Male infertility and hypogonadism

• Male infertility is the inability of a couple to conceive after 12 months of regular unprotected intercourse because of a factor in the man; hypogonadism is a separate but overlapping condition of androgen deficiency, and the two must never be managed with the same drugs. ^[5]
• Male factors contribute to infertility in up to half of all couples, so a male assessment is mandatory rather than optional even when a female factor is already known.^[1][2]
• A varicocele, the commonest surgically correctable cause, is found in roughly 35-40% of men with primary infertility and 45-80% of men with secondary infertility, but subclinical varicoceles need not be treated.^[6]
• Semen analysis is the central investigation, compared with the WHO 2021 reference values; an abnormal first sample must be confirmed, ideally 3 months later.^[3][5]
• Testosterone replacement is only for genuinely hypogonadal men: a morning fasting value below 264 ng/dL (Endocrine Society 2018) supports the diagnosis, other guidelines use 300 or 350 ng/dL, the therapeutic target is the mid-normal range at 450-600 ng/dL, and testosterone suppresses sperm production.^[7][8]

By the end of this page you should be able to:

1. Define male infertility and hypogonadism, and separate primary from secondary hypogonadism using the LH/FSH pattern.
2. Classify the causes of male infertility by level (hypothalamic-pituitary, testicular, post-testicular) and relate each to its mechanism.
3. Counsel about a varicocele, its grading, and which men should actually be offered repair.
4. Perform and interpret a semen analysis using the WHO reference values and the rules about repeating it.
5. Investigate a man with infertility or low testosterone, including when to order genetic tests such as karyotype and Y-chromosome microdeletion testing.
6. Manage hypogonadism safely: confirm it, choose the right formulation, obey the contraindications, and monitor the patient.
7. Explain the fertility-preserving alternatives to testosterone and when to refer to reproductive urology or fertility care.
8. Adapt investigation and treatment where imaging, hormones or surgery are limited.

Male infertility is the inability of a couple to conceive after 12 months of regular unprotected intercourse because of a factor in the man. It is fundamentally couple-based care: female age, ovarian reserve and the couple's time horizon shape every decision from the outset.^[4]

Hypogonadism is a clinical syndrome of androgen deficiency with symptoms, caused by low testicular testosterone production or impaired responsiveness. It is classified by where the fault lies:

• Primary (hypergonadotrophic) hypogonadism: the testis has failed, LH and FSH rise as the pituitary compensates, and the testes are small or atrophic.
• Secondary (hypogonadotrophic) hypogonadism: the hypothalamus or pituitary has failed, so LH and FSH are low or inappropriately normal despite a low testosterone.
• Functional hypogonadism: no organic defect of the hypothalamic-pituitary-gonadal axis is found; it is frequently associated with obesity, insulin resistance, chronic disease, drugs or ageing and is often reversible.
• Compensated hypogonadism: testosterone is normal with a raised LH.
• Androgen resistance: rare tissue insensitivity, with normal or raised testosterone despite symptoms.

In the testis, LH drives the Leydig cells to make testosterone and FSH drives the Sertoli cells to support germ-cell development; high intratesticular testosterone is essential for spermatogenesis. Only about 2% of circulating testosterone is free and biologically active, the rest bound to SHBG and albumin, and peripheral tissues convert testosterone to the more potent dihydrotestosterone (DHT) via 5-alpha reductase and to oestradiol via aromatase. This is why a blood testosterone in the normal range does not prove that the tubules are working, and why measures that raise systemic testosterone can still destroy fertility.

A varicocele is dilatation of the pampiniform venous plexus of the spermatic cord, almost always on the left because the left testicular vein drains into the left renal vein at a right angle. It is the commonest surgically correctable contributor to male infertility, but it is also common in fertile men, so its presence alone does not make it the cause.^[6]

• Infertility affects roughly one in six individuals worldwide, and about one in six couples have difficulty conceiving.^[1]
• Male factors contribute to infertility in up to half of all couples.^[1][2]
• A varicocele is found in about 10-20% of men in the general population, 35-40% of men with primary infertility and 45-80% of men with secondary infertility. It usually appears during the pubertal growth spurt.^[6]
• Hypogonadism becomes more common with age and comorbidity: total testosterone falls by roughly 1.6% per year with ageing and SHBG rises by about 1.3% per year; prevalence depends on definition and ranges from about 2% to over 30%.^[7]
• Klinefelter syndrome (47,XXY) is the commonest defined chromosomal cause of primary hypogonadism; see the hypogonadism and delayed puberty topic of this library for the full clinical detail.

