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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-Old
# ]: |# o) n. L+ J  mBoy Induced by Indirect Topical
6 C: M  F# D! W5 Y  M/ L6 Q( _/ kExposure to Testosterone9 ^$ a; d0 X! `5 C; x
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ w$ ~! ~5 o1 ~  ^+ v
and Kenneth R. Rettig, MD19 V, m+ T- h' Z' k# m8 K! i
Clinical Pediatrics
" Y4 Q/ m5 s" T$ S2 RVolume 46 Number 6
! E! h5 B6 T- CJuly 2007 540-543- H) z: S! `3 q- n1 u" v  M/ s
© 2007 Sage Publications  X: g9 x$ {% \0 p  H
10.1177/0009922806296651  i, ?5 b9 V4 Q) O+ }) o
http://clp.sagepub.com/ m1 T2 g2 L% C  y# e: L9 |
hosted at
$ P- W( Z- T& Y" ]) [http://online.sagepub.com
$ Z$ Q% s- B5 @2 XPrecocious puberty in boys, central or peripheral,) |( D# B7 w* _2 Z7 u  A
is a significant concern for physicians. Central
' Z* w( @; W" L% i5 J% Y1 v6 [precocious puberty (CPP), which is mediated
4 S9 q1 F, m& P" Mthrough the hypothalamic pituitary gonadal axis, has
* \* y/ c9 r& g, C: u* P1 I; Qa higher incidence of organic central nervous system0 C! O6 U' t3 v
lesions in boys.1,2 Virilization in boys, as manifested5 T. L% H' |5 m, i* l
by enlargement of the penis, development of pubic% _( U$ o# ^1 \2 l0 |! u
hair, and facial acne without enlargement of testi-# }" Q) G" j* [8 T7 F, x8 H/ _5 a
cles, suggests peripheral or pseudopuberty.1-3 We2 R# l0 U' y  B9 `- K; x
report a 16-month-old boy who presented with the
- J9 \  D) p% Y( D/ O8 j& tenlargement of the phallus and pubic hair develop-4 [3 f+ w; n; r8 t8 b
ment without testicular enlargement, which was due" |0 d' A, M$ N* W( R
to the unintentional exposure to androgen gel used by
" F. ]( z: W; Kthe father. The family initially concealed this infor-; u3 q$ N' V5 m( x& r; g
mation, resulting in an extensive work-up for this
5 C: k' W4 }' n$ schild. Given the widespread and easy availability of6 C- o1 e$ b& M9 N% N
testosterone gel and cream, we believe this is proba-. G, H# ]& Y+ j+ [$ p
bly more common than the rare case report in the4 ~" [) n4 H6 c9 G. a  F
literature.4( k7 t2 |- r0 q) ?1 U% z% a0 G: M
Patient Report/ n- M3 v% z6 g( y: w
A 16-month-old white child was referred to the0 S: j% l. j& M" @7 A) C1 I
endocrine clinic by his pediatrician with the concern: f3 C0 K9 E  [$ a- i' a; h
of early sexual development. His mother noticed
& r; D" {$ L' @& X/ V  T' G. X' Glight colored pubic hair development when he was
$ a5 ?3 A0 Q7 `, h* F' KFrom the 1Division of Pediatric Endocrinology, 2University of
' z3 P2 E% \- b0 ?3 K: o  ^South Alabama Medical Center, Mobile, Alabama.
; O4 v) S  j( a: mAddress correspondence to: Samar K. Bhowmick, MD, FACE,- h1 N8 m( @: o4 r& T) w! |, N
Professor of Pediatrics, University of South Alabama, College of
1 M0 D' @1 F9 ]/ i! B3 d7 a6 V  r% `Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
% m/ x! I0 H/ d1 F* ]/ o( me-mail: [email protected].& H9 F% o2 P7 |! i) z
about 6 to 7 months old, which progressively became/ r: f6 q% {7 ?2 U
darker. She was also concerned about the enlarge-! o7 s9 Q2 b: |1 U7 V" I" ~
ment of his penis and frequent erections. The child
$ h$ j4 h# T. Y$ ?* B$ p4 Xwas the product of a full-term normal delivery, with
7 m: n! Q4 U0 X* s9 s, R4 wa birth weight of 7 lb 14 oz, and birth length of4 e6 E* [3 W- N; z, B9 C! p
20 inches. He was breast-fed throughout the first year
% D; U0 F( ^, [6 cof life and was still receiving breast milk along with- H5 U2 C" K0 K5 W) Y& ?; m7 f- R
solid food. He had no hospitalizations or surgery,
. K% O! g# A9 A) ^# _! X  qand his psychosocial and psychomotor development
1 `  Q& P- L  o  c- Vwas age appropriate.
% u; y: @" p$ l( \& FThe family history was remarkable for the father,
4 T( x" S: K3 g/ Jwho was diagnosed with hypothyroidism at age 16,
7 b3 h4 ~- D; u4 M; m* I; _$ Qwhich was treated with thyroxine. The father’s
# ?9 W# ~* {- x; o$ Jheight was 6 feet, and he went through a somewhat% Q! d- O( \$ R
early puberty and had stopped growing by age 14.
3 p4 H( S# Q$ y7 C; VThe father denied taking any other medication. The
7 z- ?3 f- ~" w4 o3 @* Wchild’s mother was in good health. Her menarche
; ?) T4 j5 P# N' d, h5 Rwas at 11 years of age, and her height was at 5 feet! j1 c2 G2 X# E* I
5 inches. There was no other family history of pre-
- y4 x0 x3 M9 _- b( V1 Ucocious sexual development in the first-degree rela-  J) c. j! o* m7 i" s! r
tives. There were no siblings.6 g( i+ ?( i  A# g% X: n6 [
Physical Examination
* ?6 O9 m4 q* r5 G% J- O6 A- }The physical examination revealed a very active,
( j+ o" t9 q2 R( Tplayful, and healthy boy. The vital signs documented
- G! J3 z. _7 g7 B( c! h6 xa blood pressure of 85/50 mm Hg, his length was+ d% L6 n7 }' B% `2 |; H1 o
90 cm (>97th percentile), and his weight was 14.4 kg" B1 v  Q+ U1 i  p( ?5 V' N2 U
(also >97th percentile). The observed yearly growth
$ \4 y2 g% q% i+ svelocity was 30 cm (12 inches). The examination of
! p+ T3 L& b+ m" R. k5 W# mthe neck revealed no thyroid enlargement.- ^, K4 q, y, t0 s- S
The genitourinary examination was remarkable for
& |# z. u: r7 R8 ?' Xenlargement of the penis, with a stretched length of
" r" `; G( R0 J# N5 J6 k8 cm and a width of 2 cm. The glans penis was very well
8 c# t. a( m! A3 fdeveloped. The pubic hair was Tanner II, mostly around8 }, Y. L5 g8 w/ w
540
3 \- @: A7 v. i' Tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 c8 K0 L0 M/ {- Z% \; J' r& [
the base of the phallus and was dark and curled. The8 L; w- \; O+ X) P9 l' A
testicular volume was prepubertal at 2 mL each.
