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Sexual Precocity in a 16-Month-Old+ ?4 [# e. ?3 c8 i
Boy Induced by Indirect Topical6 d- P" A: y5 Y0 ]" N8 l  A! r
Exposure to Testosterone5 T& }7 F# q) Q1 l* X' Y9 d
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" d1 ], D4 F2 Q% x( p6 W; M5 o+ n! Fand Kenneth R. Rettig, MD1
& V: S* n1 I6 u/ i% p# oClinical Pediatrics0 m6 v; m  c+ m' @4 i; b2 m/ o: }
Volume 46 Number 61 @% [. R4 t: H( `$ u
July 2007 540-5431 l% B1 P3 p5 E( _% {  D% N% X
© 2007 Sage Publications  i, X9 C$ M0 k+ W# w7 N( o
10.1177/0009922806296651. b1 j( @) Z7 K( i: z) ?+ Q
http://clp.sagepub.com
  J! x# W3 q7 D7 W3 s; O- \hosted at
" a* q4 x$ V$ f: \" @http://online.sagepub.com: q1 I2 \4 [& T( H& Z! O4 [$ p
Precocious puberty in boys, central or peripheral,
; [+ B0 V& d$ L9 ~is a significant concern for physicians. Central5 v8 ~3 i) i* G2 _# d9 |* j
precocious puberty (CPP), which is mediated' W6 c! p1 H, j0 v
through the hypothalamic pituitary gonadal axis, has
$ \. q" D% S  h6 ga higher incidence of organic central nervous system0 L$ K! l7 q; \! T# R
lesions in boys.1,2 Virilization in boys, as manifested7 _9 R( e2 a! _
by enlargement of the penis, development of pubic
  ]; o' S& i! ~, r& p# V$ l$ u9 }5 mhair, and facial acne without enlargement of testi-/ `+ J, ~1 l  R& K2 ?, A, D
cles, suggests peripheral or pseudopuberty.1-3 We
6 e0 K$ j, q, P$ n1 E' M* a! \report a 16-month-old boy who presented with the
* O% X( v: r1 F  U1 Denlargement of the phallus and pubic hair develop-* e: ?7 a$ o2 n4 Z" S  l
ment without testicular enlargement, which was due! K7 ?; w) g; Q& A( `9 R0 s% q
to the unintentional exposure to androgen gel used by7 t2 B* u6 Q1 k( s4 w4 ^
the father. The family initially concealed this infor-3 q1 N+ C$ c# S! `
mation, resulting in an extensive work-up for this
1 c* b) Q+ o8 m0 A/ w( N& ]child. Given the widespread and easy availability of# ?. D( f. j+ C0 H3 o- @2 G+ M, ]
testosterone gel and cream, we believe this is proba-
" |$ Y, s2 y4 @- g( F4 o" T; o; rbly more common than the rare case report in the3 J6 c4 f; f/ t3 ^
literature.47 S8 v6 l% ~( k
Patient Report- X/ D" I) Z* @* y
A 16-month-old white child was referred to the
$ y4 ?- y& o% ]. [3 K/ ^endocrine clinic by his pediatrician with the concern' \2 ?+ w7 o% u2 W
of early sexual development. His mother noticed7 ~% E0 t. s  k* c( h& u9 s
light colored pubic hair development when he was$ h3 U, I0 z) I" Q" |# r% Z& l: V: Q
From the 1Division of Pediatric Endocrinology, 2University of9 W' q8 a0 U4 s3 L/ Y* _' j
South Alabama Medical Center, Mobile, Alabama.
; P2 I; X% S  m# jAddress correspondence to: Samar K. Bhowmick, MD, FACE,
, P( k9 B. x( n$ H; R% `Professor of Pediatrics, University of South Alabama, College of
0 l4 [8 }6 Z; V- P* oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ l: j" Z6 C6 l  @0 X
e-mail: [email protected].
( N- ?: ~) \/ X7 s" d  Wabout 6 to 7 months old, which progressively became
3 U* Y7 i' m+ w; ^& ldarker. She was also concerned about the enlarge-" |& B' }( b5 e( s
ment of his penis and frequent erections. The child
5 `( e$ v& Z4 @% r2 b1 K5 i, `was the product of a full-term normal delivery, with. n, q8 M" J0 A' R0 Q! q9 A
a birth weight of 7 lb 14 oz, and birth length of
- ]( m% {" N* g! ?. P20 inches. He was breast-fed throughout the first year5 h1 H3 }" Z' D1 i: B4 Z3 v
of life and was still receiving breast milk along with- ?; f) N! |6 G; }. c% W6 k. C
solid food. He had no hospitalizations or surgery,) K. \' f! l; ~  _% g0 C
and his psychosocial and psychomotor development- G% C4 l7 S# i" s, [
was age appropriate.; \# B3 Z* N2 M1 @" S* S+ t3 o
The family history was remarkable for the father,
) S( }; P( F& @0 F/ dwho was diagnosed with hypothyroidism at age 16,
$ }; f. i; x  e3 p) e. ?. n: gwhich was treated with thyroxine. The father’s
9 i* ^1 x/ O) e/ T0 Bheight was 6 feet, and he went through a somewhat; F+ o- @! U) O$ ?" Y, ^8 }0 r
early puberty and had stopped growing by age 14.
: a! X+ Y0 C  z+ }1 i- eThe father denied taking any other medication. The
% E, O( S! I# ?' q' n( V: ?child’s mother was in good health. Her menarche
. \0 P! X  r! a! Ywas at 11 years of age, and her height was at 5 feet
4 E0 c- Y$ n2 \* E6 n. e5 inches. There was no other family history of pre-( J1 H# k3 }" [* z8 y5 q  l
cocious sexual development in the first-degree rela-
9 H( x. E' s9 A& p, b; c% Z' Ltives. There were no siblings.
& l" x) M9 \4 w( V% hPhysical Examination
; E4 Q, I1 J) F/ GThe physical examination revealed a very active,
: k4 l$ H5 M6 _( X& s: dplayful, and healthy boy. The vital signs documented
) ?$ o- U. n+ [( Y7 D$ Da blood pressure of 85/50 mm Hg, his length was
! t2 L$ u; X, g0 g90 cm (>97th percentile), and his weight was 14.4 kg( O* A& t2 Q+ P$ c% U8 w( r# N5 Z$ h
(also >97th percentile). The observed yearly growth$ k5 E% h8 e" {, d9 r5 L
velocity was 30 cm (12 inches). The examination of
# p3 Q$ R: W4 K) n# |the neck revealed no thyroid enlargement.
7 l  K# f3 m3 y6 P, W* ~The genitourinary examination was remarkable for7 G/ ?' S9 Z# |: b
enlargement of the penis, with a stretched length of
9 o" I/ n/ h! z$ i3 `0 Y3 Q3 t8 cm and a width of 2 cm. The glans penis was very well
3 u5 D) k6 T# M5 X  |developed. The pubic hair was Tanner II, mostly around
/ B- _' W8 c7 X3 D540
* T- P, S0 L5 o* t5 U: Z1 Z( Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( ]+ N, z8 ^7 U1 Z
the base of the phallus and was dark and curled. The
! P+ X# r" b" H1 ntesticular volume was prepubertal at 2 mL each.
