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is a significant concern for physicians. Central
! \, ^5 k3 Y) _0 k3 A! B8 _precocious puberty (CPP), which is mediated6 D/ R6 u: c$ j0 E: U" J- U
through the hypothalamic pituitary gonadal axis, has2 x* U1 A: m- p! j0 Z
a higher incidence of organic central nervous system* Y6 F4 V1 ^9 |5 v
lesions in boys.1,2 Virilization in boys, as manifested
: I! u. M- O: y. y; cby enlargement of the penis, development of pubic
# J4 j5 c/ b" |: thair, and facial acne without enlargement of testi-  p, Q8 g4 h, O
cles, suggests peripheral or pseudopuberty.1-3 We" f- |! w; S0 C: M2 G3 u, `3 z" \
report a 16-month-old boy who presented with the, z. U3 A9 O1 [2 |+ I2 n
enlargement of the phallus and pubic hair develop-
6 m: M1 A0 e$ Ument without testicular enlargement, which was due& \2 L& w' w& b: X0 ^4 ]
to the unintentional exposure to androgen gel used by, g/ q% r' n2 `' z5 q! w
the father. The family initially concealed this infor-; M: r3 V7 d$ G0 x9 J, g
mation, resulting in an extensive work-up for this
! D! A1 k) I5 @* @" |child. Given the widespread and easy availability of/ s9 e. @# h# _/ w1 f
testosterone gel and cream, we believe this is proba-2 A% o8 S- f8 ]
bly more common than the rare case report in the
& `2 R/ a3 N, z/ @literature.4( {* [( N. @  \5 ]
Patient Report2 [  d% d: }" S* Y8 S2 m& p
A 16-month-old white child was referred to the  c3 d' n/ c# ]( k+ @
endocrine clinic by his pediatrician with the concern2 B$ _6 s; Q4 ]# ?- J/ m3 }
of early sexual development. His mother noticed! [6 ]7 t% _( [5 u9 u
light colored pubic hair development when he was
; C' N+ e8 ~% P! z: k4 KFrom the 1Division of Pediatric Endocrinology, 2University of) E9 I* X" k( O7 s# |  I% b" E. y% T
South Alabama Medical Center, Mobile, Alabama.
; h5 k4 o. A( {& p3 ]7 g% G- PAddress correspondence to: Samar K. Bhowmick, MD, FACE,
' D$ v* H7 D' d6 Q' e8 ], s; hProfessor of Pediatrics, University of South Alabama, College of
; V; M9 ?3 R6 }( A/ RMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( Y3 @# @7 v& |
e-mail: [email protected].& u. B5 M# s- A" {. ]2 b7 P
about 6 to 7 months old, which progressively became1 \, b7 T- A0 v+ t* U/ t$ o
darker. She was also concerned about the enlarge-/ p' L. a# u' o8 g2 i- j3 n
ment of his penis and frequent erections. The child
  U* T( C  k  Y! W# Lwas the product of a full-term normal delivery, with
! R7 S0 `! g! }* g9 p# ka birth weight of 7 lb 14 oz, and birth length of
4 c; n+ ]/ P# O+ e; c5 ~0 W" O20 inches. He was breast-fed throughout the first year
: v0 ^6 I# v& {of life and was still receiving breast milk along with+ U  q7 r6 v6 ~  t- i" W
solid food. He had no hospitalizations or surgery,) H. z+ z) q5 I( t4 l! Z
and his psychosocial and psychomotor development+ R8 z6 q0 k' Y2 w6 I7 J
was age appropriate.
