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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old8 u( L6 ^4 R% K3 P  W+ M1 S5 A
Boy Induced by Indirect Topical
0 H2 l# t) M! Z! `  Q. CExposure to Testosterone: [. i% @" b. l
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 }: w  [! @* |- l. K0 fand Kenneth R. Rettig, MD1
) o; {  R; {  T6 HClinical Pediatrics
/ n& J, G" e9 QVolume 46 Number 6. O5 a  m8 w9 n) q+ g: g
July 2007 540-543# b' q& f! s- ~
© 2007 Sage Publications
' Y, I& `+ B7 u$ B6 u, v10.1177/0009922806296651
  Z1 Y* @. Y, v: Qhttp://clp.sagepub.com, b- Z/ p6 H9 e: [
hosted at
9 T3 `6 C$ w- l( a! V/ ]http://online.sagepub.com0 F& a) }; ]  k) t& J1 K
Precocious puberty in boys, central or peripheral,
# k& W, _- Z% g$ z1 his a significant concern for physicians. Central
' g/ f% Z7 B; g* a! c& {( vprecocious puberty (CPP), which is mediated* w% b5 S# t  v  ?+ X2 g
through the hypothalamic pituitary gonadal axis, has
& Y  C. A! x* j! g4 ?3 {a higher incidence of organic central nervous system
0 d! d( p) m- o3 V2 x" s1 _lesions in boys.1,2 Virilization in boys, as manifested
$ L( F: {' k) t2 P$ H( Bby enlargement of the penis, development of pubic
. C) ^# \1 T1 s0 r$ e% ]hair, and facial acne without enlargement of testi-8 c; F# _" ]5 W) w! |; b/ X' d
cles, suggests peripheral or pseudopuberty.1-3 We
# m+ y" F! j, I" J! c4 M. m4 b2 freport a 16-month-old boy who presented with the& W4 Y# _5 S- Y/ m  Z$ \
enlargement of the phallus and pubic hair develop-
& s2 ~& k0 j4 u( ~) G( b5 O% a) oment without testicular enlargement, which was due7 X) a" B/ M  P" b# b
to the unintentional exposure to androgen gel used by
1 H: E2 u5 d! m: a) H+ t! d& M, c8 gthe father. The family initially concealed this infor-
! y+ N9 k% B2 D. ?' a9 Smation, resulting in an extensive work-up for this/ |# w' ?8 [' w- B5 ]# U
child. Given the widespread and easy availability of, S- Z! w3 g9 e. C3 V
testosterone gel and cream, we believe this is proba-, {- b" v( E& p  B8 {% g* w
bly more common than the rare case report in the
) W" r: U! [9 a; f2 Gliterature.47 E* f' m* W8 Y$ ^' D
Patient Report
: u8 W& X+ s+ U/ ^" ?' Z# E- mA 16-month-old white child was referred to the, R4 d. E4 D( P% Z8 p4 W' `/ P
endocrine clinic by his pediatrician with the concern% \& \0 i. h) {6 v
of early sexual development. His mother noticed5 U- Z1 T  Y7 A, Y' J' n1 ?2 P1 z
light colored pubic hair development when he was
0 B/ `5 p% `) hFrom the 1Division of Pediatric Endocrinology, 2University of3 q# y; ?" H3 J0 Y
South Alabama Medical Center, Mobile, Alabama.
6 @1 `6 A  C+ h+ a$ y& _5 rAddress correspondence to: Samar K. Bhowmick, MD, FACE,' q% A! _+ C! j6 n% s
Professor of Pediatrics, University of South Alabama, College of+ ^, ~9 @4 y! K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ J5 Z$ u% \* v- W/ J- j! B7 ^e-mail: [email protected].# m% O0 S7 ^+ |. ?3 H
about 6 to 7 months old, which progressively became1 E# E. K) f  f2 i4 ?2 [" D, m* n
darker. She was also concerned about the enlarge-
1 X: V. \! X+ R$ W6 ]1 n+ Wment of his penis and frequent erections. The child
8 C3 U$ C, ~; ?( Fwas the product of a full-term normal delivery, with' W1 `/ v( Z5 s- V* E4 C6 ^! U
a birth weight of 7 lb 14 oz, and birth length of
$ p! X/ n* ^4 W20 inches. He was breast-fed throughout the first year8 ?7 o; R4 j( Y
of life and was still receiving breast milk along with+ C% O7 P6 H- x, y6 ^* P2 e$ U
solid food. He had no hospitalizations or surgery,
( S7 p& z" A( @4 ?and his psychosocial and psychomotor development5 r5 u5 M. h# w7 k$ [; i6 W* r
was age appropriate.! E+ r' l# v1 h7 \! J6 j2 j2 k
The family history was remarkable for the father,
3 [  Z+ l3 R( E. \0 w$ Pwho was diagnosed with hypothyroidism at age 16,) Y/ P2 e, {# T5 o. O2 J1 o- }
which was treated with thyroxine. The father’s7 ]  m+ Z' j5 X& a- U5 Y& n# m4 e
height was 6 feet, and he went through a somewhat+ j9 L4 V# n' U1 _2 `/ d7 D7 v" y
early puberty and had stopped growing by age 14.
  m, h$ c* r0 hThe father denied taking any other medication. The
0 X* |) S& k3 \1 g3 ?1 @& schild’s mother was in good health. Her menarche
" q) ]6 s/ H* f  gwas at 11 years of age, and her height was at 5 feet
* ]$ e- ^) E  S+ H5 inches. There was no other family history of pre-$ v# r7 a( M+ H$ a( ?7 m. B- O  p2 q
cocious sexual development in the first-degree rela-
9 w' m& y8 f& g  c- ?  Etives. There were no siblings." c5 S2 ^8 |* W) I
Physical Examination  y2 ^3 t2 u1 Z2 O
The physical examination revealed a very active,
" r% Y+ K* M( T7 j% n: ]# ]. Pplayful, and healthy boy. The vital signs documented& r/ H+ p# h/ c! t
a blood pressure of 85/50 mm Hg, his length was8 {( Y% H9 x6 i% @" }, h5 T% z4 G# V
90 cm (>97th percentile), and his weight was 14.4 kg$ m% x0 V; s3 T) [4 j! z
(also >97th percentile). The observed yearly growth
' s* |2 ?8 f" w1 a1 o, Hvelocity was 30 cm (12 inches). The examination of
( ]. R, R& q% ^$ _; ~3 Athe neck revealed no thyroid enlargement.
