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is a significant concern for physicians. Central5 O* B. ^3 n8 p& t  r
precocious puberty (CPP), which is mediated5 J9 {9 ?1 u1 [, b, z; x
through the hypothalamic pituitary gonadal axis, has+ A' Y0 l' l& m
a higher incidence of organic central nervous system
! b" ]8 g- N4 D+ p* r4 Alesions in boys.1,2 Virilization in boys, as manifested2 i& K. C) F7 C
by enlargement of the penis, development of pubic% f# W: G, D' L8 d3 m! }( U
hair, and facial acne without enlargement of testi-
2 ]  E2 s# {3 C) J. W3 R+ L# Rcles, suggests peripheral or pseudopuberty.1-3 We
4 I: L$ b' M! f: ^+ @9 h, o  \3 [report a 16-month-old boy who presented with the) e: n" ]  t) \4 a
enlargement of the phallus and pubic hair develop-
* N$ @4 t8 y6 T- p2 bment without testicular enlargement, which was due4 p! Z, C2 t0 Z5 k0 V
to the unintentional exposure to androgen gel used by
7 h, I. F5 I5 z/ W% Kthe father. The family initially concealed this infor-
1 L1 X3 S" D: mmation, resulting in an extensive work-up for this
0 s; `. O5 c1 y8 y, U% g/ mchild. Given the widespread and easy availability of
; U5 a* `) P1 z2 X, J+ Otestosterone gel and cream, we believe this is proba-
- X# k* I# N2 a+ h: l: y* v$ ebly more common than the rare case report in the
) t7 s$ ~# t7 h8 g" Rliterature.4
* R8 s+ m! Y& {3 ?Patient Report+ o3 M1 Y+ E9 f' i: t2 R$ J0 r  s
A 16-month-old white child was referred to the
0 |0 S( @6 Z. x1 b) X3 D/ wendocrine clinic by his pediatrician with the concern0 C* B4 i5 g1 T" P' v
of early sexual development. His mother noticed2 D& @" m( H7 A, z# d2 X% A/ a5 i
light colored pubic hair development when he was0 {1 o" l. R; ^. u7 `
From the 1Division of Pediatric Endocrinology, 2University of
, V* Q; ?  J6 ^South Alabama Medical Center, Mobile, Alabama.
& ]  w1 s- p8 NAddress correspondence to: Samar K. Bhowmick, MD, FACE,: S( G4 m* Q, O# E
Professor of Pediatrics, University of South Alabama, College of" A$ n+ j6 I  b& H7 [. a
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 z% l% }- @% U: W4 V' V8 n% }e-mail: [email protected].
6 |6 D; H& C3 ^$ Zabout 6 to 7 months old, which progressively became3 B, W( C7 j& N  b7 u
darker. She was also concerned about the enlarge-
- b3 |5 }& Y- Hment of his penis and frequent erections. The child
; o4 p4 ]' [  F# Owas the product of a full-term normal delivery, with
( Q2 k0 ^. {* {9 I2 ~a birth weight of 7 lb 14 oz, and birth length of
$ D/ Y, x; u) ?20 inches. He was breast-fed throughout the first year
; ^, `1 X: B& }4 s0 Qof life and was still receiving breast milk along with/ ~6 @- b* n2 w7 r
solid food. He had no hospitalizations or surgery,7 P+ Q+ v# G1 i# J4 m! h/ V) F
and his psychosocial and psychomotor development
% L  z. j  H% p+ Y, nwas age appropriate.
( u( m  H& U2 b  QThe family history was remarkable for the father," Y/ O' d: [* n4 D
who was diagnosed with hypothyroidism at age 16,' f0 V8 S7 D8 \6 S$ c5 q
which was treated with thyroxine. The father’s( K. Q; A6 b" f+ ~% Q+ W: n
height was 6 feet, and he went through a somewhat
3 ^8 i* n! C, r1 I9 c. Tearly puberty and had stopped growing by age 14.
