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is a significant concern for physicians. Central
( {$ a4 P: [3 I5 Nprecocious puberty (CPP), which is mediated, m3 J. @6 F" V% n; ^
through the hypothalamic pituitary gonadal axis, has& u+ W0 v- ^4 O# W- R7 r
a higher incidence of organic central nervous system
" Y- e8 t) \$ J9 C- m; F: Llesions in boys.1,2 Virilization in boys, as manifested" H8 p. M, r/ T7 B+ [& m
by enlargement of the penis, development of pubic! l" h% f" j% Y; ~& p
hair, and facial acne without enlargement of testi-
# A4 |7 r  y# b, A$ |  c: s' ]cles, suggests peripheral or pseudopuberty.1-3 We
! S0 M( B  _: y% J- R/ \; d4 [% rreport a 16-month-old boy who presented with the
$ i3 ~) s8 Y! d6 b* Denlargement of the phallus and pubic hair develop-/ j4 q; q" W( h- `
ment without testicular enlargement, which was due
& q- M! I3 J+ M0 }# yto the unintentional exposure to androgen gel used by8 a9 D/ j2 {) Q5 C8 h/ ?  m' S
the father. The family initially concealed this infor-
+ D( L, B5 s7 a/ B( F9 Ymation, resulting in an extensive work-up for this# i4 \% o( L7 |8 R
child. Given the widespread and easy availability of. N) s* e, ^, }: G& ^, I
testosterone gel and cream, we believe this is proba-9 A8 A/ v$ c4 ~0 n2 O3 T) ~4 C( ]
bly more common than the rare case report in the
. u/ y7 k4 A+ Mliterature.4
& M; X/ u: n  Y. @( qPatient Report
" z  t2 M$ N. n* ?' k9 B+ sA 16-month-old white child was referred to the' ]9 B2 n! n9 a+ A# p7 Q. C
endocrine clinic by his pediatrician with the concern  l6 a. H$ {% D% J& ^. Y- c
of early sexual development. His mother noticed8 u# L# x+ o: S3 m' z" k- l" ?
light colored pubic hair development when he was6 H9 x( X' G+ Q, [' K, L
From the 1Division of Pediatric Endocrinology, 2University of* y" y/ N8 y* z2 s
South Alabama Medical Center, Mobile, Alabama.; R) s! z* j+ K" C
Address correspondence to: Samar K. Bhowmick, MD, FACE,
/ t  u1 Y& D5 I# _Professor of Pediatrics, University of South Alabama, College of
3 r  ?5 s: I% @" y: q% [6 P$ Z- gMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
0 y4 r  U& I: o. w- ~* m) ne-mail: [email protected].; J5 O( Y' ]! g$ b1 r4 X5 J
about 6 to 7 months old, which progressively became
9 l* _1 U, q$ d7 `) ?2 @! h- ldarker. She was also concerned about the enlarge-
9 k$ b: b) |  D) e0 _; mment of his penis and frequent erections. The child" B8 _+ x3 \& o+ ^7 x( L
was the product of a full-term normal delivery, with6 i1 c- }# T5 A
a birth weight of 7 lb 14 oz, and birth length of& a* t. }+ v( k9 N) B/ J$ r, F' e( C
20 inches. He was breast-fed throughout the first year5 T2 I  a2 Q, o! Q# A
of life and was still receiving breast milk along with7 P0 B5 s, H4 C& u3 Z
solid food. He had no hospitalizations or surgery,
' g8 Z! G: z9 z; A* ~5 {and his psychosocial and psychomotor development( p* ]5 o+ k3 ?! Q
was age appropriate.! l, B; u. B. H9 _
The family history was remarkable for the father,
4 h8 ^: C6 j# p8 e$ ^who was diagnosed with hypothyroidism at age 16,
$ B5 t* y$ ~( k2 gwhich was treated with thyroxine. The father’s6 Q6 ]7 c* C' G( g1 i+ j
height was 6 feet, and he went through a somewhat) u, f4 P: d; e. g
early puberty and had stopped growing by age 14.! |, y* i, @; k. N2 U) }
The father denied taking any other medication. The' H5 c' S6 t0 H- w; }! W/ M# l! X
child’s mother was in good health. Her menarche
' C2 `& W+ t% [: I$ [1 @2 W$ N# wwas at 11 years of age, and her height was at 5 feet
7 }: p1 w! i3 e& q" A; J% G  m5 inches. There was no other family history of pre-) l' p0 p! [/ F1 l' j# `
cocious sexual development in the first-degree rela-
* Q/ U& P( J) Ltives. There were no siblings.
