Testosterone Replacement Therapy
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Direct answer
Testosterone replacement is indicated only when characteristic symptoms meet consistently low morning testosterone — never for a number alone — and its safer execution is a matter of preparation choice plus disciplined monitoring. Injections (enanthate or cypionate 200–250 mg every 2–3 weeks; undecanoate 1000 mg every 10–14 weeks after loading) are the affordable backbone in India, gels offer steadier levels, and implants and buccal preparations are niche options. Monitoring covers haematocrit (the commonest problem — polycythaemia; interrupt or reduce above about 54%), PSA with digital rectal examination in older men, plus assessment of response at three, six and twelve months. Fertility desire, active prostate or breast cancer, untreated severe obstructive sleep apnoea and heart failure are the standing contraindications.
What you must remember
- Symptom-plus-biochemistry rule: two low morning testosterone values with a compatible clinical syndrome before the first prescription.
- Preparations: short-acting IM esters every 2–3 weeks (peaks and troughs, cheapest); testosterone undecanoate 1000 mg IM about 12-weekly (very steady); 1% gels daily (steady, transfer risk to partners and children); patches, buccal tablets, subcutaneous implants.
- Injectable peaks can cause symptoms of excess and troughs of deficiency — check levels at the midpoint and just before the next dose.
- Haematocrit: check at baseline, 3–6 months, then annually; hold therapy or venesect above roughly 54% — polycythaemia is the most frequent adverse effect.
- Prostate: baseline PSA and DRE from about age 40–50 (or earlier with family history), then PSA at 3–6 months and annually; a clear rise prompts urology referral, not silent discontinuation.
- Testosterone suppresses spermatogenesis, shrinks testes and suppresses the HPG axis — men planning fatherhood should use hCG-based therapy or clomiphene instead.
- Contraindications: active prostate or breast cancer, elevated PSA pending evaluation, desire for fertility, severe untreated sleep apnoea, haematocrit already above 54%, uncontrolled heart failure, severe lower urinary tract symptoms (relative).
- Transfer precaution with gels: cover the application site, wash hands, avoid skin contact with children and partners.
A worked monitoring cycle
A 44-year-old with confirmed secondary hypogonadism (prolactin normal, MRI clean) starts testosterone enanthate 250 mg intramuscularly every three weeks. At week six he feels better mid-cycle but reports irritability and heaviness in the week after injection — peak-and-trough pharmacology, not mystery. Options: shorten the interval at a smaller dose, switch to undecanoate, or accept a gel's daily discipline. His week-six bloods show haematocrit 52.5% (baseline 47%) and PSA 1.4 ng/mL — both acceptable, so therapy continues with annual surveillance; if haematocrit crossed 54%, the moves are dose reduction, interval extension, venesection, or a switch to a gel or transdermal patch, which raise haematocrit less.
The second scenario is the one examiners use to test judgement: the same patient, one year later, wants to start a family. Continuing testosterone guarantees further spermatogenic suppression; the correct move is a supervised transition — stop testosterone, assess semen analysis after an adequate washout, and induce spermatogenesis with hCG (± FSH if the axis is long-suppressed) or, in suitable secondary cases, clomiphene off-label. Fertility planning before the first prescription avoids this detour entirely.
The third scenario tests judgement: the asymptomatic 65-year-old with borderline testosterone and fatigue whose neighbour's gel worked wonders gets no prescription yet — weight, sleep, glycaemic control and opioid review first, since trials in this population have been mixed and long-term cardiac safety remains unsettled.
Where students slip
First slip: prescribing testosterone and never measuring haematocrit — polycythaemia is predictable, detectable and the reason for interval blood counts. Second, forgetting fertility physiology: the couple trying to conceive while the husband is on replacement is a self-inflicted subfertility diagnosis; intratesticular testosterone, not serum testosterone, drives spermatogenesis, and injections abolish it. Third, ignoring the gel transfer hazard — virilisation of a child through skin contact is documented and preventable. Finally, aim replacement at mid-normal trough levels, never supraphysiological peaks.
Frequently asked questions
Who qualifies for testosterone replacement therapy?
Men with a consistent clinical syndrome of hypogonadism plus at least two unequivocally low morning testosterone concentrations, after reversible causes (obesity, opioids, illness) and contraindications have been addressed. Low levels alone, without symptoms, do not justify treatment.
Which adverse effect most commonly interrupts therapy?
Erythrocytosis — haematocrit rising above roughly 54% — managed by dose reduction, longer intervals, venesection, or switching to transdermal delivery; baseline and interval haemat counts are mandatory.
Can a man receive testosterone while trying to conceive?
No — replacement suppresses gonadotrophins and spermatogenesis. Fertility-seeking men are treated with hCG with or without FSH, or clomiphene in selected secondary cases, to restore endogenous production.
What PSA surveillance applies on testosterone?
Baseline PSA with digital rectal examination (routinely from about age 40–50 or earlier with risk factors), reassessment at 3–6 months after starting, then annually; a clinically significant rise or abnormal DRE means urological referral before continuing.
Do testosterone preparations differ in cardiovascular risk?
Data remain contested: trials have been mixed and long-term safety unsettled. Practicable points include avoiding supraphysiological peaks, preferring steady preparations where affordable, and screening for untreated sleep apnoea and heart failure before starting.