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Sexual Precocity in a 16-Month-Old
8 A6 T. A% p) ]0 k. Q- z* yBoy Induced by Indirect Topical* J9 S6 v1 r/ N; [% p% o0 t
Exposure to Testosterone
5 Q7 W2 b0 H4 S, Z! u) gSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2+ ^1 x! X, ?# F2 h: ?1 h
and Kenneth R. Rettig, MD1 T, o5 Z# H) n! x, E9 y/ R
Clinical Pediatrics* d1 D. D# e" W5 l7 X* ]0 s
Volume 46 Number 6
, X: J0 \' ~4 V6 r2 R1 FJuly 2007 540-543
" ?$ Y* L$ ]9 Y' t& u9 c© 2007 Sage Publications
* G& W' w U0 j, C2 z$ T& \10.1177/0009922806296651
# {# }9 ~: q* \. ^3 j2 Lhttp://clp.sagepub.com
$ n/ p6 y8 _3 ^7 nhosted at! D7 ~/ E' S9 b
http://online.sagepub.com6 ?* y% \0 @% o* N4 S
Precocious puberty in boys, central or peripheral,
. O# {* R0 o4 F- p% i* u) S$ Bis a significant concern for physicians. Central) E2 Y& d Z) B5 ?8 d
precocious puberty (CPP), which is mediated
& b; s. _3 y) F. Fthrough the hypothalamic pituitary gonadal axis, has
2 l# m( D6 T& W* R. T7 V' }4 Ha higher incidence of organic central nervous system4 ~: G# |0 @ u P5 ?# Y5 H8 ? N
lesions in boys.1,2 Virilization in boys, as manifested
4 o/ _" E4 R M# `by enlargement of the penis, development of pubic
2 Y( P0 {* H2 s3 ?hair, and facial acne without enlargement of testi-9 U4 L/ ~4 N# W& j, _$ S
cles, suggests peripheral or pseudopuberty.1-3 We& X z; r4 p* y3 N+ i1 ]
report a 16-month-old boy who presented with the+ A+ w! c+ F% b& \. e
enlargement of the phallus and pubic hair develop-5 J2 t8 @$ I9 Z
ment without testicular enlargement, which was due
$ W4 Q% }% ^ H. Y0 b$ v6 Vto the unintentional exposure to androgen gel used by1 x. Z3 \5 ^, C, z. U$ ~! B4 c
the father. The family initially concealed this infor-
4 D( c( f, ^& J- b8 f3 S7 Lmation, resulting in an extensive work-up for this+ M" L5 a- f/ |6 Q
child. Given the widespread and easy availability of. |9 p7 C- w( I, z I4 b5 o7 F. c2 c
testosterone gel and cream, we believe this is proba-. p K; @, Z: }. T9 p2 c
bly more common than the rare case report in the
% l# Y8 Z0 M) ?) }: k9 z& k1 t* s" Zliterature.4; B$ N' Q0 @9 _: \% @
Patient Report2 ~& S# A4 o" Y$ P- R
A 16-month-old white child was referred to the5 h, a7 Q' r N. j, u
endocrine clinic by his pediatrician with the concern1 ?# d8 M% A( B* m1 [$ B6 w* S' c
of early sexual development. His mother noticed2 c" K; Z. C6 K' O5 l
light colored pubic hair development when he was [. d6 u7 ?6 \7 x* c
From the 1Division of Pediatric Endocrinology, 2University of: N* V* r u0 n
South Alabama Medical Center, Mobile, Alabama.
3 w1 }3 W9 H' H8 J- Y& @Address correspondence to: Samar K. Bhowmick, MD, FACE,
1 Z% E4 ]* v8 Z1 a6 @Professor of Pediatrics, University of South Alabama, College of2 Z1 D& n/ Z/ O$ P3 ~' f
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 g( u# \7 @" c7 k$ s0 i' ~
e-mail: [email protected].