& [& U) v$ l+ r% ?( kThe skin was moist and smooth and somewhat" \" [: {3 j6 S4 c8 T: F/ w
oily. No axillary hair was noted. There were no# h2 e  e1 q* I7 M0 o
abnormal skin pigmentations or café-au-lait spots.
/ @! V) _" d. j4 {( q, ~% CNeurologic evaluation showed deep tendon reflex 2+  t. B4 i4 E4 H/ y4 b& W
bilateral and symmetrical. There was no suggestion/ t' @8 o( @) v* E- h8 m- T! ?
of papilledema.$ F9 G& _. k  o
Laboratory Evaluation: \$ r/ g& {7 T) `4 L3 w
The bone age was consistent with 28 months by. G. |9 a* y! A
using the standard of Greulich and Pyle at a chrono-
6 G& _" W0 f+ D6 J9 Vlogic age of 16 months (advanced).5 Chromosomal
6 q; ^( J' d" R- Jkaryotype was 46XY. The thyroid function test
, w( a. |8 C6 P/ i, p3 Z4 ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 ~7 F9 W& K, ?; O5 n" s7 J& wlating hormone level was 1.3 µIU/mL (both normal).( I$ f* \, R) G' {2 {
The concentrations of serum electrolytes, blood# `# x3 K, {/ k+ x& M
urea nitrogen, creatinine, and calcium all were9 I; t1 c3 E: a; m$ s
within normal range for his age. The concentration4 `, A9 M9 {1 O- y
of serum 17-hydroxyprogesterone was 16 ng/dL. k# Q, s1 g: E0 o; y; V/ }. x( ?
(normal, 3 to 90 ng/dL), androstenedione was 20
5 E$ z$ M9 K; ?/ {9 lng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! i: l3 B5 F. ?7 ^( [: b/ cterone was 38 ng/dL (normal, 50 to 760 ng/dL),* z8 w7 h1 |7 n7 F
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 ^6 I7 Q; Z9 L; ]# L49ng/dL), 11-desoxycortisol (specific compound S)
2 I" x, C# \. s& r" mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
; I8 P8 w  s) W* q8 @$ Itisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total( M1 i' i" `% l7 X  ^. @( v- H
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 @$ v$ V$ x; q# Wand β-human chorionic gonadotropin was less than' j0 `. N0 Q$ Z. M, I; E* a0 I6 O1 W
5 mIU/mL (normal <5 mIU/mL). Serum follicular( o* Q" U! e0 g+ s3 R
stimulating hormone and leuteinizing hormone
7 |: q6 e$ o+ Yconcentrations were less than 0.05 mIU/mL& [( d# X7 M% A9 j2 R
(prepubertal).
7 r% z" d  R  P$ H' nThe parents were notified about the laboratory  t6 V3 O9 E' j' W# @2 ?$ A
results and were informed that all of the tests were% {0 i, R4 a0 r5 K6 I5 j
normal except the testosterone level was high. The8 x% P; N0 F5 M$ ^- D& D
follow-up visit was arranged within a few weeks to  [4 i* c! F3 o2 G; X* r
obtain testicular and abdominal sonograms; how-
" J. R1 l  J$ V( Never, the family did not return for 4 months.
5 Y# b/ ^$ L3 }# lPhysical examination at this time revealed that the
( }. m8 i" p* {child had grown 2.5 cm in 4 months and had gained' b$ x* n1 p# H4 |6 u7 p0 z4 Z
2 kg of weight. Physical examination remained0 p4 y2 Z- Y/ B/ j3 U
unchanged. Surprisingly, the pubic hair almost com-* |9 H3 y/ W1 Y+ b
pletely disappeared except for a few vellous hairs at  H. ?6 [  H! ]- m4 N
the base of the phallus. Testicular volume was still 2+ ]  J/ {$ B0 p$ `9 O; Q3 t( x
mL, and the size of the penis remained unchanged.8 q. x: X( @  {. d6 J% N. i8 J
The mother also said that the boy was no longer hav-
8 a% ]3 Q" ?1 O: Ying frequent erections.
' d1 `( k8 J4 T! `Both parents were again questioned about use of
6 D9 o- p2 C% @& Z/ P9 x/ l' h. Zany ointment/creams that they may have applied to
9 z, Y9 Z( o6 J4 i+ P: @/ `the child’s skin. This time the father admitted the( a) T* x% w, }5 x/ {7 @
Topical Testosterone Exposure / Bhowmick et al 5416 m/ C' I; Q& A/ l' m8 q$ B1 V
use of testosterone gel twice daily that he was apply-
; e/ P) V' q0 X1 Ting over his own shoulders, chest, and back area for; D: p9 R$ U  F
a year. The father also revealed he was embarrassed5 E$ X% Z% H" b; g* Z  s5 _
to disclose that he was using a testosterone gel pre-  R7 ~# O- J- s# i/ P1 \# v
scribed by his family physician for decreased libido
8 D2 M4 P! S. q% fsecondary to depression.
8 V/ h" C( n& n- M2 _; V! oThe child slept in the same bed with parents.
( \  O- B. R+ S0 L* ^The father would hug the baby and hold him on his
  S( D: u9 n7 Schest for a considerable period of time, causing sig-
; G0 p& s6 o5 x  r5 x$ t- a5 Pnificant bare skin contact between baby and father.
