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Sexual Precocity in a 16-Month-Old3 X9 O) T  c/ q
Boy Induced by Indirect Topical
+ G# r6 l/ O& ~7 FExposure to Testosterone
3 r* F& R# i/ y4 zSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 Z; ]# r" j* i' l6 |( ~! Qand Kenneth R. Rettig, MD1% j' s2 B& j% B
Clinical Pediatrics/ Z/ M! u) w% y  M3 U& G/ j
Volume 46 Number 6
6 d, u' t" \* [% d: d( uJuly 2007 540-543
$ O- K7 A# P( `© 2007 Sage Publications! d' X: Z& p$ O; o" N
10.1177/00099228062966511 z6 j2 D- \% e; o1 A3 u5 g
http://clp.sagepub.com
! E: @  X0 Z/ A3 X: A. u; Y5 `hosted at
2 g5 m% \' I* k* s' \" ?. Phttp://online.sagepub.com
+ @# b3 p% G" Y# p# _/ bPrecocious puberty in boys, central or peripheral,
. Z) ?8 Y) U3 A0 ]" k& Nis a significant concern for physicians. Central0 C1 j7 Q  d9 `0 J& x
precocious puberty (CPP), which is mediated
' h& y0 k+ ^* h, r  R( lthrough the hypothalamic pituitary gonadal axis, has3 D; T  u; A5 Q" X: V# }
a higher incidence of organic central nervous system
- s- \" t7 J; Y, e% ilesions in boys.1,2 Virilization in boys, as manifested! ~+ X" k4 Y& I* o
by enlargement of the penis, development of pubic' @$ B) D" _# f0 x+ X1 \% p
hair, and facial acne without enlargement of testi-, w+ a5 @! X! D* L: x7 K
cles, suggests peripheral or pseudopuberty.1-3 We! Y- U+ `% d* o; C* c
report a 16-month-old boy who presented with the
5 D- X* m; q; }6 ~enlargement of the phallus and pubic hair develop-
$ `  a/ E9 C7 k2 Bment without testicular enlargement, which was due
! I: m# r/ x5 L1 S2 wto the unintentional exposure to androgen gel used by7 G4 W3 N2 k, V" j- _
the father. The family initially concealed this infor-
$ `  j; i/ f# M2 U" ~mation, resulting in an extensive work-up for this5 l% l7 P' m, D/ `# E8 [
child. Given the widespread and easy availability of0 F7 M. d) s, P' y. t
testosterone gel and cream, we believe this is proba-$ L$ k  ?/ @, o+ O
bly more common than the rare case report in the6 ]$ g, K2 @# Y0 Q
literature.4
+ l: S$ y7 O' e! |! j; RPatient Report
- e8 }- r! K8 B2 t% s' \A 16-month-old white child was referred to the6 O/ l0 p4 Q1 U! B, m( ^; y
endocrine clinic by his pediatrician with the concern1 n4 f- q1 H1 n: y: A" ^- H
of early sexual development. His mother noticed
1 B. c  F  m2 D: k4 }+ G9 Zlight colored pubic hair development when he was
  p* ~) T2 V( p+ K4 V' j3 C* b. _From the 1Division of Pediatric Endocrinology, 2University of
0 H9 s# F3 a8 }( N3 c6 a* ~South Alabama Medical Center, Mobile, Alabama.
8 f8 x' }1 @! O& gAddress correspondence to: Samar K. Bhowmick, MD, FACE,# C9 `. t" S; z0 R6 Y, F/ `7 w2 s
Professor of Pediatrics, University of South Alabama, College of0 [) w2 P$ m& {1 K- N
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- }1 b3 B. G8 r. z9 F7 R, a& ^* Oe-mail: [email protected].
2 V5 H6 G8 I# j) S5 ?6 {about 6 to 7 months old, which progressively became
* t2 Y5 v9 p* R! j# Qdarker. She was also concerned about the enlarge-  [3 |# J. n1 B4 Q
ment of his penis and frequent erections. The child
, N$ R: M9 k" N* y5 y: }was the product of a full-term normal delivery, with
5 c1 f* I( k! J/ P1 F: J0 ea birth weight of 7 lb 14 oz, and birth length of
& y  o+ N* Z% U7 F& U, E6 v20 inches. He was breast-fed throughout the first year% L2 A' ]( J( e$ z
of life and was still receiving breast milk along with
8 v8 Y7 L7 O: e5 Ksolid food. He had no hospitalizations or surgery,  q, d  a( U- J, q, |$ r& n2 ~' ~+ `
and his psychosocial and psychomotor development; `3 p( Y! Q5 h
was age appropriate.
) n# b% \+ U2 A: y( HThe family history was remarkable for the father,& O/ o: U0 q. @  o7 S
who was diagnosed with hypothyroidism at age 16,+ j) z! f( I7 m+ R
which was treated with thyroxine. The father’s) Q7 M2 C% D( \) a' q
height was 6 feet, and he went through a somewhat
! [9 T& ^2 N( W- H7 |early puberty and had stopped growing by age 14.
; g. r+ B& O% }2 M& y4 bThe father denied taking any other medication. The+ e7 M' ^% @4 C$ i+ L
child’s mother was in good health. Her menarche* {- {* P% B* N8 L& f" l: M% S
was at 11 years of age, and her height was at 5 feet" y1 s8 @. b1 i
5 inches. There was no other family history of pre-
( f( Z& y9 A$ _  bcocious sexual development in the first-degree rela-% I3 P- [+ v$ l
tives. There were no siblings.
