Acne in Gender-Affirming Care

Clinical Review · CR-001

1. Why acne matters in gender-affirming care

Acne is multifactorial, but androgens are central: they enlarge the sebaceous glands and increase sebum, which — with follicular hyperkeratinisation, inflammation and Cutibacterium acnes — produces acne. Treatments that raise androgen activity can therefore precipitate or worsen it, and those that lower it can improve it. Gender-affirming hormone therapy does both, in opposite directions, placing acne squarely within it: a frequent, visible, treatable effect that is too often left unmanaged in the people most affected.^[9]

2. Acne on masculinising (testosterone) therapy

A note on the numbers first. Two kinds of figure appear in this literature and should not be run together. Clinical-examination prevalence comes from small prospective cohorts that examined participants’ skin directly; these report high figures but are small and demographically narrow. Healthcare-coded incidence comes from large electronic-records studies that count acne only when it reached a clinical encounter and was coded; these capture far more people but undercount mild acne never brought to care. Both are useful; they measure different things.

Clinical-cohort prevalence. Small prospective cohorts, with limited demographic diversity, have reported clinically assessed facial acne in roughly 80–90% of transmasculine participants by 4–6 months after starting testosterone, up from around a third at baseline.^[5]

Population incidence. A large 2026 electronic-records cohort study found higher coded incident acne in transmasculine individuals than in matched cisgender men — a five-year cumulative incidence of about 16% versus about 4% — with risk highest in the first year after testosterone.^[1] An earlier records study of 988 people found coded acne prevalence rising from about 6% to 31% after starting therapy.^[2]

Severity. Often mild, but not always: a three-year cohort found moderate-to-severe acne rising from about 12% to 39% after one year.^[3] Reported risk factors for moderate-to-severe disease include younger age at initiation (18–25), higher BMI, higher testosterone concentrations (within or above the target range), and acne already present at baseline.^[3]

A rare but important pattern. Sudden severe inflammatory flares — including acne fulminans — can occur after starting or escalating testosterone, or after starting isotretinoin on a background of severe acne. These are uncommon but matter, because they can scar quickly and may need systemic corticosteroid cover and specialist input rather than routine escalation.^[8,10]

Distribution. Testosterone-associated acne commonly involves both the face (especially the lower third) and the trunk — chest, shoulders and back. It usually appears within the first months, peaks across the first year, and often eases thereafter, though it can persist.^[1,5]

The access gap. Survey data suggest transmasculine people carry more moderate-to-severe acne than transfeminine people yet are less likely to have seen a dermatologist.^[4] Because inflammatory acne scars permanently, this supports proactive counselling and early referral over watchful waiting.

Skin of colour. In darker skin phototypes, acne more readily leaves post-inflammatory hyperpigmentation, and there is greater risk of keloidal or hypertrophic scarring — both of which raise the stakes of treating early and treating well, and shape choices such as photoprotection and caution with procedures.^[8]

3. Acne on feminising therapy

The feminising picture is largely the mirror image, though the direct dermatological evidence is thinner. Mechanistically, as testosterone activity falls, sebum and androgen-driven acne would be expected to improve — one of the more biologically plausible and commonly reported skin effects of feminising therapy. The 2026 population data are broadly consistent while adding nuance: after starting oestradiol, transfeminine people had a small early increase in coded acne risk relative to cisgender men, but lower risk than cisgender women.^[1] Some people do experience acne early in treatment, before androgen suppression is complete, or during dose or formulation changes. The specific feminising regimen may also matter — oestradiol with different anti-androgens (spironolactone, cyproterone acetate, a GnRH analogue) or oestradiol alone will differ in how completely they suppress androgen action — though this has not been compared head-to-head for acne. Cyproterone acetate warrants a specific mention, being one of the main feminising anti-androgens in the UK and Europe: as a potent androgen blocker it helps reduce sebum, and with it acne, as part of androgen suppression — an effect shown for cyproterone acetate in cisgender women with acne^[11] — so at feminising doses it contributes to the improvement rather than being a drug added for acne. Its dosing and safety profile belong to the hormone-therapy discussion rather than to acne management here (see the companion review, Feminising Hormone Therapy). Where acne persists on feminising therapy, it is managed on the principles below. The mechanism is covered in the companion review on oestrogen and skin, and why individual responses differ in Why Skin Changes Vary.

