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Sexual Precocity in a 16-Month-Old1 u7 y: U! _6 |( ^% ?1 w
Boy Induced by Indirect Topical. }% G( y. ~9 e1 t/ A1 A" [
Exposure to Testosterone
( U' B: \' G9 D+ u) ^9 r! JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. D8 r8 _% [( E3 @; W& Y
and Kenneth R. Rettig, MD1! I. D8 T! z/ X8 |4 `0 ]
Clinical Pediatrics
4 h- E4 t+ L0 R+ w5 R( sVolume 46 Number 6: {; Q A& \0 p- M' G3 t& T
July 2007 540-543/ k4 j6 c; h! a, j
© 2007 Sage Publications
5 C' Y2 q( M+ _ M8 Y10.1177/0009922806296651
/ F) ]! o- I2 d2 |: U9 xhttp://clp.sagepub.com+ q: |# M, W; q' Q
hosted at" i( b6 i- \" h. {# }% s; `
http://online.sagepub.com
1 L1 _$ T3 L2 x1 H/ e/ e/ xPrecocious puberty in boys, central or peripheral,2 t* q2 Z6 I0 o9 F
is a significant concern for physicians. Central4 b, @( p& x+ B/ h3 L
precocious puberty (CPP), which is mediated
; T; c, a' ]) O6 E; s5 V( Athrough the hypothalamic pituitary gonadal axis, has: q+ N& R9 Q8 @
a higher incidence of organic central nervous system
3 ]0 w( E, t9 ^. H5 olesions in boys.1,2 Virilization in boys, as manifested0 w) @: ~# m) v2 s8 U1 [8 `
by enlargement of the penis, development of pubic: } H* H% {5 y6 V6 {3 ?
hair, and facial acne without enlargement of testi-
# Q' N5 J6 z9 H- s+ hcles, suggests peripheral or pseudopuberty.1-3 We* d5 x' E4 j7 L3 T2 U( `) z
report a 16-month-old boy who presented with the$ P- J& c# s" b6 y) Q0 ~" m* i- ~1 E
enlargement of the phallus and pubic hair develop-
# R8 O7 h& p0 A+ Y1 x" s1 I& sment without testicular enlargement, which was due, [" Z) P' G( c" d
to the unintentional exposure to androgen gel used by% D9 q' |! B: G* Q7 D: C1 s# e2 A
the father. The family initially concealed this infor-
" R! ]' N5 g$ v. Z& k3 y' Gmation, resulting in an extensive work-up for this, Y& Q5 W, \/ R6 `
child. Given the widespread and easy availability of
3 p7 j6 }& n3 Q6 K9 s( h$ Gtestosterone gel and cream, we believe this is proba-
7 A( G$ I: ~/ S0 j! G- qbly more common than the rare case report in the
+ r' z. Z- L9 F% ^3 A" oliterature.4
* d- N( Z3 H( y- DPatient Report( b! b9 v; X! z: d8 Z! @
A 16-month-old white child was referred to the! |/ F( b4 a- D, ~, v' d: k
endocrine clinic by his pediatrician with the concern8 M5 y% H. D( w) i$ O
of early sexual development. His mother noticed
x) v7 e& U; b+ E( t. ]" ulight colored pubic hair development when he was
* h) y9 w% E* K8 J& u5 cFrom the 1Division of Pediatric Endocrinology, 2University of4 R9 x1 o% M4 T. z+ E: x1 Y: H
South Alabama Medical Center, Mobile, Alabama.
% {9 `& o9 p% o! p3 t9 J/ cAddress correspondence to: Samar K. Bhowmick, MD, FACE,
! o: w2 Q" a" h/ _" z: e" d9 F' ]Professor of Pediatrics, University of South Alabama, College of% Q! O' Y/ X1 R/ K* v& @* v
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# ~0 c/ l" \( T9 Je-mail: [email protected].
& E7 r$ v: P/ c7 W7 r5 [about 6 to 7 months old, which progressively became1 s: t" D' L G4 Q5 d3 o5 g; j
darker. She was also concerned about the enlarge-8 |( P" }' c( w$ O( o6 I/ Q# L
ment of his penis and frequent erections. The child
5 l% U$ h/ y& J( k* A$ m/ d" M( _was the product of a full-term normal delivery, with# Z( o( V7 t, i8 H* n! s
a birth weight of 7 lb 14 oz, and birth length of
8 M V9 r: {% b2 |. l4 a20 inches. He was breast-fed throughout the first year
4 ?2 k! r- F! r9 A% Q% b1 e ?of life and was still receiving breast milk along with& k, Z8 R4 }0 C, t
solid food. He had no hospitalizations or surgery,! U. w" R; A& a2 G3 u
and his psychosocial and psychomotor development
3 }8 l3 ` M hwas age appropriate.
