# Delayed Puberty > Delayed puberty for NEET-PG Paediatrics: age cutoffs, constitutional delay, hypergonadotropic vs hypogonadotropic causes and management. - Canonical URL: https://prepelephant.com/topics/neet-pg/paediatrics/delayed-puberty - Exam / course: NEET-PG · Subject: Paediatrics - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Delayed Puberty", PrepElephant, https://prepelephant.com/topics/neet-pg/paediatrics/delayed-puberty ## Direct answer No breast budding by 13 years in a girl, or no testicular enlargement (4 mL or more) by 14 years in a boy, defines delayed puberty; failure to complete puberty within five years of onset qualifies in either sex. The single commonest cause in both sexes is constitutional delay of growth and puberty — a normal variant with delayed bone age, a family history in a parent, and eventual full puberty — but the diagnosis is one of exclusion. Split the remainder by gonadotrophins: hypergonadotropic hypogonadism means the gonad is failing (Turner syndrome, Klinefelter syndrome, chemotherapy, galactosaemia), while hypogonadotropic causes span chronic illness (tuberculosis, coeliac disease, anaemia, anorexia athletica), hypopituitarism including Kallmann syndrome, and hyperprolactinaemia. ## What you must remember - **Cutoffs:** girls — no thelarche by 13 years (or no menarche by 15 with prior thelarche, i.e. more than five years from thelarche); boys — no testicular volume of 4 mL by 14 years; more than five years from onset to completion in either sex is also delay. - **Constitutional delay of growth and puberty:** commonest cause, both sexes, short but tracking with delayed bone age, positive family history in a parent, eventual spontaneous puberty; association with transient low insulin-like growth factor-1 and reduced height velocity in early adolescence. - **Hypergonadotropic (gonadal failure):** Turner syndrome (45,X — streak gonads, short stature, webbed neck), Klinefelter syndrome (47,XXY — tall, small testes), prior chemotherapy or radiation, galactosaemia, mumps orchitis, autoimmune oophoritis. - **Hypogonadotropic:** chronic systemic disease — coeliac disease, tuberculosis under the national programme's paediatric weight-band dosing era, poorly controlled diabetes, chronic kidney disease — plus anorexia nervosa and excessive training, hyperprolactinaemia, Kallmann syndrome (anosmia with gonadotrophin-releasing hormone deficiency), and craniopharyngioma or other hypothalamic-pituitary lesions. - **First-line tests:** bone age radiograph (left hand), follicle-stimulating hormone and luteinising hormone, oestradiol or testosterone, prolactin, and a systemic screen (coeliac serology, erythrocyte sedimentation rate, thyroid function); karyotype when gonadotrophins are high, MRI pituitary when low with no systemic cause. - **Turner reminders:** short female with delayed puberty needs a karyotype even without classic stigmata; echo for coarctation, renal ultrasound, and growth hormone therapy before oestrogen induction. - **Testosterone/oestrogen therapy:** boys — intramuscular testosterone 50 mg monthly for three to six months to jump-start puberty in constitutional delay; girls — very low-dose oestrogen, slowly escalated; sex steroid replacement in permanent hypogonadism. ## How to work through it A 14-and-a-half-year-old boy, third-shortest in class, humiliated in the changing room, father reports he himself "was like that, filled out by seventeen". Sequence the answer: confirm testicular volume under 4 mL, plot height and weight (constitutional delay tracks along a delayed curve), examine for syndromic clues (dysmorphism, anosmia — walk to the smell jar, visual field defects), and order bone age plus gonadotrophins. Bone age two years behind chronology with prepubertal gonadotrophins fits constitutional delay: reassure, offer a short course of monthly testosterone 50 mg for three months to accelerate maturation and morale, and review in six months for spontaneous progression. Now invert the case: a 14-year-old girl, height crossing down centiles, fatigue, and a father under treatment for tuberculosis. Delayed puberty with chronic weight loss demands coeliac serology, tuberculosis evaluation per National Tuberculosis Elimination Programme guidance, and inflammatory markers before any hormonal label — chronic disease is the great Indian impersonator of both growth failure and pubertal delay. Finally, the short 13-year-old girl with a low posterior hairline and cubitus valgus: send the karyotype that will show Turner syndrome, echo for coarctation, and plan growth hormone now, oestrogen later — sequencing matters because oestrogen fuses epiphyses. ## Where students slip Three errors recur in viva answers. First, labelling every late developer pathological: constitutional delay is the majority diagnosis, and its fingerprints — delayed bone age, familiar history, height appropriate for bone age — should be quoted, not just the exclusion. Second, forgetting that the commonest cause of delayed puberty worldwide is chronic disease and undernutrition rather than a rare syndrome; in India, tuberculosis, coeliac disease and anaemia outpace Kallmann in real clinics. Third, mismatching the therapy to the mechanism: testosterone pulses in constitutional delay versus full replacement in gonadal failure; and giving oestrogen to a Turner girl before growth hormone has done its work, sacrificing final height. ## Frequently asked questions ### What age cutoffs define delayed puberty? No thelarche by 13 years in girls or testicular volume under 4 mL by 14 years in boys; also, absence of menarche by 15 with earlier thelarche, or failure to complete puberty within five years of onset. ### What is the commonest cause of delayed puberty in boys? Constitutional delay of growth and puberty — delayed bone age, family history in a parent, and eventual spontaneous complete puberty. ### How do gonadotrophins classify the causes? High follicle-stimulating hormone and luteinising hormone indicate gonadal failure (Turner, Klinefelter); low values indicate hypothalamic-pituitary disease or chronic illness. ### Which syndrome pairs delayed puberty with anosmia? Kallmann syndrome — gonadotrophin-releasing hormone deficiency with olfactory bulb hypoplasia, treated with sex steroid replacement and gonadotrophins for fertility. ### What is the treatment of constitutional delay? Reassurance with review, plus optional short-course low-dose intramuscular testosterone in boys to accelerate puberty and relieve psychological distress.