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is a significant concern for physicians. Central
9 w0 i4 T: D+ k( Sprecocious puberty (CPP), which is mediated8 b- D: L1 [4 V: ?* F+ M' P% s- T! Z' G
through the hypothalamic pituitary gonadal axis, has
/ \* e- K7 ^9 F/ x6 va higher incidence of organic central nervous system
% r8 }2 `3 q) \- ]lesions in boys.1,2 Virilization in boys, as manifested5 w; {* o1 H6 o: w  T# z9 ]
by enlargement of the penis, development of pubic, T2 {: ^. @) @8 F
hair, and facial acne without enlargement of testi-
* N! z$ {1 r. zcles, suggests peripheral or pseudopuberty.1-3 We
  s% Z; ]& q: o# [  W1 J+ zreport a 16-month-old boy who presented with the
0 K" Z4 t" v) @) V+ Z4 Q5 r: }+ `8 Xenlargement of the phallus and pubic hair develop-/ e/ \/ y  }4 P
ment without testicular enlargement, which was due# t+ ]- K2 i; r5 c1 G
to the unintentional exposure to androgen gel used by
( o. E& F. I. o6 ~: kthe father. The family initially concealed this infor-
5 A6 u0 p6 ~" [5 h: K& s: amation, resulting in an extensive work-up for this
, o9 Q4 f& n5 u! i- K4 Xchild. Given the widespread and easy availability of
1 W7 @7 o/ O1 ~: |7 q# j! utestosterone gel and cream, we believe this is proba-
) t( s8 g( w. U1 j3 lbly more common than the rare case report in the; e1 I" U6 x3 W+ {9 w8 z
literature.4
" I2 i, g# N: Q  N& @Patient Report  a. S6 ]4 p# W: `+ y* ^( q
A 16-month-old white child was referred to the# x+ C- K$ D& A! R4 d
endocrine clinic by his pediatrician with the concern8 X+ s9 a. {9 x# B; r
of early sexual development. His mother noticed
- e0 @: Y0 v9 Qlight colored pubic hair development when he was. I4 G, [* K/ _# Y9 i
From the 1Division of Pediatric Endocrinology, 2University of( s! |5 d4 x4 ^' N
South Alabama Medical Center, Mobile, Alabama.3 t& y1 m( u( W! N
Address correspondence to: Samar K. Bhowmick, MD, FACE,5 v2 Z6 G, T' `7 P, J0 L/ f
Professor of Pediatrics, University of South Alabama, College of2 Q4 L/ h, F/ }! ^0 [. j/ ~
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. R; J; h! y+ o$ D8 z% U
e-mail: [email protected].
' ], `" T# x) oabout 6 to 7 months old, which progressively became, i/ A9 t- V* j- c1 h
darker. She was also concerned about the enlarge-
' M6 e/ n" @. I$ Zment of his penis and frequent erections. The child
( g6 ?- a& D, f, ^# k1 dwas the product of a full-term normal delivery, with" P  ?' J8 q8 E! U! _
a birth weight of 7 lb 14 oz, and birth length of8 q) @/ l1 Q  S: a. w% {
20 inches. He was breast-fed throughout the first year6 l- w: u- o6 ~" a0 |% b5 Y0 J, L
of life and was still receiving breast milk along with) K! l' H" |2 R0 H7 x- v: p, h
solid food. He had no hospitalizations or surgery,
% w& A. A2 H3 N5 x' ?% vand his psychosocial and psychomotor development
  M6 g7 B5 a9 V6 K" z0 O1 T& Pwas age appropriate.
3 s8 [8 B: G3 S$ U6 q6 BThe family history was remarkable for the father,: e5 W1 O; [7 k& a) D7 Z4 t( d1 w
who was diagnosed with hypothyroidism at age 16,$ ]' j2 f2 B! s  w! K; M/ f- y2 U
which was treated with thyroxine. The father’s
% k9 q4 p4 M  r7 O+ Dheight was 6 feet, and he went through a somewhat. c4 |6 `6 @" }7 }7 S  b+ b* Z
early puberty and had stopped growing by age 14.