1 Y/ V) t; j$ B6 W5 n) _The family history was remarkable for the father,# v. r) Z. p" S @6 P! j
who was diagnosed with hypothyroidism at age 16,
& w$ j; W0 N- y9 d+ cwhich was treated with thyroxine. The father’s0 X/ m% L. Q& I
height was 6 feet, and he went through a somewhat1 Y/ ]9 H1 W8 Z& a
early puberty and had stopped growing by age 14. Q( [" w0 A# I' v
The father denied taking any other medication. The: q+ j! [& x6 M# j- U/ W
child’s mother was in good health. Her menarche2 l, k& t B; g5 i/ i; n4 ]% w% i, x
was at 11 years of age, and her height was at 5 feet
2 F9 k6 B1 r$ {9 U8 }; n5 inches. There was no other family history of pre-
$ O0 D$ t& ]; M, w" a4 ncocious sexual development in the first-degree rela-
0 v& z: U4 H/ ptives. There were no siblings.
0 r4 @- J9 F: gPhysical Examination
; C( b( _8 I( L4 I7 iThe physical examination revealed a very active,4 {. K; X* @- j2 g
playful, and healthy boy. The vital signs documented+ H: ?6 Y# U3 D/ H8 D P* g& A% E4 h. }
a blood pressure of 85/50 mm Hg, his length was& `* S) R6 {" J+ d! R6 n* m4 Y7 a
90 cm (>97th percentile), and his weight was 14.4 kg# z( F$ v* R. X- t
(also >97th percentile). The observed yearly growth
' t+ z3 l4 D$ X7 }velocity was 30 cm (12 inches). The examination of1 j+ l9 k' r( k8 ~% q( W8 y/ H0 {
the neck revealed no thyroid enlargement.
) g4 W/ D0 |$ j3 GThe genitourinary examination was remarkable for
! s/ ]( G9 u+ f2 Henlargement of the penis, with a stretched length of
7 ]. X/ f4 {# O8 cm and a width of 2 cm. The glans penis was very well
9 e; t5 y% ^8 h8 e2 ` @developed. The pubic hair was Tanner II, mostly around
' f4 ~2 d; j' F. q540
* a8 g( ^8 m6 A! A- T( |' I2 u# ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from x( @4 X6 K- k& _' }/ @
the base of the phallus and was dark and curled. The
~3 K% M8 f5 B7 wtesticular volume was prepubertal at 2 mL each.
8 u6 K9 Z* V8 {7 k$ CThe skin was moist and smooth and somewhat, D1 `0 v# G: V9 G+ E
oily. No axillary hair was noted. There were no; D$ Y( @1 x7 W6 }, y. b
abnormal skin pigmentations or café-au-lait spots.$ S5 }' y8 a! g/ p
Neurologic evaluation showed deep tendon reflex 2+, ]9 W6 f' r8 z6 f7 Y5 M
bilateral and symmetrical. There was no suggestion
, H/ J0 r0 ]4 q+ S- O( w9 yof papilledema.
+ ^" o* F+ X+ l- T% wLaboratory Evaluation
) K/ k4 w+ H4 _1 SThe bone age was consistent with 28 months by% `6 x- T @! l' z
using the standard of Greulich and Pyle at a chrono-& d& l' d. M5 W- ^" o, \
logic age of 16 months (advanced).5 Chromosomal
' u% S5 N5 k& F Nkaryotype was 46XY. The thyroid function test
/ s; [5 o$ W& {/ r Bshowed a free T4 of 1.69 ng/dL, and thyroid stimu-+ p ]9 U: q7 x4 C- P
lating hormone level was 1.3 µIU/mL (both normal).
