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is a significant concern for physicians. Central' \4 H! _1 |- b: G& q
precocious puberty (CPP), which is mediated. E" e) M% ~* ~3 N6 o/ `
through the hypothalamic pituitary gonadal axis, has
. |2 o6 B. F( C$ x8 Va higher incidence of organic central nervous system
5 b" q0 ^9 u4 Q& g: `! p+ E# ulesions in boys.1,2 Virilization in boys, as manifested0 S8 {5 u- B. p
by enlargement of the penis, development of pubic3 J" A' z4 e: V' u7 N, u% X6 V
hair, and facial acne without enlargement of testi-
5 Y  k( r" U% K$ q; ^, Tcles, suggests peripheral or pseudopuberty.1-3 We
: O& j! a. o- d* F$ kreport a 16-month-old boy who presented with the! j( p) s  C7 i$ T
enlargement of the phallus and pubic hair develop-2 \4 J7 C. d* }. |2 X* h% G  t
ment without testicular enlargement, which was due$ F8 p$ l. r' f/ g
to the unintentional exposure to androgen gel used by
, E' H. ^( c1 f9 }. [the father. The family initially concealed this infor-
, `3 L5 H5 J% f8 I; N3 |mation, resulting in an extensive work-up for this
: D1 q# s! a& W$ ]child. Given the widespread and easy availability of
6 @7 t, E+ K& B( Y3 d- }/ x& _testosterone gel and cream, we believe this is proba-
* L4 m( b9 f# x5 s: Z( hbly more common than the rare case report in the/ W  |0 C& n4 t& w, h, q
literature.4
7 p: L2 @* u5 aPatient Report- M. ~$ a: O# Y+ S) _$ i! D
A 16-month-old white child was referred to the5 V  i7 E; M. V) w' z, W9 B* E
endocrine clinic by his pediatrician with the concern
0 ?2 P7 l, h, a0 o& vof early sexual development. His mother noticed( W* o4 Z( K  |$ a. t# a
light colored pubic hair development when he was
5 p/ p7 Q& Q' L) SFrom the 1Division of Pediatric Endocrinology, 2University of9 C6 t+ F7 `4 P  Y7 B; Y
South Alabama Medical Center, Mobile, Alabama.2 q  \/ [1 ^# G/ o/ T% O+ e
Address correspondence to: Samar K. Bhowmick, MD, FACE,
, q3 ^" v" N9 Y$ S$ A/ @3 nProfessor of Pediatrics, University of South Alabama, College of* w) \; \2 \; X" e. B& |
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) E/ N: z3 D: u2 Q/ h
e-mail: [email protected].
( _$ ?! a4 L5 a! n$ G, e+ Dabout 6 to 7 months old, which progressively became% i% w" b. z0 v
darker. She was also concerned about the enlarge-
& S" I# V- C7 n  z3 ^# ^ment of his penis and frequent erections. The child
- A/ }9 e8 j6 T; s. q5 f& o6 Fwas the product of a full-term normal delivery, with
$ w& N" f/ i7 e( j! W4 b3 p9 p* m2 Ba birth weight of 7 lb 14 oz, and birth length of
3 r5 B, z1 R" d& B" {; J, t20 inches. He was breast-fed throughout the first year4 x- w+ }! r* ?/ f
of life and was still receiving breast milk along with" Q* @% j6 q# v6 L& P
solid food. He had no hospitalizations or surgery,5 Q/ w0 X8 ?  m
and his psychosocial and psychomotor development( h$ k6 P1 i6 \' }* b6 c
was age appropriate., \( W& t' i; V5 _5 n4 p
The family history was remarkable for the father,3 \2 [0 P) K# J+ X$ a
who was diagnosed with hypothyroidism at age 16,
' F+ ~9 s5 n( L4 _- }which was treated with thyroxine. The father’s
) G- z4 ^5 N" u. o7 B( o( hheight was 6 feet, and he went through a somewhat/ T' P" C1 }) R* F3 k/ S- O
early puberty and had stopped growing by age 14.