2 n  t/ t% |' g# B1 \The genitourinary examination was remarkable for( Z- E# m1 P& K  h  o
enlargement of the penis, with a stretched length of, b/ v4 P/ _: U2 R/ i
8 cm and a width of 2 cm. The glans penis was very well
3 _4 B9 {( r6 Z9 Y0 Q8 {  L: Zdeveloped. The pubic hair was Tanner II, mostly around' U; x, b/ }- m$ d6 V2 K# n
540* I5 e* j2 ~' `9 o5 X. @, b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% ?' ~1 g+ L- s& ^( |/ Tthe base of the phallus and was dark and curled. The
5 w; \0 g/ r: P4 jtesticular volume was prepubertal at 2 mL each.- i$ a& q8 T# T9 [
The skin was moist and smooth and somewhat
, i8 @! U9 d1 ?oily. No axillary hair was noted. There were no
! k% n8 |) V6 S" R8 Babnormal skin pigmentations or café-au-lait spots.
  V" q! a; ?9 k+ S2 s, f/ PNeurologic evaluation showed deep tendon reflex 2+
! i; N4 c9 a% L/ Obilateral and symmetrical. There was no suggestion! S- S2 G$ T; P2 x
of papilledema.# Z8 q2 P$ e3 f! u
Laboratory Evaluation
+ o8 `, Y; H6 h9 sThe bone age was consistent with 28 months by+ Z) C( v  |% B
using the standard of Greulich and Pyle at a chrono-
1 S) X& a% P5 j* J1 d  Q2 elogic age of 16 months (advanced).5 Chromosomal& A$ B% b" Q7 F. f
karyotype was 46XY. The thyroid function test3 Z( `% h& Q( _
showed a free T4 of 1.69 ng/dL, and thyroid stimu-: u9 a6 x, f( |- n3 o& ]
lating hormone level was 1.3 µIU/mL (both normal).
0 {1 v2 z! L. m: r7 `" I- w  yThe concentrations of serum electrolytes, blood
3 o' ~+ [# x! E" }: \' b2 [7 ]urea nitrogen, creatinine, and calcium all were
+ y% U/ W  l0 ?5 j' a# G4 pwithin normal range for his age. The concentration3 N5 F/ |) N  S) j! d) q$ j
of serum 17-hydroxyprogesterone was 16 ng/dL
) H' H$ v7 @, q7 B; }0 w; e: a+ R) z(normal, 3 to 90 ng/dL), androstenedione was 20
1 R2 W4 w0 t: ung/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 @: {1 I. a' D- Nterone was 38 ng/dL (normal, 50 to 760 ng/dL),! l& E9 f' E) ^1 T  T
desoxycorticosterone was 4.3 ng/dL (normal, 7 to6 p4 H5 [" U" l8 y1 t
49ng/dL), 11-desoxycortisol (specific compound S)4 g. [. s* {! l) m3 O; Q% n
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 |& X7 Q/ i  R9 s9 i0 [3 @
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" X" W- M0 c& s+ I) O0 M
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 F# m) o$ S% d$ Z" Q2 o; J- T* Yand β-human chorionic gonadotropin was less than
$ ^% A5 {- b- u5 }9 n$ e- X5 mIU/mL (normal <5 mIU/mL). Serum follicular! y# }; m( ~# T
stimulating hormone and leuteinizing hormone
) W# R2 e7 @6 h# I' bconcentrations were less than 0.05 mIU/mL2 }' T$ M& i- U! c. O8 l7 C
(prepubertal).- E( ]$ ~2 v8 |4 u9 ~2 m, P( W. o
The parents were notified about the laboratory
+ e+ f6 U* [, I# Hresults and were informed that all of the tests were
* h' T$ b/ q- R; p) X+ Q+ U, k1 Lnormal except the testosterone level was high. The
, E+ N. z$ o( r0 T, `& g& bfollow-up visit was arranged within a few weeks to
3 @8 V& L, ^) U1 k. Xobtain testicular and abdominal sonograms; how-8 Q# N: k6 p0 I+ Z, s6 t# a( x
ever, the family did not return for 4 months.
! |7 A! \" W$ M5 g& mPhysical examination at this time revealed that the, J6 L# ~, I! M; B; f: I" N
child had grown 2.5 cm in 4 months and had gained9 _1 y% |1 C) }0 w7 k  m" h
2 kg of weight. Physical examination remained% u" q. u4 i. m, X; ~
unchanged. Surprisingly, the pubic hair almost com-5 E8 T2 A. h) E* O/ B" D" L9 c4 t& G3 i
pletely disappeared except for a few vellous hairs at
9 E) M0 d% t2 t( cthe base of the phallus. Testicular volume was still 2$ k6 a* x3 R" h1 }# U- [
mL, and the size of the penis remained unchanged.% I7 a6 f$ A. G; K
The mother also said that the boy was no longer hav-
& R. E; I1 Q' n8 G2 @1 y# uing frequent erections.
# H0 [: O/ @% M5 A1 qBoth parents were again questioned about use of
! \0 ~) N2 I& }" _5 ]. Q$ many ointment/creams that they may have applied to  B+ g' N9 D+ H- [9 I* q) M6 E- M: m
the child’s skin. This time the father admitted the
: X  }: @7 F# W. ~; m! M- k9 l* ~3 WTopical Testosterone Exposure / Bhowmick et al 541
+ F* @- e; k, y5 T  r0 T3 nuse of testosterone gel twice daily that he was apply-: M. @. Q! B1 A7 K
ing over his own shoulders, chest, and back area for
& w( r0 N& Y+ l( La year. The father also revealed he was embarrassed
8 W8 b& M% b) h4 l; s) eto disclose that he was using a testosterone gel pre-! R3 Y' h* X  N9 R; H8 ?! U# _
scribed by his family physician for decreased libido2 M1 m  F5 u4 R5 K/ q( d+ g
secondary to depression.
& e- T( G  }7 V& MThe child slept in the same bed with parents.
! w- H9 [, u4 X6 tThe father would hug the baby and hold him on his
" k6 a% f. n( z  Schest for a considerable period of time, causing sig-$ q' e% F% p4 k, _/ L: Y
nificant bare skin contact between baby and father.
