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is a significant concern for physicians. Central& |4 t& a' a% c. Z' m7 X
precocious puberty (CPP), which is mediated" O  f0 v3 I, ?$ A, a4 p5 [" l4 K) j
through the hypothalamic pituitary gonadal axis, has
: t# a$ J5 V; K% t( o) T2 P; ma higher incidence of organic central nervous system
4 R! B' m, k0 B- k' r2 n/ P7 jlesions in boys.1,2 Virilization in boys, as manifested" i# z+ x# Z" k( r2 U/ x( f
by enlargement of the penis, development of pubic9 H. c  v) L) }+ [
hair, and facial acne without enlargement of testi-& g: \( u% z/ v' P$ N
cles, suggests peripheral or pseudopuberty.1-3 We
. R) b; j% F% Z. W4 Vreport a 16-month-old boy who presented with the
! @# C4 \7 `& Uenlargement of the phallus and pubic hair develop-
& J* I- `( J* Z" \! |6 K7 p# vment without testicular enlargement, which was due. ~6 n# K) k) }/ k- o; S7 t
to the unintentional exposure to androgen gel used by9 q* N" h. m- Z4 E& `9 Q5 R# R
the father. The family initially concealed this infor-9 h- K: y1 P# j  t( G
mation, resulting in an extensive work-up for this
3 q" U( }; e: x  ]child. Given the widespread and easy availability of
- G% G# o% C9 n2 m8 ~testosterone gel and cream, we believe this is proba-
. H" e2 d5 @8 c$ T, H- Obly more common than the rare case report in the* o7 `/ g% v# e
literature.4
. e8 \' P! |2 ~, LPatient Report
1 d3 R2 J9 `7 G: r, |A 16-month-old white child was referred to the( B  G6 G- S3 |" R5 H& E4 z) Q$ P
endocrine clinic by his pediatrician with the concern( s9 A' C) i" o/ L5 A- u$ G
of early sexual development. His mother noticed8 I- D1 D8 c2 d, Q
light colored pubic hair development when he was
/ F, f/ i( X" F* g; E) NFrom the 1Division of Pediatric Endocrinology, 2University of3 n8 \( b6 r3 q$ t6 r8 Y0 }& Q
South Alabama Medical Center, Mobile, Alabama.
5 ~0 x3 x  E+ p1 x/ i% u" oAddress correspondence to: Samar K. Bhowmick, MD, FACE,
, i8 I# o- i0 @Professor of Pediatrics, University of South Alabama, College of2 b, a/ [8 t. O0 Z$ Z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 I1 `+ x" w8 g
e-mail: [email protected]., |9 U! N9 t; U& N
about 6 to 7 months old, which progressively became
- q* V. V. r, n; Kdarker. She was also concerned about the enlarge-# W# K4 J" |* R: K
ment of his penis and frequent erections. The child
/ r" d. Q& Q3 A; @/ k& Fwas the product of a full-term normal delivery, with% T. a* Z7 x7 `! G
a birth weight of 7 lb 14 oz, and birth length of  ]4 m+ t0 M) N  N0 t/ r
20 inches. He was breast-fed throughout the first year
& f' z5 W- d. s! Wof life and was still receiving breast milk along with
  ~- c* d1 `" O0 ssolid food. He had no hospitalizations or surgery,
; r: q; I  t8 v" oand his psychosocial and psychomotor development; ]5 u% P/ F6 B6 ?. [/ a, Z) ^6 ]
was age appropriate.