' ]+ B) v9 u- Q! uThe family history was remarkable for the father,
0 K8 g4 _1 O' {' r. q! q0 ^who was diagnosed with hypothyroidism at age 16,
( ?0 {. Y( t5 n, P) e( pwhich was treated with thyroxine. The father’s
& y; T- Q* K5 G+ zheight was 6 feet, and he went through a somewhat% A+ t' V. |6 C7 K) @
early puberty and had stopped growing by age 14.4 Z" q- h/ [% U
The father denied taking any other medication. The
% g4 O8 E6 [- K' J, U; Gchild’s mother was in good health. Her menarche; F1 L3 q4 a4 b! F% X# a
was at 11 years of age, and her height was at 5 feet
2 t! h  K* n1 t5 inches. There was no other family history of pre-
; h1 P0 [: X  X5 T$ c1 M& v% X6 rcocious sexual development in the first-degree rela-
$ ?% x4 A4 w, A- G. Rtives. There were no siblings.% w& H8 ^4 H0 Z& _
Physical Examination- M7 Z0 Y4 X1 h' K+ B5 u* i2 G
The physical examination revealed a very active,
; [' @& N  _& a! r& k( jplayful, and healthy boy. The vital signs documented# [# S- W- J. B' ~. K
a blood pressure of 85/50 mm Hg, his length was
: o$ E4 ~7 [3 r! M90 cm (>97th percentile), and his weight was 14.4 kg
2 m4 E  e  @% C4 u) m/ A, p(also >97th percentile). The observed yearly growth  |' |: Z9 Z+ z- B
velocity was 30 cm (12 inches). The examination of# l0 Z+ J6 `& Z* [; A
the neck revealed no thyroid enlargement.9 n  P9 o  X. }- O5 H, A+ \
The genitourinary examination was remarkable for% ~& i, _3 H' d: E
enlargement of the penis, with a stretched length of
& d0 ?# [4 N6 m8 cm and a width of 2 cm. The glans penis was very well9 }, j7 [6 v% x/ P
developed. The pubic hair was Tanner II, mostly around9 z( Q6 u& S! A' v$ s
5405 F5 }# f3 x2 r3 @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 i/ O) p  n0 _* F) h5 R
the base of the phallus and was dark and curled. The6 B! k( P1 f: @; [2 u  A* {
testicular volume was prepubertal at 2 mL each.
! @6 C& @% d3 W2 S6 }% y* i- EThe skin was moist and smooth and somewhat5 y6 f6 i5 R- G3 G9 K3 V
oily. No axillary hair was noted. There were no
" X! h) V1 s9 E7 j; ]' Aabnormal skin pigmentations or café-au-lait spots.) ~+ ~" v3 h& n: t) k# n4 P
Neurologic evaluation showed deep tendon reflex 2+. y+ @( V* i  Z3 c! x
bilateral and symmetrical. There was no suggestion( T; |6 v' [: k9 a& M8 s3 ]1 r' O
of papilledema.) p+ B6 [) k+ ~( w9 i. [  l6 i+ e
Laboratory Evaluation
* a' b9 w8 c& N( {& kThe bone age was consistent with 28 months by
3 V6 x$ Y' [% q) x' l5 Busing the standard of Greulich and Pyle at a chrono-5 M0 b5 q+ o% `; m" H
logic age of 16 months (advanced).5 Chromosomal6 f' {! \3 h! {: A6 m9 |; r+ Q
karyotype was 46XY. The thyroid function test
0 |+ f2 r- W$ ^9 d4 U, A4 G  oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 P; I7 b; I/ }7 P+ ~lating hormone level was 1.3 µIU/mL (both normal).
+ {5 R+ m9 ^; L: Q7 \6 RThe concentrations of serum electrolytes, blood
1 j" l) n; _" ~' c. p' K/ }" d! O$ |urea nitrogen, creatinine, and calcium all were# M/ c3 r( ^- e5 d% m4 F
within normal range for his age. The concentration
- t1 E: ~" n4 L6 C1 v3 uof serum 17-hydroxyprogesterone was 16 ng/dL: \, i6 V$ }- N; G! ^5 C
(normal, 3 to 90 ng/dL), androstenedione was 20$ J- \# q8 X# G8 v4 ?5 h! h0 l
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 p8 |. n; @4 T3 h: H3 o, D- tterone was 38 ng/dL (normal, 50 to 760 ng/dL),5 R% M: Z/ t" T; }0 R, L$ `  ]
desoxycorticosterone was 4.3 ng/dL (normal, 7 to. _+ @6 W* b9 g1 B# ?/ A4 `% T! r
49ng/dL), 11-desoxycortisol (specific compound S): F( S8 b" H7 J1 x2 y
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
! _/ `( k4 V8 E" G7 i+ r3 {tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total& g: K) R& F3 P/ v
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 x( d7 }0 W4 x4 Mand β-human chorionic gonadotropin was less than
6 H, J% \7 V7 |4 {/ H" h6 ?5 mIU/mL (normal <5 mIU/mL). Serum follicular# \7 O  }/ p' r  O
stimulating hormone and leuteinizing hormone
. ~, q/ B, T$ L& d3 W& Jconcentrations were less than 0.05 mIU/mL
; ?0 o# @; |0 g, x7 m7 b! i(prepubertal).
