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is a significant concern for physicians. Central
; s  e0 Z6 g4 c1 M9 S/ ^precocious puberty (CPP), which is mediated' C; L; n9 g% Q0 [. s9 L
through the hypothalamic pituitary gonadal axis, has" L5 V4 M4 M8 ^- k# C
a higher incidence of organic central nervous system
3 e& i6 \2 R) U; q7 Y5 Llesions in boys.1,2 Virilization in boys, as manifested
2 n( u( L+ Z. O8 u# Nby enlargement of the penis, development of pubic
  W& p* }' x$ R$ t" w; ohair, and facial acne without enlargement of testi-
6 r8 m* s; m8 Q" a+ p# V2 ccles, suggests peripheral or pseudopuberty.1-3 We0 n6 M' `& x3 W9 q: c1 d+ U
report a 16-month-old boy who presented with the, J- X4 J# t' y$ k
enlargement of the phallus and pubic hair develop-" J0 V9 Y9 t* _1 R3 S" p; t2 v" f
ment without testicular enlargement, which was due
" c& m7 `! m7 a. Yto the unintentional exposure to androgen gel used by" E% C( f3 a' w* O; |8 l
the father. The family initially concealed this infor-
. w( f5 n. X+ B1 G6 p* }4 U8 vmation, resulting in an extensive work-up for this
7 i# j3 Y1 j: b9 j, ~( M# S# pchild. Given the widespread and easy availability of7 q6 t; Z+ R& Y# h+ F
testosterone gel and cream, we believe this is proba-% H. X  C# p; b1 ~/ f& W
bly more common than the rare case report in the, v* H$ g. A! |) {! N
literature.4
. K$ R: b! B8 {! `3 iPatient Report
+ `, h* {. Q$ Y& O- BA 16-month-old white child was referred to the
6 i; m3 V4 r! G1 I$ c1 ]. h9 M) S1 Rendocrine clinic by his pediatrician with the concern/ B5 R3 }2 r1 m
of early sexual development. His mother noticed
3 y/ m: \% i1 r/ dlight colored pubic hair development when he was* M0 \6 B: B6 P/ B2 D/ b" @
From the 1Division of Pediatric Endocrinology, 2University of, ~8 t) L! ?7 ~$ \
South Alabama Medical Center, Mobile, Alabama.1 X+ [' t# d3 k* H
Address correspondence to: Samar K. Bhowmick, MD, FACE," L" X# N$ E  J: z8 v4 L5 l: M! m" j
Professor of Pediatrics, University of South Alabama, College of
! C$ v% T2 @7 I* K' K2 kMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ X0 `+ I% ~3 d+ P: le-mail: [email protected].
2 g  R' E; n+ f- s4 k- e! P! Habout 6 to 7 months old, which progressively became
5 [0 Y! z. K2 A- S5 E, ~darker. She was also concerned about the enlarge-9 Z% y5 `4 P' B! t5 d8 q# f& c
ment of his penis and frequent erections. The child
5 g: y# n( ]7 ]6 O7 r4 hwas the product of a full-term normal delivery, with$ b/ w1 @+ f9 G5 e0 g+ W) f
a birth weight of 7 lb 14 oz, and birth length of
, ]! x; O8 A  N) D9 S% ^6 K* M20 inches. He was breast-fed throughout the first year: G5 M! Z( z/ [$ P4 B7 z
of life and was still receiving breast milk along with7 G0 \# C! s/ t, o; d5 X  m: M
solid food. He had no hospitalizations or surgery," y' i4 h$ p, U* \+ T8 k2 I
and his psychosocial and psychomotor development
8 Y8 u2 m7 M. I& y4 h8 Ywas age appropriate.  ]2 R; i7 z# l% b) A
The family history was remarkable for the father,9 f/ j* f0 `" q0 n
who was diagnosed with hypothyroidism at age 16,& E1 w5 q1 t8 h/ v9 n! r
which was treated with thyroxine. The father’s
3 l; U4 }3 ?) N1 F6 d# jheight was 6 feet, and he went through a somewhat
- _4 u) }3 b8 V8 s! V. n  learly puberty and had stopped growing by age 14.# {- t0 q) G" K- n) n0 v" j  H
The father denied taking any other medication. The
3 N+ _! k) W% ]& w. Q% gchild’s mother was in good health. Her menarche9 O6 x/ l) o; z. z3 V4 N  E
was at 11 years of age, and her height was at 5 feet
3 q$ |/ e( M7 k& D& Q5 inches. There was no other family history of pre-
4 o1 |! Q# Q7 d- o6 d' n7 d' S/ dcocious sexual development in the first-degree rela-) F5 y8 V6 Q; l) U
tives. There were no siblings.
