---
title: "Low‑dose estradiol to treat persistent vasomotor symptoms after oophorectomy in a transgender man"
id: "cmaj-1-estradiol-for-persistent-vasomotor-symptoms-after-surgical-menopause-in-a"
canonical_url: "https://medichelpline.com/clinical-feed/cmaj-1-estradiol-for-persistent-vasomotor-symptoms-after-surgical-menopause-in-a"
content_type: "clinical_feed_article"
specialty: "Endocrinology"
source_name: "CMAJ"
source_url: "http://www.cmaj.ca/cgi/content/short/198/37/E1439?rss=1"
published_at: "2026-10-26T04:05:18.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Low‑dose estradiol to treat persistent vasomotor symptoms after oophorectomy in a transgender man
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/cmaj-1-estradiol-for-persistent-vasomotor-symptoms-after-surgical-menopause-in-a
- **Specialty:** [Endocrinology](https://medichelpline.com/clinical-feed/endocrinology.md)
- **Primary Source:** CMAJ
- **Source URL:** [Original Journal Publication](http://www.cmaj.ca/cgi/content/short/198/37/E1439?rss=1)
- **Published At:** 2026-10-26T04:05:18.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- A 42-year-old transgender man developed new, severe **vasomotor symptoms** and systemic complaints after total abdominal hysterectomy with bilateral salpingo-oophorectomy despite ongoing **testosterone** therapy. - Postoperative labs showed elevated FSH and LH consistent with surgical menopause; estradiol was initially elevated then fell into the cisgender male range after adjustments to testosterone dosing and formulation. - The clinical team excluded thyroid disease, adrenal pathology, pituitary abnormality and infectious or medication causes before attributing symptoms to hypoestrogenemia. - Switching injectable testosterone to transdermal gel reduced peak-to-trough variation and lowered estradiol, but headaches and hot flashes persisted. - Low‑dose transdermal **estradiol** was initiated and titrated (25 → 37.5 → 50 μg/24 h twice weekly) with symptomatic improvement: near-complete resolution of hot flashes within one month, better cognition, less musculoskeletal pain and weight stabilization. - On estradiol therapy, serum estradiol and testosterone remained within reported cisgender male reference ranges; the patient did not report feminization, worsening gender dysphoria, or thromboembolic events. - Authors noted improved HbA1c and progressive weight loss (some temporally related to later addition of tirzepatide); causality with estradiol cannot be established from this single case. - The literature on post‑oophorectomy hormone management in transgender men is sparse; available studies show variable estradiol after oophorectomy and suggest aromatization of testosterone may not reliably restore estrogen. - Transdermal estradiol was chosen to minimize thrombotic risk relative to oral formulations, but no trials have evaluated thrombotic risk of combining transdermal estradiol with physiologic testosterone in transgender men. - Unanswered questions include optimal estradiol targets for bone and cardiometabolic health in this population and longer-term safety of adjunctive estrogen therapy after surgical menopause in transgender men.
## Clinical Analysis & Structured Key Points
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Department of Obstetrics and Gynecology (Jacobson), William Osler Health System, Ont.; Division of Endocrinology (Ahmad), Department of Medicine, Toronto Western Hospital–University Health Network, Toronto, Ont. * MD * [Find this author on Google Scholar](https://www.cmaj.ca/lookup/google-scholar?link_type=googlescholar&gs_type=author&author\[0\]=Macie%2BNarbonne "Open in new tab") * [Find this author on PubMed](https://www.cmaj.ca/lookup/external-ref?apath=/cmaj/198/37/E1439.atom&link_type=AUTHORSEARCH&access_num=Narbonne%20M) * [Search for this author on this site](https://www.cmaj.ca/search/?author1=Macie%20Narbonne) * Michelle Jacobson Michelle Jacobson * Division of General Internal Medicine (Narbonne), Division of Endocrinology (Ahmad), and Department of Obstetrics and Gynaecology (Jacobson), University of Toronto, Toronto, Ont.; Department of Obstetrics and Gynecology (Jacobson), William Osler Health System, Ont.; Division of Endocrinology (Ahmad), Department of Medicine, Toronto Western Hospital–University Health Network, Toronto, Ont. * MD MHSc * [Find this author on Google Scholar](https://www.cmaj.ca/lookup/google-scholar?link_type=googlescholar&gs_type=author&author\[0\]=Michelle%2BJacobson "Open in new tab") * [Find this author on PubMed](https://www.cmaj.ca/lookup/external-ref?apath=/cmaj/198/37/E1439.atom&link_type=AUTHORSEARCH&access_num=Jacobson%20M) * [Search