Central precocious puberty results from early activation of the hypothalamic-pituitary-gonadal axis, which in a proportion of children — especially boys — is driven by an intracranial lesion such as a hypothalamic hamartoma, glioma or the sequelae of cranial irradiation. That is why a neurological examination with fundoscopy and visual fields, and attention to headache or raised-ICP features, is mandatory in the primary-care assessment.

Plotting serial growth is the single most useful primary-care step: a pubertal growth spurt that crosses centile lines supports true precocious puberty and adds urgency, whereas isolated breast development or pubic hair with normal growth velocity often represents a benign variant. The examination also screens for the syndromic clues (café-au-lait macules of McCune-Albright, neurofibromatosis stigmata) that point to a specific cause.

The history separates progressive precocious puberty (ordered, accelerating, with a growth spurt) from a non-progressive benign variant, and screens for the intracranial and exogenous causes that change management. Tanner staging plus a documented growth velocity is the objective backbone of the assessment, and testicular examination in boys can reveal asymmetric enlargement (a tumour) or bilateral enlargement (central activation) that directs the work-up.

Distinguishing central from peripheral precocious puberty determines treatment: central precocious puberty is treated with a GnRH analogue to switch the axis back off and protect adult height and psychosocial wellbeing, whereas peripheral causes require treatment of the source (e.g. a tumour, CAH). The benign variants (premature thelarche/adrenarche) need recognition so that children are reassured and monitored rather than over-investigated, but the initial referral remains appropriate because the distinction is a specialist one.

The GnRH stimulation test is the pivotal investigation because it directly demonstrates whether the hypothalamic-pituitary axis has been switched on (central) or is suppressed by a peripheral steroid source — a distinction that random hormone levels cannot reliably make. Brain MRI is essential in confirmed central precocious puberty, especially in boys and very young girls, because the pre-test probability of an intracranial lesion is high enough to mandate imaging even when the examination is normal.

The sex difference in referral urgency reflects the underlying epidemiology: in girls, precocious puberty is usually idiopathic central precocious puberty, whereas in boys an identifiable (and sometimes serious) cause is much more common — so every boy warrants urgent specialist assessment. All children are referred because the diagnosis, the need for imaging and the decision about GnRH-analogue treatment to preserve final height are specialist judgements.

GnRH analogues exploit the physiology of the axis: continuous (rather than pulsatile) GnRH stimulation desensitises the pituitary, switching gonadotrophin secretion off and arresting pubertal progression — buying time for growth and emotional maturation so final height and wellbeing are protected. The decision to treat balances predicted height loss and psychosocial impact against the burden of therapy, which is why it is specialist-led, often with the GP delivering the depot under shared care.

The impact of early puberty on the child — being physically out of step with peers, and the emotional consequences — is part of the specialist's decision about whether and when to treat, so acknowledging and supporting it is genuine management, not a soft add-on. Removing exogenous steroid exposure is a concrete, reversible cause of peripheral changes that primary care can identify and act on directly.

Serial growth data and clear safety-netting are the most valuable things primary care can add while a child waits to be seen: a documented accelerating growth velocity both supports the diagnosis and raises the urgency, and the safety-net ensures that an evolving intracranial cause is escalated rather than missed.