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is a significant concern for physicians. Central8 u. X8 Y  O* N3 h, k( c: v* Y
precocious puberty (CPP), which is mediated' J/ m% }3 F$ m  h  R
through the hypothalamic pituitary gonadal axis, has, A6 b* U0 j8 ?2 `  N6 u
a higher incidence of organic central nervous system2 Z' y; R$ I" N) m- t" v
lesions in boys.1,2 Virilization in boys, as manifested
, @; w$ }. H$ r5 @by enlargement of the penis, development of pubic
7 z8 h& I. x) }/ H. T) a% Zhair, and facial acne without enlargement of testi-: G" U4 s( K! ^/ B9 P5 E
cles, suggests peripheral or pseudopuberty.1-3 We
+ Z/ @) S4 y7 W# {& O# y7 ^report a 16-month-old boy who presented with the/ F& V# T9 j3 X/ G: o' v
enlargement of the phallus and pubic hair develop-' ~* Q6 @' l( n! t
ment without testicular enlargement, which was due+ S" @1 z- \- L' w8 E
to the unintentional exposure to androgen gel used by
9 H6 Z+ T; _+ `! i: Nthe father. The family initially concealed this infor-
& X, ~& q- F6 S& emation, resulting in an extensive work-up for this1 x* H# x6 T7 J, v& F! E+ _( c
child. Given the widespread and easy availability of+ D3 }4 E3 g* C9 {3 r1 P
testosterone gel and cream, we believe this is proba-! W9 a3 p5 X( ~, I% ?8 a) d& ]' t: d1 s
bly more common than the rare case report in the
5 q- C& D6 c. M' m' jliterature.49 ]) j0 S: _" s* A
Patient Report: W2 l0 M: `: [% B
A 16-month-old white child was referred to the
0 t; _: t+ e1 Y0 eendocrine clinic by his pediatrician with the concern
7 J5 q5 W6 d. w3 z/ ^of early sexual development. His mother noticed
4 `9 h! e' ]. O% }# |; f- Flight colored pubic hair development when he was7 }8 |$ {! V% l( n& _5 z
From the 1Division of Pediatric Endocrinology, 2University of
. d" \2 T& q, tSouth Alabama Medical Center, Mobile, Alabama.
) b; E+ u4 S" S4 o; KAddress correspondence to: Samar K. Bhowmick, MD, FACE,# U4 q1 @4 G( {# [" l
Professor of Pediatrics, University of South Alabama, College of# A% F5 W, R/ q* b  @
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 J+ [$ u' c7 ~e-mail: [email protected].# I. u" Z. z( w. v4 `
about 6 to 7 months old, which progressively became4 [* `! ^5 S; @: b' P
darker. She was also concerned about the enlarge-) q. k2 [: T' ~
ment of his penis and frequent erections. The child8 ^3 e( a7 p) w( V  R9 {5 m* w
was the product of a full-term normal delivery, with
; l) e+ I! F, E" a( o! b" V+ ]a birth weight of 7 lb 14 oz, and birth length of$ N5 P  ^- H8 t, C+ z$ m: w; _
20 inches. He was breast-fed throughout the first year' g8 @0 s# l% K
of life and was still receiving breast milk along with
* O. ?" \; P& w9 Y8 e3 isolid food. He had no hospitalizations or surgery,
6 x/ [0 c( h4 A6 ~and his psychosocial and psychomotor development$ ]6 j2 J6 r9 f3 y2 K) x) W0 ?8 {
was age appropriate.
- _* V' `3 I% Z8 rThe family history was remarkable for the father,
+ y6 Y) s: \+ R9 U6 }2 D# ?$ kwho was diagnosed with hypothyroidism at age 16,9 |- X% p7 h" g: @
which was treated with thyroxine. The father’s
& z& d: s# O- J  N: uheight was 6 feet, and he went through a somewhat5 ^, G7 e' y( D! `5 |  X
early puberty and had stopped growing by age 14.
