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Sexual Precocity in a 16-Month-Old
8 ~* Q( `% \/ f/ \Boy Induced by Indirect Topical
) _* _) D3 r) z+ A( NExposure to Testosterone
+ k5 m6 @5 C, JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
8 E. P" z3 A+ p7 E) z$ Aand Kenneth R. Rettig, MD11 y0 ` Q& X# J0 x3 T
Clinical Pediatrics
# h2 |9 U8 p; P1 ^/ @- sVolume 46 Number 6
# m; k8 ]+ u/ \ M% q+ |July 2007 540-543- W5 ~. x1 R0 Z' D
© 2007 Sage Publications3 {( }2 a$ W1 q3 h; d$ {) l H
10.1177/0009922806296651
7 N/ n" F2 H5 u. khttp://clp.sagepub.com D* y5 R1 ?( `( w+ E4 {* F
hosted at
& ~3 T& X8 V6 }; I0 R% `$ Bhttp://online.sagepub.com. j! [# i; J% {! Z: y$ @$ a
Precocious puberty in boys, central or peripheral,
1 J8 T1 i) T7 V/ O$ Sis a significant concern for physicians. Central& v9 {! s. |5 C4 \, m
precocious puberty (CPP), which is mediated
8 \. x, [+ ~: E/ Q" ]7 K. ~& A+ rthrough the hypothalamic pituitary gonadal axis, has; S/ [8 t/ G% R6 [5 ~3 e
a higher incidence of organic central nervous system
7 V/ z2 ^ P! X5 N& Glesions in boys.1,2 Virilization in boys, as manifested
4 z5 N( j8 Q3 h+ Pby enlargement of the penis, development of pubic( k& j+ |4 a- N
hair, and facial acne without enlargement of testi-
0 U) V9 G, J* f/ A# xcles, suggests peripheral or pseudopuberty.1-3 We
% w( c: a, i8 D+ N5 dreport a 16-month-old boy who presented with the
) a5 m" u3 Z9 Tenlargement of the phallus and pubic hair develop-/ D: E# s5 ^( h5 ~) z2 j* ^1 Q6 Q
ment without testicular enlargement, which was due4 ]; ~5 I( W% o! s4 U
to the unintentional exposure to androgen gel used by
* H, Z; u! q: ]+ u# x' Pthe father. The family initially concealed this infor-% [3 F& m4 l& M$ e H' s
mation, resulting in an extensive work-up for this- @2 Z3 f: r3 P1 M1 u/ _0 O
child. Given the widespread and easy availability of) _+ i$ Q: G% u/ I8 Z4 E
testosterone gel and cream, we believe this is proba-2 b/ G z( x6 E/ p6 Q
bly more common than the rare case report in the
2 {6 c8 M5 t L; }+ }8 nliterature.4
) o3 I8 o P. k+ U! NPatient Report0 A# h$ G/ |! g
A 16-month-old white child was referred to the
# a& z) { t9 q% Fendocrine clinic by his pediatrician with the concern; M* J. L% n% c0 T8 h* F, |2 c
of early sexual development. His mother noticed( S. B" ~0 v' `( r/ i: p
light colored pubic hair development when he was$ U( ~) O1 o Z ]+ {
From the 1Division of Pediatric Endocrinology, 2University of
W2 Z3 D- ^2 {+ R5 M" a3 ESouth Alabama Medical Center, Mobile, Alabama.
3 a# I0 {5 b" B, `- U. m3 lAddress correspondence to: Samar K. Bhowmick, MD, FACE,/ }$ I3 s# _% P m8 P! E
Professor of Pediatrics, University of South Alabama, College of7 K$ ?/ g7 S, c2 s0 W% l2 E4 t4 a+ R
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% V x- C7 y b% T7 B0 ]$ e
e-mail: [email protected].
3 |( g, D' S( T$ N' X7 Iabout 6 to 7 months old, which progressively became
% F& C: m* U; I: Mdarker. She was also concerned about the enlarge-
" A6 h1 a' ^" K* U* Pment of his penis and frequent erections. The child
1 \1 f) f0 L- L3 o; a& M9 twas the product of a full-term normal delivery, with5 ~& c- W" T; D
a birth weight of 7 lb 14 oz, and birth length of3 ?. h- }7 m% @ B! Z7 h4 p
20 inches. He was breast-fed throughout the first year1 X/ [5 i$ `3 e. Z+ e5 f
of life and was still receiving breast milk along with% j- i, F- ^/ M, t
solid food. He had no hospitalizations or surgery,
0 i6 E& K$ j7 ]8 A( c( E3 Gand his psychosocial and psychomotor development
5 m6 w( d l q# _* ]was age appropriate.