$ C0 V' f/ Q. n! H8 fThe family history was remarkable for the father,/ A+ q4 ~0 A! W9 u4 z
who was diagnosed with hypothyroidism at age 16,- {: X" y- e3 B3 m6 y/ m1 T
which was treated with thyroxine. The father’s% I$ ~- L: {4 J# @; H' Z: _6 j
height was 6 feet, and he went through a somewhat( Z, o' j" l" Q2 m+ t
early puberty and had stopped growing by age 14.5 s+ _; d* D4 s9 \" D( [& Q4 y
The father denied taking any other medication. The
, o5 G9 @" E# B' D" ^) r9 uchild’s mother was in good health. Her menarche
, h3 B2 s2 R/ ^% E7 o  T+ `was at 11 years of age, and her height was at 5 feet
; R4 f2 s% o. t. p* x" w5 inches. There was no other family history of pre-  I$ I1 h0 N1 y' O/ m# J
cocious sexual development in the first-degree rela-
9 F1 I" a2 j  `/ w6 K; W' z  btives. There were no siblings.1 D) i7 @! a# R) s" a! u
Physical Examination9 g% |( d3 A& E4 R( w
The physical examination revealed a very active,
7 g) S0 T* z* {playful, and healthy boy. The vital signs documented" a/ h, s; E$ ]! p
a blood pressure of 85/50 mm Hg, his length was' [/ k1 O5 y" N, e0 x* I' }
90 cm (>97th percentile), and his weight was 14.4 kg
( m" a7 G8 I' h( Y1 [/ V% [(also >97th percentile). The observed yearly growth' g' C( B" I' A
velocity was 30 cm (12 inches). The examination of
: X& Z) A$ L& }- r2 T+ v0 cthe neck revealed no thyroid enlargement.
# P4 q3 m" q2 G  L& z4 A+ DThe genitourinary examination was remarkable for
- n5 N' A( j. _( Z  nenlargement of the penis, with a stretched length of
/ A- }7 i" e1 K$ H) f8 cm and a width of 2 cm. The glans penis was very well: g% Q8 X( P5 @9 D3 m) w) c2 g: L
developed. The pubic hair was Tanner II, mostly around% ]) ?8 ~6 L9 I: O
540
  M/ e& u5 S" f7 V. y3 a! }5 tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ I# c/ H. v) ~the base of the phallus and was dark and curled. The
# P' Q: I- J% ttesticular volume was prepubertal at 2 mL each.8 q: p- M% J$ @" n9 Q0 s" _
The skin was moist and smooth and somewhat. ~- B+ e- R' M
oily. No axillary hair was noted. There were no5 k- X- w9 D$ Z" [
abnormal skin pigmentations or café-au-lait spots.
8 o; m9 l' D4 |, O' ]0 I( yNeurologic evaluation showed deep tendon reflex 2+
. |% ]6 G/ L0 ~, U7 H! b5 \2 @bilateral and symmetrical. There was no suggestion5 g- s5 ^; R7 h: K0 d* y
of papilledema.6 F& u, }) R  V- V% j; \$ W
Laboratory Evaluation7 w% I! j; Q3 K# q' e
The bone age was consistent with 28 months by. e" p) U, d3 h+ p
using the standard of Greulich and Pyle at a chrono-% d' k5 @6 M1 X2 d3 w
logic age of 16 months (advanced).5 Chromosomal
+ W9 v# n4 I( I9 kkaryotype was 46XY. The thyroid function test0 Y/ ?8 c: z  R) \! J
showed a free T4 of 1.69 ng/dL, and thyroid stimu-/ \1 p- Y/ {1 [
lating hormone level was 1.3 µIU/mL (both normal).) R# ^8 [  [; d6 _, l
The concentrations of serum electrolytes, blood
' H! m) }- D: r5 h; d' Zurea nitrogen, creatinine, and calcium all were
3 q  L. F5 y4 b9 Q) Mwithin normal range for his age. The concentration
/ M- R9 J* ^8 V0 p0 V' Mof serum 17-hydroxyprogesterone was 16 ng/dL, s1 N0 l; s* Z4 u
(normal, 3 to 90 ng/dL), androstenedione was 20
; F- W' ^% ^( i& ~0 w) U$ r/ Xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% l" `5 d9 N) Z; b! z/ ?& A  b
terone was 38 ng/dL (normal, 50 to 760 ng/dL),5 Y7 P4 e  `+ j" h; l7 u" S4 J3 \2 A
desoxycorticosterone was 4.3 ng/dL (normal, 7 to  _9 M4 o- I& {3 K9 [+ W- F, n
49ng/dL), 11-desoxycortisol (specific compound S)1 `- ^( k# {$ C0 {
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 p4 T1 h/ R. N
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; _& b3 I6 b7 g' |testosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 c- U$ O6 p/ b! [, x& b
and β-human chorionic gonadotropin was less than
8 `7 `& F1 H0 [2 D- W5 s5 mIU/mL (normal <5 mIU/mL). Serum follicular
; j0 w( Y: f1 w% [4 [  F- b& Lstimulating hormone and leuteinizing hormone$ G: T; p' j9 i, K( v
concentrations were less than 0.05 mIU/mL
( F8 F5 c2 A+ ?" J) ^+ r, k(prepubertal).
