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is a significant concern for physicians. Central) j/ {5 T: O' U+ N, ^  ~$ v# q/ ^
precocious puberty (CPP), which is mediated0 v' s# G8 @/ W  V4 m  s6 p: j
through the hypothalamic pituitary gonadal axis, has! \2 Q/ [7 r( Q: e
a higher incidence of organic central nervous system
8 ~; T" g& K' G' b# I# nlesions in boys.1,2 Virilization in boys, as manifested
. _) G$ d4 h( B2 x( g) F& j  J! Gby enlargement of the penis, development of pubic" V1 U6 p: H, Q' V$ G+ [  o
hair, and facial acne without enlargement of testi-$ s9 R( f4 f/ X* m" {7 }
cles, suggests peripheral or pseudopuberty.1-3 We
" I. n8 r4 L; z& }/ n" o7 Y( ereport a 16-month-old boy who presented with the
4 B, d- o( u: G. Yenlargement of the phallus and pubic hair develop-3 y# C2 h  L$ ~5 r
ment without testicular enlargement, which was due4 ~- X$ Z. A7 a& ]8 g
to the unintentional exposure to androgen gel used by
, O5 Z3 P) Q# \0 athe father. The family initially concealed this infor-0 H! @! f) d9 a: N8 e6 H
mation, resulting in an extensive work-up for this5 l. E' s; h* M, `2 f* w: N
child. Given the widespread and easy availability of
, ~; F% i9 h& d: f' Ktestosterone gel and cream, we believe this is proba-
0 h6 d, }7 ~% C6 h  s" hbly more common than the rare case report in the! @! T  T9 G; H, j: R- |
literature.4
! K" T, `& G# u/ D5 L1 BPatient Report
5 h7 J" ~+ D: G0 dA 16-month-old white child was referred to the
5 n% V3 {5 M' ]% rendocrine clinic by his pediatrician with the concern4 L* N. @8 l6 _5 ?7 i
of early sexual development. His mother noticed; P# C, D# ?( I7 h9 d1 M6 R/ h- g
light colored pubic hair development when he was2 w. u) V2 g. _) C& E% m
From the 1Division of Pediatric Endocrinology, 2University of- h% W0 F6 c6 B
South Alabama Medical Center, Mobile, Alabama.8 n# G* A2 L' }
Address correspondence to: Samar K. Bhowmick, MD, FACE,% p% x$ \7 o( v
Professor of Pediatrics, University of South Alabama, College of; s; l* z8 m% s
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 @% U7 I  G% d9 K7 r
e-mail: [email protected].
0 m: F, z! Q4 H  u+ [$ Pabout 6 to 7 months old, which progressively became9 i5 _0 I( j8 t+ {; q
darker. She was also concerned about the enlarge-" x. w, j( {% ^! ^  x: K2 R- ^) W
ment of his penis and frequent erections. The child
8 Z/ A7 ]6 |; [0 ^# @was the product of a full-term normal delivery, with
4 a8 N3 h" a2 |6 L9 L1 \) Na birth weight of 7 lb 14 oz, and birth length of
% h2 b  M+ L) R, [( [* h4 @" V20 inches. He was breast-fed throughout the first year( _: p8 ~. c: N, d) h  b. X
of life and was still receiving breast milk along with
5 Z' x% J  R6 E  V  E# Jsolid food. He had no hospitalizations or surgery,
  l' ^5 y7 n1 l% Pand his psychosocial and psychomotor development
- H& |8 r6 l6 U  q! dwas age appropriate.. Y$ P4 Q. ~! k( S0 N% H$ N
The family history was remarkable for the father,3 @% C, v# A' a2 N/ A6 s1 m- R
who was diagnosed with hypothyroidism at age 16,! e. y7 u1 w8 M: H0 B  V9 ^' m. b' g
which was treated with thyroxine. The father’s
" h* _, s6 r) Dheight was 6 feet, and he went through a somewhat
7 N  g1 v4 i' v! A$ learly puberty and had stopped growing by age 14.
9 c) q' m! ~) z3 d$ lThe father denied taking any other medication. The! `2 r* _4 Y5 g  L+ |3 N
child’s mother was in good health. Her menarche* ^, l% }, b8 N; I
was at 11 years of age, and her height was at 5 feet
7 j8 a. Q: E& g* ^# a0 e  V0 ]5 inches. There was no other family history of pre-
8 o6 G, ^2 L" w& U; }cocious sexual development in the first-degree rela-
+ q' A6 g& I! ^/ _. dtives. There were no siblings.