: ^( }# O- d/ P7 d+ vThe father denied taking any other medication. The
4 }* Y8 q" R1 I. C. Bchild’s mother was in good health. Her menarche" g, A  K( l9 o' x! R+ M7 P
was at 11 years of age, and her height was at 5 feet
3 o) K% O+ n" t% w: z5 inches. There was no other family history of pre-
" k- G3 B# U) G* a" ?cocious sexual development in the first-degree rela-
7 f. y0 `8 ~" |  Dtives. There were no siblings.
+ b7 c$ q0 y/ L( F5 f6 fPhysical Examination9 ]- \: Z  k4 q3 c
The physical examination revealed a very active,
  ^% m2 q- G0 G+ Kplayful, and healthy boy. The vital signs documented
* q. N, d$ G3 c8 p3 Z, V. ha blood pressure of 85/50 mm Hg, his length was
* X  U' O- t% i% [2 W0 t90 cm (>97th percentile), and his weight was 14.4 kg: m( K# \  ~4 C; R- D% O
(also >97th percentile). The observed yearly growth
- a  I8 o9 ]' n: ]/ T& j4 e' Rvelocity was 30 cm (12 inches). The examination of3 H2 g5 t7 V2 h2 }' B3 i) x% g/ S# q
the neck revealed no thyroid enlargement.
. E- {2 b. D! f' eThe genitourinary examination was remarkable for
7 K5 x3 j) B7 f8 g) Cenlargement of the penis, with a stretched length of
9 R9 M5 a( D- j% d8 cm and a width of 2 cm. The glans penis was very well
' x3 C, X+ b1 M0 \developed. The pubic hair was Tanner II, mostly around
5 V# k2 E7 K5 S5409 s) L5 t6 l5 F( B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 [* V1 G# T  ]" l* h1 z  S5 Z0 w( u- A
the base of the phallus and was dark and curled. The7 D# {) q( `: K3 E5 u& M
testicular volume was prepubertal at 2 mL each.: x/ I- U- {# G
The skin was moist and smooth and somewhat
! P, g: T5 F7 N' J+ yoily. No axillary hair was noted. There were no# z/ Z- V' [3 H/ t0 S5 t
abnormal skin pigmentations or café-au-lait spots.! Q! R# U5 E3 {" A/ Y
Neurologic evaluation showed deep tendon reflex 2+- E/ H. \7 F7 E4 w
bilateral and symmetrical. There was no suggestion
4 h& y4 X/ a* B2 C; gof papilledema.
$ n2 B1 P6 O( U1 D; A3 w3 O& yLaboratory Evaluation) w6 K' a) g4 s/ t* Q
The bone age was consistent with 28 months by7 \: B% U  N/ E7 M  r2 p. q; P
using the standard of Greulich and Pyle at a chrono-% J, X1 p9 X  h6 v
logic age of 16 months (advanced).5 Chromosomal
- K2 j" }* f. |1 {) S9 ^karyotype was 46XY. The thyroid function test* ?+ q3 y; I/ Z$ N
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 M. v9 c1 J! k+ r" Y' vlating hormone level was 1.3 µIU/mL (both normal).1 A% {# G- ^# o+ M- V
The concentrations of serum electrolytes, blood; f0 P0 \# V* q; a; o, G1 e' g
urea nitrogen, creatinine, and calcium all were: l4 g5 ~, D. M( q$ f/ n( @7 {3 `
within normal range for his age. The concentration
6 I2 Y0 N. O9 |- z& r7 u$ Yof serum 17-hydroxyprogesterone was 16 ng/dL9 E  Y, g4 t. i" Y( ?7 U% F
(normal, 3 to 90 ng/dL), androstenedione was 20
; E, ?( ^& G8 x& G" E6 G5 J- Sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
9 H1 _  R: E$ }/ t, W( l  Vterone was 38 ng/dL (normal, 50 to 760 ng/dL),
" g3 r- O; H/ H& Z! `( x* o3 _' mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to, {  C" V9 X% L0 c* t3 B5 \8 @
49ng/dL), 11-desoxycortisol (specific compound S)
% M- t' I, u$ N3 a  gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; @4 i- \) I" s7 V; g
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 x' J* K8 G4 x7 atestosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 a/ c7 q8 Z: M+ u" }. o
and β-human chorionic gonadotropin was less than3 M2 @7 q9 N9 W/ A
5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 ?# a) A) m5 S* k6 t$ w) ^1 pstimulating hormone and leuteinizing hormone
! W6 R  U, Q$ E  q1 mconcentrations were less than 0.05 mIU/mL
4 I6 o( g) }- f$ B# Y! q: S2 m(prepubertal).9 W3 V% ^( j- O0 `3 V. e/ k
The parents were notified about the laboratory
9 H/ v' @& Z  Eresults and were informed that all of the tests were8 w0 ?  D6 _7 {( v
normal except the testosterone level was high. The7 z5 [4 b$ W$ t0 H
follow-up visit was arranged within a few weeks to
8 s$ v1 k2 P! k, [4 w( Zobtain testicular and abdominal sonograms; how-
/ D; _7 `9 b: e, y3 Jever, the family did not return for 4 months.