8 q1 o: G! h; u5 X3 lThe father denied taking any other medication. The! S$ t) c' W* J6 `8 S: `% {
child’s mother was in good health. Her menarche2 R# J4 g; y/ Q6 `: v: F) U# x7 r
was at 11 years of age, and her height was at 5 feet, e% l% }. m; |' L
5 inches. There was no other family history of pre-0 Y) s  H9 S8 t: M) L% V1 ^
cocious sexual development in the first-degree rela-
8 P, o& e) N$ z2 c( ~0 M" s/ S6 w0 Ftives. There were no siblings.' v! }+ m4 X0 }" [0 f
Physical Examination
. h3 k/ p5 G/ b6 T5 u7 D7 uThe physical examination revealed a very active,
( [* k5 Y4 `" t0 G2 `4 Xplayful, and healthy boy. The vital signs documented# d" u' u6 G3 ~' K  O
a blood pressure of 85/50 mm Hg, his length was
" C: F4 r8 R- E( {' U- H90 cm (>97th percentile), and his weight was 14.4 kg5 f! A; }0 Z# H9 l
(also >97th percentile). The observed yearly growth
4 |1 ]1 W. e: o, C1 g, ^velocity was 30 cm (12 inches). The examination of
( r$ ?0 n4 s" F) P7 _the neck revealed no thyroid enlargement.$ n' v: q3 v8 X6 v
The genitourinary examination was remarkable for! F/ b* q! y1 r* z# ^
enlargement of the penis, with a stretched length of
  y7 c- z+ _+ B" }' n; W8 cm and a width of 2 cm. The glans penis was very well4 y8 U- {/ Y) C* d
developed. The pubic hair was Tanner II, mostly around4 d3 `4 K( T* C' b2 t6 J
5404 r  J6 L4 T4 W& @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, G( H/ _% w$ X) e$ e
the base of the phallus and was dark and curled. The
" z- \6 _2 ]  K. [testicular volume was prepubertal at 2 mL each.
; x. b, P6 E& X/ d4 g7 y# A$ K# |The skin was moist and smooth and somewhat
% O" o7 |" _+ m3 K/ {8 \3 |6 |oily. No axillary hair was noted. There were no4 j; S+ G2 g0 k; ~: W$ _( Y+ Y. q
abnormal skin pigmentations or café-au-lait spots.
3 l3 y7 \( K" P0 ONeurologic evaluation showed deep tendon reflex 2+9 d$ h* @. i& F+ N$ A
bilateral and symmetrical. There was no suggestion
3 h: ]& F4 c5 g5 ^1 P* w+ [% cof papilledema.& P6 }2 Y7 P3 a9 o
Laboratory Evaluation8 a* S- B( z/ K
The bone age was consistent with 28 months by+ _" Q2 C) v% `6 H
using the standard of Greulich and Pyle at a chrono-: f/ S1 x3 l3 F+ ~
logic age of 16 months (advanced).5 Chromosomal. U$ a8 N: m) ^# v7 r
karyotype was 46XY. The thyroid function test" }! D- ?! D2 S$ D# B5 W
showed a free T4 of 1.69 ng/dL, and thyroid stimu-( ^! V* X$ m; s( A2 R6 o4 M
lating hormone level was 1.3 µIU/mL (both normal).$ ~, k8 L0 i* s# z1 Y" c
The concentrations of serum electrolytes, blood
3 n" i# Q2 C8 S' K& I  Q, X3 Murea nitrogen, creatinine, and calcium all were
" f, m  i* ]; _within normal range for his age. The concentration
: D: I: C" k3 k$ ?# {2 @" rof serum 17-hydroxyprogesterone was 16 ng/dL
3 T8 u: Z* ?5 i2 Z3 I: t(normal, 3 to 90 ng/dL), androstenedione was 20
5 F9 S3 t2 a" ^4 |* n# ]4 gng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) N% R0 b3 e) e0 r
terone was 38 ng/dL (normal, 50 to 760 ng/dL),1 @$ T! u7 ~. Y- W/ D  f
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
% m! E1 n3 c& t( d" q  c49ng/dL), 11-desoxycortisol (specific compound S)
8 O2 q4 g' ^: f. twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-$ @8 h% W5 A9 `& @% o3 _1 Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 R2 M' h8 ?7 `  r: G
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; Z  @7 o: Y* E6 Zand β-human chorionic gonadotropin was less than8 x) V: ^  r- E1 h
5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 W& b  e& |8 H2 \& A! T6 mstimulating hormone and leuteinizing hormone" F' [* E8 p' h* f7 ]1 O" w+ a
concentrations were less than 0.05 mIU/mL1 z: K5 j/ Z3 X# V
(prepubertal).