; S9 c0 n$ L1 E! ^# N7 ]7 j1 IPhysical Examination
5 g/ v$ c5 l2 ^4 c- y$ xThe physical examination revealed a very active,$ `/ R3 m: U1 O! T
playful, and healthy boy. The vital signs documented; h& j2 T+ Y8 n$ _; A# H4 q
a blood pressure of 85/50 mm Hg, his length was
) b, s9 g/ d/ L90 cm (>97th percentile), and his weight was 14.4 kg$ a4 M2 I! t% s2 r
(also >97th percentile). The observed yearly growth; v5 n+ ?% h0 f0 ?$ @
velocity was 30 cm (12 inches). The examination of
) T  @7 y, {7 S; Ythe neck revealed no thyroid enlargement.6 I7 M& c6 I) c1 h  U. w  A
The genitourinary examination was remarkable for- l, S' V1 _8 a9 ~! T; f
enlargement of the penis, with a stretched length of
: ^- U7 H+ ^" |8 cm and a width of 2 cm. The glans penis was very well
, X9 @  i" K' @5 p0 u8 e. udeveloped. The pubic hair was Tanner II, mostly around
! k3 H/ y2 v9 O" Q9 ~0 L540
4 e( E  ?( B8 g! Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  @3 n4 F6 Q4 l# l1 G6 U
the base of the phallus and was dark and curled. The2 c, \8 O7 ~* i3 F
testicular volume was prepubertal at 2 mL each.2 S! S3 X4 R+ M! P2 b: f$ O  o
The skin was moist and smooth and somewhat; v' H  A# d. |2 w+ v
oily. No axillary hair was noted. There were no% Y+ e2 v* h" `7 R% _2 F, s9 M% Q
abnormal skin pigmentations or café-au-lait spots.
7 A$ Z5 h1 Y% B1 E% P! n7 INeurologic evaluation showed deep tendon reflex 2+
9 v  b" H0 @+ w" }$ ?4 Q8 T7 ?bilateral and symmetrical. There was no suggestion
- V+ e7 {1 L5 aof papilledema.5 G. L" ?4 U2 _1 j( D
Laboratory Evaluation
" T5 V; U! m$ x, tThe bone age was consistent with 28 months by
* ?/ N4 b' S' j6 gusing the standard of Greulich and Pyle at a chrono-
5 B) N8 n& h, ~+ Q' Nlogic age of 16 months (advanced).5 Chromosomal5 Q( d  ~* `' ?& j" ?
karyotype was 46XY. The thyroid function test) R% M0 R* h7 g5 y% k' N3 i7 }
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 [& @% E2 I) k
lating hormone level was 1.3 µIU/mL (both normal).# x  C3 H& f! M8 s
The concentrations of serum electrolytes, blood, u- y1 r& ?# k- d2 d
urea nitrogen, creatinine, and calcium all were
  E3 C' W! c5 Z$ Y7 M2 e  cwithin normal range for his age. The concentration
% I6 o+ p( H5 Y$ A% }  |' Rof serum 17-hydroxyprogesterone was 16 ng/dL
  _7 V5 s3 @: A7 g(normal, 3 to 90 ng/dL), androstenedione was 20
! K& |# u' u4 Z0 V/ j) n# fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- ~# p: s1 |, |1 t# O' c$ Y: `terone was 38 ng/dL (normal, 50 to 760 ng/dL),
% `5 V7 ]3 A$ Xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 u( n& e* X! M% d$ E  u49ng/dL), 11-desoxycortisol (specific compound S)
! y3 Q. c0 R; r0 r3 N4 k. twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 P7 \, q+ w0 ~: t
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 M2 C" N4 a3 f! Q  d* O9 |
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
- r2 t1 L- ?1 o7 h+ kand β-human chorionic gonadotropin was less than
- o, y( T0 M. L- f7 n  |1 I5 mIU/mL (normal <5 mIU/mL). Serum follicular- C' W" X% K/ n0 q0 a8 r; `
stimulating hormone and leuteinizing hormone3 I# g. T" f8 N7 m* S+ j
concentrations were less than 0.05 mIU/mL
* d& Y1 K/ X1 t% h" [(prepubertal).. U0 s6 Q! p4 T3 F6 M' ^9 J- M8 r
The parents were notified about the laboratory
2 o$ K' k8 I9 X3 uresults and were informed that all of the tests were* {: ?" {2 S/ B' K
normal except the testosterone level was high. The
+ F! q, o% I$ ]# Z8 z, P9 ]5 F7 R/ }follow-up visit was arranged within a few weeks to
; {5 F! ^, L9 Kobtain testicular and abdominal sonograms; how-' ?9 I* f( `/ e( x0 z; u
ever, the family did not return for 4 months.$ H/ Z& U, Y, H# ]8 {% b$ ^
Physical examination at this time revealed that the+ N( M' e* b5 _+ V$ M& ]& k: j
child had grown 2.5 cm in 4 months and had gained0 s! ~0 b% M2 v; x/ k/ O, E
2 kg of weight. Physical examination remained; w! K0 P( m5 i4 w1 k
unchanged. Surprisingly, the pubic hair almost com-+ m& D% [# v% W9 _9 L! k( _* t0 s
pletely disappeared except for a few vellous hairs at
" a& _& @0 L5 W7 J) \$ lthe base of the phallus. Testicular volume was still 2
6 X% v7 ?- [7 wmL, and the size of the penis remained unchanged.
6 T* |, O; ]& Y& o& j- _The mother also said that the boy was no longer hav-0 o) F% ]' N4 q
ing frequent erections.
& B4 b& X& ~( j- l0 g2 x3 FBoth parents were again questioned about use of/ y+ Q, A5 U3 _: X. q  p  k
any ointment/creams that they may have applied to# L9 m" e3 c  l1 k( l6 c  o' `
the child’s skin. This time the father admitted the0 M( o5 v$ m: p% m$ Z( {
Topical Testosterone Exposure / Bhowmick et al 541
7 Y1 N  @  q0 L. ]use of testosterone gel twice daily that he was apply-! \. F7 ~  j+ M/ r5 S
ing over his own shoulders, chest, and back area for& ~. |% H7 z. ^' l
a year. The father also revealed he was embarrassed
+ ]  r+ V3 B' n" x- K. \to disclose that he was using a testosterone gel pre-
; Y, P7 k4 E, E+ z* _scribed by his family physician for decreased libido7 J% k; p5 @+ \& i
secondary to depression.; p4 R1 f3 S! D! ?
The child slept in the same bed with parents.( {% q' H* ]  e( X* |2 @5 B+ w
The father would hug the baby and hold him on his
" w+ d$ N; O8 u9 |chest for a considerable period of time, causing sig-+ D5 d% Z, J2 T: `, u& e0 d6 [- T
nificant bare skin contact between baby and father.3 t2 K( s8 z  P. Y" I, M" x
The father also admitted that after the phone call,
, g- g+ z: Z8 H; mwhen he learned the testosterone level in the baby
2 S0 d; x3 ~. swas high, he then read the product information
# V4 ~: n% Y& D: Tpacket and concluded that it was most likely the rea-1 d" l$ I$ S4 a% [
son for the child’s virilization. At that time, they: a. Q5 [1 B" ?+ X2 g0 z
decided to put the baby in a separate bed, and the% A: n# p% o$ {0 g, A0 j4 ^
father was not hugging him with bare skin and had8 \7 m! Z& c, b8 d: g3 A: a! @
been using protective clothing. A repeat testosterone7 b; N5 g2 R/ ?# G
test was ordered, but the family did not go to the5 M- \7 U, p; C- ]( M; x
laboratory to obtain the test.
