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Sexual Precocity in a 16-Month-Old
9 Z. _! c$ H/ S2 N1 A. E2 {2 N% N8 \Boy Induced by Indirect Topical
& m2 g: @( R' Q2 g0 k3 N' uExposure to Testosterone4 k+ m7 g7 D4 {4 {. d
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 ?/ }8 o# ]$ J0 S, e0 k, gand Kenneth R. Rettig, MD14 C6 J7 V* K! f- C2 k+ p
Clinical Pediatrics
- b5 z. a/ }3 Z5 B% F" y0 gVolume 46 Number 6  e6 L1 K4 e2 x0 W, @) V% P
July 2007 540-543
: ]  L7 i% U+ I, N  Q: F& [8 d  G4 V© 2007 Sage Publications+ o8 \+ e+ t+ Z, T: X
10.1177/0009922806296651: K7 \/ j' i5 ]
http://clp.sagepub.com! I: K! [! z. c( j& N, z9 N
hosted at) p6 x5 G& F' s, k
http://online.sagepub.com
( r  f9 e) V0 k1 p  E5 kPrecocious puberty in boys, central or peripheral,
. V! S' s) T, S% y: Kis a significant concern for physicians. Central, a9 x- U0 j  ^9 s/ m$ \2 N
precocious puberty (CPP), which is mediated1 S* K7 X0 L7 `' n. B
through the hypothalamic pituitary gonadal axis, has
7 F/ C! {7 ?0 z7 o* z3 m) w! fa higher incidence of organic central nervous system
: |8 h$ l$ {0 q0 ]6 F7 U: Clesions in boys.1,2 Virilization in boys, as manifested  W- _+ z8 T* H/ i0 f4 M
by enlargement of the penis, development of pubic
0 {  w' w) y- m2 B) _2 `hair, and facial acne without enlargement of testi-, p( j) \& @. `( r% U
cles, suggests peripheral or pseudopuberty.1-3 We7 ~- ^1 U  g/ \: a( |% a3 U( e' |
report a 16-month-old boy who presented with the0 y3 Q% D% Y0 O( C
enlargement of the phallus and pubic hair develop-; l' `$ u6 ^0 r2 F5 r8 }$ |) @, a# r
ment without testicular enlargement, which was due
: {, G- s/ S3 H# H  T$ e& Ato the unintentional exposure to androgen gel used by5 J; C$ [+ u9 U% ^% Z
the father. The family initially concealed this infor-
; A- M: Q6 I" t- S3 e, _& Pmation, resulting in an extensive work-up for this
% ^8 I/ N# ]( ], p- a3 nchild. Given the widespread and easy availability of& h: O4 O+ u$ Z; V$ a) l% v' @! ]
testosterone gel and cream, we believe this is proba-
3 n% _4 h. x) B0 F! vbly more common than the rare case report in the
3 H( H. {& n. `+ C4 J  o( Sliterature.4
: R1 G% K7 ?, N& oPatient Report
; f3 n3 L. M9 J1 R2 ~A 16-month-old white child was referred to the; w# @" l) H  q( \" \3 l& s
endocrine clinic by his pediatrician with the concern1 _1 ^: B, \/ l4 z9 e4 u+ x# m
of early sexual development. His mother noticed
. d4 U  K5 ^+ _/ wlight colored pubic hair development when he was
8 m1 y* K; ]  z' E3 O* fFrom the 1Division of Pediatric Endocrinology, 2University of4 ]- r5 S; X3 T1 f8 h! ]9 M
South Alabama Medical Center, Mobile, Alabama.
4 N7 C. }7 T4 @5 _9 QAddress correspondence to: Samar K. Bhowmick, MD, FACE,+ g" L& b! |; ~2 k. j
Professor of Pediatrics, University of South Alabama, College of
: x, u' R2 w; u6 U, JMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( z9 b  r2 o4 l+ k: |3 Q8 Xe-mail: [email protected].
  A7 p1 D2 K; n: tabout 6 to 7 months old, which progressively became0 F& u% m" U/ e# E$ U1 X) N( w
darker. She was also concerned about the enlarge-
  i7 v  x3 T+ \8 A9 F2 S2 `7 O6 `ment of his penis and frequent erections. The child
4 ?( f. I: r' ywas the product of a full-term normal delivery, with
" |' G$ a% G. za birth weight of 7 lb 14 oz, and birth length of
/ L# T. r' d6 X6 r9 _9 d  _7 ?6 I: Q20 inches. He was breast-fed throughout the first year
$ [* ^$ e+ ~: ^) E( G2 q. ^) t- kof life and was still receiving breast milk along with
/ U5 n( q' Z* H( F  Qsolid food. He had no hospitalizations or surgery,
  R& Q0 z# g6 J* H; }6 hand his psychosocial and psychomotor development
; ]8 }2 ]5 b# z/ iwas age appropriate.
, T; a+ D# T. v+ S% j# M: x- nThe family history was remarkable for the father,
  {! L! T% N0 ~: awho was diagnosed with hypothyroidism at age 16,; B) O) ~2 g, n1 E2 r5 n* ?; b, c# k
which was treated with thyroxine. The father’s/ S; k& j9 W) Q. K! @
height was 6 feet, and he went through a somewhat
( K9 M- `. U! f2 J# P6 g1 s( n2 hearly puberty and had stopped growing by age 14.
* W% T: f0 B3 R2 R4 h( nThe father denied taking any other medication. The# {5 T! x$ Q$ e9 Q/ b  S
child’s mother was in good health. Her menarche
8 N5 J5 L4 Y7 d& o3 D) W. B% D* _" Jwas at 11 years of age, and her height was at 5 feet
6 x( Y( @: y" l/ x4 X5 inches. There was no other family history of pre-
6 X- C" z# F7 y3 ^: O, b$ a6 \9 Mcocious sexual development in the first-degree rela-' ~8 J2 K- @2 d* _: X$ Y
tives. There were no siblings.2 x- q1 X4 ?; I) J4 L% j- x
Physical Examination
5 W( O0 a' A7 [9 O9 ?The physical examination revealed a very active,4 y! r8 r0 H# l3 E! Z
playful, and healthy boy. The vital signs documented& W3 O" _5 U' ], Y
a blood pressure of 85/50 mm Hg, his length was
' M6 k" E1 i0 s: a90 cm (>97th percentile), and his weight was 14.4 kg# N) M: K! Y* N& i9 e# G
(also >97th percentile). The observed yearly growth
( X6 _! j, r1 @1 ?velocity was 30 cm (12 inches). The examination of) E' e! O, S; j
the neck revealed no thyroid enlargement.; R2 J& F9 y0 b$ l- u# v
The genitourinary examination was remarkable for& }3 N/ B3 y4 f3 s4 Z, w
enlargement of the penis, with a stretched length of
- L7 w8 _3 V1 T& t8 cm and a width of 2 cm. The glans penis was very well! b  C# j, g9 B9 b3 q1 ~
developed. The pubic hair was Tanner II, mostly around
, _6 l. b3 S0 N) A3 M& A540% C! e- P! u0 d8 p
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 ^: f# k4 A4 i% M4 a6 l0 ^8 W
the base of the phallus and was dark and curled. The4 C. z# g3 m. G% m+ m2 q
testicular volume was prepubertal at 2 mL each.
