Precocious and Delayed Puberty
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Direct answer
Precocious puberty is the onset of pubertal signs before age 8 in girls or 9 in boys, while delayed puberty is the absence of signs by age 13 in girls or 14 in boys. Central precocious puberty is gonadotrophin-dependent and usually idiopathic in girls, whereas constitutional delay is the commonest reason for delayed puberty. Measuring LH with a sensitive assay separates central from peripheral causes early in the workup.
What you must remember
- Normal onset: roughly 8 to 13 years in girls and 9 to 14 years in boys, with some variation by population.
- Central precocious puberty: gonadotrophin-dependent, with a raised LH on a sensitive assay; CNS lesions such as hypothalamic hamartoma are more often found in boys.
- Peripheral precocious puberty: gonadotrophin-independent, with suppressed LH and raised sex steroids from another source.
- Peripheral causes: congenital adrenal hyperplasia, McCune-Albright syndrome, testotoxicosis, sex steroid-secreting tumours and exogenous steroids.
- Constitutional delay: a family history of late puberty, delayed bone age and normal eventual height.
- Hypogonadotrophic hypogonadism: low LH, FSH and sex steroids, seen in Kallmann syndrome with anosmia, pituitary lesions and functional causes such as anorexia.
- Hypergonadotrophic hypogonadism: raised LH and FSH with low sex steroids from gonadal failure, as in Turner syndrome (45,X) and Klinefelter syndrome (47,XXY).
Breast development at seven: a common exam start
Breast development at 7 years in a girl is an exam staple. The next question is whether the gonadotrophin axis is switched on, and the table sets out how the main conditions differ. Growth velocity is charted alongside the signs, since accelerated growth also points to sex steroid exposure.
| Condition | LH and FSH | Sex steroids | Typical cause |
|---|---|---|---|
| Central precocious puberty | Raised | Raised | Idiopathic, or CNS lesion |
| Peripheral precocious puberty | Suppressed | Raised | CAH, McCune-Albright, tumours, exogenous steroids |
| Constitutional delay | Low, prepubertal pattern | Low | Family history, delayed bone age |
| Hypogonadotrophic hypogonadism | Low | Low | Kallmann syndrome, pituitary lesions, anorexia |
| Hypergonadotrophic hypogonadism | High | Low | Turner syndrome, Klinefelter syndrome |
A sensitive LH assay, sometimes after GnRH stimulation, separates central from peripheral causes. Bone age and family history help distinguish constitutional delay from true hypogonadism. Bone age is read from a hand and wrist radiograph, and a bone age that matches chronological age argues against constitutional delay. Prolactin and thyroid function are part of the basic workup.
Where students lose marks
These traps recur in paediatric endocrinology questions.
- Trap: calling early puberty in a girl normal because it is common. Correct: breast development before 8 years is precocious and needs evaluation, although many girls have benign idiopathic early puberty.
- Trap: treating constitutional delay with sex steroids reflexively. Correct: reassurance and observation are preferred, because growth and final height are usually normal.
- Trap: attributing hypogonadism with high FSH to a pituitary cause. Correct: raised gonadotrophins indicate gonadal failure, as in Turner or Klinefelter syndrome, so the gonads need evaluation.
Frequently asked questions
What is the normal age range for puberty onset?
Normal puberty begins roughly between 8 and 13 years in girls and 9 and 14 years in boys. Breast development before 8 years in girls, or testicular enlargement before 9 years in boys, is precocious. Nutritional and environmental factors shift timing somewhat across populations.
How is central precocious puberty distinguished from peripheral precocious puberty?
Central precocious puberty is distinguished by a raised LH on a sensitive assay, or a rise after GnRH stimulation. Peripheral precocious puberty has suppressed LH and FSH, with raised sex steroids from another source. Pelvic ultrasound and bone age help complete the diagnosis.
What is the treatment for central precocious puberty?
GnRH agonists such as leuprolide or triptorelin suppress gonadotrophin secretion in central precocious puberty. Treatment halts the progression of puberty and is aimed at protecting final adult height. It is generally stopped at an age close to the expected onset of normal puberty.
Why does Kallmann syndrome cause delayed puberty?
Kallmann syndrome causes delayed puberty because of isolated GnRH deficiency, which results from failed migration of GnRH neurons during development. It is recognised by anosmia or hyposmia alongside low gonadotrophins. Olfactory testing is therefore part of the assessment of hypogonadotrophic delay.