! f+ b/ H- s/ l+ I9 bThe father also admitted that after the phone call,2 I/ R& g5 N( X1 U  @# W; m/ z; j
when he learned the testosterone level in the baby
# H/ `0 D4 }1 P# w9 {- K2 Lwas high, he then read the product information& X6 ~7 u1 k' N3 O" [$ ?
packet and concluded that it was most likely the rea-
4 r: w* k& x# z% }" g0 Q" Json for the child’s virilization. At that time, they& C  G( i7 `9 L$ @5 v
decided to put the baby in a separate bed, and the
8 n1 o  Y% u) K8 J  Efather was not hugging him with bare skin and had- j$ q! e6 L& f  t# Y9 g5 u0 A5 P0 M% Z
been using protective clothing. A repeat testosterone# W% n0 @* ^, X
test was ordered, but the family did not go to the( X& Q0 S% d1 p2 A; e, O
laboratory to obtain the test.
3 F! i& S5 A7 A4 r3 KDiscussion* n& U* b8 b4 z: t, m6 Q' u$ Q
Precocious puberty in boys is defined as secondary
, D3 H4 H' z$ a+ J7 b& o1 Xsexual development before 9 years of age.1,4
' [+ u  N+ r$ z; U$ }5 JPrecocious puberty is termed as central (true) when
# G6 B' }/ U* j( n" Eit is caused by the premature activation of hypo-
$ ~  U2 F: ^/ p6 Qthalamic pituitary gonadal axis. CPP is more com-& q2 J6 C0 B/ G" L3 k. Z9 P% K
mon in girls than in boys.1,3 Most boys with CPP
* E# M, B' ]2 f# V: U( X$ fmay have a central nervous system lesion that is
' O4 H/ P7 N2 K2 qresponsible for the early activation of the hypothal-8 j" ]5 t$ `# x0 ?
amic pituitary gonadal axis.1-3 Thus, greater empha-
8 L# A  K9 m- s9 rsis has been given to neuroradiologic imaging in  j( a( ]% @: j3 q: Z7 B5 `: |
boys with precocious puberty. In addition to viril-2 X, B1 Y" E' o, b: H
ization, the clinical hallmark of CPP is the symmet-
/ C9 w; E5 A* N2 prical testicular growth secondary to stimulation by
! K7 \) U. ~$ Y7 R+ G$ o. Lgonadotropins.1,3, d  n, z' q7 |& C
Gonadotropin-independent peripheral preco-1 H6 V' z! |( R0 R; U
cious puberty in boys also results from inappropriate" Y3 ~8 p, _1 {3 S" `/ ^
androgenic stimulation from either endogenous or
5 k8 ^. `2 U5 {exogenous sources, nonpituitary gonadotropin stim-0 I  ]1 {/ R; J) P
ulation, and rare activating mutations.3 Virilizing
* ~; w9 T: Q& Ncongenital adrenal hyperplasia producing excessive3 `: p2 B, P) C( ~
adrenal androgens is a common cause of precocious
& D& n( I/ g: v* r' Spuberty in boys.3,49 }" ~5 g* l6 V4 D* P' i
The most common form of congenital adrenal
8 v8 E# U- }; I% ehyperplasia is the 21-hydroxylase enzyme deficiency.2 V6 r. E3 w( g
The 11-β hydroxylase deficiency may also result in: D& ~5 f' I- h3 A1 x% j. C" E
excessive adrenal androgen production, and rarely,
1 i: L( y' n/ G) e& P: Yan adrenal tumor may also cause adrenal androgen
& B, T8 N8 n7 m- J1 C+ C3 Z$ Zexcess.1,3
" d7 F0 o, P& B  s  [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 W% {( _8 {3 X8 s+ {# a
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ q  E8 x: }: B7 z& A) {% d( SA unique entity of male-limited gonadotropin-1 d4 B$ ~4 A. U9 `: i' u: Z
independent precocious puberty, which is also known
0 [! C! r2 h3 Gas testotoxicosis, may cause precocious puberty at a4 l5 Z) u' G+ s, L0 w0 \; }$ J6 E
very young age. The physical findings in these boys
4 Y+ I: k7 r# Z* [( j$ ^6 p' O4 swith this disorder are full pubertal development,0 b' O, Z4 Q) Z- q2 S; R
including bilateral testicular growth, similar to boys
; J* {/ C$ l4 c# Qwith CPP. The gonadotropin levels in this disorder) |9 P( x7 A8 j$ F  y
are suppressed to prepubertal levels and do not show* e; T$ G& p; w2 ^: x
pubertal response of gonadotropin after gonadotropin-/ I  S: G$ l0 \& V0 I
releasing hormone stimulation. This is a sex-linked" b. D9 E1 W" z1 v' p2 S
autosomal dominant disorder that affects only
+ E7 k8 X# d# U* k2 x3 Hmales; therefore, other male members of the family. k# p0 j3 m& L
may have similar precocious puberty.3
: F# x2 ~' }/ q1 J- k# j: [In our patient, physical examination was incon-2 Q! _8 y0 A, y# x
sistent with true precocious puberty since his testi-2 }6 ^$ d) e( w
cles were prepubertal in size. However, testotoxicosis
$ L. e* z+ {8 t) w5 dwas in the differential diagnosis because his father
: E0 V) v$ X" Y- estarted puberty somewhat early, and occasionally,  u. w+ |) I7 a1 j8 ?' c- W7 U* s4 y
testicular enlargement is not that evident in the
( ~$ V( m; L/ F) m6 M" abeginning of this process.1 In the absence of a neg-
. I- a& h5 }( L1 c' Jative initial history of androgen exposure, our4 n( d& a1 w; r  ?1 ^7 z
biggest concern was virilizing adrenal hyperplasia,5 [  `% b1 n, Z5 Z) M3 n+ w6 L7 G
either 21-hydroxylase deficiency or 11-β hydroxylase2 k8 y$ ^; e8 v* Y
deficiency. Those diagnoses were excluded by find-$ b# N7 o- |6 S) I! L
ing the normal level of adrenal steroids.0 N3 Q/ U9 r5 X2 P7 u: ~9 l  t
The diagnosis of exogenous androgens was strongly0 G! a$ A6 @% _# u4 l/ h7 p
suspected in a follow-up visit after 4 months because
