous gonadal activity. Additional unnecessary endocrine therapies to suppress ovarian or testicular function incur a significant expense and potential adverse effects without providing a clear change in clinical outcome.
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