4. Assessment

Assessment is mostly ordinary dermatology, done inclusively. Grade severity (a physician global assessment distinguishes mild, moderate and severe), and examine the trunk as well as the face. Ask about impact on mood and quality of life — acne’s psychosocial weight is often greater than its clinical severity, and heavier in a population with elevated baseline depression and anxiety.^[5]

Consider the differential. Not every eruption in this setting is acne vulgaris. Acne mechanica and folliculitis from chest binding, ordinary bacterial folliculitis, gram-negative folliculitis (after prolonged antibiotics), hidradenitis suppurativa and, occasionally, drug-induced or steroid acne can mimic or coexist with it, and each is managed differently.

Take an inclusive sexual and reproductive history, without assumption: gender identity does not tell you a person’s anatomy, partners or pregnancy potential, and these matter for treatment choice. Testosterone is not reliable contraception and does not by itself remove pregnancy potential; UK PPP materials define childbearing potential by uterus and ovary status unless programme-specific criteria for no expected pregnancy risk are met.^[5,7]

5. Management principles

The organising rule: treat the acne directly, and choose agents that fit the person’s goals. Most acne can be managed without reducing an effective testosterone dose; reflexive dose reduction under-treats the transition. Where hormones are genuinely implicated — for example supraphysiological testosterone or high post-injection peaks — smoothing exposure (adjusting formulation, dose interval or route) with the hormone prescriber is often preferable to simply lowering the dose, and endocrine review is reserved for selected or refractory cases.

Topical therapy is first-line for mild-to-moderate acne, as in anyone else: a topical retinoid, benzoyl peroxide, and topical antibiotics — the last always paired with benzoyl peroxide and never used as monotherapy, to limit resistance.^[8] Topical clascoterone is worth noting here: it is designed for local androgen-receptor antagonism in the skin, with no expected clinically meaningful systemic anti-androgen effect, so it can help hormonal acne without undermining masculinisation — though it has not been studied specifically in transmasculine patients, and some studies report laboratory HPA-axis changes.^[5,8]

Oral antibiotics (typically doxycycline) are a standard step up for moderate inflammatory acne — time-limited and combined with a topical retinoid and benzoyl peroxide, again for stewardship.^[8]

Truncal and binder practicalities. Truncal acne is aggravated by the friction, occlusion and sweat of chest binding. Practical measures help: a benzoyl-peroxide wash (warning patients it bleaches fabric and towels), binder hygiene and breaks where feasible, and prompt showering after sweating. These small things materially affect adherence and outcome.

Hormonal treatments need care here. Spironolactone — a mainstay of hormonal acne treatment in cisgender women — is generally avoided for acne in people using testosterone for masculinisation, because its systemic anti-androgen action may conflict with treatment goals; it should be considered only after explicit shared decision-making (some non-binary or partially-masculinising patients may weigh it differently).^[5] Combined oral contraceptives can treat acne but raise the same conflict and are often unwelcome. Contraceptive choices carry their own acne nuances — a copper IUD is hormone-neutral, while progestogen-dominant options (some implants, injectables and pills) can worsen acne in susceptible people — so where contraception is needed (including for isotretinoin), method choice is a shared decision that weighs acne effect, efficacy and acceptability.

6. Isotretinoin

For severe, nodular, scarring or treatment-resistant acne, isotretinoin is the most effective option and is entirely appropriate for trans patients, on the same indications used for anyone else.^[5,8] Because testosterone-associated acne may be severe or scarring in a clinically meaningful minority, a proportion of transmasculine patients will meet those indications. It carries specific considerations that are navigable with planning.

