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treatment in the index child was rapid progression of pubertal event (B 1 to B 3 during
6 months) and significant advancement of bone age (>2.5 SD) at presentation. GnRH
agonists are the treatment of choice for children with GDPP. However, this therapy is
preferred in children who have onset of pubertal events before the age of 6 years,
because of their potential benefit in achievement of target adult height. Long-acting
GnRH agonist depot preparations are preferred and can be administered either once a
month or every three monthly with similar efficacy. The other treatment options
include medroxyprogesterone acetate and cyproterone acetate, which can be used in
children with GDPP who present after the age of 6 years as these drugs arrest the
progression of pubertal development but have no apparent benefit on adult height
potential. The index child was treated with leuprolide acetate depot once a month
intramuscularly. The child did not report any flare after initiation of therapy. Regular
follow-up is required initially at 3 monthly interval and include clinical assessment of
secondary sexual characteristics, growth velocity, estimation of basal and stimulated
LH, and basal testosterone/estradiol in boys or girls, respectively. The biochemical
parameters are assessed on the day, when the next dose is administered. The GnRH
agonist treatment is associated with regression of secondary sexual characteristics by
6–12 months of initiation of treatment with progressive decline in growth velocity and
chronological age gradually approaches near to the bone age. The index patient had
regression of breast (B 3 to B 2 ) at 3 months. However, basal serum LH was 1.71 mIU/
ml and stimulated LH 14.7 mIU/ml (at 3h), necessitating the hike in dose of leuprolide
depot. At 6 months of follow-up, Tanner staging was A−, P 1 , B 2 , and her growth veloc-
ity was reduced to 4 cm/year. The adverse effects associated with the use of GnRH
agonist therapy include initial flare, sterile abscess, and allergic reactions. Our patient
did not experience any adverse event. The treatment is to be continued till the chrono-
logical age of 12 years. After discontinuation of GnRH agonist therapy, in girls, the
gonadotropins start rising within few weeks to months with resumption of menses by
1 year, whereas in boys, the rise in gonadotropins occurs usually by 6 months to 1 year
and testes may take a longer time to attain the adult testicular size.
6.3 Clinical Rounds
- What is precocious puberty?
Precocious puberty is defined as appearance of any secondary sexual character-
istics at an age earlier than the established normal standards for children of the
same gender and race. Although children with different race have different age of
onset of puberty, a clinically useful definition of precocious puberty is
development of any secondary sexual characteristics before the age of 8 years in
girls or 9 years in boys.- How were the age cutoffs for onset of normal puberty derived?
The normal age of onset and sequence of pubertal events were described in land-
mark studies by Tanner and Marshall in 1960s. One hundred and ninety- two British
girls between 8 and 18 years of age were serially followed up with clinical photo-6 Precocious Puberty