Every cause can be placed at one of three levels: central (brain/pituitary), testicular, or post-testicular (ducts or ejaculation).

Hypothalamic or pituitary tumours, craniopharyngioma, pituitary surgery or radiotherapy, infiltrative disease, iron overload (haemochromatosis), hyperprolactinaemia; idiopathic (isolated) hypogonadotrophic hypogonadism, usually with smell loss in Kallmann syndrome; and reversible functional causes such as severe obesity, poorly controlled diabetes, chronic illness, organ failure, malnutrition, excessive exercise, sleep disorders, chronic glucocorticoid, opioid or androgenic steroid use, alcohol and cannabis.

Genetic (Klinefelter syndrome, Y-chromosome microdeletions in the AZF regions, chromosomal translocations); developmental (cryptorchidism, anorchia); acquired (mumps orchitis, torsion, trauma, chemotherapy or pelvic/testicular radiotherapy, orchidectomy, toxins); metabolic (obesity, severe varicocele, advanced age); and structural (myotonic dystrophy, androgen insensitivity).

Obstruction of the epididymis or vas deferens after infection (chlamydia, gonorrhoea, tuberculosis), prior vasectomy, hernia or pelvic surgery, or congenital absence of the vas deferens; ejaculatory failure (erectile failure, retrograde ejaculation, anejaculation after surgery or spinal injury); and isolated semen abnormalities without azoospermia (infection, antisperm antibodies, oxidative stress).

Age, cigarette smoking, obesity (body mass index of 30 kg/m2 or more), alcohol at more than roughly 14 units per week, scrotal heat (tight underwear, sauna or prolonged laptop on the lap), certain occupations, drugs including exogenous testosterone and anabolic steroids (both suppress sperm production even when used to improve libido or physique), and recreational drugs such as cannabis.^[4]

Spermatogenesis takes about 74 days from stem cell to spermatozoon plus epididymal maturation, which is why no treatment for low sperm count can be judged for at least 3 months. Cooling matters: the testis sits outside the abdomen and runs below core body temperature, and sustained scrotal heating (varicocele, hot baths, tight clothing, fever) injures germ cells. ^[2]

In primary testicular failure the Leydig cells make less testosterone and the Sertoli cells make less inhibin B and anti-Mullerian hormone; a rising FSH is the earliest hormonal sign of germ-cell damage and is the marker of severity of spermatogenic impairment. In hypogonadism the clinical picture follows the age of onset: before puberty, androgen deficiency stops penile and testicular growth, virilisation and the pubertal growth spurt and leaves low bone mass; in adults it causes loss of muscle and bone, anaemia, fatigue, low libido, erectile problems and altered body composition. Testosterone is erythropoietic, so deficiency produces a normochromic normocytic anaemia.

Varicocele allows warm blood to reflux; the resulting hypoxia, metabolite stasis, oxidative stress and reduced intratesticular testosterone disturb spermatogenesis. It can also reduce adolescent testicular volume by more than 20%, a marker of damage. The hypothalamic-pituitary-gonadal axis can also be perturbed, lowering circulating testosterone.

Ask, in the patient's own words, how long they have been trying; previous paternity with other partners; sexual frequency and technique; contraception; childhood problems such as cryptorchidism, hernia, mumps, torsion, or testicular surgery; infections (sexually transmitted, urinary, tuberculosis), pelvic surgery and cancer treatment; drugs including anabolic-androgenic steroids and testosterone; occupational heat or toxin exposure; family history of infertility or early loss of puberty; and recent febrile illness, which depresses the count for months. Include the partner's age, menstrual history, cycles and previous pregnancies.

Sexual symptoms are fewer spontaneous and morning erections, reduced libido and infertility. General: loss of muscle and strength, increased (especially visceral) fat, breast tenderness or gynaecomastia, fatigue, low mood and poor concentration. Bone: pain or low-trauma fracture. Anaemia. In a young man the overriding features are delayed or absent puberty, small testes, scant body and facial hair, tall eunuchoid proportions and a delayed voice break.

Build, facial and body hair, gynaecomastia, fat distribution and muscle bulk; penis and testes (size, consistency, position, orchidometer volumes; a volume under 6 mL suggests androgen deficiency and Klinefelter testes feel small and firm); the cord, where a varicocele feels like a "bag of worms" and enlarges on a standing Valsalva; and a digital rectal examination where age and prostate safety screening for testosterone make it appropriate. ^[8]

Sudden loss of sexual function with severe headaches or visual field change (suspect a pituitary mass); anosmia with absent puberty (Kallmann syndrome); bilateral absent testes; testicular mass; haematospermia; chronic liver or renal disease; anaemia with low testosterone.