% ]  t  K: \4 P8 g; TThe father also admitted that after the phone call,
$ k- N" b+ E/ W9 p6 ^2 uwhen he learned the testosterone level in the baby5 {1 w) b. f  Q! b* I4 n( ~
was high, he then read the product information
* G3 G  i. k2 p. ]  mpacket and concluded that it was most likely the rea-
" F* ^1 s: A$ k( f2 Fson for the child’s virilization. At that time, they
0 m  Q3 D$ G% Pdecided to put the baby in a separate bed, and the# E; O+ ~, p4 j' l& H
father was not hugging him with bare skin and had
6 G! f, g: A! T  rbeen using protective clothing. A repeat testosterone
* C5 ~7 r' l3 ?- h! Jtest was ordered, but the family did not go to the  U% P# [4 G" i/ z
laboratory to obtain the test.6 @6 e% e$ X3 g9 U
Discussion
, c4 ^+ O$ C9 q  B$ uPrecocious puberty in boys is defined as secondary% E% P3 L: i: j: A7 ^& f. t
sexual development before 9 years of age.1,4( u5 N- [8 Y! _  J
Precocious puberty is termed as central (true) when/ g4 e; A" l- f
it is caused by the premature activation of hypo-
8 ~1 ^% \  q  l+ M7 mthalamic pituitary gonadal axis. CPP is more com-
, g7 E3 U- _, j  f/ k, B3 L$ Wmon in girls than in boys.1,3 Most boys with CPP
' S+ W  f7 V' b9 D' G% |! n- }+ Wmay have a central nervous system lesion that is
$ \. c& v! p# \: N4 Iresponsible for the early activation of the hypothal-/ P% z4 c+ D, B$ E  ^1 B  D% T
amic pituitary gonadal axis.1-3 Thus, greater empha-. u- J8 @4 w  b* d
sis has been given to neuroradiologic imaging in
. ^% ~' t( |2 N+ uboys with precocious puberty. In addition to viril-
- _0 w1 p  \; w' e9 s4 y3 B, uization, the clinical hallmark of CPP is the symmet-
' g: L4 e5 y( z3 A- `rical testicular growth secondary to stimulation by) Y4 t+ q+ O! G" m4 s' i5 |
gonadotropins.1,32 v3 a0 _1 S+ `% \. y% r( x. q+ T
Gonadotropin-independent peripheral preco-3 d) {& J. L* h6 e- C( d  D
cious puberty in boys also results from inappropriate+ h6 m: Z! x7 D! b7 z
androgenic stimulation from either endogenous or
4 N( N& s2 E+ p! s2 N/ xexogenous sources, nonpituitary gonadotropin stim-
9 G6 k* q. E8 X* Zulation, and rare activating mutations.3 Virilizing
1 B; K# j1 @2 o. ncongenital adrenal hyperplasia producing excessive
6 n$ ~* g% ]# k0 T& f! X( {adrenal androgens is a common cause of precocious
! ?/ |1 Y( C6 spuberty in boys.3,4
  L& _! @: Z& wThe most common form of congenital adrenal
5 U! m7 L7 P* uhyperplasia is the 21-hydroxylase enzyme deficiency.
0 @# ^( G  X7 ~. ]The 11-β hydroxylase deficiency may also result in0 X8 U5 h+ _9 p5 h  j7 p
excessive adrenal androgen production, and rarely,
2 D$ N/ I# v  s$ s/ j" can adrenal tumor may also cause adrenal androgen, U' o) r8 B0 {, o7 P
excess.1,3
: V) k3 N0 d, Y* H. ^6 g, }5 Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( ~" G: S/ B( M, D! x8 K542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 ]! L/ u) P1 |- l. o- s( ?A unique entity of male-limited gonadotropin-
$ {, z! ~/ e1 Kindependent precocious puberty, which is also known
7 C; `8 C' W8 D1 F  x2 yas testotoxicosis, may cause precocious puberty at a
+ J5 m2 O+ r4 e1 xvery young age. The physical findings in these boys2 t( ]; i$ E( V$ T. K
with this disorder are full pubertal development,
: M3 E$ i8 t+ d$ X8 J- Uincluding bilateral testicular growth, similar to boys
# d$ }. F; S# n, K" bwith CPP. The gonadotropin levels in this disorder- _! N8 g# i' G4 f+ l7 w
are suppressed to prepubertal levels and do not show
; g4 G4 X$ G) |1 Zpubertal response of gonadotropin after gonadotropin-% Z7 \' q+ b' }
releasing hormone stimulation. This is a sex-linked4 d  U! j; Q1 C
autosomal dominant disorder that affects only/ I' |3 @" p3 j# W
males; therefore, other male members of the family
+ N0 T, F9 L  [& ^' u# \6 Gmay have similar precocious puberty.31 D. ~* t5 [# V$ c
In our patient, physical examination was incon-" F5 ^; r, h+ A; E% R3 O* j
sistent with true precocious puberty since his testi-
! A+ R: B8 w* T7 D% ecles were prepubertal in size. However, testotoxicosis
: m# C) r/ W0 N: i3 Cwas in the differential diagnosis because his father
# S6 i  x/ c; J3 D; A/ Astarted puberty somewhat early, and occasionally,) i$ e" g0 T  K( x5 F0 h
testicular enlargement is not that evident in the
+ S5 b* {1 R6 c# j5 K9 d1 h6 _beginning of this process.1 In the absence of a neg-
; x. {. }( p2 n8 J2 v, Tative initial history of androgen exposure, our4 K5 e+ d, u& ^
biggest concern was virilizing adrenal hyperplasia,, `3 G% u7 r% _$ ?( R3 s
either 21-hydroxylase deficiency or 11-β hydroxylase
" |' u! @' P) @! |* G. {5 i3 \  ~deficiency. Those diagnoses were excluded by find-( H5 C" e7 n( M  k3 }
ing the normal level of adrenal steroids.! y: ?7 z6 K% a- l! k
The diagnosis of exogenous androgens was strongly
! y5 H+ Y# M. fsuspected in a follow-up visit after 4 months because
5 B" b9 ], R' ?9 X- dthe physical examination revealed the complete disap-
! X/ k' N& ~: u! {; ^( Qpearance of pubic hair, normal growth velocity, and
. `% z& K' ~6 xdecreased erections. The father admitted using a testos-
9 s1 F* r6 k" V* iterone gel, which he concealed at first visit. He was4 L: L" _9 ]+ f
using it rather frequently, twice a day. The Physicians’/ G  @6 j0 P  A  I
Desk Reference, or package insert of this product, gel or
1 V' u- O; J( R1 H. ?3 x" }# ?cream, cautions about dermal testosterone transfer to
0 m. X1 r. e3 O" Z4 runprotected females through direct skin exposure.