& Z" Q8 X: Z/ ~2 U2 {9 Y( kPhysical Examination' a1 A/ f0 m& U% ^# ?
The physical examination revealed a very active,
4 F* Q0 L" A8 w9 D  q! M% Rplayful, and healthy boy. The vital signs documented
& J% W# K# y  I& t: |# o) aa blood pressure of 85/50 mm Hg, his length was
% }: h( p3 `2 q/ Z0 D' x90 cm (>97th percentile), and his weight was 14.4 kg
; V. S3 m/ q; P, X(also >97th percentile). The observed yearly growth
0 ^. I, n, T% p" |8 D& o! N) S5 hvelocity was 30 cm (12 inches). The examination of) N* C3 q$ J( {, o8 i
the neck revealed no thyroid enlargement.
' u3 m2 e$ b/ c( v" O' J' TThe genitourinary examination was remarkable for
5 y/ v- r# _7 B8 L# ?enlargement of the penis, with a stretched length of- i% Z6 C! z3 T
8 cm and a width of 2 cm. The glans penis was very well
4 v0 E0 x: S8 a: }developed. The pubic hair was Tanner II, mostly around: C; p! Y4 s  f% T. a0 t
540
8 A! W% z3 {/ V9 {& n' Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! l. r* E7 P' T0 A' {5 C! x. _the base of the phallus and was dark and curled. The* I2 A. B0 [% e' {5 N
testicular volume was prepubertal at 2 mL each.
5 t! g0 y: g, A# J& ~# \& i% u6 VThe skin was moist and smooth and somewhat9 S! o6 B! b: h: e
oily. No axillary hair was noted. There were no
3 M3 O- n5 @  z$ ~/ v1 kabnormal skin pigmentations or café-au-lait spots.8 B" w8 W# S5 K* X7 _
Neurologic evaluation showed deep tendon reflex 2+
9 Q4 p" d9 T/ l- A! D6 ibilateral and symmetrical. There was no suggestion* e; C. I2 ?( x0 _) _
of papilledema.4 K. u' H$ d, o8 ]7 g5 k) y7 I* D( e
Laboratory Evaluation
2 e) l" A' v, m5 w% V! BThe bone age was consistent with 28 months by
+ W1 N4 R( t& a5 X, N/ Pusing the standard of Greulich and Pyle at a chrono-
2 N" Y9 A) x' B+ Slogic age of 16 months (advanced).5 Chromosomal- w, h- K/ h/ Y! v1 B
karyotype was 46XY. The thyroid function test
9 w8 X5 m7 P) Y) E1 D# Ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 B+ C7 m$ P/ e6 K& Z* a
lating hormone level was 1.3 µIU/mL (both normal).
* Y: k" N) l9 T! VThe concentrations of serum electrolytes, blood; Q9 H5 ^' v& o
urea nitrogen, creatinine, and calcium all were% v; ~+ G# I  J- u
within normal range for his age. The concentration& _  o& X. t9 W$ M  h' R
of serum 17-hydroxyprogesterone was 16 ng/dL
' f: |8 g" o0 m. {(normal, 3 to 90 ng/dL), androstenedione was 20, C3 u  I# h& }1 k/ U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-3 Z9 Y0 P1 D; B' L) y
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 J# Y# E4 N, ~% zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to, o% j9 E) M/ K2 w* ^/ }
49ng/dL), 11-desoxycortisol (specific compound S)
; k; `' W! b( U  hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. i, K% Q, Z/ y5 H8 l4 E
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
# h4 k2 D6 y% {& Otestosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ ?; \, p' i1 b1 `8 h
and β-human chorionic gonadotropin was less than
5 i- o1 D. b, X5 mIU/mL (normal <5 mIU/mL). Serum follicular
  s2 O) [( l9 i# K5 {$ {stimulating hormone and leuteinizing hormone6 L9 ]5 o  J# k" K( s/ O. s
concentrations were less than 0.05 mIU/mL
4 c% p  E% T' Q  w. U. d! A(prepubertal).