7 c- [' Q& x6 L: C! V9 B* d6 I# Cthe physical examination revealed the complete disap-# c" O" P' V6 _* u5 b; C  U+ h
pearance of pubic hair, normal growth velocity, and
) I8 P% R5 n$ n4 g' U, \* P8 Fdecreased erections. The father admitted using a testos-
) e3 x& ?5 A9 ?* m2 {0 \- Fterone gel, which he concealed at first visit. He was* f. Y3 H- U# C- Z
using it rather frequently, twice a day. The Physicians’
) v0 j$ d; H9 z0 n2 O9 N, fDesk Reference, or package insert of this product, gel or; d+ s- [4 S. w% _0 a
cream, cautions about dermal testosterone transfer to, P* a$ S- U: o6 \. o5 T: n
unprotected females through direct skin exposure.+ h! p0 Z/ n- k- t
Serum testosterone level was found to be 2 times the
7 f7 ?. A+ ]4 pbaseline value in those females who were exposed to) p$ R7 S* {* `7 R
even 15 minutes of direct skin contact with their male
* r& d" W" K, I" C3 xpartners.6 However, when a shirt covered the applica-( M) t* X0 N$ q3 T6 p
tion site, this testosterone transfer was prevented.  t2 A5 c: C9 y* O$ I: E
Our patient’s testosterone level was 60 ng/mL,
5 |* @) m8 M8 C5 hwhich was clearly high. Some studies suggest that
. J: L; m; y7 bdermal conversion of testosterone to dihydrotestos-
- o. }; E3 c. N! G. Nterone, which is a more potent metabolite, is more
$ I4 ?6 i' t) Y5 Yactive in young children exposed to testosterone& f: p" A  `5 U2 @
exogenously7; however, we did not measure a dihy-
0 N$ ^" U5 h6 P% Ddrotestosterone level in our patient. In addition to) S5 G- Z9 c# |/ p1 q7 M
virilization, exposure to exogenous testosterone in/ C# S  I9 f7 ~# W- y0 e
children results in an increase in growth velocity and
. n! N' a" _, r2 Iadvanced bone age, as seen in our patient.
( I! \9 Z+ w% A5 h/ r- UThe long-term effect of androgen exposure during# w! X$ J* Y9 K) J& Z  V
early childhood on pubertal development and final# Q  J. i' h9 P+ Z  @
adult height are not fully known and always remain% B! r+ t' P5 V0 v6 y# A
a concern. Children treated with short-term testos-
  S! n  W. i( W- Kterone injection or topical androgen may exhibit some
% e0 X: U0 T7 ^1 F( \6 Q2 Uacceleration of the skeletal maturation; however, after# I% k' O8 E" [" ^" u8 _9 _0 o
cessation of treatment, the rate of bone maturation( I3 o: {$ c' T: c9 z+ Y
decelerates and gradually returns to normal.8,94 n3 o- V) J  D* U$ y% d; j/ T
There are conflicting reports and controversy
: b/ v( H& H. _( c- ^over the effect of early androgen exposure on adult* @/ e3 ^- ^5 E' V6 Z( z
penile length.10,11 Some reports suggest subnormal
: {) E+ B- D, U4 H! [* oadult penile length, apparently because of downreg-2 J# q7 ?: e" G5 P# a' `: p
ulation of androgen receptor number.10,12 However,
" S4 {- T1 A  R7 w  l3 H& iSutherland et al13 did not find a correlation between
( b9 P- ^1 _0 Z2 m2 Uchildhood testosterone exposure and reduced adult
) v1 _' e4 k$ Lpenile length in clinical studies.
6 q& f' {* T6 fNonetheless, we do not believe our patient is- |+ ~; G6 C* q5 S; R
going to experience any of the untoward effects from
" S& K8 q/ ^9 s/ w6 m; n$ ctestosterone exposure as mentioned earlier because9 C7 b, \' ^2 g+ i6 R) e; ?) c
the exposure was not for a prolonged period of time.
( f+ v( q" |8 N4 HAlthough the bone age was advanced at the time of
, U- t: H0 ^; v, B1 x1 adiagnosis, the child had a normal growth velocity at
& {' L# Q/ G. y9 x  Ythe follow-up visit. It is hoped that his final adult9 d4 v* F/ q# G+ }; }: l% O3 g
height will not be affected.
& ]# q9 x  d- s4 r! NAlthough rarely reported, the widespread avail-4 L2 g* K7 _  V4 c# ?( V+ _+ P
ability of androgen products in our society may
6 S  ^! @. o7 ?1 u  J. w7 [1 Yindeed cause more virilization in male or female
8 i+ ~3 w4 \6 v6 kchildren than one would realize. Exposure to andro-
0 e3 a- j4 n3 t9 lgen products must be considered and specific ques-
0 i+ O/ t* |0 o& B2 f, f) Stioning about the use of a testosterone product or7 F/ c" i1 L( p# Q
gel should be asked of the family members during
( C3 t+ D/ S/ b" O( }/ z) Hthe evaluation of any children who present with vir-
! H) D+ w  h1 W1 H; |: i7 iilization or peripheral precocious puberty. The diag-* N' U; v' Q# E0 Q
nosis can be established by just a few tests and by
. q* |* S3 n9 G3 Q5 M3 aappropriate history. The inability to obtain such a
3 w2 Q( L7 c7 q' Q& Phistory, or failure to ask the specific questions, may
" i4 ]& f/ c# E4 presult in extensive, unnecessary, and expensive
1 T% \1 t* `! e1 Z- uinvestigation. The primary care physician should be6 i- @7 |7 L; m& k! U: F$ z
aware of this fact, because most of these children- ^  h. v& `, u- Q
may initially present in their practice. The Physicians’2 G; o$ X$ B$ p! Z) \1 c# [1 ]5 P
Desk Reference and package insert should also put a
3 O! M" Q) R+ ~( B. qwarning about the virilizing effect on a male or
/ B2 b- F& x' f' }, o" h% Kfemale child who might come in contact with some-
$ n% p2 j+ n% _  l1 Mone using any of these products.
