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Sexual Precocity in a 16-Month-Old
5 _1 P. u2 @- d4 s5 g" J5 xBoy Induced by Indirect Topical
, j4 m$ D8 X0 G: n' E, d& eExposure to Testosterone7 [3 X7 c0 p5 ?! K% f' K0 b
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2, L4 k4 C4 c. r# E6 s
and Kenneth R. Rettig, MD1
. Y) a4 Z4 i( U. g( g5 W5 xClinical Pediatrics) A3 h- w6 S# Z: f2 ?( o
Volume 46 Number 6
) w5 D+ p; ?! q8 H j/ WJuly 2007 540-543
6 [% g% K+ {: g' n6 j© 2007 Sage Publications; T8 H3 ?) ]* i& ^2 c
10.1177/0009922806296651
( o3 F4 `: E7 s. W5 whttp://clp.sagepub.com
! ~& s1 Q/ S. j* B) Fhosted at
8 \( x4 @0 d; D1 p' m5 x, Hhttp://online.sagepub.com, g1 ~& J4 n$ g! z" F! b* n8 `
Precocious puberty in boys, central or peripheral,
. C/ O9 ^: u' p$ His a significant concern for physicians. Central [# J0 Q& N6 S7 `7 m! Y
precocious puberty (CPP), which is mediated
4 O) b" u/ v2 ]+ M& K" Z0 v9 X9 @through the hypothalamic pituitary gonadal axis, has
3 V: d& f8 \( |" X8 Fa higher incidence of organic central nervous system+ H6 c& {" P# |, y7 ]
lesions in boys.1,2 Virilization in boys, as manifested2 F" E9 ?: q7 v5 P8 E
by enlargement of the penis, development of pubic$ ]8 X+ W# v4 x$ E' {& Q
hair, and facial acne without enlargement of testi- s( ~, m5 o6 ~+ F) Y$ D
cles, suggests peripheral or pseudopuberty.1-3 We
) G9 _- K6 l- ]report a 16-month-old boy who presented with the
' g' I$ A# z& P% {# q6 V1 Kenlargement of the phallus and pubic hair develop-% z# C" R2 |' N3 \: n' `/ o( D
ment without testicular enlargement, which was due
2 [3 R& P7 c' a/ g- yto the unintentional exposure to androgen gel used by) L$ I0 X9 E4 m6 f
the father. The family initially concealed this infor-
; Z, }+ l# I9 T! W' A* n+ l2 { b% Emation, resulting in an extensive work-up for this1 m, m5 Y% @( b' m( u5 r
child. Given the widespread and easy availability of E$ d7 ^0 b; z! W
testosterone gel and cream, we believe this is proba-. Q# o( v4 Q1 e7 F b$ o7 c
bly more common than the rare case report in the- ^: G4 M! i4 h; E' ~
literature.4% {7 X. G- A2 F& d
Patient Report* ~4 _. h, s1 C6 B* V$ \8 q# \# B$ a
A 16-month-old white child was referred to the% ~1 n p$ o/ y7 o% H! h
endocrine clinic by his pediatrician with the concern$ c5 T- a* a8 R& }( A% ], K9 o3 W
of early sexual development. His mother noticed+ m5 O4 I% d$ l0 I4 Y4 X
light colored pubic hair development when he was- O* J0 U' Q2 \- J7 P
From the 1Division of Pediatric Endocrinology, 2University of
7 v3 q# u9 u" N1 D$ Z- c3 w" \South Alabama Medical Center, Mobile, Alabama.5 v8 Y V/ Q* T: h% q
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 J2 x: ?6 v+ U6 I2 g4 _Professor of Pediatrics, University of South Alabama, College of
7 y6 g& M3 J, b. a' u2 o" dMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 Q3 B( B/ r2 {; Z+ K8 we-mail: [email protected].