8 f9 Q( k& I* u9 b* \1 F/ _9 lPhysical Examination3 b6 |. D6 n' q, \3 `# ?( e
The physical examination revealed a very active," k, I0 w% ~; f+ I. U
playful, and healthy boy. The vital signs documented. S/ _- a& \* P# t
a blood pressure of 85/50 mm Hg, his length was# `3 e9 S! s* i' q/ {/ w; A) A
90 cm (>97th percentile), and his weight was 14.4 kg
0 r4 E6 k% x% }' m/ O(also >97th percentile). The observed yearly growth3 P$ P  s! d5 b
velocity was 30 cm (12 inches). The examination of; z3 f' M) ]- A( w$ D
the neck revealed no thyroid enlargement.
$ C9 C; @+ g7 b, o- {The genitourinary examination was remarkable for" K2 @! B2 m+ V: \. F+ V6 d
enlargement of the penis, with a stretched length of
1 Q$ y/ L' V8 H0 H# u) R  o9 S8 cm and a width of 2 cm. The glans penis was very well
2 Q# G1 O2 n6 X! Z! }developed. The pubic hair was Tanner II, mostly around. p6 A& }1 j' g6 x
540
) S6 p$ n) c4 c/ \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& E5 Y( e& E  x; |( n! q& v4 x
the base of the phallus and was dark and curled. The! d6 s/ v* g5 v) n. m6 E- ?
testicular volume was prepubertal at 2 mL each.$ G! Q+ G$ X  p0 v/ O- P! B
The skin was moist and smooth and somewhat
$ D3 Q; q4 u% J3 V7 `- ^5 E6 F5 Ioily. No axillary hair was noted. There were no* q# e& ?6 ~# I9 {7 Y0 k; Y
abnormal skin pigmentations or café-au-lait spots.
, q- P" ?+ I) j2 zNeurologic evaluation showed deep tendon reflex 2+
) h. W* c# P( n% J# ?bilateral and symmetrical. There was no suggestion
. k" Y( y$ `! B7 wof papilledema.
+ J; |5 q4 o( Z- @Laboratory Evaluation
! v, {4 [0 J2 `) nThe bone age was consistent with 28 months by
; E0 c# v5 R: j2 a' susing the standard of Greulich and Pyle at a chrono-
1 Q$ l5 E3 B7 Glogic age of 16 months (advanced).5 Chromosomal
3 j/ f8 `- ]7 l1 u7 A; ]$ `karyotype was 46XY. The thyroid function test
7 w! z* t' B$ xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! }# t5 l1 k9 Rlating hormone level was 1.3 µIU/mL (both normal).7 q; F$ Q7 n% d6 v" D9 z1 w
The concentrations of serum electrolytes, blood+ i; B8 r8 z$ T; G" `" T1 e! t. I
urea nitrogen, creatinine, and calcium all were
( t" S  G) N) ywithin normal range for his age. The concentration
7 {0 B9 e/ C$ a' vof serum 17-hydroxyprogesterone was 16 ng/dL
- p( c" @$ w  {( M(normal, 3 to 90 ng/dL), androstenedione was 20
4 `. S2 V  w. N9 nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-9 L! w) d! a  h8 z$ M2 v
terone was 38 ng/dL (normal, 50 to 760 ng/dL),+ b4 |0 {1 [  s; x+ b! J$ k3 p
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 q5 J" z3 k: ~+ P, m9 x49ng/dL), 11-desoxycortisol (specific compound S)' Q6 {4 z. s. n' m
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
; d, [- q& z' jtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ @5 H9 N; \' \4 t
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),& k+ k# V0 `5 @) c
and β-human chorionic gonadotropin was less than6 G- h5 v1 E# y  r6 ?# h' h7 q6 ]