- \, ]5 w2 P8 J4 {References; u: \  K: p; w3 ^' G/ F  e
1. Styne DM. The testes: disorder of sexual differentiation; M  S/ A; {) x  f9 K
and puberty in the male. In: Sperling MA, ed. Pediatric3 A) v) ]0 y/ g
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 e% ?0 C( B) u2002: 565-628.. O$ p6 d3 C. z  T. V$ R' r
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ `9 K/ g- X# j. j5 y# P0 H: Z+ Fpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old2 d% C$ J9 B' u0 ]2 E
Boy Induced by Indirect Topical7 A6 Z( ?2 Y) N  u! B' `
Exposure to Testosterone- p0 `3 Z2 g' g4 Y! l
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% M( H. s. U" F3 j% [% \
and Kenneth R. Rettig, MD14 v$ u1 Q# j2 z) ~6 n; P- j
Clinical Pediatrics
  Q0 V) I7 U/ t" B$ _1 k- vVolume 46 Number 6, G; G. r* F2 U# v
July 2007 540-543
+ ?7 G5 j+ [8 p( f7 p© 2007 Sage Publications
; k1 D) u$ d9 A1 L5 L' X* Z# e10.1177/0009922806296651- D& ~" o1 r  T* w, a
http://clp.sagepub.com
  J. e) G# g6 e3 m- s7 }! ^) ihosted at
/ R0 o1 T+ u# R. z; l. s5 ghttp://online.sagepub.com! U0 z) l2 h1 R- A- ^4 u4 X
Precocious puberty in boys, central or peripheral,! z( ~/ p+ i/ `) \
is a significant concern for physicians. Central
( F( R) G, ^5 Jprecocious puberty (CPP), which is mediated
' v1 T; w  Q$ t6 L, Wthrough the hypothalamic pituitary gonadal axis, has
- j9 f# i, C% ]/ r- s% M( ?a higher incidence of organic central nervous system+ c( W- e4 P$ V) `% n; ?
lesions in boys.1,2 Virilization in boys, as manifested) d* O+ k) o. K; ?. {3 J) N
by enlargement of the penis, development of pubic
4 x, B0 c. E. P$ P8 ^2 J- m' M% xhair, and facial acne without enlargement of testi-4 A/ [0 T* `1 M' U6 h& G
cles, suggests peripheral or pseudopuberty.1-3 We. z9 s) E( n  i. X9 w
report a 16-month-old boy who presented with the! U( H! [) h9 H3 ^6 J3 l! S
enlargement of the phallus and pubic hair develop-- T/ R) m4 ]' p% _- E9 f; g
ment without testicular enlargement, which was due
' |8 s$ {* [/ ~4 b$ Yto the unintentional exposure to androgen gel used by5 l/ ]9 o  k' q% S0 I
the father. The family initially concealed this infor-; ~1 \8 k, |; G8 ]7 `
mation, resulting in an extensive work-up for this
( C6 \- n! ?) f0 {9 D: Ychild. Given the widespread and easy availability of6 l4 Y/ S9 d; z. S
testosterone gel and cream, we believe this is proba-$ }$ U, b3 q/ V. M! d
bly more common than the rare case report in the/ `/ d2 l" t- e$ |2 |' x2 X
literature.4' @" e9 E4 m# S. O4 R
Patient Report$ s; Z/ o5 K% R& h& ?' f
A 16-month-old white child was referred to the% P; ]8 \( N/ e8 N; q& O
endocrine clinic by his pediatrician with the concern, R6 ^3 L$ y9 H, O& t
of early sexual development. His mother noticed5 O6 G( F' v. Q- V
light colored pubic hair development when he was
1 G3 H: M4 G$ y" wFrom the 1Division of Pediatric Endocrinology, 2University of
5 g5 b. {6 G# }) u+ O  jSouth Alabama Medical Center, Mobile, Alabama.* v5 R2 n8 d5 A- |
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 R  N; d* B/ [# m$ s' ]! A" t% v
Professor of Pediatrics, University of South Alabama, College of
, i' N( j: E( C: M* G6 d9 C9 _) BMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 ^' {: v1 J/ V# ?' C
e-mail: [email protected].& k- ^8 p+ L5 H+ u7 w3 L) g
about 6 to 7 months old, which progressively became
6 Q) Y9 @3 y' T; s* f/ Ldarker. She was also concerned about the enlarge-4 a+ }2 @) o$ L: x, l
ment of his penis and frequent erections. The child
, G" T3 i# w  n% [* Owas the product of a full-term normal delivery, with
! r4 D* o3 P2 B: k. c- x7 Ea birth weight of 7 lb 14 oz, and birth length of$ D# u" q! z: p+ X# M' w6 X
20 inches. He was breast-fed throughout the first year" l# ~1 K3 s. `. l1 q- ~3 O) f
of life and was still receiving breast milk along with
7 l5 i- N* ~7 h  ]solid food. He had no hospitalizations or surgery,6 S1 I+ X/ S5 @4 f; p4 J
and his psychosocial and psychomotor development
5 ?6 [+ h; W3 W3 G# m: Z: Y, dwas age appropriate.
& F# ~+ u1 L) GThe family history was remarkable for the father,& _* H0 s/ }; D$ B
who was diagnosed with hypothyroidism at age 16,4 b/ x/ T9 R/ \5 \/ K6 c; T9 B
which was treated with thyroxine. The father’s% Y* e9 O3 w' w2 _( p
height was 6 feet, and he went through a somewhat: u& e0 k8 I; q& G5 s  O8 D
early puberty and had stopped growing by age 14.+ e  N$ F3 E! d. V
The father denied taking any other medication. The
9 [6 @) `) D9 e. V, s* A% Echild’s mother was in good health. Her menarche
  L* y4 h$ E# L. D6 o( Kwas at 11 years of age, and her height was at 5 feet# F" W4 C3 F  S7 ]" g
5 inches. There was no other family history of pre-+ c3 m9 k6 S% t. ?& R! a
cocious sexual development in the first-degree rela-* Y' G2 U6 b4 L$ B5 G" _
tives. There were no siblings., O9 N( d( L" b/ M! i( E
Physical Examination( @3 x9 l' P0 X+ |2 O/ M
The physical examination revealed a very active,
7 ^7 e1 o2 c4 A! lplayful, and healthy boy. The vital signs documented
* W) w# _; m( j7 U/ R, N1 m& m' {a blood pressure of 85/50 mm Hg, his length was7 _6 s! P$ B+ X) j: d* y
90 cm (>97th percentile), and his weight was 14.4 kg" a0 R8 S- C* ~
(also >97th percentile). The observed yearly growth5 c5 F  i9 J8 H! w3 p
velocity was 30 cm (12 inches). The examination of
8 l+ F% Q; c. N6 [" j6 gthe neck revealed no thyroid enlargement.: K0 L' q* J: A  o
The genitourinary examination was remarkable for4 a! J$ a) n% w' N) V
enlargement of the penis, with a stretched length of( Z& I4 T0 g0 }7 `3 D/ @
8 cm and a width of 2 cm. The glans penis was very well
$ i) c5 g: F+ Q0 x" H' F1 Ydeveloped. The pubic hair was Tanner II, mostly around; m$ T% f. I0 P  }0 C
540
. u( W: [8 N2 K# e! t" cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 R  A7 m& x( p: p$ ?the base of the phallus and was dark and curled. The
5 S) H' E0 [( g" utesticular volume was prepubertal at 2 mL each.* Q; L5 P) J8 \( f2 _8 i
The skin was moist and smooth and somewhat4 o3 c7 B. A0 `$ P7 ^3 y0 w
oily. No axillary hair was noted. There were no
+ ~" g4 H! F- Oabnormal skin pigmentations or café-au-lait spots.