An abnormal semen result is differential-diagnosed by the level of failure above. Low testosterone is differential-diagnosed first into primary (high LH/FSH) versus secondary (low or normal LH/FSH), then within secondary organic versus functional; the detailed table of organic and functional causes is summarised in the hypogonadism and delayed puberty topic of this library. ^[5]

A recurring puzzle is a dilated pampiniform plexus found on imaging. A subclinical varicocele must not be treated, and a right-sided or sudden varicocele should raise suspicion of a retroperitoneal obstruction or mass rather than an idiopathic one.

Semen analysis is the first diagnostic test and is only useful when performed to the WHO standard method (6th edition, 2021), with the same laboratory conditions when results are compared.^[3] Agree with the couple on 2-7 days' abstinence (the reference values assume 2-7 days), a fresh sample handled to the standard, and strict handling. ^[7]

Compare the result with the WHO reference values, which are 5th percentiles from men whose partners conceived within 12 months:

The medians are considerably higher (volume 3.0 mL, concentration 66 million/mL, total 210 million, total motility 64%, progressive 55%, vitality 78%, normal forms 14%), so an apparently "borderline" sample may simply sit in the normal lower tail of the distribution.^[7]

Rules that keep testing honest:^[5]

• Repeat any abnormal first sample to confirm it.
• Leave about 3 months between the test and the repeat, to let one full spermatogenic cycle complete; repeat sooner only for azoospermia or severe oligospermia. ^[5]
• Compare like with like: two analyses 3 months apart are more informative than four in a fortnight.
• After two or more abnormal semen analyses, examine the scrotum and testes and consider a testosterone and gonadotrophin panel.

• Standing physical examination first: a grade III varicocele is visible, grade II is palpable without a Valsalva, grade I is palpable only on a Valsalva, and a subclinical one is only found on ultrasound.
• Colour Doppler ultrasound is an adjunct for an uncertain examination (venous dilatation above 3 mm and reflux longer than 2 seconds on a Valsalva are widely used thresholds) or persistent or recurrent disease after repair, not a screening tool.^[6]

The same sample logic as the hypogonadism topic: a morning fasting total testosterone between 07:00 and 10:00 a.m., confirmed on a second sample about 4 weeks later and never during acute illness; LH and FSH to classify primary versus secondary disease; prolactin, thyroid function and iron studies if central disease is suspected; SHBG and a calculated free testosterone (around 6.5 ng/dL cut-off in the Brazilian consensus) when obesity, ageing, liver or renal or thyroid disease confound the result.^[7]

• Karyotype for idiopathic azoospermia, and consider it when sperm concentration stays below 5 million/mL.^[5]
• Y-chromosome microdeletion testing (AZF regions) for idiopathic azoospermia or concentration below 1 million/mL; AZFa and AZFb deletions effectively preclude sperm retrieval, while AZFc deletions permit it.^[5]
• CFTR mutation testing for idiopathic suspected obstructive azoospermia or a vasal abnormality on examination.^[5]
• Sperm DNA fragmentation testing is not currently recommended in routine practice.^[4][5]
• Antisperm antibody testing is not routine.^[5]

There is no "infertility stain"; the WHO values are lower reference limits and are only valid for samples analysed by the WHO methods. Output is summarised clinically:

• Normozoospermia: all parameters within reference.
• Oligozoospermia: concentration below 15 million/mL (or total below 39 million).
• Astheno- or teratozoospermia: motility or morphology below reference.
• Oligoasthenoteratozoospermia (OAT): all three affected.
• Azoospermia: no sperm in the ejaculate.
• Aspermia: no ejaculate.

Azoospermia is then split into obstructive (production intact, sperm cannot leave) versus non-obstructive (spermatogenic failure), on testicular size, FSH, examination of the epididymis and vas, and sometimes biopsy.