9 `; e7 O7 q% ~- Z7 o* JThe parents were notified about the laboratory' K: j; b- F. D" H
results and were informed that all of the tests were  P/ U) r7 X* z7 Q
normal except the testosterone level was high. The& p& Y3 Y  V8 R% ~
follow-up visit was arranged within a few weeks to6 i3 e  G6 m4 U, j, p
obtain testicular and abdominal sonograms; how-$ h6 v& }+ F# A: X& C
ever, the family did not return for 4 months.& ~* a# f! m* D& G% K
Physical examination at this time revealed that the
& L* P+ A! D1 e1 s8 fchild had grown 2.5 cm in 4 months and had gained" n& y' F0 T5 u2 {& C- l
2 kg of weight. Physical examination remained$ u$ X6 l! E; _+ y
unchanged. Surprisingly, the pubic hair almost com-
8 b4 {. L% m4 B5 V1 O/ Zpletely disappeared except for a few vellous hairs at* z, q$ K/ a. L; p' ~. H
the base of the phallus. Testicular volume was still 2$ m" b- E( x! B& k3 n: b
mL, and the size of the penis remained unchanged.7 g4 L2 C1 W: O$ [
The mother also said that the boy was no longer hav-
8 F5 B& K0 G: V% b7 G8 @' Ming frequent erections.
$ d* r  c. [# j! X8 J4 mBoth parents were again questioned about use of
9 c4 _& U6 g2 G& D6 P3 G9 [any ointment/creams that they may have applied to  Q1 w9 T! ^  I1 O2 Y2 \1 v  N
the child’s skin. This time the father admitted the* l! s1 r, {7 f/ g/ c) c
Topical Testosterone Exposure / Bhowmick et al 541
! H$ ^! q3 N  w4 V( buse of testosterone gel twice daily that he was apply-
1 T  K: W) H$ Q- Ring over his own shoulders, chest, and back area for' ?4 W# L( Z) w/ E
a year. The father also revealed he was embarrassed
7 R, {3 o3 @; p4 J& T$ _& zto disclose that he was using a testosterone gel pre-# P" y- F. s3 p( P, `- I
scribed by his family physician for decreased libido" n6 L2 d# _" h; J
secondary to depression.& l% c6 q! H( A" [" u
The child slept in the same bed with parents.1 n/ {8 K3 R7 R" }8 |+ J
The father would hug the baby and hold him on his- r8 w4 [6 K- f# E5 l% F7 z2 b
chest for a considerable period of time, causing sig-
$ Y$ a9 E, y2 r3 ^. Mnificant bare skin contact between baby and father.- K/ Q+ V1 i. j
The father also admitted that after the phone call,
, [# x8 j6 |4 kwhen he learned the testosterone level in the baby
4 o" b+ F; v: M4 K) m" x8 a7 m2 I/ Swas high, he then read the product information
& b  l0 ^8 o( m/ k# K/ bpacket and concluded that it was most likely the rea-0 w' N5 F2 \$ m2 |
son for the child’s virilization. At that time, they5 H6 \# e2 ?* Q+ T& G5 ]
decided to put the baby in a separate bed, and the
4 V5 O1 D6 i7 G1 Q& b3 E. ?- dfather was not hugging him with bare skin and had
5 \+ }5 e7 @" A, O8 S' Q: N1 s8 n. pbeen using protective clothing. A repeat testosterone2 k/ X$ g/ l% U1 J- D
test was ordered, but the family did not go to the" K, F; I  _9 g$ m! t9 e
laboratory to obtain the test.
9 i1 {+ e$ e- W: a& C& i% u* ~, Z3 U# ]; hDiscussion1 _3 {, Y! w% b4 U* M' ?