+ C: Q- d: O) X5 ?, M5 @The family history was remarkable for the father,8 z( a4 q6 Q X* ~) o9 l3 F
who was diagnosed with hypothyroidism at age 16,
4 c# ? m* V0 i' Qwhich was treated with thyroxine. The father’s
% J: p2 A$ g I) O; i& M+ Cheight was 6 feet, and he went through a somewhat
! @+ l9 l0 N7 X+ Zearly puberty and had stopped growing by age 14.
- {8 M% L; o0 C) I; f& uThe father denied taking any other medication. The
4 @4 @/ l1 _; c; Z* i1 Qchild’s mother was in good health. Her menarche
# t1 A: K& t; h/ t% u9 swas at 11 years of age, and her height was at 5 feet. A6 Y1 W7 h. v `) O+ X2 _! ~% P: \
5 inches. There was no other family history of pre-
! S; f: G8 X, H w. D+ G9 |( icocious sexual development in the first-degree rela-
3 U! u2 e9 O# C( ?tives. There were no siblings.
* [. c. v/ C7 h: \8 X3 oPhysical Examination: S3 C' j8 t, R' r* H8 o: B7 N: N& ]
The physical examination revealed a very active,
4 W) l/ W4 B _; c% b4 W2 @1 zplayful, and healthy boy. The vital signs documented
1 d1 I0 ]- w1 }6 k q& L. Ba blood pressure of 85/50 mm Hg, his length was6 o+ m6 D# @) M* h1 i* f
90 cm (>97th percentile), and his weight was 14.4 kg% T1 B, `% K* P
(also >97th percentile). The observed yearly growth
! C! s2 j9 ]! b4 i+ [velocity was 30 cm (12 inches). The examination of
/ m& J0 S u2 r6 t" Cthe neck revealed no thyroid enlargement." I. j+ b! v0 P# B
The genitourinary examination was remarkable for) u. T+ E- _8 Z8 b; S
enlargement of the penis, with a stretched length of
8 ^" x3 v! J( ?7 S! g7 \, F8 cm and a width of 2 cm. The glans penis was very well
. {) [/ R, l5 K5 p2 a; Edeveloped. The pubic hair was Tanner II, mostly around
5 C2 I1 X- s* W$ H Q540+ U/ k, {4 t, P: x! w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# {; i4 H% p& k8 w' C" \ t* Q, `) I
the base of the phallus and was dark and curled. The
, A7 p3 q) O: T3 Ztesticular volume was prepubertal at 2 mL each." Y, U5 O0 z6 c- O3 ?
The skin was moist and smooth and somewhat
) c) N) S: P0 G0 _1 Koily. No axillary hair was noted. There were no
2 h/ H8 Y5 b/ q5 v/ habnormal skin pigmentations or café-au-lait spots.0 R( T5 V; I, x' G
Neurologic evaluation showed deep tendon reflex 2+
3 V8 @; P% F( d3 X* Rbilateral and symmetrical. There was no suggestion" |9 F- w7 s! y" P
of papilledema.0 X9 D' i9 R8 V [& @* P( `6 k
Laboratory Evaluation
# [) u( o P5 U6 w# _The bone age was consistent with 28 months by
9 a: x; |! q2 a1 L5 | ^; H0 gusing the standard of Greulich and Pyle at a chrono-2 g+ p1 ] a5 P$ n7 i$ x
logic age of 16 months (advanced).5 Chromosomal
# N1 @: U6 D0 z, E/ m2 A8 Ukaryotype was 46XY. The thyroid function test
' Q+ Z3 e* }$ h) ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 ~" q) z; W: ~lating hormone level was 1.3 µIU/mL (both normal).7 U$ O' R1 U) e2 \; C
The concentrations of serum electrolytes, blood
- R! n" v. j$ P: R. nurea nitrogen, creatinine, and calcium all were
" x# N: v0 T9 kwithin normal range for his age. The concentration( {4 }& J9 E% k0 x4 |
of serum 17-hydroxyprogesterone was 16 ng/dL0 p% G% K6 i |6 \: o