For hypogonadism the guideline numbers genuinely differ and should be stated rather than fudged:^[7][8]

• Endocrine Society 2018: 264 ng/dL (9.2 nmol/L) as the lower limit of normal total testosterone for healthy non-obese men; diagnose with unequivocally and consistently low morning values. ^[7][8]
• American Urological Association 2018: 300 ng/dL. ^[7]
• European, andrological and sexual medicine societies (EAU, EAA, ISSM): around 350 ng/dL. ^[7][8]
• In practice a morning total testosterone below 264 ng/dL supports the diagnosis, a value above 350 ng/dL usually excludes it, and intermediate values call for calculated free testosterone and clinical context. ^[7]

Morning sampling (07:00-10:00, fasting; roughly a 4-week gap between samples) is required because levels fluctuate with time of day and with illness; an afternoon "low testosterone" alone is usually an artefact.

The single commonest management error is treating the man for months while the partner's fertile window passes. At the first visit set a horizon: 3-6 months for potentially reversible measures such as varicocele repair, weight loss or lifestyle change, then reassess pregnancy and move promptly toward assisted reproduction if nothing has happened. Sperm need one full spermatogenic cycle (about 74 days) to respond.^{[2] [6]}

Weight loss for obese men with oligospermia, smoking cessation, reducing alcohol, loose breathable clothing and avoiding laptop-on-lap heat, treating chronic illness, and stopping anabolic steroids or exogenous testosterone. Review every prescribed drug, including GLP-1 receptor agonists, testosterone-replacement therapy and finasteride, plus over-the-counter and recreational drugs for their fertility impact.^[2][4]

• Repair only clinical (palpable) varicoceles in an infertile man with abnormal semen parameters, taking the female partner into account.^[4][6]
• Do not treat subclinical (ultrasound-only) varicoceles; neither AUA/ASRM nor EAU recommends it.^[6]
• In NOA with clinical varicocele the evidence is genuinely inconsistent: tell the couple there is no definite evidence that varicocele repair before assisted reproduction helps, although a recent meta-analysis found improved sperm retrieval (odds ratio 2.65, 95% CI 1.69-4.14) after varicocelectomy.^[2][6]
• Technique: microscopic subinguinal or inguinal varicocelectomy is the standard (AUA/ASRM and EAU prefer it for the lowest recurrence rate). Sperm parameters improve in roughly 60-80% and spontaneous pregnancy in 26-37% of treated men, and expect results 3-6 months after surgery. Scrotal pain responds in about 80%. Adolescents with greater than 20% testicular volume loss are also usually considered for repair.^[6]
• Varicocele repair before IVF/ICSI is worth doing if the varicocele is palpable, the couple is infertile, the female partner has normal or treatable fertility, and the man has abnormal semen parameters; when a woman is 37 or older, repair and assisted reproduction are often done in parallel so neither is delayed.^[2][6]

• Hypogonadotrophic hypogonadism: the disease-specific therapy is gonadotrophin replacement (hCG with or without FSH, or pulsatile GnRH) to induce spermatogenesis.^[4]
• Do not give testosterone for abnormal semen parameters: it suppresses spermatogenesis and is contraceptive in most men.^[4]
• Functional hypogonadism (often obesity-related): lifestyle optimisation is foundational; phenotype-driven medical therapy, such as clomiphene citrate or aromatase inhibitors, is only a time-limited option within specialist care, with the honest proviso that high-quality evidence linking these directly to live birth is limited.
• Antioxidants are optional adjuncts with uncertain benefit; low- or very-low-certainty evidence supports possible improvement in pregnancy outcomes, and they should not delay definitive treatment when time-to-pregnancy is critical.^[2]
• Antibiotics only for confirmed or strongly suspected infection; routine antibiotics for leukocytospermia alone do not improve pregnancy rates and should not be given.^[4]

Testosterone replacement is indicated only in men with consistent symptoms and unequivocally low morning total testosterone after reversible causes have been sought; classify the failure as primary or secondary first.^[7][8] The patient must understand that starting it will usually shut down his own spermatogenesis.

Contraindications (obey these): fertility desired in the near term; breast or prostate cancer; an unevaluated palpable prostate nodule, induration or elevated age-adjusted PSA; baseline haematocrit elevated; untreated severe obstructive sleep apnoea; a stroke or myocardial infarction in the previous 6 months; and, as a relative contraindication, a major cardiovascular event in the past 3-6 months. Do not prescribe testosterone simply to improve energy, vitality, physical function or cognition in older men or for "anti-ageing".^[8]

Before starting, screen for benign prostatic hyperplasia, prostate cancer risk, an elevated haematocrit, sleep apnoea, hypertension and cardiovascular/venous thromboembolic disease, and counsel on HPG axis suppression and impaired spermatogenesis.^[8]

Formulation and dosing (individualised by age, SHBG, preference and cost; not all formulations exist in every country):^[8]

