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is a significant concern for physicians. Central
) R) N8 G! p! a0 f8 i0 R  _precocious puberty (CPP), which is mediated/ t0 B, Y% u1 l  e8 D- A- U
through the hypothalamic pituitary gonadal axis, has' x% l+ _' ]3 v. v
a higher incidence of organic central nervous system: A! }% {, p0 z9 t: W6 s4 U
lesions in boys.1,2 Virilization in boys, as manifested0 C; k3 S! d0 Z( O% P' W/ t% Q8 A
by enlargement of the penis, development of pubic
* F# L- I; ~6 z. |2 r  shair, and facial acne without enlargement of testi-# X0 C1 t8 }3 h
cles, suggests peripheral or pseudopuberty.1-3 We: x# Y3 }7 W  O9 m0 w7 T3 ?
report a 16-month-old boy who presented with the
( c6 t8 b$ T3 k4 k8 jenlargement of the phallus and pubic hair develop-2 [' b( l& D- p, L( h" W0 P
ment without testicular enlargement, which was due
9 `5 |* w3 Y$ v6 `0 l- {3 Eto the unintentional exposure to androgen gel used by
7 y, d' t& t- x, p' Nthe father. The family initially concealed this infor-
/ m6 P; _  ?2 X7 l0 rmation, resulting in an extensive work-up for this4 n/ C8 K  M" \. R; u7 b
child. Given the widespread and easy availability of/ f0 q1 X) ~7 o: t3 X, F
testosterone gel and cream, we believe this is proba-! B; w; Y* b$ t4 j! P
bly more common than the rare case report in the
& D# D8 H8 J4 _, Sliterature.44 R  {, i3 ~5 e+ w4 r' h8 l
Patient Report
! {& m8 T/ e  e$ _4 s7 zA 16-month-old white child was referred to the
' y* ]+ g) q4 P- v. A% c; j2 aendocrine clinic by his pediatrician with the concern$ {/ L3 R' E8 p) i% o* A4 R7 P
of early sexual development. His mother noticed: _) \2 u3 W% A3 s0 _* F2 S2 j
light colored pubic hair development when he was9 d0 y# C2 e: z3 V( E  ?
From the 1Division of Pediatric Endocrinology, 2University of2 ]$ Q) t3 }3 W8 M
South Alabama Medical Center, Mobile, Alabama.
- v8 s/ R7 ^' l8 PAddress correspondence to: Samar K. Bhowmick, MD, FACE,/ C% t5 m, x3 |/ g
Professor of Pediatrics, University of South Alabama, College of
  b' Q/ G  l; w$ }' K% O: zMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 d8 G& \6 [- [: D" T- Z
e-mail: [email protected].. C" m4 ]+ p5 {7 ]: O! v5 T0 b' T4 r
about 6 to 7 months old, which progressively became- g, Z: G% O, r# p- }# Q
darker. She was also concerned about the enlarge-
0 a( ^5 r( D: G+ qment of his penis and frequent erections. The child
% P* V- w" G1 N. e- i+ Ewas the product of a full-term normal delivery, with( y1 @9 S" n1 e1 X% R0 k
a birth weight of 7 lb 14 oz, and birth length of5 P- n3 `% U, Y3 P; U# ?8 v; b
20 inches. He was breast-fed throughout the first year
$ f  T- a1 }$ D" @0 ^5 a5 p/ uof life and was still receiving breast milk along with$ H# ^4 E8 L, w0 F
solid food. He had no hospitalizations or surgery,9 u7 L" L: @9 b5 F4 R- L3 s4 Y
and his psychosocial and psychomotor development. }7 r( y6 D, A7 Y6 O5 r3 x
was age appropriate.
