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is a significant concern for physicians. Central
8 t$ L1 h6 n7 z# s( rprecocious puberty (CPP), which is mediated
6 r# t1 s5 ~: B8 @through the hypothalamic pituitary gonadal axis, has
4 |2 U% n: p0 `a higher incidence of organic central nervous system. V6 M4 ^, J5 O' N% e# M3 _6 \
lesions in boys.1,2 Virilization in boys, as manifested- k7 I" t! b4 z* k9 N: ~
by enlargement of the penis, development of pubic
1 x* W$ q) P3 X9 v; q6 Q  q1 bhair, and facial acne without enlargement of testi-5 k5 g0 ?; \: k4 c
cles, suggests peripheral or pseudopuberty.1-3 We% q/ m  F% `) Z- u; d( ]1 \
report a 16-month-old boy who presented with the3 o5 ]- S+ V6 Q& Y
enlargement of the phallus and pubic hair develop-
) F# W: r. C$ H& e1 \% e* zment without testicular enlargement, which was due0 k; r$ Y; g- Q4 v" f# s
to the unintentional exposure to androgen gel used by7 p" |% g% {, t$ D
the father. The family initially concealed this infor-% Y; p) H9 M* W2 o) h" I& j# E
mation, resulting in an extensive work-up for this
; s9 Q' p8 B7 R: }) D( dchild. Given the widespread and easy availability of% i+ z0 ]0 `4 E* Y; u
testosterone gel and cream, we believe this is proba-8 r3 p6 L: d  r3 o# z/ j
bly more common than the rare case report in the5 w3 y2 o; v% N5 [. M2 X
literature.4& a! s" W2 R3 y& |
Patient Report
+ u. v" f+ |$ @" Z1 uA 16-month-old white child was referred to the
$ L5 i6 M8 ?! O: {* [3 q: f7 eendocrine clinic by his pediatrician with the concern
; L9 |. r" ~( B! Z4 mof early sexual development. His mother noticed
$ @2 E6 N. h1 P1 r+ ^3 q4 q, _2 clight colored pubic hair development when he was
+ W: z' I% M% r) qFrom the 1Division of Pediatric Endocrinology, 2University of
! l5 D/ C5 u3 w( l. i5 ]) }# kSouth Alabama Medical Center, Mobile, Alabama.
* D4 Y! @1 f  C2 hAddress correspondence to: Samar K. Bhowmick, MD, FACE,
4 W0 P  U& f# j  S9 \( z7 f4 j9 qProfessor of Pediatrics, University of South Alabama, College of, ~( K, n6 t6 @0 Y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 R+ s! \) s6 G3 k7 |2 E  ye-mail: [email protected].
+ |. x" v) n6 B# f% k; P, b" i' tabout 6 to 7 months old, which progressively became
; O- e3 F* T9 X( Ndarker. She was also concerned about the enlarge-
% U/ j1 w! y9 x! I$ i2 J2 gment of his penis and frequent erections. The child
7 ^* _' r1 Y! p) @$ V9 Xwas the product of a full-term normal delivery, with- L: ?$ E/ b' H! z% L: L9 d* }
a birth weight of 7 lb 14 oz, and birth length of
% S8 `8 E# R* K2 o4 e0 o; j+ u4 \- E20 inches. He was breast-fed throughout the first year2 d/ K, G5 y2 i5 ]
of life and was still receiving breast milk along with% T' }/ y( B8 Y
solid food. He had no hospitalizations or surgery,
$ [% {- p/ U5 A, iand his psychosocial and psychomotor development
+ L' ~- J# f& F7 |was age appropriate.+ H% V. @" ?0 r# F; ~; j6 Q- ?/ L; \
The family history was remarkable for the father,
+ Z9 d4 [+ e  bwho was diagnosed with hypothyroidism at age 16,
8 i( `; u' ~7 |4 s, gwhich was treated with thyroxine. The father’s: U7 e8 A, `/ T* [9 o4 Q
height was 6 feet, and he went through a somewhat& m+ d; E8 I+ J7 N7 v+ y! Q
early puberty and had stopped growing by age 14.