. S- o9 A: k( v# Sabout 6 to 7 months old, which progressively became
& o0 s4 R; Q* [& Wdarker. She was also concerned about the enlarge-
/ ~8 I0 V# P, {& b. [ment of his penis and frequent erections. The child
+ z" `- Z; H; U( T+ Rwas the product of a full-term normal delivery, with7 U7 }" q% O7 p( x, U
a birth weight of 7 lb 14 oz, and birth length of
- H- ?3 J, W& `% \20 inches. He was breast-fed throughout the first year' r* i! r. B ^7 V" f
of life and was still receiving breast milk along with- J. s4 H( L& `' W7 }' ^& c" g7 @1 T
solid food. He had no hospitalizations or surgery,
0 B* x4 d0 Z2 u7 [and his psychosocial and psychomotor development9 [/ ^/ j3 u! M/ S9 S2 z
was age appropriate.- H- `/ t2 L; o" X
The family history was remarkable for the father,& w) h8 N: q+ O5 H( K3 _* d
who was diagnosed with hypothyroidism at age 16,$ `. U' ~) t2 j% I% f; o5 ?' D
which was treated with thyroxine. The father’s- s# Y4 n5 j% j3 _, r
height was 6 feet, and he went through a somewhat$ t) m9 e; h7 @% \- ^1 r j
early puberty and had stopped growing by age 14.
* @7 S# R, ?) Z6 ~1 s# s- lThe father denied taking any other medication. The" K# q5 ~/ O. h# S
child’s mother was in good health. Her menarche
: z/ a( ^ U nwas at 11 years of age, and her height was at 5 feet* w7 g- x& y0 C; S
5 inches. There was no other family history of pre-& e3 o& E5 B7 E5 O' M! f F& X
cocious sexual development in the first-degree rela-
& }& T4 T1 t! Gtives. There were no siblings.0 o* e, j% y9 U. g
Physical Examination5 t5 F* E' j; N3 {$ |% D9 Y
The physical examination revealed a very active,7 Z7 G; q1 |/ S) {- c" u7 f
playful, and healthy boy. The vital signs documented* L2 ?; }) w( `( s7 Q) ?+ J9 |
a blood pressure of 85/50 mm Hg, his length was
/ z7 z1 H1 m1 l90 cm (>97th percentile), and his weight was 14.4 kg
+ b& @3 `% F+ p+ ~6 f(also >97th percentile). The observed yearly growth
: S9 H8 F& k; V+ a' I0 l0 s% zvelocity was 30 cm (12 inches). The examination of% S1 O, `+ k0 b
the neck revealed no thyroid enlargement.
+ e4 q8 n E6 f4 _; \ wThe genitourinary examination was remarkable for
2 P/ E8 c6 U! J" N& Z4 n( Y% V7 Jenlargement of the penis, with a stretched length of" D) O4 F. @4 m) P: _+ n. l8 U
8 cm and a width of 2 cm. The glans penis was very well0 X3 H# d; Q/ ~( u+ |3 I
developed. The pubic hair was Tanner II, mostly around
* y, B; }% ?. V540
3 Q6 v! s# c! D" N |2 N/ W5 G; Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! l7 O5 O, U; X0 g5 othe base of the phallus and was dark and curled. The, S7 g0 a* B5 P& ?1 R% T
testicular volume was prepubertal at 2 mL each.
; x4 ~4 l, Q _The skin was moist and smooth and somewhat) G/ N" c: e* Q/ C& r
oily. No axillary hair was noted. There were no
. Q* A5 _# I. Q1 l2 q2 rabnormal skin pigmentations or café-au-lait spots.8 `! @- H% E+ m! I) P
Neurologic evaluation showed deep tendon reflex 2+
; a$ w" X3 L6 t/ xbilateral and symmetrical. There was no suggestion
: N! W+ f0 c' [$ f5 Jof papilledema.