+ Y* Y5 ]  S2 ?. r4 t4 BDiscussion- T2 x  T$ `5 a" l- S* }) |/ v
Precocious puberty in boys is defined as secondary
3 G: }, z1 [+ U; R( U. d4 Usexual development before 9 years of age.1,45 x& ~* y, Q4 |4 o
Precocious puberty is termed as central (true) when* A* N) I+ m2 r) ?$ Y* D8 M$ S
it is caused by the premature activation of hypo-; o- A3 V! b5 k2 o. S8 Y
thalamic pituitary gonadal axis. CPP is more com-
4 m9 Y+ ^6 }+ y5 H' K: }7 Mmon in girls than in boys.1,3 Most boys with CPP0 j2 j# `" X" m9 V5 U
may have a central nervous system lesion that is/ X9 @, {$ Z5 H& U  F  y
responsible for the early activation of the hypothal-  o' J- @4 y5 C- F
amic pituitary gonadal axis.1-3 Thus, greater empha-
3 [9 ^9 O  ?) f% {4 E/ Osis has been given to neuroradiologic imaging in
6 S' r  Y8 @( M  e% B! zboys with precocious puberty. In addition to viril-! T# A- [' j& G$ V3 z
ization, the clinical hallmark of CPP is the symmet-
. @" J$ g& d* }2 Vrical testicular growth secondary to stimulation by, V" @) U4 L, P- p- Y
gonadotropins.1,36 Q0 l; A- W4 c9 d1 \
Gonadotropin-independent peripheral preco-
3 `. f# l1 Z; T2 X9 Kcious puberty in boys also results from inappropriate9 @0 l' X) ~$ q1 y$ E4 ?
androgenic stimulation from either endogenous or
( z, i' D0 m$ Uexogenous sources, nonpituitary gonadotropin stim-
! u# V  i1 f$ [; Wulation, and rare activating mutations.3 Virilizing" p! N! }8 X# `" ?
congenital adrenal hyperplasia producing excessive0 r2 F# [9 _; o% m, k
adrenal androgens is a common cause of precocious5 F  }6 T; B7 \( Q& ]/ \
puberty in boys.3,47 O+ A# U1 e& a- A
The most common form of congenital adrenal1 t! d9 {+ i5 D3 W7 }3 |( h
hyperplasia is the 21-hydroxylase enzyme deficiency.- l. j1 N2 F: |$ f& x3 z5 j: Q/ F
The 11-β hydroxylase deficiency may also result in
: M: H/ F& F! v6 a: _5 mexcessive adrenal androgen production, and rarely,
% x- b- T" x, o' R2 Uan adrenal tumor may also cause adrenal androgen: f5 L6 z/ c4 K
excess.1,3: {* [6 t% R- i. l; z4 V. }$ ?
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! Y8 \! L" P2 q% j3 o8 j542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! J- D( m  V% U; b  E
A unique entity of male-limited gonadotropin-
; q( z7 S7 i" v4 ~* B. Yindependent precocious puberty, which is also known  }2 i; x9 @" j* S$ S; _
as testotoxicosis, may cause precocious puberty at a
$ [9 m: O8 z- P& f6 ?: t) @very young age. The physical findings in these boys
2 N/ j$ z; i, i) P# Ywith this disorder are full pubertal development,
$ |7 l4 J' X3 `) Aincluding bilateral testicular growth, similar to boys7 E0 m# B9 n" X9 J/ ]
with CPP. The gonadotropin levels in this disorder7 q6 d7 V/ d/ z, J8 z" f% B7 v& V- B
are suppressed to prepubertal levels and do not show
# Y, @. C! j$ P; E% qpubertal response of gonadotropin after gonadotropin-' M  I& G  H$ f/ u6 n
releasing hormone stimulation. This is a sex-linked- l# t* E% P/ q7 O4 v
autosomal dominant disorder that affects only
3 z, P1 j) Y+ ?( v0 |males; therefore, other male members of the family/ s# U+ O# }1 Q; a/ a
may have similar precocious puberty.3
" Z! }: |& w# S; q& G- f* }In our patient, physical examination was incon-
' y; P! [) `! j$ m8 x0 dsistent with true precocious puberty since his testi-2 }/ j* `5 u$ _, B$ u. D
cles were prepubertal in size. However, testotoxicosis, [7 O4 X  k7 I" C7 ?$ _
was in the differential diagnosis because his father
0 m) `9 K6 |$ r; g: gstarted puberty somewhat early, and occasionally,1 m1 ]  l6 B9 n: q1 D/ v; {
testicular enlargement is not that evident in the. O8 w; q! |- Q. K* ]. x
beginning of this process.1 In the absence of a neg-8 G8 C) g# n8 z9 F, a9 D9 b
ative initial history of androgen exposure, our
; A. _2 c* U4 t7 B1 N+ Nbiggest concern was virilizing adrenal hyperplasia,
4 J. H. U8 Y9 n& [8 u8 L" g9 _either 21-hydroxylase deficiency or 11-β hydroxylase+ @+ {; n+ ]) E; O
deficiency. Those diagnoses were excluded by find-
$ P; x, u1 X9 H4 D8 u. xing the normal level of adrenal steroids.