+ u% \$ x; u3 ^8 o( nabout 6 to 7 months old, which progressively became* w5 M( h6 S6 d# o/ B+ B* R
darker. She was also concerned about the enlarge-# L% R8 _0 J9 I& E8 H! Z" I9 l
ment of his penis and frequent erections. The child& D) X# p' S$ X7 K I$ J8 q2 l
was the product of a full-term normal delivery, with
0 P% N' P6 X# r2 D7 w, W2 ^a birth weight of 7 lb 14 oz, and birth length of+ S6 K- ^" Y' L" ]7 k# ?6 `. z0 X
20 inches. He was breast-fed throughout the first year6 M! L* r% q9 s+ T2 i- K
of life and was still receiving breast milk along with8 j/ ^2 C3 N& g* _( F9 x
solid food. He had no hospitalizations or surgery,
% a3 a5 T& m$ q- N; W$ Q# Sand his psychosocial and psychomotor development
- i# K" x0 S9 w/ R& u8 F9 mwas age appropriate.
8 o, {, r0 c" v3 n c5 {The family history was remarkable for the father,
9 q% ?' \' e, P6 B; E0 owho was diagnosed with hypothyroidism at age 16,
. m+ L! l4 Z" [. A' lwhich was treated with thyroxine. The father’s
. `) o) p9 G+ v! n5 iheight was 6 feet, and he went through a somewhat, ^4 q: ]( m4 P/ E
early puberty and had stopped growing by age 14.6 ]6 Y6 L1 M. K, p2 y( ^
The father denied taking any other medication. The
8 N r5 ~. r9 V7 qchild’s mother was in good health. Her menarche
7 @/ ^ M; G8 Pwas at 11 years of age, and her height was at 5 feet* b; q/ H$ i! Q: q A+ t
5 inches. There was no other family history of pre-+ @8 r. _7 c% X8 z+ q: A" `
cocious sexual development in the first-degree rela-
8 q. [$ f, W* y- I$ Q4 a: z$ r9 Ltives. There were no siblings.( j1 F! W) A4 \# Z- R
Physical Examination
- z$ E6 l% ?9 e& D' w0 ^The physical examination revealed a very active,, [; t$ G ?4 T
playful, and healthy boy. The vital signs documented E( l6 p/ R1 W! T8 P) I1 `: |4 q) `
a blood pressure of 85/50 mm Hg, his length was
: V, f1 j! Y G" X4 I90 cm (>97th percentile), and his weight was 14.4 kg4 I* m% y. M; |, }9 R
(also >97th percentile). The observed yearly growth" z+ D* ~$ u ^) W# O; a7 c
velocity was 30 cm (12 inches). The examination of
: D; B* }9 }. A# rthe neck revealed no thyroid enlargement.* h# N( z% ]4 b6 n2 t
The genitourinary examination was remarkable for3 l9 O1 Z, q `, r, t
enlargement of the penis, with a stretched length of
5 U ^; g8 `5 u5 K" n7 C8 cm and a width of 2 cm. The glans penis was very well
: N: x/ f& J- W6 U9 }1 Q2 H4 Z0 Xdeveloped. The pubic hair was Tanner II, mostly around
) i0 i- ^$ V1 F7 u- R- T5409 {* j1 g' N0 u; D+ @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 R9 Q# t* d- _0 I/ }* @7 Q; P bthe base of the phallus and was dark and curled. The
% {. q; L5 i1 D0 H# Ztesticular volume was prepubertal at 2 mL each.