! \3 A; P& D5 y, [0 h' eThe parents were notified about the laboratory
( W, \, Q' w! T3 [1 ]  T/ Bresults and were informed that all of the tests were: v3 a# A" j3 K0 e2 M4 U( C+ k) o
normal except the testosterone level was high. The6 I0 X  M# I/ ]( ?. r8 l
follow-up visit was arranged within a few weeks to; L5 _: q( y0 x* |3 G+ ?' }' h
obtain testicular and abdominal sonograms; how-: l0 a2 j( ?+ s* M/ S
ever, the family did not return for 4 months.. y0 B" \% G6 h1 `4 w- L% A
Physical examination at this time revealed that the
3 k. ]) r0 u0 Y7 Z% d& xchild had grown 2.5 cm in 4 months and had gained& d, B! B4 X  u% p( U
2 kg of weight. Physical examination remained! P$ g5 d7 F( _# x  M2 A% _) n
unchanged. Surprisingly, the pubic hair almost com-) |8 w4 M0 Y( U$ \  w  z
pletely disappeared except for a few vellous hairs at
2 M# I8 u. m& I& cthe base of the phallus. Testicular volume was still 2
' P2 d! ^& O& }( i( H# c3 @mL, and the size of the penis remained unchanged.
# T6 s" Y4 |, k) A7 \4 k3 sThe mother also said that the boy was no longer hav-
- k! r. y* n- L/ L, i% I1 k  ^6 hing frequent erections.
7 y: L" L8 D/ u- B. K# Z3 c& pBoth parents were again questioned about use of  Z- O9 {/ `7 z& D" t; i  g
any ointment/creams that they may have applied to% N- L6 f) k- Y! P% X) K. ]" e& L
the child’s skin. This time the father admitted the
% Z+ h" W' s# M5 t3 r6 J( V; rTopical Testosterone Exposure / Bhowmick et al 541
' x; h7 Z1 o4 n; D* q: Iuse of testosterone gel twice daily that he was apply-/ P0 n6 ^. v; [" W; m: j2 P0 F$ B
ing over his own shoulders, chest, and back area for
+ N% F; c' v1 q! j( R+ ha year. The father also revealed he was embarrassed
+ a  O& Q! ]/ `6 b, vto disclose that he was using a testosterone gel pre-5 Q0 |/ J7 ~9 A$ j
scribed by his family physician for decreased libido% e& O" F# ?$ f3 M2 E
secondary to depression.
/ @. x+ z; l* d4 PThe child slept in the same bed with parents.
# l- l; n- d( t( v2 u! O, cThe father would hug the baby and hold him on his, I+ z$ G) g* F0 b4 f1 [7 r- m* n
chest for a considerable period of time, causing sig-
; n. `7 y# ?( N/ a% Lnificant bare skin contact between baby and father.