- R, k5 S& s9 H. F, r+ r3 ^The family history was remarkable for the father,5 ]# {  m* w( n( J0 I8 F
who was diagnosed with hypothyroidism at age 16,
) v3 T" ?  F: `- u4 Dwhich was treated with thyroxine. The father’s
! J9 @$ `! D! ?" G/ [4 Sheight was 6 feet, and he went through a somewhat4 _8 ~0 t, I# s
early puberty and had stopped growing by age 14.7 b' Q. j  a+ V4 e1 f) G6 h
The father denied taking any other medication. The9 v" D% d4 q) v) a, y, _
child’s mother was in good health. Her menarche
* F! }6 T4 A! m1 E! U$ g! iwas at 11 years of age, and her height was at 5 feet
$ M1 o3 n! q( f4 Q7 }+ ^+ s5 inches. There was no other family history of pre-9 }- R" |, i# i* O. @
cocious sexual development in the first-degree rela-
# K0 Q' j; l6 Y! ]' Mtives. There were no siblings.
+ i# J/ q, ^6 T' Z* s0 aPhysical Examination5 g( u: z3 ?" s1 c) O; y. q3 g1 w
The physical examination revealed a very active,
" N( y4 J4 W3 jplayful, and healthy boy. The vital signs documented1 P! h1 m* @1 e* U" t; u8 j+ V
a blood pressure of 85/50 mm Hg, his length was0 g: _, y- F2 F: N0 t5 V
90 cm (>97th percentile), and his weight was 14.4 kg
. _$ W( I- O2 {4 G. A7 _9 c(also >97th percentile). The observed yearly growth
# j4 p4 c- ~" L% m- [7 _; H7 K& Bvelocity was 30 cm (12 inches). The examination of7 P& M% H# T7 S, j! W7 X
the neck revealed no thyroid enlargement.
# A) I* r! B. j. b; X- J* \The genitourinary examination was remarkable for3 y: U4 C$ n6 N8 ]* g' D( W* N
enlargement of the penis, with a stretched length of2 t  ?" z0 h+ E* [
8 cm and a width of 2 cm. The glans penis was very well2 l" X8 o, \) O( n/ s4 x& L  t
developed. The pubic hair was Tanner II, mostly around# S: p1 L# ~* `
540: b  a6 f4 _1 C7 p* u& Y* Z( a9 c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 t$ Y0 m! {; N' lthe base of the phallus and was dark and curled. The
$ q% N7 T0 [' i) otesticular volume was prepubertal at 2 mL each.
" {" K! P2 W) l- Q0 y( xThe skin was moist and smooth and somewhat
* y+ A6 H) Y# z; |' Doily. No axillary hair was noted. There were no% e6 i9 o3 d* J; z3 `  N. H
abnormal skin pigmentations or café-au-lait spots.
; t  D! O- P. A% Z  I7 Y  KNeurologic evaluation showed deep tendon reflex 2+
7 g2 `) s% b6 F$ Tbilateral and symmetrical. There was no suggestion% u, o' S: y2 ]5 c
of papilledema.8 {& c! y8 L; U& A; _
Laboratory Evaluation' P2 @) D. |% f2 j+ `2 C! n2 f; f# i
The bone age was consistent with 28 months by: _0 h- _0 g5 L
using the standard of Greulich and Pyle at a chrono-# a4 A" I4 e2 s# `- S
logic age of 16 months (advanced).5 Chromosomal# `0 O7 q4 s5 j8 Q. D/ s' K+ r
karyotype was 46XY. The thyroid function test0 N8 }5 v" D3 U  ]
showed a free T4 of 1.69 ng/dL, and thyroid stimu-: r$ i! J, n  N& ?% E
lating hormone level was 1.3 µIU/mL (both normal).# [# K/ z! J2 T! q
The concentrations of serum electrolytes, blood) i& h0 M  p& X$ `/ r
urea nitrogen, creatinine, and calcium all were( M! Y% [9 `, f+ P7 b# d* s( I
within normal range for his age. The concentration5 R! x! O1 u: M( _7 u3 ]6 o
of serum 17-hydroxyprogesterone was 16 ng/dL
' O7 {! d' Q  s4 W: z(normal, 3 to 90 ng/dL), androstenedione was 20# n+ \4 \1 P% a1 M
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! p' W( k) A8 P! n* ~terone was 38 ng/dL (normal, 50 to 760 ng/dL),# s. Y1 U, R4 l3 g1 a
desoxycorticosterone was 4.3 ng/dL (normal, 7 to0 Y! j7 ?( @& f
49ng/dL), 11-desoxycortisol (specific compound S)1 O9 `  Y) r; a% z& T
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 t5 c5 I$ \9 b( m) y  }3 a
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 n; z9 w$ N* l' o* j  ?' |testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
. M& x# m( |5 \5 J. qand β-human chorionic gonadotropin was less than
, E% y8 h, W: P5 mIU/mL (normal <5 mIU/mL). Serum follicular- ?6 G6 K. m% f8 k# h
stimulating hormone and leuteinizing hormone
0 E5 d$ k4 s4 nconcentrations were less than 0.05 mIU/mL4 o& o$ y& t# w( W9 k9 w' {' x5 d5 e
(prepubertal).