% \4 M: S0 Y4 s- s& GLaboratory Evaluation1 o1 f/ A* }1 _
The bone age was consistent with 28 months by
3 V' R# ?# v. V6 ?+ Busing the standard of Greulich and Pyle at a chrono- k2 P* K4 L1 g2 l/ P4 ?/ Q. ^
logic age of 16 months (advanced).5 Chromosomal& u* K% D5 P0 \7 ^5 s, p' G
karyotype was 46XY. The thyroid function test' d- t3 n6 R8 Y( j6 b- N3 k
showed a free T4 of 1.69 ng/dL, and thyroid stimu-! E2 s i7 @8 W0 F. Q4 H
lating hormone level was 1.3 µIU/mL (both normal).# z- P S$ V4 _/ W+ N# {: u1 n9 T
The concentrations of serum electrolytes, blood2 g( @/ _( Z8 i9 W& Z' Z7 [& F
urea nitrogen, creatinine, and calcium all were0 A2 z! x2 n, ?) {; L
within normal range for his age. The concentration
0 c$ k& w$ a1 e/ [- Wof serum 17-hydroxyprogesterone was 16 ng/dL
' w. ?9 w4 S* X8 k(normal, 3 to 90 ng/dL), androstenedione was 206 ~& q9 s. O9 q0 R, c
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( N, t/ U G1 Z# Y/ ]* _terone was 38 ng/dL (normal, 50 to 760 ng/dL),6 s2 e6 N8 E2 J2 l+ t" G: v( t
desoxycorticosterone was 4.3 ng/dL (normal, 7 to2 Q6 _* n& O% l7 |
49ng/dL), 11-desoxycortisol (specific compound S)! x- k5 `2 C# f- n3 s7 l7 L
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-7 R3 \- ?) y [: F
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ A+ f& h M( b; H) ]6 Qtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),& N1 h! A* B' A$ h5 k; V* u
and β-human chorionic gonadotropin was less than
" ~0 x$ E, ^6 V, f3 v1 O; X$ |5 mIU/mL (normal <5 mIU/mL). Serum follicular+ ]2 F; N" @0 W! @
stimulating hormone and leuteinizing hormone
: \ x+ n3 `6 I4 `concentrations were less than 0.05 mIU/mL8 r- m6 u3 n' ?$ C J2 e* T
(prepubertal).
8 O4 ^5 q" V- H: }) I% Y$ J4 GThe parents were notified about the laboratory
0 x' ~1 U, j$ V9 C5 Y+ Wresults and were informed that all of the tests were
# c9 N1 t. n( x! T3 y; p0 Pnormal except the testosterone level was high. The6 v) c5 R, k# y, z
follow-up visit was arranged within a few weeks to7 d: t2 s% p4 c* \! x5 x
obtain testicular and abdominal sonograms; how-9 m% w% |3 x8 l6 ? m
ever, the family did not return for 4 months.
- r# z4 k4 r4 n9 V2 s7 oPhysical examination at this time revealed that the4 R) L6 a9 n# d* n s/ M+ [
child had grown 2.5 cm in 4 months and had gained
2 i( U; @# T4 m/ e3 B2 kg of weight. Physical examination remained
$ S9 I, ~. V E% runchanged. Surprisingly, the pubic hair almost com-
/ r' S2 I0 q1 L/ N% Z, e0 [& Cpletely disappeared except for a few vellous hairs at9 n: Z, K$ T1 |( k4 n
the base of the phallus. Testicular volume was still 20 e; j" N& `) E7 `( ?3 e6 t9 Z
mL, and the size of the penis remained unchanged.
! a+ H* }5 W, c, P a( CThe mother also said that the boy was no longer hav-
# L* a) H! U4 H/ ~6 ting frequent erections.. G2 S' k1 w; |6 |" O* {- B
Both parents were again questioned about use of- {4 s i6 p# g5 q: b" d; f$ b# W; e) G
any ointment/creams that they may have applied to W6 h1 Q: J L+ v# p; O
the child’s skin. This time the father admitted the
: _3 t( ?2 f3 S9 S7 K+ t$ E5 KTopical Testosterone Exposure / Bhowmick et al 541
/ a5 x* _' S% ] yuse of testosterone gel twice daily that he was apply-
2 f# ^1 u. d& Y+ ~; U, \ing over his own shoulders, chest, and back area for
- ?; d% r$ o8 F1 M6 Fa year. The father also revealed he was embarrassed
+ | O( j- t2 y' d6 \to disclose that he was using a testosterone gel pre-: R3 q: X" S c) w- C) X, V
scribed by his family physician for decreased libido3 y& E& H! w& h. X2 G5 L0 \
secondary to depression.% b/ S9 ^% h- w! q+ c% [7 P# s
The child slept in the same bed with parents./ l) c- a) R7 r6 ^$ L; C
The father would hug the baby and hold him on his, V( u) @5 |/ f' w y) T* ^0 C. b# N
chest for a considerable period of time, causing sig-2 _% N9 P5 D# {) m& x* N0 [" K
nificant bare skin contact between baby and father.* c( }( L7 w4 Z, V
The father also admitted that after the phone call,
+ H j$ W# q: \when he learned the testosterone level in the baby$ P# m" U6 @2 k4 r# z2 }) q
was high, he then read the product information( G; K( ~& d! r6 g# t2 V
packet and concluded that it was most likely the rea-" K- L' {& K5 W9 d6 A
son for the child’s virilization. At that time, they
) Y$ K. o; ]9 {2 d6 y. q; L/ ]decided to put the baby in a separate bed, and the& e2 `+ J3 z5 Y5 Y$ E1 a5 y
father was not hugging him with bare skin and had
9 v+ S& u$ _& q1 d4 bbeen using protective clothing. A repeat testosterone6 P9 H6 C7 g7 E; v: r( q! Q
test was ordered, but the family did not go to the
8 f) h) ]- h% C5 a$ y% T, Z7 olaboratory to obtain the test.
