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is a significant concern for physicians. Central/ O$ ]& Q% K) T+ K% `& d* d, f$ |7 C
precocious puberty (CPP), which is mediated+ K1 @1 B; f. K- U8 K) |
through the hypothalamic pituitary gonadal axis, has. l+ h$ o: T. |3 p
a higher incidence of organic central nervous system
: R6 g) e6 g$ l! g' `lesions in boys.1,2 Virilization in boys, as manifested. S  B; {' e* V5 ?" [
by enlargement of the penis, development of pubic
' y% |" i. R. G( khair, and facial acne without enlargement of testi-1 s( }) \6 r% a, J8 d0 u
cles, suggests peripheral or pseudopuberty.1-3 We% {; L5 O4 m, F" q
report a 16-month-old boy who presented with the9 O& f2 ~# R  @# r$ l! z+ W8 c( t  a
enlargement of the phallus and pubic hair develop-
8 ~9 }0 s$ w: y5 }0 G" Tment without testicular enlargement, which was due
+ y" M! j, ~, Y$ gto the unintentional exposure to androgen gel used by) W/ z7 M3 @  V  X  m- V
the father. The family initially concealed this infor-1 c3 R2 o( L; W4 I$ B+ u5 c, e
mation, resulting in an extensive work-up for this+ H  Q- W% k6 Q7 P7 C
child. Given the widespread and easy availability of
* c9 X5 C6 U3 T  i; a  n5 wtestosterone gel and cream, we believe this is proba-. P4 R( S# F* Z: J% T. K% R1 X* m- z
bly more common than the rare case report in the8 S  W" c3 I+ H. x7 d7 _3 j
literature.4; k. b0 S6 i- H) T
Patient Report; e  X/ z' L& q2 A2 {: ~
A 16-month-old white child was referred to the/ g3 X3 Y% F7 @3 L
endocrine clinic by his pediatrician with the concern! Y0 E. a! X5 P1 E+ G
of early sexual development. His mother noticed) M7 x3 v/ s. b5 U+ Y
light colored pubic hair development when he was: _' [. O2 @8 i# K; V$ M
From the 1Division of Pediatric Endocrinology, 2University of0 }  j5 C% N! v2 ~, `" d8 u
South Alabama Medical Center, Mobile, Alabama.! a( l: k0 J# z# ^4 F* J( ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,
3 m1 F3 @3 A0 y- d1 P+ c, S, T, _Professor of Pediatrics, University of South Alabama, College of# y* v8 F5 P9 k3 w
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# j. L: T: K7 Z+ m6 S5 c- me-mail: [email protected].5 ~. a/ Q5 ]* b" @" `/ }( h
about 6 to 7 months old, which progressively became! `5 J# D/ r- o6 `  ]. P0 y8 w
darker. She was also concerned about the enlarge-* B( @2 F  H9 l: c0 B
ment of his penis and frequent erections. The child1 o2 O' Z& B7 {) {% @6 ?2 I1 r
was the product of a full-term normal delivery, with2 x: ^* X0 A$ v; v; A
a birth weight of 7 lb 14 oz, and birth length of7 n4 `; @. Z6 L2 A/ h2 |1 _6 ~
20 inches. He was breast-fed throughout the first year
3 H$ w. \( a' [( G/ Dof life and was still receiving breast milk along with
1 [+ n& {9 t! t$ Qsolid food. He had no hospitalizations or surgery,
+ J5 u8 d. |7 F# land his psychosocial and psychomotor development7 A4 l* _. R7 O5 [) {3 i4 I6 [
was age appropriate.
) K: {: I! v6 }! hThe family history was remarkable for the father,  V" z" \+ n/ b' M' G
who was diagnosed with hypothyroidism at age 16,
" r0 k/ ^- P  u( Rwhich was treated with thyroxine. The father’s# a8 p9 `% E6 T$ q
height was 6 feet, and he went through a somewhat# A) u, ~& |* Q/ B" X% \
early puberty and had stopped growing by age 14.
