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is a significant concern for physicians. Central
; o! G3 d) A6 }/ `precocious puberty (CPP), which is mediated
2 W! _4 I9 b1 _5 j, c/ l+ g; J# Tthrough the hypothalamic pituitary gonadal axis, has
: r3 V- W. o8 z3 B6 ja higher incidence of organic central nervous system- _9 ~5 X/ k5 ?! L  F; D& u
lesions in boys.1,2 Virilization in boys, as manifested
- v1 y4 `  E8 `6 A3 ^8 Zby enlargement of the penis, development of pubic! V9 Y/ c, C6 v/ [
hair, and facial acne without enlargement of testi-
5 s; l: c; Y. g; f+ O' R. L+ scles, suggests peripheral or pseudopuberty.1-3 We% r% s; K; q5 L: B# P( l
report a 16-month-old boy who presented with the" Q3 C- ~9 U/ V! s
enlargement of the phallus and pubic hair develop-4 C- C) r3 [8 n3 j+ r
ment without testicular enlargement, which was due# D: T' E6 a: P& E- t, C, f8 ]
to the unintentional exposure to androgen gel used by
. n" p  L9 f& E1 Q/ }the father. The family initially concealed this infor-! E! U% G! g4 |6 z/ x" @1 Q( z
mation, resulting in an extensive work-up for this/ E/ ]6 L) f( c5 t$ H3 i
child. Given the widespread and easy availability of! O; A. |+ `; q! d, x
testosterone gel and cream, we believe this is proba-9 Q2 M# D: z! X1 Z2 z
bly more common than the rare case report in the, I9 Z4 [8 Q+ w$ y% Z
literature.4) V8 S! f6 Q' y$ {" i
Patient Report
" n' w, r, A; H' @1 IA 16-month-old white child was referred to the7 E+ D" @! P4 |: q( B
endocrine clinic by his pediatrician with the concern$ L- K" U2 W' F( y
of early sexual development. His mother noticed( U- @& K5 _/ O9 Q: t) J6 q% Y
light colored pubic hair development when he was/ X6 a7 p! b& C# p+ n
From the 1Division of Pediatric Endocrinology, 2University of
4 h# a5 N  x+ H, j1 PSouth Alabama Medical Center, Mobile, Alabama.
* q# p7 K; _7 z4 PAddress correspondence to: Samar K. Bhowmick, MD, FACE,
' }) r$ c$ S4 g0 K+ AProfessor of Pediatrics, University of South Alabama, College of; ?, V( E" C! ^) o$ {6 V' r
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ L& z" m1 m  e; V
e-mail: [email protected].+ X  f/ p' l) V
about 6 to 7 months old, which progressively became
8 \; l% D7 l% f- odarker. She was also concerned about the enlarge-
+ {1 Y; B2 n8 M: Q5 p$ A% `& Fment of his penis and frequent erections. The child
/ K( |/ j. S1 l0 Iwas the product of a full-term normal delivery, with
5 b8 m( d# T9 }0 Ia birth weight of 7 lb 14 oz, and birth length of% Y' e1 r) C1 E+ A
20 inches. He was breast-fed throughout the first year, L! z  Y  }, @; ?5 @. J2 u# G
of life and was still receiving breast milk along with3 s* @- x; W& \
solid food. He had no hospitalizations or surgery,
2 O. R: V* A8 I$ L2 pand his psychosocial and psychomotor development5 U  A" `. ~8 m3 t
was age appropriate.+ S- j; n. f6 n* f1 s  ]
The family history was remarkable for the father,6 g+ q1 c2 r6 ^8 x  L
who was diagnosed with hypothyroidism at age 16,
0 V0 D  s& Z2 S1 t- }+ owhich was treated with thyroxine. The father’s- \. |+ \4 [, `7 @! u" f
height was 6 feet, and he went through a somewhat
* L. ?3 h1 Z! B4 V" F% j) }early puberty and had stopped growing by age 14.
, d4 u$ A7 ^# ]The father denied taking any other medication. The* r) B8 D9 W2 j5 M
child’s mother was in good health. Her menarche
# I& C% c5 V/ a' Zwas at 11 years of age, and her height was at 5 feet$ ^. ]# E; L4 e1 k
5 inches. There was no other family history of pre-
+ B4 F1 X- J0 c) V+ s4 Y+ ycocious sexual development in the first-degree rela-
' X1 }3 O" O1 ctives. There were no siblings.