2 \9 f0 `. i  w) c( S: P8 yThe skin was moist and smooth and somewhat6 w$ k$ ~( [) Y
oily. No axillary hair was noted. There were no; b2 C9 p# K3 a: {" j
abnormal skin pigmentations or café-au-lait spots.
/ W& ^9 F  g' _" eNeurologic evaluation showed deep tendon reflex 2+
2 w; E  Q  W. |4 Bbilateral and symmetrical. There was no suggestion
3 s6 o  [3 L7 d( _: |5 ^of papilledema.; U% o0 E4 h1 P2 Y$ Y
Laboratory Evaluation
9 E! @. ]; R* W& N8 j( B& |1 MThe bone age was consistent with 28 months by
% _3 R1 |- V3 G% E; t2 Pusing the standard of Greulich and Pyle at a chrono-
9 l, a7 @" a/ h7 G3 G* Blogic age of 16 months (advanced).5 Chromosomal/ z3 t0 X( c% V3 {  J$ c, `1 o
karyotype was 46XY. The thyroid function test
* J% N5 i/ H& e  g# \1 N& {showed a free T4 of 1.69 ng/dL, and thyroid stimu-( ^" k0 F$ D" f& W
lating hormone level was 1.3 µIU/mL (both normal).$ ^- P) P' @" G0 T5 n# o. O
The concentrations of serum electrolytes, blood/ s& C6 G/ ~' m" f) T
urea nitrogen, creatinine, and calcium all were1 v8 ]3 C0 W% O# v% P
within normal range for his age. The concentration
- a! k+ V$ U% j" Pof serum 17-hydroxyprogesterone was 16 ng/dL
$ h" W" u1 l6 p(normal, 3 to 90 ng/dL), androstenedione was 20$ D% _$ {& L, I# s% B& T% H7 Z
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 N+ i2 E2 w& h3 A5 S# C
terone was 38 ng/dL (normal, 50 to 760 ng/dL),9 p" ]6 [5 M/ V; f7 C6 T3 i7 b& C
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
. j& [' f1 L# x# R& O. y; r, n49ng/dL), 11-desoxycortisol (specific compound S)( e+ r- r/ R% J+ {* p. g4 u1 U* g+ u- N
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-1 S( {2 G# q  e; n3 Y9 E
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total  S2 N, S. I0 s8 |6 @# [
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( Y, L6 [- M$ c- M
and β-human chorionic gonadotropin was less than
) W. ?) v0 n. h3 F3 M5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 ?3 N4 _# L+ L" o8 ^2 W: ^$ Ystimulating hormone and leuteinizing hormone
) d$ }0 f& ?# dconcentrations were less than 0.05 mIU/mL
0 Y$ |8 \8 {1 v& O(prepubertal)., \+ B" g) w' b/ k
The parents were notified about the laboratory
! e$ s, ^) `% Y) ^+ s' d8 @) Q$ S  Aresults and were informed that all of the tests were
* [* w* ~% Y# A: e8 Inormal except the testosterone level was high. The, J, d2 H% Y/ i7 I7 O- j
follow-up visit was arranged within a few weeks to
: G% G2 K5 O; N- iobtain testicular and abdominal sonograms; how-
' D5 a! n0 @- }8 g/ Cever, the family did not return for 4 months.
% T. _" s+ s* b' N2 ^) \Physical examination at this time revealed that the
+ O" \, q- b4 B# j7 C7 Echild had grown 2.5 cm in 4 months and had gained
# y$ E& H" ?6 Q4 ~! V0 L2 kg of weight. Physical examination remained- }/ h: X$ h7 w0 @2 ]/ g; N' v
unchanged. Surprisingly, the pubic hair almost com-7 A3 ^( }% n1 N) Z- u. H. I) r$ G
pletely disappeared except for a few vellous hairs at( |$ Z9 Q! U4 K4 t  u; S
the base of the phallus. Testicular volume was still 2# s. ?+ p9 J" e$ _) `, @
mL, and the size of the penis remained unchanged.
% n* @+ X( K  ZThe mother also said that the boy was no longer hav-! ^7 u# T! e  R* o' \- s
ing frequent erections.
4 E9 |7 J8 k  |Both parents were again questioned about use of/ ^; @* L' @" t( x
any ointment/creams that they may have applied to! @% _, N) ]3 Y3 k
the child’s skin. This time the father admitted the! d0 P8 t1 f# p1 t9 j1 V! e. d
Topical Testosterone Exposure / Bhowmick et al 541
5 ^! V& d# w4 Y8 R1 G" @3 J# Nuse of testosterone gel twice daily that he was apply-& X1 n$ _8 k+ Q( _5 L6 g
ing over his own shoulders, chest, and back area for" A  ^) H4 k( r
a year. The father also revealed he was embarrassed
2 u) M1 O3 e1 @( h- dto disclose that he was using a testosterone gel pre-
" [0 |( ^  Q' u7 Cscribed by his family physician for decreased libido
* s4 Z1 N4 Z! l- d$ Qsecondary to depression.6 C( W& m! |* \  I3 g+ E3 A0 t
The child slept in the same bed with parents.