* F! _' n$ [% H! W/ c$ RThe father denied taking any other medication. The
& i* L* y$ |1 `, Pchild’s mother was in good health. Her menarche
, G; g. y2 d+ [9 Mwas at 11 years of age, and her height was at 5 feet
/ t5 ~5 q) `* ~# l, Q8 s* w7 D$ o5 inches. There was no other family history of pre-3 F+ C+ t8 |' v. t9 V, t8 w0 S- D
cocious sexual development in the first-degree rela-
! G% Y0 H; l3 h" R) F0 {tives. There were no siblings.0 }3 R7 n# e4 R: y& w% x
Physical Examination' |3 ~2 X: a1 h4 @* x$ \' O
The physical examination revealed a very active,4 Y5 l  L9 G1 S5 I" @1 _9 N% K
playful, and healthy boy. The vital signs documented
4 p, A( r6 ]5 F3 va blood pressure of 85/50 mm Hg, his length was
7 o$ R( u/ m, d90 cm (>97th percentile), and his weight was 14.4 kg5 |& F: \/ a5 p# T( [: P. u
(also >97th percentile). The observed yearly growth0 d" A) p; R' L6 n
velocity was 30 cm (12 inches). The examination of8 l& f9 {6 \- v2 e7 o. C
the neck revealed no thyroid enlargement.
' }. N# q, @2 k# H# O1 s6 {The genitourinary examination was remarkable for( K2 V+ T. n* P7 a$ ^, H
enlargement of the penis, with a stretched length of
* A  T! `  K2 {: X! B4 U; \8 cm and a width of 2 cm. The glans penis was very well5 C8 E# o. r. i. @" {$ `' p2 i8 \/ y+ @
developed. The pubic hair was Tanner II, mostly around
# d+ x" E0 Y) h7 N. \+ d4 r! V- b3 H5404 ?6 c8 S" U4 E- ]; l; S1 {- G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! G) x& I7 s- C1 _. q/ gthe base of the phallus and was dark and curled. The- K6 i. p9 i3 V
testicular volume was prepubertal at 2 mL each.
& [; D$ q6 m3 d1 _) u- ]6 pThe skin was moist and smooth and somewhat0 ]+ \7 g  ?0 j8 T% ]
oily. No axillary hair was noted. There were no
: l) x) H& F/ |' y$ s# G4 l6 eabnormal skin pigmentations or café-au-lait spots.
9 W, ?5 J2 e7 D3 }' VNeurologic evaluation showed deep tendon reflex 2+
; D- x6 m2 B3 {; z, f- qbilateral and symmetrical. There was no suggestion
; \0 w& c; Q4 |5 J4 qof papilledema.( V# u' o4 b5 ~4 d) E5 C
Laboratory Evaluation& s& [+ G. s8 o9 J  m
The bone age was consistent with 28 months by
5 X& t; j! N! s) n$ `6 u. R! W. ousing the standard of Greulich and Pyle at a chrono-8 C- H3 m) ?; T5 j6 w! V
logic age of 16 months (advanced).5 Chromosomal& w5 `; e& m* |9 v( J. b) |
karyotype was 46XY. The thyroid function test
" j/ a3 x/ i: i3 f( qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 T) l% f2 W+ }8 g7 m8 Zlating hormone level was 1.3 µIU/mL (both normal).% a/ I  X8 l1 c6 ~% u0 {
The concentrations of serum electrolytes, blood, t8 D  K, d7 V' f1 A
urea nitrogen, creatinine, and calcium all were
- W$ t9 H: E+ m) C  t4 N2 r, kwithin normal range for his age. The concentration0 C5 G! ^, K7 `& e1 o2 _
of serum 17-hydroxyprogesterone was 16 ng/dL; R0 D9 M) m% s+ s9 G0 |( H+ r
(normal, 3 to 90 ng/dL), androstenedione was 20& G0 L3 }. @9 M/ Y- A/ H& [7 x" U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, H! r+ w  w% kterone was 38 ng/dL (normal, 50 to 760 ng/dL),+ }  {& l( W# f! j2 t2 J
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ V7 n4 e  w$ g* _# Q# y" J- w; P49ng/dL), 11-desoxycortisol (specific compound S)
7 w$ y  d" t' K: O7 E5 cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 T* Q% P: H3 H/ U: t0 Qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- v' ?; w) u% k' P8 u. r
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
% V5 z5 r; ]+ H9 C1 Oand β-human chorionic gonadotropin was less than2 U) m5 q4 y* Y  T# @: s- t( W8 W% q
5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ B2 y* }+ ~- \! `stimulating hormone and leuteinizing hormone. Y* y, j. D8 U- N* H
concentrations were less than 0.05 mIU/mL
* w3 @& Q& y, S(prepubertal).