- q( r1 ?% i, h+ j9 ~: qSerum testosterone level was found to be 2 times the
9 |' X8 j( D# i: Obaseline value in those females who were exposed to1 w5 Y, @1 W( n$ N* c) Z  R2 U! W" P
even 15 minutes of direct skin contact with their male1 b: ~3 B; R2 H  r
partners.6 However, when a shirt covered the applica-* {5 x2 ?+ D/ f* k
tion site, this testosterone transfer was prevented.
6 d3 n, M& d1 u. |/ XOur patient’s testosterone level was 60 ng/mL,! x. u2 y$ Q3 `7 P
which was clearly high. Some studies suggest that
/ M% Y8 m2 F6 g1 @, v0 `' Rdermal conversion of testosterone to dihydrotestos-+ B7 D% z1 K* v+ F' [  c9 C  I
terone, which is a more potent metabolite, is more7 a) p8 t% ~+ K1 y
active in young children exposed to testosterone
1 f! I5 M/ Q, o/ Rexogenously7; however, we did not measure a dihy-% r" J0 j# T8 }" P( _
drotestosterone level in our patient. In addition to6 i  v$ ?7 K% T) R
virilization, exposure to exogenous testosterone in% q7 ]% G  i- ?9 S
children results in an increase in growth velocity and
/ r9 s2 V- j. x& ]advanced bone age, as seen in our patient.
8 R& L0 r2 z) ^( y) p1 c, I: }The long-term effect of androgen exposure during
* a' k* x1 H' Wearly childhood on pubertal development and final
! |1 H9 e0 |) D3 l8 t1 wadult height are not fully known and always remain
4 k, |" `! `, }a concern. Children treated with short-term testos-$ y  T; b4 W. y, _( f
terone injection or topical androgen may exhibit some
- ]0 A  O8 `/ v8 ^) _) aacceleration of the skeletal maturation; however, after
; ]+ ^& s+ f8 wcessation of treatment, the rate of bone maturation
9 a  L$ a- C' `: Udecelerates and gradually returns to normal.8,9' U8 k2 f( ~' @
There are conflicting reports and controversy
! ]. c1 g# P. {) A; Mover the effect of early androgen exposure on adult
: p* N2 u3 x9 @8 [4 \penile length.10,11 Some reports suggest subnormal4 x5 w" s2 r9 K1 i
adult penile length, apparently because of downreg-$ A3 z0 n/ f% b* p: A! h
ulation of androgen receptor number.10,12 However,3 B7 C+ z) n! g+ O9 D/ a
Sutherland et al13 did not find a correlation between% W- w, u2 c* t' z
childhood testosterone exposure and reduced adult! l% {$ @; b1 e: S) C, U
penile length in clinical studies.
4 c8 ]( ?- l/ P8 r; q' l6 hNonetheless, we do not believe our patient is! e, a9 Z8 c' R7 [% _
going to experience any of the untoward effects from# y" H: v% [$ n* ~5 |8 A7 _# a
testosterone exposure as mentioned earlier because7 G8 I: o' i. ?
the exposure was not for a prolonged period of time.; e( j- M9 e+ h  }- f
Although the bone age was advanced at the time of
; n* D3 n! r& i! _* d: q- x. Adiagnosis, the child had a normal growth velocity at
7 s8 I' I% W4 R7 `the follow-up visit. It is hoped that his final adult9 Z6 c) H7 L! E1 i; q1 J2 R# z- V* Z
height will not be affected.+ q& f+ R% h0 M( \6 }1 u% m& |
Although rarely reported, the widespread avail-
3 x  V6 D  t+ I* z1 Z; _ability of androgen products in our society may
9 I* C# p. A) M# oindeed cause more virilization in male or female
3 ?3 e' w$ O9 }# V- {. D( `children than one would realize. Exposure to andro-. N% s4 E. r3 j# j" i
gen products must be considered and specific ques-/ s0 O9 L3 h6 c$ D7 e+ J
tioning about the use of a testosterone product or
) X3 w5 N& ^5 Z4 [6 n# ^gel should be asked of the family members during: O4 M  }; m" V) N! V: P
the evaluation of any children who present with vir-% z0 U( [! ]/ a0 d) H
ilization or peripheral precocious puberty. The diag-
; y3 \9 ~; T/ s! w( f: i  Onosis can be established by just a few tests and by9 n4 i  U2 s5 c8 c" F/ o4 d
appropriate history. The inability to obtain such a/ u8 K$ j" h, f! L* V; T* I; [
history, or failure to ask the specific questions, may% V1 d# R) C9 B" F6 Q: a% o
result in extensive, unnecessary, and expensive0 Y9 A7 m/ y: T0 G8 G, O4 t8 e1 r( [" O
investigation. The primary care physician should be3 I0 H5 K) y" w: u5 W( U' G: h0 v
aware of this fact, because most of these children8 U8 V! G3 D: e
may initially present in their practice. The Physicians’
3 P; V8 t) _6 d9 D$ l" V0 zDesk Reference and package insert should also put a5 B' u3 T- U, P# c) j! V* y0 B. U) B
warning about the virilizing effect on a male or
9 P. j. m: \$ M7 k, V) U$ a$ Jfemale child who might come in contact with some-/ H! Z" ?' V0 S9 M" {
one using any of these products.# Z, A9 Q4 @2 r" D6 x6 ^, x
References" `7 ]" p" F! S; S0 A9 z
1. Styne DM. The testes: disorder of sexual differentiation
: D* {; O$ g: o( w1 k& Rand puberty in the male. In: Sperling MA, ed. Pediatric$ i$ v+ u- e' ~: O5 Z
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  Z6 h3 `8 ?! D6 ]' x+ c
2002: 565-628.