# m- r; W' G3 `4 k" A0 |2 [7 MThe parents were notified about the laboratory& I/ v) k% A  _, ]
results and were informed that all of the tests were
/ {$ ^  \! j+ }  [1 m( dnormal except the testosterone level was high. The
- M4 v7 F7 R8 S3 e8 `6 J& }follow-up visit was arranged within a few weeks to; {" e( ^2 ?) q  e5 R
obtain testicular and abdominal sonograms; how-6 {6 |" m7 E) U/ {& W0 V0 s* `
ever, the family did not return for 4 months.
- }, L2 o  u! F- [Physical examination at this time revealed that the
( y( a/ i" [, Kchild had grown 2.5 cm in 4 months and had gained
" w$ j8 u6 o/ I8 j) u8 H0 a; L2 kg of weight. Physical examination remained8 a) r) `1 B" d% |  |
unchanged. Surprisingly, the pubic hair almost com-
6 L' Q7 t2 H, T/ X; gpletely disappeared except for a few vellous hairs at
  Z3 e+ _9 U6 }7 u; D6 gthe base of the phallus. Testicular volume was still 2
5 t* Z* m& u  D5 c/ imL, and the size of the penis remained unchanged.6 k1 H4 g, j) p2 {. A1 m
The mother also said that the boy was no longer hav-
- b# G5 F6 ~* t. hing frequent erections.2 o) m, k7 R! l6 B: a7 Q
Both parents were again questioned about use of
/ z) U  N* ^4 e* H9 u( H! C# |any ointment/creams that they may have applied to7 D$ {3 `' ~; \$ b) U" @9 w
the child’s skin. This time the father admitted the
! c" q3 ~3 {& k5 D( ?Topical Testosterone Exposure / Bhowmick et al 541& O& F. t. o6 [4 r# c/ q
use of testosterone gel twice daily that he was apply-
. z3 Z8 Y$ n7 b' {2 ming over his own shoulders, chest, and back area for
  j8 \' @9 _5 Ta year. The father also revealed he was embarrassed
" Y5 R) G  |5 m2 ?3 Lto disclose that he was using a testosterone gel pre-
. G+ v+ K  F& yscribed by his family physician for decreased libido6 u' e$ s! i+ q: `; ]# D
secondary to depression.( U4 E7 l3 c5 }' l% t/ Q) q/ ?- i+ r
The child slept in the same bed with parents.
/ b* g/ ?& S: p8 e9 v  D; SThe father would hug the baby and hold him on his% k5 @2 }6 R9 ^# C  d2 a/ _
chest for a considerable period of time, causing sig-
( |+ B+ y+ {2 _2 y! knificant bare skin contact between baby and father.5 h4 P( H7 ]' C( K; U" p+ B
The father also admitted that after the phone call,
- |3 }3 _9 y" O, J* z! a8 @  Twhen he learned the testosterone level in the baby" V) e; M7 A8 f/ u# D7 q
was high, he then read the product information
. n6 P3 J; r/ C* g7 {- Tpacket and concluded that it was most likely the rea-' A4 I# z1 e3 ^* x( c1 m
son for the child’s virilization. At that time, they$ u0 S- Q* n5 E- Y) }) d# e* _
decided to put the baby in a separate bed, and the
4 w9 z+ k6 y: p) \$ tfather was not hugging him with bare skin and had
$ R( O+ E: [, o  q' ^9 U+ Kbeen using protective clothing. A repeat testosterone# ^' d# ]: K+ f+ c; e# e
test was ordered, but the family did not go to the
* B+ Q2 ?0 C; c" |; M/ Rlaboratory to obtain the test.