$ u$ v0 ^5 e5 G- T: E' ~2 E. gThe parents were notified about the laboratory! K5 n/ U5 }8 x+ K
results and were informed that all of the tests were( T; Y, i5 S' A+ X/ Z" ^+ O
normal except the testosterone level was high. The
2 ~0 K* o" i3 J( d& g5 w8 tfollow-up visit was arranged within a few weeks to1 j! k! f- k1 G+ i- e+ L
obtain testicular and abdominal sonograms; how-
6 C" @. Q& ^4 kever, the family did not return for 4 months.
0 P5 f) S, L; GPhysical examination at this time revealed that the  B3 g. R( G. G" K) I
child had grown 2.5 cm in 4 months and had gained
/ d* F6 Z/ e, l2 ^) ^+ ]4 [3 ^2 kg of weight. Physical examination remained2 Y  h' D4 K$ c: q+ X
unchanged. Surprisingly, the pubic hair almost com-
! C2 T! S' q, O1 p& y6 D4 gpletely disappeared except for a few vellous hairs at
, D8 @# K; t! _the base of the phallus. Testicular volume was still 2
" w, g6 t  P3 o+ h; lmL, and the size of the penis remained unchanged.# c# e: J8 Z, v+ J
The mother also said that the boy was no longer hav-0 l# x4 t" X2 {$ u
ing frequent erections.) ^1 ]6 i, H/ j- g, W) Y- p* v+ D
Both parents were again questioned about use of
  Y3 k2 c" u2 }2 Vany ointment/creams that they may have applied to* G% v6 n  z0 m4 x" }' f
the child’s skin. This time the father admitted the
3 v" Z& C! R/ s, I& zTopical Testosterone Exposure / Bhowmick et al 541/ a6 {" R+ M# {; v
use of testosterone gel twice daily that he was apply-  k. i, @( x- |9 s5 ?6 w
ing over his own shoulders, chest, and back area for- t1 }+ k& @, ?4 ~
a year. The father also revealed he was embarrassed
) f7 ^/ u6 j* S4 r* {  ?to disclose that he was using a testosterone gel pre-
6 m2 n9 K! z( Iscribed by his family physician for decreased libido$ [2 z! E  \8 S( q: F9 f' z. s2 `
secondary to depression.
$ e2 h( B# h$ k1 L, D& UThe child slept in the same bed with parents.$ b& k1 K/ u! \' r+ j/ Z
The father would hug the baby and hold him on his: R; i/ n: l. z. y4 X/ G& D
chest for a considerable period of time, causing sig-
4 |6 q  s0 G" z. z, c9 k  j/ E; K; ~nificant bare skin contact between baby and father.