) Z" U1 _' o8 ?! G" A( A; fThe father denied taking any other medication. The; R% G$ v. ?6 K# \+ H2 V
child’s mother was in good health. Her menarche
% ]7 z5 {( y5 O; qwas at 11 years of age, and her height was at 5 feet
: m$ M) T' U/ n9 Q& B# C5 inches. There was no other family history of pre-
5 e2 i4 |1 N5 v5 w' rcocious sexual development in the first-degree rela-
% O" s& z- u: _) Btives. There were no siblings.8 ^, K/ N# [8 s
Physical Examination
) i+ q2 x; k% n- EThe physical examination revealed a very active,
& [  k- N% n5 \; I6 f2 Nplayful, and healthy boy. The vital signs documented
% ~; s) Z) s% }0 P* oa blood pressure of 85/50 mm Hg, his length was5 X. |4 a% d2 B  e
90 cm (>97th percentile), and his weight was 14.4 kg
/ T1 G( N$ C& K. a6 [(also >97th percentile). The observed yearly growth
; D+ I! d7 I: P0 k! t$ y/ ]velocity was 30 cm (12 inches). The examination of
3 r+ p+ v$ _& Q; A$ sthe neck revealed no thyroid enlargement.+ b! c" V0 v2 t4 d( R
The genitourinary examination was remarkable for1 o7 ]0 j5 y% K5 x! R: P
enlargement of the penis, with a stretched length of
) c/ z/ Q, G* D4 w, {! L8 cm and a width of 2 cm. The glans penis was very well
% g% G  a+ [! C8 D; _' b/ U" |developed. The pubic hair was Tanner II, mostly around" z9 `" s8 y6 E' e6 g6 U9 U
5403 e+ M% V9 Y! M; P/ Z- `! \' W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 C; i3 ?- C. o, ]) w
the base of the phallus and was dark and curled. The- O1 ~1 t* J% q! w
testicular volume was prepubertal at 2 mL each.$ B" o* a9 U; J4 i8 u5 ]" j
The skin was moist and smooth and somewhat
# O) P: ~! e7 ^oily. No axillary hair was noted. There were no
- G8 T* a: d9 }4 H# g& `: |# V% O+ Mabnormal skin pigmentations or café-au-lait spots.7 R7 L0 P, o4 A3 c- y0 x& P
Neurologic evaluation showed deep tendon reflex 2+
3 {4 C* r9 [+ }% ~+ Vbilateral and symmetrical. There was no suggestion7 ^# S. d" Z, p6 R( ^
of papilledema.+ V, _4 r1 t, L' M+ S* y  W
Laboratory Evaluation2 P9 t, A; w  Q
The bone age was consistent with 28 months by
: G' x  g& @5 D" T5 Y# U, U& ~1 cusing the standard of Greulich and Pyle at a chrono-* \, ]; V: v( l0 @
logic age of 16 months (advanced).5 Chromosomal
1 m1 j6 \% q9 X( j. O* `, y0 X. ^karyotype was 46XY. The thyroid function test
, q+ O; q, i4 S+ O9 Xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-4 S7 s' k  l. Y5 \/ }& j6 C- f
lating hormone level was 1.3 µIU/mL (both normal).
; g# n5 D( t: Y+ M* g; w$ MThe concentrations of serum electrolytes, blood6 k2 h# t1 c! k
urea nitrogen, creatinine, and calcium all were
# L% M" i7 Q6 zwithin normal range for his age. The concentration
; a8 H: o/ H8 g  \* v+ D# W5 rof serum 17-hydroxyprogesterone was 16 ng/dL
" d7 F) o, G* @: ^(normal, 3 to 90 ng/dL), androstenedione was 20
, g/ x( M& G* M+ G( U8 ung/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 Z* H6 V" U; Vterone was 38 ng/dL (normal, 50 to 760 ng/dL),
  E4 p" _  E0 t- X9 S( gdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
, E9 f& W, f, a- N" i- k% y49ng/dL), 11-desoxycortisol (specific compound S)
# {, U! j% I( L$ swas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* B3 T: w/ h, W! q$ k0 _( ^2 @# ]tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
6 U$ I7 N) m4 R/ o- Ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
: x% O" S9 l2 {* y% N* G( E* t4 }and β-human chorionic gonadotropin was less than
8 \4 I: [! P% J: z4 I5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 X+ ^  Z3 e5 F4 Q/ p( q1 _stimulating hormone and leuteinizing hormone9 ^5 \8 L0 i5 i
concentrations were less than 0.05 mIU/mL! Z4 G2 _3 e6 U. }4 p; b# B
(prepubertal).