4 X8 y, q! Y# MThe parents were notified about the laboratory
% P1 B6 ^+ U' qresults and were informed that all of the tests were
( w1 b. ~. D9 k8 J( ~( G5 v2 F, unormal except the testosterone level was high. The( h2 W; N6 B% G
follow-up visit was arranged within a few weeks to: J* S. R4 L0 v! ~' ?! T  N% |: M8 w+ N! U
obtain testicular and abdominal sonograms; how-
% M6 @! h! H. p% s  `& q! J. B  oever, the family did not return for 4 months.
2 s9 `0 [9 [% N4 b, FPhysical examination at this time revealed that the
6 A4 o3 C# P  p: v; Gchild had grown 2.5 cm in 4 months and had gained
9 k# p/ r# p* [0 i1 P2 kg of weight. Physical examination remained5 n5 h, L# g; o& O4 p  d3 j
unchanged. Surprisingly, the pubic hair almost com-
  s  F; ~% A# }1 C8 Apletely disappeared except for a few vellous hairs at( O/ o( }) S) W! C' C& r6 U
the base of the phallus. Testicular volume was still 2
& K, u/ {4 G( i" cmL, and the size of the penis remained unchanged.7 `- ?2 ~3 H+ R" b& d8 L
The mother also said that the boy was no longer hav-1 i2 ~5 V* f; l1 W& {7 A1 X
ing frequent erections.) Z1 S; A% k4 G2 `7 D5 {
Both parents were again questioned about use of- D' c8 i: ]4 h. c
any ointment/creams that they may have applied to- T9 _" G. e1 y' ^/ V2 H5 s
the child’s skin. This time the father admitted the8 m& O4 @3 W! g4 I+ \2 |% h
Topical Testosterone Exposure / Bhowmick et al 541' f8 ]! t" h" F$ v; I) N
use of testosterone gel twice daily that he was apply-; ]/ S* t: a1 p3 O" d
ing over his own shoulders, chest, and back area for
( U/ g& C* ^  u( [7 s+ oa year. The father also revealed he was embarrassed: y/ c# r" g3 n, T# E3 x) J
to disclose that he was using a testosterone gel pre-: d: ?0 V9 K  N7 x. o
scribed by his family physician for decreased libido, v( y) E" V7 v/ s. T- ]2 X
secondary to depression.
: u* P: h  O6 w; Q' YThe child slept in the same bed with parents.
# E: f5 D+ f. A7 J2 L; hThe father would hug the baby and hold him on his
  E0 ~& R; {9 y2 f1 k. I3 Lchest for a considerable period of time, causing sig-! u. f5 m5 ~; j% i: c
nificant bare skin contact between baby and father.
$ N. M' C5 D% O9 ~. C; z' XThe father also admitted that after the phone call,
$ p  o+ P: O/ N7 ^: _$ i4 s- E& s7 Xwhen he learned the testosterone level in the baby3 I# N2 {' e2 N4 e6 c: R: x" ?
was high, he then read the product information
. o3 a; c8 P% x# l/ C# q  fpacket and concluded that it was most likely the rea-+ Q* I& d' Y9 O9 D5 z
son for the child’s virilization. At that time, they
& w4 p6 c8 t( T( ^; c  p4 }# Ldecided to put the baby in a separate bed, and the: ~% s% Q) l. `8 i. Z( {/ ?
