Gynaecomastia

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Breast gland grows when oestrogenic stimulation outweighs androgen inhibition. This can follow normal hormonal transitions, reduced testicular testosterone, increased aromatisation, impaired hepatic hormone metabolism, thyrotoxicosis, hCG stimulation or receptor-blocking medicines. The finding may be unilateral or asymmetric even when benign. Tenderness suggests active proliferation but is not a cancer discriminator by itself.

The clinical task is first to distinguish a symmetrical subareolar disc from diffuse fat and from a discrete breast lesion. Breast cancer in men is uncommon but often presents as a painless unilateral hard mass, nipple change or nodes. A testicular tumour, Klinefelter syndrome, cirrhosis, chronic kidney disease, hyperthyroidism and medicine exposure are important secondary causes.

The central decision is whether this is a typical physiological or medicine-associated presentation suitable for observation, a secondary endocrine or organ disorder requiring treatment, or a suspicious breast or testicular lesion requiring urgent triple assessment. The person's pain and distress determine treatment need even when pathology is benign.

Key points

True gynaecomastia is benign proliferation of glandular breast tissue, usually felt as a rubbery or firm concentric subareolar disc; adipose enlargement without gland is pseudogynaecomastia.
Physiological gynaecomastia occurs in newborns, puberty and later life, but the age does not remove the need to investigate a suspicious eccentric mass or systemic clue.
The mechanism is increased oestrogen effect relative to androgen action from gonadal failure, liver or thyroid disease, tumours, medicines or exogenous hormones.
Take a complete prescribed, over-the-counter, private and substance history, including spironolactone, anti-androgens, finasteride, antipsychotics, anabolic steroids, cannabis and supplements.
A unilateral tender subareolar disc can still be benign; cancer is more concerning when hard, irregular, eccentric, fixed or associated with nipple, skin or nodal change.
Examine testes because an hCG- or oestrogen-producing testicular tumour can present through breast enlargement before the patient reports a testicular symptom.
Laboratory testing is targeted by age, duration and findings; testosterone with LH and FSH, oestradiol, hCG, prolactin, thyroid, liver and renal tests are not an automatic panel for every pubertal case.
New tender glandular tissue may respond to removal of the cause or specialist medical treatment, while long-standing fibrotic tissue is less likely to regress pharmacologically.
Persistent pain, marked asymmetry or psychological distress deserves active care and a surgical discussion where appropriate, although NHS commissioning criteria vary locally.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Physiological hormone transition

Puberty and later-life changes can temporarily shift the oestrogen-androgen balance and stimulate benign subareolar glandular tissue.

Reduced androgen effect

Testicular failure, increased aromatisation, liver disease, kidney disease or receptor-blocking medicines reduce androgen influence relative to oestrogen.

Hormone-producing disease

Testicular tumours, thyrotoxicosis or hCG-related disease can increase oestrogenic stimulation and require cause-directed assessment when supported by the surrounding clinical evidence.

Medicine or substance exposure

Several prescribed and non-prescribed agents alter hormone production, metabolism or receptor action, making a complete exposure history essential.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Oestrogenic signalling predominates
Breast stromal and ductal tissue receives more oestrogenic stimulation relative to androgen inhibition, regardless of the absolute hormone concentration.
2
Glandular tissue proliferates
A rubbery subareolar disc develops and may be tender during active proliferation, sometimes asymmetrically despite a benign mechanism.
3
Fibrosis may become established
Persistent enlargement becomes less hormonally responsive over time, leaving pain, contour change or distress even after the initiating factor resolves.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Subareolar glandular disc

A mobile rubbery or firm disc centred beneath the nipple, sometimes tender and bilateral, is the typical examination finding of true gynaecomastia.

Pseudogynaecomastia

Diffuse soft adipose tissue without a discrete subareolar gland commonly accompanies higher body fat; both conditions can coexist and examination may be difficult.

Male breast cancer patternRed flag

A hard irregular eccentric mass, skin dimpling, nipple inversion, unilateral bloody discharge or axillary nodes is suspicious and needs urgent breast referral.

Testicular tumour clueRed flag

A firm intratesticular mass, asymmetry, heaviness or recent rapid gynaecomastia can reflect hCG or oestrogen production and requires urgent testicular assessment.

Primary hypogonadism

Small firm testes, reduced shaving, infertility, low libido and raised gonadotrophins suggest testicular failure such as Klinefelter syndrome or treatment injury.

Liver or thyroid phenotypeRed flag

Jaundice, spider naevi, ascites, muscle loss or testicular atrophy suggests liver disease; tremor, weight loss, heat intolerance and tachycardia suggests thyrotoxicosis.

Medicine relationship

Onset after spironolactone, an anti-androgen, finasteride, dopamine blockade or anabolic steroid withdrawal supports a drug mechanism but does not cancel examination for malignancy.