" z+ r/ E& s1 a% c& c+ TThe diagnosis of exogenous androgens was strongly
: V$ F+ d$ ^0 ]+ b( `" Bsuspected in a follow-up visit after 4 months because
; j/ y. b0 I! {8 W+ Sthe physical examination revealed the complete disap-
2 c, E- ?6 t* g4 U% I1 |! f" tpearance of pubic hair, normal growth velocity, and% i7 x- F4 z$ M' v3 o
decreased erections. The father admitted using a testos-
- u" F7 T- ]; [* I9 \! Kterone gel, which he concealed at first visit. He was
1 q/ D' ^1 }. S$ t' L' [$ _2 L4 qusing it rather frequently, twice a day. The Physicians’& s+ N: _% {7 k
Desk Reference, or package insert of this product, gel or6 k( y7 C$ c1 f8 \+ Q* H
cream, cautions about dermal testosterone transfer to5 x: Q# h1 \' C4 G9 D
unprotected females through direct skin exposure.7 W+ B0 L) c! Y1 t5 C0 B
Serum testosterone level was found to be 2 times the* W+ e1 O1 v  C) ?
baseline value in those females who were exposed to) g# [5 c& K0 {( |
even 15 minutes of direct skin contact with their male
+ l7 c& B9 t+ t: Spartners.6 However, when a shirt covered the applica-
. t. ]1 Y  {# E, U% H4 Qtion site, this testosterone transfer was prevented.
+ R2 a6 H1 T6 t8 M4 V" pOur patient’s testosterone level was 60 ng/mL,$ T8 `. Y$ M! m  }$ c! L6 M9 ]
which was clearly high. Some studies suggest that! O8 Z2 v0 ~: J( r4 I, }; U) M+ u
dermal conversion of testosterone to dihydrotestos-' X  o' J8 W" [7 h' w+ L
terone, which is a more potent metabolite, is more; c: C5 ^; }# p
active in young children exposed to testosterone
$ y& v  y  g$ dexogenously7; however, we did not measure a dihy-
% |& G& \; w7 Odrotestosterone level in our patient. In addition to
* l9 Z$ x$ k1 k* cvirilization, exposure to exogenous testosterone in3 T" A4 h, w3 H) D2 s
children results in an increase in growth velocity and: s+ }/ z8 C* }) {
advanced bone age, as seen in our patient.8 W. w- N+ }; `/ }; {8 |9 I
The long-term effect of androgen exposure during
% K: ]4 a+ R) Q. g/ wearly childhood on pubertal development and final
1 r5 V- |) k5 a, {% xadult height are not fully known and always remain, G1 X, D# D" D: g/ i4 A
a concern. Children treated with short-term testos-7 N) C9 r; w- y6 p2 V
terone injection or topical androgen may exhibit some
* q2 w2 k7 ]7 vacceleration of the skeletal maturation; however, after
9 O& R/ w* x& l! g7 @% zcessation of treatment, the rate of bone maturation
/ Z6 L; Q) k( v6 S$ Ydecelerates and gradually returns to normal.8,9
0 W* [- i3 q* s0 hThere are conflicting reports and controversy
9 M6 s, w. b6 \* m3 w6 yover the effect of early androgen exposure on adult
# I& z8 U3 ?- i% Zpenile length.10,11 Some reports suggest subnormal( P8 e% F( K+ r; t/ P/ u! R; C
adult penile length, apparently because of downreg-  Q) J; F' n2 X- O$ }
ulation of androgen receptor number.10,12 However,
7 W6 w& }# d1 D9 l2 t$ K8 X) TSutherland et al13 did not find a correlation between  H+ N3 T( \' @/ a# b9 D4 Y8 @
childhood testosterone exposure and reduced adult( z0 Y" B; `) |5 z
penile length in clinical studies./ j7 q0 F4 A+ p6 a  E
Nonetheless, we do not believe our patient is! G3 f7 Y- F" {/ c) v
going to experience any of the untoward effects from) a# H0 I, B2 k+ B8 T+ U# H8 O0 }
testosterone exposure as mentioned earlier because
/ U& Z+ r4 D9 c% G# x: r2 F. b8 zthe exposure was not for a prolonged period of time.  I0 ?4 D0 v. P/ N- M
Although the bone age was advanced at the time of! H- K" `0 t* T8 d5 H6 \4 `9 x
diagnosis, the child had a normal growth velocity at5 ]6 t1 a9 L9 @" V6 u( `
the follow-up visit. It is hoped that his final adult
- W7 E* X$ `+ |, J2 Q/ pheight will not be affected.
4 L( W; s5 K6 f- c: h3 OAlthough rarely reported, the widespread avail-- j8 r6 U' `9 F; T
ability of androgen products in our society may- y8 |+ Q4 h# D
indeed cause more virilization in male or female
$ }+ T6 _/ h' i4 b* `children than one would realize. Exposure to andro-8 T9 ^8 O6 ?# F2 U7 i, q2 M
gen products must be considered and specific ques-
, A, w3 c$ g- ?8 W# Q* Ltioning about the use of a testosterone product or
" S5 ?9 @/ ]& k" }. C1 x( Fgel should be asked of the family members during
+ j6 J. M& q; ]+ s1 [; X9 Ythe evaluation of any children who present with vir-
* P4 G; ?' O; J0 ?3 d. y0 ~ilization or peripheral precocious puberty. The diag-% f- X, p% X; w0 `5 F# H
nosis can be established by just a few tests and by8 p7 L1 f8 ~) w, f# c
appropriate history. The inability to obtain such a9 X  S. ~; A  m) N( \
history, or failure to ask the specific questions, may
. T! T8 Q, k- A# q4 ]result in extensive, unnecessary, and expensive/ H: y: Z+ e+ X3 ^- t, \( |5 ]
investigation. The primary care physician should be
7 r, y% ^* G% p9 y; E; x8 q6 F( {aware of this fact, because most of these children
( b' q/ P" r4 ]$ Z+ S5 l% t3 Cmay initially present in their practice. The Physicians’
# h+ c+ A. B  N" ~. mDesk Reference and package insert should also put a5 d. B1 H* G( S! P6 U
warning about the virilizing effect on a male or0 l7 u/ ?% g9 b; y1 f
female child who might come in contact with some-6 c! E: J: R7 c. ^& H
one using any of these products.
' a$ o" P3 V3 N# n; N$ p; X: dReferences4 @" m% Q3 g3 {1 R1 Q' [$ M
1. Styne DM. The testes: disorder of sexual differentiation
( f" ]/ q2 y3 y9 G" aand puberty in the male. In: Sperling MA, ed. Pediatric# w( ]$ m/ o5 ~
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 P: P2 u' J1 ?7 `
2002: 565-628.