  V5 D6 `" E; N0 o2 Y' m. UPhysical Examination
1 c! e1 G6 j5 h* w$ _7 \- N6 Q2 Z; pThe physical examination revealed a very active,
# T1 V5 `4 A, qplayful, and healthy boy. The vital signs documented# G6 r* H3 @) z% U- L( H
a blood pressure of 85/50 mm Hg, his length was
2 m" I& F/ Z% ^/ w90 cm (>97th percentile), and his weight was 14.4 kg
1 j3 |0 |0 S- ~' i0 }- k: ^(also >97th percentile). The observed yearly growth
0 q7 H" B) E7 R) h# p) z1 mvelocity was 30 cm (12 inches). The examination of
( [" H" u: A( b  W% Z  Ethe neck revealed no thyroid enlargement.! {6 |7 e. w1 q# ^" P- Z2 O
The genitourinary examination was remarkable for( Z+ F4 \+ k" M/ t1 u
enlargement of the penis, with a stretched length of
0 U/ B7 P8 @3 o( C8 cm and a width of 2 cm. The glans penis was very well: N+ y' M# {. U1 Y/ ?
developed. The pubic hair was Tanner II, mostly around! f: ]+ k! M; [4 _
540
8 P$ c+ A, I. o  dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) {0 K! z  R1 |4 T) |$ ~' H
the base of the phallus and was dark and curled. The; Q$ b$ Z7 I4 ?
testicular volume was prepubertal at 2 mL each.% y3 X2 C' h9 d7 |! D" `
The skin was moist and smooth and somewhat
& a/ L4 o5 b  ^4 G6 eoily. No axillary hair was noted. There were no
. j0 w$ ~( i: k* @abnormal skin pigmentations or café-au-lait spots.2 _$ h- U% e4 o
Neurologic evaluation showed deep tendon reflex 2+
  R- x/ r$ R+ q2 |( A% Y" x  ]bilateral and symmetrical. There was no suggestion
! G, }/ q* o$ Mof papilledema.; N1 m2 H4 Y) j; k
Laboratory Evaluation" ?4 a" z9 u% \4 A. O" u
The bone age was consistent with 28 months by( M( B/ n, g" v+ E' S
using the standard of Greulich and Pyle at a chrono-
4 H2 D' n9 y8 `7 Q" flogic age of 16 months (advanced).5 Chromosomal
5 X8 F! a) h/ V- w8 `karyotype was 46XY. The thyroid function test  B# F! N- e. n( r8 h
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
2 W. q# L6 H9 h. e- \! e- u6 Clating hormone level was 1.3 µIU/mL (both normal).% _- u' i, N& Z3 q0 A/ e; Q$ `
The concentrations of serum electrolytes, blood$ e0 A- N  C! o
urea nitrogen, creatinine, and calcium all were& V. c: W% b  `4 r" N. G5 K7 U
within normal range for his age. The concentration+ d: o' w0 ^+ y
of serum 17-hydroxyprogesterone was 16 ng/dL/ l! }( N3 G) b. S; M) [- y3 g8 c
(normal, 3 to 90 ng/dL), androstenedione was 20
3 f; d* w+ q, x' Mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
; \8 d9 D" [4 {5 ], w* [terone was 38 ng/dL (normal, 50 to 760 ng/dL),7 V5 A4 u5 h' @) {) l+ C& g
desoxycorticosterone was 4.3 ng/dL (normal, 7 to% t* {$ A, u' t% h% @+ z4 N& l
49ng/dL), 11-desoxycortisol (specific compound S)1 \% G; T3 u/ d; U
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( l$ U. H% t, n5 r
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ G7 z0 C% p4 o6 s
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# x" a/ t6 v. eand β-human chorionic gonadotropin was less than
% O5 x" j$ v# |7 s& u" J) i5 mIU/mL (normal <5 mIU/mL). Serum follicular' I: ?, d; Z/ Q$ U6 e9 T
stimulating hormone and leuteinizing hormone$ D3 c# ]5 J% ]$ J9 j1 W
concentrations were less than 0.05 mIU/mL
' C" [$ s7 d$ ]) J(prepubertal).