( E+ y" _) B& `0 ]: w* XThe father denied taking any other medication. The- p$ y+ p$ }4 t, C7 f, J! H
child’s mother was in good health. Her menarche# l; ?% p' w% ]9 p! H
was at 11 years of age, and her height was at 5 feet: K5 z( T: y1 h) ~
5 inches. There was no other family history of pre-0 F9 e2 A& N  |: C8 [4 g
cocious sexual development in the first-degree rela-- J' B* U" ^! C2 R9 _6 i/ P% ]$ Y2 Z
tives. There were no siblings.9 k; ~3 n) V, ]8 U0 u
Physical Examination  ?. O# Z% }  l& o6 [; q
The physical examination revealed a very active,+ @7 S5 [. U3 N: [9 S) p
playful, and healthy boy. The vital signs documented8 N/ K  n$ x7 |
a blood pressure of 85/50 mm Hg, his length was+ P, G+ F7 P: T; d/ G4 ^6 m. }
90 cm (>97th percentile), and his weight was 14.4 kg
3 C! u: Q: E  P1 }; g  R7 N" |. r(also >97th percentile). The observed yearly growth) W! h1 Q3 t+ J5 |$ \, I3 G  n
velocity was 30 cm (12 inches). The examination of5 e, p, W3 @- H7 p; c
the neck revealed no thyroid enlargement.( v8 ^8 m, [: D, B& J- g
The genitourinary examination was remarkable for8 U! V3 G1 r5 k# ^8 Y- _1 S, ^
enlargement of the penis, with a stretched length of
5 q+ ]2 A  Q- s5 m. Q8 cm and a width of 2 cm. The glans penis was very well. M5 i8 }; n( f2 U" [
developed. The pubic hair was Tanner II, mostly around
. S8 z6 G# k) e" p4 r5404 z0 s( G5 c0 U& @4 b  y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 |; h4 ]. h% q3 X) l! g: o
the base of the phallus and was dark and curled. The5 {& B  a2 H! R* o
testicular volume was prepubertal at 2 mL each.
" x1 |" Q) S  K7 OThe skin was moist and smooth and somewhat. @7 w" \0 V+ ]8 i
oily. No axillary hair was noted. There were no
+ w& i+ e+ Q+ r$ V  f) rabnormal skin pigmentations or café-au-lait spots.
/ j2 ]4 ]& s* q+ m$ y0 aNeurologic evaluation showed deep tendon reflex 2+8 \8 w" n% o; M1 `: O' P6 @' {: a
bilateral and symmetrical. There was no suggestion
1 y! J* i  Z2 t9 d. R3 k4 x! hof papilledema.; C2 p& _  \# |$ v/ ~* V
Laboratory Evaluation
6 z  j7 E" y3 i' S+ \The bone age was consistent with 28 months by/ z7 }. Y5 Q2 S+ r+ ^* j
using the standard of Greulich and Pyle at a chrono-+ B3 H, }. O' {
logic age of 16 months (advanced).5 Chromosomal
6 {& j1 V4 ^8 }4 b: A- @3 {% v, c* Rkaryotype was 46XY. The thyroid function test
: }' C" t3 k* A$ R" r' Yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
& @+ b6 d6 _+ |  o, Olating hormone level was 1.3 µIU/mL (both normal).1 ?1 I8 j- `! s" i' y
The concentrations of serum electrolytes, blood: n9 z# t+ H6 J6 P6 E
urea nitrogen, creatinine, and calcium all were
% `" j+ G; F3 r8 G8 L: Qwithin normal range for his age. The concentration4 F- k% N. D' e6 ?* I  p. Z
of serum 17-hydroxyprogesterone was 16 ng/dL
4 F" A2 _" y$ s# p8 |3 @6 ~(normal, 3 to 90 ng/dL), androstenedione was 20
+ P2 O0 ]$ {! _8 E6 ~9 n4 A7 Dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
+ a) o2 F/ [* U$ o4 kterone was 38 ng/dL (normal, 50 to 760 ng/dL),# C/ T) R2 G; t+ N
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
( y" \% H- C1 \6 J* I# v49ng/dL), 11-desoxycortisol (specific compound S)
% V7 j( h: P) g/ J5 ]0 Gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% N& K3 \2 E: |
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, R% h  ~7 y3 g+ W0 k# `
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& A: \6 }$ L! i2 Z. d/ A: ?7 n* Mand β-human chorionic gonadotropin was less than
8 ]$ S0 R. U5 E3 k; ^5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 Y& ]4 F: L: x3 {  c4 W$ \stimulating hormone and leuteinizing hormone4 @% R: f! g: q4 u8 n) A$ N) u! A4 f
concentrations were less than 0.05 mIU/mL
6 W! C5 @% U' r7 A& i. W(prepubertal).. D& w( M! Q1 g4 e$ Y$ t- }
The parents were notified about the laboratory" w6 M% Q8 U( ^
results and were informed that all of the tests were
( a9 P5 M  ^" w' C! ]normal except the testosterone level was high. The% i0 V: `& g1 o4 }
follow-up visit was arranged within a few weeks to
& f2 k& ?9 T1 F: M* @% w6 m. qobtain testicular and abdominal sonograms; how-/ f" B4 q# g" d9 ?3 Y2 W+ G. }" ?
