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is a significant concern for physicians. Central5 q# j8 I5 O: W) I
precocious puberty (CPP), which is mediated
- \5 k% O8 m0 N' e; Y: uthrough the hypothalamic pituitary gonadal axis, has
# ^+ v+ x6 x$ ta higher incidence of organic central nervous system
% ?; }$ Y+ V4 Vlesions in boys.1,2 Virilization in boys, as manifested6 E0 [- C2 e& ?# s1 X2 W: ~- A
by enlargement of the penis, development of pubic% K/ _9 R' e# j$ p3 X) C
hair, and facial acne without enlargement of testi-' c& E0 K' k" M, k
cles, suggests peripheral or pseudopuberty.1-3 We
0 h$ e, K, s- a! Z8 rreport a 16-month-old boy who presented with the  b- ]7 e( E1 Y0 }3 \0 Q  e+ c+ D
enlargement of the phallus and pubic hair develop-4 M" t& }" e: g$ g5 s. e( g5 o- C
ment without testicular enlargement, which was due1 r1 Q4 j' m9 e! [
to the unintentional exposure to androgen gel used by* v, t, j; k4 I$ G( _/ @( j
the father. The family initially concealed this infor-
, H1 \8 T) q8 R3 m0 M' V! F1 cmation, resulting in an extensive work-up for this
+ _2 A% q1 y. f& g5 G  _child. Given the widespread and easy availability of% i/ \  ]/ y" B0 A" u! O4 @
testosterone gel and cream, we believe this is proba-& N2 h8 v7 ^8 C% c2 Q
bly more common than the rare case report in the2 S/ R: m/ O/ Y* ]3 E
literature.4
& G7 ~2 i$ C4 D2 DPatient Report2 }/ l! R' U. {" U+ b
A 16-month-old white child was referred to the
5 f# s8 K, g6 g! _. G2 \4 Z! xendocrine clinic by his pediatrician with the concern! `5 z% a2 ], }2 M
of early sexual development. His mother noticed' R6 ?# I, x" e# y- m
light colored pubic hair development when he was' |9 h) e# P; @  a4 B
From the 1Division of Pediatric Endocrinology, 2University of
' p2 M' o) L* k8 [South Alabama Medical Center, Mobile, Alabama.5 w( O0 q4 m& L4 u& ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,
: c3 t1 A5 U6 @" `+ DProfessor of Pediatrics, University of South Alabama, College of
+ R' H; i$ e5 o  w$ S% mMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;& I+ l2 v6 j9 a; Q% U
e-mail: [email protected].
# ?0 _( |- ]3 t! G8 c$ Oabout 6 to 7 months old, which progressively became; x2 c- S3 g' T
darker. She was also concerned about the enlarge-
8 B5 R& p$ D) Y: ument of his penis and frequent erections. The child3 P# k6 ~! D* I/ _/ o  x
was the product of a full-term normal delivery, with
% y0 C! S/ r% R* ha birth weight of 7 lb 14 oz, and birth length of1 p# d# y) j& _9 X! r4 _
20 inches. He was breast-fed throughout the first year! \2 S7 z8 Y5 Q3 Z! g: j
of life and was still receiving breast milk along with- C* j- L) E, Y/ K
solid food. He had no hospitalizations or surgery,
" @$ y+ R9 X3 O6 Z' `# e" P: vand his psychosocial and psychomotor development
* K' l) S. ^3 Y7 `was age appropriate.! l6 r% J9 P/ c9 g( T2 U0 s+ S
The family history was remarkable for the father,
: w& h& g- \; Z' Q9 m, Dwho was diagnosed with hypothyroidism at age 16,
* F8 ~7 t) e9 ~9 {  X. K0 o+ [which was treated with thyroxine. The father’s$ [1 G  F  P' ^1 P% o* q4 U
height was 6 feet, and he went through a somewhat; x6 Q! `7 z+ C7 j/ c
early puberty and had stopped growing by age 14.4 O# f7 \6 Q1 ~5 _! v
The father denied taking any other medication. The' C+ C: T  w8 a
child’s mother was in good health. Her menarche8 f, \9 }9 m2 @: d/ ~
was at 11 years of age, and her height was at 5 feet
* {, `- _; R$ H* h5 inches. There was no other family history of pre-6 _3 c: {4 J! m- o( Q  Y
cocious sexual development in the first-degree rela-
  c  Q8 _& |8 s+ A9 itives. There were no siblings.