3 s$ @5 `: ^" q9 WPhysical Examination
9 z  [7 a2 [2 F' {The physical examination revealed a very active,* L+ Q' m$ k  D  l# t3 \) s
playful, and healthy boy. The vital signs documented! y  l7 X) u4 I/ n1 J8 u
a blood pressure of 85/50 mm Hg, his length was
2 ~% g6 W5 N* E3 c3 ]90 cm (>97th percentile), and his weight was 14.4 kg
5 F. ^  K6 H: \8 v  F(also >97th percentile). The observed yearly growth3 H; U5 ~& ]% \! W. J% s
velocity was 30 cm (12 inches). The examination of( u. d4 E4 [; ]; a$ i) V
the neck revealed no thyroid enlargement.
6 r7 `- R+ v$ k( FThe genitourinary examination was remarkable for7 `7 C2 [( @; R, i! z. p4 n
enlargement of the penis, with a stretched length of
/ H/ J" k& P* W2 k" H8 cm and a width of 2 cm. The glans penis was very well
& d/ G3 A3 u6 h- N$ A! Kdeveloped. The pubic hair was Tanner II, mostly around
& `5 T1 e5 d) I6 N* I, H540
- g2 e6 B1 }! ^$ t: iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- A' L' z$ I3 C! `4 dthe base of the phallus and was dark and curled. The! `5 d# z+ A2 n6 C
testicular volume was prepubertal at 2 mL each.
. X4 `0 |. a( N. ^) S" f+ B2 _( t& ]The skin was moist and smooth and somewhat
7 H8 I4 G- r6 F( A( x& [oily. No axillary hair was noted. There were no7 }; v  Q5 z! Z! Q% a- K/ a
abnormal skin pigmentations or café-au-lait spots.
4 G* l7 L6 b( c4 m" PNeurologic evaluation showed deep tendon reflex 2+' N* W$ I5 G" A4 N8 o/ Y; i, H
bilateral and symmetrical. There was no suggestion+ u4 [; O2 o- g/ a
of papilledema.
# o5 h3 p7 ?+ q8 h5 k8 SLaboratory Evaluation
- }' s' _1 C1 q$ y; [The bone age was consistent with 28 months by
( S8 |& ~, p! \) _( `$ E! Dusing the standard of Greulich and Pyle at a chrono-
5 _+ R" ?) {' D' tlogic age of 16 months (advanced).5 Chromosomal
# K1 }9 `9 W( p5 ~& _karyotype was 46XY. The thyroid function test
. u$ S8 b% \" k7 }. v* Jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-( v' q* o+ c8 Q. ?3 \' \
lating hormone level was 1.3 µIU/mL (both normal).
) C" l  T' n  c8 A8 a+ zThe concentrations of serum electrolytes, blood  }# f- y/ z8 w' c
urea nitrogen, creatinine, and calcium all were
! r4 `. m+ C+ a. Gwithin normal range for his age. The concentration. q5 Z* h6 W! c/ B0 l/ I
of serum 17-hydroxyprogesterone was 16 ng/dL
* \7 {0 a9 o1 z) O(normal, 3 to 90 ng/dL), androstenedione was 20
, r1 j; e+ \- ^* V  r% z  V5 Xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 h4 l' ~' l0 }2 e1 {3 e2 Kterone was 38 ng/dL (normal, 50 to 760 ng/dL),8 w+ h8 K6 l: f  P7 H- I
desoxycorticosterone was 4.3 ng/dL (normal, 7 to% r' ~& i9 b# U0 q; e9 }
49ng/dL), 11-desoxycortisol (specific compound S)# q8 K9 W# ]- e2 r9 T) _
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) _3 f3 g& l6 g/ U* ]' U8 L
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 O8 A, Y' I7 S! W2 C6 E/ v/ D
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 P# R. u; W; V3 X- b+ c  j. H) ], A
and β-human chorionic gonadotropin was less than8 s- G$ O' P: _
5 mIU/mL (normal <5 mIU/mL). Serum follicular
+ p% x" U. G3 ~3 S/ }, B1 ^stimulating hormone and leuteinizing hormone# P/ x% L- z% Z
concentrations were less than 0.05 mIU/mL
/ u1 v9 {: X& B, j# p( q(prepubertal).