( S# \; ?. x* n. lThe father also admitted that after the phone call,( F4 j% a% ]' i* [! x
when he learned the testosterone level in the baby
  X2 b4 T6 t/ v$ A9 G- Y1 @0 P4 Hwas high, he then read the product information
$ K  J9 b0 |3 w2 H9 ~packet and concluded that it was most likely the rea-
2 m- Y' W. t6 O, ?- P% Sson for the child’s virilization. At that time, they
! |" w' A7 n' Y+ W5 H0 L2 y9 idecided to put the baby in a separate bed, and the) `/ L1 p/ L- F/ J8 i+ j
father was not hugging him with bare skin and had- N# ?6 L4 S# a# V) H  {% }
been using protective clothing. A repeat testosterone' E+ j* D7 z7 R) _
test was ordered, but the family did not go to the
# }. m9 x/ K; Zlaboratory to obtain the test., Y2 t6 @: L2 w" b& e9 e7 S" R
Discussion
2 q8 X, x! V( C7 A; l' hPrecocious puberty in boys is defined as secondary$ S0 n) t5 K( u) A- c
sexual development before 9 years of age.1,4
- G; n) U. p0 Z0 Q: P( C, l! A$ @Precocious puberty is termed as central (true) when; i/ H3 W* E: |5 c! K9 o  V
it is caused by the premature activation of hypo-
/ @4 B8 v# a- S$ w2 K: kthalamic pituitary gonadal axis. CPP is more com-
% [; ]; C5 r  U( v( ^9 ?mon in girls than in boys.1,3 Most boys with CPP
0 X' P6 v) F  a, Umay have a central nervous system lesion that is
+ R9 S5 Q' e1 d" cresponsible for the early activation of the hypothal-# I' Z0 }  A  L% z
amic pituitary gonadal axis.1-3 Thus, greater empha-( X  X8 e  F6 m8 D8 d
sis has been given to neuroradiologic imaging in5 j  a) Q1 V2 D
boys with precocious puberty. In addition to viril-4 S9 v/ @- k6 h+ I' L: R# }
ization, the clinical hallmark of CPP is the symmet-) B. h8 m  Q$ U3 s
rical testicular growth secondary to stimulation by
. i$ k' R! `0 G# e9 }1 xgonadotropins.1,31 r( k# }+ y& ~3 e
Gonadotropin-independent peripheral preco-. F1 e+ B6 K3 ~  ~$ r, z/ a6 i4 o- ]
cious puberty in boys also results from inappropriate
- O! m6 L$ d- X9 vandrogenic stimulation from either endogenous or
; H1 F' ?" {4 Cexogenous sources, nonpituitary gonadotropin stim-7 L7 E: g7 }! f8 P  i: C
ulation, and rare activating mutations.3 Virilizing, R% u& n8 f& e: g3 Y
congenital adrenal hyperplasia producing excessive
+ q( {  t2 h6 b2 j# kadrenal androgens is a common cause of precocious- k2 l6 |( Q) A! B2 z- w
puberty in boys.3,4
0 R/ u* a% j* f' h. ^0 H# s/ a& A4 ]The most common form of congenital adrenal. H  f* `/ o2 D  r) o- K- M
hyperplasia is the 21-hydroxylase enzyme deficiency.9 E9 A! }( P- G+ G/ v$ |% L
The 11-β hydroxylase deficiency may also result in+ W3 ^' b; }6 B
excessive adrenal androgen production, and rarely,  L+ r+ I# I& _, [' F* p* N! r3 j6 q
an adrenal tumor may also cause adrenal androgen/ J  i* Z0 L3 H; {. x0 a- ], |& s
excess.1,3
5 f$ M! Z7 h; a7 E1 h. |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 o: ?" B, `0 w* L8 z* @( q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, u# R6 u- p' G
A unique entity of male-limited gonadotropin-6 F( P1 S* L9 o6 G3 ~8 l) x
independent precocious puberty, which is also known8 T- a3 r+ L& ~  v$ V
as testotoxicosis, may cause precocious puberty at a
3 F) e5 p/ V3 T4 X3 Overy young age. The physical findings in these boys, S% y$ b, T9 g6 @2 n2 |7 y
with this disorder are full pubertal development,3 r* e; T1 @7 u* f, g! J% L1 C& C- x