• Transdermal 1% gel, starting about 50 mg daily. ^[8]
• Testosterone cypionate or enanthate intramuscularly, about 200 mg/mL once weekly (older short-acting esters in escalation schemes). ^[8]
• Long-acting testosterone undecanoate by intramuscular injection, where available.
• Subdermal pellets: about six 75 mg pellets. ^[8]
• Intranasal gel: one 5.5 mg pump per nostril three times daily. ^[8]
• Clomiphene citrate 25 mg every other day, anastrozole 0.5 mg weekly and hCG 500 IU subcutaneously every other day are used when fertility must be preserved (below). ^[8]

Target: mid-normal serum testosterone, typically 450-600 ng/dL, measured appropriately for the formulation (trough before injections; 2 hours after gel).^[8]

Monitoring: reassess symptoms within 6 months, recheck serum testosterone and haematocrit during treatment, and assess prostate cancer risk per local screening policy; a raised haematocrit during treatment warrants dose reduction and further assessment. Follow-up intervals depend on formulation and local guidance.

• Hypogonadotrophic hypogonadism: replace hCG plus FSH, or use pulsatile GnRH; intratesticular testosterone is restored and sperm counts rise over 12-24 months. Gonadotrophin therapy and its dosing belong to specialist care. Testosterone alone never restores fertility.^[8][2]
• Klinefelter syndrome: microsurgical testicular sperm extraction (micro-TESE) plus intracytoplasmic sperm injection can retrieve sperm in many non-mosaic 47,XXY men; referral is best made before testosterone is started if fertility matters, and many men still enter puberty spontaneously.^[2]
• Functional hypogonadism: treat the underlying condition first (weight loss, disease control, drug review); weight loss alone has been shown to raise endogenous testosterone. A therapeutic trial of testosterone gel in functional hypogonadism should be re-evaluated within 6 months, but exogenous testosterone is contraindicated while the man is trying to conceive, so fertility concerns should be disclosed to the patient from the start.^[8]
• Obstructive azoospermia: both microsurgical reconstruction and surgical sperm retrieval plus intracytoplasmic sperm injection are acceptable; the choice follows obstruction site, female partner age and reserve, family size, cost and expertise. Cryopreserve sperm at retrieval wherever possible.^[4]
• Non-obstructive azoospermia: micro-TESE is preferred where expertise exists; hormonal "pre-treatment" aimed solely at retrieval has uncertain benefit but may be offered as a monitored, time-limited trial after counselling. Y-chromosome AZFa and AZFb deletions indicate sperm will not be found; AZFc deletions allow it, with genetic counselling and discussion of male offspring risk.

• Total motile sperm count is a useful predictor of intrauterine insemination (IUI) success and should be combined with partner age and ovarian reserve.^[2]
• ICSI should be reserved for clear indications: severe male factor, prior fertilisation failure, very low sperm numbers, or surgically retrieved sperm. Routine ICSI does not improve live-birth outcomes compared with conventional IVF in couples without severe male factor, and it should not be a surrogate for treating the underlying male condition.^[2]
• Minimise maternal and neonatal risk: single embryo transfer policies, avoidance of multiple pregnancy, awareness of ovarian hyperstimulation, preterm birth and low birth weight.

• Reassess semen parameters after a full spermatogenic cycle; compare trends rather than single values because semen parameters have wide within-man variability.
• Monitor bone mineral density, haematocrit, prostate safety, cardiovascular and metabolic risk in hypogonadal men; testosterone "cures" androgen deficiency but does not cure infertility.
• Psychological support and couple counselling throughout; treatment burden and decision regret are genuine outcomes.

• Progressive testicular damage and rising FSH if a significant varicocele is left untreated or infertility is diagnosed late.
• The important medical complication of prolonged hypogonadism is osteoporosis, anaemia, metabolic syndrome, increased adiposity and impaired bone health, along with infertility.
• Post-surgical: hydrocele, recurrence, rarely testicular atrophy, slow improvement until the recovery window.
• Testosterone therapy complications: polycythaemia (raised haematocrit), worsening sleep apnoea, acne or oedema, suppression of spermatogenesis and the HPG axis, possible cardiovascular and thrombotic risk (reported but the evidence continues to develop).
• Genetic: transmission of AZFc microdeletions and CFTR-related disease to sons; Y-deleted men need counselling.
• Psychological: anxiety, depression and relationship strain; infertility is a couple condition.