(normal, 3 to 90 ng/dL), androstenedione was 202 m# V. A# C, Z4 g! Y) m
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-+ M+ }' y; A3 s8 H9 F
terone was 38 ng/dL (normal, 50 to 760 ng/dL),' `" y" F8 i/ P' P+ S* f, z1 A3 g$ w
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
% S \ w: d; v* x8 r49ng/dL), 11-desoxycortisol (specific compound S), i; W7 F% l7 u; g u
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 P* ?( S* G' T$ L2 W% ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
! q' d/ d) K4 m/ E' mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),* H2 [, Q4 }* v# n# |4 D3 L
and β-human chorionic gonadotropin was less than' ^$ N: e7 W4 p: E- A. l
5 mIU/mL (normal <5 mIU/mL). Serum follicular
C3 {: [7 k8 l1 W' Bstimulating hormone and leuteinizing hormone+ {' s6 }/ @5 M( O* I" l r Z6 c
concentrations were less than 0.05 mIU/mL
! O% Q" y* y2 e2 C! H& |9 H; @9 M(prepubertal).
) i3 H$ d4 e4 k# S. {1 I9 QThe parents were notified about the laboratory) \- v0 l3 w: W) l
results and were informed that all of the tests were% V/ H& x, Q8 h) O/ q# c7 p/ K
normal except the testosterone level was high. The$ C. Y/ u. j# y5 i
follow-up visit was arranged within a few weeks to; l3 x: \3 @% z1 v* H" ^
obtain testicular and abdominal sonograms; how-
8 ^& \4 H" f7 o- Q5 i, ^/ uever, the family did not return for 4 months.3 \( J( D5 _$ l6 y" ]% ?
Physical examination at this time revealed that the
% R2 C! G- P7 y6 h5 a! ~$ pchild had grown 2.5 cm in 4 months and had gained3 T O9 c" Z) y& \4 ~: x) z
2 kg of weight. Physical examination remained4 o6 ? x# Q' ?0 Z" x
unchanged. Surprisingly, the pubic hair almost com-0 f' \$ H3 |" g" n$ i7 K5 @4 V
pletely disappeared except for a few vellous hairs at0 x( x3 h* z5 T8 r4 ]
the base of the phallus. Testicular volume was still 2
5 n# d' w7 k+ f% u" I+ R6 Q! ~mL, and the size of the penis remained unchanged.8 w K. ~( L5 Z7 Y+ ?+ D# f. o+ o* a
The mother also said that the boy was no longer hav-+ F, Q+ Z) i7 C! q3 e/ s/ a
ing frequent erections.
; n2 b. Z+ b( C, Y5 S% n( g/ jBoth parents were again questioned about use of7 h/ Z! v; p5 `1 ^
any ointment/creams that they may have applied to8 n' f# i( Y. M3 i" ]! d
the child’s skin. This time the father admitted the y9 |3 H* L, \4 F1 \, U, d' a
Topical Testosterone Exposure / Bhowmick et al 541
W/ m3 C/ I- r* |2 P! }use of testosterone gel twice daily that he was apply-
. Z1 f& n% P( @' D; ring over his own shoulders, chest, and back area for" o. W6 X% u$ |& \
a year. The father also revealed he was embarrassed
' A% X( p. D/ m/ X! @, y, fto disclose that he was using a testosterone gel pre-
6 L2 R! Z6 U" |scribed by his family physician for decreased libido" T1 _4 m; L1 p" ]. Q8 k
secondary to depression.: e% x2 l+ c: n! _9 T
The child slept in the same bed with parents.
r/ f4 Y. F' N$ s/ I# a& q/ I5 CThe father would hug the baby and hold him on his
* g1 s) x+ K) @2 ^chest for a considerable period of time, causing sig-+ c7 \/ R+ b; |5 w
nificant bare skin contact between baby and father.