1 _, j" P0 z7 b* F4 r5 J2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! ~7 Q1 ^+ m8 a
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old7 j: ?+ ?2 E( f" G+ ]: G
Boy Induced by Indirect Topical
/ E! N% Z( `6 z& R3 }" uExposure to Testosterone
' Z0 t+ H; w- r: Z$ i  }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 a) W  F: ?4 l; V* |
and Kenneth R. Rettig, MD1
* B" v1 v8 Z8 xClinical Pediatrics
: H8 q( {+ X/ P7 T( n2 e1 }; qVolume 46 Number 61 O9 l3 v! A& m3 ^
July 2007 540-5430 D  r8 ]6 v# B/ e
© 2007 Sage Publications
' m2 I0 L+ A, C8 u10.1177/0009922806296651
: w/ }0 U; e- jhttp://clp.sagepub.com! A: B$ `0 a0 V, s4 ^8 L
hosted at/ }8 f5 F5 v6 {& e. o; {
http://online.sagepub.com* ]2 @6 r" ^6 r; X/ E( f+ f
Precocious puberty in boys, central or peripheral,
" E+ R$ s8 C& a) o* j  dis a significant concern for physicians. Central# V' n' K$ E" ]
precocious puberty (CPP), which is mediated
3 W6 D  M* V' Y5 Q& ithrough the hypothalamic pituitary gonadal axis, has
9 k3 q' O5 t  {. {. ]' a/ [a higher incidence of organic central nervous system
- }1 a+ I9 T: A- ]' `& i  v' wlesions in boys.1,2 Virilization in boys, as manifested
' q/ Q3 F8 E2 L+ M. y! Uby enlargement of the penis, development of pubic  q6 ^! ~# |+ L2 I# C* f
hair, and facial acne without enlargement of testi-/ Q! k5 I8 g' _% k5 L/ K
cles, suggests peripheral or pseudopuberty.1-3 We
, y& a) z% a" ]$ Xreport a 16-month-old boy who presented with the7 X: r; \4 L1 d# M. p
enlargement of the phallus and pubic hair develop-: h6 @& x1 i6 U# X; Q5 P' w. s. s  @
ment without testicular enlargement, which was due
4 }" k9 B5 C+ ?9 oto the unintentional exposure to androgen gel used by
8 l9 j6 k& R# Y5 q; ^. k! Pthe father. The family initially concealed this infor-
" w: @6 R2 J! d8 Imation, resulting in an extensive work-up for this
8 O/ @4 [7 Q' g3 C& W7 n2 N( w7 Kchild. Given the widespread and easy availability of$ b! v9 R0 P+ r0 b2 P$ x9 I
testosterone gel and cream, we believe this is proba-
# t% @, ~( z5 {4 y- C/ Z+ `- Vbly more common than the rare case report in the, X& {  o" r0 b
literature.43 }' X, G4 _/ k( \  ?+ U' |- ~$ L; h
Patient Report
1 k0 h. A. I! ~6 }- l3 z% _A 16-month-old white child was referred to the
/ g9 g' I) e. e& \* l6 P0 Tendocrine clinic by his pediatrician with the concern
8 b$ S4 S; s- Y2 {# w2 Jof early sexual development. His mother noticed7 Q: E, g- T$ X! |
light colored pubic hair development when he was
3 g8 @' U$ J' {7 ?From the 1Division of Pediatric Endocrinology, 2University of! [$ h/ q% j: [  e" Z
South Alabama Medical Center, Mobile, Alabama.
5 m% t, z6 x9 nAddress correspondence to: Samar K. Bhowmick, MD, FACE,9 s2 t! R: m3 ]
Professor of Pediatrics, University of South Alabama, College of
9 |6 {. `8 J- `% m- ?  I- ~) h& V0 VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) n/ y% O  u  Ge-mail: [email protected].2 E. B! d3 z3 h* B- n
about 6 to 7 months old, which progressively became
0 L3 ]2 v6 X. y5 `% V, `darker. She was also concerned about the enlarge-
$ q% S. J) U6 |) o7 Zment of his penis and frequent erections. The child, p( b' P0 @/ Y; r) M
was the product of a full-term normal delivery, with
" ~/ [* C: ~, p, l" \a birth weight of 7 lb 14 oz, and birth length of
! \! {( t- B5 U7 T: [% ^3 X2 I, `20 inches. He was breast-fed throughout the first year: y9 ~4 ~# u$ j9 s9 v$ F
of life and was still receiving breast milk along with  x4 f& i/ ^; K3 K, s
solid food. He had no hospitalizations or surgery,& ]( S# g( Q/ I8 d
and his psychosocial and psychomotor development$ b. X: `9 ]$ C: W
was age appropriate.
0 P  M9 Q; p! o, c& S  jThe family history was remarkable for the father,) r& h( M" ]! \: P; p
who was diagnosed with hypothyroidism at age 16,
  ], }3 d) Q& j( w8 K' w6 ?4 B3 |( z& awhich was treated with thyroxine. The father’s) c  n1 Y. T, ~! {$ U
height was 6 feet, and he went through a somewhat
& Z* l3 j! i4 v5 ]0 }- ?' H& q' Zearly puberty and had stopped growing by age 14.& t. N4 d: f2 N- H
The father denied taking any other medication. The/ U6 _3 c3 O* o& Q1 W+ P
child’s mother was in good health. Her menarche2 I( H: L5 B% o! `
was at 11 years of age, and her height was at 5 feet  F( A$ T& G7 N& ]% o5 k
5 inches. There was no other family history of pre-" r8 r+ Q* i/ q
cocious sexual development in the first-degree rela-/ ~/ T8 Q* u4 B. Y, N' @9 x% ^; }
tives. There were no siblings.% Z# }5 K4 T+ O+ A  C6 ~/ I" N5 Y
Physical Examination2 l2 U. v  O  [, n& T- S6 ~5 }
The physical examination revealed a very active,
5 v* x/ V2 W0 y* ?9 c  ^playful, and healthy boy. The vital signs documented
8 C1 A4 {- K7 F2 x& y& Ya blood pressure of 85/50 mm Hg, his length was& Z* Z. A# z2 r" I
90 cm (>97th percentile), and his weight was 14.4 kg
" v3 J8 R* z7 n3 P1 F" s(also >97th percentile). The observed yearly growth
* k2 }( x4 _  c5 x5 F. q9 I! J) c' fvelocity was 30 cm (12 inches). The examination of" [( U* c/ m/ w  V' p
the neck revealed no thyroid enlargement.: D; C; [" ]8 l+ o9 i: N/ h: d+ l
The genitourinary examination was remarkable for7 Z0 E# U, H4 V
enlargement of the penis, with a stretched length of
, [2 G) s8 S6 U8 cm and a width of 2 cm. The glans penis was very well# s$ n& z2 g' Q' H
developed. The pubic hair was Tanner II, mostly around% d& v$ W4 k7 W. X! e# K
540
! L' _& O! _4 q/ v, l: Z$ `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& G! v* ?. F. [: Z3 P' D6 k1 ^
the base of the phallus and was dark and curled. The
6 ]$ G$ H; X/ M' c' a! x1 dtesticular volume was prepubertal at 2 mL each./ n" W  k# @& }8 k0 T+ |' V5 t8 d
The skin was moist and smooth and somewhat9 D2 F- n) ^6 L; Q' \
oily. No axillary hair was noted. There were no& E, ]9 W2 M" Q0 k3 I: S
abnormal skin pigmentations or café-au-lait spots.4 f$ d% j6 Z6 n/ B
Neurologic evaluation showed deep tendon reflex 2+
1 w) b, g/ U2 v# I2 B6 Obilateral and symmetrical. There was no suggestion' I, s, T! w- a0 {- N! u- d
of papilledema.