: U$ m6 G0 \4 p% r; C! A, ~9 SThe parents were notified about the laboratory; d7 y; T7 g7 o* K+ [4 d. l2 l% ~
results and were informed that all of the tests were
# A0 k/ N. L1 ~8 r- \7 Vnormal except the testosterone level was high. The7 t2 j: a; \% z& U
follow-up visit was arranged within a few weeks to
: m5 K8 e  \* W+ i( r; wobtain testicular and abdominal sonograms; how-7 I) h  y. M# F* v4 W) f3 H% s& \
ever, the family did not return for 4 months.9 q4 V$ w1 l) j
Physical examination at this time revealed that the$ q5 J$ V- g1 u* ^$ _
child had grown 2.5 cm in 4 months and had gained, m1 D- _4 B0 w6 P% Y9 h
2 kg of weight. Physical examination remained8 X( \4 ~/ ^# [; G
unchanged. Surprisingly, the pubic hair almost com-. ?0 `/ o* \. N% c- D
pletely disappeared except for a few vellous hairs at
0 i, g6 M$ F7 {# Athe base of the phallus. Testicular volume was still 26 X; h( t, I' U! I) T6 H4 U( x5 d6 D
mL, and the size of the penis remained unchanged.
! \8 ?. s9 Z6 R1 k5 T) \/ Z  kThe mother also said that the boy was no longer hav-% ]3 a# k7 o) _2 |
ing frequent erections.
) @2 r0 J  v/ A8 A# j" O* Q$ p  C4 sBoth parents were again questioned about use of6 E8 f( b1 c! w# n5 v
any ointment/creams that they may have applied to. M" w% H$ W: N0 p; U6 w" \
the child’s skin. This time the father admitted the
, H8 _# ?) ]3 o2 Z( z0 r9 U. |Topical Testosterone Exposure / Bhowmick et al 541# i7 [9 T5 n$ C
use of testosterone gel twice daily that he was apply-: o2 L0 F( P. I/ Y( f: K8 N
ing over his own shoulders, chest, and back area for. g2 X8 x( W6 C+ x
a year. The father also revealed he was embarrassed4 Z& l. S/ f0 }4 i
to disclose that he was using a testosterone gel pre-
$ ?4 ^( u) `+ J. bscribed by his family physician for decreased libido$ o$ }  M" _5 ?" E% C
secondary to depression.
+ c7 U1 q8 ]! x+ x( _, R& }' eThe child slept in the same bed with parents.
) I, ~0 F7 [1 E: UThe father would hug the baby and hold him on his
% G; \: q& |8 L2 Q% Ochest for a considerable period of time, causing sig-! U; A* T% f- p5 B& M
nificant bare skin contact between baby and father.
% M6 R) P7 _+ ?2 s% UThe father also admitted that after the phone call,8 O/ O- f7 @5 d4 K3 O. b' f, C$ y
when he learned the testosterone level in the baby4 t& C% o3 L# _* M* a
was high, he then read the product information
7 |: H, `4 m' E+ ~' Epacket and concluded that it was most likely the rea-
. Z# C0 u# m2 L, E" i3 d3 k- S; Cson for the child’s virilization. At that time, they( U% `: V# h7 B  P9 D
decided to put the baby in a separate bed, and the
" I! @! i/ c  g# A0 D7 vfather was not hugging him with bare skin and had
% P* {, L9 P& `been using protective clothing. A repeat testosterone* p, {/ O8 r$ I1 Y
test was ordered, but the family did not go to the0 ^6 b: m" w3 V2 X2 \9 A
laboratory to obtain the test.3 W" {. F8 O7 H% |
Discussion
' e+ w6 G) Z' [0 N1 RPrecocious puberty in boys is defined as secondary
# L- C4 J( N; Zsexual development before 9 years of age.1,4
: _! ]. w$ }# X, [+ rPrecocious puberty is termed as central (true) when
# @* g9 l: y3 |: _0 r3 xit is caused by the premature activation of hypo-$ X7 Q) T* ]( `! f# d
thalamic pituitary gonadal axis. CPP is more com-5 X: Y$ V4 ?1 ?% e* @: d: `. h