* U/ @0 U7 D) e+ SThe parents were notified about the laboratory
7 z# A1 H8 k- p7 mresults and were informed that all of the tests were
0 q, N, P0 t. j1 J% m2 Xnormal except the testosterone level was high. The
2 j$ J8 R- d7 S1 W  ^follow-up visit was arranged within a few weeks to
: u  ]. U& G# i, N* F$ Yobtain testicular and abdominal sonograms; how-
* G& c- _; p$ h3 |! g2 N6 Rever, the family did not return for 4 months.5 ~, j5 E0 a4 C8 ]  z/ K+ T
Physical examination at this time revealed that the/ M" y- V4 A$ e  _' W! p
child had grown 2.5 cm in 4 months and had gained
/ H8 {4 {" t: H3 z+ j7 ?2 kg of weight. Physical examination remained
- m$ ~6 O  F) i' t% p4 F( q3 Junchanged. Surprisingly, the pubic hair almost com-* q9 `8 w$ q( I: a$ c
pletely disappeared except for a few vellous hairs at8 j" ^5 N/ q+ ~3 u* u
the base of the phallus. Testicular volume was still 2
) o4 c; n! F4 U) W2 B- y/ l6 emL, and the size of the penis remained unchanged.
% H  o4 Q- P0 h* r3 aThe mother also said that the boy was no longer hav-8 o6 v' Z5 ?* j: @, e* e
ing frequent erections.: T( Z; a& Y! e( A$ H9 C" q& }
Both parents were again questioned about use of
- q) q! o& ~( Z$ U, many ointment/creams that they may have applied to. N& N& R2 F! |: ]
the child’s skin. This time the father admitted the: C2 l! e8 c! o+ u
Topical Testosterone Exposure / Bhowmick et al 541' T! |" c# F. i- T7 E& w
use of testosterone gel twice daily that he was apply-+ Q! x) N# G% U3 X
ing over his own shoulders, chest, and back area for
4 i: {/ K( t" y5 f: |/ Oa year. The father also revealed he was embarrassed- z( B0 \, x- ?, J0 J7 _/ V5 W
to disclose that he was using a testosterone gel pre-
4 o. k$ N4 F$ g: F/ yscribed by his family physician for decreased libido  z0 d" W1 z8 B# F
secondary to depression.
1 e" A6 T" L6 k: P. @; SThe child slept in the same bed with parents.
6 h( r, f3 b1 {+ UThe father would hug the baby and hold him on his
. n1 v" v5 h; nchest for a considerable period of time, causing sig-
5 ?! F) O1 j" |nificant bare skin contact between baby and father." x0 m: Z' x7 y6 n- K2 e; W
The father also admitted that after the phone call,! R- z0 H6 s& B, r, h
when he learned the testosterone level in the baby
  y- J' W3 f( g0 E, d% fwas high, he then read the product information- C& U. d/ Y  i
packet and concluded that it was most likely the rea-
6 f$ B  P8 M  Ison for the child’s virilization. At that time, they# U0 v- e6 o! J/ q* ~# I( m# G8 e* I
decided to put the baby in a separate bed, and the
# h$ u, ?5 b; O% N$ H+ Q: Ffather was not hugging him with bare skin and had' q* y0 P/ |$ W' ^8 h8 Y; u
been using protective clothing. A repeat testosterone7 T+ [4 `! D7 S7 z) M: y( Z
test was ordered, but the family did not go to the
- M+ j7 X- P4 c5 w+ glaboratory to obtain the test.