5 mIU/mL (normal <5 mIU/mL). Serum follicular
( E" v$ n; H" x! b) nstimulating hormone and leuteinizing hormone
  x1 q# D' _' p  Tconcentrations were less than 0.05 mIU/mL) [& V0 j1 W* i! \" K: ^* _4 k
(prepubertal).! l5 K: c! m1 z3 ^
The parents were notified about the laboratory
; A1 c; f+ C* t$ K& N" G) H+ ^3 Rresults and were informed that all of the tests were8 A* w" E7 u5 Z, C
normal except the testosterone level was high. The5 o% s) w4 k& n4 a
follow-up visit was arranged within a few weeks to% W% `% M) R" s, v$ [6 k
obtain testicular and abdominal sonograms; how-" l. E; {* d% B4 Q1 r& o
ever, the family did not return for 4 months.* l! U$ ~7 G8 I5 X- Z9 O- l% a
Physical examination at this time revealed that the4 I" `3 y* y( R2 T4 @
child had grown 2.5 cm in 4 months and had gained
* l# ^, e# m6 L5 K, ]4 W3 f2 kg of weight. Physical examination remained5 {3 x4 K) E$ R' a& _# I2 T
unchanged. Surprisingly, the pubic hair almost com-9 ~" v1 V3 R" Y, R; S
pletely disappeared except for a few vellous hairs at
( @% L& f8 a/ d" X' ?9 pthe base of the phallus. Testicular volume was still 21 a7 L. O0 {5 B8 [7 f
mL, and the size of the penis remained unchanged.9 U7 |9 A. g+ o
The mother also said that the boy was no longer hav-3 e2 m# ~/ t; _! D6 k$ |+ \
ing frequent erections.
, u0 z$ ]0 O; i4 J. G9 ABoth parents were again questioned about use of
- H* J7 S1 @9 T, g% Pany ointment/creams that they may have applied to
+ f( ^3 J0 h9 ^5 P9 O" T  Vthe child’s skin. This time the father admitted the
! ]: e4 V4 x& U! H- h! L5 i6 ?1 wTopical Testosterone Exposure / Bhowmick et al 541- G+ r7 g" [$ T
use of testosterone gel twice daily that he was apply-
2 \: ?$ A7 q; Y' Z3 z3 f1 ting over his own shoulders, chest, and back area for
0 u: N3 l" O3 ?& _( ha year. The father also revealed he was embarrassed, _& Q8 ?& ^- Y6 c6 M
to disclose that he was using a testosterone gel pre-
( A4 n& ^) x( i  I. X/ ]scribed by his family physician for decreased libido
+ D- Q; a, C1 U/ v* d1 I9 lsecondary to depression.
) c3 [) E; s! A1 `) {8 o. jThe child slept in the same bed with parents.; Y" r" ^, f3 R3 K% r: A0 C
The father would hug the baby and hold him on his- G0 w, C1 m$ r& h$ p
chest for a considerable period of time, causing sig-
; ?8 w, `) q* A8 Ynificant bare skin contact between baby and father.* L* k* I1 j0 P& f% E) W3 {
The father also admitted that after the phone call,! ~( Q, V; [' P; `* c' Y: P; {  ^
when he learned the testosterone level in the baby
/ o! z5 ?( ?+ Y& b  gwas high, he then read the product information+ ?8 V# `, x$ H; b# _5 `
packet and concluded that it was most likely the rea-* P8 T9 L" y' C6 o2 c/ [0 L
son for the child’s virilization. At that time, they
% u% h) g; V8 p5 c8 Ddecided to put the baby in a separate bed, and the+ K. @1 O* q" }
father was not hugging him with bare skin and had: P4 M# k' X3 J4 F
been using protective clothing. A repeat testosterone$ ]  y2 n1 U! R7 _3 I" }* s# ?