3 x* z! K& p# ]The concentrations of serum electrolytes, blood
: ^7 @! g4 f7 |- h1 surea nitrogen, creatinine, and calcium all were
) X9 j k, G* Wwithin normal range for his age. The concentration: D E7 o5 j% J" X$ U2 \0 c
of serum 17-hydroxyprogesterone was 16 ng/dL
[! m( F7 X, g. Q) _' n7 u. O( x% g7 D(normal, 3 to 90 ng/dL), androstenedione was 200 f* Y" [5 @5 Z# G: x1 d' N' K
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-+ D) b" z" q8 q }( j6 a4 F; O
terone was 38 ng/dL (normal, 50 to 760 ng/dL),7 W3 R; W; y0 x5 Z# X2 k8 g
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 ~0 V# W$ a: \( }: E49ng/dL), 11-desoxycortisol (specific compound S), c2 G- h0 Q/ m& ?- G& I& S
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
/ q9 U, o* W5 ], M! Ctisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( o- t/ }, l) z2 Gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL), x, o* P/ J: s
and β-human chorionic gonadotropin was less than
0 w) k! G8 f: H2 L7 \5 mIU/mL (normal <5 mIU/mL). Serum follicular
) K/ T+ y$ n2 q( {' X$ astimulating hormone and leuteinizing hormone
+ k0 D" }& a& l$ Xconcentrations were less than 0.05 mIU/mL
6 L( g Q" N, I2 Q1 f1 S& m(prepubertal).
4 V/ u0 Y9 o8 f3 X0 {* {The parents were notified about the laboratory
3 [0 a' n2 C5 u# qresults and were informed that all of the tests were
0 C. _# o" h6 A) }" V6 k% O: E& Jnormal except the testosterone level was high. The
& Q* _5 s- f6 b& p) ofollow-up visit was arranged within a few weeks to; S, ^" a/ j" j& c8 o% _
obtain testicular and abdominal sonograms; how-6 u6 s" R3 [; M# ]
ever, the family did not return for 4 months.
/ u. F; u0 j" bPhysical examination at this time revealed that the
) h0 Z9 O2 h8 }5 wchild had grown 2.5 cm in 4 months and had gained4 W, c' J+ K0 G& S
2 kg of weight. Physical examination remained* M0 ^$ x Y% j6 \ Z+ f3 D" z
unchanged. Surprisingly, the pubic hair almost com-5 N$ E' f" Z' c) G* E
pletely disappeared except for a few vellous hairs at
' `1 M# f& P" Q+ W# F2 f% Rthe base of the phallus. Testicular volume was still 2
% R0 C; G7 H: K5 dmL, and the size of the penis remained unchanged.& i Z! B8 Z [. Y5 s2 Z
The mother also said that the boy was no longer hav-
, M( W8 o+ t* o' R! Iing frequent erections.; w) v& S/ }; P- {
Both parents were again questioned about use of7 a( E: J! G: S0 ?' \' A
any ointment/creams that they may have applied to
" R6 q# Z. G1 h7 N" s$ D# B; [the child’s skin. This time the father admitted the
* L2 X& \/ b4 T6 v0 UTopical Testosterone Exposure / Bhowmick et al 5416 B, r; H6 u! Z$ T, X$ a: b( Y
use of testosterone gel twice daily that he was apply-
* C% x; I: |9 |0 s+ sing over his own shoulders, chest, and back area for X. L! l7 ~' a) `
a year. The father also revealed he was embarrassed3 P+ d% `2 x& P3 c; C' J5 k2 ?
to disclose that he was using a testosterone gel pre-
# t- f% C: z. A* b$ `! j/ ]2 wscribed by his family physician for decreased libido/ R/ K W4 o2 w0 t
secondary to depression.
7 a% L2 o, I* p( _9 E/ b1 m( O. R1 P8 xThe child slept in the same bed with parents.
8 a2 I" S& S6 y9 r/ S" _3 YThe father would hug the baby and hold him on his8 u( B9 X% m! P, X L: c; n/ Y
chest for a considerable period of time, causing sig-
$ i) I1 \( L/ L& x5 M) Hnificant bare skin contact between baby and father.