: m, m6 `. {, J, u3 J/ h" CDiscussion# S7 b2 g2 T7 D9 B, W
Precocious puberty in boys is defined as secondary
; @9 c8 \$ E$ H% K! E; h2 @) Tsexual development before 9 years of age.1,4
: U  Z5 U9 W  J% C9 Z$ FPrecocious puberty is termed as central (true) when. x5 D' U  K) v8 D
it is caused by the premature activation of hypo-. b8 p0 k6 D& P( ]- R" U1 T
thalamic pituitary gonadal axis. CPP is more com-! H% C/ i# r, r3 {) w2 f6 `. z+ a$ N( u
mon in girls than in boys.1,3 Most boys with CPP
1 y: t, i2 \) [! A7 m! A7 L! Omay have a central nervous system lesion that is* C' B; a+ @. o: a
responsible for the early activation of the hypothal-
+ I! L& Y0 t# z) g* Damic pituitary gonadal axis.1-3 Thus, greater empha-' T  H, q4 B1 w8 p) x
sis has been given to neuroradiologic imaging in. h8 `; f9 w; b
boys with precocious puberty. In addition to viril-/ b  U! n2 `9 X4 }( o- }
ization, the clinical hallmark of CPP is the symmet-
5 z  M: \5 p  O! w$ P% z# trical testicular growth secondary to stimulation by
% G- g# t! i* z& Ugonadotropins.1,39 ]. _4 J9 _# q+ h0 m% l
Gonadotropin-independent peripheral preco-& ]% W/ I0 u0 F# l
cious puberty in boys also results from inappropriate
2 g1 n& ^# K+ ~* U9 F/ wandrogenic stimulation from either endogenous or
& }  z& }6 @% U: D7 N* n3 ]exogenous sources, nonpituitary gonadotropin stim-
8 R* @# m, k4 @* G$ [9 |( S' qulation, and rare activating mutations.3 Virilizing
3 U2 L/ M# r7 M; ~* c6 zcongenital adrenal hyperplasia producing excessive, I4 X/ ^" x! x+ Q- ]7 d2 K
adrenal androgens is a common cause of precocious
5 Y+ U( K, b- w2 b. qpuberty in boys.3,41 [0 |4 U; Q4 V
The most common form of congenital adrenal
" i! d% x) y/ ]* Jhyperplasia is the 21-hydroxylase enzyme deficiency.
5 }+ E' ?8 ^# r9 }The 11-β hydroxylase deficiency may also result in
* e) i5 U( ~: y9 r9 e* Lexcessive adrenal androgen production, and rarely,
* ?! `* n( Z5 i8 ean adrenal tumor may also cause adrenal androgen
5 O$ C1 a2 x/ p6 sexcess.1,36 b. u3 m( ]% H" U) j+ p
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 ~1 ]7 a! y4 L4 o542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! [& G6 _9 ~# u) ~% S9 N8 ^" bA unique entity of male-limited gonadotropin-) f: s( d, P6 C. {8 G
independent precocious puberty, which is also known
! }. y; T, f* x" i% ]! Q. J/ Ras testotoxicosis, may cause precocious puberty at a, b( [! ~- |  Y$ U4 _# H: k
very young age. The physical findings in these boys; W- C) P$ r8 O6 ^% _: h
with this disorder are full pubertal development,
  _& H. |6 q% p+ h- r6 A2 ?. \including bilateral testicular growth, similar to boys
0 r7 n  K3 Z! k/ ]3 Pwith CPP. The gonadotropin levels in this disorder
) y; J6 q  d0 c) S4 b; A' Hare suppressed to prepubertal levels and do not show
/ p: b9 C6 i5 j# X( t! m, ^pubertal response of gonadotropin after gonadotropin-
# J. k: W/ z. greleasing hormone stimulation. This is a sex-linked
3 ~; S( Q3 y3 x0 Q6 Gautosomal dominant disorder that affects only
/ v  X- O6 \$ C: ?$ emales; therefore, other male members of the family
' R9 _. [* u0 Q' L3 k$ q- c% r3 xmay have similar precocious puberty.3
1 q. Q( n3 N) `( t3 u; c, I# }' |In our patient, physical examination was incon-
0 [# ~; w! c7 O2 M1 O/ c' [( R% o+ Esistent with true precocious puberty since his testi-
/ M0 ]+ r* E4 V8 {cles were prepubertal in size. However, testotoxicosis1 p% {2 J3 [+ V
was in the differential diagnosis because his father
4 o7 P! l  f+ G) Ustarted puberty somewhat early, and occasionally,
: w, ~$ _) V7 ~/ I* h7 ?testicular enlargement is not that evident in the
& ]- O. P- I' L' N1 \beginning of this process.1 In the absence of a neg-
, c5 p; K2 o- D$ Qative initial history of androgen exposure, our
9 \/ o, @2 Z2 _+ i8 A1 Jbiggest concern was virilizing adrenal hyperplasia,
, Q! r8 R( t- b6 E3 T- P$ qeither 21-hydroxylase deficiency or 11-β hydroxylase  \/ l0 W' I! B: B1 T' \5 G6 F
deficiency. Those diagnoses were excluded by find-9 t) t& L/ g- m9 P$ f2 j
ing the normal level of adrenal steroids.