' p$ Y% X( ^: B3 u5 }9 bPhysical Examination
. `! R7 r$ P: A/ n% v5 mThe physical examination revealed a very active,( Y% l1 A. q& ~9 ?, z) X- G: E
playful, and healthy boy. The vital signs documented" J5 s# b+ b" [4 a$ d/ H
a blood pressure of 85/50 mm Hg, his length was
1 A8 [7 @3 l- b* A% ~, z3 U( b90 cm (>97th percentile), and his weight was 14.4 kg
% z  |1 Z1 Q8 g. v2 t(also >97th percentile). The observed yearly growth6 ]+ |( q1 L0 P- D! x! `  Y
velocity was 30 cm (12 inches). The examination of
# g9 P. z4 A" ^6 n0 Q: m1 `the neck revealed no thyroid enlargement.6 b2 @- v7 F3 {
The genitourinary examination was remarkable for
4 I. C+ z6 {, q( |. ~enlargement of the penis, with a stretched length of, k! `& z. E5 X! |: i' n
8 cm and a width of 2 cm. The glans penis was very well
# O% T( F, z/ `9 Y$ U! C  `developed. The pubic hair was Tanner II, mostly around
" ]5 h6 ?9 c8 K: O# Z, S0 b540
: s8 p3 |2 @, T; C" t, cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( l- S4 u3 v& f0 ^$ ?the base of the phallus and was dark and curled. The
7 U6 Y& j; c+ w) C' t7 rtesticular volume was prepubertal at 2 mL each.
/ b4 o0 t4 G/ H, U! W. ]The skin was moist and smooth and somewhat
! W9 y- Z; R7 a/ P" J! S- aoily. No axillary hair was noted. There were no' g  c9 @  D6 l2 F" H  Q9 t; L. h
abnormal skin pigmentations or café-au-lait spots.
& s* n0 |; k: [/ `9 N5 gNeurologic evaluation showed deep tendon reflex 2+& |- S- u& u& J! H# L9 G
bilateral and symmetrical. There was no suggestion
' v9 f5 Q3 l' @* x. Qof papilledema.
/ }( |+ S! K/ H6 S' [2 e  i4 Z; `Laboratory Evaluation  U" J9 Z3 _' T/ g
The bone age was consistent with 28 months by4 n  i9 a- w3 q! U$ T4 p
using the standard of Greulich and Pyle at a chrono-
6 R2 a( C( M) ?  y7 A) alogic age of 16 months (advanced).5 Chromosomal
' z' I' `; A4 i! j* ]karyotype was 46XY. The thyroid function test
: m: b5 a: C8 R1 wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
* h! B/ u: ^8 u% ilating hormone level was 1.3 µIU/mL (both normal).5 h$ P% V9 s9 g  l1 n3 K" Q3 P
The concentrations of serum electrolytes, blood
: a5 b6 g' h  j( [; O8 Kurea nitrogen, creatinine, and calcium all were
! ^" @2 C* d# Z' Y& ^+ |# p& fwithin normal range for his age. The concentration
* j! B$ H7 G+ _7 O1 c  ~of serum 17-hydroxyprogesterone was 16 ng/dL
, b0 n7 x& A4 j/ W(normal, 3 to 90 ng/dL), androstenedione was 204 [8 ?5 n6 x- D! R/ O
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& H; X* B# M$ u8 J! p' ]3 K3 @& C
terone was 38 ng/dL (normal, 50 to 760 ng/dL),1 Z# S  _) ]' N5 W0 n
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
# R! }. t/ }) C49ng/dL), 11-desoxycortisol (specific compound S)' M4 J. v: u1 k5 F
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! O$ ?9 T! \* C  d! y% R- e9 S1 h
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& v9 J2 ^3 q7 e4 x+ Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 C$ w! l  F# B6 E1 h0 \4 Vand β-human chorionic gonadotropin was less than
& x  i! y7 N! I6 i5 mIU/mL (normal <5 mIU/mL). Serum follicular, z; @  f+ ]3 }! f7 o- v& E
stimulating hormone and leuteinizing hormone
5 [" }' F* s4 M  K  sconcentrations were less than 0.05 mIU/mL
/ h6 C7 v+ w% ?' Q# W  E(prepubertal).