father was not hugging him with bare skin and had0 E" D% v/ \! J0 G  V1 A$ Y# M( H
been using protective clothing. A repeat testosterone1 N, J  H, K$ h1 S
test was ordered, but the family did not go to the$ P4 K3 w7 \/ S# t' A6 H
laboratory to obtain the test.# G6 s* N; |" g1 }# P
Discussion
# M. q" h: y3 E$ \Precocious puberty in boys is defined as secondary
7 O8 L1 O4 e2 m) _9 v2 W7 k4 csexual development before 9 years of age.1,4) K7 x( S% o/ Q$ l
Precocious puberty is termed as central (true) when
' o" k# Z' Z* P( E, Cit is caused by the premature activation of hypo-
3 f" c0 p0 g( Gthalamic pituitary gonadal axis. CPP is more com-" P; _) N! m* v6 D; p  N$ I
mon in girls than in boys.1,3 Most boys with CPP
1 j- {$ l" }. y1 Rmay have a central nervous system lesion that is
6 M# b9 {! Y1 _5 Kresponsible for the early activation of the hypothal-
  v, n7 j+ T1 O3 n5 Lamic pituitary gonadal axis.1-3 Thus, greater empha-/ `9 C3 Q8 K' }- A* I
sis has been given to neuroradiologic imaging in; A# p- e; a5 @
boys with precocious puberty. In addition to viril-* I9 t7 {: b6 M: @- r
ization, the clinical hallmark of CPP is the symmet-
: G7 w5 ?! X# f5 [  _( Irical testicular growth secondary to stimulation by
( R! h) H6 N7 G: zgonadotropins.1,37 f2 W1 Q2 {. F$ N2 d9 G
Gonadotropin-independent peripheral preco-
" r- D" b( j5 R. ]8 [8 k& w2 Ecious puberty in boys also results from inappropriate1 B, [" u9 E* \, H( B$ u
androgenic stimulation from either endogenous or
$ A% ]1 t* y5 e) Z/ uexogenous sources, nonpituitary gonadotropin stim-8 x( ]5 f* B/ X  M
ulation, and rare activating mutations.3 Virilizing
3 J7 G+ D2 G& Y6 p- Wcongenital adrenal hyperplasia producing excessive8 h. j; D8 g2 K+ A1 \6 H* ^
adrenal androgens is a common cause of precocious8 p5 h& o2 p. A& B! Z% \. z* ~
puberty in boys.3,4
4 J1 |. g" z5 p3 p- _! x  b" \The most common form of congenital adrenal4 g" X. @5 x# e; _: i% d3 d9 g
hyperplasia is the 21-hydroxylase enzyme deficiency.3 S8 h' ~* w3 [7 l1 R
The 11-β hydroxylase deficiency may also result in
3 s- L. N7 J& x7 z: zexcessive adrenal androgen production, and rarely,4 o) H7 s% K; d* g: R5 e; U, ?3 t
an adrenal tumor may also cause adrenal androgen
1 \( w; M# ?9 n9 K0 ~8 p& yexcess.1,3' c7 E; r+ U: g7 x/ p( k4 _
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- Q4 P, R9 G* e& t) Q542 Clinical Pediatrics / Vol. 46, No. 6, July 20071 K0 `, a9 g+ @7 ?( T
A unique entity of male-limited gonadotropin-% k8 ]/ ~. O+ h$ R% O
independent precocious puberty, which is also known+ V. [. v* M# q5 ?: m& `8 V* p
as testotoxicosis, may cause precocious puberty at a" g! Y. E2 P! H* Z* }$ e, p) J
very young age. The physical findings in these boys
. a* j2 G4 ]5 Y# w5 ?! qwith this disorder are full pubertal development,
0 V7 o, H& z- I! H# ~# Nincluding bilateral testicular growth, similar to boys
+ Z, {% z8 {( iwith CPP. The gonadotropin levels in this disorder
1 b/ t' b) _4 T% P. Fare suppressed to prepubertal levels and do not show
: c# P: I! i& a% _pubertal response of gonadotropin after gonadotropin-0 q* y6 d$ `& S; F
releasing hormone stimulation. This is a sex-linked
1 |2 W  F. y* R3 e/ ?autosomal dominant disorder that affects only( f& K3 _* H( v  y
males; therefore, other male members of the family1 w: [- \; q) D- Z
may have similar precocious puberty.3
& l8 s. F) i6 Z' U1 I. nIn our patient, physical examination was incon-
8 a" ]8 o" r+ h' H- P* A8 d1 csistent with true precocious puberty since his testi-9 {/ \0 ?5 }' d5 E1 {
cles were prepubertal in size. However, testotoxicosis
& z7 M5 Z* d' q. l% K: dwas in the differential diagnosis because his father