3 T5 L: O# \6 C# \  DThe parents were notified about the laboratory
6 a# a& Z" b, J! r  ^results and were informed that all of the tests were
8 T( g! u) P" G2 y- inormal except the testosterone level was high. The
) f$ E. X) ^4 `' t  Sfollow-up visit was arranged within a few weeks to/ D4 N% f6 W0 W0 x4 ^
obtain testicular and abdominal sonograms; how-
1 N/ y( Q; h+ a. R6 U& c* Zever, the family did not return for 4 months.! Q0 |+ n0 f6 l' z4 c
Physical examination at this time revealed that the6 l) E. G# F' s6 S. E/ i1 g
child had grown 2.5 cm in 4 months and had gained" Q. v, Y1 L0 v: _8 H
2 kg of weight. Physical examination remained) Q' |$ R% C$ P2 x5 r' @5 k, @
unchanged. Surprisingly, the pubic hair almost com-
0 T- A. Y; D" fpletely disappeared except for a few vellous hairs at
9 @5 c% a: x" Q' z  y. uthe base of the phallus. Testicular volume was still 2
- ]: y; b6 V; }: UmL, and the size of the penis remained unchanged.
. P( {4 d% `, E) y0 l  h# zThe mother also said that the boy was no longer hav-
- a2 Y9 a7 T4 O, s0 I' J# ]; Jing frequent erections.( |' G  |8 \& w- e: u9 b
Both parents were again questioned about use of0 q* D) Q5 C! D8 e$ A( y5 a* Y+ e
any ointment/creams that they may have applied to
3 z) V0 I5 ?" }8 a/ ^! Wthe child’s skin. This time the father admitted the( ]2 _  h/ D. P
Topical Testosterone Exposure / Bhowmick et al 541
0 B  B0 w/ I3 o. o0 ruse of testosterone gel twice daily that he was apply-# B8 a3 u0 i* H# ~; B/ N
ing over his own shoulders, chest, and back area for
3 ~7 ^, e3 k' Ca year. The father also revealed he was embarrassed, w2 u7 O0 a, h: B' @
to disclose that he was using a testosterone gel pre-
' N( w% K, {" |) I- ?scribed by his family physician for decreased libido
: g- l! W9 W* Q9 }8 rsecondary to depression.
: @1 u7 \8 }/ h7 F2 @3 G/ qThe child slept in the same bed with parents.: H& ~- s3 Y- Y0 i9 B. i
The father would hug the baby and hold him on his) J, l3 F0 b4 N; J3 Q4 b. w
chest for a considerable period of time, causing sig-
8 O7 Y, V$ k; `9 {nificant bare skin contact between baby and father.
5 F9 M5 a6 r& S# yThe father also admitted that after the phone call,1 b/ a1 u4 ?! a; E3 T& n% i
when he learned the testosterone level in the baby$ k! J$ _; C  j! x: t
was high, he then read the product information
# C' Z: l! a" G" y% Ypacket and concluded that it was most likely the rea-
  V& E  t4 u+ v) T. bson for the child’s virilization. At that time, they2 D1 F' u) S- e
decided to put the baby in a separate bed, and the
" \" J; z' n$ T3 o" c! U0 A% x# @father was not hugging him with bare skin and had
6 O# N& t; g% T! R7 Lbeen using protective clothing. A repeat testosterone2 V3 k  m# I8 D* R& G
test was ordered, but the family did not go to the: Y/ b- @9 r; S  F) L- f
laboratory to obtain the test.