for this author on this site](https://www.cmaj.ca/search/?author1=Michelle%20Jacobson) * and Tehmina Ahmad Tehmina Ahmad * Division of General Internal Medicine (Narbonne), Division of Endocrinology (Ahmad), and Department of Obstetrics and Gynaecology (Jacobson), University of Toronto, Toronto, Ont.; Department of Obstetrics and Gynecology (Jacobson), William Osler Health System, Ont.; Division of Endocrinology (Ahmad), Department of Medicine, Toronto Western Hospital–University Health Network, Toronto, Ont. * MD MScCH * [Find this author on Google Scholar](https://www.cmaj.ca/lookup/google-scholar?link_type=googlescholar&gs_type=author&author\[0\]=Tehmina%2BAhmad "Open in new tab") * [Find this author on PubMed](https://www.cmaj.ca/lookup/external-ref?apath=/cmaj/198/37/E1439.atom&link_type=AUTHORSEARCH&access_num=Ahmad%20T) * [Search for this author on this site](https://www.cmaj.ca/search/?author1=Tehmina%20Ahmad) * CMAJ * October 26, 2026 * 198 * (37) * E1439-E1442; * DOI: https://doi.org/10.1503/cmaj.261004 [PDF](https://www.cmaj.ca/content/cmaj/198/37/E1439.full.pdf)[Help](https://scholar.google.com/scholar/help.html#access) * [Article](https://www.cmaj.ca/content/198/37/E1439#tab-group-article) * [Figures & Tables](https://www.cmaj.ca/content/198/37/E1439#tab-group-figure) * [Responses](https://www.cmaj.ca/content/198/37/E1439#tab-group-eletter) * [Metrics](https://www.cmaj.ca/content/198/37/E1439#tab-group-metrics) * [ PDF](https://www.cmaj.ca/content/cmaj/198/37/E1439.full.pdf) Key points * Persistent vasomotor symptoms after oophorectomy should prompt evaluation for hypoestrogenemia, even in transgender men receiving adequate testosterone therapy. * Low-dose transdermal estradiol may be an effective option for refractory vasomotor symptoms in transgender men without causing feminization or worsening gender dysphoria. * Evidence to guide hormone management after oophorectomy in transgender men is limited, highlighting a need for individualized, symptom-based care. * Data from cisgender populations suggest that prolonged estrogen deficiency after bilateral oophorectomy may have long-term health implications; whether these findings apply to transgender men requires further study. A 42-year-old transgender man was referred to our endocrinology clinic for management of masculinizing hormone therapy. His medical history included type 1 diabetes, hypertension, and dyslipidemia. His medications included an insulin pump, amlodipine 10 mg daily, atorvastatin 20 mg daily, and testosterone enanthate (200 mg/mL) 60 mg intramuscularly weekly. He had undergone gender-affirming bilateral mastectomy several years earlier. Two years before presentation, he underwent total abdominal hysterectomy with bilateral salpingo-oophorectomy for chronic pelvic pain of uncertain etiology, in addition to gender affirmation. Although his pelvic pain resolved postoperatively, recovery was complicated by new symptoms, including frequent hot flashes (3 to 6 episodes per day), night sweats, headaches, fatigue, memory impairment, sore joints, and tight muscles. He gained 13.6 kg within 12 months of surgery, most within 5 months after surgery, contrasting with only 4 kg gained during the preceding 8 years of testosterone therapy. We evaluated him for secondary endocrine causes of weight gain, fatigue, and vasomotor symptoms with measurement of thyroid-stimulating hormone, free thyroxine, adrenocorticotropic hormone, and serum cortisol levels (dexamethasone suppression test was negative), together with a magnetic resonance imaging scan of the sella; all findings were unremarkable. Infectious causes and medication adverse effects were also excluded. After surgery, the patient had elevated follicle-stimulating hormone of 49.9 to 63.9 (reference range 1.0 to 12.0) IU/L and luteinizing hormone of 27.7 to 31.4 (reference range 0.6 to 12.1) IU/L, consistent with surgical menopause ([Table 1](https://www.cmaj.ca/content/198/37/E1439#T1)). In February 2024, testosterone was 36.6 (reference range 8.4 to 28.8) nmol/L, with estradiol elevated at 292 (male reference range 37 to 147) pmol/L, presumed to reflect peripheral aromatization of exogenous testosterone to estradiol. Despite elevated estradiol, his vasomotor symptoms continued. Testosterone dosing was subsequently reduced (from 80 mg to 60 mg intramuscularly weekly) through his family physician, with both testosterone and estradiol thereafter remaining within physiologic cisgender male ranges. However, his symptoms worsened. View this table: * [View inline](https://www.cmaj.ca/content/198/37/E1439) * [View