' K' _7 m- V* _% r4 _The skin was moist and smooth and somewhat& M; E/ `6 `) X6 U
oily. No axillary hair was noted. There were no
! {# F- T/ d( t/ d8 }" B8 Dabnormal skin pigmentations or café-au-lait spots.- k/ O, O8 H1 h; k
Neurologic evaluation showed deep tendon reflex 2+- |" I* v  Y- Q: \
bilateral and symmetrical. There was no suggestion
1 S4 F' l% P- j9 xof papilledema.; J" o9 ?0 e# \4 p
Laboratory Evaluation$ e, S# A8 \2 A! X4 {! y( K
The bone age was consistent with 28 months by
. N! L9 |$ |& \5 P3 kusing the standard of Greulich and Pyle at a chrono-" J, X! B- A) A1 N
logic age of 16 months (advanced).5 Chromosomal
6 ]4 Z" v3 F: x6 }karyotype was 46XY. The thyroid function test
; S/ P0 g, U% Q( zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
4 I& S* O( C3 H" n, S. ilating hormone level was 1.3 µIU/mL (both normal)." g- ?/ i( K$ K2 ~9 c
The concentrations of serum electrolytes, blood$ B% D0 r0 o& Z6 n" X, N) o
urea nitrogen, creatinine, and calcium all were7 }9 d" ~+ l' ^1 U( k+ }! y, J
within normal range for his age. The concentration
6 o" z1 _3 ^1 w  [of serum 17-hydroxyprogesterone was 16 ng/dL( A% O+ q" a, F/ u" V  o! V( i/ Z
(normal, 3 to 90 ng/dL), androstenedione was 20% s1 v3 p' \( o- w9 k
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 O9 f; u, k/ Y! m+ z2 R. s1 K( Yterone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ q5 @7 ]1 g% L/ Z, e# X2 ^: ]desoxycorticosterone was 4.3 ng/dL (normal, 7 to% G6 b. Y2 d1 _5 [. y: B
49ng/dL), 11-desoxycortisol (specific compound S)' J- ^! L! ]( t; O; y8 p7 F6 X+ u
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
# C' ]5 G9 M. u" \tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% U! j( ?7 Q5 A& h: Ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# o. j& x% ~0 Nand β-human chorionic gonadotropin was less than# t9 u9 ]" R; ]1 b# S; q
5 mIU/mL (normal <5 mIU/mL). Serum follicular) H/ [8 Z, T" x9 u/ w/ h
stimulating hormone and leuteinizing hormone
. [! h5 E, Z( {5 f  K" gconcentrations were less than 0.05 mIU/mL' b% f, \6 F0 p% g
(prepubertal).
( z2 M1 A% H  x8 R/ [The parents were notified about the laboratory
6 r( J3 p9 N( Fresults and were informed that all of the tests were" G5 L3 n/ A, u6 Z5 P$ d
normal except the testosterone level was high. The9 ~; m4 Q) s+ w3 d3 U+ o' [
follow-up visit was arranged within a few weeks to
% B" o3 @% C3 i. f: t3 ^) r0 |obtain testicular and abdominal sonograms; how-; T" V4 ^* V4 o' K7 Q
ever, the family did not return for 4 months.
6 L# q% }4 f% Y! j- D$ UPhysical examination at this time revealed that the: I8 M1 z+ ~5 ~$ t9 s1 a
child had grown 2.5 cm in 4 months and had gained
# h6 D8 J; D$ d7 L! L2 kg of weight. Physical examination remained
' B% v  Y, N, t6 a7 i! _unchanged. Surprisingly, the pubic hair almost com-
/ U8 D" @6 D: F- X; U7 Ipletely disappeared except for a few vellous hairs at2 R4 H! R9 l# s4 c+ @" n( A
the base of the phallus. Testicular volume was still 2
0 d( Z% z# z$ T, T: h  mmL, and the size of the penis remained unchanged.3 v* y9 h: `: M$ ?& r
The mother also said that the boy was no longer hav-( }' [7 G  Y! f( ]3 r% K- o  w' Y
ing frequent erections.0 p0 G" S" K/ I  l7 ?+ D; m: g5 F% C
Both parents were again questioned about use of
& l) |* P$ {4 Cany ointment/creams that they may have applied to- v& ?0 b- ]' m8 Y. p
the child’s skin. This time the father admitted the
: l6 v. y2 Q+ W+ ]+ F9 YTopical Testosterone Exposure / Bhowmick et al 5412 M( d4 a- H! D' Z' g+ C1 f
use of testosterone gel twice daily that he was apply-
  ^3 X8 R& ]9 R( F* iing over his own shoulders, chest, and back area for
( m7 [8 {7 i* R8 L" Aa year. The father also revealed he was embarrassed
4 y& b6 f, ~# v& Dto disclose that he was using a testosterone gel pre-
9 K$ F' i: H( |  }# ~scribed by his family physician for decreased libido
( e# b+ n/ a( b; o. ^: a1 W- n8 zsecondary to depression.