8 G9 y: c6 i. k% y7 vThe parents were notified about the laboratory$ s( T! E( _6 a  x4 g+ {
results and were informed that all of the tests were
+ E3 u0 F9 p. I  w' ]1 A3 j5 tnormal except the testosterone level was high. The8 a  ]0 h: I* P) x
follow-up visit was arranged within a few weeks to
) l; e, p" Y- A  g; yobtain testicular and abdominal sonograms; how-
/ i  i( s8 d& Cever, the family did not return for 4 months.  T+ [, B* z1 N+ ^& u' `
Physical examination at this time revealed that the( M5 t. ]' C  `' w1 H- e9 R
child had grown 2.5 cm in 4 months and had gained
5 y  r' ~" ~) E9 B2 kg of weight. Physical examination remained
3 D) r8 F$ O8 o/ punchanged. Surprisingly, the pubic hair almost com-7 a5 I9 {- ~$ h; R& O  }4 r
pletely disappeared except for a few vellous hairs at1 {$ S/ b2 R- |
the base of the phallus. Testicular volume was still 2
+ Y2 X9 x0 @( I2 F( ~% smL, and the size of the penis remained unchanged.
) d8 G: s7 E: p" h+ J- ?The mother also said that the boy was no longer hav-7 t# W% q" C1 u4 M# u% R, B
ing frequent erections.+ ~' B" l8 _  E8 ^
Both parents were again questioned about use of7 x" D# S7 ]2 I6 H
any ointment/creams that they may have applied to
6 E+ Q, i/ A6 y5 H% Rthe child’s skin. This time the father admitted the
! h- ~; s9 }& D" x8 {& ~, {Topical Testosterone Exposure / Bhowmick et al 541% g5 s/ L$ P. a0 r
use of testosterone gel twice daily that he was apply-. f: n+ K7 u! z
ing over his own shoulders, chest, and back area for
9 {* K2 i( e% l) F9 `* _a year. The father also revealed he was embarrassed
; O; q  [' J0 h, U; J6 m5 M9 T2 jto disclose that he was using a testosterone gel pre-
, ~) p& Q0 g2 q+ X, \; nscribed by his family physician for decreased libido
9 v- c  O+ s3 h" Z. I( T) \secondary to depression.) G' U: q1 U) P! a4 b
The child slept in the same bed with parents.
( m2 ^  i- x6 M: N1 FThe father would hug the baby and hold him on his
$ }( s5 q3 m7 h' ]1 B  \1 ~1 z( uchest for a considerable period of time, causing sig-. }0 _" @( i/ i# j, {1 Q$ _
nificant bare skin contact between baby and father.