Precocious puberty in boys is defined as secondary* [1 j  J: f6 H" g
sexual development before 9 years of age.1,4
2 d; [! @) a" ~* E7 oPrecocious puberty is termed as central (true) when
; H- A/ k' E( d% M: Mit is caused by the premature activation of hypo-
+ o) I! h7 z6 cthalamic pituitary gonadal axis. CPP is more com-
! o+ _6 y! O1 xmon in girls than in boys.1,3 Most boys with CPP
4 y0 f( ?7 ~/ c4 ~+ `. j( Qmay have a central nervous system lesion that is
% z5 i' Z; b& g. o* F8 g, Nresponsible for the early activation of the hypothal-
! Q" A" Y7 n2 e. R+ Pamic pituitary gonadal axis.1-3 Thus, greater empha-! j0 f/ `4 n0 {
sis has been given to neuroradiologic imaging in. u0 Q2 U: c1 D+ \
boys with precocious puberty. In addition to viril-
3 ~( N) B0 k/ H+ A6 E( H: Q. yization, the clinical hallmark of CPP is the symmet-
8 j8 N: V4 M7 D! _rical testicular growth secondary to stimulation by
/ C6 k1 j7 y6 i- p+ }gonadotropins.1,3% D* e7 K% s# V! f5 {
Gonadotropin-independent peripheral preco-
' j; i( H  B0 ]' Lcious puberty in boys also results from inappropriate# G0 X& ^6 `$ y* z
androgenic stimulation from either endogenous or6 Q1 R( u5 x: e! s0 }
exogenous sources, nonpituitary gonadotropin stim-) V# d# Z) @# u2 @/ ~0 {  m7 H
ulation, and rare activating mutations.3 Virilizing7 E; }  w% ]; c; U% E) n
congenital adrenal hyperplasia producing excessive( O8 c' x/ w+ J4 X3 [
adrenal androgens is a common cause of precocious% p/ T( c( G. w
puberty in boys.3,4
9 D  ]0 `7 L6 B" S7 {" }The most common form of congenital adrenal) |$ h# R7 \6 X2 v
hyperplasia is the 21-hydroxylase enzyme deficiency.
1 s; ~2 v+ V% |. W% ?The 11-β hydroxylase deficiency may also result in6 j4 c0 f+ u- M) d8 _; l# L& ^2 C
excessive adrenal androgen production, and rarely,
& U1 n: Y/ g  f- v$ zan adrenal tumor may also cause adrenal androgen/ {0 E9 C! p3 r
excess.1,3
' a) o% w# R4 B+ r5 |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) q1 Q- H0 Z/ N. Y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 T. ], J  H0 QA unique entity of male-limited gonadotropin-
* n0 e, ^8 r* v! m& P0 `independent precocious puberty, which is also known* }- H* E8 N% h
as testotoxicosis, may cause precocious puberty at a
* g7 Q6 [# d1 W2 p4 z: q, |. xvery young age. The physical findings in these boys3 ^3 R) h9 s. c' {2 A: a; F8 _# N9 N
with this disorder are full pubertal development,0 A3 d8 v# e4 Q( h( ~! C" g# f
including bilateral testicular growth, similar to boys
1 z/ b3 U0 l/ A- P; ]( r% Twith CPP. The gonadotropin levels in this disorder
2 k9 M( Z9 s+ Q  k2 F: @) `are suppressed to prepubertal levels and do not show
! Y' n; {6 V" c4 h  wpubertal response of gonadotropin after gonadotropin-
! V% v6 o0 Y# [1 P7 G" m$ Ireleasing hormone stimulation. This is a sex-linked+ y+ o( |4 J% [  w% |' O
autosomal dominant disorder that affects only+ `9 u0 {, l; e1 F5 g
males; therefore, other male members of the family7 ?8 t+ D- ^, M3 `
may have similar precocious puberty.3
- T& _+ f" Z  ^% Y) [In our patient, physical examination was incon-' Z* Y* s( m, a8 G2 @8 F2 d' h
sistent with true precocious puberty since his testi-
$ C/ u( j, |9 F& a7 y& Hcles were prepubertal in size. However, testotoxicosis) r" p3 W1 C, `; j# p
was in the differential diagnosis because his father$ x2 T, ]! ]( J# s$ X( T( Q
started puberty somewhat early, and occasionally,6 y: p! r! w' b6 [
testicular enlargement is not that evident in the
7 ]8 d- w; O7 \: r. t$ Q, Mbeginning of this process.1 In the absence of a neg-
( r9 _) |, K0 E* y. a4 f5 [ative initial history of androgen exposure, our
) d- t; l5 k) z& qbiggest concern was virilizing adrenal hyperplasia,3 h; n( |5 A) z5 }( t2 N
either 21-hydroxylase deficiency or 11-β hydroxylase& M1 ]% U5 V2 F" @  g- |: ~
deficiency. Those diagnoses were excluded by find-
( A, h5 a3 `  H( g2 u. |ing the normal level of adrenal steroids.