9 z7 G% A9 s' u  |3 q' v  n4 {4 YThe father denied taking any other medication. The5 \' [" d+ g* i2 y5 B, U2 P
child’s mother was in good health. Her menarche. j: j# }% U$ R3 d
was at 11 years of age, and her height was at 5 feet
  \/ S! E! B: n  r7 C, u; A% u5 inches. There was no other family history of pre-7 h1 ^1 q1 S) d& q
cocious sexual development in the first-degree rela-
- `: \" V7 x, z7 \tives. There were no siblings.7 r9 }) T: h: o4 o& q; C: p
Physical Examination  K* }, {8 [# ^. M  r
The physical examination revealed a very active,
; h% R6 W/ h3 y8 V6 \' Hplayful, and healthy boy. The vital signs documented
) S" v) b. |5 B! ua blood pressure of 85/50 mm Hg, his length was  F+ C1 M& m$ ~5 a8 ?
90 cm (>97th percentile), and his weight was 14.4 kg
! J' b2 e% L# B$ V/ x) V(also >97th percentile). The observed yearly growth6 J$ E7 h! b1 s% k5 T! x$ X& E
velocity was 30 cm (12 inches). The examination of
3 g6 p/ I( O/ [( j( b1 Hthe neck revealed no thyroid enlargement.
6 W0 t* j  r, N- R) IThe genitourinary examination was remarkable for  p: C; e' E9 B  \# ^0 Z% `
enlargement of the penis, with a stretched length of& P7 }2 _3 v$ \" H7 M
8 cm and a width of 2 cm. The glans penis was very well+ o! T9 `$ S( {( `
developed. The pubic hair was Tanner II, mostly around6 x' L1 `# P( c+ k
540
. }) K+ R$ P2 \( t5 G5 S, k7 {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: d' b% V, j3 R1 r9 i5 `9 zthe base of the phallus and was dark and curled. The2 H: C9 N8 m* L7 L  \# y- Y
testicular volume was prepubertal at 2 mL each.
( ?* Z& v$ I( d0 }+ z' BThe skin was moist and smooth and somewhat
" ?+ G0 }/ \1 }. @/ i8 D+ M7 Noily. No axillary hair was noted. There were no+ M, e. H4 m& ^3 @5 L
abnormal skin pigmentations or café-au-lait spots.
4 k' A( ?9 V+ {" {2 C( }" FNeurologic evaluation showed deep tendon reflex 2+; Z0 F0 ^$ Q" i' F' B
bilateral and symmetrical. There was no suggestion+ l; q# M- p" K) Y" L
of papilledema.
2 {1 J$ X# R. hLaboratory Evaluation
+ _. J- W& v2 oThe bone age was consistent with 28 months by% e4 L  B" `( c- g/ j; f# Q8 X  L
using the standard of Greulich and Pyle at a chrono-- Q1 F: D; h8 r- y7 p
logic age of 16 months (advanced).5 Chromosomal3 V3 \) R' |% H/ N% x( z. A
karyotype was 46XY. The thyroid function test
7 {  T1 j+ R: B: Oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
1 x8 \% |" u0 ^4 Jlating hormone level was 1.3 µIU/mL (both normal)., H/ m/ r8 B" U* B
The concentrations of serum electrolytes, blood
% X3 I* O5 q1 H' burea nitrogen, creatinine, and calcium all were
8 A3 F" w6 E5 O) p9 O4 V' Ewithin normal range for his age. The concentration
9 _2 M! g" u7 N; ]( wof serum 17-hydroxyprogesterone was 16 ng/dL
/ b5 T5 M# r9 ^(normal, 3 to 90 ng/dL), androstenedione was 20
1 Q0 }* M- o4 Fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 R' T+ p1 `, D2 m7 ~, r6 E
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 H: Q  S6 F3 cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ @/ L; Q- x' d: u49ng/dL), 11-desoxycortisol (specific compound S)  b, W- B5 ~- M. x( n1 T; c
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
! n9 }% a. G* etisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% v" x5 G9 `2 X/ l" otestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ }3 z6 {( v' E! jand β-human chorionic gonadotropin was less than% m( H& V! U& ]" u; Q, b
5 mIU/mL (normal <5 mIU/mL). Serum follicular
( \: P1 {' F- ~) zstimulating hormone and leuteinizing hormone) K- r( C! K  \+ e5 T( I
concentrations were less than 0.05 mIU/mL
/ s6 j6 u4 u1 v3 D* p(prepubertal).