& |+ j5 L2 o5 U1 J' XThe skin was moist and smooth and somewhat9 X: ^9 F/ X7 D5 y x# y8 C8 J
oily. No axillary hair was noted. There were no- Q* X! K' i5 `6 f0 c8 t
abnormal skin pigmentations or café-au-lait spots.9 h$ a0 {, Q* u# N& l6 E3 r
Neurologic evaluation showed deep tendon reflex 2+- N) X8 T f% M5 k5 |
bilateral and symmetrical. There was no suggestion5 K- l- n L. s6 J9 m* v
of papilledema.6 u, c: V8 H0 ]# t
Laboratory Evaluation; R: N' ]* g( _ C
The bone age was consistent with 28 months by
0 T+ i0 h2 N" Xusing the standard of Greulich and Pyle at a chrono-
2 t( ?' O0 H2 w2 K/ Nlogic age of 16 months (advanced).5 Chromosomal
( ^ [& D% F( s4 m- Ikaryotype was 46XY. The thyroid function test
0 p& a" L$ J9 p L1 e, qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-4 }, A0 E1 i! d& k# F3 L! k# ?7 D8 l d: @
lating hormone level was 1.3 µIU/mL (both normal).# E3 J, ^" E# k' \3 J9 X
The concentrations of serum electrolytes, blood
% [, p" J; R" {) E% a! l9 ~urea nitrogen, creatinine, and calcium all were' ~' X: y. {4 N7 x u9 V% W
within normal range for his age. The concentration
; t+ H0 C) f9 R$ M/ d6 y/ E& ^of serum 17-hydroxyprogesterone was 16 ng/dL0 t4 \3 G$ b- Z* s% x
(normal, 3 to 90 ng/dL), androstenedione was 20! T! ]) H& I( P. H) I" U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& B5 A3 F3 g( |% Xterone was 38 ng/dL (normal, 50 to 760 ng/dL),+ I( _* ~: c2 i+ i+ s7 d
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 l7 L0 |) F, F8 j49ng/dL), 11-desoxycortisol (specific compound S)
+ G7 `# C, A$ Rwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 T7 K2 N1 q! Z3 z$ s! y1 o8 {
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total2 O# M6 O0 H+ G' H+ ~) U! m. g
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
3 `2 }7 L. Q6 R3 F7 B; ]) e8 kand β-human chorionic gonadotropin was less than2 \. \( ~1 @8 s' ^
5 mIU/mL (normal <5 mIU/mL). Serum follicular9 l1 \3 |6 W& n) }( j* K0 Y( K
stimulating hormone and leuteinizing hormone- R+ y) d- {: @! D- J
concentrations were less than 0.05 mIU/mL
4 x) H/ U& v9 U |* E(prepubertal).
/ k- l; C7 _% p3 I _& wThe parents were notified about the laboratory
7 G3 p/ S, j I5 l8 H; uresults and were informed that all of the tests were
* Y7 P+ I: k; E+ ~) _9 Fnormal except the testosterone level was high. The
4 G% p: X' J7 S/ q, n& n$ Y4 ifollow-up visit was arranged within a few weeks to. d5 {& r R5 Z
obtain testicular and abdominal sonograms; how-. c& `, {* i V
ever, the family did not return for 4 months.
9 |+ a1 P: b9 n' ~/ W" M) VPhysical examination at this time revealed that the* s- q8 C8 W. g% w
child had grown 2.5 cm in 4 months and had gained' z% G+ E) T: D9 \. O
2 kg of weight. Physical examination remained
* a# |# h% W; ?8 Q1 lunchanged. Surprisingly, the pubic hair almost com-
" }6 r+ Q6 R- c4 ~' j, l ?- qpletely disappeared except for a few vellous hairs at
+ H: k3 [6 P0 _- h: I1 [the base of the phallus. Testicular volume was still 2
. }* D) i6 ~1 V9 v1 ymL, and the size of the penis remained unchanged.
* S$ {) N% A7 R* X$ R5 GThe mother also said that the boy was no longer hav-& G( \' _0 e# z1 k, I9 V, T6 \
ing frequent erections.
" l# w1 e& O7 [Both parents were again questioned about use of. g) V$ }$ ^/ H, T1 z, |# U/ y" t
any ointment/creams that they may have applied to
# d, x. b( R' t; S$ w$ h! Bthe child’s skin. This time the father admitted the7 u1 l8 y' Z2 Y# {/ `; C
Topical Testosterone Exposure / Bhowmick et al 541. {5 E9 H+ }+ l- ^
use of testosterone gel twice daily that he was apply-4 ]% Q: s) L, r) T6 P$ R5 Z: ^
ing over his own shoulders, chest, and back area for
" S) q( {- m" g# l! {a year. The father also revealed he was embarrassed
! {0 X7 x; \0 ^& Qto disclose that he was using a testosterone gel pre-
" w0 O# Q& f& tscribed by his family physician for decreased libido
) T/ f* j+ ?/ b; `+ _, [secondary to depression.: M0 J) |3 r* n4 s# O# a. f
The child slept in the same bed with parents.( f' E$ h5 l @& C
The father would hug the baby and hold him on his
3 ?( ^+ }6 `4 w9 n) m- _- S5 [( dchest for a considerable period of time, causing sig-
% @4 _6 b, h1 Jnificant bare skin contact between baby and father. \: g L4 g0 _: @; q. D
The father also admitted that after the phone call,
2 P! x8 q, T& q8 B2 j; V; `- ^when he learned the testosterone level in the baby
3 c y6 x4 r* |5 ]7 k' Zwas high, he then read the product information
: I- w; [! D; T6 a8 \5 u2 v/ ~# q3 fpacket and concluded that it was most likely the rea-4 T! }: b8 W* k) b y N
son for the child’s virilization. At that time, they
4 {: o! Q0 }9 Pdecided to put the baby in a separate bed, and the
4 m' u6 s: o# P7 kfather was not hugging him with bare skin and had& P' s4 w3 D$ a9 b* q. c