8 D; x9 {( l! c' ], a- xThe father would hug the baby and hold him on his3 |! V  b* `: m- Z1 z; s- V
chest for a considerable period of time, causing sig-/ D3 ^- @9 v( d: J4 Z
nificant bare skin contact between baby and father.% r, M& Q8 a5 o
The father also admitted that after the phone call," b& v! w7 ^5 I& c4 D. v
when he learned the testosterone level in the baby, D; H  p# X1 R( L- v
was high, he then read the product information
; x% r/ E/ h# N: Vpacket and concluded that it was most likely the rea-
9 Q6 e5 Q  \" [! V! v0 Qson for the child’s virilization. At that time, they
( g0 {9 _* D# W5 ^0 K2 [3 Edecided to put the baby in a separate bed, and the
0 b# C8 d1 r& P3 h! j7 e7 e- Kfather was not hugging him with bare skin and had
% U/ z0 i7 U; T5 v8 Zbeen using protective clothing. A repeat testosterone
4 E: h3 `: K- ~$ O3 Vtest was ordered, but the family did not go to the
: |# l6 ]( E) ?+ R5 K% `laboratory to obtain the test.
( g2 u+ @6 z/ wDiscussion" M& E+ q% K- i7 x+ [# V) T$ }
Precocious puberty in boys is defined as secondary
7 |2 v9 t+ c: {, h, lsexual development before 9 years of age.1,4( {/ @& r' \5 }  R
Precocious puberty is termed as central (true) when4 j) V0 o8 ]) g3 H% e4 Q
it is caused by the premature activation of hypo-+ X2 [  W/ Z& P5 a0 L" V7 A4 t5 a; p
thalamic pituitary gonadal axis. CPP is more com-
$ J# I1 e3 S! ^3 B: i4 {' _' ?. n* }mon in girls than in boys.1,3 Most boys with CPP
/ g. `# E* A6 s+ q2 t, s4 [. Dmay have a central nervous system lesion that is1 J7 h& K# |# Z  Z' p+ x
responsible for the early activation of the hypothal-9 R: y  a# D" j! J! E, z% ?
amic pituitary gonadal axis.1-3 Thus, greater empha-
3 X* j7 O; [% csis has been given to neuroradiologic imaging in$ t* D  P. h* X2 ]3 f- j0 M
boys with precocious puberty. In addition to viril-& u7 O2 [( I* L* b
ization, the clinical hallmark of CPP is the symmet-
( `2 _: D# C$ r+ N; vrical testicular growth secondary to stimulation by
- F' O# h4 n  {2 P8 r. W4 u$ dgonadotropins.1,3
: T. F! f( B* A* b! }' z; UGonadotropin-independent peripheral preco-4 ]' f. d( m! s% i1 w
cious puberty in boys also results from inappropriate0 F' ~) c% d7 A4 V+ {
androgenic stimulation from either endogenous or0 l: D6 J1 K6 ^5 f9 S, I. B
exogenous sources, nonpituitary gonadotropin stim-
9 O% J1 g! P& {: l  C8 U( Rulation, and rare activating mutations.3 Virilizing* ~" ]1 b3 R2 v
congenital adrenal hyperplasia producing excessive' E: E" r" z& ?; Y
adrenal androgens is a common cause of precocious
7 Y# j" B, @0 N0 Z- d; Spuberty in boys.3,43 C$ n$ K. I0 O) N0 k
The most common form of congenital adrenal
( }& U- g$ u- O- ?+ }hyperplasia is the 21-hydroxylase enzyme deficiency.: [0 B- y! G0 S* ]5 Z; j7 b) n
The 11-β hydroxylase deficiency may also result in  ?6 T' i* |4 t8 J4 L
excessive adrenal androgen production, and rarely,
$ c0 _& I2 b# K  I% j- ean adrenal tumor may also cause adrenal androgen
+ L  Z. |) h2 D7 _* P1 Nexcess.1,3
5 l- B( a. s8 X& V) I8 H* ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 Z7 B2 r  T( T) T542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' O& o- E- A1 m" X  c( ?% }
A unique entity of male-limited gonadotropin-4 k8 B* [# T) |& V) `
independent precocious puberty, which is also known# ]) w( ?% ?8 N( W3 A
as testotoxicosis, may cause precocious puberty at a  Y5 X$ P0 c, G7 A# X
very young age. The physical findings in these boys6 n4 m1 X! u% W% a& m8 R6 m5 c0 V
with this disorder are full pubertal development,
, i9 j* @# q1 L6 Bincluding bilateral testicular growth, similar to boys5 x$ a. _1 X2 d- r
with CPP. The gonadotropin levels in this disorder
* a8 ^4 _1 D' w2 w6 O- x  i0 zare suppressed to prepubertal levels and do not show5 x- v/ I& q! a" s. h0 l! F% ^
pubertal response of gonadotropin after gonadotropin-
7 c4 i( J! d; f5 ]5 a6 e0 b" k4 ]releasing hormone stimulation. This is a sex-linked+ M, Y% Z" M% z# Q
autosomal dominant disorder that affects only
7 J, A: y4 @7 imales; therefore, other male members of the family7 f# g$ T7 F" g  m; ]+ S
may have similar precocious puberty.3
- C6 [/ {, d% {# c5 d, p3 V* o, yIn our patient, physical examination was incon-, `' V( s' D  g) V. J. v+ p( w
sistent with true precocious puberty since his testi-
4 T3 k5 E4 s6 i; D, L$ ocles were prepubertal in size. However, testotoxicosis5 h0 a9 g! \+ q4 Y
was in the differential diagnosis because his father3 e7 @4 a& T% H) [$ F- Y6 Q
started puberty somewhat early, and occasionally,
$ L: {5 e! e( ~- P$ v/ s& mtesticular enlargement is not that evident in the
( g" B, v' W$ I: y0 m0 R! Ibeginning of this process.1 In the absence of a neg-
$ t5 N9 w0 Q  d3 D" s5 O; mative initial history of androgen exposure, our
0 O6 T$ F$ ]$ Q, t( A: g% sbiggest concern was virilizing adrenal hyperplasia,
1 P, G: N; Z/ _$ s3 a$ Y' n. {either 21-hydroxylase deficiency or 11-β hydroxylase& [$ g$ }, H6 [4 p& z
deficiency. Those diagnoses were excluded by find-5 s6 w% u. B+ ?
ing the normal level of adrenal steroids.