$ e) S3 H3 `$ A" E2 y5 k, u2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 L& t6 D9 u3 {! w: w% _puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
1 Y8 x" t2 d4 c# vBoy Induced by Indirect Topical
, V6 ^8 u! ^# eExposure to Testosterone
- t7 H! z: i" J. A0 _Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( W- G0 R6 D& ~- ]3 p- C
and Kenneth R. Rettig, MD1* h, O7 s1 Z4 u' ?, ^: _5 y# @
Clinical Pediatrics
7 M1 E1 E; R* j. f1 L$ W, FVolume 46 Number 6
7 [. R# D5 U* y2 {July 2007 540-543
" Q1 X% P5 H# L  p7 |' l# R; v© 2007 Sage Publications9 ?; }9 _9 b' x  s3 b% Y% d6 ]! z
10.1177/00099228062966519 s# b7 ~9 w, L# L1 o
http://clp.sagepub.com
4 ?0 A( o9 O  I6 }& |hosted at
& K* t9 Z3 a( ~http://online.sagepub.com5 V& _2 ]4 ?5 j
Precocious puberty in boys, central or peripheral,- t0 ]$ K, j. E" U
is a significant concern for physicians. Central* D8 L* i, W8 k3 P8 y2 [' r
precocious puberty (CPP), which is mediated
) @  w* q+ ~$ g& K: ]& i% Ethrough the hypothalamic pituitary gonadal axis, has
: z8 E( t, I$ v0 y& P+ ya higher incidence of organic central nervous system
) o4 v8 R9 }* \+ Z( ~6 [) ~lesions in boys.1,2 Virilization in boys, as manifested
: Z- u/ c  r7 Y; nby enlargement of the penis, development of pubic
2 ^% h: M2 i1 H- x% lhair, and facial acne without enlargement of testi-
5 N" C$ X& E2 |9 f) p, Pcles, suggests peripheral or pseudopuberty.1-3 We
/ I  @+ _- d- A; `. @report a 16-month-old boy who presented with the" F8 Z& x! p, j- I
enlargement of the phallus and pubic hair develop-8 y4 o* f2 C" R  Z1 }6 _' t: v/ S
ment without testicular enlargement, which was due
# Z. n. q9 f% Z9 J8 Sto the unintentional exposure to androgen gel used by- ]7 R( c+ ~: l' Z. w
the father. The family initially concealed this infor-
. [4 H5 Q  O: \' n4 p3 I9 ^( o6 Tmation, resulting in an extensive work-up for this
. {. Y/ h' W. k" S  c- |4 Mchild. Given the widespread and easy availability of! h; L: b0 r  \) K$ \9 w* x
testosterone gel and cream, we believe this is proba-
- A' }% p) k; o+ B* e  Lbly more common than the rare case report in the
7 ]2 u8 e; Z4 N  U, fliterature.4
- P$ I' Y7 s8 \' F1 c1 `: zPatient Report6 t3 W; x$ a  ?0 N2 r$ N
A 16-month-old white child was referred to the5 h( ]# t7 E+ Y" S
endocrine clinic by his pediatrician with the concern0 E# V: o+ n! j7 U% M
of early sexual development. His mother noticed
2 q. j' O" a3 |5 Klight colored pubic hair development when he was6 I, e+ B+ W) n# H4 k: m# K7 A* i8 j
From the 1Division of Pediatric Endocrinology, 2University of
% D, [- V% E) |South Alabama Medical Center, Mobile, Alabama.8 V) O+ A! }. y4 r8 \2 X
Address correspondence to: Samar K. Bhowmick, MD, FACE,5 W' O1 C* d: ~3 K& A
Professor of Pediatrics, University of South Alabama, College of
3 c3 H/ P7 l3 U- B9 D9 WMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;5 F$ l' @6 u3 \
e-mail: [email protected].
' l. [% _1 D$ t5 xabout 6 to 7 months old, which progressively became
. F3 I- A7 Z8 u1 t4 [darker. She was also concerned about the enlarge-" u% b7 ~  ~; m
ment of his penis and frequent erections. The child
. Y0 g- Y9 W& q) Zwas the product of a full-term normal delivery, with- p8 M: i: J& [9 H% H. j6 t' v+ D, x
a birth weight of 7 lb 14 oz, and birth length of' l( s1 w" J6 |. m+ T
20 inches. He was breast-fed throughout the first year. Q6 h+ U+ a, H% v0 W  f8 d3 z( n
of life and was still receiving breast milk along with$ n& k# z% j7 a9 x6 y
solid food. He had no hospitalizations or surgery,) Z) L! ]" a, U- T9 E, j; D/ F
and his psychosocial and psychomotor development4 |( t  E5 |8 B" P% b% E
was age appropriate.
8 b! m' ~, x3 iThe family history was remarkable for the father,7 L! ?7 j" z; J: n& E- a, T& ~
who was diagnosed with hypothyroidism at age 16,8 r! M) ?1 G2 `/ ]5 R% y
which was treated with thyroxine. The father’s' x: z8 D3 g2 F9 t2 R" b) u7 w& p
height was 6 feet, and he went through a somewhat  k: m, n7 M- E( R* W, T
early puberty and had stopped growing by age 14.
5 s9 x, h1 G( T+ H) rThe father denied taking any other medication. The; s; _9 \# P& l. D
child’s mother was in good health. Her menarche% ?7 p8 \" I* ~
was at 11 years of age, and her height was at 5 feet9 S  k, p. ~  b0 T- ?5 o$ N
5 inches. There was no other family history of pre-
2 H7 w+ ^3 ~! \8 d* C: fcocious sexual development in the first-degree rela-' p% q+ C8 V$ A# `3 M# K
tives. There were no siblings.5 X  |* \; W9 _4 {  i. W$ A7 M
Physical Examination3 q, y! L5 ]. ~5 a0 _; z6 b; ?
The physical examination revealed a very active,9 L% y- S4 x  c, M9 U
playful, and healthy boy. The vital signs documented! j7 |7 h5 N( H8 D
a blood pressure of 85/50 mm Hg, his length was
7 {7 ^# t* H% X4 Q90 cm (>97th percentile), and his weight was 14.4 kg( O( K) k% d" d2 t7 a- p
(also >97th percentile). The observed yearly growth. I1 Z8 {' }, ]  R( m: q
velocity was 30 cm (12 inches). The examination of
& |. P6 L' \4 P( |+ O9 h% @8 nthe neck revealed no thyroid enlargement.