1 {9 E+ }# T6 M- L" Z9 J( I3 lThe father also admitted that after the phone call,
1 a0 P8 t' B! o: V2 C) lwhen he learned the testosterone level in the baby
; w* B% i5 ~$ F$ B9 A, K8 V" C/ rwas high, he then read the product information
) e4 h( a7 R) p- Rpacket and concluded that it was most likely the rea-
9 S$ Y1 d1 D3 ~6 n7 Y7 {son for the child’s virilization. At that time, they' \" z1 X S0 M, d
decided to put the baby in a separate bed, and the
3 L, N' O/ A5 S$ {) vfather was not hugging him with bare skin and had9 A* O! X! h0 H7 }9 B& `+ z
been using protective clothing. A repeat testosterone
6 Q6 W7 E6 p% S5 ]% T' Wtest was ordered, but the family did not go to the3 n/ m7 Z! o, ]& Z/ \% U
laboratory to obtain the test.: V+ l( b# { S( h t, E
Discussion
4 G1 [# K! O8 }2 d6 D* `) [Precocious puberty in boys is defined as secondary
4 D/ x2 A6 v) Q' q9 r `sexual development before 9 years of age.1,4: s+ C# H$ l/ U
Precocious puberty is termed as central (true) when
: z% `$ G: E/ B4 e5 W0 }it is caused by the premature activation of hypo-+ G7 j2 o! o5 G" G. x8 U/ V
thalamic pituitary gonadal axis. CPP is more com-
) o; o4 j T q3 [mon in girls than in boys.1,3 Most boys with CPP
* o9 N4 F7 S5 y( jmay have a central nervous system lesion that is3 Y, a! u) _7 e. T# s# d8 {
responsible for the early activation of the hypothal- `9 i3 T; S; p; i5 `9 u: u
amic pituitary gonadal axis.1-3 Thus, greater empha-
4 a( D/ k: r/ A; b+ K# U: d/ X6 Osis has been given to neuroradiologic imaging in/ K6 K) b- H2 w7 i
boys with precocious puberty. In addition to viril-1 I3 o& G; r* m. k( h& x
ization, the clinical hallmark of CPP is the symmet-: q: c. j; ^) k# f; B# f% Y1 w S. d
rical testicular growth secondary to stimulation by5 `: Z5 S2 j; g7 n4 g5 J G
gonadotropins.1,3
- d3 S/ Y3 h8 q/ C3 }Gonadotropin-independent peripheral preco-
" T8 j- g A& m- W0 x! [2 {* U3 {cious puberty in boys also results from inappropriate9 M1 _2 r5 T% Y: q
androgenic stimulation from either endogenous or
( h1 L$ m1 q) T9 B; zexogenous sources, nonpituitary gonadotropin stim-, B. [6 j; u2 p( H8 H
ulation, and rare activating mutations.3 Virilizing
# n/ t: A% |5 g4 N$ @8 W8 U9 ^congenital adrenal hyperplasia producing excessive. {' U) Y( u/ _* g* u* [
adrenal androgens is a common cause of precocious
: T5 b: u. z2 z; s0 m8 ]# j* e$ Upuberty in boys.3,4; i$ U4 Q) D$ m7 k" w' g B, Q, @
The most common form of congenital adrenal7 W, `1 |% s o
hyperplasia is the 21-hydroxylase enzyme deficiency.
) K" f' r/ L! L# |( M: e2 q/ nThe 11-β hydroxylase deficiency may also result in
9 G- m3 }4 ^. w: C1 u: \5 U( gexcessive adrenal androgen production, and rarely,: h4 G. l+ B% \8 B5 W
an adrenal tumor may also cause adrenal androgen
+ M' `4 x3 J5 j" |6 B0 V& yexcess.1,3
) {* J6 k( L& I2 s3 dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% D3 u1 O2 u) f
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ q4 c L, b& Q9 kA unique entity of male-limited gonadotropin-9 H6 y: X/ `9 A& }6 V/ x* s
independent precocious puberty, which is also known
/ {9 ^4 a- |! ]as testotoxicosis, may cause precocious puberty at a
9 \8 g* e3 U+ D" R) ~* every young age. The physical findings in these boys% \0 e0 n2 P/ K" |
with this disorder are full pubertal development,6 w4 a4 v+ j/ e# a- Z; g
including bilateral testicular growth, similar to boys
; v% L' O2 }- b# P) w" Y( {with CPP. The gonadotropin levels in this disorder
0 u8 N& N- \' ?# B5 Aare suppressed to prepubertal levels and do not show
$ d! Q' ]: z) i2 Ppubertal response of gonadotropin after gonadotropin-
4 R! g7 U. t' P; E8 D- m6 Lreleasing hormone stimulation. This is a sex-linked5 d; ]8 v2 u6 c1 f! \6 ]
autosomal dominant disorder that affects only
$ i: b4 [+ ]4 @ [2 @males; therefore, other male members of the family* A5 j9 P& L% N* q1 w- I! N l T5 h
may have similar precocious puberty.39 v, C8 Y' B% \/ [
In our patient, physical examination was incon-& O. p! \4 ]( x4 X
sistent with true precocious puberty since his testi-% n2 W% t$ W% @. X* l1 ~ F% j