$ b6 t' s8 n: b! WThe child slept in the same bed with parents.' J: W3 X9 Z, z& O  z( c* d% `0 q2 B
The father would hug the baby and hold him on his, }+ i: n. n& y0 q
chest for a considerable period of time, causing sig-
8 i; {1 e0 Y6 }  q- e: m" fnificant bare skin contact between baby and father.$ i" o4 u, B5 n7 z
The father also admitted that after the phone call,
4 j5 b$ p% i) z& A6 y. u% U5 R5 ]when he learned the testosterone level in the baby
0 i+ A- C8 L: k6 ?( U5 Y8 }" Cwas high, he then read the product information9 Z9 \4 U+ x: @% e9 g) t# I
packet and concluded that it was most likely the rea-
  [3 ]2 [% M' b; p6 Yson for the child’s virilization. At that time, they
  u+ R6 I1 D* b+ \+ ]( Xdecided to put the baby in a separate bed, and the# q2 N5 o! h) v1 c0 D
father was not hugging him with bare skin and had8 [6 N7 w# y3 d7 @3 K
been using protective clothing. A repeat testosterone* J5 G8 ~" k- E$ I; l/ N& n0 G6 ]
test was ordered, but the family did not go to the
% l8 |8 s, ]1 V! B4 G0 U1 {0 Zlaboratory to obtain the test.6 H) b4 F1 b% Z' s- N) C* a: O* _' U
Discussion1 d+ D4 R$ Q' R
Precocious puberty in boys is defined as secondary8 v2 e8 l4 t! p" q
sexual development before 9 years of age.1,4
; w0 k% [) R/ t; Z% t& R( ePrecocious puberty is termed as central (true) when
3 O2 X/ W3 Z8 E! P" n- _it is caused by the premature activation of hypo-0 b6 T# b3 |/ A. e) K9 ^9 r, u( Y$ }
thalamic pituitary gonadal axis. CPP is more com-: i3 C* W1 W" m5 U, l4 o
mon in girls than in boys.1,3 Most boys with CPP
+ D3 {  n* c% x( Smay have a central nervous system lesion that is
+ c& W" {" Q% {6 R# {+ Jresponsible for the early activation of the hypothal-
0 P' [% C& {4 @amic pituitary gonadal axis.1-3 Thus, greater empha-
& s. h5 K" h& H+ g# B% F) W% z3 ksis has been given to neuroradiologic imaging in, z5 Y6 D0 }7 U- d1 V: N
boys with precocious puberty. In addition to viril-5 d  x- j. B# @- |3 l
ization, the clinical hallmark of CPP is the symmet-
2 k. Q1 }% q+ b8 |' Y! Crical testicular growth secondary to stimulation by
/ |* n( h2 b% v, Dgonadotropins.1,3
* w  u! R4 d" L; ]/ b, y, E) SGonadotropin-independent peripheral preco-6 t( {* i2 Y" m- V
cious puberty in boys also results from inappropriate
8 X  H1 k+ A# g% d2 Randrogenic stimulation from either endogenous or
& P, i& n1 A1 h9 L2 Vexogenous sources, nonpituitary gonadotropin stim-
; [% _7 E" M9 S9 v9 n+ S* wulation, and rare activating mutations.3 Virilizing
" r! I  y" K6 d( J. B# Bcongenital adrenal hyperplasia producing excessive9 X- }( P& a1 J5 ]& M) A+ V5 l. l) E
adrenal androgens is a common cause of precocious1 E% {5 C; s1 l( y
puberty in boys.3,4
5 F8 C% _% D& A# z, v0 M/ GThe most common form of congenital adrenal3 ]# E2 k0 `6 u& L3 D6 r  j
hyperplasia is the 21-hydroxylase enzyme deficiency.! [$ I% q7 q* N: C! g, g  E
The 11-β hydroxylase deficiency may also result in
. M+ V5 S& L& I# M. ?# vexcessive adrenal androgen production, and rarely,0 R* I! @' Q" N2 [# w- x1 s# c$ N( r
an adrenal tumor may also cause adrenal androgen6 j; E+ g0 l5 |- U5 l4 O
excess.1,3
: S1 E- U/ {/ G% [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. W) N% H! O3 S) T- y: [542 Clinical Pediatrics / Vol. 46, No. 6, July 20074 V$ g: G8 ~0 r; y
A unique entity of male-limited gonadotropin-
) t; f' F' h0 Findependent precocious puberty, which is also known' u7 A0 Y! g1 |: j* ^4 o& A
as testotoxicosis, may cause precocious puberty at a
  x! b3 [* \9 Mvery young age. The physical findings in these boys% M: _* q- ?: l9 F
with this disorder are full pubertal development,
6 |/ z7 U( a! F& ^4 S5 oincluding bilateral testicular growth, similar to boys, s3 H* L9 v! Z; W5 j3 N
with CPP. The gonadotropin levels in this disorder
* Q& {  u+ h# Q$ N9 e4 j& aare suppressed to prepubertal levels and do not show
0 Z6 m* a# m. w9 E1 ipubertal response of gonadotropin after gonadotropin-# v: B$ e: x: }  h- d
releasing hormone stimulation. This is a sex-linked
& C8 h$ d% S8 F- s0 W# Xautosomal dominant disorder that affects only' A0 P, O2 o: t' `- X/ K
males; therefore, other male members of the family
" r- k0 Q8 _9 ^( C: E( B* U" T" X8 g+ r: Wmay have similar precocious puberty.32 \# X. `9 g* @
In our patient, physical examination was incon-
& G% k- o% w' f' gsistent with true precocious puberty since his testi-/ A, ?4 y' H! P! Y2 O- T+ q
cles were prepubertal in size. However, testotoxicosis
6 B- M5 o# D1 L: ^  g* A* G" `was in the differential diagnosis because his father( Q/ M* {/ G6 j) m1 G! i
started puberty somewhat early, and occasionally,
6 ]0 H: K- [# e8 }testicular enlargement is not that evident in the
' f0 Y- o: `+ A4 ]beginning of this process.1 In the absence of a neg-
6 w- S) B% z/ P0 B/ ^  ?( gative initial history of androgen exposure, our
/ m5 g* A9 _) zbiggest concern was virilizing adrenal hyperplasia,
- q" z" z# K) W8 g9 t! xeither 21-hydroxylase deficiency or 11-β hydroxylase
  B( g# G3 s2 ^1 \  Fdeficiency. Those diagnoses were excluded by find-
  z/ Q' W8 u) zing the normal level of adrenal steroids.