mon in girls than in boys.1,3 Most boys with CPP% n* _- [0 q5 F4 d7 q. N- Q
may have a central nervous system lesion that is
7 ^1 e; f# P8 T' sresponsible for the early activation of the hypothal-
4 H  i: g9 N/ y- E4 c. Famic pituitary gonadal axis.1-3 Thus, greater empha-2 i8 r! M+ T) n+ _# U( l0 Q
sis has been given to neuroradiologic imaging in# F/ @* V& W, ~3 ]  i
boys with precocious puberty. In addition to viril-$ V! S+ J1 L6 P6 Z
ization, the clinical hallmark of CPP is the symmet-
4 K. @! k7 [5 @2 rrical testicular growth secondary to stimulation by8 P8 }' A6 O- y4 g& u/ N
gonadotropins.1,3
" K* r2 \* b0 F" q/ P  O' }4 vGonadotropin-independent peripheral preco-. r  C  O5 j% K3 J: k7 m
cious puberty in boys also results from inappropriate# _+ V0 w; D  z
androgenic stimulation from either endogenous or+ J8 E; ^- j8 \) H$ f# I
exogenous sources, nonpituitary gonadotropin stim-4 j+ [/ Z: ~! J. F* Z6 M
ulation, and rare activating mutations.3 Virilizing
2 F/ c% |9 q) Pcongenital adrenal hyperplasia producing excessive" U& t- F3 [3 j
adrenal androgens is a common cause of precocious8 u6 G6 @2 W( F5 D! t  d9 e8 @
puberty in boys.3,4
- V0 o! g; N# `- ]( lThe most common form of congenital adrenal
* J9 }- y3 u6 B3 a2 p, Khyperplasia is the 21-hydroxylase enzyme deficiency., n7 b9 b( Y2 {" f0 Q% ?. I
The 11-β hydroxylase deficiency may also result in: \1 x) y# n  [9 v# ^
excessive adrenal androgen production, and rarely,
) n( G, M) `) F! r5 R( `an adrenal tumor may also cause adrenal androgen6 a. b2 i0 D1 A1 I( N9 l# ^; |4 v
excess.1,38 z! j; \, q' g6 W+ L
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  V; D7 t0 Z- v2 F9 g
542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 L" l8 k1 l& |# e& G, M
A unique entity of male-limited gonadotropin-* V) C. X$ o  ?; f$ E
independent precocious puberty, which is also known1 S% k* S; ]! Z+ K1 J# O
as testotoxicosis, may cause precocious puberty at a
  y/ ^& I" q' a  Uvery young age. The physical findings in these boys  c$ G/ m- o. o3 Q
with this disorder are full pubertal development,0 }6 M5 o' ~6 u' L' L7 `9 j& n% `
including bilateral testicular growth, similar to boys
5 y$ t9 S# E1 F4 l7 ]with CPP. The gonadotropin levels in this disorder
* b1 E+ e9 L% o0 A, C' H0 aare suppressed to prepubertal levels and do not show0 d" M; N) S) k; g. S
pubertal response of gonadotropin after gonadotropin-
$ J0 \- w' Q( H8 M4 v) E1 P) Xreleasing hormone stimulation. This is a sex-linked
: D4 T" K: z( Uautosomal dominant disorder that affects only
0 K- J& I7 p' ]+ [7 S" Dmales; therefore, other male members of the family
8 t0 k) l. e5 zmay have similar precocious puberty.3
. b& _0 J$ w- s7 g. z0 JIn our patient, physical examination was incon-" D. ?1 h& K" E. w% E/ M" U
sistent with true precocious puberty since his testi-
0 H/ c" l) w4 @cles were prepubertal in size. However, testotoxicosis
) U* O# l$ {: E5 Kwas in the differential diagnosis because his father; B# Y9 X" U. S+ J. Q) o2 }0 o" c
started puberty somewhat early, and occasionally,( a$ N+ X$ u# X! V( [
testicular enlargement is not that evident in the' [! F& O' f' D& r  ?