0 j% d9 C! G, v' T3 Q7 }: H1 EThe parents were notified about the laboratory
0 l/ o, l5 D4 yresults and were informed that all of the tests were9 X* P7 n% N$ H7 A5 a3 I) R
normal except the testosterone level was high. The
. Y) U( B$ W, w4 O& ~* ~; P) nfollow-up visit was arranged within a few weeks to) Z. I) F1 e/ J3 O9 D5 N9 F
obtain testicular and abdominal sonograms; how-
# m* r/ R/ F4 h+ Cever, the family did not return for 4 months.: M7 j# A. p' P! y0 L$ `( h
Physical examination at this time revealed that the. U0 f- `' v& l7 t
child had grown 2.5 cm in 4 months and had gained) j1 ]' N, S: a3 ], \% n
2 kg of weight. Physical examination remained+ j# a, ^. N8 i) A8 k" F3 u
unchanged. Surprisingly, the pubic hair almost com-
( b* N% m# R0 u4 Epletely disappeared except for a few vellous hairs at
: h1 G5 H4 S  h8 O0 l- j3 dthe base of the phallus. Testicular volume was still 2
. K! v. E/ c) W( WmL, and the size of the penis remained unchanged.5 l6 `# P! k0 H8 w% H1 }
The mother also said that the boy was no longer hav-
) d7 K$ F1 H) {) ]! Aing frequent erections.
! C8 z3 s* q. BBoth parents were again questioned about use of' ^$ O& ]% n: v% v
any ointment/creams that they may have applied to& Y7 n) m) I6 o6 f9 g5 A+ m
the child’s skin. This time the father admitted the8 ]$ |2 o, K& m. h3 g' _3 B
Topical Testosterone Exposure / Bhowmick et al 541, B' @; v8 m! Q: ?+ Y5 Q, W
use of testosterone gel twice daily that he was apply-& B/ O8 {( S9 e) m6 _. Q
ing over his own shoulders, chest, and back area for( `4 z' i% n' Z
a year. The father also revealed he was embarrassed
/ p1 n) @7 p% T' w% j5 ]7 [1 Ato disclose that he was using a testosterone gel pre-. M. J' O4 J1 |* J1 t
scribed by his family physician for decreased libido: b1 @5 S: }) h7 U% d1 n6 D
secondary to depression.
4 H, o  O4 R% K$ k* s/ B+ D. qThe child slept in the same bed with parents.( l# _; ^' G" I* c$ i
The father would hug the baby and hold him on his' _3 V: y7 _$ _$ y0 k
chest for a considerable period of time, causing sig-, B( ~7 ~( P7 _: H0 y
nificant bare skin contact between baby and father.1 k8 p% {# V+ E, e: N
The father also admitted that after the phone call,
5 O' b  h7 \- A7 `, N& {5 q7 Gwhen he learned the testosterone level in the baby6 A7 q5 J1 J$ r; N% E; ?
was high, he then read the product information
$ `* _* C8 f. i& a, _9 `  Hpacket and concluded that it was most likely the rea-
( p5 N$ m; l3 T5 B! ?son for the child’s virilization. At that time, they
$ M$ l* k/ M" u% v: ddecided to put the baby in a separate bed, and the
8 u5 m& M1 f2 o+ a& ofather was not hugging him with bare skin and had. m5 E& W9 t0 v& c) G' {( g! O
been using protective clothing. A repeat testosterone
# M* a) O5 p" E3 w. ^) Y8 \test was ordered, but the family did not go to the
' D1 ^3 `" Y+ C% f- @1 o7 flaboratory to obtain the test.1 B3 s; n# h* {& @# k" I