" @1 I1 z6 w1 RThe diagnosis of exogenous androgens was strongly
0 }# f* v9 B+ }! W6 ssuspected in a follow-up visit after 4 months because% @. z" t% P* R7 c" [' @
the physical examination revealed the complete disap-& `/ y3 @4 c) ~  \6 U' y7 m& R
pearance of pubic hair, normal growth velocity, and' C) B; r' ], h2 k& h; ]
decreased erections. The father admitted using a testos-; a: y6 G  D  @. S. p4 n9 Q
terone gel, which he concealed at first visit. He was
- U7 k2 z& r8 Q8 Z) ousing it rather frequently, twice a day. The Physicians’
- s& ]9 J6 ]( }. f# N  `; YDesk Reference, or package insert of this product, gel or
2 f# `  E- b$ |3 Tcream, cautions about dermal testosterone transfer to# w( `! Q- }, c! S% o
unprotected females through direct skin exposure.
3 i( V  I+ F( p( }* X) fSerum testosterone level was found to be 2 times the
5 r9 H% P: ?; Y. T7 ^; b1 s- Rbaseline value in those females who were exposed to( y  d$ T+ @& g  _! W2 W* t
even 15 minutes of direct skin contact with their male
8 u$ F" x6 j7 z( u5 Y) {) ^6 Qpartners.6 However, when a shirt covered the applica-
0 K/ ?6 x1 s+ U" Y4 X  S4 G5 z- Ption site, this testosterone transfer was prevented.) t: M$ Q; {8 P- j/ ^! |
Our patient’s testosterone level was 60 ng/mL,
6 B- [! X- I( D, Bwhich was clearly high. Some studies suggest that
; e, {! P$ @9 E+ s4 ^, ~7 @dermal conversion of testosterone to dihydrotestos-
) \8 f& A2 D$ Sterone, which is a more potent metabolite, is more
2 H4 \( ?2 Q0 x5 Y4 n3 Uactive in young children exposed to testosterone; }  f+ g, K/ e+ R4 n4 ?
exogenously7; however, we did not measure a dihy-
, o7 ^7 ~# h) l; P0 ~drotestosterone level in our patient. In addition to
+ ?4 u7 g: D: W) v! Gvirilization, exposure to exogenous testosterone in1 S9 f+ r( p5 s% X6 l" f" \) k
children results in an increase in growth velocity and5 ~8 R, D- c: ^. P0 e3 `* N
advanced bone age, as seen in our patient.5 k! a1 ?9 u' F/ O2 o, n& E. y9 V! V
The long-term effect of androgen exposure during/ U- C" k' P7 z
early childhood on pubertal development and final
3 ?1 b6 j* J7 X9 I$ Yadult height are not fully known and always remain7 ^( `  {  _( C5 u: r
a concern. Children treated with short-term testos-
+ S9 h! s& d4 ?( [7 G* `; eterone injection or topical androgen may exhibit some5 q; ]4 ~! J: ~  O7 C
acceleration of the skeletal maturation; however, after7 b# P/ R- t( G/ I) W
cessation of treatment, the rate of bone maturation* J$ ?$ v6 w9 l9 j
decelerates and gradually returns to normal.8,9- T0 Y& P  n6 t8 D& p
There are conflicting reports and controversy
* e6 y: @: u4 i! o2 I8 e* f1 u$ uover the effect of early androgen exposure on adult# n" O, }* [. O  X
penile length.10,11 Some reports suggest subnormal
/ _6 B- [+ O& [# E8 U' wadult penile length, apparently because of downreg-' E% c4 b3 R/ |
ulation of androgen receptor number.10,12 However,
# W2 l' A2 r, `" D0 t3 NSutherland et al13 did not find a correlation between4 b6 Y1 I& M7 _. l1 W
childhood testosterone exposure and reduced adult
9 y6 B1 |+ z7 j: _9 _9 r; Openile length in clinical studies.$ n' Y  E$ E# ]/ F3 P
Nonetheless, we do not believe our patient is
6 F0 K% M! t$ C( p$ U, i: kgoing to experience any of the untoward effects from
: o: u! O' J3 w. Ctestosterone exposure as mentioned earlier because2 G1 f8 @8 O8 Q. y) }0 k
the exposure was not for a prolonged period of time.