+ h# p& `4 \. I+ u+ q, iPhysical examination at this time revealed that the
3 C, _4 O7 P% z) lchild had grown 2.5 cm in 4 months and had gained) \1 F. g* ?+ z) y7 [
2 kg of weight. Physical examination remained- P7 m& I/ g' a, n. l1 I: @2 J
unchanged. Surprisingly, the pubic hair almost com-1 R5 p% @9 V, b- K: a7 }! }1 y
pletely disappeared except for a few vellous hairs at8 n4 h8 ?9 }7 o. {
the base of the phallus. Testicular volume was still 23 c! b/ A9 k& q: l! g% b1 F
mL, and the size of the penis remained unchanged.
# Q" V6 m+ O% AThe mother also said that the boy was no longer hav-
% j: u; S- p' T6 M& m& {, M: Q* M* Jing frequent erections.
1 H- R/ w8 q6 c7 c: J. s' zBoth parents were again questioned about use of
9 D- P8 N4 ?0 K0 ?any ointment/creams that they may have applied to% X% c2 V. }- K- }) ~& Y
the child’s skin. This time the father admitted the" ]7 D. `5 X$ y# a
Topical Testosterone Exposure / Bhowmick et al 541* i5 S7 d* ^; Q9 W- j  U# \
use of testosterone gel twice daily that he was apply-
( }- `7 `# ]0 `$ k6 @ing over his own shoulders, chest, and back area for0 m; q7 q4 F& J1 j7 U& {: t
a year. The father also revealed he was embarrassed
" W( P+ d7 i0 Zto disclose that he was using a testosterone gel pre-
& u7 F- `* k% G9 A5 I0 s3 ^scribed by his family physician for decreased libido/ ?# Q( w, a' x" f
secondary to depression.
, t# d- {3 Q: F; R; KThe child slept in the same bed with parents./ V5 g8 ~3 c5 b6 H0 ?/ f0 D
The father would hug the baby and hold him on his
+ s' A- D* w* ^" Rchest for a considerable period of time, causing sig-  J# n* I3 }/ l
nificant bare skin contact between baby and father.! K' u) p4 ~  [2 b: @
The father also admitted that after the phone call,
$ u' v4 N7 J( O2 C' p, D; Gwhen he learned the testosterone level in the baby) P5 |6 i; t8 V' L/ e
was high, he then read the product information9 _, E8 v, D0 C0 R
packet and concluded that it was most likely the rea-
* j, P9 Y9 O5 U: F0 I8 B+ Fson for the child’s virilization. At that time, they- _  o2 `+ ~8 S# n& R) L8 E
decided to put the baby in a separate bed, and the
3 [8 j$ C6 ?% Q* q! c( m, Ifather was not hugging him with bare skin and had4 E  f# c# G  y+ D, f
been using protective clothing. A repeat testosterone
. t; y% l) \2 {, [: D! ztest was ordered, but the family did not go to the
% i, o1 S3 k( t6 Ulaboratory to obtain the test.5 i  E; w  d: u1 h; U
Discussion: |* @: `# N# q9 Z
Precocious puberty in boys is defined as secondary
3 d0 P2 W/ g0 O4 f# [5 X) S) ~& n& @sexual development before 9 years of age.1,4
; R9 F9 u3 b7 ?Precocious puberty is termed as central (true) when
8 C9 o" K8 Y, S, [it is caused by the premature activation of hypo-
/ N# i# e* [7 e! [7 z7 m0 H" {thalamic pituitary gonadal axis. CPP is more com-
. D# b: ~2 }/ Nmon in girls than in boys.1,3 Most boys with CPP0 y& z) }' w" W' i0 a2 I
may have a central nervous system lesion that is: p3 u( G% Y  |: G% l+ E8 ^
responsible for the early activation of the hypothal-# Q3 p, A  s. s. Q. {' b! ?