& |% F' a* ]( c# N" G$ N4 K( eLaboratory Evaluation& m6 _/ [& I5 ]! H+ `4 I, W, S
The bone age was consistent with 28 months by2 e. V5 T+ s& J
using the standard of Greulich and Pyle at a chrono-+ V% l" ?/ P; u% W! W  R, e
logic age of 16 months (advanced).5 Chromosomal
+ D: l# D( p, R% a8 Nkaryotype was 46XY. The thyroid function test
9 e. e, x8 V* D& T0 b7 Kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-& Z4 {$ M# y+ K4 E
lating hormone level was 1.3 µIU/mL (both normal).& h& e  T& [1 z+ q
The concentrations of serum electrolytes, blood9 Q1 F$ f& A/ [- |2 _4 E# K( V# O. g' H
urea nitrogen, creatinine, and calcium all were
# i/ Z9 M3 D, N! u4 C+ P# o  s' p  hwithin normal range for his age. The concentration
; c( Q+ W* [; w0 ]7 h7 B% Tof serum 17-hydroxyprogesterone was 16 ng/dL
( n8 T7 g! m( j4 c" f( _(normal, 3 to 90 ng/dL), androstenedione was 20
8 A3 d/ ?: C" O9 ~2 I, L: o* Png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- r- ^9 r+ Z: p) ]2 J  n
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 H8 b0 W& @) X: @4 b9 I9 ]desoxycorticosterone was 4.3 ng/dL (normal, 7 to- |) t3 ?+ Z# q$ I" g" ]9 m1 c6 n
49ng/dL), 11-desoxycortisol (specific compound S)) i& e$ X) P0 {) w: ?9 b  f5 Q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( t1 W! J( W; l" R* l# _
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# v, B: F/ a9 Z& @2 j! W! u( k
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 m- T+ N7 [0 C$ u
and β-human chorionic gonadotropin was less than
7 V; I: Q% P0 [8 z5 D5 mIU/mL (normal <5 mIU/mL). Serum follicular
- S- ?- R" Q1 q7 Sstimulating hormone and leuteinizing hormone
6 L( Q9 T& z4 W7 f# ?0 ^" Y3 gconcentrations were less than 0.05 mIU/mL( w' w4 Z1 f3 e, [& \5 c$ z
(prepubertal).
* [. {+ w7 g# G3 I% D. {6 q* h. n+ LThe parents were notified about the laboratory
4 ]- P+ O4 c2 Uresults and were informed that all of the tests were
7 O5 v" r( e/ w& R( G5 \normal except the testosterone level was high. The1 I5 d, [. O: {
follow-up visit was arranged within a few weeks to3 D3 F0 W" ~, O) l; P/ ^) B* r
obtain testicular and abdominal sonograms; how-
0 `* E4 i6 V! dever, the family did not return for 4 months.& w( K% V: ?. R& c  ~
Physical examination at this time revealed that the
: ~( [3 A# p! M* I( O" ^3 Cchild had grown 2.5 cm in 4 months and had gained
$ x% R0 K" ~" X6 z5 g2 kg of weight. Physical examination remained
7 f. i  |# \6 j' U4 O% P2 Z0 bunchanged. Surprisingly, the pubic hair almost com-
3 [" c5 i& r1 ^1 I$ Vpletely disappeared except for a few vellous hairs at3 }1 u! z6 E4 Q3 {; N2 C& y
the base of the phallus. Testicular volume was still 2
8 X' P% k, c$ Q0 imL, and the size of the penis remained unchanged.5 j! E3 `* S6 Y. F
The mother also said that the boy was no longer hav-! A& P( s$ _' M# {! n- a. h
ing frequent erections.
: p! j; `: H2 h$ \8 q! dBoth parents were again questioned about use of) x, m5 G! W$ _% X
any ointment/creams that they may have applied to
) H: `1 T7 f( x0 Fthe child’s skin. This time the father admitted the) D: ^- U+ H, _& }4 ~
Topical Testosterone Exposure / Bhowmick et al 541
0 {5 j$ X, ?. a# X9 L' z& _# Q+ kuse of testosterone gel twice daily that he was apply-) r, p4 V& [* |5 |7 T+ a& N
ing over his own shoulders, chest, and back area for7 D7 J5 S5 r+ h
a year. The father also revealed he was embarrassed
9 X) S" w5 b( H* [to disclose that he was using a testosterone gel pre-
6 n* k- @; A/ j* U1 ?2 Yscribed by his family physician for decreased libido
+ V( B; R6 c9 k9 _/ @2 C4 \secondary to depression.
/ A" s7 g0 y( S+ g$ C2 dThe child slept in the same bed with parents.
) Q9 I. S% p1 J! k: Y9 ]- U) ]The father would hug the baby and hold him on his
  b$ B# U, F' O% q( kchest for a considerable period of time, causing sig-
. E$ H4 b1 s0 T8 p  [7 F5 S: Lnificant bare skin contact between baby and father.: J- \% X4 Z* V$ r" Q, ]9 n
The father also admitted that after the phone call,1 Y7 t: o  s* A* J
when he learned the testosterone level in the baby6 u# C+ a- E& Z6 R
was high, he then read the product information
3 G8 X' E8 f6 M4 e4 O/ g. jpacket and concluded that it was most likely the rea-4 k; l2 L: j: L9 u
son for the child’s virilization. At that time, they3 r- r# O; G" P7 @9 v
decided to put the baby in a separate bed, and the
* v4 ]* ^5 k4 Afather was not hugging him with bare skin and had4 |, \! w3 N; o6 X& ~2 }
been using protective clothing. A repeat testosterone
: |7 x  R0 Z& j# otest was ordered, but the family did not go to the: s9 g+ {$ i, E! H( n7 _
laboratory to obtain the test.