& N$ t; Q( R+ F3 ]# IDiscussion
( k2 a* p9 V5 s+ Z* b5 A2 ?Precocious puberty in boys is defined as secondary
, h& q& T- Y% x% c& M+ Msexual development before 9 years of age.1,4. j5 X3 A$ b0 N  S- F$ K7 w' j
Precocious puberty is termed as central (true) when
1 Q4 B( N- L- ]5 M. dit is caused by the premature activation of hypo-; ~& a  g8 l+ k" g3 ?
thalamic pituitary gonadal axis. CPP is more com-
7 u! i3 T+ E  G- ^9 W) x2 u$ c0 ^+ umon in girls than in boys.1,3 Most boys with CPP$ M" W. v0 N4 [* C! I* X
may have a central nervous system lesion that is+ M. J5 Y2 L; C8 s1 a2 [
responsible for the early activation of the hypothal-
$ V. t* M& B- c- m4 r, U- N. lamic pituitary gonadal axis.1-3 Thus, greater empha-; ^, n) O0 [1 \2 T
sis has been given to neuroradiologic imaging in
) w& E; R3 i$ O+ Q5 tboys with precocious puberty. In addition to viril-, {$ A& B& w3 N. r
ization, the clinical hallmark of CPP is the symmet-
& Z6 _3 T3 ^: f8 Q( i: Irical testicular growth secondary to stimulation by: ]& R/ O( v( f$ W
gonadotropins.1,3  y) J- q. j$ E# D
Gonadotropin-independent peripheral preco-
3 K5 \6 e7 Z/ R7 y* ]1 Icious puberty in boys also results from inappropriate
: F+ k% \# i. H' l5 [8 K3 gandrogenic stimulation from either endogenous or* _. J9 _  r* q& x! U7 C
exogenous sources, nonpituitary gonadotropin stim-1 E: V: r* J. ?# \' k( i' T% _
ulation, and rare activating mutations.3 Virilizing
) u( ~: V$ S' w1 Ocongenital adrenal hyperplasia producing excessive
1 Q9 R5 o0 I% Yadrenal androgens is a common cause of precocious
2 M/ F' u. {6 F; L- |& Q2 Epuberty in boys.3,4
' r( k# ]2 }& a) v9 TThe most common form of congenital adrenal
! |" e8 ]( H4 h. w) ~" [hyperplasia is the 21-hydroxylase enzyme deficiency.$ t: e( o6 m+ G
The 11-β hydroxylase deficiency may also result in5 h- Y( k5 W6 V" y3 U
excessive adrenal androgen production, and rarely,
& F) {0 z" i& p: f1 gan adrenal tumor may also cause adrenal androgen
0 S+ `5 T7 J+ O  E0 hexcess.1,38 n+ {4 o6 C8 h6 N: Q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 @6 y9 ^: v- f) L4 n  R9 c
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007  M) j& E5 `4 b+ x+ s/ `+ y, B2 u  ~
A unique entity of male-limited gonadotropin-
4 i( P6 U6 n4 ~0 \. Mindependent precocious puberty, which is also known9 w( A1 ?" ]% b  p! ]: x: ?
as testotoxicosis, may cause precocious puberty at a
# i. j! A; ^3 B# o' U- dvery young age. The physical findings in these boys
" M3 R$ _/ _. b! P8 ]; }5 |# S7 Fwith this disorder are full pubertal development,1 w) C7 @6 I* L  D% S3 B( L
including bilateral testicular growth, similar to boys
: o9 d! G7 m" t4 k, K+ Jwith CPP. The gonadotropin levels in this disorder- A4 O( N7 y" s0 j8 Q
are suppressed to prepubertal levels and do not show. |$ l/ h% \6 _  s
pubertal response of gonadotropin after gonadotropin-
7 G: Y, d  X0 q. Q5 u' N! [releasing hormone stimulation. This is a sex-linked3 t" b6 h$ s: I7 m5 ^
autosomal dominant disorder that affects only1 a$ U6 [! t$ H3 _( Z: \) M
males; therefore, other male members of the family1 m- {/ M" V- }
may have similar precocious puberty.3" G+ k* l; f' `9 P* |
In our patient, physical examination was incon-
$ T; d+ |! j9 ssistent with true precocious puberty since his testi-4 {9 q+ y0 L+ X. r6 P
cles were prepubertal in size. However, testotoxicosis
' ^  U* x+ q* G  o* I# ywas in the differential diagnosis because his father7 f; Z/ V+ I& }1 _2 \1 Y
started puberty somewhat early, and occasionally,
: [; U7 C! J: M& z) Y0 otesticular enlargement is not that evident in the6 K5 B' W0 F5 @5 }. M( P
beginning of this process.1 In the absence of a neg-
) ?. }0 h& Z; _( U; l$ E6 f( Kative initial history of androgen exposure, our
/ q5 j8 |' R6 d- S' j% J4 nbiggest concern was virilizing adrenal hyperplasia,( R5 @+ Y( q4 ]$ `# G$ N/ X
either 21-hydroxylase deficiency or 11-β hydroxylase8 k' K- P. z: p
deficiency. Those diagnoses were excluded by find-
: h& F/ w$ Z! _( T, sing the normal level of adrenal steroids.