8 v+ s! h9 `& Q5 K9 b" Z+ S; yThe diagnosis of exogenous androgens was strongly
: q- O% V1 Z7 G+ Tsuspected in a follow-up visit after 4 months because" w: K. Y" w6 ^: K% I
the physical examination revealed the complete disap-( i( b0 i- x. V3 c3 H. F
pearance of pubic hair, normal growth velocity, and% Q- J% d7 i6 N' n8 _/ u
decreased erections. The father admitted using a testos-
/ i  S* }! _' oterone gel, which he concealed at first visit. He was
7 I! H2 s# _) N* I2 rusing it rather frequently, twice a day. The Physicians’
- j' d3 ~5 m$ y# \Desk Reference, or package insert of this product, gel or7 g9 `2 [* h8 u2 Q* J  x6 g% m6 ]
cream, cautions about dermal testosterone transfer to3 {# g( S$ {$ _: x7 ~6 K1 z( a
unprotected females through direct skin exposure.% c( w. F' \- M' x( R& c- r4 R
Serum testosterone level was found to be 2 times the
8 I% A- ]; e0 e# S  j( S! T& wbaseline value in those females who were exposed to9 a& n0 ?5 F& I8 p# V" @2 F' ]: q
even 15 minutes of direct skin contact with their male
# f1 L0 ?1 R% mpartners.6 However, when a shirt covered the applica-8 [7 {0 a* b: t( g
tion site, this testosterone transfer was prevented.) u# s/ j& K: q: h$ o+ M& L
Our patient’s testosterone level was 60 ng/mL,) j- r. i! s1 R. m6 G! _
which was clearly high. Some studies suggest that3 M* }; _1 p( C" |7 F
dermal conversion of testosterone to dihydrotestos-; J9 k' v* \+ y* Q4 @. j) d) j
terone, which is a more potent metabolite, is more" d* V; S+ e4 N. ~# {$ n5 a' v
active in young children exposed to testosterone' Y8 l1 v& G7 `
exogenously7; however, we did not measure a dihy-
: o( u% z5 @# d$ x7 e; y0 ]drotestosterone level in our patient. In addition to" Z1 n3 c$ j; _! |6 j
virilization, exposure to exogenous testosterone in
5 l% Q0 q- M- k9 \" |children results in an increase in growth velocity and
0 U7 H4 \( `0 r& r& |advanced bone age, as seen in our patient.2 ~6 V) N! w, v$ S
The long-term effect of androgen exposure during8 {. {* \! H3 t; m1 B8 f
early childhood on pubertal development and final" {- h: G5 {0 c0 O- r& O
adult height are not fully known and always remain
. |: p4 I  d8 @% E1 F8 Na concern. Children treated with short-term testos-
/ [$ [( s  o4 d% }3 G# aterone injection or topical androgen may exhibit some) H8 s- T- t" N
acceleration of the skeletal maturation; however, after
3 r9 \0 M5 r; g" ?* {cessation of treatment, the rate of bone maturation$ y) B0 z* b! |- ]- p
decelerates and gradually returns to normal.8,9
2 [( H* h. Q8 I+ rThere are conflicting reports and controversy3 \& b' j, T  [3 r. g1 l/ p9 c: c
over the effect of early androgen exposure on adult) ?; K4 e' V/ v9 v
penile length.10,11 Some reports suggest subnormal* X0 I* s( V) {# F
adult penile length, apparently because of downreg-! M) z+ Y- }. ?: O9 B3 x! F
ulation of androgen receptor number.10,12 However,
3 I( I& Q9 G5 H  H3 SSutherland et al13 did not find a correlation between
2 ~. N  m4 A. \" W/ s+ e/ zchildhood testosterone exposure and reduced adult  z2 t/ @1 T; x1 p, p
penile length in clinical studies.
7 b- o- v0 U: X; E' b7 ONonetheless, we do not believe our patient is, @* Z+ l" T/ T
going to experience any of the untoward effects from7 B2 J1 `3 y5 A
testosterone exposure as mentioned earlier because+ L2 Q7 L1 i. D: ^
the exposure was not for a prolonged period of time.
) ]$ ~" i- D) {4 qAlthough the bone age was advanced at the time of/ M% r4 y7 N' k! B* w
diagnosis, the child had a normal growth velocity at; w# m% C- t% _6 J$ O
the follow-up visit. It is hoped that his final adult
' B. H1 F3 Z0 gheight will not be affected.5 s+ @9 r, E5 N( A% a
Although rarely reported, the widespread avail-. t- g1 E: U* Z9 J: O; H, ^# `0 p
ability of androgen products in our society may
6 z* a1 L( Y. Q* Q! [- xindeed cause more virilization in male or female# _7 H. a& F9 w, \1 z1 E
children than one would realize. Exposure to andro-
2 `6 e+ I$ E% L7 ^+ K: u7 s2 ^gen products must be considered and specific ques-5 I; ~! R% Y0 W
tioning about the use of a testosterone product or2 h/ d) {) }5 i( t
gel should be asked of the family members during
+ \; z" Z" X9 dthe evaluation of any children who present with vir-9 C- ^' z& \8 V  R0 N
ilization or peripheral precocious puberty. The diag-
1 z( d3 t8 f; inosis can be established by just a few tests and by
9 x* G5 i1 B$ e9 Z2 Lappropriate history. The inability to obtain such a5 |# ?9 T3 P- ]' E/ L
history, or failure to ask the specific questions, may* Y, W- d/ ?' I5 ~: w- x! b/ J% c5 \
result in extensive, unnecessary, and expensive0 o. D4 t! C$ k" J+ o) k
investigation. The primary care physician should be
! ^7 \/ w6 N$ B) B, Uaware of this fact, because most of these children
! ^3 \" h" z! @5 }may initially present in their practice. The Physicians’0 \+ L, H% v9 }
Desk Reference and package insert should also put a( u0 E, {: M+ }" L* {5 B2 d
warning about the virilizing effect on a male or
' a# H1 V' n! h1 T3 v$ W1 n* o5 s2 Cfemale child who might come in contact with some-
( B# a* e& H# w0 m" ^5 Eone using any of these products.6 v$ M# Y) Z! p7 _0 K
References
, j0 A* c5 ^0 K4 F1. Styne DM. The testes: disorder of sexual differentiation