# r; T( w( W, O' y# W5 QThe father also admitted that after the phone call,
/ J) J- G& G4 m9 W1 Cwhen he learned the testosterone level in the baby: g/ _$ N2 ?! G1 B
was high, he then read the product information; T; `4 q. f- O. l- K% p& K4 w  R# D. q
packet and concluded that it was most likely the rea-
$ ~% V- \+ F# \- l9 a* V  ~son for the child’s virilization. At that time, they8 G" D- k8 {2 c; L$ r; }- {
decided to put the baby in a separate bed, and the
. e9 X+ I9 @/ c/ }3 p- C' L) c5 O* Hfather was not hugging him with bare skin and had
. b( r( Q/ E5 z! O, z0 D5 G9 X  {: a; [been using protective clothing. A repeat testosterone. o  i* g( J. ?& @
test was ordered, but the family did not go to the) N6 e2 f  R6 g; E+ m
laboratory to obtain the test.2 {; X. P$ d4 o3 R
Discussion  D) G; q4 B  G# O  [; F; i# j) W
Precocious puberty in boys is defined as secondary7 Q) e7 @1 e# ~+ e$ c
sexual development before 9 years of age.1,4
( J$ L: j* F7 G+ ]Precocious puberty is termed as central (true) when1 d8 L$ t: e. R5 W! S; O2 {
it is caused by the premature activation of hypo-6 Q0 y9 m' q$ i1 u/ E5 {
thalamic pituitary gonadal axis. CPP is more com-
# w; g) V  h  o" Z+ ?mon in girls than in boys.1,3 Most boys with CPP, J  I- k9 i1 H/ b; j
may have a central nervous system lesion that is( s4 p# X# r0 e" o1 V
responsible for the early activation of the hypothal-6 r" l; t- j2 k2 _. y
amic pituitary gonadal axis.1-3 Thus, greater empha-
7 R5 [' K8 l, F4 K* P1 m5 N( y$ j, gsis has been given to neuroradiologic imaging in$ }) v# v8 A! M5 u' T3 A, b8 }
boys with precocious puberty. In addition to viril-
% |; G0 Q3 X* bization, the clinical hallmark of CPP is the symmet-+ i* G4 V6 q& B2 T) ~# {4 j
rical testicular growth secondary to stimulation by- p6 q; }1 ~& p: @/ m# g
gonadotropins.1,3
& H# j" G' ~  ?! k: UGonadotropin-independent peripheral preco-" s) H. p# S9 M2 x3 p) T3 Q
cious puberty in boys also results from inappropriate
: T% v8 b; `( c: candrogenic stimulation from either endogenous or
5 @4 C5 |0 @4 c& @4 h1 p) m2 u8 aexogenous sources, nonpituitary gonadotropin stim-$ D# V8 T5 C* B' h9 f# v
ulation, and rare activating mutations.3 Virilizing
/ }' ^: Z2 ?! Q/ N. U  K5 Xcongenital adrenal hyperplasia producing excessive
7 b& L8 o8 U$ U4 B3 ^adrenal androgens is a common cause of precocious, I& {. H& d. J# q& B6 L0 T; m5 n
puberty in boys.3,4( Q* `/ Z' L2 @* I( ^: V- u
The most common form of congenital adrenal9 y/ @9 F3 A4 J; ?7 w* N% u- \
hyperplasia is the 21-hydroxylase enzyme deficiency.4 x, r. p9 e3 L1 F
The 11-β hydroxylase deficiency may also result in
, r9 b! ]* Y  p& m& F2 R) S, C; ~, Gexcessive adrenal androgen production, and rarely,1 N# b$ w  t% _; B) ~
an adrenal tumor may also cause adrenal androgen
( r- X/ J+ s) fexcess.1,3( ?) K7 v' k# ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 i' T! v% Q* C1 E6 ]' I0 z
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! E  Z( J/ J, ^- \6 l: [A unique entity of male-limited gonadotropin-. Z& K4 I& y+ F  n
independent precocious puberty, which is also known
4 w4 [0 I$ G7 W: o: n! T5 fas testotoxicosis, may cause precocious puberty at a2 r6 {- y7 o. S* u" h
very young age. The physical findings in these boys1 T4 f! K6 `1 |# P4 y' T0 j1 D' I
with this disorder are full pubertal development,% [* }5 }% R( {7 Q
including bilateral testicular growth, similar to boys) _0 M  k0 s; ^0 f8 k# s
with CPP. The gonadotropin levels in this disorder
1 k/ i# D& a* L& h, d# _. fare suppressed to prepubertal levels and do not show8 |' |: X' `6 l" y. D) c
pubertal response of gonadotropin after gonadotropin-8 t2 d+ c7 X2 }8 ^2 i. _2 I
releasing hormone stimulation. This is a sex-linked
& u& k# i8 S) I0 \& {( n1 F5 Cautosomal dominant disorder that affects only7 l+ B4 S+ ?) p) g
males; therefore, other male members of the family! Z3 N# Q6 q3 l( e) l
may have similar precocious puberty.36 Y0 t' @+ ~; I6 z0 \) O
In our patient, physical examination was incon-& U) w5 X* B9 x# `' }2 h
sistent with true precocious puberty since his testi-
1 B3 K7 {' G9 t% K( m% ccles were prepubertal in size. However, testotoxicosis
+ M+ c6 V5 J8 F, q3 `& dwas in the differential diagnosis because his father
+ a3 V4 P) y5 `3 l- dstarted puberty somewhat early, and occasionally,9 f  `; Y$ n# L, x& f
testicular enlargement is not that evident in the
0 o* V9 T+ n1 R- U* M3 Sbeginning of this process.1 In the absence of a neg-
( K- x  P/ x# z4 c$ ?) V7 R( S4 [4 _4 xative initial history of androgen exposure, our
3 t7 }- j+ Z3 S  V4 S9 m3 @biggest concern was virilizing adrenal hyperplasia,, L" T+ J" Q$ [! Q. }2 `" T