amic pituitary gonadal axis.1-3 Thus, greater empha-8 g# f7 b! H' z; n- i; s4 @7 F7 {& {
sis has been given to neuroradiologic imaging in8 ~: m8 U3 I" _4 M$ v
boys with precocious puberty. In addition to viril-
& L& c3 `+ M! h8 R9 R; S! `ization, the clinical hallmark of CPP is the symmet-/ \  t7 j1 K0 W7 F7 _
rical testicular growth secondary to stimulation by' Y( p- r$ j( a6 [( J2 {# S4 ?$ U
gonadotropins.1,3* c5 o) \. [7 ?  D
Gonadotropin-independent peripheral preco-0 s% o' A  B1 v+ N
cious puberty in boys also results from inappropriate
' l2 X  W% A; T3 [" ]3 wandrogenic stimulation from either endogenous or
  O7 l& b$ N' g& Rexogenous sources, nonpituitary gonadotropin stim-
( X! Q$ ]2 s( B5 T$ S  }" g& h' Julation, and rare activating mutations.3 Virilizing3 {$ ~1 G4 x0 S1 C3 p3 g
congenital adrenal hyperplasia producing excessive
0 N& K4 K1 m+ e) Zadrenal androgens is a common cause of precocious
  M% I( G) V* S- R- gpuberty in boys.3,4; U- p7 y4 x4 g$ T
The most common form of congenital adrenal
5 }- ~+ b0 V3 s4 \5 }hyperplasia is the 21-hydroxylase enzyme deficiency.  ]* i: V1 v8 x- H' o" K" N5 Y
The 11-β hydroxylase deficiency may also result in/ r. }8 }. w/ V% n
excessive adrenal androgen production, and rarely,7 t) Z. F& S) P7 s  h" ~
an adrenal tumor may also cause adrenal androgen# s* U/ W) i3 @. w) s# {
excess.1,3
4 A# }' s: O' A; Q# a* A& t( Dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 x. n; m0 |& F* S- ?2 r
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% }9 U3 G3 k# a3 j" X: L5 yA unique entity of male-limited gonadotropin-. o: }0 `9 [2 B8 R
independent precocious puberty, which is also known
* [! s6 H" X9 N! I9 |as testotoxicosis, may cause precocious puberty at a+ Y: {0 v! Y- C4 `
very young age. The physical findings in these boys; h9 v( Z1 k# Y7 b& T8 n; A5 Q9 e
with this disorder are full pubertal development,/ ^' J: }  e) U
including bilateral testicular growth, similar to boys
' y; V; G8 M) R$ t; P$ Lwith CPP. The gonadotropin levels in this disorder
4 h7 o7 b: v# {' t) y1 [! care suppressed to prepubertal levels and do not show
$ O' w0 d" N2 l* p( fpubertal response of gonadotropin after gonadotropin-
) o8 H( m" {4 q, I+ ^0 }. h% ~* Dreleasing hormone stimulation. This is a sex-linked* m+ r- o* m* W
autosomal dominant disorder that affects only
2 Y4 F6 l- J8 d% f8 b- h1 E3 q7 emales; therefore, other male members of the family
2 Q0 I! r5 I: f; ~8 Xmay have similar precocious puberty.3, e. R1 v# f. A! f. S
In our patient, physical examination was incon-! o' G1 ~. S0 Y, M5 I  C# m/ z) m
sistent with true precocious puberty since his testi-! d& g' m  t7 J, x7 y( R