test was ordered, but the family did not go to the2 [  L$ m6 Z- _2 b, `+ z7 x
laboratory to obtain the test.5 w0 c, \1 b3 s$ B2 R6 B) ]
Discussion' p9 x( q4 z1 n- m+ B) b
Precocious puberty in boys is defined as secondary1 [7 o0 ^/ E3 S0 Y) \- r$ Y2 k
sexual development before 9 years of age.1,40 f+ E$ Y% J+ D  m& e& C# O5 g( e
Precocious puberty is termed as central (true) when
$ a" o2 X& O% y$ V7 d9 o, j0 Hit is caused by the premature activation of hypo-  Q* I" v+ m4 p& K
thalamic pituitary gonadal axis. CPP is more com-
0 g0 d/ X- b. i% ?mon in girls than in boys.1,3 Most boys with CPP  p& [% z' ]# U* y- X0 u% e/ R
may have a central nervous system lesion that is: ~- F6 G  ?2 O" i8 i& J' P
responsible for the early activation of the hypothal-
0 w" I1 U7 |; Samic pituitary gonadal axis.1-3 Thus, greater empha-; W/ Y& p) a) N% ]; F" j. U
sis has been given to neuroradiologic imaging in" t' Y& \8 _: n- b% V/ x7 A5 F: h" {4 u
boys with precocious puberty. In addition to viril-  N' T6 H4 N0 s8 y, V3 z7 ]/ [
ization, the clinical hallmark of CPP is the symmet-5 z- J% |% X3 c7 |, s) W
rical testicular growth secondary to stimulation by
: k/ g0 B! r' S1 z$ d9 u, P$ y0 R  C, Wgonadotropins.1,3
& Z; E+ N5 d5 @# w& f3 j# _Gonadotropin-independent peripheral preco-+ ]7 n, \1 o1 s# C- A, ~- k
cious puberty in boys also results from inappropriate
1 P6 Z% P! X- e; zandrogenic stimulation from either endogenous or8 V% p2 a8 H! p3 f+ T
exogenous sources, nonpituitary gonadotropin stim-% |: i" s% S, s5 _7 W, \0 x
ulation, and rare activating mutations.3 Virilizing1 j, n0 N: u* ]  \% E: U
congenital adrenal hyperplasia producing excessive
; `( E! L/ M1 u# {( g- a' Nadrenal androgens is a common cause of precocious
% j4 n$ l, [' n  v9 qpuberty in boys.3,4
% X/ ~( R6 c  O" ^The most common form of congenital adrenal- `, l$ O( [& |5 R: a
hyperplasia is the 21-hydroxylase enzyme deficiency.5 a9 f/ V! N" e3 O( J+ {) e, w
The 11-β hydroxylase deficiency may also result in; Y  I. H# @6 l
excessive adrenal androgen production, and rarely,
; p% B5 P. y: I" r  R' n, xan adrenal tumor may also cause adrenal androgen
3 B  n7 T/ g8 K: dexcess.1,3! Z3 Y- I6 F& c  r" w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  U* `3 _9 a; `2 U% x2 U
542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 n( U3 v. c7 v' n1 m1 q
A unique entity of male-limited gonadotropin-, ]( \! n( P$ m5 f/ W: U. N
independent precocious puberty, which is also known
" Q1 @+ @  ]$ E- m  R, e2 tas testotoxicosis, may cause precocious puberty at a  Z' O+ M9 s, Q7 q9 Y8 Q2 s
very young age. The physical findings in these boys5 A( X  ?5 m7 g1 G
with this disorder are full pubertal development,- `# S# ]0 t- T$ n2 U
including bilateral testicular growth, similar to boys7 N/ ^9 e- T5 N4 L3 v- s
with CPP. The gonadotropin levels in this disorder
5 Q& v; p5 a# _% {3 ]are suppressed to prepubertal levels and do not show- G0 V. h5 o+ c, |; s  X4 |
pubertal response of gonadotropin after gonadotropin-* J; U* A" Q5 ~, [. A4 h
releasing hormone stimulation. This is a sex-linked. B( ]4 |2 p$ I9 O/ {8 f  T: o; I. e
autosomal dominant disorder that affects only6 {) N: S: D5 ^. [& L- ~- a
males; therefore, other male members of the family
" i& s) _7 |! O. Rmay have similar precocious puberty.3$ h( k9 D  e4 e! W
In our patient, physical examination was incon-
' D2 o, Q2 F3 C7 U, n, Rsistent with true precocious puberty since his testi-3 E, _9 ?" |. e' U, \" r
cles were prepubertal in size. However, testotoxicosis6 o6 ~( b+ J2 B+ s$ f& r5 _
was in the differential diagnosis because his father: b9 m" q( o2 |: P. ~- S2 o. [