8 F2 F3 Z) H8 \/ F: L( jThe parents were notified about the laboratory
+ j, S' p% S! N9 v: nresults and were informed that all of the tests were
; h  O# n) ?. L& D5 Rnormal except the testosterone level was high. The
) u1 }  z5 H1 {. s' I9 afollow-up visit was arranged within a few weeks to
; m  G: [  l) d: E2 q5 yobtain testicular and abdominal sonograms; how-
9 t$ p5 p. e' ~ever, the family did not return for 4 months.8 g: u4 V8 x& z8 M3 l& V
Physical examination at this time revealed that the
+ _8 Z- u4 i5 k# P2 Xchild had grown 2.5 cm in 4 months and had gained+ B7 r9 c: h% ~
2 kg of weight. Physical examination remained
( I- \$ ]7 v0 {0 C* v+ ?- A+ funchanged. Surprisingly, the pubic hair almost com-
+ l. ^2 m/ ~. X+ u. G5 Rpletely disappeared except for a few vellous hairs at
* d" A- b1 e; N; T. o0 J" P. y% xthe base of the phallus. Testicular volume was still 2& n+ E5 _2 r4 _- G4 [1 ?
mL, and the size of the penis remained unchanged.
& G5 D; D* r- Y4 tThe mother also said that the boy was no longer hav-
3 A4 u3 ]9 ?- ning frequent erections.
+ R2 J, ~$ w0 y. }, z! BBoth parents were again questioned about use of
, ~, O% J" \" `4 L+ Q% sany ointment/creams that they may have applied to- [5 Q$ f1 V' V- y, N9 ?) c
the child’s skin. This time the father admitted the
/ x, S4 L7 s! ]& @# q  s( l5 wTopical Testosterone Exposure / Bhowmick et al 541
1 v6 B7 l$ I2 y4 K6 w8 euse of testosterone gel twice daily that he was apply-8 t0 Z( X; N9 s  Y; [
ing over his own shoulders, chest, and back area for
& |- q: H! x% N# r& r+ z' n. {a year. The father also revealed he was embarrassed
0 B' t  h; ]0 @9 F1 S+ {6 Eto disclose that he was using a testosterone gel pre-
* y* a' ]% Q. c' dscribed by his family physician for decreased libido
; G/ p  C" U( V* ^secondary to depression.
/ q2 m4 |) N0 N+ Y4 B8 bThe child slept in the same bed with parents.3 U. c& b) W: u, `- f" }' c
The father would hug the baby and hold him on his) b0 i# z8 u- i) t' u. H
chest for a considerable period of time, causing sig-/ K' \, J* p. e' @0 s  |. A6 F
nificant bare skin contact between baby and father.9 O- l; m5 k' M) _5 U: h9 k. L2 N
The father also admitted that after the phone call,
! Q+ [5 L9 S& k$ X3 d' J  wwhen he learned the testosterone level in the baby
9 _  _$ j1 ^& _* A5 y! k2 @was high, he then read the product information  k- x, N( a/ _& L+ E" z" n2 X
packet and concluded that it was most likely the rea-
1 }1 L. W- I! i+ c6 {4 qson for the child’s virilization. At that time, they; i% U8 I4 r* }7 [
decided to put the baby in a separate bed, and the, h# _( e# F' H  M6 z
father was not hugging him with bare skin and had% K2 S3 C; n5 ]  e; _
been using protective clothing. A repeat testosterone
0 `+ t. Z4 s' p' A' }- t* t/ o- dtest was ordered, but the family did not go to the