. v. O! v  x# ?& ?5 E3 n8 U5 ]The diagnosis of exogenous androgens was strongly
/ H2 y  Y8 r9 r" y8 ^8 u  N4 x( m& Vsuspected in a follow-up visit after 4 months because0 K% Y3 c) M( h/ R$ ^1 f
the physical examination revealed the complete disap-
# N% _3 T& p9 m) w( O5 k' R# m1 Upearance of pubic hair, normal growth velocity, and+ [  h1 ?% u- B' a: y9 D& k  c, ?
decreased erections. The father admitted using a testos-
8 g; ~0 L/ q7 J+ _; S3 qterone gel, which he concealed at first visit. He was, d) ?7 ?' F3 K! D1 t2 k
using it rather frequently, twice a day. The Physicians’
  }; F3 _: r- y$ K+ ?Desk Reference, or package insert of this product, gel or/ f( x: s3 Q  T; ]: o
cream, cautions about dermal testosterone transfer to7 M* P$ y0 `) H1 O
unprotected females through direct skin exposure.
. K) o/ \8 U& s5 k) |( L$ XSerum testosterone level was found to be 2 times the, ]6 k- B. _/ _7 h2 _+ Q, |  Z
baseline value in those females who were exposed to. h2 c8 [* O% r7 A+ A
even 15 minutes of direct skin contact with their male8 x( T0 X: K8 ]+ U) X& W/ L8 U
partners.6 However, when a shirt covered the applica-. M2 T+ A, l; G0 a0 g) `5 }2 q
tion site, this testosterone transfer was prevented.
+ H" e& u$ L( a3 TOur patient’s testosterone level was 60 ng/mL,- h. c, _9 r  @2 Y+ ^9 Y3 V
which was clearly high. Some studies suggest that
8 t* N) j3 M& |dermal conversion of testosterone to dihydrotestos-' d% V7 r6 E1 f$ q0 C
terone, which is a more potent metabolite, is more
8 ^: ]7 ]" `1 B/ i6 j( ]% factive in young children exposed to testosterone
% Y7 q$ g/ ]* o  y5 Qexogenously7; however, we did not measure a dihy-! ^3 W, [* W# X  k9 D+ p6 c# \
drotestosterone level in our patient. In addition to
. \+ d" |1 m  \( J8 L. a& Tvirilization, exposure to exogenous testosterone in
% e6 ?; F' O4 a/ Vchildren results in an increase in growth velocity and
" F1 e8 V$ }. c; M& ?( a9 \advanced bone age, as seen in our patient.# O9 q2 j/ \9 g
The long-term effect of androgen exposure during+ G" e) K, p% B+ e2 ~' `$ u0 u
early childhood on pubertal development and final
+ J+ y1 B- d9 h" B( Kadult height are not fully known and always remain6 L) d3 z5 ~( H5 S  e6 M
a concern. Children treated with short-term testos-3 g# M4 G7 d$ m4 b" O# H. k0 O+ j
terone injection or topical androgen may exhibit some
% i+ q4 b5 [1 e' Racceleration of the skeletal maturation; however, after% v) ^9 X/ K: s( E9 f# V
cessation of treatment, the rate of bone maturation
$ D! t; z9 n  N  `% ^$ C; t7 i+ ]decelerates and gradually returns to normal.8,9
7 q; t, _3 {0 E. E0 p1 j( H" kThere are conflicting reports and controversy
3 n! s. A. M4 `% i; z$ mover the effect of early androgen exposure on adult2 l. n: v% m0 \* E+ ]* Y- M1 s
penile length.10,11 Some reports suggest subnormal2 [! Z. ?( p& ?- m
adult penile length, apparently because of downreg-
4 q' q) P% O. x+ d! q* Zulation of androgen receptor number.10,12 However,
! F& _- d( {2 W9 n2 nSutherland et al13 did not find a correlation between
2 Y5 r4 B  `6 X9 m: [- Y7 hchildhood testosterone exposure and reduced adult
% Y- x7 p* u9 P# _4 X) bpenile length in clinical studies., W, {# k% J5 I0 Y& z  f
Nonetheless, we do not believe our patient is2 e+ n3 q4 G. k& |4 S; x
going to experience any of the untoward effects from
) I1 t$ B. |) A' q0 ctestosterone exposure as mentioned earlier because
. i2 s& m; [7 k0 B1 [0 xthe exposure was not for a prolonged period of time.
; X9 G3 w4 Z* F5 F1 EAlthough the bone age was advanced at the time of
) l6 |5 ]0 O$ M0 O9 o* Q4 Zdiagnosis, the child had a normal growth velocity at
* t; v3 b# P. U- g; T& U7 athe follow-up visit. It is hoped that his final adult
, w( ~" S+ y! j  P) j! k* Qheight will not be affected.
) S6 w0 x! n3 [* J2 uAlthough rarely reported, the widespread avail-, ^& m0 S4 G( Q& j- u3 v6 \6 p# ]
ability of androgen products in our society may
) X$ H8 O+ U% O( C# `8 {indeed cause more virilization in male or female
& _% }, w7 `4 Y# G* z- ~0 echildren than one would realize. Exposure to andro-8 p; N' P0 y* _
gen products must be considered and specific ques-8 N3 Q+ d4 l- D( e7 t
tioning about the use of a testosterone product or
) G% J+ a8 M2 u0 Z" B+ [gel should be asked of the family members during
0 Q% s  l$ M3 o8 f6 p1 _the evaluation of any children who present with vir-& L1 C4 |- N/ X
ilization or peripheral precocious puberty. The diag-) ]- A. M$ [# x/ ^& P8 i
nosis can be established by just a few tests and by
: X& Q2 L; X9 c2 J- c  G: ]appropriate history. The inability to obtain such a
: P9 v/ j1 q/ K& W) H+ `; G/ uhistory, or failure to ask the specific questions, may
) v+ O. a/ @4 _. P; _$ _" b3 bresult in extensive, unnecessary, and expensive  H: F( |/ c) [& w
investigation. The primary care physician should be* J0 g. e4 c' x" g: j
aware of this fact, because most of these children5 d1 M0 P6 K) ?+ v; p
may initially present in their practice. The Physicians’
: O3 ~9 C) s$ n! PDesk Reference and package insert should also put a% {4 T- T: O" d* H, y! r" |* V; b