ever, the family did not return for 4 months.) _1 b- D  ]( U7 D
Physical examination at this time revealed that the
- b8 H6 z. f% e) v8 u, @; ichild had grown 2.5 cm in 4 months and had gained* u) [3 u# b) Y3 _5 l
2 kg of weight. Physical examination remained
# G2 g7 o8 z/ T7 l; x6 tunchanged. Surprisingly, the pubic hair almost com-
, o4 E- L" m( E2 V. p; P% }" h) bpletely disappeared except for a few vellous hairs at1 A6 i$ |3 ]" Q2 P) L' N
the base of the phallus. Testicular volume was still 2
7 G) j7 \) W$ Q1 G% o- y- VmL, and the size of the penis remained unchanged.
, i7 N4 _5 z6 r. a0 M4 \5 eThe mother also said that the boy was no longer hav-& Q/ w6 R: e4 Q% O  E7 `: {
ing frequent erections.4 L8 u2 n( E2 s6 A$ t4 ~7 R
Both parents were again questioned about use of
- D. I8 k; p+ Uany ointment/creams that they may have applied to  ^7 K: n$ E& Q" Q
the child’s skin. This time the father admitted the
' M! n- P6 f& X, V- A6 R0 KTopical Testosterone Exposure / Bhowmick et al 541
- ^7 }, l: d. ~0 ?, W2 O: Tuse of testosterone gel twice daily that he was apply-$ M/ v8 y2 N$ j* Z
ing over his own shoulders, chest, and back area for
0 Y7 |, i( c6 _9 n$ \7 e& [a year. The father also revealed he was embarrassed" u5 b1 x/ \, U/ c7 E
to disclose that he was using a testosterone gel pre-
9 i6 L1 i* D) H7 k; o' |scribed by his family physician for decreased libido
3 ]3 A: v& `4 R6 H1 K5 Usecondary to depression.
; C6 {: o0 g3 fThe child slept in the same bed with parents.
9 \* ^# p, u  \' G$ vThe father would hug the baby and hold him on his1 e: `& D% d  Z- `" }
chest for a considerable period of time, causing sig-
" n& H9 P% G6 A; inificant bare skin contact between baby and father.( W7 p) e1 n+ r- B) v# {
The father also admitted that after the phone call,2 R7 S5 G1 ?. ?1 W
when he learned the testosterone level in the baby0 }( |. V/ f& ?! Y; a
was high, he then read the product information
6 y5 z3 }4 q" H/ i" x  ?* _0 fpacket and concluded that it was most likely the rea-: h. K* r$ s! k+ N; U
son for the child’s virilization. At that time, they2 e, J4 ^: a% a5 G2 w( K: u9 u- j
decided to put the baby in a separate bed, and the3 d( ?, j+ H- S$ o) z1 r
father was not hugging him with bare skin and had( U: ^) r. n9 O5 Y. q& I4 U- V" M6 a3 S
been using protective clothing. A repeat testosterone
& A7 c6 V( l  r, V* |- Ctest was ordered, but the family did not go to the' T2 R$ P. O( h& l0 F' g0 [; w# _& h
laboratory to obtain the test.* r4 Q( Q% B$ J; L- r! C; J
Discussion  H  h0 x7 t" |- P- Q
Precocious puberty in boys is defined as secondary+ f# l- J1 e3 w7 Q& p9 @8 @
sexual development before 9 years of age.1,4- m: B: [( H, W" p  `2 Z% U
Precocious puberty is termed as central (true) when4 H6 g1 U! x! W3 H" [- s" Z
it is caused by the premature activation of hypo-2 X6 L, l4 E% f9 \/ l. y9 _
thalamic pituitary gonadal axis. CPP is more com-
0 I4 G' Q7 l+ ]: D8 ^. smon in girls than in boys.1,3 Most boys with CPP
/ P. _- |& g; ^6 dmay have a central nervous system lesion that is
7 I9 f; f# [/ h* ^4 ~# xresponsible for the early activation of the hypothal-
+ M# w* M5 [" x/ z. Vamic pituitary gonadal axis.1-3 Thus, greater empha-- a" q2 [. ^, B) n% ?