4 {) \7 g/ q2 d* A1 P) L2 gDiscussion* T( v. K8 \( U5 {
Precocious puberty in boys is defined as secondary
  o  S+ c8 K0 ]$ `8 Jsexual development before 9 years of age.1,4% u: y$ T5 G( u% j9 }/ E
Precocious puberty is termed as central (true) when6 o. u& q7 Y5 d" w0 ^) ]3 A
it is caused by the premature activation of hypo-
2 X& K; W- t/ H( w0 z7 l% cthalamic pituitary gonadal axis. CPP is more com-6 U0 y0 U. u. L$ S
mon in girls than in boys.1,3 Most boys with CPP& R0 W% ~" b% r
may have a central nervous system lesion that is
' k, O+ T7 ~, U8 ~! [responsible for the early activation of the hypothal-- X0 K# P- u) u$ O
amic pituitary gonadal axis.1-3 Thus, greater empha-# e! J7 O, L  T+ b
sis has been given to neuroradiologic imaging in
4 ?  f4 O- C6 }/ x# v, C+ ?boys with precocious puberty. In addition to viril-! ]$ J" u- ^/ n+ w% T8 Z
ization, the clinical hallmark of CPP is the symmet-. x  t9 ^7 q) R7 h
rical testicular growth secondary to stimulation by
5 T  @4 t" s3 w, u7 \6 b0 @& Dgonadotropins.1,3; m- Q* E0 |/ X- t. |
Gonadotropin-independent peripheral preco-" C: G2 x: U0 F% H
cious puberty in boys also results from inappropriate( d. X/ V0 [$ y  j
androgenic stimulation from either endogenous or
+ Q- L# O/ w7 {. ~9 l- ^. ]exogenous sources, nonpituitary gonadotropin stim-
1 N! V/ E& o  M4 j: W. Xulation, and rare activating mutations.3 Virilizing+ B4 Y5 y6 q& a: x1 R: K
congenital adrenal hyperplasia producing excessive
: e) u8 Y5 o# [+ }! ?+ r1 aadrenal androgens is a common cause of precocious! e) n  y; f  c. y
puberty in boys.3,4; y0 m4 m3 [) i# ^; P& J- M
The most common form of congenital adrenal
- t. M- `. j" b( c& rhyperplasia is the 21-hydroxylase enzyme deficiency.; P8 X) Y. W6 M: g: o& K1 G
The 11-β hydroxylase deficiency may also result in
4 A3 e* D  d" Q) f5 C/ Vexcessive adrenal androgen production, and rarely,
8 L' m& A* E. b) c8 f, Wan adrenal tumor may also cause adrenal androgen/ Y% }5 o- T* Y. [4 Q
excess.1,3
$ O4 ~6 F8 O7 d) fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; I+ [8 w( V! S# o! }  U* [" _542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! i( I; W% ]7 j; V8 s5 A. HA unique entity of male-limited gonadotropin-1 Y2 B9 S& a: C  \4 ^
independent precocious puberty, which is also known
6 G1 x- S2 v! q* k: Mas testotoxicosis, may cause precocious puberty at a: y& c& j) t  O/ {- r/ ~
very young age. The physical findings in these boys8 j3 g: W# @' ?
with this disorder are full pubertal development,& U) I. [' P/ Y& D, P
including bilateral testicular growth, similar to boys
0 O9 m& O3 T: ]" X5 \with CPP. The gonadotropin levels in this disorder
/ i1 E! U- {8 e4 |9 ]are suppressed to prepubertal levels and do not show
9 a# z3 M: n- Mpubertal response of gonadotropin after gonadotropin-
2 h3 ~  p2 I1 @; a5 c3 [/ T; Mreleasing hormone stimulation. This is a sex-linked
; |( V1 M; r. G9 H; Hautosomal dominant disorder that affects only
: Q- @3 ~: w7 `males; therefore, other male members of the family
6 |# _$ a1 H6 Q% {8 R5 ymay have similar precocious puberty.3! s$ _' p2 t4 m5 ]
In our patient, physical examination was incon-' R; n' F" i) w
sistent with true precocious puberty since his testi-7 r  S3 s) I% m, o4 x( T9 T9 \- M
cles were prepubertal in size. However, testotoxicosis8 V3 _& Q9 L- Z8 E
was in the differential diagnosis because his father
/ {, x# S/ r# {# O& M( d3 m' t, Istarted puberty somewhat early, and occasionally,
$ ?6 l0 B: i' }& b1 m; t" P9 V* rtesticular enlargement is not that evident in the
" `  X2 b( V1 E# ibeginning of this process.1 In the absence of a neg-
' u0 Z' B$ k8 l9 sative initial history of androgen exposure, our3 o9 i1 R5 e. a# W. Y
biggest concern was virilizing adrenal hyperplasia,* o$ [8 Y( r5 d3 h# c( {+ L$ \
either 21-hydroxylase deficiency or 11-β hydroxylase4 n1 ?  L/ \* t8 x; r
deficiency. Those diagnoses were excluded by find-2 J4 T. L% _# X
ing the normal level of adrenal steroids.