including bilateral testicular growth, similar to boys
$ @  V( O1 t0 fwith CPP. The gonadotropin levels in this disorder
" T' J+ J$ i; z! @1 ~6 H3 _are suppressed to prepubertal levels and do not show3 `5 A: N4 l- I" A  ~
pubertal response of gonadotropin after gonadotropin-5 ?, ], ]! K/ {- B( a
releasing hormone stimulation. This is a sex-linked
8 e/ C. L, I' p6 z, ^+ rautosomal dominant disorder that affects only
9 N9 J+ n# m8 W! v7 o# qmales; therefore, other male members of the family
& ]" h8 x: o3 u" L* W& X3 k9 t5 kmay have similar precocious puberty.37 {$ n$ W) Q- r9 M
In our patient, physical examination was incon-" W6 H+ e$ v* x9 k0 x
sistent with true precocious puberty since his testi-
. n2 K1 Y$ H) X' e7 ]cles were prepubertal in size. However, testotoxicosis
' _( Y( q2 ^5 z- e+ J5 hwas in the differential diagnosis because his father) ?6 Y: ^  U+ n7 V6 n
started puberty somewhat early, and occasionally,& j, m* s  V# c
testicular enlargement is not that evident in the- ]9 n7 [; A. i! s' P; r
beginning of this process.1 In the absence of a neg-
- [* b. d# k# D) x  rative initial history of androgen exposure, our0 Y. N) P4 t* P8 A, {& k' i
biggest concern was virilizing adrenal hyperplasia,: {% c  P6 q! ^9 C" r1 [: w
either 21-hydroxylase deficiency or 11-β hydroxylase
) J4 j2 a: K1 G$ N' ^! `deficiency. Those diagnoses were excluded by find-! u, I* u6 N6 z8 o1 E- }% g
ing the normal level of adrenal steroids./ E+ ~- v) z/ A( p+ \4 d
The diagnosis of exogenous androgens was strongly* w, s. o" U- T/ Q! S
suspected in a follow-up visit after 4 months because$ \8 p( t/ t3 v2 [
the physical examination revealed the complete disap-
( h9 y- T* q5 t( s: d+ z* Q. {pearance of pubic hair, normal growth velocity, and
5 c+ b# d, ?/ W% n  ~  Z. Mdecreased erections. The father admitted using a testos-
2 k2 h' E4 p! e6 P; g  r5 h& y2 sterone gel, which he concealed at first visit. He was
+ n1 _4 @- y( @( x9 _& F5 Pusing it rather frequently, twice a day. The Physicians’) z' E) K; ^. ~1 v
Desk Reference, or package insert of this product, gel or8 X& P9 q# |& m  Y
cream, cautions about dermal testosterone transfer to
1 _9 ]! t+ X7 ~$ f5 _unprotected females through direct skin exposure.4 }& v2 {1 y+ k: p' N
Serum testosterone level was found to be 2 times the9 ]. R3 q) Z3 k7 c
baseline value in those females who were exposed to
0 c. @$ [: B) H6 G7 |( U7 ieven 15 minutes of direct skin contact with their male
6 ?3 L5 I( `( C* O# r' Qpartners.6 However, when a shirt covered the applica-
* Q3 X. F; k1 b, Z: qtion site, this testosterone transfer was prevented.
. V6 v( A: @( G9 b5 d( a! rOur patient’s testosterone level was 60 ng/mL,
3 A4 [/ x. f/ V* `+ J7 Wwhich was clearly high. Some studies suggest that
' T. \% r2 ^) ddermal conversion of testosterone to dihydrotestos-
0 h  G9 x3 j, a0 S" o$ Bterone, which is a more potent metabolite, is more
8 I8 ?! Y/ R( X; @7 T+ Nactive in young children exposed to testosterone
" f& _( G! O: Z2 iexogenously7; however, we did not measure a dihy-
; q- F. D; G! Y/ ^' X3 k6 kdrotestosterone level in our patient. In addition to. h. S% x% f5 T1 g2 G
virilization, exposure to exogenous testosterone in  n8 d! S! D' r' B5 Y
children results in an increase in growth velocity and
% D3 h  q/ {% y$ i' }advanced bone age, as seen in our patient.