. }- K" v: N7 d; o# h! sDiscussion. r1 d8 _" X+ i- J2 I5 |
Precocious puberty in boys is defined as secondary  V# Z' l- P6 f/ H3 y
sexual development before 9 years of age.1,4
% n* B! o$ d+ D2 r3 RPrecocious puberty is termed as central (true) when: C; i# I5 \' w; [5 r; w
it is caused by the premature activation of hypo-: P5 l( b: J3 E2 {6 \( V
thalamic pituitary gonadal axis. CPP is more com-; r. T: O6 i" [& _! o2 r/ d6 h
mon in girls than in boys.1,3 Most boys with CPP; C0 M  T% x1 |7 _9 K# Z: e5 x
may have a central nervous system lesion that is
( z, g6 m$ N1 x0 T6 _% G  @responsible for the early activation of the hypothal-
, v  b& x- G" C) n" z1 f2 q1 K6 eamic pituitary gonadal axis.1-3 Thus, greater empha-2 }( i: J5 W5 _6 w
sis has been given to neuroradiologic imaging in
, R- K9 D- e& F/ C. c  Tboys with precocious puberty. In addition to viril-
$ B2 Q+ t+ G1 C4 o! X9 [; sization, the clinical hallmark of CPP is the symmet-
* C. d. U! \0 b. h9 b2 P+ Arical testicular growth secondary to stimulation by* R7 u9 L& k/ g& e% s6 u8 q/ t
gonadotropins.1,3
) e& j1 n1 J- F9 GGonadotropin-independent peripheral preco-
/ x4 q' w9 P$ n% q# T7 tcious puberty in boys also results from inappropriate; z. W# f( P, e& a& E8 F, ]3 e
androgenic stimulation from either endogenous or
* S( p/ G' N0 Cexogenous sources, nonpituitary gonadotropin stim-+ L  Z+ t4 F( b
ulation, and rare activating mutations.3 Virilizing" c: P. D# E/ I1 k
congenital adrenal hyperplasia producing excessive2 b. o! h& d6 _. M1 ^$ q
adrenal androgens is a common cause of precocious1 i5 X6 R6 }0 Q) l; n- y
puberty in boys.3,47 i2 r7 L2 G$ I/ \
The most common form of congenital adrenal4 F3 R, g( S- R) `0 H: A) h8 \. N
hyperplasia is the 21-hydroxylase enzyme deficiency.
& E* U0 W# u9 @! `The 11-β hydroxylase deficiency may also result in
; ]! m! X0 ~- x5 s. Bexcessive adrenal androgen production, and rarely,+ u6 ^9 i* z' M
an adrenal tumor may also cause adrenal androgen2 Z* Q* P7 _- q
excess.1,3
5 S- s7 s) Q( w+ sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ f5 D& v4 Z6 I542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& N- @  H; X' \& f4 {& Q2 S1 A$ c( v7 uA unique entity of male-limited gonadotropin-9 k( h* ]; Z, z5 N; n$ W# d
independent precocious puberty, which is also known
" _. E) q& ^5 e9 C. Ras testotoxicosis, may cause precocious puberty at a+ F( d% H& t/ D, r5 S. d, I
very young age. The physical findings in these boys
# G4 |0 ^+ p! r6 C- X9 P8 F" cwith this disorder are full pubertal development," Q: z  r5 m' F
including bilateral testicular growth, similar to boys
- b; ]0 h% s& a( zwith CPP. The gonadotropin levels in this disorder& Z4 g: g9 A1 b4 B/ H4 }) p
are suppressed to prepubertal levels and do not show
. y0 ]  p( z# J! vpubertal response of gonadotropin after gonadotropin-) b6 Z3 l7 T- u7 O+ ]% _! m
releasing hormone stimulation. This is a sex-linked
. M* o" W3 r9 A! `$ i$ Aautosomal dominant disorder that affects only
( T, ?, i5 ?" }4 Y% Fmales; therefore, other male members of the family
# B% g. n8 @8 |7 c4 `' R, M, ]& b; c& Dmay have similar precocious puberty.33 ~4 j" {8 A' v1 t' I
In our patient, physical examination was incon-
* A; c6 m4 l7 L- \- i8 F/ {sistent with true precocious puberty since his testi-$ P/ ~1 J! s. z% T6 ~- h& E+ w
cles were prepubertal in size. However, testotoxicosis
7 R- ~! O3 A" o' A7 v8 Z4 Awas in the differential diagnosis because his father$ U8 Q" p9 J; E2 W% y
started puberty somewhat early, and occasionally,
0 S+ v7 h4 V$ g. O" n& @testicular enlargement is not that evident in the8 s, l" r+ J! _
beginning of this process.1 In the absence of a neg-
$ ~3 e% R8 J. Cative initial history of androgen exposure, our
2 [) H) [+ f" S& _% X6 tbiggest concern was virilizing adrenal hyperplasia,  ^* I) g7 y* _# A
either 21-hydroxylase deficiency or 11-β hydroxylase
" l6 F" i' d; E- t$ i* mdeficiency. Those diagnoses were excluded by find-
( b" H5 v/ k/ d/ U/ Eing the normal level of adrenal steroids.
& M, f$ r. e4 L2 ?/ ]; I# PThe diagnosis of exogenous androgens was strongly
3 |* N3 O* G% I9 {' E: N( ?suspected in a follow-up visit after 4 months because
/ l( ]# u+ M4 u! R' Lthe physical examination revealed the complete disap-
3 U/ |) V$ X6 I) upearance of pubic hair, normal growth velocity, and
" t$ R4 Q% p$ U0 i# {/ |8 O& Adecreased erections. The father admitted using a testos-
& i3 q: W( S$ v. g+ E6 ?; C) lterone gel, which he concealed at first visit. He was
, t4 P5 g) U6 G  @using it rather frequently, twice a day. The Physicians’
3 P5 e+ M# s4 H* S8 s3 SDesk Reference, or package insert of this product, gel or
' Z1 ~5 r" ~4 s7 e- l+ B3 a3 a  ncream, cautions about dermal testosterone transfer to2 o1 k9 |/ `  u' M9 G. {
unprotected females through direct skin exposure.