warning about the virilizing effect on a male or
  }+ R7 Q  D8 O3 L3 F) p6 b$ g2 Nfemale child who might come in contact with some-
) x6 f  T# E4 B3 N  r% T3 wone using any of these products.4 p* T" p& N- |
References1 A' T' E; y3 Q7 i9 u, `
1. Styne DM. The testes: disorder of sexual differentiation- i& U4 E2 O6 Q, q" I! o. ?$ Z' p
and puberty in the male. In: Sperling MA, ed. Pediatric) D1 X3 l: _# Z, ^( W/ ]! u$ R' u
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 u/ ]5 @' @! {% J8 t0 }( f2002: 565-628., M7 {2 l" z9 a) p
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  C% u9 ?2 f- K. {puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
: M9 k7 @1 `- ?  g. `6 ?! lBoy Induced by Indirect Topical! ^, f( a; J& g( M. X5 c
Exposure to Testosterone
8 {- U8 H8 q7 p* z" ySamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
$ F' R5 O0 T5 A! {( i$ Xand Kenneth R. Rettig, MD18 f  G/ f+ C# T! N( X
Clinical Pediatrics7 b2 e/ f! J5 F: M8 J7 H7 G
Volume 46 Number 6
; I0 V* |# h3 l' p3 C3 f6 N& tJuly 2007 540-543
+ x* F" C& w  t© 2007 Sage Publications1 [7 w4 ]0 V/ v/ U8 _4 `2 _
10.1177/0009922806296651
, i; c8 l, L6 H  H# rhttp://clp.sagepub.com
& O3 m4 @# F! b* Ohosted at
5 x% U. ?& x+ V  j( s3 ehttp://online.sagepub.com
" ]1 f- x; l6 @5 R/ n. g% pPrecocious puberty in boys, central or peripheral,
- I5 d6 w4 R9 X, j) @, ^3 pis a significant concern for physicians. Central% Z; T# h2 D" t4 l8 d
precocious puberty (CPP), which is mediated7 F* g( C( _* `2 W
through the hypothalamic pituitary gonadal axis, has
8 ?& u) r. \2 la higher incidence of organic central nervous system
. I0 `. C/ d% w4 D2 jlesions in boys.1,2 Virilization in boys, as manifested$ o+ C* W- O0 X. E/ f0 J- ~( C* c
by enlargement of the penis, development of pubic
8 o1 y5 ~$ X& ~) ^% }  Xhair, and facial acne without enlargement of testi-
+ J, T4 d: \& r/ x, u& q6 [cles, suggests peripheral or pseudopuberty.1-3 We" O; {! U+ O; O- I; z
report a 16-month-old boy who presented with the
, Q2 R  U! e$ e  u  w5 O  C. Denlargement of the phallus and pubic hair develop-1 x* [& s3 |& h2 {
ment without testicular enlargement, which was due
$ w# T9 W2 l- h  \) N9 ito the unintentional exposure to androgen gel used by
# m) V( A0 a3 e1 I. dthe father. The family initially concealed this infor-
$ o: l) l4 u3 tmation, resulting in an extensive work-up for this5 b: _. k3 m* j" |" C3 @  |
child. Given the widespread and easy availability of. T# ?* B0 f5 t) [: `
testosterone gel and cream, we believe this is proba-, b$ G9 Q9 b, x. ?- v
bly more common than the rare case report in the
  _( D1 H+ A8 `0 }" b- d5 Y( cliterature.47 t0 t* M+ Q% C( d0 `' |
Patient Report) t+ ~: a0 d. D- I- `
A 16-month-old white child was referred to the6 U$ k! f; r* J7 X: ]; p' a
endocrine clinic by his pediatrician with the concern
8 x7 k% w4 R: Q, j, y8 fof early sexual development. His mother noticed
+ R; _: C  ~6 Llight colored pubic hair development when he was
4 W  {5 U2 W) b$ E& c" B1 |From the 1Division of Pediatric Endocrinology, 2University of  l: d; {# v/ c  l, S( w# Y! f
South Alabama Medical Center, Mobile, Alabama.
' E  J) T8 ^: l0 `% zAddress correspondence to: Samar K. Bhowmick, MD, FACE,: P7 b- e6 t- j& A( W
Professor of Pediatrics, University of South Alabama, College of5 p# G% |4 Z/ D" U2 r, H" i
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
* _6 d( h+ U( S+ D( x( N5 Xe-mail: [email protected].
8 t- x4 c- h0 [% Tabout 6 to 7 months old, which progressively became
/ x3 C$ b  z2 J0 I8 A( Mdarker. She was also concerned about the enlarge-
( k# d$ K' K4 ~5 qment of his penis and frequent erections. The child$ i9 u2 P4 J2 b8 a3 S3 q
was the product of a full-term normal delivery, with* t* y, P. w8 C/ F
a birth weight of 7 lb 14 oz, and birth length of- F8 h, i( Z0 R3 A6 J! r
20 inches. He was breast-fed throughout the first year+ U" Q) e3 d% r7 S' i* J, R2 g
of life and was still receiving breast milk along with
/ T7 F7 J+ R8 P4 l! F5 P5 k! v# e6 xsolid food. He had no hospitalizations or surgery,2 u5 e1 c: k8 s2 k* v- Q
and his psychosocial and psychomotor development3 B  E) P2 v: w3 G
was age appropriate.0 j. K2 T# H2 k# S9 K# i2 J
The family history was remarkable for the father," k( x. L! M9 g; z. x6 N9 n
who was diagnosed with hypothyroidism at age 16,
. P0 r4 q' t" u. }5 L& i$ fwhich was treated with thyroxine. The father’s2 |6 k( c5 j+ z$ z# v
height was 6 feet, and he went through a somewhat
$ j, Z. t! x9 j4 U' v( aearly puberty and had stopped growing by age 14.
0 S8 N2 z$ Z! `7 h4 J. MThe father denied taking any other medication. The
% E+ r- o2 T+ U3 z8 Bchild’s mother was in good health. Her menarche3 Z# {# g7 ]$ g% \1 f
was at 11 years of age, and her height was at 5 feet# Y; k, `# R6 f5 Y7 r
5 inches. There was no other family history of pre-
9 w, A. |0 p' F0 L% t+ q" fcocious sexual development in the first-degree rela-
) Q, O+ g$ z. |0 o' ^/ ?tives. There were no siblings.