Discussion9 H1 ^4 W0 a9 x/ D1 I) a6 ^6 N% s+ H$ X
Precocious puberty in boys is defined as secondary3 {" P3 ~2 q9 @4 J0 {  e
sexual development before 9 years of age.1,40 @" Y4 ~( P5 k- z( V6 O
Precocious puberty is termed as central (true) when
1 A7 W3 i. i! \$ vit is caused by the premature activation of hypo-3 l) F; r  M8 C% n: o' m8 ?
thalamic pituitary gonadal axis. CPP is more com-; N/ N# G& c3 c/ L  ~  T
mon in girls than in boys.1,3 Most boys with CPP
6 p: k" F3 \: a. g6 Lmay have a central nervous system lesion that is
6 M3 O2 Z  r3 z5 @* gresponsible for the early activation of the hypothal-
7 E" P7 S6 H+ _  D  e, `amic pituitary gonadal axis.1-3 Thus, greater empha-; x3 ~! i8 B% i( J# X
sis has been given to neuroradiologic imaging in
- _3 K# j8 `# {& h% ^0 jboys with precocious puberty. In addition to viril-
$ |% r* T4 Q) o2 U+ b5 N* F. Cization, the clinical hallmark of CPP is the symmet-5 v* N9 C! m4 G: Q
rical testicular growth secondary to stimulation by
/ z% {% L$ S5 J' j3 _gonadotropins.1,37 t- @+ _# Y  H( [& r
Gonadotropin-independent peripheral preco-+ _- C9 `' m" c2 D
cious puberty in boys also results from inappropriate  J' T1 r6 R9 h% C( L% A" y
androgenic stimulation from either endogenous or9 Y$ c( k% Z! D/ t* ?3 f
exogenous sources, nonpituitary gonadotropin stim-
' ]! E2 q: e* M* wulation, and rare activating mutations.3 Virilizing% v* m: ^6 |( p1 `
congenital adrenal hyperplasia producing excessive
5 I" l9 i+ T/ B4 s  m9 _3 Padrenal androgens is a common cause of precocious
" A+ r, `- e/ T& F2 I0 A" qpuberty in boys.3,4
8 n; g8 O3 k8 W  N% l+ y; JThe most common form of congenital adrenal2 a/ h4 u: Y) \- q* q  V
hyperplasia is the 21-hydroxylase enzyme deficiency.
0 S0 H- ~% V. @The 11-β hydroxylase deficiency may also result in2 E: \. M3 {9 X% L
excessive adrenal androgen production, and rarely,
7 b: {  R- a4 E7 R5 c2 Nan adrenal tumor may also cause adrenal androgen  J, d1 C  Y2 O
excess.1,30 ^# c6 \: g" O6 G! V$ b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 D2 J0 E" T6 x& @8 o542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 z" z& r9 Y' e: ]! ?: M2 m& mA unique entity of male-limited gonadotropin-/ @6 v: B. \1 o6 f
independent precocious puberty, which is also known
* s. q3 X: C' G; m' Fas testotoxicosis, may cause precocious puberty at a# X% w0 x- j3 p4 d, X2 V
very young age. The physical findings in these boys
5 i6 }8 x1 {' Swith this disorder are full pubertal development,) }' P8 N' H# g. z2 Z. H3 W
including bilateral testicular growth, similar to boys
. C" P* b2 V( v! C) }  Jwith CPP. The gonadotropin levels in this disorder
/ n6 B  ?8 ?3 q/ e" Care suppressed to prepubertal levels and do not show
0 U9 i3 C- w, X/ q. K% Xpubertal response of gonadotropin after gonadotropin-
# K% z. R3 g7 X; j& ureleasing hormone stimulation. This is a sex-linked( X! L* p- G' `+ v/ H
autosomal dominant disorder that affects only
8 {: u3 N/ s$ \- E. V9 L. qmales; therefore, other male members of the family1 R( {$ w, Q! {  J3 f
may have similar precocious puberty.3, a& t) l4 W5 f5 y/ N. h. C5 K: U
In our patient, physical examination was incon-, m: q5 o% H! F3 E
sistent with true precocious puberty since his testi-
+ m5 g" j; [5 bcles were prepubertal in size. However, testotoxicosis/ {, Y6 S1 H2 b
was in the differential diagnosis because his father% ~' o1 g- |6 I( W* s' U
started puberty somewhat early, and occasionally,
* @+ q, R' H4 |' Ktesticular enlargement is not that evident in the
