Blood tests are how we confirm you get the levels you need, and they catch the one common silent side effect before it matters. This page covers what gets tested, how often, red-flag symptoms, and how to read your own results.
The monitoring schedule
The usual schedule looks like this:
| When | What gets checked |
|---|---|
| Baseline (before starting) | Testosterone, hematocrit/hemoglobin; often lipids, LFTs, glucose/A1c, and (in AusPATH/NHS protocols) LH, FSH, estradiol12 |
| Year 1 | Every ~3 months and with any dose change: testosterone + hematocrit (Endocrine Society / SOC8)13 |
| Once stable | 1-2×/year: testosterone + hematocrit13 |
| Ongoing | Blood pressure, weight at visits; cancer screening by anatomy (see FTM Long-Term Health); bone density per risk |
There is a lot of variance in when different standards of care recomend you getting blood tests; the Endocrine Society and WPATH SOC8 recommend labs about every 3 months through year 1, then 1-2×/year.13 While UCSF disagrees: “Endocrine Society guidelines recommend monitoring of hormone levels every 3 months. In practice this is not realistic and not likely to add value once a stable dosing has been achieved”, UCSF checks at 3 and 6 months, then yearly once you’re in range.2
Note from Aria:
I have opinions again! if you are somewhere blood tests are cheap or better yet free (Australia if you have a free GP/NP clinic near you) I would recomend, once stable, to at least get 2 tests a year, if you’re on a long acting formulation like undecanoate 1000mg I would recomend getting a blood tests around your injection time basically every time!
What’s tested
Testosterone. Interpreted against draw timing (mid-interval for weekly injections; trough-only for undecanoate; >=2 h after gel) and the target ranges in FTM Target Ranges.13
Hematocrit / hemoglobin. This is the only transmasculine lab with its own formal WPATH recommendation (SOC8 statement 12.17): “health care professionals monitor hematocrit (or hemoglobin) levels in transgender and gender diverse people treated with testosterone,” with the expected rise kept consistent with cisgender-male reference ranges.3 Testosterone drives red-blood-cell production; too much (erythrocytosis/polycythemia) thickens the blood. It’s the most common dose-limiting side effect and usually symptom-free until it’s not.
Lipids, glucose, LFTs. (That’s cholesterol and other blood fats, blood sugar, and liver-function tests.) The Endocrine Society suggests cardiovascular risk-factor screening (fasting lipids, diabetes screening).1 UCSF’s monitoring table states the opposite: “No evidence to support lipid monitoring at any time; use clinician discretion” (same for A1c - screen per general-population guidance instead).2 NHS and Canadian (Rainbow Health Ontario) protocols include lipids/A1c routinely; some include LFTs, while the Endocrine Society notes serious liver toxicity “is not anticipated” with bioidentical testosterone and UCSF’s table omits LFTs entirely.24
Bone density (DEXA): not routine on stable T - recommended when risk factors exist, specifically if someone stops hormones after gonadectomy.1 See FTM Long-Term Health.
The hematocrit thresholds
Three different answers exist to “when do we act?”, and none has been validated specifically in trans people:
- >50% - the Endocrine Society flags hematocrit above 50% as a “very high risk” baseline condition for testosterone therapy (a risk-stratification flag, not a management cut-off).1
- >=54% - the common action threshold (reduce dose, consider therapeutic phlebotomy/venesection - removing some blood, like a donation), imported from cisgender-male testosterone-therapy guidance (MSD Manual; European Association of Urology).5 Some institutional protocols operationalize it: 50-54% → hydrate and recheck in 1-3 months; >54% → phlebotomy plus dose/route change.6
- No number - SOC8 says only that the rise should stay “consistent with reference ranges in cisgender males.”3
How common is it really? Across large cohorts, ~11-20% of people on T exceed 50% at some point, but only ~0.5% exceed 54%, severe erythrocytosis is rare.78 Causality to clots is also weaker than often assumed: the link is “correlational rather than causal,” and the erythrocytosis effect washed out when smoking, blood pressure, and obesity were accounted for.7 Risk is higher with injectables than gel (see FTM forms of HRT), higher doses/peaks, smoking, untreated sleep apnea, and higher BMI.