9 k. a; g$ ~- N( o7 Y1 dstarted puberty somewhat early, and occasionally,
/ h! I3 R8 K  mtesticular enlargement is not that evident in the+ o$ K" l# u  v+ _
beginning of this process.1 In the absence of a neg-8 |4 b# A% r+ v+ P+ f
ative initial history of androgen exposure, our
0 T( t2 y+ s  @; Abiggest concern was virilizing adrenal hyperplasia,
3 i7 o9 L* f9 I) ?: d, [either 21-hydroxylase deficiency or 11-β hydroxylase1 A0 B( e( k. Y
deficiency. Those diagnoses were excluded by find-
2 I  D1 N4 |) ^/ {ing the normal level of adrenal steroids.1 D+ ~7 N* |$ G- S" \, [/ Q9 z3 a
The diagnosis of exogenous androgens was strongly' A& o: x3 a6 I) W! G2 t5 A
suspected in a follow-up visit after 4 months because
: D! ], x7 e  ^: Lthe physical examination revealed the complete disap-
. g; ^4 X- a. Wpearance of pubic hair, normal growth velocity, and, w0 B$ b7 c5 z* g3 ?! S& e& |
decreased erections. The father admitted using a testos-' D* a; n1 L3 S/ I- F% L, a
terone gel, which he concealed at first visit. He was/ P3 U6 g1 g% x! Z/ U+ r) W
using it rather frequently, twice a day. The Physicians’; P( c: t. f5 m6 t' [' f% C. P  @
Desk Reference, or package insert of this product, gel or2 H+ i3 |  C- K4 c. N
cream, cautions about dermal testosterone transfer to
" m6 [9 }5 h. Y1 y- ?0 uunprotected females through direct skin exposure.
4 J- \3 e: k3 e5 ?$ Y. H- l  LSerum testosterone level was found to be 2 times the
+ O/ g+ z8 ?: G+ E  U; Dbaseline value in those females who were exposed to# T: U1 L9 C! l, r
even 15 minutes of direct skin contact with their male( e' O9 m% [8 e% p1 Q5 Y1 X9 Y
partners.6 However, when a shirt covered the applica-
6 M5 t# Y* q, _" D0 q9 [) Ption site, this testosterone transfer was prevented.* Y& u: T" K6 Q- X" P
Our patient’s testosterone level was 60 ng/mL,; w0 W; G% {7 i% c. P
which was clearly high. Some studies suggest that
% F: t/ t7 B+ P. q+ M2 `( h- bdermal conversion of testosterone to dihydrotestos-
; l/ x4 A' Q9 {& P& ?% |2 oterone, which is a more potent metabolite, is more
( F$ R1 C$ X( A, S  m5 \+ s8 [active in young children exposed to testosterone1 ]6 j' J! F4 r* o0 o) C+ l
exogenously7; however, we did not measure a dihy-
! }3 [9 H$ I$ t/ r6 Qdrotestosterone level in our patient. In addition to
. ]0 \2 |" ~6 s5 fvirilization, exposure to exogenous testosterone in
" H" ^* U* u# m& l/ v  fchildren results in an increase in growth velocity and7 B5 t/ X7 I& P' l1 \* s2 k
advanced bone age, as seen in our patient.
, F, f/ p' f) OThe long-term effect of androgen exposure during4 r4 n, x- _+ ~0 P- {8 Y
early childhood on pubertal development and final
  g. w9 k) h4 M, D; Cadult height are not fully known and always remain
2 W1 t$ L! K% J6 |: f! G( u, Wa concern. Children treated with short-term testos-6 [+ \2 G5 t. u/ C% Q1 G
terone injection or topical androgen may exhibit some6 T9 S$ a$ g2 d' E9 o$ E
acceleration of the skeletal maturation; however, after% s# e) a: |! A0 b# p
cessation of treatment, the rate of bone maturation
4 L1 \- Z/ A  t' J% Pdecelerates and gradually returns to normal.8,92 O5 i5 T, s. Q9 b+ a+ ^. J
There are conflicting reports and controversy
  `! B7 Q/ k  J! r  B. d5 ]6 s) xover the effect of early androgen exposure on adult0 Y2 b7 n$ T$ j9 H
penile length.10,11 Some reports suggest subnormal' @8 p, c8 e/ o* A2 s6 [
adult penile length, apparently because of downreg-: a' A/ ^- M, w' U: f4 a
ulation of androgen receptor number.10,12 However,: _( p6 X! R# i; u/ C
Sutherland et al13 did not find a correlation between- }+ j$ z) ^7 M* ?8 k
childhood testosterone exposure and reduced adult
. K; z% p3 Y4 Q/ y$ U- Dpenile length in clinical studies.