( D4 t$ K, h) _5 p1 k$ f& ubeginning of this process.1 In the absence of a neg-
+ Q: |1 z9 n/ [( D; F& Y0 Hative initial history of androgen exposure, our
( q' e0 k& \4 d2 ]: b3 C9 z2 cbiggest concern was virilizing adrenal hyperplasia,- A% f0 X, H7 a: A- T
either 21-hydroxylase deficiency or 11-β hydroxylase
: F4 j/ t/ [' w  `7 @, w9 E" Cdeficiency. Those diagnoses were excluded by find-8 S" C  d# e) G+ S2 Q' v0 r4 l2 B
ing the normal level of adrenal steroids., ^! c  `/ y7 w/ }7 V. e8 P
The diagnosis of exogenous androgens was strongly1 p) O1 N6 u8 s, Q
suspected in a follow-up visit after 4 months because
; _( t7 @+ S  D3 I, Y5 o/ ?9 pthe physical examination revealed the complete disap-
, g. [7 G. _2 T: R2 [pearance of pubic hair, normal growth velocity, and
; L: F! e! {9 Bdecreased erections. The father admitted using a testos-
& J9 e5 f9 ]5 B( M$ E1 hterone gel, which he concealed at first visit. He was6 k$ O: |$ Z, g) M
using it rather frequently, twice a day. The Physicians’  w* L, H2 F8 }  U/ G
Desk Reference, or package insert of this product, gel or
/ X! G' g& d1 [# i, ccream, cautions about dermal testosterone transfer to" Y, B, s- _  @3 d# m( u
unprotected females through direct skin exposure., H4 Q* Q. O2 n
Serum testosterone level was found to be 2 times the# C5 ?' ^! t1 ]8 k: G6 n
baseline value in those females who were exposed to
& \( C- U5 b% w( ^( Oeven 15 minutes of direct skin contact with their male
6 }0 H' f+ Q2 z" q' b; Rpartners.6 However, when a shirt covered the applica-
3 Y. K1 w! V) _- i% q3 m: Y; Ction site, this testosterone transfer was prevented.% v8 c0 a- A  W- H! `/ E$ U. x: K) }
Our patient’s testosterone level was 60 ng/mL,: k3 H7 b5 W- w" i3 K
which was clearly high. Some studies suggest that
/ t$ y( [( M8 z6 Fdermal conversion of testosterone to dihydrotestos-
! R) k5 g/ l9 q$ Rterone, which is a more potent metabolite, is more# u& a  s6 o& b! _6 n* {+ P* h7 \
active in young children exposed to testosterone
" z5 L( F1 l' S$ j+ j8 [+ Z% L% Kexogenously7; however, we did not measure a dihy-7 ]1 B% p# T) G1 _! Y* D; C2 e: m
drotestosterone level in our patient. In addition to
/ T0 |0 q5 l9 J5 k7 @6 lvirilization, exposure to exogenous testosterone in+ S& T( {+ L& v; h
children results in an increase in growth velocity and/ t2 P7 i# h: ^" Y2 p2 M9 F3 `
advanced bone age, as seen in our patient.$ N3 U& G& c7 }8 ?7 P! v5 ~
The long-term effect of androgen exposure during
6 L9 e4 N. J, O5 J8 w. ~! eearly childhood on pubertal development and final
% h0 p5 z1 ?) z2 r7 n+ ?& Fadult height are not fully known and always remain
) L. Z! }$ s# za concern. Children treated with short-term testos-; z9 s7 X. l7 S0 A+ T! }0 @8 b" n
terone injection or topical androgen may exhibit some* Z. W9 V0 Z& @/ i. V: z
acceleration of the skeletal maturation; however, after
- j2 t: B8 i- Wcessation of treatment, the rate of bone maturation& s5 h; ]3 O1 R; t1 L+ Q/ \
decelerates and gradually returns to normal.8,9
$ u3 I( \1 v7 [0 r" c1 L2 SThere are conflicting reports and controversy
: ^7 E* z. ^9 O  j- |6 yover the effect of early androgen exposure on adult1 R" ~' C9 T! b8 S/ k
penile length.10,11 Some reports suggest subnormal( w5 K$ @: u7 A" L
adult penile length, apparently because of downreg-
5 r( ~: [3 G  s. c* r& K' _ulation of androgen receptor number.10,12 However,! t# ^! _( I4 O$ e, X/ ^1 X+ Y
Sutherland et al13 did not find a correlation between  ?! y: ~4 O8 j" g2 y& T
childhood testosterone exposure and reduced adult! x' a; y, [; V9 C0 l- T
penile length in clinical studies.