been using protective clothing. A repeat testosterone1 [9 N/ i# g( X% ?3 B9 N
test was ordered, but the family did not go to the
# |" o. v/ w1 v% x+ o! q1 [6 Ilaboratory to obtain the test.
# e; l( t; P, X- h9 W& a- dDiscussion
& C# u( V8 U& F5 lPrecocious puberty in boys is defined as secondary
; \ D+ V" _. Hsexual development before 9 years of age.1,4( s% t/ T$ a. R2 p
Precocious puberty is termed as central (true) when- |5 g( V) J- g/ D% }
it is caused by the premature activation of hypo-' ?3 w/ E# |! e
thalamic pituitary gonadal axis. CPP is more com-
( d8 s5 y& a9 }: b: jmon in girls than in boys.1,3 Most boys with CPP4 ]" F& Z6 F* h6 K9 m! C( E7 v
may have a central nervous system lesion that is
" I& W: }' i4 v' h$ t- D5 D7 Fresponsible for the early activation of the hypothal-) J' x& o0 a9 i* o
amic pituitary gonadal axis.1-3 Thus, greater empha-
1 A: I1 Y/ @ _sis has been given to neuroradiologic imaging in+ @$ k' [: @0 f
boys with precocious puberty. In addition to viril-
8 S' k9 m( J! t) ^( bization, the clinical hallmark of CPP is the symmet-$ N; a. q( X: G
rical testicular growth secondary to stimulation by7 X5 ^! H- x) o& b5 C
gonadotropins.1,3" B& ?3 Q' `4 U$ H% s9 ~/ D- K. C: z
Gonadotropin-independent peripheral preco-1 e5 m X2 U& ^4 L+ j& s4 o; s' Y
cious puberty in boys also results from inappropriate9 Z) J& ]; x/ Y6 y
androgenic stimulation from either endogenous or. w2 |& X' w3 g) \
exogenous sources, nonpituitary gonadotropin stim-& `- u9 I$ n* s$ t( k
ulation, and rare activating mutations.3 Virilizing
6 I5 h* r4 X& s5 L- d& C( {, N; acongenital adrenal hyperplasia producing excessive
7 l% W. u0 _: w1 ?9 ]adrenal androgens is a common cause of precocious0 C. v h, C4 s% g6 E
puberty in boys.3,4
) C! t8 g" o9 `* R JThe most common form of congenital adrenal+ l+ {, r7 C- G
hyperplasia is the 21-hydroxylase enzyme deficiency.
