Synopsis
Identify ovarian and central oestrogen deficiency early, establish the cause and fertility implications, and provide physiological sex-steroid replacement that protects bone, cardiovascular and genitourinary health.
- Female hypogonadism means inadequate ovarian sex-steroid action from ovarian failure, deficient hypothalamic-pituitary stimulation or treatment-related suppression; amenorrhoea is a presentation, not the complete diagnosis.
- Premature ovarian insufficiency is ovarian dysfunction before age 40 with disordered cycles and biochemical evidence; ovarian activity may be intermittent, so the term does not mean irreversible absence of every ovulation.
- NICE advises against diagnosing POI from one blood test and uses two elevated FSH results obtained four to six weeks apart after clinical assessment; hormonal treatment can make the tests uninterpretable.
- Do not use anti-Müllerian hormone routinely to diagnose POI; it measures aspects of follicular reserve but does not replace the required clinical and gonadotrophin assessment.
- High FSH with low oestrogen supports primary ovarian insufficiency, whereas low or inappropriately normal FSH suggests functional hypothalamic, pituitary or systemic suppression.
- Offer sex-steroid replacement to people with POI unless contraindicated and normally continue until at least the average natural-menopause age, even when vasomotor symptoms are mild.
- A uterus requires progestogen protection with systemic oestrogen; transdermal oestradiol is often favoured when venous thrombosis or metabolic considerations make oral exposure less suitable.
- HRT is not contraception. Intermittent ovulation and spontaneous pregnancy can occur in POI, so discuss both fertility wishes and pregnancy prevention.
- Bone, cardiovascular, sexual, psychological and fertility care should begin at diagnosis, with genetic and autoimmune investigation selected by age, phenotype and specialist guidance.
Key red flags
Headache, visual field loss, diplopia, galactorrhoea, polyuria or additional cortisol and thyroid deficits suggests sellar disease; abrupt severe symptoms may represent apoplexy.
Vitiligo, autoimmune thyroid disease, weight loss, postural hypotension, pigmentation or electrolyte disturbance raises concern for associated adrenal or thyroid autoimmunity.
Investigation priorities
Exclude pregnancy before interpreting amenorrhoea or prescribing replacement and progestogen.
Management branches
Disordered cycles or oestrogen-deficiency symptoms before age 40 with no physiological explanation.
- Exclude pregnancy, record hormonal treatment, surgery, cancer therapy, autoimmune and family history, and assess pubertal development, vasomotor, genitourinary and fertility concerns.
- Obtain FSH on two occasions four to six weeks apart under current NICE guidance, with oestradiol, LH, thyroid and prolactin as clinically useful.
- Refer for cause assessment including genetic and autoimmune testing where eligible, and address urgent adrenal or pituitary features immediately.
- At diagnosis, discuss hormone replacement, contraception, fertility, bone and cardiovascular health and psychological support rather than arranging an isolated annual blood test.
Key medicines
Transdermal oestradiolUse the licensed patch or gel regimen titrated to physiological replacement and symptom control through specialist guidance.A uterus requires progestogen. Review unexplained bleeding, hormone-sensitive cancer, liver disease and thrombosis context; transdermal delivery avoids first-pass exposure but still needs individual assessment.
Oral micronised progesterone or alternative progestogenGive continuously or cyclically in the licensed or specialist regimen matched to systemic oestrogen exposure.Adherence is essential; unscheduled bleeding follows the current BMS and local pathway. Sedation, mood effects and product-specific thrombosis considerations inform choice.