% \" d: k1 x( j  ]' c; _The father also admitted that after the phone call,
* ?. E6 n0 T& _0 P8 wwhen he learned the testosterone level in the baby( W3 q- F& q! v4 w1 f! M
was high, he then read the product information
+ A. [6 ?- V% ]( T( u7 {+ v. ^packet and concluded that it was most likely the rea-1 U5 H7 o& w: W; C9 Q' J% b
son for the child’s virilization. At that time, they
- r$ f1 L+ g" i$ Pdecided to put the baby in a separate bed, and the6 f1 s* g! B3 S7 t
father was not hugging him with bare skin and had/ _5 t& L" }4 q: ]+ c2 ?/ J
been using protective clothing. A repeat testosterone
8 M- _# h) w4 ]; Y3 h( Atest was ordered, but the family did not go to the5 S( S" a$ ], u$ Z$ B1 a0 c6 r
laboratory to obtain the test.6 Y% ^% m. b, q3 S. B. V. V. @" N1 i
Discussion
' I0 J( u% ~; {8 O. zPrecocious puberty in boys is defined as secondary
' c) Z% B% L8 u+ K% i$ f  O  [3 Usexual development before 9 years of age.1,4/ K$ w0 |' @/ y0 e
Precocious puberty is termed as central (true) when
- a: r( ?) \) }& Q! l+ L5 _: tit is caused by the premature activation of hypo-
' O$ k6 `- Y1 l6 u- s3 e9 tthalamic pituitary gonadal axis. CPP is more com-* T2 ^4 q- t$ U9 y7 G5 a
mon in girls than in boys.1,3 Most boys with CPP7 {" m2 {# Q, b6 q( a/ I
may have a central nervous system lesion that is
: p: j, a/ h, ?  c2 {4 [6 qresponsible for the early activation of the hypothal-
) ^! V  D2 U  t; H0 Samic pituitary gonadal axis.1-3 Thus, greater empha-
* o1 A  a0 |, G( C! G  [) Msis has been given to neuroradiologic imaging in' Q" u; k# y& u  c  E0 R8 _
boys with precocious puberty. In addition to viril-/ ~" n. e1 O/ R! k) R
ization, the clinical hallmark of CPP is the symmet-8 k8 q4 h+ P& c; b5 z! R
rical testicular growth secondary to stimulation by
, A$ ^& I; n4 a  e# a  Sgonadotropins.1,3
( f4 S/ v; L7 R" `) TGonadotropin-independent peripheral preco-9 J: D9 `% l: F9 z: \
cious puberty in boys also results from inappropriate
. [& t5 H4 N1 s2 ^androgenic stimulation from either endogenous or
' }* W3 J$ @* iexogenous sources, nonpituitary gonadotropin stim-/ {' x. W; A% H: q  T
ulation, and rare activating mutations.3 Virilizing
3 D  I9 i. Z1 }: dcongenital adrenal hyperplasia producing excessive
" K# j7 p) x6 T; ]% uadrenal androgens is a common cause of precocious
) S0 D- Y3 @, E4 opuberty in boys.3,4! s: X6 o' Z2 Y* T9 X" D6 Y
The most common form of congenital adrenal! ?/ Z5 g4 C" N" T) Q% V( a
hyperplasia is the 21-hydroxylase enzyme deficiency.+ @7 {% ~( M5 g, g  u
The 11-β hydroxylase deficiency may also result in
5 @5 Y  u) D3 Q: ~" ^' ]: o( Xexcessive adrenal androgen production, and rarely,
8 p# o6 _' q; H% C& L7 y( ?an adrenal tumor may also cause adrenal androgen: j* @% F# Z; z
excess.1,39 U; M/ ]& ^. E3 N* ?+ ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 |( E* o: p. x% ~! h& L* ^
542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 P( |2 t. \( p3 y1 V
A unique entity of male-limited gonadotropin-* d3 r$ Q+ u- I: m/ {) J
independent precocious puberty, which is also known( w% l8 u+ W0 P: W/ ]3 [+ U
as testotoxicosis, may cause precocious puberty at a
" }9 Y4 g2 O% s/ ^; P7 lvery young age. The physical findings in these boys
* O, p/ n5 ^. \, l" x; Dwith this disorder are full pubertal development,# w( o4 `& s  C1 i
including bilateral testicular growth, similar to boys* e3 @+ b0 U! u
with CPP. The gonadotropin levels in this disorder4 ~/ D* Y( I; Q2 z! T, O5 C
are suppressed to prepubertal levels and do not show
9 F4 q, s) M7 ]# Y; B; n- K% lpubertal response of gonadotropin after gonadotropin-
) ?& p8 ]- ?+ @3 g6 Y! Kreleasing hormone stimulation. This is a sex-linked
( Q3 {' h: L. S7 a1 i+ @autosomal dominant disorder that affects only2 S7 g8 V6 n3 b' G# D
males; therefore, other male members of the family
( ]& c9 \0 r5 m. j1 k4 S* imay have similar precocious puberty.30 M/ G1 D( H. y, l
In our patient, physical examination was incon-
- V& N, M, v; U  b# s( l$ S0 M: M7 ysistent with true precocious puberty since his testi-: p7 ?+ T$ a. C, ]% d9 T5 G8 N
cles were prepubertal in size. However, testotoxicosis7 i: N1 U6 H; L1 x3 N
was in the differential diagnosis because his father
. O5 v  a1 J! Z8 O9 R  _3 _; ?started puberty somewhat early, and occasionally,
9 U% f  i9 W( [; z0 O& O% xtesticular enlargement is not that evident in the6 v5 t$ g1 d  f" S) t3 _4 A
beginning of this process.1 In the absence of a neg-- l6 j, f2 }1 T) K8 q# B: u  t
ative initial history of androgen exposure, our& @& P9 Z0 Q" ^' M9 A4 ]
biggest concern was virilizing adrenal hyperplasia,
0 b& {2 |0 z3 e# P0 ^either 21-hydroxylase deficiency or 11-β hydroxylase; l& @. k3 O+ X/ @4 @' S. q
deficiency. Those diagnoses were excluded by find-
% w* C5 J% j: N( U  F" [. @5 m7 f# Xing the normal level of adrenal steroids.