1 ]5 X" h9 E7 [! B; y& ?" aPhysical Examination
  h3 V* ~& @5 g; Z5 u6 [The physical examination revealed a very active,
- d. B8 n1 C5 w, W! o) D; Xplayful, and healthy boy. The vital signs documented' X; ~) U4 c+ n. }
a blood pressure of 85/50 mm Hg, his length was
! n7 a# m. Y% X: `9 t) x/ J6 R3 H3 Q90 cm (>97th percentile), and his weight was 14.4 kg
! ]% M+ Y  M. X9 `(also >97th percentile). The observed yearly growth% E1 M# C/ M3 L7 J. t! L/ U: D
velocity was 30 cm (12 inches). The examination of0 f* E7 y) g& T7 c
the neck revealed no thyroid enlargement.: K8 I; R$ K3 L" j$ N
The genitourinary examination was remarkable for2 _( a* j9 |- V6 g7 B5 H$ _
enlargement of the penis, with a stretched length of
( V% d( b3 Z! Z" G2 F8 cm and a width of 2 cm. The glans penis was very well! F' v& c9 [9 w( Z- ^% k
developed. The pubic hair was Tanner II, mostly around
+ G! v- x' v: [  j& L! U; {5407 V, S( n( `- v+ _& Z: Y3 y* G" H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: J' B' q  W  L
the base of the phallus and was dark and curled. The
* R! q- f# X; S- Q4 H" W" }testicular volume was prepubertal at 2 mL each.
4 |4 M& S" a/ Q, {( y. O4 TThe skin was moist and smooth and somewhat: }/ [$ U7 J: m9 e. ?
oily. No axillary hair was noted. There were no
, S6 o; ]8 _. L) p& D7 Aabnormal skin pigmentations or café-au-lait spots.
$ g1 L' @$ }- p. H' sNeurologic evaluation showed deep tendon reflex 2+/ L; A. z6 O6 {
bilateral and symmetrical. There was no suggestion4 W' [4 V/ N! d  O2 T
of papilledema.$ l5 P, r+ }( Q4 N
Laboratory Evaluation
" P8 A4 W4 I% S( O' aThe bone age was consistent with 28 months by
& o- c; M; c* v# Q. i, fusing the standard of Greulich and Pyle at a chrono-
4 M4 k( h$ O1 z& C# Clogic age of 16 months (advanced).5 Chromosomal* ]$ T& B$ }- d$ C- A
karyotype was 46XY. The thyroid function test
; D7 S9 ~$ B3 e6 zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-0 E. H, V3 d  f: u; }0 t& C
lating hormone level was 1.3 µIU/mL (both normal).
; p: w4 p: o7 {* ?- A6 J6 n/ A" XThe concentrations of serum electrolytes, blood
* G: w# ?/ M. C! \4 W: f: rurea nitrogen, creatinine, and calcium all were& n6 c- v. j, M) O) J" B
within normal range for his age. The concentration
, v- [+ W  m- V: Oof serum 17-hydroxyprogesterone was 16 ng/dL
# ]1 {$ f* w- h( |8 a$ d) N3 A. U8 o(normal, 3 to 90 ng/dL), androstenedione was 20
5 R5 T% J/ e* S- F7 f  @& \) L0 [ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
+ |) K& T. p1 q! s( I/ lterone was 38 ng/dL (normal, 50 to 760 ng/dL),- ~1 d# z, u  ?. j/ G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 W$ N* v- I2 r0 _/ W& C+ @  S49ng/dL), 11-desoxycortisol (specific compound S); t' D) n* L. i4 z3 k) ~
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-1 N9 c$ D" f8 K4 @. J
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 w8 z; S% [0 H5 _( y6 Q
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 q3 E8 H* D  J0 l4 Z* u: G# ~
and β-human chorionic gonadotropin was less than1 Y$ [% `& V  M5 ?, }
5 mIU/mL (normal <5 mIU/mL). Serum follicular  {" _+ y% p6 }* |
stimulating hormone and leuteinizing hormone
( c% M5 m. a! _3 L! I( `" dconcentrations were less than 0.05 mIU/mL+ p- z( p" U6 w( H" `9 c. r
(prepubertal).
  p3 }( G. T- t- X+ S" T4 H7 k* ?The parents were notified about the laboratory
" Z" |" M6 Y* w3 presults and were informed that all of the tests were& @4 S3 e9 O& t4 V
normal except the testosterone level was high. The
3 I2 p( R8 D. R/ m3 L. A( hfollow-up visit was arranged within a few weeks to
* E+ J1 {# @5 c6 a' u  @( xobtain testicular and abdominal sonograms; how-
! b" V2 @9 H. z3 cever, the family did not return for 4 months.
" B. O2 e- K% x1 i, P3 RPhysical examination at this time revealed that the7 I$ G5 e. m9 ^! x
child had grown 2.5 cm in 4 months and had gained
/ L0 D; G" s8 J! ~2 kg of weight. Physical examination remained
, N# @' M0 ~. \  Cunchanged. Surprisingly, the pubic hair almost com-
1 K: s* ~2 u* K! v9 H; @; epletely disappeared except for a few vellous hairs at
' `$ }8 v: K. C1 U7 W8 zthe base of the phallus. Testicular volume was still 2$ [5 `' G" p7 u
mL, and the size of the penis remained unchanged.
  b1 U4 X' s3 i& _8 @The mother also said that the boy was no longer hav-
" y( a" x" }( t, bing frequent erections.
6 |% }3 Z7 n( i- `' yBoth parents were again questioned about use of# h2 f$ v7 d* G4 ], |
any ointment/creams that they may have applied to, K% z& J( R# i- W
the child’s skin. This time the father admitted the
% \' k- W- j. I4 ATopical Testosterone Exposure / Bhowmick et al 541
' u' ?0 m2 }1 b# s1 Z4 H5 _* duse of testosterone gel twice daily that he was apply-3 {  I6 m0 [! {3 o
ing over his own shoulders, chest, and back area for
! W' d7 g1 K$ N, wa year. The father also revealed he was embarrassed
) v  _6 J5 |6 Z* Q/ H* oto disclose that he was using a testosterone gel pre-
; Y. p! R5 `5 I1 b! v& @scribed by his family physician for decreased libido
) M# ^9 C6 r. C& j$ N* Ssecondary to depression.
" i1 g: q7 i& x8 ?9 ?( t4 tThe child slept in the same bed with parents.. E0 t; K) |( Z& r' b4 F0 W  n/ {
The father would hug the baby and hold him on his% s( x3 O/ k# l0 b- f4 v3 D
chest for a considerable period of time, causing sig-
) G  v5 p$ ]" s9 Z6 {nificant bare skin contact between baby and father.