/ g4 S1 m9 k) {and puberty in the male. In: Sperling MA, ed. Pediatric
/ Q5 c9 C: z! g( p6 h$ gEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ \9 z  K* r& i  a8 q$ p  r& \2002: 565-628.$ |3 g. U; a! v2 Y2 `8 i9 R0 P" e* V2 Y
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; v) `) [8 d( m+ w1 F" Z: _
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
. N- m8 J' Z5 Q; C8 \/ d1 B7 xBoy Induced by Indirect Topical
# n2 ?$ {/ v* G7 eExposure to Testosterone  Z( g6 A) x, r- f
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' q+ |/ P* }) \% ]7 B+ A) |and Kenneth R. Rettig, MD19 s9 q* h1 L' {/ A9 N
Clinical Pediatrics9 T) b2 @" `8 l
Volume 46 Number 67 M) J/ |  O$ v. ~
July 2007 540-5439 D; T4 l* X9 ~3 g# O" V- \
© 2007 Sage Publications
0 m9 E( l6 n7 u; I5 g: s* G  {10.1177/0009922806296651
5 T" K( Z( ~- [2 U0 U; f6 s5 l1 Ahttp://clp.sagepub.com
$ \& S( @! R8 S5 \* n2 Ohosted at2 `) F5 [7 Y& T! `
http://online.sagepub.com
0 B. f8 @5 S; k' e) _7 \4 Q7 EPrecocious puberty in boys, central or peripheral,
- K8 ^) i6 U3 Z  Wis a significant concern for physicians. Central
9 @5 S3 E3 d" ~& Yprecocious puberty (CPP), which is mediated6 g+ r$ c6 t# s+ Y' A  l
through the hypothalamic pituitary gonadal axis, has' P# X- J2 a# T' ^
a higher incidence of organic central nervous system
/ g# E5 X) l+ u  N1 I# Ilesions in boys.1,2 Virilization in boys, as manifested
6 B- X3 \/ L; {5 N2 Uby enlargement of the penis, development of pubic
3 a  Q* B) I( S7 @; zhair, and facial acne without enlargement of testi-6 @! m6 {, |' ~4 G
cles, suggests peripheral or pseudopuberty.1-3 We. Z- C, h9 A+ m! n
report a 16-month-old boy who presented with the
+ n0 H1 ?2 k. p; K0 ~enlargement of the phallus and pubic hair develop-
5 P6 ?' E) }' \1 a, {8 Gment without testicular enlargement, which was due, X* Y( V: F( C5 v. L+ [* G
to the unintentional exposure to androgen gel used by5 y( O$ u& Q# g( X
the father. The family initially concealed this infor-6 [1 f0 d8 v: |1 k3 {
mation, resulting in an extensive work-up for this8 O% }8 o8 D( F9 V" y' |" w% t) F9 E7 H
child. Given the widespread and easy availability of  c' K" |7 A- w6 n1 v2 k& d: f
testosterone gel and cream, we believe this is proba-
4 |( i. A, M. C$ W9 u- ~bly more common than the rare case report in the0 y# p2 m* Y& C5 d. h
literature.4; }* w" f% g$ |6 Y$ ^
Patient Report
* l) o+ R) D) }, a9 f5 A8 n5 `A 16-month-old white child was referred to the
  K. p3 Z* o9 t8 \endocrine clinic by his pediatrician with the concern! o% e( h! ^) x
of early sexual development. His mother noticed& C$ E2 E( R9 u+ W2 }5 T! W, B7 @
light colored pubic hair development when he was
+ \3 Z& e) Y+ R. r; X9 `From the 1Division of Pediatric Endocrinology, 2University of
4 n1 O  _) B5 M* ~6 f6 ySouth Alabama Medical Center, Mobile, Alabama.7 j" w3 J3 D' I; K
Address correspondence to: Samar K. Bhowmick, MD, FACE,
3 y$ [  H9 _# o' l+ F2 tProfessor of Pediatrics, University of South Alabama, College of
" g+ b' i+ }1 I+ e" DMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;+ F$ L9 w! Y* W/ r2 s- V( C) Q
e-mail: [email protected].
, M$ V! f' Y3 b4 [9 P4 ^+ s! ^4 Eabout 6 to 7 months old, which progressively became
5 p+ @' N( D, g7 Wdarker. She was also concerned about the enlarge-& T" e) q/ R0 T) f6 m( b! l9 w
ment of his penis and frequent erections. The child
& _- h  _5 ^$ nwas the product of a full-term normal delivery, with/ j4 P! I/ G+ F- J6 j" U: _! Q% t  h/ I
a birth weight of 7 lb 14 oz, and birth length of
1 b* b" n6 E- R1 I; {8 o) L% Y20 inches. He was breast-fed throughout the first year
3 a% H5 M" v4 Rof life and was still receiving breast milk along with
0 K9 z: [: I: Gsolid food. He had no hospitalizations or surgery,0 o, U8 X' }; z3 g
and his psychosocial and psychomotor development
2 u$ a; \6 f: q* |) Mwas age appropriate.8 o+ g6 _& C% t+ r" N5 \3 I# t
The family history was remarkable for the father,: w2 J$ u5 q, \. [& r8 j/ w% a
who was diagnosed with hypothyroidism at age 16,+ P  e& L8 E& O) B$ ?9 D
which was treated with thyroxine. The father’s
8 s) h( ^7 y( cheight was 6 feet, and he went through a somewhat4 B, u! U2 f* j
early puberty and had stopped growing by age 14.
2 Y* j: x4 r& ~0 ^" z! C: HThe father denied taking any other medication. The8 B9 Q7 P, R0 ]0 H; T) [" g/ F/ R: H
child’s mother was in good health. Her menarche
: m6 q3 v1 q+ s- R& Z" N- kwas at 11 years of age, and her height was at 5 feet
# Z. X; ^; o. e# A' ~5 inches. There was no other family history of pre-
% a0 e0 D, ]% N- p5 [" d+ N+ d  r+ ~cocious sexual development in the first-degree rela-$ L$ q: V, }" V
tives. There were no siblings.) X, c; s& K- r5 R
Physical Examination
- k8 F+ I. g. MThe physical examination revealed a very active,
; L* a2 ]$ W5 A- L5 eplayful, and healthy boy. The vital signs documented2 R; |4 T. L0 Y7 U4 A0 R# }. Q( R
a blood pressure of 85/50 mm Hg, his length was
  y9 \5 f9 o7 g+ Y1 T90 cm (>97th percentile), and his weight was 14.4 kg
  q5 F) D4 O4 b8 {(also >97th percentile). The observed yearly growth
7 w+ A, G9 e- Y  F; kvelocity was 30 cm (12 inches). The examination of
7 k. R1 \6 h* S# [# X" zthe neck revealed no thyroid enlargement.