( N4 a) E7 l' N9 U0 hThe diagnosis of exogenous androgens was strongly# v# m* C' y# S
suspected in a follow-up visit after 4 months because; Z* K* m4 q* g( x
the physical examination revealed the complete disap-  @4 I* w' |6 l
pearance of pubic hair, normal growth velocity, and% K. n2 N0 {& b, _: B. \
decreased erections. The father admitted using a testos-
" M( v1 p0 D; Pterone gel, which he concealed at first visit. He was
7 ^  v' E. l0 ~9 d( y( fusing it rather frequently, twice a day. The Physicians’
+ A6 q0 L  \, N8 L/ s1 wDesk Reference, or package insert of this product, gel or
+ l5 M# V: P# ucream, cautions about dermal testosterone transfer to0 v4 \. a+ v- V
unprotected females through direct skin exposure.
' s8 M1 i0 z" USerum testosterone level was found to be 2 times the8 K4 K* X7 L8 }, N
baseline value in those females who were exposed to
8 [3 \. c: D  M. w+ u  @: Z7 w6 }even 15 minutes of direct skin contact with their male
- b: Z/ W" f3 B4 c  U6 X1 o/ U% npartners.6 However, when a shirt covered the applica-4 C' B1 N* d6 [) f& O- C
tion site, this testosterone transfer was prevented.% h, N: p+ E* D/ n! {
Our patient’s testosterone level was 60 ng/mL,
8 m% n) ^% L3 W2 Pwhich was clearly high. Some studies suggest that: J" {* q1 G  }  ~9 t& v$ t
dermal conversion of testosterone to dihydrotestos-
5 P1 ~! I  N9 T, n" ?terone, which is a more potent metabolite, is more
) i$ s% j' c. E! B7 H  s  \: pactive in young children exposed to testosterone
7 ?; @! G1 u/ ?: r2 yexogenously7; however, we did not measure a dihy-
6 E) J+ B6 c+ Wdrotestosterone level in our patient. In addition to6 w) l5 R0 P# Q
virilization, exposure to exogenous testosterone in
  w6 A$ p9 |+ C0 G5 S  {  q. Hchildren results in an increase in growth velocity and6 `) X+ b% l' C0 t4 a
advanced bone age, as seen in our patient.
8 y% [. O  g' kThe long-term effect of androgen exposure during
$ {6 I- u! u: U6 i6 _early childhood on pubertal development and final
( b9 u# X! x2 R5 G# Nadult height are not fully known and always remain
, P% M6 C9 M: b3 S( Ga concern. Children treated with short-term testos-" I$ w0 A0 L9 Y6 ]- W
terone injection or topical androgen may exhibit some
% u5 o8 S% N) X% Vacceleration of the skeletal maturation; however, after5 |( X2 ^7 @; Y7 f0 K% o
cessation of treatment, the rate of bone maturation
. u" D; V% {& odecelerates and gradually returns to normal.8,9
, [) C# w1 A$ T. @& j( KThere are conflicting reports and controversy
  R9 R. R4 A9 `over the effect of early androgen exposure on adult
/ ~/ j; N6 f5 q, L0 ?# v1 A7 }' {+ Qpenile length.10,11 Some reports suggest subnormal! S9 G8 o8 n6 {9 R1 W7 V. A4 E
adult penile length, apparently because of downreg-2 L0 }* H0 J) y9 G4 C0 b, t: C0 C9 v
ulation of androgen receptor number.10,12 However,; t& _1 y2 {6 E; l) Y: W) s+ b
Sutherland et al13 did not find a correlation between
' d( x- `; u# D) V' q+ `- Gchildhood testosterone exposure and reduced adult" f" Q. o( u( Y, ]
penile length in clinical studies.2 V% T( x& P5 D, Q4 @2 f2 S' R9 S1 a
Nonetheless, we do not believe our patient is- U( |9 Q/ K3 `9 `/ R
going to experience any of the untoward effects from
, p7 N' }7 A' \4 \. o. E3 Rtestosterone exposure as mentioned earlier because. u. V5 J7 d" j2 m
the exposure was not for a prolonged period of time.