5 T& w& K9 Z+ H8 B" S: uThe father also admitted that after the phone call,, k& z0 g! ~, A- ?! P* P4 p, Q
when he learned the testosterone level in the baby% [- n! P1 [$ f# Q
was high, he then read the product information' b) K/ v  V8 U4 j3 s; C2 a6 ?
packet and concluded that it was most likely the rea-
  I1 x- {+ T; N: d& Gson for the child’s virilization. At that time, they* g, h0 Z# A" T! U' q8 E5 y7 m
decided to put the baby in a separate bed, and the* y( Z' F0 j& L- T# ~2 j  K
father was not hugging him with bare skin and had( f0 N) |( V/ j( z% D
been using protective clothing. A repeat testosterone8 T5 T" B  X# f5 Y
test was ordered, but the family did not go to the
, `" S4 k3 l3 `* F& Vlaboratory to obtain the test.
) j+ X" ]% ?5 f# j, w) t; cDiscussion# Q5 ]6 S1 B+ w6 Y! @  X' S3 h
Precocious puberty in boys is defined as secondary
6 d( ]) c5 h% D* O6 Msexual development before 9 years of age.1,4; A0 o+ P$ B: C9 i$ s0 N
Precocious puberty is termed as central (true) when7 ^. q* ?! G) z! t  Q4 f. R- B
it is caused by the premature activation of hypo-2 A/ [1 n: p; l  e: R/ e
thalamic pituitary gonadal axis. CPP is more com-, [8 t0 @2 {1 b, ~+ f. j
mon in girls than in boys.1,3 Most boys with CPP9 H* t3 E! u3 i) ~  {& l0 p
may have a central nervous system lesion that is0 C0 u2 C0 D2 G4 C0 u9 ~* b
responsible for the early activation of the hypothal-
2 s1 P' @& y+ W6 K$ x9 Oamic pituitary gonadal axis.1-3 Thus, greater empha-" K5 ]  s. W' @2 y( C% \
sis has been given to neuroradiologic imaging in/ h' a' o3 [9 k
boys with precocious puberty. In addition to viril-
# u2 S+ o8 N; k; B, |! i0 S7 aization, the clinical hallmark of CPP is the symmet-
8 z' B8 }7 y/ P9 W) srical testicular growth secondary to stimulation by; J) l( D! F# q5 r
gonadotropins.1,3) R2 n/ a0 l, _: J  I$ X
Gonadotropin-independent peripheral preco-
3 d) c& ]+ O* F7 A3 M/ L: Y) T4 Ycious puberty in boys also results from inappropriate2 m' Y+ E, t/ f/ W2 p
androgenic stimulation from either endogenous or: R; x3 ^: ?$ T7 k' T
exogenous sources, nonpituitary gonadotropin stim-: i1 E) `( h1 u# g& D
ulation, and rare activating mutations.3 Virilizing/ u; \; d2 J( x( `
congenital adrenal hyperplasia producing excessive, p6 @3 a8 z) b7 k
adrenal androgens is a common cause of precocious; D2 f: X$ k5 x5 l8 W
puberty in boys.3,4% m! _* J: _$ b3 g
The most common form of congenital adrenal! E9 E  h4 U( r, J
hyperplasia is the 21-hydroxylase enzyme deficiency.
8 x' y5 T3 U4 X6 A' H5 O0 E, c$ ]The 11-β hydroxylase deficiency may also result in
" K( F$ H* X/ o3 p% Kexcessive adrenal androgen production, and rarely,* h" V9 s- J2 `' ], c
an adrenal tumor may also cause adrenal androgen
. e9 C3 J/ ^$ n- b" fexcess.1,3: v. T4 b" E' R) x1 a1 B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! J$ X- A# \& n) _; n" f
542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 X( {( [, j& u5 g1 l
A unique entity of male-limited gonadotropin-
) E' `7 j. p0 h& T8 Z, Qindependent precocious puberty, which is also known+ X( {! z. Q9 L0 J
as testotoxicosis, may cause precocious puberty at a
' H& C. L( q; ?% v$ G; fvery young age. The physical findings in these boys
- s# e7 u. E8 {; b- d5 V& Iwith this disorder are full pubertal development,$ N/ C2 K; P' q5 e7 {% P% T
including bilateral testicular growth, similar to boys
% _9 x0 s" P6 @* r5 Q& `" i8 J1 [* Twith CPP. The gonadotropin levels in this disorder
( l$ s, ~; h4 O- care suppressed to prepubertal levels and do not show9 @+ P/ y% L: m, @8 X
pubertal response of gonadotropin after gonadotropin-
3 M+ w! j; a  n; rreleasing hormone stimulation. This is a sex-linked
; a/ R) d; \; u* {- n( l& Jautosomal dominant disorder that affects only
4 v5 h- G; D" A6 m, f9 Y# h: \males; therefore, other male members of the family8 `3 o+ Y# H% ]6 ~( L3 h2 t$ U
may have similar precocious puberty.3
) c6 ]9 s2 k+ }( \In our patient, physical examination was incon-
, ~5 z" J5 C( m8 N* n  D  Psistent with true precocious puberty since his testi-6 K3 F0 ?) D( Q! A6 `/ g7 `
cles were prepubertal in size. However, testotoxicosis$ b/ n2 ?+ x  |' V5 q
was in the differential diagnosis because his father- {, B- z6 h  @6 l
started puberty somewhat early, and occasionally,
$ n* G/ |9 Z4 p0 ]$ [% T' Ltesticular enlargement is not that evident in the
" ?7 M. N" ~1 D$ B4 Mbeginning of this process.1 In the absence of a neg-9 W0 F3 _" e1 }6 n6 Y; N7 T& C, @8 ~
ative initial history of androgen exposure, our
3 E' a$ N1 O0 ?$ m2 _( Tbiggest concern was virilizing adrenal hyperplasia,
9 |5 f. k1 H9 w7 [8 R* }either 21-hydroxylase deficiency or 11-β hydroxylase
9 z0 D; q  n7 [( v, R# {deficiency. Those diagnoses were excluded by find-! h" O* F, _( N9 u4 _
ing the normal level of adrenal steroids.: t- W% \' @! l5 D' A1 ~  l
The diagnosis of exogenous androgens was strongly
+ t& t& h* t6 j, p* o; ?2 F) R! osuspected in a follow-up visit after 4 months because
/ o+ o5 y$ |* |$ J! G! M2 P- nthe physical examination revealed the complete disap-
7 ?" O; G3 U% s& [/ mpearance of pubic hair, normal growth velocity, and5 F) H4 J: @3 e( {
decreased erections. The father admitted using a testos-
+ ]+ R0 p; ^; x5 D; O% }terone gel, which he concealed at first visit. He was
* F5 N# e# u: K5 l8 cusing it rather frequently, twice a day. The Physicians’
5 a2 Y5 j" ]* vDesk Reference, or package insert of this product, gel or
* C/ x* W# z( _' i2 {cream, cautions about dermal testosterone transfer to4 E* t! M+ L" s7 N* i7 z6 E
unprotected females through direct skin exposure.: D. o2 ~$ b* o8 W: J1 Z- ^3 g
Serum testosterone level was found to be 2 times the  a8 Q9 u! z0 I& p* a7 i6 Y1 s& G1 `- Q
baseline value in those females who were exposed to9 _- r: c9 H8 Z% H5 [: B+ i! K
even 15 minutes of direct skin contact with their male- @4 c, X6 Y8 m% ]; h
partners.6 However, when a shirt covered the applica-
8 b/ k! ?& Y% Q: \% D; ztion site, this testosterone transfer was prevented.