0 d6 R# n5 f. D6 R, w- uThe diagnosis of exogenous androgens was strongly# n: g5 `" M2 Y
suspected in a follow-up visit after 4 months because, m2 `/ h# S; E8 F5 e9 i2 g0 D: z5 C
the physical examination revealed the complete disap-! ~+ d9 J8 T) X3 V/ p' B
pearance of pubic hair, normal growth velocity, and
4 m6 O) P! n; W2 @  l" g. fdecreased erections. The father admitted using a testos-
  D2 i% I" p& P! T; dterone gel, which he concealed at first visit. He was
4 ~# C/ c1 o- p! x4 D; r0 C: vusing it rather frequently, twice a day. The Physicians’! P* m& M5 _& J. s9 L2 ], f% u
Desk Reference, or package insert of this product, gel or
1 U. n5 D6 O3 c) H& m6 t* r* ncream, cautions about dermal testosterone transfer to
! M; Y; C: @) Z1 m( q/ b7 wunprotected females through direct skin exposure.
! s9 @1 Q3 W* ^+ NSerum testosterone level was found to be 2 times the
3 w: [) d& J0 U, l- w4 I* Tbaseline value in those females who were exposed to# ^0 }7 j, A9 ]
even 15 minutes of direct skin contact with their male# m% f2 Y! e4 k" b
partners.6 However, when a shirt covered the applica-
, i, C9 g$ C% b: ^tion site, this testosterone transfer was prevented.
2 R* q* g) e8 H- U+ w/ f' y+ JOur patient’s testosterone level was 60 ng/mL,
" `1 P  s9 Q" w9 r2 }which was clearly high. Some studies suggest that
8 W3 P% Z: x0 Q1 Vdermal conversion of testosterone to dihydrotestos-
7 J# E) V3 _( u% o  i" u1 yterone, which is a more potent metabolite, is more; s6 u8 J  k9 l+ C$ ^
active in young children exposed to testosterone. H3 s, h0 h9 n: W1 O$ }$ p
exogenously7; however, we did not measure a dihy-
  S# a' O) h5 v+ T: i2 ]8 |drotestosterone level in our patient. In addition to4 y- H" G. `  ^' v4 q. f8 w& x
virilization, exposure to exogenous testosterone in8 v  B8 W: H8 h
children results in an increase in growth velocity and
4 }$ ?: u2 U" y3 G2 c: ~advanced bone age, as seen in our patient.( \% D' D5 Q% g: m0 [% {
The long-term effect of androgen exposure during
4 n2 A, [, Y; b; D7 aearly childhood on pubertal development and final( N* T; M" U! {
adult height are not fully known and always remain+ d" n6 I" @, `6 z# H5 L
a concern. Children treated with short-term testos-2 G# z$ j1 I1 x5 p; m/ r5 a& H  n
terone injection or topical androgen may exhibit some
, `/ p' h, u9 \" i( s6 m( F5 nacceleration of the skeletal maturation; however, after2 i; m1 ?$ M: ], f% `2 f1 p2 R- I
cessation of treatment, the rate of bone maturation$ h" T! ^7 m' C8 _1 K2 `8 @) ]
decelerates and gradually returns to normal.8,93 k2 \0 ^1 A2 }8 I6 f
There are conflicting reports and controversy7 V; ~7 G+ u* E8 D+ T% @4 A' A
over the effect of early androgen exposure on adult
5 n0 d1 ^  Y7 [7 e% j9 u5 }penile length.10,11 Some reports suggest subnormal
% `0 q( G& D1 J: W2 Aadult penile length, apparently because of downreg-
8 k& w. a! M2 G" H! X( _( S1 g' zulation of androgen receptor number.10,12 However,
5 q) u% e  _% X* `0 RSutherland et al13 did not find a correlation between
" S- |) P: Z$ p) B! d- Cchildhood testosterone exposure and reduced adult. w+ d+ X1 l" ~# D8 Y1 ]
penile length in clinical studies.