: s* W5 T+ o# l6 Q3 r0 a+ UThe father also admitted that after the phone call,1 c; {! t3 ]& P4 Y
when he learned the testosterone level in the baby
' Z% A' F& g1 P' Ewas high, he then read the product information2 M; D4 y( @$ s( W. m8 L- f8 I
packet and concluded that it was most likely the rea-$ l U" S$ ]8 v, `
son for the child’s virilization. At that time, they2 P& V1 m, P* z
decided to put the baby in a separate bed, and the
( K: Y" L9 C* D. Q8 ofather was not hugging him with bare skin and had
* x3 D) O& [+ K/ X2 `been using protective clothing. A repeat testosterone- V0 h7 s g' p$ @* M
test was ordered, but the family did not go to the0 ~4 `! D: ?9 `( S0 P) W! Z7 ~
laboratory to obtain the test.2 v& M1 G2 v. i# M9 V) }
Discussion% ], G, Z" O/ C' u
Precocious puberty in boys is defined as secondary' y% M- e, ?- V( r- W
sexual development before 9 years of age.1,4
; g; k. j' N" z! ~. _) j. _Precocious puberty is termed as central (true) when; { [# q( g) l5 s
it is caused by the premature activation of hypo-
( E4 u9 m( k0 a, Vthalamic pituitary gonadal axis. CPP is more com-
" ?% Q& u, n$ P4 ^$ Z! `9 U" bmon in girls than in boys.1,3 Most boys with CPP
$ b: O. _3 _ L& Z3 @( a4 h( E7 Bmay have a central nervous system lesion that is; o/ b* J, x" y( z
responsible for the early activation of the hypothal-$ T3 @: k& r+ }" Y
amic pituitary gonadal axis.1-3 Thus, greater empha-
" b$ u* ?5 h5 M8 S Osis has been given to neuroradiologic imaging in& v2 \+ r2 W0 [; }2 w; p/ L- O
boys with precocious puberty. In addition to viril-: V( [- l( l+ O5 B1 V: V$ m
ization, the clinical hallmark of CPP is the symmet-
( f8 C4 b$ m0 b$ e) Brical testicular growth secondary to stimulation by
; T* j4 k4 X( Q$ z( U8 cgonadotropins.1,3
5 v- ^& \4 o' v# tGonadotropin-independent peripheral preco-; e _) {. J/ ]6 E. A
cious puberty in boys also results from inappropriate9 j8 N( }& h3 ^2 [/ m! R
androgenic stimulation from either endogenous or
- I: e8 F& B( Q2 ]exogenous sources, nonpituitary gonadotropin stim-3 Z. R1 Q: E2 @: A4 x, c; ]
ulation, and rare activating mutations.3 Virilizing7 V% B9 [4 e0 T. I" u
congenital adrenal hyperplasia producing excessive
3 _4 i8 Y0 E8 N; n2 `' D+ Zadrenal androgens is a common cause of precocious+ @5 ~3 G1 e2 M w. p- K
puberty in boys.3,4
- P( f) t2 |8 w; g9 {& RThe most common form of congenital adrenal) c3 Y7 x- M, ^- n: j k( @
hyperplasia is the 21-hydroxylase enzyme deficiency.
9 A2 u+ _8 r* U" V2 U* f; b/ e$ HThe 11-β hydroxylase deficiency may also result in( U" S! N) U9 p
excessive adrenal androgen production, and rarely,
6 H- A! C+ f6 g. u" q# ban adrenal tumor may also cause adrenal androgen
& U( g1 U9 z" b. _excess.1,3 J+ Q- \+ ]$ P6 F! |* J5 @6 D
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 p5 b& G6 o; i. l! H
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 @' A3 o; {! m `% ~( IA unique entity of male-limited gonadotropin-
, B# I; L7 d* [6 }, ?/ M) yindependent precocious puberty, which is also known
( V1 J) `5 `% e: Ras testotoxicosis, may cause precocious puberty at a/ A f* z: g4 i( |
very young age. The physical findings in these boys
* r3 K' ]8 g/ g; ^- twith this disorder are full pubertal development,7 r2 n+ ] T, q( a7 r$ w+ a$ ?