' W7 c* B9 q, r( I& b$ WThe diagnosis of exogenous androgens was strongly
( f2 c; u% J' F" C+ k8 U. ?$ Ysuspected in a follow-up visit after 4 months because
. Z' u# O* X3 W" Z* Lthe physical examination revealed the complete disap-
+ G6 B) l, @; |6 e. P1 npearance of pubic hair, normal growth velocity, and
3 i2 t+ j/ G5 @4 U) P; e! g8 Jdecreased erections. The father admitted using a testos-
" M2 x- I8 W0 d4 d( c# {terone gel, which he concealed at first visit. He was* D1 a% _" C" m# i: Y3 ~1 W9 ?
using it rather frequently, twice a day. The Physicians’0 h& k6 b0 v; X* N+ b" z4 |' B
Desk Reference, or package insert of this product, gel or( L' _/ _$ o9 e# ]& |, O7 K
cream, cautions about dermal testosterone transfer to8 q( t$ p! \5 I: N( _0 q; V7 P
unprotected females through direct skin exposure.
( K" M- {. Y, @Serum testosterone level was found to be 2 times the" l$ ?4 g% j! U9 q
baseline value in those females who were exposed to
7 b: A7 n& t+ v  G+ n. V% meven 15 minutes of direct skin contact with their male$ W, ]( x( n, k. u" e9 \
partners.6 However, when a shirt covered the applica-
; Z1 Z6 Z& {. z# Gtion site, this testosterone transfer was prevented.
7 B3 p6 A! U% u) qOur patient’s testosterone level was 60 ng/mL,
3 W/ u3 R* l: uwhich was clearly high. Some studies suggest that
9 X+ Q; \+ K4 n' S9 d7 e. o6 j) Hdermal conversion of testosterone to dihydrotestos-* ~' e5 ]1 @' N3 R
terone, which is a more potent metabolite, is more! y; ]. c9 X0 r$ W
active in young children exposed to testosterone/ i: O# R* m* I, I: R
exogenously7; however, we did not measure a dihy-
2 h4 |  J- h- v- H4 H7 F; {drotestosterone level in our patient. In addition to* G  l) x2 _  n8 L$ i7 V
virilization, exposure to exogenous testosterone in% U/ s* E6 c( `
children results in an increase in growth velocity and- q$ E1 y* l3 c1 G! u8 r5 A
advanced bone age, as seen in our patient.* V! k# U6 d7 ]
The long-term effect of androgen exposure during* C2 r. K2 E; D! W& g
early childhood on pubertal development and final
. U% F5 j1 R. }4 ~: \% t4 c  ~adult height are not fully known and always remain3 P- N7 f& Y8 t: v1 D; _( s1 T/ b
a concern. Children treated with short-term testos-6 B$ l' R& ]) @: S5 X
terone injection or topical androgen may exhibit some
  g' l; ?8 w. z2 `acceleration of the skeletal maturation; however, after5 O6 V% a1 E6 i' c3 q2 ?4 `+ |
cessation of treatment, the rate of bone maturation
. P# U# u" |' Q; W4 O' t4 i+ Ddecelerates and gradually returns to normal.8,98 n+ T( F" L1 W3 G- w" x! b
There are conflicting reports and controversy
) }: G7 m6 o; K3 M- t) Nover the effect of early androgen exposure on adult9 ]' Y! N* |# E! l0 w0 i! q
penile length.10,11 Some reports suggest subnormal3 {. D8 u& b0 c. y
adult penile length, apparently because of downreg-! N9 ~# y8 ^, C, n2 ^
ulation of androgen receptor number.10,12 However,
$ u  I* i% Q& g2 W  r& U: `7 m$ {Sutherland et al13 did not find a correlation between+ ~; E* \- [( D! A9 G6 I0 P% T- _7 J% z
childhood testosterone exposure and reduced adult  J% e9 ^( l1 G! t
penile length in clinical studies.) g& f: k9 \# j. M# O6 v2 m
Nonetheless, we do not believe our patient is* Y) f% u0 ?' v/ Y. k/ O( x) f
going to experience any of the untoward effects from
; ]7 i1 I6 V" ^/ htestosterone exposure as mentioned earlier because
- f% m$ D- \5 K/ N8 ]the exposure was not for a prolonged period of time.