sis has been given to neuroradiologic imaging in: ^; k0 n5 w$ ?9 d/ P
boys with precocious puberty. In addition to viril-
, I( K: v: p' u; |, x. ?2 M( Fization, the clinical hallmark of CPP is the symmet-
) x% N- L0 M* T& R/ m3 }0 V! D/ krical testicular growth secondary to stimulation by
/ ~4 G, n% u8 k1 sgonadotropins.1,3. o2 U: q  g4 U' n
Gonadotropin-independent peripheral preco-
6 N$ A' `) g( a# }cious puberty in boys also results from inappropriate
9 O- S# n8 t0 G1 N% Zandrogenic stimulation from either endogenous or
/ U6 g  h  x, N6 G$ c8 A! Oexogenous sources, nonpituitary gonadotropin stim-
# \& d8 ^& G0 D/ F; r  F$ G4 O7 `; q9 y9 Sulation, and rare activating mutations.3 Virilizing
7 R' ?5 T4 D) R3 l/ \- Ocongenital adrenal hyperplasia producing excessive# `* z/ H2 K4 i* [2 }$ ?
adrenal androgens is a common cause of precocious
- z3 x. v/ F( A) S+ z% Z5 ~# Rpuberty in boys.3,4
6 o# T. u! v2 R) O4 ~0 o' YThe most common form of congenital adrenal
3 }7 k# Y' [% f5 G+ W' |hyperplasia is the 21-hydroxylase enzyme deficiency.2 A6 ~, ~$ I( @4 l- l% F- D
The 11-β hydroxylase deficiency may also result in
4 V1 D3 Z, ]& H/ `+ Nexcessive adrenal androgen production, and rarely,, K" e- Q4 ^- W  o! Z5 p
an adrenal tumor may also cause adrenal androgen7 ]: ?" O$ T0 D8 i9 y
excess.1,3
$ B& K) \0 G9 h. Q# ]at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: J. S8 c7 t, l* f7 j  W) L3 s" e& e542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! L$ p1 u# v0 \A unique entity of male-limited gonadotropin-( T. d; J0 B4 S* N1 |
independent precocious puberty, which is also known, P  R8 \! ?% `3 f! K+ d( }. e/ U
as testotoxicosis, may cause precocious puberty at a0 ]- ^5 p$ K- l, q: c5 g
very young age. The physical findings in these boys
/ `. k( H6 O; F7 K& g, b- Qwith this disorder are full pubertal development,/ S# g+ F# {5 T2 m& B, M
including bilateral testicular growth, similar to boys: X$ D5 A! f6 o
with CPP. The gonadotropin levels in this disorder
  f( J8 q: {6 W7 c& H8 Care suppressed to prepubertal levels and do not show4 b6 v# W) A: e0 x/ `! A) {6 s$ z
pubertal response of gonadotropin after gonadotropin-7 u7 Q" B- Z- z+ q- k
releasing hormone stimulation. This is a sex-linked
$ B3 e* e% D: b) f1 G8 eautosomal dominant disorder that affects only9 }( Y- N" f! r
males; therefore, other male members of the family$ m0 q; T6 |; n) V5 G: M
may have similar precocious puberty.3
" E3 G* V+ @7 t9 Z. i5 l' hIn our patient, physical examination was incon-  i& p' T( |* u3 e
sistent with true precocious puberty since his testi-& E2 I1 L/ u/ p% Y) f
cles were prepubertal in size. However, testotoxicosis
4 j, i- ?/ _- v6 B& y# Ywas in the differential diagnosis because his father
) _2 {$ u3 i0 \+ ?% S/ n* t* fstarted puberty somewhat early, and occasionally,
* E1 [. d! t; gtesticular enlargement is not that evident in the  W9 P4 o  o# Y" n* s" c
beginning of this process.1 In the absence of a neg-/ Q* M+ X; p" G% ?: I
ative initial history of androgen exposure, our
7 ^4 F8 F6 |$ l) e) \3 @biggest concern was virilizing adrenal hyperplasia,
) ^' m: X1 P. n7 _+ b/ X2 V# ~$ H  zeither 21-hydroxylase deficiency or 11-β hydroxylase
5 E+ o/ h4 |( m$ @9 Q8 o- m: y" p9 r' Cdeficiency. Those diagnoses were excluded by find-6 y4 M& d* u- u. \3 p2 b
ing the normal level of adrenal steroids.