If a result comes back high, the standard clinical goto is: confirm it (hydration affects this), check T levels including a peak, adjust dose/interval, consider switching to more frequent injections or transdermal, use phlebotomy/blood donation as a short-term bridge, and rule out other causes (sleep apnea, tobacco).2
Red flags - don't wait for your next scheduled draw
Possible thickened blood (book a prompt review + a CBC, a full blood count): persistent or worsening headaches, dizziness or ringing in the ears, blurred vision, facial flushing/ruddy complexion, itching especially after warm showers, burning/tingling in hands or feet, unusual fatigue or breathlessness, nosebleeds or easy bruising.9 Emergency now: chest pain or pressure; sudden shortness of breath; one-sided leg swelling/pain (possible clot in the leg); coughing blood (possible clot in the lung); face droop, arm weakness, or speech difficulty (stroke). Prompt, non-emergency: any vaginal bleeding after sustained amenorrhea (a long stretch with no periods) not explained by a missed or reduced dose, guidelines are clear this warrants evaluation (see FTM Periods and Fertility); periods persisting past ~6 months; hot flashes or regressing virilization (masculine changes sliding backwards, signs of possible underdosing); spreading redness, heat, pus, or fever at an injection site.24
LH, FSH, and the post-gonadectomy trick
LH and FSH (the two hormone signals your brain sends to the ovaries) are partially suppressed on T, not abolished (e.g., LH ~4-5 IU/L in cohorts on T), and no guideline uses them routinely.10
Estradiol and progesterone
No guideline schedules routine E2 or P4 checks for people on T but there is measured data: on testosterone, E2 falls or stays low (~100-175 pmol/L across nine cohorts; it does not rise into female ranges), P4 collapses to the floor - yet ~1 in 3 amenorrheic people still show signs of recent ovulation, which is why T is not contraception. Immunoassay (standard lab-test) E2 results at male-range levels are unreliable (LC-MS/MS, a more precise mass-spectrometry method, is the accurate one). Checking E2 can matter in specific situations: breakthrough-bleeding workups, post-oophorectomy low-dose regimens, and baseline PCOS workups. The full evidence walk-through is at What about estrogen and progesterone?.
How to read your own results
Patient portals mean you’ll often see your labs before your clinician calls. Some orientation:
- Reference ranges (the lab’s “normal” bands) follow the recorded sex marker on the lab order not your body. If your record says “F,” a healthy male-range testosterone will be flagged “HIGH” and a healthy male-range hematocrit may be flagged too. That flag is an artifact and not a finding. You can ask your prescriber or the pathology lab for affirmed-gender reference ranges.211
- Hematocrit/hemoglobin on T should be read against the male range if you’re amenorrheic, UCSF is explicit that the male upper limit is the right comparison, and conversely a value sitting between the female and male lower limits can hide genuine anemia (too few red blood cells).2
- Check draw timing before panicking. A testosterone drawn the day after your shot (a peak) can look supraphysiologic (above the male range) and mean nothing; one drawn at trough can look low. Compare like with like, see the timing table in FTM Target Ranges.
- Convert units before comparing to anything online. US labs use ng/dL (testosterone) and pg/mL (estradiol); Australia/UK use nmol/L and pmol/L. Full conversion table at Unit conversions (for reading your own results).
- Trend beats point. One out-of-range result is a question, not a verdict. hydration, illness, draw timing, and assay noise all move numbers. The pattern over time, plus how you feel, is what you/your clinician titrate against.
- Bring your results into the conversation. Knowing your trough level and where it sits in the male range is the single most effective piece of self-advocacy on this page. see Underdosing for why it matters.