popup](pending:yes) Table 1: Serial measurements of body weight, testosterone, and estradiol levels of a 42-year-old transgender man during gender-affirming hormone therapy and after surgical menopause Given the patient’s ongoing symptoms, we transitioned testosterone from weekly injectable therapy (60 mg) to transdermal 1% gel (75 mg daily) to minimize peak-to-trough fluctuations, owing to concern that supraphysiologic testosterone peaks were contributing to his headaches. However, the headaches persisted and his estradiol level decreased. A neurologist diagnosed migraine without aura, thought to be exacerbated by hypoestrogenism after surgical menopause. We initiated low-dose transdermal estradiol (25 μg/24 h twice weekly) to address persistent vasomotor symptoms while minimizing feminizing effects. The potential thromboembolic risk of adjunctive estrogen therapy was discussed. Given the lower thrombotic risk associated with transdermal than with oral estradiol, we selected a low-dose transdermal preparation. After 1 week of therapy, the patient estimated a 10% reduction in hot flash frequency and reported a mild reduction in headache frequency. As vasomotor symptoms persisted, 2 weeks later, we increased transdermal estradiol to 37.5 μg per 24 hours twice weekly. The patient noted mild additional benefit, prompting further increase to 50 μg per 24 hours, twice weekly. After 1 month of estradiol treatment, the patient reported near-complete resolution of vasomotor symptoms, improved cognition, reduced muscle and joint pain, improved energy, and weight stabilization. In the months following, his estradiol remained stable at 116 to 123 (male reference range 37 to 147) pmol/L, with testosterone at 8.1 to 13.8 (reference range 8.4 to 28.8) nmol/L. His weight stabilized, and his glycated hemoglobin (HbA1c) level improved on estradiol replacement therapy. At his peak postoperative weight, he weighed 79.8 kg. Before initiation of low-dose estradiol replacement therapy, his weight was 78.0 kg. Within 4 months of initiating and up-titrating low-dose estradiol therapy, his weight decreased and plateaued at about 74.5 kg. Although the weight loss occurred before the patient met with a dietitian, he had been making more effort to track his caloric intake. After 4 months of estradiol treatment, tirzepatide (2.5 mg subcutaneously, weekly) was then initiated to facilitate weight loss, and within a few months, the patient’s weight further decreased to 70.5 kg. His HbA1c remained stable at 7.5% postoperatively before estradiol initiation, then improved to 6.9% within a few months of starting the patch, before tirzepatide initiation. At the patient’s last follow-up (13 mo after estradiol initiation), his symptom control was maintained, and his weight had decreased to 68.5 kg without any dose escalation of tirzepatide. He did not report any feminizing physical changes (including mastalgia or gynecomastia), worsening gender dysphoria, or thromboembolic events. ## Discussion A current international guideline recommends testosterone monotherapy as the standard gender-affirming hormone therapy for most transgender men.[1](https://www.cmaj.ca/content/198/37/E1439#ref-1) A common assumption is that exogenous testosterone provides adequate peripheral aromatization to estradiol to mitigate physiologic sequelae related to estrogen deficiency, including vasomotor symptoms, following surgical menopause, in which case testosterone largely prevents symptoms associated with estrogen deficiency. However, emerging data call this assumption into question. A study of transgender men on long-term testosterone therapy found that participants’ serum estradiol levels often remained within the typical male range, suggesting that aromatization alone may not reliably restore estrogen levels.[2](https://www.cmaj.ca/content/198/37/E1439#ref-2) Worth noting is that estradiol may be an imperfect marker of total estrogen activity in this context, as peripheral aromatization in adipose tissue predominantly produces estrone, which is not routinely measured in clinical practice. Another study showed that serum estradiol levels decreased significantly after oophorectomy in transmasculine individuals despite ongoing testosterone therapy.[3](https://www.cmaj.ca/content/198/37/E1439#ref-3) Data on estradiol levels after oophorectomy in transgender men remain limited; available evidence suggests estradiol concentrations may remain within the typical male range despite ongoing testosterone therapy. Research on hypogonadal cisgender men showed that vasomotor symptoms were more closely associated with estradiol deficiency than with androgen deficiency, which suggests estrogen as the key mediator of vasomotor symptoms in hypogonadal men.