" y+ E2 k2 S1 ^" ~( e: q" l$ J& DNonetheless, we do not believe our patient is
' S( w6 A. \1 a4 {going to experience any of the untoward effects from/ n0 o0 V; ^' h: z' D# A
testosterone exposure as mentioned earlier because* T% q. c/ n% |: F$ k+ O4 [
the exposure was not for a prolonged period of time.# E: G1 [, G# t+ U
Although the bone age was advanced at the time of
3 k; m' H& O" o' Z' @diagnosis, the child had a normal growth velocity at
' _9 m. n/ Z2 Q1 Tthe follow-up visit. It is hoped that his final adult
% j% m* ^  I7 K5 D( y  }) d  W/ lheight will not be affected.% I# C+ l% g. v6 W. \3 I
Although rarely reported, the widespread avail-, w& v) @0 r- X' p! g
ability of androgen products in our society may* P, Y* H1 h! x) |
indeed cause more virilization in male or female
! M7 }6 f) q) Tchildren than one would realize. Exposure to andro-
/ J2 K! ?6 J8 t8 tgen products must be considered and specific ques-( Y7 f, B4 x* }2 K+ Y( {
tioning about the use of a testosterone product or& s6 Q/ s# Y9 `
gel should be asked of the family members during
' I6 A  D; X6 l0 }% O" ~& \$ sthe evaluation of any children who present with vir-
  N* f4 j2 a7 N+ b4 ~* Y  W: filization or peripheral precocious puberty. The diag-
9 q( B: Q- V* I7 O8 R5 b6 cnosis can be established by just a few tests and by; U8 u8 L" K% ~
appropriate history. The inability to obtain such a2 b. I7 L/ L+ t$ k3 M) Y1 \
history, or failure to ask the specific questions, may1 T) E8 Z  \$ w6 v+ N( G
result in extensive, unnecessary, and expensive
  a8 I9 V: z  j+ X) U% Linvestigation. The primary care physician should be. ^, l* [% K- `3 R: s
aware of this fact, because most of these children
- G$ c. w/ E. e+ O/ r& I+ ?3 Bmay initially present in their practice. The Physicians’
; z5 S: k* ^' t0 t# }Desk Reference and package insert should also put a; o. Z' ^$ N" g2 G7 e+ S
warning about the virilizing effect on a male or
6 y8 d7 Q- t: T- P$ K: Q% Sfemale child who might come in contact with some-
: a' V" J" `- M1 H: }! W; Y0 {& _one using any of these products., X' `; M, S2 L0 u! ^9 [
References
1 k$ {. N: G, Q6 k1. Styne DM. The testes: disorder of sexual differentiation
/ d; J/ ?1 @1 p/ }and puberty in the male. In: Sperling MA, ed. Pediatric) B4 M5 \8 Y8 V
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 p, t3 k4 R- d6 B8 \2002: 565-628.
0 a3 p" c7 J4 Z' D2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, }$ W# c0 x0 P: q
puberty in children with tumours of the suprasellar pineal9 C" u( L5 ^3 `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ d4 r% Z* h# h4 O6 nTopical Testosterone Exposure / Bhowmick et al 543
* w9 }# a! y8 {3 e5 Pareas: organic central precocious puberty. Acta Paediatr.
0 Q' @" t8 q$ A/ H2001;90:751-756.; g" H& h3 \; s( z% U) W0 |: I
3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
' C/ E* ?9 U  g4 e: l2 |4 M& H3 kPediatric Endocrinology. 4th ed. New York, NY: Marcel
/ s) L3 Q4 `2 u+ h% t7 p7 LDekker Inc; 2003:211-238." }7 q, q+ z1 |
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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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