either 21-hydroxylase deficiency or 11-β hydroxylase
' B7 w$ R  g6 q& Z3 \( I; kdeficiency. Those diagnoses were excluded by find-
5 G* f3 D! B1 c0 x: [2 ^5 ?6 G' _ing the normal level of adrenal steroids.
2 e4 P, d9 v! p: \1 d) cThe diagnosis of exogenous androgens was strongly
2 V& `; a( X9 _2 p5 ]- Q( zsuspected in a follow-up visit after 4 months because
5 p$ Y! d6 @, bthe physical examination revealed the complete disap-7 m8 ^# l, ]" t9 B% a9 V
pearance of pubic hair, normal growth velocity, and
% l0 M2 C" P1 G3 a& W5 G+ H0 Z- Hdecreased erections. The father admitted using a testos-( Z. @+ K/ \$ x  g: D9 [: x
terone gel, which he concealed at first visit. He was6 X9 P( o+ u: v: v7 c$ B. n/ z' i
using it rather frequently, twice a day. The Physicians’0 a1 c) C" N+ `$ v* b5 `7 R
Desk Reference, or package insert of this product, gel or
: |% z8 s" Y' Z" u7 h+ u8 icream, cautions about dermal testosterone transfer to
) W9 Y5 u% b( [unprotected females through direct skin exposure.! O2 _- x# p* p1 @9 A
Serum testosterone level was found to be 2 times the- O& I) J. z; O, q( J/ `1 N
baseline value in those females who were exposed to
( q4 {! w8 C7 ^# D, F- X3 Ieven 15 minutes of direct skin contact with their male5 V% K7 h" m  v9 r) \
partners.6 However, when a shirt covered the applica-
6 M4 R' L4 W8 ^; T  b! Y0 _tion site, this testosterone transfer was prevented.
4 B( U+ w$ D/ L! B) B# O( [Our patient’s testosterone level was 60 ng/mL,! T' B5 J" E& }* s! ?% R
which was clearly high. Some studies suggest that2 R, l9 u6 n. a! ]5 Y2 u( b
dermal conversion of testosterone to dihydrotestos-! x' }5 W& |- E/ e
terone, which is a more potent metabolite, is more
# ~5 t2 u0 i  j$ q' o& Q  A% k- S- ~! kactive in young children exposed to testosterone- m0 S& a. E2 l* Y: N/ V
exogenously7; however, we did not measure a dihy-
# ~' P; e0 n- M9 R7 G$ W: Hdrotestosterone level in our patient. In addition to$ o# a$ _8 E& N2 j' n
virilization, exposure to exogenous testosterone in4 U3 t# ~& Z( C( O/ \+ @$ P
children results in an increase in growth velocity and/ K) c, t! i) r; q
advanced bone age, as seen in our patient.
. _) E/ V; z6 `  L3 HThe long-term effect of androgen exposure during; ]7 N5 l* v$ a/ k4 C+ t
early childhood on pubertal development and final4 G4 h9 u/ t& r
adult height are not fully known and always remain
5 T/ T. D. m7 ba concern. Children treated with short-term testos-& }9 I& \3 ^& f( l
terone injection or topical androgen may exhibit some" D& g/ t0 L, _/ h" g
acceleration of the skeletal maturation; however, after# x3 r1 p5 j3 _  b
cessation of treatment, the rate of bone maturation
9 g8 g1 c/ y2 n+ p( Gdecelerates and gradually returns to normal.8,9# n% j+ b7 m& h  F. _% b
There are conflicting reports and controversy
7 m: `9 n3 ^7 H2 iover the effect of early androgen exposure on adult
. T9 t$ ]/ L) q$ r. j, Bpenile length.10,11 Some reports suggest subnormal
. d6 [2 }' N$ V5 H$ hadult penile length, apparently because of downreg-7 e4 h; G5 i3 R; p+ ?
ulation of androgen receptor number.10,12 However,
9 W0 B( Z+ `) @- ?. LSutherland et al13 did not find a correlation between4 T. T# w3 D6 g5 r  B
childhood testosterone exposure and reduced adult. s0 q7 I8 E* r( H
penile length in clinical studies.