including bilateral testicular growth, similar to boys% @5 V' N. x$ n' W
with CPP. The gonadotropin levels in this disorder
4 _! x# |; G7 y/ Xare suppressed to prepubertal levels and do not show
j- d6 G, G1 z, m& y5 d: d8 ^pubertal response of gonadotropin after gonadotropin-; C* b( A. ~4 R8 d1 m$ T0 m
releasing hormone stimulation. This is a sex-linked% A/ y L a# c4 a8 [' `4 E! @
autosomal dominant disorder that affects only* _) Z! v) A5 O2 p, F6 z
males; therefore, other male members of the family1 G( B, W: y2 {5 s
may have similar precocious puberty.3
3 D5 N9 C0 D7 YIn our patient, physical examination was incon-
/ c' `$ G% ] \" D8 q: G' osistent with true precocious puberty since his testi-1 o6 ^- A8 O3 X0 [" T6 A
cles were prepubertal in size. However, testotoxicosis
5 q) ?6 G2 k) E- i! Rwas in the differential diagnosis because his father' c) x- e4 t8 r
started puberty somewhat early, and occasionally, q+ V, s2 \$ e9 V8 j' K
testicular enlargement is not that evident in the" y- H% P% E+ y: ], C4 D$ z
beginning of this process.1 In the absence of a neg-
0 m/ g6 ]! x, `" l, ~- z7 i$ @ative initial history of androgen exposure, our
5 c9 C( c+ W) Y$ e2 jbiggest concern was virilizing adrenal hyperplasia,
: k/ Y7 W" C1 Y5 ?7 X6 ]. ?+ Reither 21-hydroxylase deficiency or 11-β hydroxylase
1 `9 R3 n2 J8 O$ Y' s) ]4 Z" ^deficiency. Those diagnoses were excluded by find-
& H5 d( P) ]. d; c( Ring the normal level of adrenal steroids./ ^, H* J$ D% ?; i5 B7 {$ @7 O
The diagnosis of exogenous androgens was strongly
8 D& P! }& J5 v/ Qsuspected in a follow-up visit after 4 months because
) h& F x, `' y$ E3 M3 fthe physical examination revealed the complete disap-" t! n. r% ?/ V! x
pearance of pubic hair, normal growth velocity, and& S" L) D6 A/ H* K8 `* M2 V
decreased erections. The father admitted using a testos-
1 j2 @' H5 j: x+ o) ~5 q% n( A) Nterone gel, which he concealed at first visit. He was3 v q$ W. f, L$ D5 O9 m' e
using it rather frequently, twice a day. The Physicians’7 n5 `6 S) n1 i+ |; G/ w
Desk Reference, or package insert of this product, gel or
& n+ ~% h1 a5 L( l0 y' P9 q2 o3 _cream, cautions about dermal testosterone transfer to
* C( T6 F) z( C0 f7 e/ Ounprotected females through direct skin exposure.
4 `* y( S! I2 g0 D- u SSerum testosterone level was found to be 2 times the; Y. D% L) s6 x- W
baseline value in those females who were exposed to
" S) m* Z7 Q1 ?" s) `0 T2 v+ keven 15 minutes of direct skin contact with their male
* U# u) h( m- u$ u0 opartners.6 However, when a shirt covered the applica-6 X, i/ h4 N/ ^3 @( h4 }3 @( V
tion site, this testosterone transfer was prevented.
. a' q* E( W1 N, FOur patient’s testosterone level was 60 ng/mL,
) h1 C: _" m% f, P/ V" b _" mwhich was clearly high. Some studies suggest that
# D" a% ]5 N* D9 E2 w5 y6 edermal conversion of testosterone to dihydrotestos-2 f, S" X. b) b7 K8 F
terone, which is a more potent metabolite, is more; Y ^2 Q4 p7 g( b& ]
active in young children exposed to testosterone X) I) i' H L5 h! @
exogenously7; however, we did not measure a dihy-
0 l, {1 Q0 V& w7 A, Z N1 s* jdrotestosterone level in our patient. In addition to
. g4 P1 _, S) }6 i8 A* y+ wvirilization, exposure to exogenous testosterone in
6 X+ [+ P, P6 @. Q. qchildren results in an increase in growth velocity and: o' X. g% q8 A2 m- b+ c
advanced bone age, as seen in our patient.0 F# s# Q: U, A" U
The long-term effect of androgen exposure during" v" V9 G6 \7 ?* M/ \
early childhood on pubertal development and final; i6 h. K! t i, R7 z
adult height are not fully known and always remain2 V0 `: [ s; E4 V% n& F
a concern. Children treated with short-term testos-
. v- y7 j( }' a& v8 F% w" Aterone injection or topical androgen may exhibit some( M: k' Y$ Y0 Z: m9 c8 p, V' a
acceleration of the skeletal maturation; however, after3 l' w9 p# Z$ }$ c
cessation of treatment, the rate of bone maturation% S9 G. P- `* R/ x
decelerates and gradually returns to normal.8,9. M: ?! A% g$ P' B
There are conflicting reports and controversy
. ?9 L3 t ^' _3 K' U6 j6 Y! Aover the effect of early androgen exposure on adult9 L# `8 X8 V r, ^3 S: K5 `, u
penile length.10,11 Some reports suggest subnormal+ T0 {) `) I: {, b9 g2 m
adult penile length, apparently because of downreg-
`( n- B, ~/ @' z- v/ rulation of androgen receptor number.10,12 However,
+ P' ^; n/ a& K$ R* `Sutherland et al13 did not find a correlation between
" J. r' p, n; u# B% Kchildhood testosterone exposure and reduced adult' H$ d b/ [& v: d8 S
penile length in clinical studies.