# w" R- J% r, j7 }The genitourinary examination was remarkable for" C- B( X8 [( a$ M1 ]
enlargement of the penis, with a stretched length of
4 x) y! R4 K+ L8 cm and a width of 2 cm. The glans penis was very well
% ^6 N0 b+ J5 P! ~' d! k7 Sdeveloped. The pubic hair was Tanner II, mostly around. o3 Q, A+ T+ t7 T: X9 S
540
1 ]9 G+ y/ k' _/ v$ G) }3 `# Zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* E- |6 o; B! F4 B8 R+ {5 Z4 bthe base of the phallus and was dark and curled. The
, w& q# Q+ U$ H1 }9 Utesticular volume was prepubertal at 2 mL each., I+ k6 \' A; x) H& U& \1 G
The skin was moist and smooth and somewhat
. z" V. x4 Q% j. u' W8 Xoily. No axillary hair was noted. There were no* `6 ^8 b- {" P" @7 s6 A
abnormal skin pigmentations or café-au-lait spots.+ j6 ~1 n. j0 z  O; n9 _" ~
Neurologic evaluation showed deep tendon reflex 2+
; k' q: ]- G5 bbilateral and symmetrical. There was no suggestion" g$ a# |; T3 b. D( ^* T( C
of papilledema.
7 }/ f' I# R' \/ G5 ILaboratory Evaluation
/ }  g5 j2 e5 y$ y7 J* s5 @6 }The bone age was consistent with 28 months by9 j* [) X1 }+ h: F# i1 s* j6 ~4 R
using the standard of Greulich and Pyle at a chrono-9 a+ K' \) m% |. O! e: q4 e! Z
logic age of 16 months (advanced).5 Chromosomal
0 B) o6 I- K" Z7 n# U+ ]  Q: kkaryotype was 46XY. The thyroid function test- ?+ M! z5 q5 `! x7 b" I
showed a free T4 of 1.69 ng/dL, and thyroid stimu-0 C1 ^- H  [! ~- \' q3 z
lating hormone level was 1.3 µIU/mL (both normal).
! S/ |, m$ J: Y" Q, S2 k8 E! UThe concentrations of serum electrolytes, blood2 ^, v9 C1 D; T& \+ o
urea nitrogen, creatinine, and calcium all were
' J; G4 u, L; L4 T4 b$ |( Owithin normal range for his age. The concentration- [; D" T+ c. N$ l: `1 y3 T7 ]0 D
of serum 17-hydroxyprogesterone was 16 ng/dL# v8 }9 V4 {: w1 ]4 R- G( |
(normal, 3 to 90 ng/dL), androstenedione was 20( N9 p4 U. S* Z# m! t. p: ]" @5 _; G; K
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) q3 D! N  {5 a
terone was 38 ng/dL (normal, 50 to 760 ng/dL)," x4 c* |( c$ d# |8 ^8 b  c$ J
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 N9 |* L4 u" d2 Y4 |% ?. D49ng/dL), 11-desoxycortisol (specific compound S)
3 `9 [" y/ o6 X  E" pwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: F& X/ m/ F  P' R
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# c6 q; f) l* S! M( B0 a
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 _6 P" x4 C2 i) N7 ^8 j* M* a0 F% I) }and β-human chorionic gonadotropin was less than8 x, _+ k/ p1 Z) N
5 mIU/mL (normal <5 mIU/mL). Serum follicular
( ^: F  R( `4 ~) G' [- G0 L( ?* ^stimulating hormone and leuteinizing hormone
% J4 ^) J/ b; F$ F+ z, w6 Vconcentrations were less than 0.05 mIU/mL
  |* [( _2 R7 y; f& R9 K(prepubertal).
2 O- b  ?, Z! R* ~& P( mThe parents were notified about the laboratory$ c  u7 Y' N+ G: q. Z5 Q
results and were informed that all of the tests were
$ f) B& j9 I# a" H2 vnormal except the testosterone level was high. The1 L$ _5 x) K  _0 B" |6 G" r
follow-up visit was arranged within a few weeks to
3 m2 s3 a6 \7 Y5 vobtain testicular and abdominal sonograms; how-( c4 d! E* d' `9 P3 N( x' t
ever, the family did not return for 4 months.
; j% b# o6 U" p# F% I( iPhysical examination at this time revealed that the  N1 r; V+ L0 z: m' B
child had grown 2.5 cm in 4 months and had gained
: R3 i# ?) E" g8 p" Z2 kg of weight. Physical examination remained
7 s% y4 Z1 {# a8 H) punchanged. Surprisingly, the pubic hair almost com-8 n! q1 B' r  A
pletely disappeared except for a few vellous hairs at/ F) X  h$ Y* e0 K$ i  t4 d& F$ ~
the base of the phallus. Testicular volume was still 28 p( S& S8 L  G) C# y$ x; L+ e" u; z
mL, and the size of the penis remained unchanged.
1 h6 n" T1 W% @, g! ?. M2 Y  A* iThe mother also said that the boy was no longer hav-6 j- r. ]* M0 l9 L/ o1 l6 j* f& Q5 o2 q
ing frequent erections.4 f& a2 j4 g( W) [$ T- Z  g$ G
Both parents were again questioned about use of8 A/ y' y6 T, Q
any ointment/creams that they may have applied to
" b) h& v8 \3 R& |" N7 Lthe child’s skin. This time the father admitted the
$ Q& \2 h0 H" Y8 \6 c6 }5 yTopical Testosterone Exposure / Bhowmick et al 541
1 e3 b% V3 D; zuse of testosterone gel twice daily that he was apply-# H. d- F" ~5 `! h4 e5 O
ing over his own shoulders, chest, and back area for+ r/ D8 H1 X3 K6 C! R- ^
a year. The father also revealed he was embarrassed7 n) ?/ V# e3 z& C4 \/ X# l; T! `
to disclose that he was using a testosterone gel pre-& B3 T# u3 z8 q# g# M6 y8 y2 N
scribed by his family physician for decreased libido
5 ~, D( }" \$ T. Qsecondary to depression.4 H4 r! x* {) D+ ^4 }
The child slept in the same bed with parents.; h2 E1 @; d2 V  E' o  W
The father would hug the baby and hold him on his4 u- I1 L* V( j# h6 j
chest for a considerable period of time, causing sig-& w7 ]/ `9 f2 {# k3 O# ]
nificant bare skin contact between baby and father.3 H9 w$ w, s9 m- L% x
The father also admitted that after the phone call,0 E! \: O/ C! [6 p: q7 P
when he learned the testosterone level in the baby
5 ~5 c: k" V6 z" F  s/ P% Dwas high, he then read the product information* I% A8 @6 f/ N4 ]1 ^# m( P
packet and concluded that it was most likely the rea-' @3 h: u" }% f+ y
son for the child’s virilization. At that time, they# b5 A! O. J1 Y6 f( Q+ J+ v- U
decided to put the baby in a separate bed, and the" _3 \& O" H, y7 s  b. w1 @
father was not hugging him with bare skin and had
' l/ n' [& a5 t4 |been using protective clothing. A repeat testosterone
: J$ @# T  q: C% k/ stest was ordered, but the family did not go to the3 I$ F+ C+ h8 u5 f7 A( s& x
laboratory to obtain the test.4 f+ |6 l# a& j, \8 t; c- G; Y$ G* ?