! [" Y4 Y# O- g8 S- |; ZDiscussion/ ]3 H5 l2 c6 ^( N( W3 w4 D
Precocious puberty in boys is defined as secondary1 k4 Y% T7 F! M2 _, @* }# w
sexual development before 9 years of age.1,4
4 k" E" ?% Q# A* S3 ]Precocious puberty is termed as central (true) when
4 c- c5 ]8 Q( }- j) k$ tit is caused by the premature activation of hypo-
6 s: b, y4 A8 }" A# _2 _2 rthalamic pituitary gonadal axis. CPP is more com-! f8 j$ U- e8 B' a' C
mon in girls than in boys.1,3 Most boys with CPP+ d Y' W5 O7 \
may have a central nervous system lesion that is, z3 k( q+ {# B3 `
responsible for the early activation of the hypothal-
3 w6 q5 w0 {0 j. d; B# Jamic pituitary gonadal axis.1-3 Thus, greater empha-
- ?# L- v( X0 w' N$ v+ [sis has been given to neuroradiologic imaging in# Y0 S7 q% G0 h b- Q
boys with precocious puberty. In addition to viril-
* ]8 Y# I1 @( N+ Y# ?+ Yization, the clinical hallmark of CPP is the symmet-1 k. g' ~- R- {& e% T1 z; ^
rical testicular growth secondary to stimulation by, D0 `) u1 [, ?
gonadotropins.1,3/ e! Y5 l! m C6 t7 x& p9 O4 x7 w
Gonadotropin-independent peripheral preco-
2 ?7 o7 e! j- mcious puberty in boys also results from inappropriate; s1 e& _& {; L" d
androgenic stimulation from either endogenous or
- D, k) E1 a/ {7 X* U7 a# pexogenous sources, nonpituitary gonadotropin stim-
b b+ T/ U2 m& j8 nulation, and rare activating mutations.3 Virilizing5 N$ Z y9 s; P j7 d6 h! Q/ [$ q
congenital adrenal hyperplasia producing excessive
1 Y% S* {4 k% F ~: k& R/ wadrenal androgens is a common cause of precocious5 f8 `% ]. p4 S& E
puberty in boys.3,4 _- E: X! Y, d, ?2 z T4 N. p
The most common form of congenital adrenal
1 g* x9 W) q; N0 phyperplasia is the 21-hydroxylase enzyme deficiency.! P: n7 W3 @# V% F. t! \
The 11-β hydroxylase deficiency may also result in- m7 W. t0 k& z
excessive adrenal androgen production, and rarely,5 D l8 G3 Y* P) P" {( _
an adrenal tumor may also cause adrenal androgen# K( X( m" B7 R% H& W: D7 |
excess.1,3
* h; v1 ~& T" c3 S) Bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! F( j, ?3 n2 j" k4 o
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. t: B$ m- `9 l# O" ^. I9 W3 Q
A unique entity of male-limited gonadotropin-
! `: V9 `( ~2 R# cindependent precocious puberty, which is also known
* G, b: D3 @% t Y* e4 ras testotoxicosis, may cause precocious puberty at a8 M& o1 i) Z! K& B( ?, v4 n7 f
very young age. The physical findings in these boys; S7 L3 F0 B3 m, a/ F
with this disorder are full pubertal development,
6 |8 P* a& K$ t) k% U; a5 K. |including bilateral testicular growth, similar to boys
: p2 X6 C. d" b( ]with CPP. The gonadotropin levels in this disorder/ N. a# m. |$ H7 g' E
are suppressed to prepubertal levels and do not show
% R2 W2 k$ {" R+ m6 I0 Cpubertal response of gonadotropin after gonadotropin-
! f1 W. A( c1 ]8 v. @% n" ereleasing hormone stimulation. This is a sex-linked) B$ M1 k2 K, }1 T+ {6 G
autosomal dominant disorder that affects only$ ~# g% Q4 X) \& }6 I+ Q
males; therefore, other male members of the family
$ b' j' J8 W9 P" Umay have similar precocious puberty.3
$ r" s' i" p* r/ p9 S1 pIn our patient, physical examination was incon-
! y/ w1 R. e6 I# k l( Esistent with true precocious puberty since his testi-