- t1 Y* v% I1 V; n) v* UThe diagnosis of exogenous androgens was strongly/ w$ z/ q3 Q  \* o* r
suspected in a follow-up visit after 4 months because
7 {. \# U2 @+ c" z  Jthe physical examination revealed the complete disap-
  {0 j0 N4 D( C5 [# Qpearance of pubic hair, normal growth velocity, and8 x. O5 r9 }: N7 z; a
decreased erections. The father admitted using a testos-% c; _' Z7 j" n5 t0 L% M
terone gel, which he concealed at first visit. He was/ _  W1 S0 S0 @; m" G2 X
using it rather frequently, twice a day. The Physicians’
/ V; x$ N+ K$ w) I3 `" R/ LDesk Reference, or package insert of this product, gel or5 t/ k( ?& n9 _' s) F' r) _8 l7 P7 U
cream, cautions about dermal testosterone transfer to
# l  q1 l1 n) E  C  |unprotected females through direct skin exposure.. _5 M  I' K" B4 v$ d4 t: m
Serum testosterone level was found to be 2 times the8 ]9 H: w+ w7 e; ?
baseline value in those females who were exposed to) ~8 T7 o5 n% V5 h( ]5 B: E& Q% c, I
even 15 minutes of direct skin contact with their male
& b! U9 _8 y3 a- S: a6 l- \+ Wpartners.6 However, when a shirt covered the applica-
1 C: a/ x, }/ |' c1 Xtion site, this testosterone transfer was prevented.3 m# }2 s# ]; Z6 q1 T  k
Our patient’s testosterone level was 60 ng/mL,( i7 I2 \! Y* Y4 N: T3 N
which was clearly high. Some studies suggest that5 n5 i( l+ o" ^% ^5 r8 X/ ^6 L
dermal conversion of testosterone to dihydrotestos-
( V) M' L8 r- d9 \/ Eterone, which is a more potent metabolite, is more
4 W# S9 t5 p5 Y$ q/ H+ eactive in young children exposed to testosterone+ |! _& V/ O3 B) D; V- o( ]; A
exogenously7; however, we did not measure a dihy-
+ D! S" ^  e# Xdrotestosterone level in our patient. In addition to
& L, ?: ?/ w8 v/ V1 [& \) R' yvirilization, exposure to exogenous testosterone in
. w) m7 a" n% a  y/ z* \& L0 B) _! Schildren results in an increase in growth velocity and
; e4 o8 Z3 g( R! j! Vadvanced bone age, as seen in our patient.
: `7 H2 j5 f0 n' n" {The long-term effect of androgen exposure during
' Z- R( J. K7 Z0 Xearly childhood on pubertal development and final$ H/ k# c# P' \
adult height are not fully known and always remain
* R3 n' q9 k# r& ka concern. Children treated with short-term testos-
' I$ Z9 g% C- Y. H3 m! mterone injection or topical androgen may exhibit some8 F0 k& G* }. e0 y6 G/ ]! }/ N
acceleration of the skeletal maturation; however, after7 m( m& f9 Q: |- |% I
cessation of treatment, the rate of bone maturation
+ [2 {9 D% ]5 udecelerates and gradually returns to normal.8,9
* w4 H4 d+ E9 wThere are conflicting reports and controversy9 @3 G4 L8 Z$ k5 _& E
over the effect of early androgen exposure on adult
* W! S" s+ b" ]penile length.10,11 Some reports suggest subnormal
+ D" H3 A! _3 g. ~adult penile length, apparently because of downreg-
/ i0 Q+ }; R+ ~ulation of androgen receptor number.10,12 However,% Q1 ^) D/ f) r& N% V: Q8 h
Sutherland et al13 did not find a correlation between+ \' H0 s4 G; n, b
childhood testosterone exposure and reduced adult
- V* s$ [( L6 K% o; mpenile length in clinical studies.