Discussion6 G0 G2 j5 w$ n$ L6 ^3 e% D/ ~
Precocious puberty in boys is defined as secondary
: O# w1 b0 Q6 ^sexual development before 9 years of age.1,4
9 O/ _7 b0 `( r1 i; d  a+ PPrecocious puberty is termed as central (true) when
* _" M& X( T2 u+ a0 a& X" ?it is caused by the premature activation of hypo-
! ?( ?# ^4 t9 A2 k4 _% @' o6 Ythalamic pituitary gonadal axis. CPP is more com-
. q9 E; z/ ~( [( B# j$ rmon in girls than in boys.1,3 Most boys with CPP
2 H4 a: S+ }( q1 _. }may have a central nervous system lesion that is4 X  U; h! j- z) f; P8 N3 }7 @
responsible for the early activation of the hypothal-
) Q& W4 I7 \) w4 x+ m8 k; `amic pituitary gonadal axis.1-3 Thus, greater empha-' C- S, a1 m* _3 p, k$ P
sis has been given to neuroradiologic imaging in
5 x& d# g) J) ]' T4 E; @: w9 i/ rboys with precocious puberty. In addition to viril-# ]5 ?) i5 h" g! D$ Z1 y
ization, the clinical hallmark of CPP is the symmet-* B' r# q" r6 H( r/ ^
rical testicular growth secondary to stimulation by
' k; g+ S" l) J5 wgonadotropins.1,3( z! o0 Y6 b8 |4 Q' B. F
Gonadotropin-independent peripheral preco-
) F  a2 s7 [2 t9 k5 v0 }cious puberty in boys also results from inappropriate
8 z, L/ S9 ~& e( W2 V7 Y$ aandrogenic stimulation from either endogenous or
% E& a% T! ?0 S% G& _6 l5 Iexogenous sources, nonpituitary gonadotropin stim-
, G% w" d$ W0 `3 [ulation, and rare activating mutations.3 Virilizing- y8 M* {/ X% F% A4 W
congenital adrenal hyperplasia producing excessive$ r- b% h: z) j# r# U5 v
adrenal androgens is a common cause of precocious
" P8 R  z0 W$ [, _7 _! L1 Bpuberty in boys.3,41 n0 j1 m/ X  w5 P3 s9 W" a
The most common form of congenital adrenal
- l" [% q# v) x3 k1 ?  |5 Fhyperplasia is the 21-hydroxylase enzyme deficiency.
; a: ^9 Q8 U5 ^The 11-β hydroxylase deficiency may also result in
9 I1 K* e9 u/ I) `; Y* C7 Wexcessive adrenal androgen production, and rarely,) M( U  P/ f" o5 Z) D7 x5 w( x5 G
an adrenal tumor may also cause adrenal androgen$ [  x3 s) r- c. I! C7 t  H
excess.1,3: i" F6 ^/ `0 b5 O1 g) c4 ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 S0 b9 ?$ T7 F! N4 A) Y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' M  A5 I3 S. i2 J9 x8 g3 FA unique entity of male-limited gonadotropin-
" k. A; B. E) Q# X; l6 n  C7 X' Nindependent precocious puberty, which is also known! r! Z) o- D  \# r2 w
as testotoxicosis, may cause precocious puberty at a/ E3 I" H7 |, ?7 F! f0 x' a0 M
very young age. The physical findings in these boys
( I6 T5 i7 ^- G0 F7 ^: b7 ^" ewith this disorder are full pubertal development,; U3 L9 ~4 d- @0 W/ F5 E! f4 W7 \- q% R
including bilateral testicular growth, similar to boys- u1 [* x4 v3 m1 A
with CPP. The gonadotropin levels in this disorder
' c+ G6 |% K$ ]: I% U: yare suppressed to prepubertal levels and do not show/ e' M) n  O+ y
pubertal response of gonadotropin after gonadotropin-: d" f3 R6 E& ~8 m# j+ K/ ~8 K1 z
releasing hormone stimulation. This is a sex-linked
! r& L3 U0 @6 b$ J% bautosomal dominant disorder that affects only
4 @4 d, ^, A' H. U6 jmales; therefore, other male members of the family
- u$ O7 R( C3 L1 X" s, v1 xmay have similar precocious puberty.36 L( v) A* J- f( Q# ?
In our patient, physical examination was incon-
3 r- Z: T$ a( i7 C; Tsistent with true precocious puberty since his testi-
( t' m+ V; Z( \& ecles were prepubertal in size. However, testotoxicosis- B( k0 k  Z9 O( O: L, {
was in the differential diagnosis because his father
0 q/ e& f5 F- n6 Qstarted puberty somewhat early, and occasionally,# U: m7 U8 S- E% n- x
testicular enlargement is not that evident in the: o8 h, ?! O' X$ W1 _0 q1 R
beginning of this process.1 In the absence of a neg-
1 {: X" _! ]$ @5 ~' xative initial history of androgen exposure, our
* E$ e; b1 n  A" f" ubiggest concern was virilizing adrenal hyperplasia,1 ~6 T( o$ v* x/ U6 z, p
either 21-hydroxylase deficiency or 11-β hydroxylase2 c! O7 b: j; e/ a+ i- P
deficiency. Those diagnoses were excluded by find-
5 O1 b4 u* C) g; i" ving the normal level of adrenal steroids.9 F+ W. i+ S1 h3 j+ y+ H" |
The diagnosis of exogenous androgens was strongly5 {/ i) U, ]- [* B2 {
suspected in a follow-up visit after 4 months because
# U5 N. R) S" l6 x$ i) Bthe physical examination revealed the complete disap-8 C+ V  y. O, O, G- c# B3 I+ _
pearance of pubic hair, normal growth velocity, and
, }7 P% M9 G. ]5 a- P- M9 Cdecreased erections. The father admitted using a testos-5 ~. ?. i+ Q) F. w' j6 x
terone gel, which he concealed at first visit. He was2 V  ^( u% D2 g4 I% S
using it rather frequently, twice a day. The Physicians’% B# i7 [; r- _1 A# t: Y7 V) e$ f2 v
Desk Reference, or package insert of this product, gel or
+ Z* }1 }; @* I3 }5 rcream, cautions about dermal testosterone transfer to" E7 x) u! s& P' R$ h, g  \. Z
unprotected females through direct skin exposure.4 @* }) R9 w/ ]& ]$ O3 R
Serum testosterone level was found to be 2 times the
) T  A) G/ Q, H7 @" }  Sbaseline value in those females who were exposed to! N$ X8 ~# x8 W% A
even 15 minutes of direct skin contact with their male$ r4 z* O6 o6 ~! ], o* `# s3 D
partners.6 However, when a shirt covered the applica-
1 ]! |. L3 t- W; j( `tion site, this testosterone transfer was prevented.