+ [% @5 z& f% \4 y) l3 V2 Bcles were prepubertal in size. However, testotoxicosis
- O- }- v% @7 Q6 ]% ~4 c" q% Kwas in the differential diagnosis because his father: x8 i! g7 }" b3 U* S# i
started puberty somewhat early, and occasionally,3 B5 m, G" @1 }$ L! z3 p
testicular enlargement is not that evident in the
& I* f9 I% E* t! H1 ?! _- Sbeginning of this process.1 In the absence of a neg-
) o. W/ G3 Y8 d% s$ N# T: r2 sative initial history of androgen exposure, our. l" y. |- q7 q' G; f) n9 N
biggest concern was virilizing adrenal hyperplasia,
. G* k8 j, n: {& d( r! Weither 21-hydroxylase deficiency or 11-β hydroxylase
/ \- ]9 z7 j; ]' Adeficiency. Those diagnoses were excluded by find-
4 g: q% k# |' oing the normal level of adrenal steroids.
. x( ~ X* n5 {* N/ D0 [6 [The diagnosis of exogenous androgens was strongly
6 l! A6 T$ H% `suspected in a follow-up visit after 4 months because
$ U& r" @8 X' @- q- ]0 sthe physical examination revealed the complete disap-
) S7 S5 L# O+ j8 E6 A3 g2 ?/ L: Mpearance of pubic hair, normal growth velocity, and
9 I, j, ^1 j! w. ydecreased erections. The father admitted using a testos-/ S8 ?; S6 |7 n& D5 |
terone gel, which he concealed at first visit. He was
: x" T, c1 |2 @# h: q5 b5 susing it rather frequently, twice a day. The Physicians’' E$ ^6 S" y9 A8 M2 T6 q$ M- o7 ?9 {
Desk Reference, or package insert of this product, gel or2 x/ b) I; f, U% N
cream, cautions about dermal testosterone transfer to
C5 T7 j2 h$ s( w4 I1 d2 Iunprotected females through direct skin exposure.
& k3 R! O; F4 t7 B; M) N' ^3 sSerum testosterone level was found to be 2 times the" r5 r$ y% ?' p7 G
baseline value in those females who were exposed to
6 u, D3 A4 O4 i9 t( D; aeven 15 minutes of direct skin contact with their male
: Q3 Z# u+ x" K- j5 W% vpartners.6 However, when a shirt covered the applica-
! b) _8 Q$ n# [! B9 r) k b: jtion site, this testosterone transfer was prevented.7 _) ^& w+ Q' q% d. h" w
Our patient’s testosterone level was 60 ng/mL,
4 e" g, {3 s( J! |which was clearly high. Some studies suggest that
! m: W/ R$ O3 a) C0 wdermal conversion of testosterone to dihydrotestos-( C! g7 B0 d; k& N! h
terone, which is a more potent metabolite, is more: j* q$ s& A, ]- e
active in young children exposed to testosterone: e3 d4 c3 ?2 ]+ q% X6 a/ n; y$ v
exogenously7; however, we did not measure a dihy-
8 \- G) B9 [$ k. f+ Pdrotestosterone level in our patient. In addition to
H9 s9 G/ g/ q9 D5 Zvirilization, exposure to exogenous testosterone in
W% b/ S# z/ O$ Y9 e4 C% Z, j1 zchildren results in an increase in growth velocity and
5 h6 [& R& ~/ I1 O; xadvanced bone age, as seen in our patient.' G2 N, o6 E' S7 ~; G5 n s- s
The long-term effect of androgen exposure during' G9 w5 F* i, L
early childhood on pubertal development and final
( _: @# f* a. Y1 i, t4 k0 y5 dadult height are not fully known and always remain
# `8 E: n i' r, L% e; _: W, j0 S8 e qa concern. Children treated with short-term testos-
, O) y6 V. I! ~! X9 yterone injection or topical androgen may exhibit some
8 X; D. z3 O! s8 ~acceleration of the skeletal maturation; however, after