! U( n' _" N7 e; M: o/ w3 uThe diagnosis of exogenous androgens was strongly
% D, i$ l" ]& b) n" K" wsuspected in a follow-up visit after 4 months because
* T. d0 {( u2 F9 W: k+ Tthe physical examination revealed the complete disap-5 D" Y9 U& A8 [, n
pearance of pubic hair, normal growth velocity, and3 G$ I, j8 d0 ]/ a8 M( f
decreased erections. The father admitted using a testos-8 J( Q7 G; U5 B: ]( X2 T
terone gel, which he concealed at first visit. He was: w. q0 S' @. \) o5 T  Z
using it rather frequently, twice a day. The Physicians’
( d( W( P: ?" ~Desk Reference, or package insert of this product, gel or
5 b# D2 r* V8 l3 n$ A. T2 D; Kcream, cautions about dermal testosterone transfer to1 V* o3 g; R( r+ v$ |
unprotected females through direct skin exposure.8 |  ~6 `2 D1 D; Z+ p
Serum testosterone level was found to be 2 times the
+ Y! g) ?0 e# i6 l0 b+ ~, _baseline value in those females who were exposed to. e+ @  y1 h2 w
even 15 minutes of direct skin contact with their male
- `' i. I0 }& _# M# S0 M! \partners.6 However, when a shirt covered the applica-
5 a/ _+ z9 i0 v% a4 V* M" Ution site, this testosterone transfer was prevented.% O& H; j0 V5 k# M5 S
Our patient’s testosterone level was 60 ng/mL,
1 N( f7 }- ^2 e. |- C6 i" C4 q9 nwhich was clearly high. Some studies suggest that
8 D% ~5 G, v6 fdermal conversion of testosterone to dihydrotestos-
/ u( l6 [* f8 Z+ T0 \& p6 uterone, which is a more potent metabolite, is more5 h0 r$ f* d( }' Q8 L& Z4 }
active in young children exposed to testosterone
- g& N: T9 i3 n6 Y2 ]' Hexogenously7; however, we did not measure a dihy-( c# L# Y9 K) Q, M$ `- @: Q! Y
drotestosterone level in our patient. In addition to
3 X/ ]# n. H9 i5 Y/ w  y9 `% Wvirilization, exposure to exogenous testosterone in0 Y4 }* R" D4 [$ l
children results in an increase in growth velocity and
. }/ g8 W# C' b# F+ S" A1 m+ ]( i0 k, Kadvanced bone age, as seen in our patient.4 D$ w4 ~0 _* W* l- D* G, {# W2 d- y
The long-term effect of androgen exposure during. O; @; s: W3 U( R1 H+ c
early childhood on pubertal development and final$ b- x/ I+ X- @
adult height are not fully known and always remain
+ `2 B+ r' E4 H4 w! h- U% ?a concern. Children treated with short-term testos-
! k( N& U. L/ X+ u: U/ u& Gterone injection or topical androgen may exhibit some
3 M1 b5 U/ F% l. |' e9 D7 @acceleration of the skeletal maturation; however, after
$ P5 M7 A: P. ccessation of treatment, the rate of bone maturation
+ A7 E" J5 a, Q3 i. @1 K+ k1 d" Ddecelerates and gradually returns to normal.8,9
7 S3 {) W- G) d3 S& BThere are conflicting reports and controversy
) Q3 x7 i8 F, k: Lover the effect of early androgen exposure on adult" |  h+ v) r+ [
penile length.10,11 Some reports suggest subnormal
2 q  r" C" g  F% v* ^# yadult penile length, apparently because of downreg-
0 Q5 \1 w5 R3 }* D0 n5 v/ lulation of androgen receptor number.10,12 However,2 g6 e, ]4 B3 |/ x
Sutherland et al13 did not find a correlation between
) j! |9 _$ n" C" \5 p; O/ f! Wchildhood testosterone exposure and reduced adult
- L6 {6 R" }" M* jpenile length in clinical studies.# b) ~0 v1 q( A, R
Nonetheless, we do not believe our patient is2 B, R! W( `) h
going to experience any of the untoward effects from0 y& s: t6 Y; y3 x
testosterone exposure as mentioned earlier because
- p, }) `# }  f5 @: Z+ x7 Tthe exposure was not for a prolonged period of time.& ^/ A4 J- n( ]1 p+ }
Although the bone age was advanced at the time of* w1 r2 O% m5 m0 p- K% f
diagnosis, the child had a normal growth velocity at- M& p% |: r) L1 V. y. z
the follow-up visit. It is hoped that his final adult' N$ B) I2 D- q% D
height will not be affected.