' l& i6 z8 a' C" DSerum testosterone level was found to be 2 times the- _9 B2 a7 q  [2 D0 B2 k
baseline value in those females who were exposed to1 ]) B. @$ Z$ F1 S
even 15 minutes of direct skin contact with their male
$ T% S9 l$ W6 |$ j: rpartners.6 However, when a shirt covered the applica-
. ]/ q7 C7 ?! B( F7 K1 O1 mtion site, this testosterone transfer was prevented.
- f9 o2 c- g9 ]( P9 p5 Z0 j1 AOur patient’s testosterone level was 60 ng/mL,
( K: E# d, N; A$ |. [8 `which was clearly high. Some studies suggest that
6 E2 [8 W% S$ H8 g1 R! ~0 Adermal conversion of testosterone to dihydrotestos-: `( B  j6 n  l0 X2 Z4 G# \  a  q6 k
terone, which is a more potent metabolite, is more4 F- S" `, p. j& e3 J" D
active in young children exposed to testosterone5 e' Q: I4 r0 f! y
exogenously7; however, we did not measure a dihy-
- _" ?/ T4 a( e1 U3 x( \3 ydrotestosterone level in our patient. In addition to
" ]# D$ I" k  H4 f- [' T) j# Mvirilization, exposure to exogenous testosterone in  W" o* t( \( A' {* q
children results in an increase in growth velocity and3 o' b. E/ M/ @5 x4 ^
advanced bone age, as seen in our patient.
5 Q- |; U1 f, W  l# {0 q- m* w1 YThe long-term effect of androgen exposure during) |- X1 ?2 p0 v) W1 z
early childhood on pubertal development and final
4 i1 s/ @3 O: Y, b* fadult height are not fully known and always remain5 v; \! w& S: h2 H1 B
a concern. Children treated with short-term testos-
# r- f% R7 r6 Gterone injection or topical androgen may exhibit some
2 @5 M4 u, _8 F: b/ u) H5 O5 u# @acceleration of the skeletal maturation; however, after
  _+ W5 x5 B2 _: ucessation of treatment, the rate of bone maturation' o/ e+ E6 `% B
decelerates and gradually returns to normal.8,9* \4 Q; {0 n% A* t* U
There are conflicting reports and controversy: w9 g3 `. \" a! s- v
over the effect of early androgen exposure on adult0 c+ S9 @% K* r' m& V( X- J
penile length.10,11 Some reports suggest subnormal/ q8 k; _. T- A2 \8 _# l
adult penile length, apparently because of downreg-0 [# G5 f# R! Z, |1 U5 j) A% e8 ^! y2 {
ulation of androgen receptor number.10,12 However,
0 l- r! D; j! G7 v8 E" nSutherland et al13 did not find a correlation between
* Y6 v( E% s) _) i8 Q: ^4 Q) t' @childhood testosterone exposure and reduced adult
- S' s, X. J. N: f; s2 e% w' Dpenile length in clinical studies.3 R3 R6 w& n5 Z  r& K( N
Nonetheless, we do not believe our patient is+ o/ a/ z$ M$ S) V, [4 N4 [5 y
going to experience any of the untoward effects from
% t% t' J1 {" U# t- E8 R7 y. w+ F, ttestosterone exposure as mentioned earlier because
" n9 K% b* U& q4 R4 `the exposure was not for a prolonged period of time.
7 q- Q2 Q9 D$ f2 e7 ]! T) ]& @Although the bone age was advanced at the time of
2 K6 y+ h/ ^9 E7 y. h  Udiagnosis, the child had a normal growth velocity at
# R4 p  f1 e3 r/ t3 vthe follow-up visit. It is hoped that his final adult( p0 p+ ^0 l) i: y; {& D$ b( {& A, O
height will not be affected.
$ C7 W- I: `$ a( P/ a) X; X& hAlthough rarely reported, the widespread avail-. D  m( C1 L) j+ c) X1 z/ b( l
ability of androgen products in our society may
  F  o8 l$ J: e/ Rindeed cause more virilization in male or female
3 n3 s, W; a5 g. J" q. Rchildren than one would realize. Exposure to andro-
2 H; B6 q5 x% G0 S& F6 I2 B' g' Pgen products must be considered and specific ques-# v2 E; m. z' ]# U
tioning about the use of a testosterone product or
4 [# n0 `6 M: a8 F6 F, tgel should be asked of the family members during
( f( Q) v) W! N9 othe evaluation of any children who present with vir-9 S/ [2 F9 }5 h5 }$ f
ilization or peripheral precocious puberty. The diag-4 m# b0 Q" `' j8 F1 x3 r
nosis can be established by just a few tests and by7 ]( \4 E* A* y! ]+ p
appropriate history. The inability to obtain such a7 \2 b3 t7 _# L4 |; y. n
history, or failure to ask the specific questions, may
2 J5 M7 e1 h1 C, t1 k; tresult in extensive, unnecessary, and expensive
8 w7 d: U0 m( }- B) O) Linvestigation. The primary care physician should be
( i- J+ K# i; o& i. E" G: Qaware of this fact, because most of these children
2 I/ z( u+ b; X, o% jmay initially present in their practice. The Physicians’
+ C+ A* m* g5 o2 s! l$ |Desk Reference and package insert should also put a
# [9 g5 h5 \; T6 j2 h0 bwarning about the virilizing effect on a male or
3 t6 c+ \' ~$ B1 u# [0 @female child who might come in contact with some-, T1 W* \  ]0 |3 e' Q# R& m% C
one using any of these products.
9 g, O+ p5 h1 M. H6 CReferences: W% ~6 _/ s& n" g% F4 J4 x
1. Styne DM. The testes: disorder of sexual differentiation0 R9 ]3 O1 W' p, H; R! s; {
and puberty in the male. In: Sperling MA, ed. Pediatric* E0 N* O/ y. f: m0 {( g
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' `. B0 u3 W6 P, [' N1 ^- D2002: 565-628.
: g- Y8 ^$ |) F: _8 K1 J8 x4 h2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious5 f) s' ?+ n) G% A
puberty in children with tumours of the suprasellar pineal
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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 2025-1-10 10:43:39 | 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
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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!
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
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?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

8 V/ r9 J- c; P4 {精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
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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