Prognosis depends on the level of failure: mild idiopathic oligospermia may improve with lifestyle change; clinical varicocele repair improves semen parameters in 60-80% of men and spontaneous pregnancy in 26-37%; NOA is the most severe form, yet micro-TESE still finds sperm in some carefully selected cases; hypogonadotrophic hypogonadism has the best outlook with gonadotrophins. Female partner age is often the limiting factor and should shape counselling from the first visit. ^[6]

• There is no routine screening for hypogonadism in the asymptomatic general population; diagnose only when symptoms co-exist with two low morning values. ^[7]
• Pre-conception counselling about smoking, alcohol, weight, heat and drug exposure for both partners.
• Adolescent varicocele: monitor testicular volume; repair adolescent varicoceles with persistent testicular asymmetry greater than 20%, abnormal semen analysis or pain.
• Fertility preservation (sperm cryopreservation) before gonadotoxic therapy such as chemotherapy, radiotherapy or orchidectomy, and before vasectomy, using the same WHO collection standards.
• Cross-check with endocrinology: anything that looks like hypogonadism should be classified primary versus secondary and functional versus organic before any treatment is given; do not give testosterone as anti-ageing therapy.

• Adolescents: most adolescent varicoceles need observation only; testosterone exposure before completing growth needs specialist care, and a teenager presenting with "delayed puberty" needs the full hypogonadism work-up.
• Older men: testosterone can be offered to a confirmed hypogonadal man for specific organ benefits if he has no contraindications; it should not be offered for low energy or "feeling older" alone.
• Cancer survivors: remember orchidectomy, radiation and chemotherapy; check semen before treatment where possible and follow-up after.
• Sexual medicine and orientation: the inclusive framing used in modern guidelines refers to people with male reproductive organs; respect identity, adapt language and involve both partners, and the principles (WHO thresholds, contraindications, repeat testing) remain the same.
• Men with functional hypogonadism and obesity: endocrinology and andrology should coordinate; weight loss is the most effective endocrine treatment available.

• Where standard care for infertility is unavailable, a structured history, standing scrotal examination and WHO-standard manual semen analysis still allow categorisation of most couples; WHO publishes a 6th edition manual expressly to standardise the test.
• When testosterone assays are unavailable, clinical assessment (Tanner stage, testicular volume, growth curve) carries most of the diagnostic weight; a bone-age radiograph and a single morning testosterone, where available, change management.
• Karyotype and microdeletion testing are often unavailable; prioritise them for azoospermia and non-mosaic Klinefelter suspicion, and counsel without them.
• Where micro-TESE, microscopy and andrology surgery are unavailable, explain the limits honestly and support referral timing for IVF/ICSI; avoid invasive varicocele surgery without a microscope where recurrence rates are high.
• Shared language with generalists and midwives about the 12-month definition and male-first examination prevents years of female-only treatment.

• Male infertility is multifactorial and is the cause in up to half of infertile couples; always assess the man.
• The three levels of failure are central, testicular and post-testicular; FSH is the earliest marker of testicular damage.
• Semen analysis is a linchpin and must be done, and repeated, to the WHO 2021 method; interpret values using its 5th percentile limits, not arbitrary "normal".
• Always repeat an abnormal first sample, leaving about 3 months for a full spermatogenic cycle.
• A palpable varicocele with abnormal semen in an infertile man is the commonest surgical target; subclinical varicoceles are not treated. ^[6]
• Testosterone is for hypogonadism, never for low sperm count; it suppresses spermatogenesis.
• Hypogonadism thresholds differ by guideline (264, 300, 350 ng/dL); diagnose with two morning fasting samples and symptoms.
• Fertility wishes dictate the drug choice: gonadotrophins restore sperm, testosterone does not.
• Treat reversible causes (weight, heat, drugs) before invasive or hormonal therapy, with a 3-6 month horizon and early escalation to assisted reproduction in older female partners.
• Genetic testing (karyotype, Y-deletion, CFTR) is guided by azoospermia and very low counts, and must be accompanied by counselling.
• Assisted reproduction complements rather than replaces male-factor treatment; reserve ICSI for severe disease.
• In low-resource settings, history, examination and WHO-standard semen analysis carry most of the diagnosis; genetic and micro-surgical tests come second.

Hypogonadism and delayed puberty. Infertility and Bartholin gland disease. Acute scrotum and testicular torsion. Testicular tumours. Chronic kidney disease. Fertility preservation and oncology. Sexual dysfunction. Obesity and metabolic syndrome.