* Z+ o& y9 t. N3 I. }$ A* Z7 FThe genitourinary examination was remarkable for5 n3 q) J) k" ?0 l- o
enlargement of the penis, with a stretched length of
# d1 P; R, d! c: k3 N8 cm and a width of 2 cm. The glans penis was very well
5 G$ j. D  Q; A& M# zdeveloped. The pubic hair was Tanner II, mostly around5 S4 n6 Z/ i. {: d
5406 K4 E1 a  j3 y+ G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 |$ O! y8 @0 r: t
the base of the phallus and was dark and curled. The
& N& U; P) @' u8 [+ x! D6 Utesticular volume was prepubertal at 2 mL each.& R/ b" c, e2 e: C
The skin was moist and smooth and somewhat6 i: f; K5 [$ n, a1 \5 S
oily. No axillary hair was noted. There were no
, Z# [, y/ o/ Vabnormal skin pigmentations or café-au-lait spots.
! T; k- h4 a4 h& hNeurologic evaluation showed deep tendon reflex 2+5 a1 X$ f2 }+ k+ i
bilateral and symmetrical. There was no suggestion2 X, E( _$ V2 O
of papilledema.# a7 p. y1 C3 ]( u# l2 f
Laboratory Evaluation
  {1 a+ I& a* T( L3 s. yThe bone age was consistent with 28 months by
2 E% _+ @9 o2 G+ v2 h( V& Jusing the standard of Greulich and Pyle at a chrono-0 \+ P/ {! n, c2 w! y
logic age of 16 months (advanced).5 Chromosomal3 f! ^) w' P! w* r8 x- Z: L
karyotype was 46XY. The thyroid function test
) f* F( N+ |! p8 oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-- t) n. a) C; E3 P
lating hormone level was 1.3 µIU/mL (both normal).! A- f+ T) Y! K9 `
The concentrations of serum electrolytes, blood/ J2 h( D( Y) `7 s$ V$ S, {! e- c8 l
urea nitrogen, creatinine, and calcium all were
4 j& X8 h! O. ^3 r7 E2 owithin normal range for his age. The concentration" e/ B. l6 @+ M6 q9 c( `$ e
of serum 17-hydroxyprogesterone was 16 ng/dL- z' x, d9 M; @/ Q
(normal, 3 to 90 ng/dL), androstenedione was 20
' T6 T0 A+ |* E6 s! Nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
2 j+ m" A9 {2 q1 Y- R* O" Oterone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 a) V, z4 L2 }) r8 [desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 w6 k" S, P' F. O49ng/dL), 11-desoxycortisol (specific compound S)! E  m: N8 m7 _4 e" C
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. m* I" X( H, `8 i* L2 p6 t/ J6 mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- c2 ~) B  ?3 a0 x
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, J  @8 k7 q1 {" A0 j6 l
and β-human chorionic gonadotropin was less than$ C8 ^; `8 ?- G" b- W8 j' D2 y
5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 g, ?; e0 \! T0 Estimulating hormone and leuteinizing hormone! a1 U7 U: h1 h; D( x! l- P
concentrations were less than 0.05 mIU/mL$ f* e, q- D0 w+ U/ B
(prepubertal).: y; Z+ ^( p/ l1 p
The parents were notified about the laboratory: C4 T5 ~- ]( b
results and were informed that all of the tests were
8 m5 U! E6 Z% Z6 Ynormal except the testosterone level was high. The
" K. r1 v! f4 W3 h9 Sfollow-up visit was arranged within a few weeks to
0 Y0 [4 y5 G8 Y  ^: i6 d' vobtain testicular and abdominal sonograms; how-7 @9 V3 G& K' A1 c4 P
ever, the family did not return for 4 months.( ^* z  N$ v/ I) M! k! D8 B
Physical examination at this time revealed that the
" ~' B9 p1 Z# g* D# X, u( ^child had grown 2.5 cm in 4 months and had gained. O- F, E( }# d* k+ `: y
2 kg of weight. Physical examination remained7 ~/ M5 d' v& i9 J8 s# L
unchanged. Surprisingly, the pubic hair almost com-
- |7 \& Z( [+ Q' mpletely disappeared except for a few vellous hairs at
, e9 {# {" S; b. g3 lthe base of the phallus. Testicular volume was still 2
6 M* ?! G' p: ], X: I, {mL, and the size of the penis remained unchanged.
$ Q9 d2 i  [* g+ W+ wThe mother also said that the boy was no longer hav-
0 u% T+ @7 R0 S' K/ xing frequent erections.
: S  W) `! q/ H7 lBoth parents were again questioned about use of" n/ X& b) k  c3 C7 I3 I$ `
any ointment/creams that they may have applied to
- C4 S" \* Y. K8 g0 _% {- Zthe child’s skin. This time the father admitted the. f' v- @4 U# p; r- q
Topical Testosterone Exposure / Bhowmick et al 541) n( V8 H" m$ X' \5 \% E
use of testosterone gel twice daily that he was apply-
$ _% K9 f% U6 y4 m( Q) _ing over his own shoulders, chest, and back area for
* ~& N) L0 L5 C! @# Ha year. The father also revealed he was embarrassed
$ B$ n/ }6 G, u5 F: e+ _3 gto disclose that he was using a testosterone gel pre-4 ^1 _9 A& \! K* J. J; p, K' H# W" t
scribed by his family physician for decreased libido# w5 ~) N7 ?$ E6 O2 Y7 n
secondary to depression.
+ i$ I  t# j2 S; j: bThe child slept in the same bed with parents.& l/ q  k6 D' a% O) {5 \% a- J* x9 r
The father would hug the baby and hold him on his
8 v% e# ?: c  I$ X/ p5 N2 nchest for a considerable period of time, causing sig-* T2 a6 o& B9 ^- a! Q" f6 t
nificant bare skin contact between baby and father.
0 T& x, z$ a: X9 x7 ]The father also admitted that after the phone call,/ Q2 R$ J) d, Y5 U4 e
when he learned the testosterone level in the baby: k, P1 X/ _  x
was high, he then read the product information$ ]4 H+ C, a+ `  r
packet and concluded that it was most likely the rea-2 Z, f/ ^2 @& k( K  C, K
son for the child’s virilization. At that time, they1 l! k3 u* k9 O+ V3 {
decided to put the baby in a separate bed, and the, E# E  T- p9 ?' F0 h' u  z- `
father was not hugging him with bare skin and had
/ J' p9 h9 r% g$ \- v  a* Q0 lbeen using protective clothing. A repeat testosterone
. q( G: O7 b4 u3 A, w: m% I6 Mtest was ordered, but the family did not go to the; A' b1 D' d  |0 X# e
laboratory to obtain the test.