Pubertal physiological change

A tender mobile subareolar disc during otherwise normal puberty is common and often resolves, but prepubertal onset, very rapid enlargement or incomplete puberty needs specialist assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Breast, node and testicular examinationFirst step
Why
Distinguish gland, fat and suspicious masses and identify a gonadal source.
Interpretation and limitations
Document position relative to the nipple, texture, mobility, skin, discharge and nodes. A discrete eccentric or fixed lesion enters the breast-cancer pathway regardless of presumed hormonal cause.
02
Breast ultrasound and mammography
Why
Characterise a clinically indeterminate or suspicious male breast lesion.
Interpretation and limitations
The symptomatic breast service selects age- and finding-appropriate imaging under Royal College of Radiologists guidance. Typical clinical gynaecomastia may not need both; suspicious imaging proceeds to tissue diagnosis.
03
Core needle biopsy
Why
Establish histology when examination or imaging cannot safely exclude malignancy.
Interpretation and limitations
Triple assessment aligns clinical, imaging and pathology findings. A benign imaging label should not overrule discordant nipple, skin or nodal findings.
04
Morning testosterone, LH, FSH and SHBG
Why
Identify primary or central hypogonadism when sexual, pubertal or testicular features suggest it.
Interpretation and limitations
Low testosterone with high gonadotrophins supports testicular failure, while low or normal gonadotrophins directs pituitary and functional assessment. Confirm low testosterone on separate standardised samples.
05
Serum hCG and oestradiol
Why
Detect a hormone-secreting testicular, extragonadal or adrenal process in rapid or unexplained cases.
Interpretation and limitations
An abnormal tumour marker or substantially raised oestradiol requires urgent specialist localisation. Assay interference and prescribed hCG use should be considered without delaying a credible cancer pathway.
06
Prolactin and thyroid function
Why
Assess galactorrhoea, central hypogonadism, dopamine-blocking medicine effects and thyrotoxicosis.
Interpretation and limitations
Repeat prolactin appropriately and review medicines and renal function. Hyperprolactinaemia is not itself a common direct cause of gland growth but can produce hypogonadism.
07
Liver and renal profile
Why
Identify impaired hormone metabolism and chronic organ disease that alters oestrogen-androgen balance.
Interpretation and limitations
Interpret with alcohol, nutrition and medicine context. Treating the organ disease may halt progression but established fibrotic breast tissue may persist.
08
Testicular ultrasound
Why
Evaluate a palpable abnormality, asymmetry or biochemical tumour-marker concern.
Interpretation and limitations
Arrange urgently through urology when a solid intratesticular lesion is suspected; a normal scan does not explain a suspicious breast mass and both pathways may be needed.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Pseudogynaecomastia

Diffuse soft fatty enlargement lacks the discrete subareolar glandular disc and usually follows overall adipose distribution rather than active breast proliferation.

Male breast cancer

A hard eccentric mass, nipple change, skin tethering or nodes is suspicious and requires urgent breast assessment rather than endocrine observation.

Breast abscess or inflammation

Focal erythema, warmth, fluctuation and systemic symptoms favour infection over hormonally driven glandular enlargement when supported by the history and examination.

Chest-wall mass

A lesion fixed beneath breast tissue or unrelated to the nipple-areolar complex may arise from skin, muscle or rib rather than breast gland.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01TriageMale breast enlargementFirst stepA person presents with unilateral or bilateral breast swelling, tenderness or a lump.

1Clarify duration, pain, nipple change, weight change, puberty, sexual and fertility symptoms, organ disease, family cancer risk, radiotherapy, medicines, anabolic agents, alcohol and supplements.
2Examine both breasts and nodes and distinguish subareolar gland from diffuse fat or an eccentric lesion; examine testes and secondary sexual characteristics with consent.
3Send any suspicious breast feature to the urgent NICE breast pathway and any testicular mass to urgent urology rather than ordering a routine endocrine panel first.
4For a typical benign presentation, decide whether age and history support observation or targeted testosterone, gonadotrophin, hCG, oestradiol, prolactin, thyroid, liver and renal testing.

02MedicineLikely drug-associated gynaecomastiaGlandular enlargement follows exposure to a medicine or exogenous hormone known to alter androgen-oestrogen balance.

1Confirm the temporal relationship, indication, dose changes and non-prescribed products and ensure examination contains no cancer or testicular red flag.
2Discuss stopping, reducing or substituting the suspected drug with its prescriber; do not abruptly withdraw essential antipsychotic, anti-androgen, heart-failure or endocrine treatment.
3Treat pain conservatively and reassess gland size after the expected biological interval, recognising that regression is less likely once tissue is longstanding and fibrotic.
4If enlargement progresses despite withdrawal or the causal link is weak, reopen endocrine, testicular and breast investigation rather than anchoring on the medicine.

03SecondaryEndocrine or organ diseaseSymptoms, examination or laboratory results suggest hypogonadism, thyroid, liver, kidney or tumour-related gynaecomastia.