0 Y: O3 ^/ w) G( m) u0 S( v7 cNonetheless, we do not believe our patient is
) k- M: n7 I2 M, e8 j# rgoing to experience any of the untoward effects from
) N! @) S3 J$ ^+ s9 Ktestosterone exposure as mentioned earlier because7 o* s4 k0 m  o9 q0 I
the exposure was not for a prolonged period of time.6 l4 N) o& [8 O, L
Although the bone age was advanced at the time of
* X& T! \6 G' Kdiagnosis, the child had a normal growth velocity at; w/ ~" ]+ }0 C4 u5 E! N
the follow-up visit. It is hoped that his final adult
0 o. T9 J- F% q0 l5 _( P% `height will not be affected.) c; i1 U, t: \$ |0 }
Although rarely reported, the widespread avail-! Z7 E; a- D1 o2 t& ]
ability of androgen products in our society may
( Q8 E4 |8 V( Z+ {& [' M3 h9 n# Vindeed cause more virilization in male or female
9 H* _0 j- x4 [1 W$ u" fchildren than one would realize. Exposure to andro-  l4 F7 W- E. Q- K1 B3 g
gen products must be considered and specific ques-
2 |6 S5 @; Z+ g, xtioning about the use of a testosterone product or
8 S5 P, j4 J7 Bgel should be asked of the family members during# l6 d' |1 W8 a2 Q
the evaluation of any children who present with vir-
: ]9 t( Q  |, r# }ilization or peripheral precocious puberty. The diag-/ H2 e/ {# Z) @, K4 H. n
nosis can be established by just a few tests and by
1 }) {- d  R4 B2 F; tappropriate history. The inability to obtain such a  g( y! l* ^; G# j
history, or failure to ask the specific questions, may1 V& x% i* A' u1 b, h; }
result in extensive, unnecessary, and expensive
7 B. d9 Q) v4 f7 P3 R8 _! T5 ninvestigation. The primary care physician should be) e. R/ A, q3 L1 S
aware of this fact, because most of these children$ Q: o+ a6 L7 _7 q
may initially present in their practice. The Physicians’$ o: D' R! \6 E7 j
Desk Reference and package insert should also put a7 f. c! f$ _6 ^1 K
warning about the virilizing effect on a male or2 W4 B7 t- e3 I9 O4 w0 B' r
female child who might come in contact with some-
1 w$ K/ a2 S3 o3 e2 e7 Y6 Jone using any of these products.
$ y: q( P' m5 I. e  TReferences- m+ l/ b& T8 w, ?7 Q+ q
1. Styne DM. The testes: disorder of sexual differentiation% v- q- e% N# t) m8 J
and puberty in the male. In: Sperling MA, ed. Pediatric
( a+ T+ }: q6 |0 R0 X, ]- ~Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ ~$ j: ?6 d* C" @$ x; i% w6 Y2002: 565-628.
0 Y; h( ~$ p1 e0 a5 T! Y2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  l$ g% p. S% t1 s3 p! q) a% d
puberty in children with tumours of the suprasellar pineal
* H2 P+ D9 z3 L+ Q' [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 A2 o' M+ }- z. }- b3 CTopical Testosterone Exposure / Bhowmick et al 543
3 {6 A) N4 l0 y- R  Iareas: organic central precocious puberty. Acta Paediatr.
% K- X3 J# p, F) h0 f, f4 R/ t2001;90:751-756.
- S; a2 w' m$ @; D* `9 b3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.! W1 N9 f4 {* X3 ^1 v1 q( [  s
Pediatric Endocrinology. 4th ed. New York, NY: Marcel; v( a1 e: e6 P8 h  p4 T* z
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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!
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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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