5 ~2 z( s+ ^7 q1 f% m; j5 z8 [The long-term effect of androgen exposure during7 y+ [4 y) a, u( o5 M, }9 [
early childhood on pubertal development and final$ I* ^4 Y, v* ]4 r3 J; L4 e
adult height are not fully known and always remain
, T9 w1 l, Z3 C% P! l3 pa concern. Children treated with short-term testos-
* z9 n5 L0 l& C  b9 Pterone injection or topical androgen may exhibit some2 g8 O+ [' z( U8 N; I( Q. l
acceleration of the skeletal maturation; however, after8 i% P, q. ~. [; b
cessation of treatment, the rate of bone maturation
4 e, d# s: B$ m: `decelerates and gradually returns to normal.8,9
8 g9 ~( _2 O$ e  |2 kThere are conflicting reports and controversy- E& U" Z/ V# {! U
over the effect of early androgen exposure on adult
+ n# i" e2 u& g. z6 n5 Apenile length.10,11 Some reports suggest subnormal
5 Y7 A- M0 U0 L2 Q0 oadult penile length, apparently because of downreg-7 |8 U6 N5 a3 D
ulation of androgen receptor number.10,12 However,
* K: N: h' E: hSutherland et al13 did not find a correlation between
9 W7 ?3 M" m/ o; k* }childhood testosterone exposure and reduced adult+ h; v- T/ s: \( k9 [
penile length in clinical studies.. d3 D! c! A$ Q) ^
Nonetheless, we do not believe our patient is
( J9 m% J" C2 R) t  igoing to experience any of the untoward effects from7 j2 X5 P2 s9 Z+ v+ H( L3 ^
testosterone exposure as mentioned earlier because5 e6 l6 z8 e7 R, y  K& M" S
the exposure was not for a prolonged period of time.7 q  V/ }- t  n! Z, V6 p+ \
Although the bone age was advanced at the time of8 G' R) P7 x' h0 m' A
diagnosis, the child had a normal growth velocity at2 }# A3 b, h0 x/ Q
the follow-up visit. It is hoped that his final adult
% r9 b2 t8 b( Q8 w" f- B3 }height will not be affected.  s" k3 _- d: x2 a
Although rarely reported, the widespread avail-- ^7 n" _. }9 @. y) r
ability of androgen products in our society may
& K! T9 w/ u9 c; J0 Xindeed cause more virilization in male or female! f. {! l! W3 K. e/ z
children than one would realize. Exposure to andro-7 x0 V% I& m3 X* v1 k: f
gen products must be considered and specific ques-( S- y# J/ f& G; x% S0 Z' c
tioning about the use of a testosterone product or
! Q* U3 \; I( `gel should be asked of the family members during
  c" G6 g2 U/ _  Jthe evaluation of any children who present with vir-
* V6 S! Y- W' s$ w' h0 milization or peripheral precocious puberty. The diag-/ U4 _! X1 g  l8 d% x
nosis can be established by just a few tests and by: r2 Q6 H" L; j; ]' ~9 l
appropriate history. The inability to obtain such a# V5 Z! n4 a! F' F: X- Q$ ^% ?- L) i
history, or failure to ask the specific questions, may6 b0 o, D) M6 Q# g% r' h& X
result in extensive, unnecessary, and expensive
& e1 V( w( W. n8 K8 O6 q: rinvestigation. The primary care physician should be6 y9 [2 K8 N1 W( Y8 G7 i
aware of this fact, because most of these children
7 c( ~+ c4 U+ X$ O* L2 Dmay initially present in their practice. The Physicians’
6 {2 r; }9 B- Q9 F8 t  YDesk Reference and package insert should also put a( u. U; T7 N* ?+ s. y, N
warning about the virilizing effect on a male or7 n1 _/ [# [3 j3 @
female child who might come in contact with some-) B; N& q: V5 i% G) r' h& ^
one using any of these products.
- w) o5 Q' _: j. cReferences
9 ?, c! K, z" r% z1. Styne DM. The testes: disorder of sexual differentiation% A  t/ ^8 y% O, O
and puberty in the male. In: Sperling MA, ed. Pediatric- q: O/ \6 ?9 n/ {
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" j2 Y! m* y9 d9 t' B4 N$ J
2002: 565-628.8 v# o. d. u+ l6 C) p
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, A, c- @& X) s1 |, x
puberty in children with tumours of the suprasellar pineal1 W% z! b& F8 y8 q) j' P2 q- k
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( f  S. A" |$ j( L4 L0 XTopical Testosterone Exposure / Bhowmick et al 543
5 M& Y1 u3 {; k( v0 e0 pareas: organic central precocious puberty. Acta Paediatr.( Y1 n# S. G6 N/ M( T
2001;90:751-756.
6 j* |. V! }2 K0 o7 O6 }3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
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Dekker Inc; 2003:211-238.% T* ~1 Q$ k" _  W: s/ P8 }
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