started puberty somewhat early, and occasionally,
& A/ k, }9 ]( i; _- N9 ltesticular enlargement is not that evident in the+ ?0 A7 m4 S  |
beginning of this process.1 In the absence of a neg-
" \' T4 a+ K4 C5 q: J- t! hative initial history of androgen exposure, our; m( O2 E* X/ _" g9 ]
biggest concern was virilizing adrenal hyperplasia,
0 y* U+ K! k" a9 Z! o  meither 21-hydroxylase deficiency or 11-β hydroxylase
6 z& E0 P9 g- |* i) o0 m. qdeficiency. Those diagnoses were excluded by find-, z: D$ e1 _" W& j$ a: F
ing the normal level of adrenal steroids.* h$ [7 l" O4 k8 I
The diagnosis of exogenous androgens was strongly6 n' r; j. h6 B4 }% b
suspected in a follow-up visit after 4 months because
) v6 A( t5 S. W0 Q- m8 |9 }the physical examination revealed the complete disap-
+ L2 U( ]- K' z2 H, Ipearance of pubic hair, normal growth velocity, and/ m* x* b# v& U7 H' b
decreased erections. The father admitted using a testos-
6 k/ u: b' o# qterone gel, which he concealed at first visit. He was
) Q7 ~8 I# E& tusing it rather frequently, twice a day. The Physicians’
* K0 j' b; S+ l) s5 L0 ^( f: iDesk Reference, or package insert of this product, gel or2 B* _% l/ L$ z' Z. u! t5 X* m9 O
cream, cautions about dermal testosterone transfer to7 Z5 k) k' ^: ^0 \5 {1 R
unprotected females through direct skin exposure.  H3 F' |. g/ c& f  |- ~% i( T
Serum testosterone level was found to be 2 times the1 `' C6 j+ e: T% M/ E
baseline value in those females who were exposed to
4 E9 @: ]" V) h+ aeven 15 minutes of direct skin contact with their male. \* }( Q" {' n% y9 o7 M
partners.6 However, when a shirt covered the applica-
/ |) ?8 A7 X2 c5 A( U$ J+ ntion site, this testosterone transfer was prevented.  f$ `' z, Q8 N$ t
Our patient’s testosterone level was 60 ng/mL,
2 I5 ~. o0 W" q5 P0 D% C2 twhich was clearly high. Some studies suggest that
8 v& ?, B0 p& D5 Y  Hdermal conversion of testosterone to dihydrotestos-# L1 B6 L) g% Z8 @/ Q6 j- e# ~6 j
terone, which is a more potent metabolite, is more
3 Q% X1 I4 Y; f0 I- iactive in young children exposed to testosterone
" C; U( l- a6 S# R  J! j+ Eexogenously7; however, we did not measure a dihy-' Q$ x6 ~3 U! H1 ~, p$ u
drotestosterone level in our patient. In addition to! r/ D  ^. O$ U8 |3 K3 p* {
virilization, exposure to exogenous testosterone in
, i4 `3 \% H; @children results in an increase in growth velocity and
  Z' g  j* S4 Y+ L% x7 T* _* aadvanced bone age, as seen in our patient.
9 I: ?6 d5 p9 a  K! X1 kThe long-term effect of androgen exposure during: R  p+ @4 c" o8 Z
early childhood on pubertal development and final" O" o( s  S' F. N& S5 G2 k
adult height are not fully known and always remain" _0 C7 O) @4 t
a concern. Children treated with short-term testos-( I3 G; s. u% i  }$ P
terone injection or topical androgen may exhibit some" Z0 ]( l- W8 X0 s7 q
acceleration of the skeletal maturation; however, after$ J: `: M  d7 ?! d( ~9 C# r
cessation of treatment, the rate of bone maturation6 \3 w2 G( \) i5 i9 z
decelerates and gradually returns to normal.8,9
1 i! }5 u- [9 ~- |. v- DThere are conflicting reports and controversy
" g* ]/ K+ t6 y5 w- B. C% uover the effect of early androgen exposure on adult9 H9 @  J8 m* L5 A9 D/ i8 [
penile length.10,11 Some reports suggest subnormal7 Q. R9 _) b7 P" z
adult penile length, apparently because of downreg-
7 e* ~- g6 [" [- nulation of androgen receptor number.10,12 However,
( E5 V8 q/ h) P' S0 G5 xSutherland et al13 did not find a correlation between
3 [: p; i' q4 {childhood testosterone exposure and reduced adult% l8 W0 M- a8 i4 |/ V& E
penile length in clinical studies.