! z8 t. ?$ h+ u; v7 q7 q9 ?0 JNonetheless, we do not believe our patient is
! v8 u& m3 v, Z! N/ f4 U* p. lgoing to experience any of the untoward effects from. f/ |  t4 X4 Y$ i6 p8 i" I+ Z
testosterone exposure as mentioned earlier because- `( N/ m& J9 H5 @' J- l
the exposure was not for a prolonged period of time.% \6 B+ F" g. U# c
Although the bone age was advanced at the time of2 i( c' a0 A' a% F4 m& w6 A
diagnosis, the child had a normal growth velocity at
" n' g; F5 ^8 B/ Jthe follow-up visit. It is hoped that his final adult
0 X' D% |8 l* r+ K5 v8 Yheight will not be affected.: z( Z5 U! c; N$ J4 B: C
Although rarely reported, the widespread avail-
6 E9 {% E& F! Uability of androgen products in our society may" _- F' W8 x/ n: w" h% k
indeed cause more virilization in male or female1 z: k: ~  q7 F: H9 Q4 H, g
children than one would realize. Exposure to andro-* O, H! R8 U3 T9 m
gen products must be considered and specific ques-
( d% @$ b# t6 J2 _tioning about the use of a testosterone product or. K0 c  X# ^, L+ i" B# K$ ?% N
gel should be asked of the family members during- B6 ~) e& u. S, a: J( ]8 }* K) S
the evaluation of any children who present with vir-
" i% ^6 e4 b" w% U( i/ }7 bilization or peripheral precocious puberty. The diag-) M" m! v& J2 p) I' c  Q% [
nosis can be established by just a few tests and by
3 a! S1 i- k3 X8 h+ {& a$ _: Bappropriate history. The inability to obtain such a, e4 z+ f0 J8 M% @' c. M
history, or failure to ask the specific questions, may
- i* l) U- y8 h  [: t3 y1 zresult in extensive, unnecessary, and expensive: a8 t5 J: G' f
investigation. The primary care physician should be
8 R7 e% r8 u( n3 h7 b3 oaware of this fact, because most of these children1 t, X; V) ^1 d! z
may initially present in their practice. The Physicians’# |# ^  P" P6 O/ D+ |
Desk Reference and package insert should also put a' ^* t2 h1 I4 V7 ^
warning about the virilizing effect on a male or
( \# ~; k  y, x; _female child who might come in contact with some-3 U0 _1 F! @, z0 [, h* A" a6 z" R
one using any of these products.9 P5 z  p5 M3 N- Z( R/ E
References4 D/ ^" Y0 r1 d7 M! n
1. Styne DM. The testes: disorder of sexual differentiation
  a8 T5 f" g# y; ]1 W/ B2 c' _and puberty in the male. In: Sperling MA, ed. Pediatric3 a' S# {! c3 Y7 q7 e3 |
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
$ R1 |. c) T  M) c4 D' n9 [2002: 565-628.
  D1 O  m  d1 h9 U+ z2 N/ e: [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 g9 e8 @1 k! s* ~- w0 v$ ?puberty in children with tumours of the suprasellar pineal2 V, j/ {, ~8 x/ T6 G" D
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" }& G; b: G6 g! N" M
Topical Testosterone Exposure / Bhowmick et al 5432 P$ I9 S. @4 M
areas: organic central precocious puberty. Acta Paediatr.. V& v. z, W. A" M
2001;90:751-756.
( H& p  }: T2 {( @1 u2 W7 K3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.. E: a, n' r" i% R- D
Pediatric Endocrinology. 4th ed. New York, NY: Marcel! l' v$ m( s/ x" v- [* d( V
Dekker Inc; 2003:211-238.
0 Z* I  ^4 |& }5 ?) `4. Yu YM, Punyasavatsu N, Elder D, D’Ercole AJ. Sexual# s  A* @- b8 C0 \
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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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