Further reading
Don’t just take our word for it - here’s where the monitoring advice comes from.
- UCSF’s monitoring guidance - the practical, less-is-more monitoring schedule, plus how to read your labs
- WPATH Standards of Care v8 - the hematocrit-monitoring recommendation (statement 12.17) lives here
- Porat et al. 2023 - erythrocytosis in gender-affirming care - the open-access study on how common high red blood cells really are
- Trans Harm Reduction - blood tests - what to test, and when, if you’re doing this outside the system
- TransHub - clinician guidance - Australian monitoring and lab-range guidance
Footnotes
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Endocrine Society Clinical Practice Guideline (Hembree WC, et al.), J Clin Endocrinol Metab 2017;102(11):3869-3903 - Recs 4.1-4.4, Table 14 - https://academic.oup.com/jcem/article/102/11/3869/4157558 ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8
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UCSF Gender Affirming Health Program, “Overview of masculinizing hormone therapy” (monitoring tables, erythrocytosis, post-gonadectomy, lab interpretation) - https://transcare.ucsf.edu/guidelines/masculinizing-therapy ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8
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WPATH Standards of Care v8 (Coleman E, et al., 2022), Statements 12.9 and 12.17, Chapter 12 Table 5 - https://pmc.ncbi.nlm.nih.gov/articles/PMC9553112/ ↩ ↩2 ↩3 ↩4 ↩5 ↩6
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Rainbow Health Ontario, “Masculinizing Hormone Therapy” (monitoring table; bleeding workup); Nottinghamshire APC (NHS), “Masculinising Hormones Information Sheet” (2022) - https://www.rainbowhealthontario.ca/TransHealthGuide/gp-mascht.html ; https://www.nottsapc.nhs.uk/media/gxfnn13a/masculinising-hormones-information-sheet.pdf ↩ ↩2
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MSD Manual Professional, “Male Hypogonadism” (>=54% threshold); EAU Guidelines on Male Hypogonadism (2017) - https://www.msdmanuals.cn/en-in/professional/genitourinary-disorders/male-reproductive-endocrinology-and-related-disorders/male-hypogonadism ; https://d56bochluxqnz.cloudfront.net/media/Male-Hypogondism-2017-pocket-1.pdf ↩
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Johns Hopkins Center for Transgender Health, “Dosing Guide: Gender Affirming Hormone Therapy” (hematocrit action thresholds) - https://www.hopkinsmedicine.org/-/media/center-for-transgender-health/documents/adolescentdosingguide41224.pdf ↩
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Porat AT, et al., “Erythrocytosis in Gender-Affirming Care With Testosterone,” Ann Fam Med 2023 - https://pmc.ncbi.nlm.nih.gov/articles/PMC10519768/ ↩ ↩2
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Madsen MC, et al. (Amsterdam cohort, n=1073; 11% >0.50, 0.5% >0.54), summarized by The Blood Project, “Hematology and the transgender patient” (2022) - https://www.thebloodproject.com/cases-archive/a4/hematology-and-the-transgender-patient/ ↩
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Mayo Clinic, “Polycythemia vera - Symptoms & causes”; StatPearls, “Polycythemia” (hyperviscosity symptoms; physiology applies to secondary erythrocytosis) - https://www.mayoclinic.org/diseases-conditions/polycythemia-vera/symptoms-causes/syc-20355850 ; https://www.ncbi.nlm.nih.gov/books/NBK526081/ ↩
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Grouthier V, et al. (QTrans), JAMA Network Open 2025 (LH/FSH on T); Spinder T, et al., JCEM 1989 - https://pmc.ncbi.nlm.nih.gov/articles/PMC12311718/ ↩
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TransHub (ACON, Australia), clinician guidance (lab ranges and recorded sex markers) - https://www.transhub.org.au/clinicians/endocrinology/ ↩