; M' i7 g! ?, KAlthough rarely reported, the widespread avail-! }& l! v. f3 Q6 x2 _6 }3 u6 r$ r& U
ability of androgen products in our society may4 i; G& S* }$ g; R# f6 o$ r
indeed cause more virilization in male or female
. d5 r( X; A! @* p. S# }# m8 p; |children than one would realize. Exposure to andro-
/ }, j4 J& x: z( r& sgen products must be considered and specific ques-
. d0 D1 Q1 p! {' G% Ptioning about the use of a testosterone product or5 @  @% z  w( g' e
gel should be asked of the family members during# b2 A  b3 c' I% N
the evaluation of any children who present with vir-) y, J* O9 v. ]/ E
ilization or peripheral precocious puberty. The diag-
1 F" ^) ?% V5 N2 U' b, T- wnosis can be established by just a few tests and by
$ ^+ @( D3 h  H$ F  b7 _appropriate history. The inability to obtain such a1 r9 @) q& B* k- U
history, or failure to ask the specific questions, may
* h* c' p. b0 s% `result in extensive, unnecessary, and expensive0 x: z! i$ O2 k" \7 I
investigation. The primary care physician should be2 J. q+ r8 B% e! I
aware of this fact, because most of these children+ r: r, t/ J1 Z: |) `  u
may initially present in their practice. The Physicians’; f6 m& x! }8 I( k
Desk Reference and package insert should also put a' J% \2 ?9 Z6 ]4 F8 f( X
warning about the virilizing effect on a male or
  ?) L$ [, M3 R4 \4 h4 N* s& }female child who might come in contact with some-0 `) x: t. U9 O1 n1 T) O
one using any of these products.. V: w1 m* t; `1 _* h
References
7 H( h* P9 W% k* P' d1. Styne DM. The testes: disorder of sexual differentiation4 S/ B# c9 O3 w, U% `- F
and puberty in the male. In: Sperling MA, ed. Pediatric
* T5 D5 U) R2 W) M- X9 ?$ AEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* }+ n( J- e/ `( @2 T( ]9 F% n' f2002: 565-628.
3 s0 f& Y9 M$ h3 A0 {2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* {/ {) g3 l/ U9 h9 v5 F, a( v) Mpuberty in children with tumours of the suprasellar pineal& U# N/ s1 ]4 h  [/ a" R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  V. _! S1 Q, l+ B5 P+ e. oTopical Testosterone Exposure / Bhowmick et al 5434 l! \0 f7 W$ o1 T$ g9 q. j6 X
areas: organic central precocious puberty. Acta Paediatr.
# U1 {7 v2 W+ p, S# L5 k) y2001;90:751-756.( `, |/ q3 {! @$ A' D- d3 `  I
3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
' }( U- @3 {) l8 x, C& iPediatric Endocrinology. 4th ed. New York, NY: Marcel
9 c* s/ C- k" s3 l: eDekker Inc; 2003:211-238." S+ V  r5 w3 q, H  W; C
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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!
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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!
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感谢楼主无私分享
 分享同時學會感恩,一句感謝的話語,就是最大的支持!  歡迎交流討論
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