cles were prepubertal in size. However, testotoxicosis
5 c2 d2 w$ {- a: Rwas in the differential diagnosis because his father) b5 W+ P" u# r$ t5 q. F2 j$ B
started puberty somewhat early, and occasionally,: m  i, ^/ D4 l- d% A
testicular enlargement is not that evident in the
4 V3 U- T" H3 w3 l! Pbeginning of this process.1 In the absence of a neg-8 e/ U$ Y" X+ h
ative initial history of androgen exposure, our" \- Z( O% `# n2 ~
biggest concern was virilizing adrenal hyperplasia,
9 t( T# q/ P6 y0 t- `7 Zeither 21-hydroxylase deficiency or 11-β hydroxylase
/ J& B. V- c0 G5 Kdeficiency. Those diagnoses were excluded by find-
  g" }  ?$ q, U  o( Ling the normal level of adrenal steroids.# J9 ]1 Q' k4 J4 r' \! T
The diagnosis of exogenous androgens was strongly# f# Q2 T, ]  f5 v) E, C" C
suspected in a follow-up visit after 4 months because7 K$ _: e& U- Z  x6 X
the physical examination revealed the complete disap-$ L+ O6 _4 b$ j% q2 E+ C! d* T7 x
pearance of pubic hair, normal growth velocity, and
) g' e$ \8 P; D2 Q( o9 u6 fdecreased erections. The father admitted using a testos-' C6 r% ^* F, `/ U8 r
terone gel, which he concealed at first visit. He was2 R) ~0 h0 Y  c3 z( L3 c; e5 i
using it rather frequently, twice a day. The Physicians’
2 q. i6 y; n$ C5 e+ J; L: ?( N( BDesk Reference, or package insert of this product, gel or/ a9 c  d3 T, D3 P9 V
cream, cautions about dermal testosterone transfer to, X3 A! B; v; a7 |
unprotected females through direct skin exposure.
! q7 x" C) ^- u5 }$ M# d' D: ^3 r$ tSerum testosterone level was found to be 2 times the' C* H3 N7 ?4 ^! x" B( T8 h9 }" Y
baseline value in those females who were exposed to8 R/ h8 ?6 v8 p( ?  V0 ^
even 15 minutes of direct skin contact with their male+ v1 n* |+ h6 D" t' h5 {
partners.6 However, when a shirt covered the applica-- H4 i0 m7 y3 N6 I9 n8 |
tion site, this testosterone transfer was prevented.- Z  }. w9 J) C* }
Our patient’s testosterone level was 60 ng/mL,3 \; x. D4 v6 N  E
which was clearly high. Some studies suggest that& s' c1 ^1 |: V; ~' i  ~
dermal conversion of testosterone to dihydrotestos-5 Y, Q0 B, O% J, B. m2 \/ q. b
terone, which is a more potent metabolite, is more0 M% o. k( o) c' r. m
active in young children exposed to testosterone7 B; i8 W- p; b. \
exogenously7; however, we did not measure a dihy-
) b# r% B1 t, J* p3 ?' [+ @5 ddrotestosterone level in our patient. In addition to
7 `! {, z0 ^: h% Qvirilization, exposure to exogenous testosterone in
3 D7 z% G: O- ]% J* T( Z- ~; bchildren results in an increase in growth velocity and
7 c% y7 E2 ?5 Z/ {advanced bone age, as seen in our patient.