0 i0 y+ n4 W2 q! P4 l$ Acessation of treatment, the rate of bone maturation& c8 J* S2 u+ V k
decelerates and gradually returns to normal.8,9
2 z$ b6 r. X( Y4 \There are conflicting reports and controversy
& t- }, a* u$ |over the effect of early androgen exposure on adult
4 c+ N& _% d0 ^$ Apenile length.10,11 Some reports suggest subnormal; @) B0 E y& l5 e [ J; p
adult penile length, apparently because of downreg-
& J# S: v: v. j. R3 l' o0 z" U/ r! d4 Xulation of androgen receptor number.10,12 However,
- t; J7 z# h$ O! O7 d$ `( ZSutherland et al13 did not find a correlation between# g0 S `: h' L# P. G# U1 z8 V1 k' K
childhood testosterone exposure and reduced adult2 M X# e7 G0 n
penile length in clinical studies.
$ Q- d/ V# s I2 s/ c- }1 ^' t1 R. MNonetheless, we do not believe our patient is
& U/ [2 l- a$ V3 rgoing to experience any of the untoward effects from
0 v, b6 n* J! b" d8 Ktestosterone exposure as mentioned earlier because
& D- h: h! p+ W; M& `the exposure was not for a prolonged period of time.7 _4 O& j. y/ g" w7 f/ e8 d
Although the bone age was advanced at the time of" `, ~4 @1 C! Z8 ^+ D
diagnosis, the child had a normal growth velocity at
$ L2 s, N8 M* U- E Pthe follow-up visit. It is hoped that his final adult/ M F& }$ z0 H0 j
height will not be affected.
. w+ S" B9 P) G2 Z# ]6 oAlthough rarely reported, the widespread avail-
H; d! ^, D: \: Y, m9 D+ f+ X: ?8 Rability of androgen products in our society may( l9 D" ~8 N& w$ j
indeed cause more virilization in male or female9 Y U4 u1 z/ E2 q
children than one would realize. Exposure to andro-
% s0 O! q) \ Z/ n. Z5 Vgen products must be considered and specific ques-& j/ z& T, v, r3 _0 c6 |1 P
tioning about the use of a testosterone product or
+ f0 ]* _6 Q K5 r# t/ ]gel should be asked of the family members during
2 a% D2 U$ }& `7 r4 T, Vthe evaluation of any children who present with vir-& j: G0 |' u. P3 J# v" P0 i
ilization or peripheral precocious puberty. The diag-
9 z" @, y* R2 D3 ynosis can be established by just a few tests and by
( p3 ]* d& }2 a* k2 D: eappropriate history. The inability to obtain such a
. `# {! T) ]* ?- rhistory, or failure to ask the specific questions, may: m, E+ C$ {1 Q
result in extensive, unnecessary, and expensive' L- j' ]4 K7 |
investigation. The primary care physician should be! k/ j. S+ c8 G0 f7 [
aware of this fact, because most of these children
! R, v+ e/ N; j, gmay initially present in their practice. The Physicians’
. i: P$ ~& _+ G- ^& hDesk Reference and package insert should also put a
7 d& h# e% M- P" r1 v2 Lwarning about the virilizing effect on a male or; m6 W* Q& w3 P% \' Y
female child who might come in contact with some-+ c" w/ m s: k6 w
one using any of these products.3 P1 s; u$ N7 ~* x/ l: Q( t! M2 q
References7 u" S) C1 e( U: Q L
1. Styne DM. The testes: disorder of sexual differentiation
& M2 o6 A4 }6 d1 `) eand puberty in the male. In: Sperling MA, ed. Pediatric6 a5 o! C. _( Y, f6 a
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* X I- t2 d. ?' k
2002: 565-628.
+ M$ d# g9 p5 |2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! p0 ^% {9 z+ n6 z# A
puberty in children with tumours of the suprasellar pineal |
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