$ _+ j4 i# @( ~4 m1 V: EAlthough the bone age was advanced at the time of8 }7 ?* v2 q% @9 T4 h' R
diagnosis, the child had a normal growth velocity at3 A+ Q8 Q$ R' d. X& t& e
the follow-up visit. It is hoped that his final adult
3 a4 l' O7 T3 i8 o& D/ ^height will not be affected.
$ q$ [5 [2 ~- C; U  ~' z; oAlthough rarely reported, the widespread avail-2 \9 z9 T% n* \7 K2 i/ w, F  h
ability of androgen products in our society may
3 ^, I" Q3 m# M( gindeed cause more virilization in male or female
7 x9 O7 I/ Y: \- [( s' m' ]children than one would realize. Exposure to andro-4 ]$ a4 [: I" |3 v  g6 j7 ^
gen products must be considered and specific ques-
% I- l% X) f  E; Z' _9 U3 Ztioning about the use of a testosterone product or. J- H# c' ?( F6 S  U
gel should be asked of the family members during
6 T1 o. u* c" p8 U9 Xthe evaluation of any children who present with vir-4 l: N, t9 v7 d+ p9 s
ilization or peripheral precocious puberty. The diag-( m0 J2 F, ]/ Q" p, I" L) B
nosis can be established by just a few tests and by
2 x" g+ U1 d# ~! D/ R4 U$ B3 eappropriate history. The inability to obtain such a
8 p: U" _- G+ E* |$ b2 nhistory, or failure to ask the specific questions, may
) `! F8 `2 V& o2 K+ [result in extensive, unnecessary, and expensive: |" ]6 }4 h% Y: U+ A- l
investigation. The primary care physician should be2 N  D, s/ A, }; m. F4 n) k6 }& R2 r2 B$ g
aware of this fact, because most of these children
! U4 u( t; E8 J& ]5 amay initially present in their practice. The Physicians’7 U& U  m5 a9 ^1 l7 W
Desk Reference and package insert should also put a5 b8 i% c& V5 k5 T" c% Y# W
warning about the virilizing effect on a male or
! U% A  k7 n% h% ?2 N$ u9 mfemale child who might come in contact with some-' j4 V# U% E) z, F3 \
one using any of these products.5 r" o7 D, \1 O& f2 j
References
" w8 x: D+ J' w2 `' |1. Styne DM. The testes: disorder of sexual differentiation
$ `2 A5 }/ ~& ?0 Zand puberty in the male. In: Sperling MA, ed. Pediatric4 Q7 i; j, [" ?' O: r0 I$ M
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
) I4 N% F; A" O( _1 ~2002: 565-628.
- d& q$ l+ F. K, u! @2 p" k; P2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious+ H8 O9 @; }* t/ f
puberty in children with tumours of the suprasellar pineal4 h' x: B. N4 B; l" N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 U) `, R9 H: m2 C
Topical Testosterone Exposure / Bhowmick et al 543, ?6 n0 y& i4 p) H
areas: organic central precocious puberty. Acta Paediatr.
. {! o6 J6 z1 @, ~$ A2001;90:751-756.
& b( ^. q# S1 P3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
  D- F5 Q# A, V4 O, [Pediatric Endocrinology. 4th ed. New York, NY: Marcel
" S' n/ ^9 g6 o) b1 {Dekker Inc; 2003:211-238.
* p. Z; c7 y& A, J6 [4. Yu YM, Punyasavatsu N, Elder D, D’Ercole AJ. Sexual
9 p% n& _# M5 i) B. @development in a two-year-old boy induced by topical9 o; a. _  S# o* Z
exposure to testosterone. Pediatrics. 1999;104:e23.
' P  F- l( R0 Q# S5. Greulich WW, Pyle SI, eds. Radiographic Atlas of
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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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