# Q- U; W4 r0 q% ^' Elaboratory to obtain the test.
  C  b  U' k& c! f/ x/ F2 T) LDiscussion  e7 ^7 T: A4 h
Precocious puberty in boys is defined as secondary
+ ]' Q7 Y: s) G0 c- i4 nsexual development before 9 years of age.1,4
" x, W) _8 n% h* Y7 t# @- ZPrecocious puberty is termed as central (true) when: H9 l3 z) t7 c# \  K
it is caused by the premature activation of hypo-  t! D; b  g. {0 P0 Z
thalamic pituitary gonadal axis. CPP is more com-  B% M0 w5 X- c6 M) v# ]* |3 Z2 d& D" j
mon in girls than in boys.1,3 Most boys with CPP
, z) P3 }) [8 w, Cmay have a central nervous system lesion that is1 e& }( l" b2 \0 E, \2 Z
responsible for the early activation of the hypothal-' K/ E. i) J0 ]+ ~
amic pituitary gonadal axis.1-3 Thus, greater empha-
) K) U- t& j' E3 X  @7 bsis has been given to neuroradiologic imaging in. Q! M7 G. p, A, G" E
boys with precocious puberty. In addition to viril-0 H7 `2 q7 E0 H4 b/ J
ization, the clinical hallmark of CPP is the symmet-
9 f* }/ k1 z* xrical testicular growth secondary to stimulation by1 Q# g; Z7 {8 F6 Q- H- d" {- i+ v
gonadotropins.1,3
4 h9 l: ?# v1 Z' C* p* `$ BGonadotropin-independent peripheral preco-6 K9 `/ L1 |* Q9 ?8 u  ]$ M
cious puberty in boys also results from inappropriate
1 k: v% H* r" s1 Z* ?androgenic stimulation from either endogenous or
& i7 O/ V1 O/ M( _8 Texogenous sources, nonpituitary gonadotropin stim-
. _; }; y  r5 T" M! h2 a& Aulation, and rare activating mutations.3 Virilizing6 |" A/ X1 }( X) c6 C0 ]3 x. g
congenital adrenal hyperplasia producing excessive
- r+ `$ ]( ~8 w* r: zadrenal androgens is a common cause of precocious- y  w! b& j! ^# _
puberty in boys.3,4
3 x. q2 g8 i2 L3 k/ m2 r7 WThe most common form of congenital adrenal0 Y, g2 B" I. O# U7 e/ A$ O
hyperplasia is the 21-hydroxylase enzyme deficiency.9 Z7 g- F+ C, R
The 11-β hydroxylase deficiency may also result in
& ]7 `% e7 ?) Hexcessive adrenal androgen production, and rarely,. J4 Z- K; N  P) k' n% ]# v' W& _
an adrenal tumor may also cause adrenal androgen; i0 {2 m4 \0 [- W0 z2 c3 g
excess.1,3' I) a% H' i& _1 ?
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 [2 E# g! o7 A# k( u: h  |% r0 J
542 Clinical Pediatrics / Vol. 46, No. 6, July 20077 M* D! s) i% o0 i( i, V) J
A unique entity of male-limited gonadotropin-
% S  Z' ?$ |6 V8 }  E9 Gindependent precocious puberty, which is also known0 m2 p: P; o7 R" s
as testotoxicosis, may cause precocious puberty at a
' ~  m' k' _6 \/ r" T: Mvery young age. The physical findings in these boys$ z, B6 A4 \) }1 ]
with this disorder are full pubertal development,$ e8 [) X8 a1 s
including bilateral testicular growth, similar to boys
0 W% G, E+ ?8 \& T9 ?8 S, twith CPP. The gonadotropin levels in this disorder
: Y) ^! o  b/ I* bare suppressed to prepubertal levels and do not show& ~1 A) ?2 U- b; q
pubertal response of gonadotropin after gonadotropin-$ E9 R' S5 A  `! a/ f# h. V
releasing hormone stimulation. This is a sex-linked
2 J+ y7 s* r( [0 p, tautosomal dominant disorder that affects only
% i) G; U! C3 f5 R; O% R  Cmales; therefore, other male members of the family
# t2 ~8 j( X1 A/ E% k: q# bmay have similar precocious puberty.3- N* D/ x. \  [% x( ?, b
In our patient, physical examination was incon-
/ A. `  Z. x4 b) a1 {$ Ysistent with true precocious puberty since his testi-2 @9 _( }" p* v/ D5 ^
cles were prepubertal in size. However, testotoxicosis
- }0 v9 Y' ?( c! G) e8 Ewas in the differential diagnosis because his father
5 [" j# l  x% N0 C  Lstarted puberty somewhat early, and occasionally," s7 k$ S9 ~# D5 G0 W
testicular enlargement is not that evident in the6 P# V6 K4 Z, Q" Q0 `* m
beginning of this process.1 In the absence of a neg-