; U& E5 T. k' X0 p9 x1 OThe long-term effect of androgen exposure during
8 d9 h! V* v4 k  kearly childhood on pubertal development and final
! ~% K& |- v5 V  xadult height are not fully known and always remain
: N- w% [0 d& }1 {a concern. Children treated with short-term testos-
. X* X% @, F& O+ y$ q7 V8 Yterone injection or topical androgen may exhibit some
8 \4 V- c! `  |+ g, a; m# b4 `acceleration of the skeletal maturation; however, after
" F, }$ U& B$ b5 |/ ]cessation of treatment, the rate of bone maturation) @) L$ \% I( _3 H$ \% J
decelerates and gradually returns to normal.8,9
3 G4 H+ _7 ~! V# M* ^There are conflicting reports and controversy- b' g% R" ^, r* x. k) k  q( A
over the effect of early androgen exposure on adult/ f8 d" P# J) I! v/ D! \9 v
penile length.10,11 Some reports suggest subnormal4 H2 X- d3 c+ }6 F( n+ g
adult penile length, apparently because of downreg-
6 i" ^6 y2 r1 V7 Q0 K+ V$ |ulation of androgen receptor number.10,12 However,9 p  H' {2 @, R  Y; z2 y* F( }
Sutherland et al13 did not find a correlation between
2 U/ C/ ]$ d  \+ {* Bchildhood testosterone exposure and reduced adult
. F8 f3 I9 `; m  M! Spenile length in clinical studies.: V0 f+ |( @5 U, Q! B1 n- X
Nonetheless, we do not believe our patient is
; h6 K% o/ _$ E+ c* {( {2 Xgoing to experience any of the untoward effects from) R/ w5 S' ]0 t$ ~' V3 ~0 H9 p
testosterone exposure as mentioned earlier because/ @3 {# }/ |* x# L# N/ v  J
the exposure was not for a prolonged period of time.* [3 J3 l+ C, ~1 U  i
Although the bone age was advanced at the time of
1 h4 F9 j( j" d/ K2 |diagnosis, the child had a normal growth velocity at
% {2 ]' N: \6 t; S5 }! N2 Xthe follow-up visit. It is hoped that his final adult. E5 u2 y7 K5 k1 t; m
height will not be affected.
& i6 t& I  i2 i  ~7 R, s, _Although rarely reported, the widespread avail-% \1 R2 b6 t5 p2 v
ability of androgen products in our society may
+ k3 N1 w9 p1 ~) Q" J, dindeed cause more virilization in male or female
( D+ k* C* c+ P4 cchildren than one would realize. Exposure to andro-
/ G* \2 X6 v$ T1 d% _3 c* sgen products must be considered and specific ques-
6 |9 |' m& F+ c/ n( @6 xtioning about the use of a testosterone product or2 b+ F# V, J8 r0 g5 y& R/ H
gel should be asked of the family members during) ~, z, A! k& I
the evaluation of any children who present with vir-
+ e/ o4 e; U9 @/ d2 vilization or peripheral precocious puberty. The diag-
  i! r) w1 c) Q; U$ `2 b4 Xnosis can be established by just a few tests and by1 C: U8 X* S) m6 k2 v+ |
appropriate history. The inability to obtain such a
* f3 N5 }3 b4 L9 D# i- ehistory, or failure to ask the specific questions, may6 h+ `  W. r/ L9 g, p5 D1 r5 S
result in extensive, unnecessary, and expensive
% [2 D8 c& C8 i7 {$ i& ~! H/ }8 Winvestigation. The primary care physician should be5 X. Y3 k; C  h4 q6 p: r* ~" j
aware of this fact, because most of these children
& D; b5 o+ C& G* bmay initially present in their practice. The Physicians’
0 _" v) B' l  K( C4 rDesk Reference and package insert should also put a0 R- m4 S" w, ]' Z6 O5 Z
warning about the virilizing effect on a male or$ X, ^. [' Y+ n& Z- f) b! t
female child who might come in contact with some-
; B9 g9 M8 h% ^* Pone using any of these products.% ?) g2 p2 k: F) ?) m( {& K) B
References: U# U+ C' R" [5 T4 j
1. Styne DM. The testes: disorder of sexual differentiation
; c( i* E5 |3 f* yand puberty in the male. In: Sperling MA, ed. Pediatric5 I" q9 O. w' B6 L
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;; d/ F% g/ N$ o! A3 h" {
2002: 565-628.& Q/ p' D* H* i: I2 w0 p
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& v; k" a8 h! i  Y7 k# l& V# _puberty in children with tumours of the suprasellar pineal  B# H' r" @4 \( s2 {! T* k2 e
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 S# Y& R# ~4 j; }/ c, M! F
Topical Testosterone Exposure / Bhowmick et al 543' f  ~( c9 _$ Z1 b3 `) w
areas: organic central precocious puberty. Acta Paediatr.1 x1 f7 A  A% |* S: V: m5 c
2001;90:751-756.
2 e8 S% M5 g  j+ h( ?1 z$ G3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
2 P# U. a$ W  y- jPediatric Endocrinology. 4th ed. New York, NY: Marcel
! |- @: y4 `; t* yDekker Inc; 2003:211-238.
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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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