8 ^% U. a, a, u- _# y* ROur patient’s testosterone level was 60 ng/mL,$ Q0 ]8 |% G% w7 Q' p0 G
which was clearly high. Some studies suggest that
9 P2 u2 y. ]" sdermal conversion of testosterone to dihydrotestos-9 @- z% y' [( K  L- m& f9 ?, s
terone, which is a more potent metabolite, is more  X4 F6 a/ E% b
active in young children exposed to testosterone1 u* O( {3 o" V4 ]8 p9 j
exogenously7; however, we did not measure a dihy-
2 S# a  J' }$ y- s9 z% K; Udrotestosterone level in our patient. In addition to1 f# i" a6 T" ?* l
virilization, exposure to exogenous testosterone in. P9 E" T! u- v- ?* m' i- F
children results in an increase in growth velocity and
( Z9 _9 D) W3 R. @1 E- F/ }. f3 Ladvanced bone age, as seen in our patient.
9 Z0 E' U, p$ _, T9 h* ^8 aThe long-term effect of androgen exposure during- Q3 A/ O! D" o1 N0 D% `! D$ `
early childhood on pubertal development and final$ ~( }" i+ n5 b) _5 V) D: m
adult height are not fully known and always remain
: n% u4 e/ ~8 j, da concern. Children treated with short-term testos-
$ q) f8 o' b( ^* z5 _terone injection or topical androgen may exhibit some# a6 R5 r* l0 A; [$ s& P/ r
acceleration of the skeletal maturation; however, after6 N9 @) Y7 q) m# ?0 {. o
cessation of treatment, the rate of bone maturation) I' n, i6 p1 L2 |5 E
decelerates and gradually returns to normal.8,95 D! A6 n& Q3 \# Z
There are conflicting reports and controversy5 ?" h8 s* i* Q
over the effect of early androgen exposure on adult/ o& ?- S' K+ R" o
penile length.10,11 Some reports suggest subnormal
; I- w/ Y) ?* y- ^; ~adult penile length, apparently because of downreg-
% I( i3 ^# I% E* f' xulation of androgen receptor number.10,12 However,
$ G9 ?) ?- m0 m5 wSutherland et al13 did not find a correlation between; @1 ^2 O0 h9 k( B; E
childhood testosterone exposure and reduced adult7 k2 p5 `. A* u) ~
penile length in clinical studies.
; ?. D$ `8 @, \' h% z5 S7 INonetheless, we do not believe our patient is
; [2 ~& _' y9 Q" _going to experience any of the untoward effects from
3 l+ T' A8 d' t( Ftestosterone exposure as mentioned earlier because
+ ?: _  z5 I" p! {5 y! n- tthe exposure was not for a prolonged period of time.% U- e% ]9 _) S$ D' b8 L0 Y: j
Although the bone age was advanced at the time of; y: W" S# Q6 Z# V+ d8 V% c
diagnosis, the child had a normal growth velocity at
/ b" E8 A# Z! H7 qthe follow-up visit. It is hoped that his final adult
$ {" J: Q% z% h* N( \+ n( R/ bheight will not be affected.2 W" W/ @& K6 x% V: {0 S
Although rarely reported, the widespread avail-  K+ C: V2 w, S3 c; r2 l
ability of androgen products in our society may% e) F8 L. M5 S3 c
indeed cause more virilization in male or female
; g5 R" p# u, }. o" vchildren than one would realize. Exposure to andro-, R+ h# Q) v3 |( W
gen products must be considered and specific ques-- y  ^* h- ~( l2 f4 ~8 L: Z
tioning about the use of a testosterone product or' Y2 {* m6 V2 G! R1 @  Q3 U% O
gel should be asked of the family members during/ E3 F2 P$ Q5 e/ y* v
the evaluation of any children who present with vir-" u/ k$ r  C! r2 _
ilization or peripheral precocious puberty. The diag-9 K4 f4 U7 z0 Z4 D' [
nosis can be established by just a few tests and by
# B0 y3 y# B  g" a4 i- V- Cappropriate history. The inability to obtain such a/ m5 `3 \) ?# D' i5 O
history, or failure to ask the specific questions, may; X5 n8 H/ k; V! V4 O/ Q  z0 _) V
result in extensive, unnecessary, and expensive
( m. j# }" [# @  Q  ^4 e, cinvestigation. The primary care physician should be
" B+ U( i/ m7 s( B1 t  L4 o0 `aware of this fact, because most of these children/ ^; s( E  C2 b2 d
may initially present in their practice. The Physicians’4 z: P9 \3 y8 k, W1 K' |# N- r
Desk Reference and package insert should also put a' g& @# H4 x  ]8 a& d1 p$ l
warning about the virilizing effect on a male or+ t* m: c/ [& `
female child who might come in contact with some-% r2 K' v3 W  Y9 B+ r  i# E
one using any of these products.  k! p4 e4 k2 R1 l/ J" S2 _
References6 A" }" `2 [- r1 x1 D
1. Styne DM. The testes: disorder of sexual differentiation
6 i. K) H# j7 B  s' `and puberty in the male. In: Sperling MA, ed. Pediatric
$ m% |' N/ y) F0 d6 A) CEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 U- @2 `/ ^: V2002: 565-628.( B  F* y  y8 f- ?0 M
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% q" m5 W! I6 Y* vpuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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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
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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

' j0 R2 V$ B  w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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