8 \- A$ g, b. TNeurologic evaluation showed deep tendon reflex 2+
4 d# ~0 r6 N& v1 X* c+ E$ Wbilateral and symmetrical. There was no suggestion( i5 F. g: y7 \) i+ P* R
of papilledema.
3 A6 v8 N; D' {2 _Laboratory Evaluation
; `9 g( ^/ I1 f; B) j/ n; P: _- XThe bone age was consistent with 28 months by
/ d  N5 ~8 `% K' wusing the standard of Greulich and Pyle at a chrono-" H( x1 I! ?7 ]0 |
logic age of 16 months (advanced).5 Chromosomal& y" j7 s6 O, o
karyotype was 46XY. The thyroid function test
. W9 p2 i& z0 U. u$ H7 y7 s2 `, Lshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
- M. H- A( o  y* X; i! Vlating hormone level was 1.3 µIU/mL (both normal).* x: r' W; O7 [% ~, V1 G
The concentrations of serum electrolytes, blood* u/ O4 M# O+ j/ K2 D" b- x
urea nitrogen, creatinine, and calcium all were: J# k' O/ U& I% N3 k# [" V3 E
within normal range for his age. The concentration
, W# p& _. K, J: ?" F# M3 {, Mof serum 17-hydroxyprogesterone was 16 ng/dL
4 s1 m5 l6 P3 V& l' [9 {; g& G(normal, 3 to 90 ng/dL), androstenedione was 20& p' a% y" ]9 `. n, ]
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  g. ?/ n/ L+ k+ Q6 A  M
terone was 38 ng/dL (normal, 50 to 760 ng/dL),* \/ f8 o8 u5 q% x. j
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 `! Q9 B7 \2 H4 |: g) X49ng/dL), 11-desoxycortisol (specific compound S); M6 K$ J) d# ^8 V* _
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
0 }( A4 o) B( [1 a& `+ _tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; b4 K' K9 h* b# s! h# B3 j" G; z' Ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),  \4 }8 Y, u  ~) i
and β-human chorionic gonadotropin was less than) o# S+ j2 V, d/ M
5 mIU/mL (normal <5 mIU/mL). Serum follicular7 D. S) V4 Y3 q0 U8 g* e
stimulating hormone and leuteinizing hormone- c" i) a9 n; [. T( \
concentrations were less than 0.05 mIU/mL6 \/ y7 ], t& J; |. R1 y1 }
(prepubertal).
! Y' f* n& |  d- s$ B$ O, N3 }) Y* kThe parents were notified about the laboratory
$ Y& e* t4 ~0 r. K4 S' Wresults and were informed that all of the tests were
/ N$ T8 B1 W0 s$ bnormal except the testosterone level was high. The/ R$ G9 T* {, w1 A
follow-up visit was arranged within a few weeks to
& C* r) |4 [2 o. Cobtain testicular and abdominal sonograms; how-$ m& `: o& w# g, H0 O
ever, the family did not return for 4 months.( L( W8 {  {' z4 m7 j
Physical examination at this time revealed that the# n( y( G8 f& {* O, S
child had grown 2.5 cm in 4 months and had gained9 i% }+ N4 T; L8 q% {4 v
2 kg of weight. Physical examination remained
6 z5 r$ Q8 k: Lunchanged. Surprisingly, the pubic hair almost com-: h8 _0 W( J/ a
pletely disappeared except for a few vellous hairs at, o7 s; b1 s, H4 T7 B
the base of the phallus. Testicular volume was still 22 b0 E9 A" W0 r- ?2 S% W
mL, and the size of the penis remained unchanged.
4 A/ k+ J) t& p) w0 QThe mother also said that the boy was no longer hav-$ G0 T+ j5 k" K# l
ing frequent erections.9 k+ N2 ?) K+ _8 N  E, ~6 Q* I
Both parents were again questioned about use of
# _$ R# S) L9 l- Iany ointment/creams that they may have applied to9 i( ~0 u1 L- C+ W+ A0 c' b
the child’s skin. This time the father admitted the  g+ X' I5 [) o4 `; K$ p; [4 a* _2 p
Topical Testosterone Exposure / Bhowmick et al 5418 v; f1 _' G* W! A" g
use of testosterone gel twice daily that he was apply-
! N: f% K7 `# A% M* x% \ing over his own shoulders, chest, and back area for
/ a2 `" C5 {0 l& s' S& e' ^a year. The father also revealed he was embarrassed! {) P% f/ ^& f. m  U
to disclose that he was using a testosterone gel pre-
3 B0 i+ V1 I* A+ ?3 ~6 ?scribed by his family physician for decreased libido
) y, \* F" s2 Q% \$ N- Hsecondary to depression.
" @7 H/ R4 d4 x9 s! t0 IThe child slept in the same bed with parents.
" t2 Q+ V4 k% g& Z( OThe father would hug the baby and hold him on his& P% V7 K$ K- W: a
chest for a considerable period of time, causing sig-
- k4 e6 @/ |# tnificant bare skin contact between baby and father.