6 Z! L6 x& g3 n* Y, kNonetheless, we do not believe our patient is' V$ W( p; J0 O1 z: B+ y) \
going to experience any of the untoward effects from
; b9 e+ p3 i0 T" W9 ktestosterone exposure as mentioned earlier because1 B1 V4 j2 ^; `- u3 J3 f/ J
the exposure was not for a prolonged period of time.
3 N& ~$ C: [  v% rAlthough the bone age was advanced at the time of# H. p! f' \# ~, _: I1 Q* ^, @
diagnosis, the child had a normal growth velocity at
; w# s8 R/ i) c. t6 r0 Uthe follow-up visit. It is hoped that his final adult6 Y: k0 x2 a0 @) f% q& b
height will not be affected.
- \) G+ z  S  A2 [' k" ]& E: RAlthough rarely reported, the widespread avail-
: W. _+ n: h! L/ ^6 |ability of androgen products in our society may
9 f4 w3 Q9 V. Y2 h3 \; z! s# ?indeed cause more virilization in male or female
. @% s& S/ x, Gchildren than one would realize. Exposure to andro-
; p8 }/ X' Y4 A+ P. e' Mgen products must be considered and specific ques-
. B0 b9 i' B3 v; A: F7 [4 Rtioning about the use of a testosterone product or
0 j2 g/ z4 R. t7 [: P2 kgel should be asked of the family members during
8 G1 I/ b$ E* ^4 c# y+ h: B; g5 ~the evaluation of any children who present with vir-2 E7 `$ v) w  w3 g; `* a6 j
ilization or peripheral precocious puberty. The diag-
5 A1 U  s2 [* G* D( Q3 jnosis can be established by just a few tests and by: n. ~" G0 g, z* U4 t  _
appropriate history. The inability to obtain such a
) \* u( s$ m' {/ {5 }0 T6 ihistory, or failure to ask the specific questions, may
/ e! v0 N* K, ]9 _result in extensive, unnecessary, and expensive( F! `2 i- ~- G/ D5 V( I7 l
investigation. The primary care physician should be
' J4 m4 M5 n/ f  o/ _+ [' kaware of this fact, because most of these children% k0 O7 ]6 a8 S) T4 T  p& X
may initially present in their practice. The Physicians’
, i6 `* r& H7 JDesk Reference and package insert should also put a
* H+ c1 D  P/ Ewarning about the virilizing effect on a male or
9 s; h) R6 _: y" y. v, k( cfemale child who might come in contact with some-
6 z; j. N- e, j3 y1 l5 I8 Oone using any of these products.
# F5 Z" D1 r3 w' n8 p5 GReferences; k3 J6 o4 H$ ?5 ~0 ]& i; R
1. Styne DM. The testes: disorder of sexual differentiation$ _1 Q" N. W) g. W& u
and puberty in the male. In: Sperling MA, ed. Pediatric% }( Y! |, H$ T$ a. T  ]+ j
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;9 y% z6 {2 ^9 k' }. |' @+ J
2002: 565-628.$ E, q2 @# i4 `; O) c7 O
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( {. F7 J8 H. s) i- w8 rpuberty in children with tumours of the suprasellar pineal
, H0 E$ G. \6 Z# L: lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# o, K" N9 c7 u. ?Topical Testosterone Exposure / Bhowmick et al 543- v3 S3 E& N2 U7 d$ A$ [
areas: organic central precocious puberty. Acta Paediatr.% ^1 j2 @: Z: L& [: ?* g3 k. X, j
2001;90:751-756.
5 X$ X  D1 J  V3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
( Y/ M8 C& P1 ]/ e  qPediatric Endocrinology. 4th ed. New York, NY: Marcel
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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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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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