, F" s. O6 f0 s& @4 _ative initial history of androgen exposure, our5 W3 _, o& w' }* v4 Z( R
biggest concern was virilizing adrenal hyperplasia,
0 O' _) Z6 R3 |/ {3 l' @  heither 21-hydroxylase deficiency or 11-β hydroxylase, Q" y3 M1 I1 _8 m( `
deficiency. Those diagnoses were excluded by find-
# L# ^- _3 T4 I. P2 Hing the normal level of adrenal steroids.- Z, u2 `# l4 j! `$ U% E4 V: r5 P
The diagnosis of exogenous androgens was strongly
6 a, O' w1 ~/ _1 l- E! A7 Bsuspected in a follow-up visit after 4 months because
4 \  p5 Y4 B. B5 f3 `& T2 o/ gthe physical examination revealed the complete disap-
( M9 }9 U# a* w  H8 I8 qpearance of pubic hair, normal growth velocity, and
. `* A  d# {1 ?2 D8 k% Gdecreased erections. The father admitted using a testos-& |, ^1 C( o" M0 q9 y4 t5 E
terone gel, which he concealed at first visit. He was
' k6 ]$ l3 j' _0 o8 C2 Z5 C. musing it rather frequently, twice a day. The Physicians’
4 \, I3 f) C8 U+ {& {Desk Reference, or package insert of this product, gel or
9 D8 V3 B; `) k! F0 w  Acream, cautions about dermal testosterone transfer to7 m, f0 b+ ^% Y9 K
unprotected females through direct skin exposure.
! V  {* P9 h7 p4 |1 \Serum testosterone level was found to be 2 times the
9 \0 Z! x" P& c5 ebaseline value in those females who were exposed to5 n5 L& p. F0 L
even 15 minutes of direct skin contact with their male% C1 s& Z5 F6 k
partners.6 However, when a shirt covered the applica-) X; ?3 g: c; f
tion site, this testosterone transfer was prevented.! C* n2 o5 r2 a, ^
Our patient’s testosterone level was 60 ng/mL,9 X0 X6 ?( j8 y- U: B
which was clearly high. Some studies suggest that, Q& P5 V2 g+ }! ~7 j; _
dermal conversion of testosterone to dihydrotestos-
  z( _7 a5 S! `  I! ?6 Vterone, which is a more potent metabolite, is more# H) O* z/ H9 P# ~
active in young children exposed to testosterone& m5 T$ O! U4 _; X2 O
exogenously7; however, we did not measure a dihy-
9 x1 v" J, R" a7 P) c' r! @% ddrotestosterone level in our patient. In addition to3 X1 d9 l. F" B- s
virilization, exposure to exogenous testosterone in
, v. R9 P1 {% L& M% X# Wchildren results in an increase in growth velocity and4 V7 u( c4 S' m( b1 d) ?0 c; b8 i) E
advanced bone age, as seen in our patient.
, n9 \5 f+ m* P: s; N# Y; @2 {The long-term effect of androgen exposure during
' m& _! G- _; S. j) Vearly childhood on pubertal development and final% @$ ?% q  B4 x# U
adult height are not fully known and always remain
. D3 K, m4 t& y4 M4 v  Za concern. Children treated with short-term testos-
. K5 G7 l! ?; i" @terone injection or topical androgen may exhibit some
6 h0 Z% @* \& h5 z: Racceleration of the skeletal maturation; however, after2 e( U; Y) t* p6 _- _' f* b
cessation of treatment, the rate of bone maturation
+ D8 g1 x- L; K  B- o9 Sdecelerates and gradually returns to normal.8,9
) y; }3 v5 l% _# {There are conflicting reports and controversy
! n, O& O3 B/ C  [over the effect of early androgen exposure on adult
+ u' I0 m/ ~, A- h# V" g5 ipenile length.10,11 Some reports suggest subnormal8 F: }8 G0 W1 W7 B0 M  q' l. z5 ^
adult penile length, apparently because of downreg-
( N9 U: [. G* o1 @ulation of androgen receptor number.10,12 However,! {' M0 @* l: s; X/ p- e3 c
Sutherland et al13 did not find a correlation between
" {4 q3 E: n2 l/ P2 n* Kchildhood testosterone exposure and reduced adult
. d9 A5 t, I" Spenile length in clinical studies.. d6 W7 \4 Z: G6 Z4 Q9 s
Nonetheless, we do not believe our patient is
" {" e& u1 {  |going to experience any of the untoward effects from+ l2 x; L' Z5 r& t) g. q8 V, ~
testosterone exposure as mentioned earlier because
! q! `' O9 P# k$ Othe exposure was not for a prolonged period of time.