beginning of this process.1 In the absence of a neg-2 e. o1 e( S% A; h1 C
ative initial history of androgen exposure, our
" G/ d9 `" O. j; g" J$ ~biggest concern was virilizing adrenal hyperplasia,1 ^( g' _* X. K" O7 V
either 21-hydroxylase deficiency or 11-β hydroxylase
' D: d; k& i: _6 Q7 C( Fdeficiency. Those diagnoses were excluded by find-5 `  W% J" ~% E; R2 t
ing the normal level of adrenal steroids.* d$ ~/ U& t+ m- w
The diagnosis of exogenous androgens was strongly
; R4 [1 f9 K+ Q# K+ m" bsuspected in a follow-up visit after 4 months because8 }% B" Y; T% H3 D3 Q% q- S
the physical examination revealed the complete disap-# ?* C- M7 i: ?: U
pearance of pubic hair, normal growth velocity, and
: `# p- U& U; ?" ]- {decreased erections. The father admitted using a testos-
; \/ _/ Q& M7 Mterone gel, which he concealed at first visit. He was
2 c6 ]$ X4 T( q, y! [/ j$ o9 @using it rather frequently, twice a day. The Physicians’
  G! [6 n/ O. M: I5 V& ^Desk Reference, or package insert of this product, gel or+ r. \+ H! J3 D
cream, cautions about dermal testosterone transfer to3 g; o- B+ R0 u  T
unprotected females through direct skin exposure.$ r: `/ Q0 A( f& O1 J4 p1 [
Serum testosterone level was found to be 2 times the% v) `: Y1 J3 `+ B7 }
baseline value in those females who were exposed to) y; F$ W) F0 t
even 15 minutes of direct skin contact with their male
0 d6 h" ]# t* Z4 k7 v7 o% h7 bpartners.6 However, when a shirt covered the applica-
, b. E& z9 n& ltion site, this testosterone transfer was prevented.
: b. }% ]5 X7 ROur patient’s testosterone level was 60 ng/mL,
& N/ U1 [; q0 H8 P, ^  q7 L8 L$ pwhich was clearly high. Some studies suggest that
* a2 @7 u2 u# N: Z0 @dermal conversion of testosterone to dihydrotestos-
6 |; y: A  |& U2 L: `  i0 J" [4 cterone, which is a more potent metabolite, is more
5 S: y7 F% {* v5 z, Tactive in young children exposed to testosterone
( l/ D* o: W, l  bexogenously7; however, we did not measure a dihy-
+ A7 x3 E3 s1 k6 \7 hdrotestosterone level in our patient. In addition to' U) _, \. g: A# `+ B" a9 r: {
virilization, exposure to exogenous testosterone in/ j7 Y4 |9 w* @# e1 {- p
children results in an increase in growth velocity and* x3 q, P) D5 A: l
advanced bone age, as seen in our patient.; z% W% {& [- P% o
The long-term effect of androgen exposure during
0 L/ n* |/ k% e/ C) H$ ^early childhood on pubertal development and final
1 ]4 u6 s4 F6 Qadult height are not fully known and always remain7 f8 F1 q3 I$ w# N
a concern. Children treated with short-term testos-
4 g8 M/ }" {/ o& T; `terone injection or topical androgen may exhibit some
+ j! S9 a3 T, Y+ Lacceleration of the skeletal maturation; however, after
( Y$ R3 x) d/ ?cessation of treatment, the rate of bone maturation
/ e2 g. d' ]4 `  ^6 ?( z4 Vdecelerates and gradually returns to normal.8,94 [' f$ W8 X% g& `8 x! y3 ^  W
There are conflicting reports and controversy
/ f: v0 u% L' @/ k( L! ^  ~over the effect of early androgen exposure on adult' y3 d# A: D' D7 t, h5 m3 U
penile length.10,11 Some reports suggest subnormal) F- }% e% A8 r! ]8 W
adult penile length, apparently because of downreg-' \& |( k9 h+ Q+ L/ e7 v5 X$ J
ulation of androgen receptor number.10,12 However,8 a# G' C0 O8 q' ]
Sutherland et al13 did not find a correlation between
, e' g6 z" W0 ^; [0 T6 X6 ~childhood testosterone exposure and reduced adult' I  X+ E) x3 ]: N0 A# k9 y
penile length in clinical studies.