- ]3 H  f& g7 |) r0 ?Discussion* b% e* D! d9 W6 C( h* U
Precocious puberty in boys is defined as secondary
5 F) J& o! u, |; C& osexual development before 9 years of age.1,4
, d/ S* {" U- p! t, V* cPrecocious puberty is termed as central (true) when
5 I. x- \6 h% L# ]+ R$ S: n# {0 Lit is caused by the premature activation of hypo-- L) @/ b3 Y: P/ {2 P5 B
thalamic pituitary gonadal axis. CPP is more com-
; [. d/ [: U# l! k, qmon in girls than in boys.1,3 Most boys with CPP
: ~/ p7 i1 x+ A! V% L1 T8 Fmay have a central nervous system lesion that is6 ^  X, {; o  y% k( s2 ^
responsible for the early activation of the hypothal-. u" W, b: _  }* A* u8 c1 y- t# ]
amic pituitary gonadal axis.1-3 Thus, greater empha-- \  h- k3 a7 n; e* c- y3 f
sis has been given to neuroradiologic imaging in
2 M3 a# B4 M- E4 e$ t3 Tboys with precocious puberty. In addition to viril-8 W: \+ I( |( [& T/ t
ization, the clinical hallmark of CPP is the symmet-
" g9 G# V8 o) ~) p$ Hrical testicular growth secondary to stimulation by3 j6 n% Z0 d; E3 q
gonadotropins.1,30 M# a5 A6 C- X6 t. n( L. Y* ]9 N1 o
Gonadotropin-independent peripheral preco-# d. H0 \+ F0 K: ?; U
cious puberty in boys also results from inappropriate
5 o9 v5 F  y6 J( I3 f4 Nandrogenic stimulation from either endogenous or
# E5 @6 y4 e% z: U; ^exogenous sources, nonpituitary gonadotropin stim-8 \7 A- d, h& A, m
ulation, and rare activating mutations.3 Virilizing+ h) K; p6 U! G1 `. a9 |
congenital adrenal hyperplasia producing excessive% u' Z. n% b: `! v. m; w6 Z
adrenal androgens is a common cause of precocious
* o/ @/ w( ~! \; o, n2 I: @puberty in boys.3,4: N9 @9 I$ ^% f
The most common form of congenital adrenal
6 o3 ?6 T( b+ g9 [  c! w6 A7 dhyperplasia is the 21-hydroxylase enzyme deficiency.7 f! N, V6 f7 |, C( V
The 11-β hydroxylase deficiency may also result in
: M8 |# \# g0 Z5 I5 z9 A" dexcessive adrenal androgen production, and rarely,$ ^5 Q( r2 a5 b  N6 W3 ]
an adrenal tumor may also cause adrenal androgen
& S* O) N$ U- G# N5 \excess.1,3
6 K- ~8 }2 _8 u7 xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) o) F' }8 ]1 X7 w542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& R$ U3 `  U+ H0 G+ R" HA unique entity of male-limited gonadotropin-. \3 y7 C; m# A' i6 K8 b6 T7 k' w
independent precocious puberty, which is also known3 O* M$ }! o) r, `/ J4 e, e; Y
as testotoxicosis, may cause precocious puberty at a& I5 p0 D% A1 L
very young age. The physical findings in these boys" c1 w* g& v) g) j8 o: K: f$ ~
with this disorder are full pubertal development,( M/ I( b% m1 b  o7 g2 K8 v
including bilateral testicular growth, similar to boys5 s4 ]  o1 M2 b8 m/ m
with CPP. The gonadotropin levels in this disorder
( p7 k, K, b! |) V* [  L* hare suppressed to prepubertal levels and do not show
- R  I; j8 U/ ^8 `1 wpubertal response of gonadotropin after gonadotropin-
( V- u: o# a. z+ \" D: _5 jreleasing hormone stimulation. This is a sex-linked) M0 M8 H9 w) E3 J
autosomal dominant disorder that affects only/ ^$ c/ Z' ^; d* l7 y. K* Z
males; therefore, other male members of the family. {! B8 K7 l# t* V# g
may have similar precocious puberty.3
( I& u+ [# |2 W" vIn our patient, physical examination was incon-# h, F' l5 M) b2 D
sistent with true precocious puberty since his testi-
- {' J" h3 ^$ H- V, h8 Ucles were prepubertal in size. However, testotoxicosis
4 U1 Y! G# Y* r1 d$ n( Hwas in the differential diagnosis because his father9 }7 Q$ e& z& W3 Y8 y9 H
started puberty somewhat early, and occasionally,( ^" }, g: a# j8 V- u
testicular enlargement is not that evident in the4 U1 A+ J8 [+ S1 u% S% p! u8 G
beginning of this process.1 In the absence of a neg-6 I# m9 q$ m7 w, @% g+ y
ative initial history of androgen exposure, our, |- K, R3 }4 g; h' c  W, o
biggest concern was virilizing adrenal hyperplasia,- r0 q/ @" K) n. q
either 21-hydroxylase deficiency or 11-β hydroxylase
( d7 \" z4 L( B% F" X, o& G, ddeficiency. Those diagnoses were excluded by find-
6 w( ]' [) g* }4 p: _$ ring the normal level of adrenal steroids.