) x# O* J+ F: E4 v- D5 xNonetheless, we do not believe our patient is
- U) M" U- h& r1 ~: `going to experience any of the untoward effects from
' m f! U" w4 B! W, c, @& X2 R0 u0 Htestosterone exposure as mentioned earlier because
: i' R. P; }! h. A6 `5 y' M7 D. ]4 kthe exposure was not for a prolonged period of time.1 ?2 y& a5 i- y& G* z
Although the bone age was advanced at the time of8 {4 Q$ S4 n) V( M2 }# e
diagnosis, the child had a normal growth velocity at
. {! e" `2 s3 `4 Vthe follow-up visit. It is hoped that his final adult& `0 y8 r) ` s7 e3 [0 z
height will not be affected.7 L1 Y* }, L$ C; b- E) g w9 Q
Although rarely reported, the widespread avail-
! Y$ [8 O( v6 \& q+ \! T+ Oability of androgen products in our society may
+ P- k& u" F, y- E- F2 Nindeed cause more virilization in male or female
2 J; S3 @: o+ s2 F. Jchildren than one would realize. Exposure to andro-
# S1 K# u; ~, n$ R' y% \gen products must be considered and specific ques-7 T+ r( D+ H/ c$ Q
tioning about the use of a testosterone product or; L: S g$ F3 ^- t! I
gel should be asked of the family members during8 c4 U/ R! r8 q; J2 d8 _: X
the evaluation of any children who present with vir-
% ~- B: j; h% r5 d' E2 Ailization or peripheral precocious puberty. The diag-9 d4 Y. r0 G" _; F2 x2 t- C% y
nosis can be established by just a few tests and by$ e* j f0 y$ c3 Q7 r1 X! J
appropriate history. The inability to obtain such a. J$ D/ y' ?2 w& p7 e1 M; }/ f
history, or failure to ask the specific questions, may
( d) E/ N- \0 Y" cresult in extensive, unnecessary, and expensive
( l/ c5 Z) v! C1 k( U6 t" Y. ]% T. Pinvestigation. The primary care physician should be
0 D1 z8 c( o# I- |( Z' F& k. baware of this fact, because most of these children
! h+ F" B8 L4 N8 c/ e* p! s9 V; ~may initially present in their practice. The Physicians’
% X; y. S! _" q. lDesk Reference and package insert should also put a0 e8 l* `# E: z# n$ W; O
warning about the virilizing effect on a male or
& U( q3 T( u( q, v9 Sfemale child who might come in contact with some-2 z+ R; t. c; K$ R* O3 V) N! c# m( t
one using any of these products.4 E( e/ W, _+ b5 a5 w
References7 x5 O* P4 d, s% Y4 e. ?: U- C
1. Styne DM. The testes: disorder of sexual differentiation
- h5 S' \' z( P8 M0 Kand puberty in the male. In: Sperling MA, ed. Pediatric
' x" \* {* M% I; @9 fEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 J4 P/ @' w; ^
2002: 565-628.3 r* v/ i1 J; M8 [, U6 q
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
4 w5 r1 T' R0 J ~7 ipuberty in children with tumours of the suprasellar pineal |
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