& q: t, `: _+ FOur patient’s testosterone level was 60 ng/mL,: Y/ [* }7 M# w; s* ~
which was clearly high. Some studies suggest that/ W# J( [) z$ h( S
dermal conversion of testosterone to dihydrotestos-
, W( F+ Q, Z9 y5 x/ Sterone, which is a more potent metabolite, is more4 Q1 y( X. r7 `
active in young children exposed to testosterone1 m! f7 b9 e1 |% A) ]8 {. [# O
exogenously7; however, we did not measure a dihy-
7 T- L+ j9 Z7 ndrotestosterone level in our patient. In addition to
9 ^% }, P+ ^/ Z! Hvirilization, exposure to exogenous testosterone in1 J9 w- |2 y- M( J. j5 F
children results in an increase in growth velocity and
" o6 g7 f5 g1 {3 K  w5 Aadvanced bone age, as seen in our patient.& W& b. L) s5 ?& T
The long-term effect of androgen exposure during$ A1 C3 Y8 E; C
early childhood on pubertal development and final- w1 W& s% i- E
adult height are not fully known and always remain$ k, Z/ C: X. J# C% v* ~" s
a concern. Children treated with short-term testos-0 R- K' X/ k! F8 {) C! y- E
terone injection or topical androgen may exhibit some
3 Q# Z" K: H" \: F$ X% [+ jacceleration of the skeletal maturation; however, after
  E- {* V2 s6 D6 Ucessation of treatment, the rate of bone maturation
- a5 g  a8 K' o9 ^& z7 Edecelerates and gradually returns to normal.8,9
9 V$ m# U8 w) x& _; z( K6 tThere are conflicting reports and controversy
; g1 ?6 ]8 L2 H+ n2 c9 h1 }* i1 ?over the effect of early androgen exposure on adult
/ h# [$ |% E- l. \; V3 cpenile length.10,11 Some reports suggest subnormal* n& N, s* Y& A% [
adult penile length, apparently because of downreg-, t- g! d8 o0 N! |0 \( F9 `8 N* r
ulation of androgen receptor number.10,12 However,
' J6 `8 g8 j1 E. v' GSutherland et al13 did not find a correlation between
1 J. e  K% i; V3 |childhood testosterone exposure and reduced adult
. p, s( E- f; z% W* Epenile length in clinical studies.
- H9 x5 b9 [/ oNonetheless, we do not believe our patient is
, N$ V7 o  U; h/ X- kgoing to experience any of the untoward effects from
. N- Y. D; g+ E0 [6 itestosterone exposure as mentioned earlier because2 c7 H6 v" @0 y/ ?
the exposure was not for a prolonged period of time.
& ]4 ~& V' ?$ [  m2 BAlthough the bone age was advanced at the time of; |: U# ?0 J+ P7 l
diagnosis, the child had a normal growth velocity at4 i, B: Y/ F/ u* e
the follow-up visit. It is hoped that his final adult2 D3 R" x. Q2 b' s8 R
height will not be affected.
9 n" b" n+ j. B0 r. ]) `Although rarely reported, the widespread avail-
& B; r; l! t9 L0 ]: @5 [) v* Kability of androgen products in our society may- `/ v7 R6 X+ w
indeed cause more virilization in male or female
' s" I. l# J$ Uchildren than one would realize. Exposure to andro-2 s. s6 ^4 C$ ~) H+ }$ k
gen products must be considered and specific ques-4 ^5 u& J6 \' F4 |; N; p4 r
tioning about the use of a testosterone product or
" K- O- N4 E" W  x; s& egel should be asked of the family members during  Q8 _' m# ^; W
the evaluation of any children who present with vir-
9 E) s! ~' ?3 Q! j+ A4 Xilization or peripheral precocious puberty. The diag-! ~. a! ^1 T& Y' T% U
nosis can be established by just a few tests and by- ?8 m' w2 `: T2 M
appropriate history. The inability to obtain such a" s; I) U1 F) f- w' ]
history, or failure to ask the specific questions, may
' }: d6 T  g6 N, U. oresult in extensive, unnecessary, and expensive. o! D- U" R" u5 b6 ^/ r* ~
investigation. The primary care physician should be% _1 N2 L4 O  a' |2 t, d
aware of this fact, because most of these children
- G4 _8 {# F# c! V. Y9 Imay initially present in their practice. The Physicians’9 h" k- i" r% R5 b
Desk Reference and package insert should also put a
/ R1 j3 H1 s- H5 ?$ a6 ?+ n5 ywarning about the virilizing effect on a male or8 q6 y9 m. ?( j* F! N/ U! [
female child who might come in contact with some-
- i; _  k- x, U5 k1 R! h, f4 ^; pone using any of these products.
+ z9 A$ ^; v; i8 f0 [8 U) YReferences; q/ g- Q: K2 B) V3 w: ]/ i& N& a  ^3 r7 z
1. Styne DM. The testes: disorder of sexual differentiation
- V$ M- ~2 @2 @( l/ Yand puberty in the male. In: Sperling MA, ed. Pediatric
$ I+ {8 v  N, a" c1 X/ i( F2 [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' G2 A( B7 ~0 A; }2002: 565-628.+ y4 C% _7 ~4 y( A2 Y- n! q  j
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( g# x+ I- C5 t8 i& ^puberty 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

$ o4 _4 T- k. F1 ^+ g" p. e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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