; I+ Y" {$ d7 d& j4 W% A7 s2 |2 n. \Although the bone age was advanced at the time of8 n  b/ h* a! m
diagnosis, the child had a normal growth velocity at5 x" o# e9 Y& P6 l, r; E
the follow-up visit. It is hoped that his final adult0 X" e# N& W/ C' R* E
height will not be affected.0 @  b5 k8 X$ q1 }3 b
Although rarely reported, the widespread avail-
) f# P% y( v. a& a; a. a, }ability of androgen products in our society may4 o2 G6 n1 U' i, b, \
indeed cause more virilization in male or female7 n* \. l: J1 I$ o2 G
children than one would realize. Exposure to andro-( |! b2 d; b8 P1 z8 M
gen products must be considered and specific ques-
# m- r3 g- U- otioning about the use of a testosterone product or
* V3 f( `9 _5 B- I# d. vgel should be asked of the family members during
# z0 w4 E2 P' c( j0 `the evaluation of any children who present with vir-8 n* c( ]0 w. _+ `8 G0 N& h$ ?
ilization or peripheral precocious puberty. The diag-1 M% n  \. D3 B& ~3 s! {
nosis can be established by just a few tests and by
9 K4 Q; a. ?. H) ~& G; ^( Q9 ^appropriate history. The inability to obtain such a8 `$ l& D3 {5 }, T
history, or failure to ask the specific questions, may) p& [- j: s/ X1 M, n1 _- x- z
result in extensive, unnecessary, and expensive1 R3 k  S7 R- G. d4 A2 X
investigation. The primary care physician should be
+ t+ t( v1 B4 U' A: o3 oaware of this fact, because most of these children
, q( x% x/ b* M0 _may initially present in their practice. The Physicians’
4 P+ v) b! j" R* O9 ^- kDesk Reference and package insert should also put a* ?' j2 g( ^( R; c3 v, t, g
warning about the virilizing effect on a male or
% c: X/ }4 R! D  Q  m/ hfemale child who might come in contact with some-# }2 k3 }9 Z3 @* C7 s% T
one using any of these products.
& d. j! r* {, S: O; Y# hReferences) T* \/ i7 J; N* C5 m0 x" S
1. Styne DM. The testes: disorder of sexual differentiation, n% Y8 R3 ]  s; o, w
and puberty in the male. In: Sperling MA, ed. Pediatric
2 R9 Z4 P% u/ m# H# G* hEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* s% ~+ ]3 {* [' }% {2002: 565-628.
, c: `' h! M; p; V2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 a  N) \# y/ }$ B) Apuberty in children with tumours of the suprasellar pineal
3 l* T. l& H( c! F; U( c# o' Lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( a' M6 p1 V4 ^Topical Testosterone Exposure / Bhowmick et al 5433 j; E" _; O3 Q$ |- Z6 M
areas: organic central precocious puberty. Acta Paediatr.( R$ ~3 O% p# Y% \
2001;90:751-756.; K% P6 M3 Y4 h
3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
; c2 h7 r3 u/ `- O; pPediatric Endocrinology. 4th ed. New York, NY: Marcel
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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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