1Confirm the hormone pattern with appropriately timed reliable tests and image testes, breast, pituitary or adrenal glands only when the phenotype indicates.
2Treat the underlying disorder through endocrinology, hepatology, renal, urology or oncology while addressing pain and psychosocial impact concurrently.
3Use testosterone only for confirmed symptomatic hypogonadism after fertility and prostate or haematocrit safety assessment; replacement may not reverse established tissue.
4EscalationEscalate rising hCG, oestradiol, a mass or rapid progression to the relevant multidisciplinary cancer service without waiting for symptom treatment to work.

04PersistentPainful or distressing benign gynaecomastiaSerious causes are excluded, but pain, asymmetry or psychosocial burden persists.

1Explain benign pathology and natural history without minimising impact, and offer support for clothing, body image, school, work, relationships and mental health.
2Consider specialist tamoxifen for selected recent tender proliferative disease after off-label consent and thrombosis and interaction review; avoid indiscriminate long-term prescribing.
3Refer to breast or plastic surgery for established large, painful or severely distressing tissue when conservative measures fail, explaining scar, contour and sensation risks.
4Check local NHS commissioning criteria early and document functional and psychological impact; inability to fund surgery does not end supportive care.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Blocks oestrogen receptors in breast tissue and may reduce tenderness and gland size before fibrosis becomes established.

Tamoxifen specialist treatment

Use only the short specialist-selected off-label course for recent painful proliferative gynaecomastia.

Assess venous thrombosis, visual symptoms, liver disease and interacting medicines and explain off-label use. It is not a substitute for evaluating cancer, testicular mass or endocrine cause.

Corrects androgen deficiency that contributes to gynaecomastia and other hypogonadal health effects.

Testosterone replacement

Use a licensed formulation and specialist-titrated regimen only after symptomatic hypogonadism is repeatedly confirmed.

It suppresses spermatogenesis, needs haematocrit and prostate monitoring and can aromatise to oestradiol; it may not shrink chronic glandular tissue and is not empirical breast-lump treatment.

Relieves tenderness while a recent benign process resolves or definitive cause treatment takes effect.

Simple analgesia

Use the lowest effective formulary paracetamol or anti-inflammatory regimen for a short symptomatic period.

Analgesia must not delay assessment of an eccentric mass. Review liver, renal, gastrointestinal, cardiovascular and interaction risks before selecting an anti-inflammatory drug.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Persistent pain

Active tissue proliferation can cause tenderness that interferes with clothing, exercise or sleep even when the pathology is benign.

Psychological distress

Visible breast enlargement can affect body image, relationships and social participation, making the person's priorities relevant to treatment need.

Missed underlying disease

Assuming every enlargement is physiological can delay recognition of hypogonadism, a testicular tumour, thyrotoxicosis or male breast cancer.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Document breast size, tenderness and examination features at a defined interval; any new eccentricity, fixation, nipple or nodal change triggers breast reassessment.
Track the relevant endocrine marker and clinical features after treatment of hypogonadism, thyrotoxicosis, liver disease or a tumour rather than repeating a generic panel.
After withdrawing a suspected medicine, review whether breast activity stabilises and whether the underlying condition remains controlled on the alternative regimen.
For tamoxifen, monitor thrombosis symptoms, vision, interactions and clinical benefit and stop at the planned specialist endpoint.
For testosterone, follow timed levels, haematocrit, prostate safety, sleep apnoea, symptoms and fertility under the replacement protocol.
Ask directly about pain, clothing, exercise, relationships, bullying and mood; referral need is determined partly by functional and psychological impact, not centimetres alone.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Tender can still be benign

New gland proliferation is often sore, while breast cancer may be painless. Pain alone neither proves benignity nor determines referral.

Concentric versus eccentric

A subareolar disc favours gynaecomastia; a hard lesion displaced from the nipple is more suspicious. Imaging and biopsy resolve clinical uncertainty.

Check the testes

Breast enlargement can be the presenting endocrine effect of a testicular tumour. Omitting testicular examination is a high-consequence shortcut.

Medicines need context

Spironolactone and anti-androgens may be essential for heart failure or cancer. Substitute collaboratively rather than trading breast symptoms for disease destabilisation.

Old tissue becomes fibrotic

Removing the hormonal driver early can halt or reverse active tissue, whereas established dense gland is much less responsive and may need surgery.

Fat and gland coexist

Weight change can reduce adipose bulk but not necessarily the subareolar gland. Promising that weight loss alone will cure true gynaecomastia is inaccurate.

Benign does not mean trivial

Pain, shame and avoidance of sport or intimacy can be profound. Validation and treatment discussion are appropriate after malignancy is excluded.

11Common pitfallsFrequent interpretation and management errors.

01
Calling every enlarged male breast obesity without palpating for gland.
02
Reassuring a hard eccentric mass as gynaecomastia.
03
Omitting nipple, node and testicular examination.
04
Ordering broad hormone panels for typical transient pubertal tissue without clinical indication.
05
Stopping essential spironolactone or antipsychotic treatment abruptly.
06
Starting testosterone before confirming hypogonadism and fertility plans.
07
Using tamoxifen without first excluding malignancy and reviewing thrombosis risk.
08
Dismissing psychological distress after benign histology.