! B7 m( J; L0 ~* b7 ]: I: A' K. i4 {Nonetheless, we do not believe our patient is6 _, m* Z+ X- C  k5 y' S
going to experience any of the untoward effects from) ^# i8 e1 ]1 J7 L& s8 q8 h
testosterone exposure as mentioned earlier because: r5 T. a# q* e. \
the exposure was not for a prolonged period of time.) E6 k4 e; t, F1 Q
Although the bone age was advanced at the time of
' Q1 _! L8 l0 a# {5 S$ Xdiagnosis, the child had a normal growth velocity at
# ^9 \( m6 P8 w+ i- A, ^+ F* ?the follow-up visit. It is hoped that his final adult
. V" c& H. A3 i+ N$ e2 }+ R5 Z. u, Eheight will not be affected.
( [1 J7 c' e( QAlthough rarely reported, the widespread avail-) V1 E5 H' u0 D9 {4 w. d
ability of androgen products in our society may
4 n6 i8 X% u, i5 M) t8 jindeed cause more virilization in male or female1 v: x3 o5 t5 V7 ^" ]
children than one would realize. Exposure to andro-
  L4 t5 n" R5 I- K7 P: A! @# Ggen products must be considered and specific ques-. ]0 z- h8 ^* `9 D, g: j3 ~
tioning about the use of a testosterone product or% ~5 D. y$ ?1 c( p0 y% {: x7 s5 {* P
gel should be asked of the family members during
5 E. g( J6 z3 P$ i0 Pthe evaluation of any children who present with vir-
% \$ M/ N0 q; B* T. ]: X0 J4 g- Iilization or peripheral precocious puberty. The diag-
. t6 L" H& a; A  r) I( enosis can be established by just a few tests and by# u8 a( S2 x- u1 j* Q0 ~
appropriate history. The inability to obtain such a; I2 L! \8 G# h8 q( ^1 M1 c9 O
history, or failure to ask the specific questions, may
+ L8 u( Z7 Y# tresult in extensive, unnecessary, and expensive
% G8 [# v) Y; b* ninvestigation. The primary care physician should be6 u5 E% A" p5 ]- P3 h% |
aware of this fact, because most of these children; h. i- b" ]' {4 L3 p( U
may initially present in their practice. The Physicians’
1 q8 ^  R7 a# ], B( `, S0 lDesk Reference and package insert should also put a8 T) R+ j$ H5 b
warning about the virilizing effect on a male or
, J/ f8 S! L+ C  afemale child who might come in contact with some-7 c  \4 Y; w. t" A1 ?
one using any of these products.0 m2 D& ?1 B0 S1 j- k1 X1 ]
References
% g# q) _$ U2 o& _. A- P1. Styne DM. The testes: disorder of sexual differentiation+ T" A# G: y+ @; p, `7 C
and puberty in the male. In: Sperling MA, ed. Pediatric
7 P6 A% P9 L, ~& x7 r) a2 ]+ GEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: V9 v) g% e7 r2 \" f. U& Z2002: 565-628.
% V$ ?/ x8 Z' I+ [; E8 M2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* ?* E$ F! ]# o2 b! z" N
puberty in children with tumours of the suprasellar pineal) }! W3 {  |; K* A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. }; e2 s8 h/ |5 n- R; y; [+ n
Topical Testosterone Exposure / Bhowmick et al 543! f7 D* I& v5 v3 I6 w5 |
areas: organic central precocious puberty. Acta Paediatr.
# F2 c1 N% k+ ~: V! }0 K, Q2001;90:751-756.0 K) u8 ^. \2 K  F( c
3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
8 `' P5 x5 M4 g* t7 g# D5 X! QPediatric Endocrinology. 4th ed. New York, NY: Marcel
* M" V0 g* @* K. M3 C9 c6 Y- hDekker Inc; 2003:211-238.7 s9 B& U* I7 |" Y
4. Yu YM, Punyasavatsu N, Elder D, D’Ercole AJ. Sexual2 o  Z  i# R4 I; z9 g# k3 }
development in a two-year-old boy induced by topical
% P* O+ t# u; j7 Q$ }' Iexposure to testosterone. Pediatrics. 1999;104:e23.# ~) m' e2 H) v
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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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