$ X8 t% L: E1 r4 t3 R4 ?The diagnosis of exogenous androgens was strongly
6 S- r  \; `. b$ ~# P6 tsuspected in a follow-up visit after 4 months because
- _; n, N6 D2 dthe physical examination revealed the complete disap-
/ Y1 \3 l6 `! V) P# N$ Lpearance of pubic hair, normal growth velocity, and4 F* q, ]9 i7 ]6 h$ E; j# x2 f
decreased erections. The father admitted using a testos-6 Q7 ~, o( Y2 }! e* w
terone gel, which he concealed at first visit. He was2 Z+ @8 G8 z- ^+ n" }4 x
using it rather frequently, twice a day. The Physicians’
$ Z2 f- p" w' w, v, P, hDesk Reference, or package insert of this product, gel or
( N0 t) B& |; q5 t% fcream, cautions about dermal testosterone transfer to! I: ~: N; t* t9 J1 n
unprotected females through direct skin exposure.( b2 q: i8 w$ |& _$ C% C+ ]. \: H
Serum testosterone level was found to be 2 times the
$ r0 R2 X& z4 J& obaseline value in those females who were exposed to2 l, |! C" S. f7 c2 {% P
even 15 minutes of direct skin contact with their male
' T' E1 `1 h, W; J( b7 H# r# c6 hpartners.6 However, when a shirt covered the applica-7 e1 ]- {! a$ Y' d* G7 O! B
tion site, this testosterone transfer was prevented.4 B) B8 y& f. O  V5 z7 W
Our patient’s testosterone level was 60 ng/mL,
2 Q& }9 S" s% {* U9 I; P8 D0 lwhich was clearly high. Some studies suggest that; i; M3 d  x6 w
dermal conversion of testosterone to dihydrotestos-9 L. A, ?  L- s9 o/ ^4 ~) R
terone, which is a more potent metabolite, is more
2 i8 `+ ?% C- R: X% p% ~% }& v3 iactive in young children exposed to testosterone" g# q# d9 b( `2 @- j% r
exogenously7; however, we did not measure a dihy-8 F* |/ k0 l; U8 S; _# ?1 T
drotestosterone level in our patient. In addition to
9 @* O! P* b5 J& c/ Nvirilization, exposure to exogenous testosterone in
$ w1 F" w+ R9 z6 P! V! achildren results in an increase in growth velocity and( R- i2 A! T' R& @* K) T
advanced bone age, as seen in our patient.% T* Q+ p. F. J+ P
The long-term effect of androgen exposure during
7 H9 W/ k: u4 V6 pearly childhood on pubertal development and final
; ^  b/ A9 a0 ?6 H! w9 Eadult height are not fully known and always remain$ T: R+ G  X5 L5 [/ ^2 F
a concern. Children treated with short-term testos-. F- [8 y2 o3 U+ [4 K1 L6 l
terone injection or topical androgen may exhibit some
' W$ U. s8 u: F  `( e2 cacceleration of the skeletal maturation; however, after
' `, x9 ^0 e# [3 d$ Hcessation of treatment, the rate of bone maturation/ o4 v* N- r6 M* S+ B6 B0 ?
decelerates and gradually returns to normal.8,9
! h9 A: d: C1 i& hThere are conflicting reports and controversy* S8 j, Z2 `0 r6 k
over the effect of early androgen exposure on adult! I+ B! \( q$ R# u  K+ h
penile length.10,11 Some reports suggest subnormal, y6 R2 c3 R$ s: Y3 L, z7 K
adult penile length, apparently because of downreg-5 t$ Y3 D& t9 D; N
ulation of androgen receptor number.10,12 However,
, p  J+ j! }+ N- R' dSutherland et al13 did not find a correlation between  ^' ^2 K3 f2 |4 J
childhood testosterone exposure and reduced adult$ C4 S# f" ^4 Q, {3 n/ J$ y$ g5 H
penile length in clinical studies.
8 M- f9 S) Z7 j( v& O# k# SNonetheless, we do not believe our patient is
! {! c, l9 U& I& mgoing to experience any of the untoward effects from
: N+ Y3 E) T3 D4 e2 ftestosterone exposure as mentioned earlier because
5 }3 m( M' x' M% I3 p9 L6 ithe exposure was not for a prolonged period of time.
+ d4 ^( G9 Z# j' w7 m) y! T  [0 m/ sAlthough the bone age was advanced at the time of2 S0 j$ q: k4 c
diagnosis, the child had a normal growth velocity at1 I! @( `' S$ z
the follow-up visit. It is hoped that his final adult2 e. P0 \5 u; F3 a, ~) N
height will not be affected.% t& r- T. R. D) k4 v# V
Although rarely reported, the widespread avail-
" r6 t; c+ }" z. M+ wability of androgen products in our society may
. u" s8 K* f1 d( @2 E( P$ kindeed cause more virilization in male or female
" B, @: M/ @1 `8 s4 H+ Qchildren than one would realize. Exposure to andro-# E6 u3 Q. e! j4 S6 y3 o2 v$ L
gen products must be considered and specific ques-5 Q3 [9 t# J3 B  _3 Y, A5 o3 h
tioning about the use of a testosterone product or' P7 `0 K5 \/ A5 I' N4 o
gel should be asked of the family members during
* w; v' ~* d' F, J* j* O- B+ O* y4 Athe evaluation of any children who present with vir-( Y9 x# |3 p* `  ~- v* b" O
ilization or peripheral precocious puberty. The diag-4 S, V5 C$ n. u! B
nosis can be established by just a few tests and by! w) ]: }/ x4 g. N: x/ {' J; k
appropriate history. The inability to obtain such a
" X# ^3 w9 i, ]( [0 h6 R, yhistory, or failure to ask the specific questions, may: {8 m  a" ~& W$ L. y4 W
result in extensive, unnecessary, and expensive
+ P" [4 g8 w4 r- L% I% f, v! B1 iinvestigation. The primary care physician should be
) }8 w3 `+ T5 x* f$ e3 ]+ a7 naware of this fact, because most of these children
3 o; e2 Y6 N5 ?  @- a3 Cmay initially present in their practice. The Physicians’3 j: I+ G* e* ~
Desk Reference and package insert should also put a
/ T" R) d" Z2 V& ~$ jwarning about the virilizing effect on a male or+ i: j8 X, n5 N
female child who might come in contact with some-
* ]  f( O* k: K7 b3 M1 Q; qone using any of these products.
2 @% E( V( Q0 {References
2 V& w/ d3 b  k4 R1. Styne DM. The testes: disorder of sexual differentiation
- Q. Y9 }: m! V) Land puberty in the male. In: Sperling MA, ed. Pediatric  s: A# T) U# {5 ^0 X5 k! V. E
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 r. q7 A" g0 d2 ^' y$ H2 F2002: 565-628.
4 o9 X4 ]! A: d- w- `2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 t$ i" n5 q( Lpuberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
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發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点

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發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
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發表於 2025-1-19 02:41:05 | 顯示全部樓層

# E2 q0 G, c7 o* G精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!

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發表於 2025-3-8 22:04:50 | 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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