" T, m) n8 X5 q) w P( j' yThe 11-β hydroxylase deficiency may also result in
; A& C7 O" H N% u. Sexcessive adrenal androgen production, and rarely,8 E' r: ^+ k* E1 ?6 d. S+ F6 D
an adrenal tumor may also cause adrenal androgen8 v6 Z9 F) @. f. D7 D" T# _- A
excess.1,3& F. x9 @; S7 j# N3 x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, L* M/ Y: a% U @: N: A" G542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& r0 a4 L6 R( y7 Q0 N8 M/ lA unique entity of male-limited gonadotropin-
- N0 P" J: O Kindependent precocious puberty, which is also known
- ^$ Y! \( f1 Z c4 H. A+ O* aas testotoxicosis, may cause precocious puberty at a6 Z3 s6 l: @7 X1 \; q
very young age. The physical findings in these boys
( l7 @' _- ]9 c `# ?3 `with this disorder are full pubertal development,
! Z9 L2 n- ^3 N. hincluding bilateral testicular growth, similar to boys
9 k9 @! w" z; K8 j6 l: G rwith CPP. The gonadotropin levels in this disorder
9 \' j T ]. h6 t2 e" C; B# Dare suppressed to prepubertal levels and do not show
& N: I. g2 i: f& _& ]6 f$ S2 [pubertal response of gonadotropin after gonadotropin-; A) T3 k! l7 e3 p0 ]8 [, x, j2 A
releasing hormone stimulation. This is a sex-linked
3 I( K L+ \* j2 C7 R) Aautosomal dominant disorder that affects only! C" \# a, L f3 _9 }; I: m
males; therefore, other male members of the family
. I( P7 d9 m' r# Cmay have similar precocious puberty.3
- V- e1 N6 o% X5 }% h: dIn our patient, physical examination was incon-, G$ P8 F9 G2 d# V5 t/ Q* F, y
sistent with true precocious puberty since his testi-
/ z6 j4 p4 B" a) f3 Z Ecles were prepubertal in size. However, testotoxicosis
3 G6 G+ q3 G' G6 N% p5 ^4 rwas in the differential diagnosis because his father9 E+ J) k' ], Z2 v) a9 `* r3 v5 A
started puberty somewhat early, and occasionally,
! T3 z2 K, c$ S2 c4 b3 P" Dtesticular enlargement is not that evident in the
+ M* B9 ^5 |3 b4 Ybeginning of this process.1 In the absence of a neg-4 Z' C* \( C3 s2 @! L- r
ative initial history of androgen exposure, our1 |& m& R p5 P) t3 x
biggest concern was virilizing adrenal hyperplasia,
3 V5 ^' ]1 m, C6 f4 Feither 21-hydroxylase deficiency or 11-β hydroxylase
, {0 |1 \2 U7 Z: N+ Mdeficiency. Those diagnoses were excluded by find-
p0 t! w% Z% o# \ing the normal level of adrenal steroids." U @) D9 ]% [
The diagnosis of exogenous androgens was strongly+ b' i( L5 ~+ ~ F( G7 a
suspected in a follow-up visit after 4 months because4 w" E4 u' }6 |1 |" d
the physical examination revealed the complete disap-
) n6 Q- V( C. F1 hpearance of pubic hair, normal growth velocity, and
7 s$ I7 S" X1 _1 |decreased erections. The father admitted using a testos-
# k. X) l4 h6 F1 }$ [terone gel, which he concealed at first visit. He was
3 B- z# E% y- B. V- {using it rather frequently, twice a day. The Physicians’* c5 o; V" O# g6 F6 f0 `- m& [- P
Desk Reference, or package insert of this product, gel or
; U. I( J& I, b# t* gcream, cautions about dermal testosterone transfer to. F! E4 R1 l* B( j- d
unprotected females through direct skin exposure.0 h% ^4 g( M' B
Serum testosterone level was found to be 2 times the1 M& j/ c+ L, M2 U4 ?* m
baseline value in those females who were exposed to$ ?3 b: v$ b8 V3 F% F
even 15 minutes of direct skin contact with their male
( G( }' b, `1 l$ S7 apartners.6 However, when a shirt covered the applica-
6 N4 B F* A" O# Ltion site, this testosterone transfer was prevented.
P/ g S3 {5 xOur patient’s testosterone level was 60 ng/mL,
, R; O5 e6 e. k, s( C' ]which was clearly high. Some studies suggest that, Q+ O+ |0 b5 Q' p0 W8 D) N
dermal conversion of testosterone to dihydrotestos-% h: m) l w9 L' t
terone, which is a more potent metabolite, is more2 n5 F6 P6 [. \3 O% E
active in young children exposed to testosterone
/ G1 o( l2 y* a! Nexogenously7; however, we did not measure a dihy-9 z. f7 f2 u: _1 j( ~
drotestosterone level in our patient. In addition to. M2 f$ d5 k8 p, F/ @
virilization, exposure to exogenous testosterone in
& D6 u3 I4 b/ z# r1 ]6 tchildren results in an increase in growth velocity and1 ]# E5 E8 t+ C& A
advanced bone age, as seen in our patient.