[4](https://www.cmaj.ca/content/198/37/E1439#ref-4) Although these findings provide valuable insights, a gap in the literature remains on the management of menopause in transgender men after oophorectomy. To date, only 1 published case report describes severe vasomotor symptoms in a transgender man on stable testosterone therapy post-oophorectomy, with symptoms resolving after the addition of low-dose estradiol.[5](https://www.cmaj.ca/content/198/37/E1439#ref-5) Despite this, literature suggests that the manifestations of hypoestrogenemia can be quite pronounced in cisgender women after surgical menopause.[6](https://www.cmaj.ca/content/198/37/E1439#ref-6) With this in mind, and no clear guidelines, we took an individualized approach to our patient’s hormone regimen by adding low-dose transdermal estradiol. Our approach required considering potential feminizing effects with adjunctive estrogen therapy. Although our patient is a transgender man, he maintained serum testosterone concentrations at or near the lower end of the physiologic male range while on testosterone gel therapy. In individuals within the physiologic cisgender male range, androgen receptor signalling suppresses estrogen-mediated breast epithelial proliferation, thereby limiting the development of gynecomastia despite endogenous or exogenous estrogen exposure.[7](https://www.cmaj.ca/content/198/37/E1439#ref-7) A transdermal estradiol patch delivering 50 μg/day typically produces serum estradiol concentrations of approximately 184 to 220 pmol/L,[8](https://www.cmaj.ca/content/198/37/E1439#ref-8) overlapping with or modestly exceeding the upper limit of the normal male reference range of 37 to 147 pmol/L, according to the American Urological Association (AUA).[9](https://www.cmaj.ca/content/198/37/E1439#ref-9),[10](https://www.cmaj.ca/content/198/37/E1439#ref-10) Notably, circulating estradiol concentrations in healthy cisgender men may occasionally exceed those observed in postmenopausal women. Estrogen receptors are widely expressed in male tissues; however, adequate circulating testosterone is thought to limit clinically significant feminization through predominant androgen receptor signalling.[9](https://www.cmaj.ca/content/198/37/E1439#ref-9) Accordingly, clinically evident feminization would not be expected in a transgender man maintained on physiologic testosterone receiving low-dose transdermal estradiol for vasomotor symptoms. The principal anticipated adverse effect would be mild mastalgia or breast tenderness. In men who develop breast symptoms while receiving testosterone therapy, measurement of serum estradiol is reasonable. The AUA recommends measuring serum estradiol in symptomatic patients, recognizing concentrations of more than 147 pmol/L as above the normal male reference range, although no specific therapeutic estradiol target is recommended.[10](https://www.cmaj.ca/content/198/37/E1439#ref-10) Another important consideration is thromboembolic risk. Transdermal 17β-estradiol has been associated in observational studies and meta-analyses with a lower risk of venous thromboembolism than with oral estrogen, although no randomized trial has been designed to evaluate this.[11](https://www.cmaj.ca/content/198/37/E1439#ref-11) No studies have assessed the thrombotic risk of combining low-dose transdermal estradiol with physiologic testosterone in transgender men; however, extrapolation from these observational data suggests that transdermal estradiol is the preferred estrogen formulation when adjunctive therapy is considered,[12](https://www.cmaj.ca/content/198/37/E1439#ref-12) with attention to concurrent risk factors such as testosterone-induced erythrocytosis.[10](https://www.cmaj.ca/content/198/37/E1439#ref-10) Beyond symptom management, the long-term health effects of estrogen deficiency also warrant consideration. Evidence from cisgender female populations demonstrates that surgical premature ovarian insufficiency increases the risk of cardiovascular disease, accelerated bone loss, and possibly earlier cognitive decline.[13](https://www.cmaj.ca/content/198/37/E1439#ref-13) Although recent literature has explored potential serum estradiol concentrations of approximately 220 to 550 pmol/L to optimize bone health during hormone therapy for postmenopausal cisgender women, whether similar targets apply to transgender men receiving physiologic testosterone therapy after oophorectomy is not known.[14](https://www.
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