* c1 C  u; W% EAlthough the bone age was advanced at the time of+ c9 r7 e- x) e" U, ]6 V
diagnosis, the child had a normal growth velocity at: d/ I. M+ a$ d) x! e, g, U
the follow-up visit. It is hoped that his final adult
. H) u* H! w5 k8 M+ p6 Dheight will not be affected.
8 D& T$ R% p. a" UAlthough rarely reported, the widespread avail-
4 {# G& c5 L# r9 z2 x8 t* Z/ N, T0 hability of androgen products in our society may
0 {' [) o4 k* s4 eindeed cause more virilization in male or female& |2 Y4 d. j, w8 C" N2 w& [
children than one would realize. Exposure to andro-
5 y3 V. w- [( y8 X2 ~; H4 \gen products must be considered and specific ques-
  p5 I2 z" z% s  Utioning about the use of a testosterone product or
( i  \$ z( [) j$ Z% qgel should be asked of the family members during
6 X# S; d( @) Y* J; q- R7 Pthe evaluation of any children who present with vir-: V/ q8 z5 {' D
ilization or peripheral precocious puberty. The diag-6 s3 o  l# }, q, _9 ^3 C& n
nosis can be established by just a few tests and by0 i: N! M& f4 L* Q- ^
appropriate history. The inability to obtain such a
8 {$ g6 @( ^9 Z/ y1 dhistory, or failure to ask the specific questions, may
' m; C5 R$ D6 t4 aresult in extensive, unnecessary, and expensive: R* G2 l% H& e: E7 p- U9 n
investigation. The primary care physician should be6 N/ p7 {$ t, G
aware of this fact, because most of these children
( f" j$ C. G, L% x/ N9 wmay initially present in their practice. The Physicians’
2 |5 s# i+ s6 t: u! iDesk Reference and package insert should also put a  F( _3 Z9 L' v0 b5 ^$ u
warning about the virilizing effect on a male or
3 i# N* q- E. T/ Xfemale child who might come in contact with some-
( e0 m# _1 V" U- g  e, ^one using any of these products.7 V* f, F& B. F* ~# X: f( c  @
References
% o0 J: c1 O' l1. Styne DM. The testes: disorder of sexual differentiation9 Y; ?1 A$ v* w/ }7 ~8 N0 ]
and puberty in the male. In: Sperling MA, ed. Pediatric
& h& e1 s) H; LEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; d$ ]8 w# m' P# X/ }2002: 565-628./ y  ?! L& K- A. d" R% s' c
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
# H, W0 Y2 `* u: xpuberty in children with tumours of the suprasellar pineal. h3 r5 X( X# r" z5 v
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 w2 [# j  N! b4 v# fTopical Testosterone Exposure / Bhowmick et al 543
, h( z3 u4 ?9 z' Z; S( t% [areas: organic central precocious puberty. Acta Paediatr.
- T) a& @, u3 ~0 Z) a' y2001;90:751-756.
" j3 q7 r) u. e  B4 ]) ^6 e9 H6 f3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
& s+ t& P+ u6 j2 B% h- T6 nPediatric Endocrinology. 4th ed. New York, NY: Marcel1 Q% I' c& C0 h. Y
Dekker Inc; 2003:211-238.: d9 V% a+ y/ R$ f2 p  b
4. Yu YM, Punyasavatsu N, Elder D, D’Ercole AJ. Sexual
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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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