1 E+ d! h( w  ?4 T2 H1 aThe father also admitted that after the phone call,
# e4 q1 v0 a3 ?: f' awhen he learned the testosterone level in the baby6 J, j: _( S: S  t& H* L# h3 t
was high, he then read the product information( K& U- k9 z- i, g2 a
packet and concluded that it was most likely the rea-
9 Y' m' v7 s; i7 fson for the child’s virilization. At that time, they1 q3 N" T( S( y7 q
decided to put the baby in a separate bed, and the
! D( M4 H* j  Q$ a( V" ifather was not hugging him with bare skin and had
3 {8 [8 m0 r" A. X/ X- @. sbeen using protective clothing. A repeat testosterone6 t6 ^7 C7 K. \- b: E5 t" _" ^
test was ordered, but the family did not go to the
& Y; o- n. p9 \laboratory to obtain the test." a) K  g& w: Z0 W6 X. |: w
Discussion
- O# U) R( P+ Z+ T# dPrecocious puberty in boys is defined as secondary
; \, [$ J" P+ Lsexual development before 9 years of age.1,4
2 R5 V1 V. @8 W+ ]/ mPrecocious puberty is termed as central (true) when" |4 w# K5 J- F" S2 k3 T! k# U
it is caused by the premature activation of hypo-' N, A# w0 M+ t" j
thalamic pituitary gonadal axis. CPP is more com-
4 i9 ?. A2 J% }  v6 u8 m' [+ \5 Jmon in girls than in boys.1,3 Most boys with CPP
' [  K: ?/ y3 I6 x: gmay have a central nervous system lesion that is0 l' h6 l. U1 c; A! h1 o0 X
responsible for the early activation of the hypothal-: H: t5 K8 m* K) \* }
amic pituitary gonadal axis.1-3 Thus, greater empha-8 p$ S# j$ l" x- c; S/ F
sis has been given to neuroradiologic imaging in6 T3 `0 W( ?' f; k  N/ s
boys with precocious puberty. In addition to viril-
7 N0 J* u8 q( {8 d* E! oization, the clinical hallmark of CPP is the symmet-$ Z6 {* O4 c" h: H, `
rical testicular growth secondary to stimulation by1 ~2 N# b) a$ {0 T. D" I: a/ n
gonadotropins.1,3" F2 P. o0 r; l5 _3 _2 b* G
Gonadotropin-independent peripheral preco-
( @' l' p5 s* e/ L0 xcious puberty in boys also results from inappropriate! E/ w1 g, F: o9 E0 u- G
androgenic stimulation from either endogenous or8 X  w( ~2 T& x9 z5 \2 j1 x
exogenous sources, nonpituitary gonadotropin stim-1 E. v* z2 J1 o( v2 H1 P
ulation, and rare activating mutations.3 Virilizing
2 z+ \% k2 Y3 w( z( p) k: [  M! d8 U/ Vcongenital adrenal hyperplasia producing excessive
3 j& w! H  ]& Z$ kadrenal androgens is a common cause of precocious
: a5 `$ B' ^+ s9 X2 B6 p* upuberty in boys.3,46 J& L6 r/ Y& ^4 j( C. G" m8 z
The most common form of congenital adrenal
; x  B4 O0 ]2 r+ \  v/ chyperplasia is the 21-hydroxylase enzyme deficiency.1 \3 Y! \3 q% [1 g- @2 w, e
The 11-β hydroxylase deficiency may also result in
+ n5 Y* R% `% _3 U& Uexcessive adrenal androgen production, and rarely,7 N0 w/ r3 Z- X$ ?6 M+ t; n
an adrenal tumor may also cause adrenal androgen
$ \. V- b+ z6 T2 \: Vexcess.1,3& K0 P' `' k! W8 B# u* [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& P" [" s" N) @6 w1 p4 \
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& t9 a& d6 ~  G6 M( C* k( Q& QA unique entity of male-limited gonadotropin-
5 T! {* ^! @9 @; Rindependent precocious puberty, which is also known
- v) {% s+ o) z, vas testotoxicosis, may cause precocious puberty at a" \) E0 G" k& d: N
very young age. The physical findings in these boys& L# ~* s3 \! Q) J) c
with this disorder are full pubertal development,
* Q; b2 l& v: A" g, }! \# p" ~4 t4 Cincluding bilateral testicular growth, similar to boys
  s1 \3 b$ x) R. awith CPP. The gonadotropin levels in this disorder
- W. z3 N$ J- Q# Mare suppressed to prepubertal levels and do not show! u* Z9 J# f0 N
pubertal response of gonadotropin after gonadotropin-
# ]! `% q' ?  [  ireleasing hormone stimulation. This is a sex-linked
, D4 |' O! p- X) gautosomal dominant disorder that affects only
) r2 K" F( W8 {4 O" Y. tmales; therefore, other male members of the family
: `' {) k; `. R0 Imay have similar precocious puberty.3
( i) G1 ]# ]+ q$ ^0 d& F9 d! WIn our patient, physical examination was incon-1 O7 g6 m5 ^5 e  U5 f; Z2 p4 a
sistent with true precocious puberty since his testi-4 b% [; y- d$ c  N: {+ K  d6 F
cles were prepubertal in size. However, testotoxicosis
, ]1 R/ A* C$ `% [# k  vwas in the differential diagnosis because his father
6 O4 ]8 }! L2 U% N7 J# g8 Y) Jstarted puberty somewhat early, and occasionally,' p9 }6 W4 i6 _1 c+ y) G
testicular enlargement is not that evident in the
+ |- P0 h( u  Z! Kbeginning of this process.1 In the absence of a neg-8 x0 F! l" P$ Q+ T  p, I
ative initial history of androgen exposure, our
2 C+ z6 Q- d+ d2 Vbiggest concern was virilizing adrenal hyperplasia,- w$ n% j# X& p  ^3 W
either 21-hydroxylase deficiency or 11-β hydroxylase
" B6 B# B) i( _4 _: kdeficiency. Those diagnoses were excluded by find-# R+ D% A; P. k/ H, D
ing the normal level of adrenal steroids.( b$ f/ Q2 t" i' o
The diagnosis of exogenous androgens was strongly
4 B- j& _) m" `, O3 @suspected in a follow-up visit after 4 months because8 [8 y4 E2 Q: p( F; x& h
the physical examination revealed the complete disap-$ @' `2 P# w% `
pearance of pubic hair, normal growth velocity, and; w/ l# P; K9 B. g% ]8 n/ x& V
decreased erections. The father admitted using a testos-
( S8 N! |# R1 w" i4 u) ]0 Tterone gel, which he concealed at first visit. He was; _0 ~( O0 E* @1 A  c
using it rather frequently, twice a day. The Physicians’
- F3 n& z# N. M  t9 ]0 z" w* RDesk Reference, or package insert of this product, gel or- ^. X$ d; A: y' H* D
cream, cautions about dermal testosterone transfer to
6 Y+ m, p# r. M! Aunprotected females through direct skin exposure.! M' I/ @" W* F
Serum testosterone level was found to be 2 times the
' d# J- j+ O6 m  R/ zbaseline value in those females who were exposed to6 @" U3 O1 x) P/ C! {+ ?
even 15 minutes of direct skin contact with their male$ c. ]2 M5 W% u' G- }
partners.6 However, when a shirt covered the applica-
8 k1 [0 O6 o, W# t6 btion site, this testosterone transfer was prevented.