- n4 O5 ?0 P) lAlthough the bone age was advanced at the time of
6 E' u" O5 c! E& s( z4 g  kdiagnosis, the child had a normal growth velocity at
' }7 i7 x; n3 X; n# Wthe follow-up visit. It is hoped that his final adult5 C  ]5 `8 M& |- `! i2 _
height will not be affected.
! ]4 I' I: J' c# N( bAlthough rarely reported, the widespread avail-  m+ T9 r  M: s& V$ P- r
ability of androgen products in our society may/ p3 e* B5 Z. ~, R! `$ w# Y3 X
indeed cause more virilization in male or female
' \, B  s7 `' D$ xchildren than one would realize. Exposure to andro-" p7 T+ k5 q: B; g! e5 B
gen products must be considered and specific ques-! y: a" k. ?) O' n& [! o2 H8 M9 t
tioning about the use of a testosterone product or! q) W; K8 {& h
gel should be asked of the family members during
/ ^2 p6 \# N- n9 Z' X8 D' dthe evaluation of any children who present with vir-
8 C% s; W$ W% q$ Bilization or peripheral precocious puberty. The diag-$ Z$ y  S. n6 n
nosis can be established by just a few tests and by5 E( d( q! q( p1 ^
appropriate history. The inability to obtain such a
" T2 {  u3 r+ q, u! ^history, or failure to ask the specific questions, may
5 C! _+ o2 ^. S+ y2 Q8 [3 _result in extensive, unnecessary, and expensive
5 N7 ~: t1 T" X" L  B) {investigation. The primary care physician should be
! K8 I% @9 a' h4 f. Y5 o7 M' I8 @aware of this fact, because most of these children, s% n+ _( j) `$ h& I  l1 a2 L' F
may initially present in their practice. The Physicians’
2 p& n1 _: D- f" pDesk Reference and package insert should also put a
9 I1 n  T( G, y9 t; Ewarning about the virilizing effect on a male or
8 i1 v) F0 k/ ~6 m& k2 m7 qfemale child who might come in contact with some-
' S/ P& j, B5 B; ]6 X- G3 J% z. F. sone using any of these products.- {' x6 e2 o3 d$ h& t
References
& A/ C) y: z# I/ H) s; I1. Styne DM. The testes: disorder of sexual differentiation1 W9 a/ V  l5 g
and puberty in the male. In: Sperling MA, ed. Pediatric
$ d3 s% k: y9 q( f3 ^+ Q! _7 ?' vEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 S0 q- y' s+ s/ X" J2002: 565-628.
- s8 L9 T; {( ~6 o% s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious+ y, l" m. O& e: g8 j% v, F
puberty in children with tumours of the suprasellar pineal: B! ~3 D& f& f8 T: z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( }8 u7 v4 t. N: k, l# E/ |- ?
Topical Testosterone Exposure / Bhowmick et al 543
" Z* U; I1 l0 g: ^. C/ iareas: organic central precocious puberty. Acta Paediatr.0 c" S- L" G8 G. o$ }" P8 N
2001;90:751-756.
) ^. R) E& g0 `/ w2 Q6 o) B2 K3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
+ U) M+ @0 G1 \6 I0 a) i2 W$ N+ nPediatric Endocrinology. 4th ed. New York, NY: Marcel' |: _: x8 w3 M7 V) z8 y3 v" T
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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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