Synopsis
Recognise puberty that starts too early, progresses too rapidly or fails to start, distinguish central activation from peripheral sex-steroid exposure and separate constitutional delay from gonadal or hypothalamic-pituitary disease using growth, staging and ordered endocrine investigation.
- Precocious puberty means secondary sexual development before 8 years in girls or 9 years in boys; rate, sequence, growth acceleration and neurological symptoms determine urgency as well as age.
- Delayed puberty is absence of breast development by 13 years in girls or testicular enlargement by 14 years in boys; absent menarche by 15 years or more than three years after breast onset also requires assessment.
- True central puberty follows the normal sequence with growth acceleration and advanced bone age; isolated early breast or pubic-hair development can be benign but needs trajectory review.
- Rapid virilisation, vaginal bleeding without breast progression, testicular asymmetry or Cushingoid features suggests peripheral hormone production or exposure rather than simple early central puberty.
- First-line assessment documents serial height velocity, Tanner stage, testicular volume, body proportions, BMI, neurological findings, chronic disease, nutrition, exercise, medicines and family pubertal timing.
- Bone age estimates sex-steroid exposure and remaining height potential. Basal LH, FSH and estradiol or testosterone are timed and interpreted using paediatric, pubertal and assay-specific ranges.
- A GnRH stimulation test can confirm central activation when basal results and progression are unclear; random sex hormones or adult laboratory ranges create misleading conclusions.
- Brain MRI is urgent for neurological signs and usually indicated in boys with central precocious puberty and in very young girls or atypical rapid progression according to specialist assessment.
- Long-acting GnRH agonist can pause central precocious puberty when progression threatens height or causes important psychosocial burden; treat peripheral puberty by correcting the underlying adrenal, gonadal, tumour or exposure source.
- Constitutional delay is a diagnosis supported by healthy slow tempo, delayed bone age and family history after exclusion of chronic disease; high gonadotrophins indicate gonadal failure, while low or normal gonadotrophins require hypothalamic-pituitary and functional assessment.
Key red flags
Pubertal signs with headache, vomiting, visual loss, seizure or focal deficit requires urgent intracranial evaluation.
Precocious puberty in a boy is more likely to have an identifiable pathological cause and needs prompt specialist work-up.
Rapid virilisation, clitoral enlargement, deep voice or very rapid growth suggests substantial androgen exposure or tumour.
Vaginal bleeding without expected breast progression or a palpable abdominal mass requires urgent peripheral-cause assessment.
A hard or asymmetric testis, testicular pain or mass needs urgent ultrasound and tumour-aware referral.
Delayed puberty with anosmia, polyuria, visual symptoms or multiple pituitary features suggests central hormone deficiency.
Weight loss, restrictive eating, excessive exercise or chronic diarrhoea can suppress puberty and requires systemic and safeguarding-aware care.
Headache, vomiting, visual or focal signs accompanying early or stalled puberty suggests intracranial pathology requiring urgent imaging.
Investigation priorities
Document onset, tempo, sequence, testicular volume, height velocity, proportions and pubertal stage accurately.
Management branches
Secondary sexual features appear before 8 years in a girl or 9 years in a boy.
- Record sequence, rate, exposures, neurological symptoms, height velocity, Tanner stage and testicular or pelvic findings.
- Obtain bone age and mechanism-directed basal hormones, using stimulation testing when central activation remains uncertain.
- Arrange risk-based brain or gonadal imaging and observe only genuinely non-progressive isolated variants with a dated review.