+ D- |( h; |" Y. B8 ?' lOur patient’s testosterone level was 60 ng/mL,
& S+ l* s) B- p! [8 i, `which was clearly high. Some studies suggest that( \( H7 ~* w8 Z! X3 y
dermal conversion of testosterone to dihydrotestos-9 n" `/ ^* S) J
terone, which is a more potent metabolite, is more; ^. x. H, Q3 q0 \* G+ J' G
active in young children exposed to testosterone
" t7 W+ u- N# `7 Uexogenously7; however, we did not measure a dihy-
5 n# E+ P/ w" hdrotestosterone level in our patient. In addition to
3 l7 f: a- p0 z5 @6 }( g) t  Avirilization, exposure to exogenous testosterone in
# o; D& U6 k, J$ _children results in an increase in growth velocity and# `* K4 g; h) i! N; J4 w* R, F
advanced bone age, as seen in our patient.. g3 W1 H6 j' _
The long-term effect of androgen exposure during& _# G4 E* \3 `8 f; L: w/ y
early childhood on pubertal development and final1 X6 b( u. @; Q7 W, \+ ^, F
adult height are not fully known and always remain
# ?* U; `- t! s2 P  |" @; Ga concern. Children treated with short-term testos-5 ?0 ]9 X1 y9 @" K
terone injection or topical androgen may exhibit some
$ X& i* E, h# P; @+ sacceleration of the skeletal maturation; however, after
# a& q, S4 D  H# Ecessation of treatment, the rate of bone maturation
+ A( b' x2 L  Odecelerates and gradually returns to normal.8,9( P& ?8 x7 C0 _- G) C% ]! Y
There are conflicting reports and controversy% p1 Z5 f4 ^* b! W  g+ w' G' G
over the effect of early androgen exposure on adult( _3 m5 R" p. s( b4 Y- [" s
penile length.10,11 Some reports suggest subnormal
; S3 ]( H1 ^5 i9 ]adult penile length, apparently because of downreg-4 v+ G( \- `2 M! Q( w4 h9 c
ulation of androgen receptor number.10,12 However,
7 W  s& p* h  ~& K, v7 U; [. @Sutherland et al13 did not find a correlation between
* E6 y8 n: `3 F% y; T8 tchildhood testosterone exposure and reduced adult0 b5 v% o/ g2 Y5 [& Z: Z
penile length in clinical studies.2 q2 _7 a' M" r& r6 p
Nonetheless, we do not believe our patient is7 H* t' i/ e; [# ?9 r
going to experience any of the untoward effects from1 O% z5 I, a" k. H
testosterone exposure as mentioned earlier because) o3 m. G; `$ v7 Q0 S7 Q. G( \* h+ Z
the exposure was not for a prolonged period of time.: A* c3 C. Q- f7 R3 G3 f
Although the bone age was advanced at the time of
# D4 u7 y( L1 z2 Rdiagnosis, the child had a normal growth velocity at
' s. v+ u4 x& @' Z- {5 e/ Fthe follow-up visit. It is hoped that his final adult
$ o0 L  b0 y! b0 Z' P2 y: bheight will not be affected.: u  p, x+ r# `9 j
Although rarely reported, the widespread avail-% g8 L1 \  g2 h
ability of androgen products in our society may
1 T4 ~8 ^* v. ?5 |: r" ^2 ]indeed cause more virilization in male or female
: b* b0 K) E+ Z3 p1 r1 Nchildren than one would realize. Exposure to andro-
5 G8 ^2 T( r! Z+ X$ cgen products must be considered and specific ques-$ X2 A$ m" d. `6 M
tioning about the use of a testosterone product or9 ?4 z" \( w6 }, F# D5 E- ^
gel should be asked of the family members during5 _9 N' E% c1 k
the evaluation of any children who present with vir-
" H! m% B2 u( E* b* ]8 j8 Uilization or peripheral precocious puberty. The diag-( |; {8 B7 W( I. |! \
nosis can be established by just a few tests and by$ ?+ g$ b" X8 L) o8 O: D
appropriate history. The inability to obtain such a2 o; {: [" \$ |$ p" T  H3 S9 |/ J  D
history, or failure to ask the specific questions, may8 C3 T6 l$ x% ~# g% x' V- b8 A
result in extensive, unnecessary, and expensive- h' G9 V4 ~, S, i$ a
investigation. The primary care physician should be1 W0 V1 U: C: G
aware of this fact, because most of these children9 q4 ^  c1 c. U, b- K4 p
may initially present in their practice. The Physicians’
# |+ b4 H/ `7 D+ f2 p' NDesk Reference and package insert should also put a
* x5 E  V: Y% ewarning about the virilizing effect on a male or
/ Z- B3 j1 C! Y& w, [, f9 ?female child who might come in contact with some-, e8 X7 h' k  G& g% z- n, C% @
one using any of these products.% G, V3 J8 b, Q7 q! w
References
& ?4 j5 k0 Z  l# s2 ?0 ?1. Styne DM. The testes: disorder of sexual differentiation
8 P% B5 B8 Z0 r3 cand puberty in the male. In: Sperling MA, ed. Pediatric
6 x, p: N' {' ~Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 A, y0 E- Q  P  d
2002: 565-628.
, W7 ?. Z; K4 B1 J2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious3 N) N. o! H& M% ~. u
puberty 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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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

2 X  |5 }" Y5 `$ E/ x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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