6 E8 m# {3 }) {5 P$ a- |; XNonetheless, we do not believe our patient is
& V9 X- \6 i; }2 {& Ugoing to experience any of the untoward effects from) u; n( G0 w! K( J, M$ v
testosterone exposure as mentioned earlier because, ^9 b- Z* L' C  s# o
the exposure was not for a prolonged period of time.8 W5 u% l* R" }7 u6 Q! G6 K  O4 a; h. q
Although the bone age was advanced at the time of' ^; S; i) j6 S, A$ O1 B/ o) [
diagnosis, the child had a normal growth velocity at
. x7 Y+ Q8 g% p8 @) Gthe follow-up visit. It is hoped that his final adult
- s8 E- N/ f: [) E' v3 W+ x2 `" `height will not be affected.
! B6 V) j3 }( G6 I. WAlthough rarely reported, the widespread avail-; M( |. {% ~- A6 L! K
ability of androgen products in our society may
- C! f" y7 L! ]& w/ @' Y4 oindeed cause more virilization in male or female( z1 z- w" |8 k/ I
children than one would realize. Exposure to andro-1 S+ Y& E/ b0 r  {' a( ?$ F/ h
gen products must be considered and specific ques-9 @4 B% f# w8 @2 ?. U
tioning about the use of a testosterone product or
4 X, _# q$ g# a' {1 |' Bgel should be asked of the family members during. p9 W: Y) c  V# w+ ^; i8 J+ A
the evaluation of any children who present with vir-
6 Y5 a; l6 j7 V$ U! milization or peripheral precocious puberty. The diag-
) z1 _9 \9 ~) e9 s# {# @nosis can be established by just a few tests and by0 g. Z% q- M5 C1 ?" i
appropriate history. The inability to obtain such a
5 J* m, m" E' y5 y+ ^7 phistory, or failure to ask the specific questions, may, h' v; g" m8 G1 [* p- `' ~
result in extensive, unnecessary, and expensive
+ }( O+ {! L' S& A( B/ einvestigation. The primary care physician should be! J: C7 x7 }& b' ~2 c; x9 b
aware of this fact, because most of these children* V& y/ u* ^8 q
may initially present in their practice. The Physicians’- ?$ c3 M) B- c# P
Desk Reference and package insert should also put a
1 Y8 X$ o8 Y# M9 D$ @warning about the virilizing effect on a male or  i) I  F& s- s, I% o7 l( v
female child who might come in contact with some-
; m, ^3 y' d) C0 ^/ v1 Ione using any of these products.) f+ P, x3 z  z8 X1 Y; o2 C
References
% o7 M$ V* G  p& ]" h8 a, X1. Styne DM. The testes: disorder of sexual differentiation
/ S5 O! v$ J1 Tand puberty in the male. In: Sperling MA, ed. Pediatric
& ?' j5 r+ W# uEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
2 h( H6 g/ O$ N2 I$ v0 ?2002: 565-628.* Q; S, i, B! y/ Z& \! S
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- x' b  I: w2 E# h" M" n6 upuberty in children with tumours of the suprasellar pineal
% h" `, v; W" k- e4 N% uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! ~* o9 f; Q. v% X2 e
Topical Testosterone Exposure / Bhowmick et al 5431 B8 z8 B1 {% X; [# }  H! x
areas: organic central precocious puberty. Acta Paediatr.- L6 I* f; L" l1 r0 p# P
2001;90:751-756.
: j' E% y: @) y, N' z7 r$ L3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.3 u0 ?3 |; {/ a" R0 o
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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!

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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!
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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!
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感谢楼主无私分享
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