Teratogenicity and pregnancy-prevention programmes. Isotretinoin is severely teratogenic, so regulators require pregnancy-prevention frameworks for anyone of childbearing/pregnancy potential — the iPLEDGE programme in the United States and the Pregnancy Prevention Programme (PPP) in the UK. Eligibility is based on pregnancy potential as defined by the relevant programme, not gender identity. In the US, the FDA states that from 13 December 2021 iPLEDGE assigns patients to two categories — “patients who can get pregnant” and “patients who cannot get pregnant” — replacing the earlier gender-based scheme.^[6] In the UK, the PPP uses “childbearing potential” with programme-defined categories and allows for people with no expected risk of pregnancy. Many transmasculine people with a uterus and at least one ovary will fall within these requirements — programme-specific contraception and pregnancy-testing rules — unless they meet the programme’s criteria for no expected pregnancy risk.^[7] Two points are commonly got wrong: testosterone is neither reliable contraception nor a contraindication to other contraception, so effective, programme-appropriate contraception can be used alongside it.^[5] These conversations are best had directly and inclusively, since the programmes’ framing can otherwise feel invalidating.

Procedure and surgery timing. Historical practice often delayed elective procedures (dermabrasion, laser resurfacing) and surgery for 6–12 months after isotretinoin over wound-healing concerns, but the evidence for impaired healing is limited and procedure-specific, and modern reviews challenge a blanket delay. Incisional gender-affirming surgery is not the same as laser resurfacing. Timing should therefore be discussed between the patient, dermatologist and surgeon rather than automatically deferred.^[5]

Monitoring. Standard isotretinoin monitoring applies — lipids and liver enzymes, mucocutaneous effects (dryness, cheilitis), and awareness of relapse — alongside a sensible dosing approach. Hair-removal timing matters too: laser and electrolysis around a course need procedure-specific counselling, which connects to the person’s wider hair-removal plan.

Mood. Mood symptoms should be monitored during treatment, particularly in those with prior mental-health concerns — while acknowledging that a causal link with isotretinoin remains debated and that acne itself is associated with psychological morbidity.^[5] In a population with elevated baseline depression and suicidality, this monitoring matters without assuming causation either way.

Team. Severe acne here is best managed as a multidisciplinary effort — dermatology, the hormone prescriber, and, where relevant, surgical, reproductive and mental-health colleagues.^[5]

7. The bigger picture: burden and access

Two facts should shape practice. First, acne’s harm is not only cosmetic: it scars — more readily, and with more pigmentary and keloidal consequence, in darker skin — and it weighs on mood at a stage when many people are already navigating a great deal. Second, the group most likely to get significant acne from treatment is among the least likely to reach dermatological care.^[4,5] Proactive counselling before starting testosterone, a low threshold for referral, and an affirming manner are therefore not extras — they are how this common, treatable, scarring condition is kept from doing lasting harm.

8. Evidence quality

The evidence here is stronger than for most trans-dermatology topics, but uneven, and its numbers need honest labels. That testosterone commonly precipitates acne is well supported, now including large population-level data — but those population figures are healthcare-coded incidence, dependent on people presenting to care and on coding, and they undercount mild acne; they are not interchangeable with the higher clinical-examination prevalence from small cohorts.^[1,2,3,5] The feminising-therapy expectation rests more on mechanism and cross-sectional data than on prospective transfeminine dermatology. The management guidance is largely sound general dermatology applied to this setting rather than trans-specific trial evidence: clascoterone is mechanistically apt but unstudied in trans patients, and no trials compare acne treatments head-to-head in this population. The isotretinoin and regulatory content is practice-and-policy guidance, not experimental finding. In short: the epidemiology is solid but must be read by measure; the therapeutics are extrapolated from general dermatology with reasoned, not trialled, trans-specific adjustments.

Clinical bottom line

1. Acne is a common, clinically predictable effect of masculinising therapy — usually worst in the first year — and would be expected to improve on feminising therapy.^[1,3]
2. Counsel early, examine the trunk, mind skin-of-colour scarring risk, and refer promptly; the most affected group is the least likely to reach care.^[4]
3. Treat acne directly and choose agents that fit transition goals; smooth testosterone peaks rather than reflexively lowering an effective dose, and avoid spironolactone for acne on testosterone absent shared decision-making.^[5]
4. Isotretinoin is appropriate for severe or scarring acne on standard indications, with attention to pregnancy-prevention programmes, procedure timing (not automatic deferral) and mood.^[5,6,7]