2 T# S$ ?4 |0 N' z4 M! [The long-term effect of androgen exposure during" Q" m& Z) D+ ?# [2 J0 k( U! L3 |
early childhood on pubertal development and final
; V0 ?( U: i# Z1 E2 M; E ]adult height are not fully known and always remain
1 V( s" Q! v: Qa concern. Children treated with short-term testos-
2 V6 l5 ]8 O6 q: Z" g+ W, Q6 d* p$ Nterone injection or topical androgen may exhibit some
~" w4 w; j6 h+ Z& b+ eacceleration of the skeletal maturation; however, after
$ e( ]( s) U( @3 c2 F0 N1 Lcessation of treatment, the rate of bone maturation
Z- Z" z5 ^! q2 Z4 }8 Y3 xdecelerates and gradually returns to normal.8,93 {( d- Q$ k, l; Y: l+ X# U( Q% a
There are conflicting reports and controversy
* |2 B: w' `) j; H" L3 V' [over the effect of early androgen exposure on adult
9 n. X: V& \4 k0 H9 npenile length.10,11 Some reports suggest subnormal
' r# Q7 c, [1 F( F) Padult penile length, apparently because of downreg-/ c9 B# G, j4 L9 F- F8 V
ulation of androgen receptor number.10,12 However,
* W5 J' z! Z& Q: ySutherland et al13 did not find a correlation between* G9 L0 D# w) D( s8 I2 I6 V( l- a
childhood testosterone exposure and reduced adult9 x1 s1 @% z& n0 e/ i" k
penile length in clinical studies.
" n, g* S. P3 k: INonetheless, we do not believe our patient is
n: s* g+ P4 d, ggoing to experience any of the untoward effects from
9 S6 N' r' J) t% O" `, t6 Dtestosterone exposure as mentioned earlier because
* _" n0 p2 w1 e0 I% a! lthe exposure was not for a prolonged period of time.) p$ j) K7 O5 v) h5 J6 e# r
Although the bone age was advanced at the time of
g7 @1 X1 V. ~4 F6 H, I+ A/ o: ~. ?diagnosis, the child had a normal growth velocity at
) Z" E6 k% P$ V0 Othe follow-up visit. It is hoped that his final adult
0 w# Q6 I2 A! V7 Z; l: kheight will not be affected.
) a/ {' P8 r; q7 D% wAlthough rarely reported, the widespread avail-7 n, H5 B& } ?) ]
ability of androgen products in our society may
. G( ^; h- g7 x& @. G) xindeed cause more virilization in male or female. H8 ?) R/ h, W
children than one would realize. Exposure to andro-
/ s2 G0 m% M9 }3 Y- s Kgen products must be considered and specific ques-$ \# h0 u! {% `6 c" o) x
tioning about the use of a testosterone product or8 @$ S+ U6 s& L# f4 W
gel should be asked of the family members during
. y' g4 l; m# J2 Qthe evaluation of any children who present with vir-
6 R1 y% W) D2 d/ e9 T7 wilization or peripheral precocious puberty. The diag-
" I$ \7 e: N0 e+ tnosis can be established by just a few tests and by, j% x2 ?9 g+ [# G* h7 {8 R6 b7 Z
appropriate history. The inability to obtain such a& ]: v3 _2 r% W- j& G1 f: x
history, or failure to ask the specific questions, may8 s' y: m+ A* w- N) Y
result in extensive, unnecessary, and expensive5 M1 b( j9 ~; g
investigation. The primary care physician should be% i6 i: X J1 n& o' u" [( s$ `
aware of this fact, because most of these children
3 c. J2 _- ^, [1 S! }9 r3 ^may initially present in their practice. The Physicians’
' x" |' u; \" M% f3 O1 ODesk Reference and package insert should also put a
; }1 O5 ^% @6 |; X$ ?: pwarning about the virilizing effect on a male or, X' r$ q- U) j9 g
female child who might come in contact with some-' o5 N/ N. T S8 Q: |
one using any of these products.- y4 R" _1 m8 z: a
References9 f$ _% s4 j) e* p/ L
1. Styne DM. The testes: disorder of sexual differentiation
6 S% h$ S8 P# fand puberty in the male. In: Sperling MA, ed. Pediatric F: l4 ?$ O' E& z# ]
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' Q' r1 |& Q% N: O2002: 565-628.
4 ^( }5 [4 H( I$ q1 L2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
; a {3 B, ` u! npuberty in children with tumours of the suprasellar pineal |
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