( V- d& o! O+ [Nonetheless, we do not believe our patient is
' O0 o8 e1 ]0 T0 E! b8 N* y4 Dgoing to experience any of the untoward effects from  a+ o" N( U$ b, f: m
testosterone exposure as mentioned earlier because) l( U. r, J2 n8 F! @1 n- |4 s) K
the exposure was not for a prolonged period of time.& m! Z% J, B& u8 t
Although the bone age was advanced at the time of
% R. V: o" A1 H- y: U! h3 wdiagnosis, the child had a normal growth velocity at# V. z7 b) \6 Q, w- i
the follow-up visit. It is hoped that his final adult$ {/ c7 o( z/ h# e+ n5 b$ [# l
height will not be affected.) [- |: E' T/ E" W% S
Although rarely reported, the widespread avail-! ?+ s; b4 ~1 @0 `
ability of androgen products in our society may
' t8 }8 b1 J! B- |& ^2 }indeed cause more virilization in male or female7 {; J0 u7 s* ?& Z# G4 m& W: V! X
children than one would realize. Exposure to andro-
0 W+ q1 ?( I8 s8 p- M* t& agen products must be considered and specific ques-8 S; r3 `& k7 ]" L- t
tioning about the use of a testosterone product or
: A) A3 [$ i# Bgel should be asked of the family members during# C8 E3 g/ ~/ X1 |: n$ A% z% r- s
the evaluation of any children who present with vir-
7 s: i; z6 R( I& m* ?ilization or peripheral precocious puberty. The diag-
9 R/ l* T! b9 p! pnosis can be established by just a few tests and by4 q( k' }/ G& U0 M) A: z
appropriate history. The inability to obtain such a* |; O8 I4 l4 t
history, or failure to ask the specific questions, may
3 R1 F4 c3 ]$ c8 H. [1 c( Oresult in extensive, unnecessary, and expensive0 O; d+ I) _0 w3 @3 I7 J6 J# H/ g
investigation. The primary care physician should be
+ o4 o% v3 g+ ]9 }& M) M' ~8 qaware of this fact, because most of these children
: g, U  p; u; p) M9 Mmay initially present in their practice. The Physicians’; E0 H, t1 }/ W& a
Desk Reference and package insert should also put a  [4 O  W* H4 G6 G8 F
warning about the virilizing effect on a male or8 H6 ?5 W% N* U5 w# A
female child who might come in contact with some-2 v! c! z# \; y+ I2 Y
one using any of these products.
- t: j3 w3 U5 aReferences$ Z: W+ O( X* }
1. Styne DM. The testes: disorder of sexual differentiation  L* B  e, c, l0 |% k
and puberty in the male. In: Sperling MA, ed. Pediatric' z- _8 w- o8 _, q! Y
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
) `3 {9 G7 V  K2002: 565-628., e* G7 U2 Y* g" G& ~
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! E: K  M! i- h# W+ b. d
puberty in children with tumours of the suprasellar pineal
; R% k* O( x7 s- }# A! z' xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' U) _* a. y& j; j% P1 xTopical Testosterone Exposure / Bhowmick et al 543
- o5 e* W! e7 S+ }+ j* r3 Aareas: organic central precocious puberty. Acta Paediatr.
, k! m; B- O" c1 F# M4 N2001;90:751-756.
6 l7 b% y* a% M0 L. ]# l3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed./ {6 k; n$ Q' U
Pediatric Endocrinology. 4th ed. New York, NY: Marcel
1 J8 L% s, o+ z9 |' ]* J9 {% J( UDekker Inc; 2003:211-238.
% `0 u3 j9 ]4 W  J* ~# m4. Yu YM, Punyasavatsu N, Elder D, D’Ercole AJ. Sexual
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發表於 2025-1-4 13:25:11 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
發表於 2025-1-5 09:19:02 | 顯示全部樓層
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發表於 2025-1-26 17:11:43 | 顯示全部樓層
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-27 16:30:49 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-29 20:38:58 | 顯示全部樓層
感谢楼主无私分享
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