cles were prepubertal in size. However, testotoxicosis8 O+ W }8 r7 Z) i6 a t7 {# V: o
was in the differential diagnosis because his father
' r# u- L1 ~* q& q( wstarted puberty somewhat early, and occasionally,; i" s7 G: l1 E+ p( B! S$ {8 P: Q
testicular enlargement is not that evident in the
- c% o) _: W. D2 b1 R; wbeginning of this process.1 In the absence of a neg-5 G1 }$ t& l1 V! h- w' \
ative initial history of androgen exposure, our N; ]7 Q! d% o* y2 `0 ~+ O/ V( T
biggest concern was virilizing adrenal hyperplasia,
! D" G# y, x& zeither 21-hydroxylase deficiency or 11-β hydroxylase2 k6 ^5 K4 m( l0 H) y- y% i
deficiency. Those diagnoses were excluded by find-" k! Y9 G2 e, T: E
ing the normal level of adrenal steroids.5 R- { M9 G$ h5 M& d
The diagnosis of exogenous androgens was strongly
/ Q4 f5 | m; X) Msuspected in a follow-up visit after 4 months because
3 G/ U6 z) H X; f9 w; ethe physical examination revealed the complete disap-
* l3 k L! u* ]- _# G) f1 Cpearance of pubic hair, normal growth velocity, and
' P( F8 T: B2 Q7 _decreased erections. The father admitted using a testos-8 E) \( F$ ?% g) V
terone gel, which he concealed at first visit. He was
) L. Z7 G8 B# z7 ?0 l, z9 Husing it rather frequently, twice a day. The Physicians’
: H6 @2 s' K! I$ wDesk Reference, or package insert of this product, gel or
8 |* M& r: v2 v4 K) H2 P& y6 Y q( Fcream, cautions about dermal testosterone transfer to6 h: u# T1 P X( z+ I% t
unprotected females through direct skin exposure.6 S5 |& c3 }2 \; y) O7 m: O
Serum testosterone level was found to be 2 times the4 n% K- [+ S6 p' d0 p) U- s& A
baseline value in those females who were exposed to
* L7 X6 t& G5 P5 \3 o/ Reven 15 minutes of direct skin contact with their male+ p. {- M0 B% u6 K% X) S
partners.6 However, when a shirt covered the applica-: H8 z4 _' M4 q. T0 H" N
tion site, this testosterone transfer was prevented.5 M9 u: W* x) v
Our patient’s testosterone level was 60 ng/mL,4 [3 [# {) {$ U" J- |" J2 b$ n1 y
which was clearly high. Some studies suggest that+ \' e. ^% {& M5 X0 S1 _
dermal conversion of testosterone to dihydrotestos-& P" V [/ V1 A% {) n/ V
terone, which is a more potent metabolite, is more# ?' z* R2 ]3 y' H0 B- K
active in young children exposed to testosterone
; q# f) p8 P* V7 Sexogenously7; however, we did not measure a dihy-! \! U1 E0 ?: v! i T0 a7 k
drotestosterone level in our patient. In addition to! f& \, d9 e/ y4 J$ a b+ k7 H
virilization, exposure to exogenous testosterone in7 H" u5 U; \; F
children results in an increase in growth velocity and; ~4 |2 X5 _; T8 L# A v0 _
advanced bone age, as seen in our patient.5 g& V0 R0 F) a, @
The long-term effect of androgen exposure during0 L5 D2 e8 n$ n% {, c; n3 P
early childhood on pubertal development and final
# T% p( X0 ^& G+ madult height are not fully known and always remain
% A0 r+ p4 h$ F/ La concern. Children treated with short-term testos-
7 E9 G3 i" | ?5 ?9 `; Vterone injection or topical androgen may exhibit some( b7 X( B$ o1 j' M" T$ N- H
acceleration of the skeletal maturation; however, after
0 k( i. A; M5 acessation of treatment, the rate of bone maturation
/ _ y. f( i/ M, o3 H% e, ldecelerates and gradually returns to normal.8,99 u4 M( H' o" l' s
There are conflicting reports and controversy8 d: i4 S9 s) w$ B- r- g$ A
over the effect of early androgen exposure on adult
, ~2 P/ J% T. `penile length.10,11 Some reports suggest subnormal- }% s# z) b# Z: {" b% K
adult penile length, apparently because of downreg-
8 q6 o# r& E1 Z! g$ Wulation of androgen receptor number.10,12 However,. S9 K& z' }3 O2 q* Z: h% n
Sutherland et al13 did not find a correlation between
" w2 G% h( T' O; b4 Dchildhood testosterone exposure and reduced adult, m. [% Z1 z3 v- t& V$ b( i
penile length in clinical studies.
& k4 U2 |4 R2 j+ x- o% v& w5 |Nonetheless, we do not believe our patient is* p4 _2 q' D9 R
going to experience any of the untoward effects from
6 @6 r+ y6 u6 Dtestosterone exposure as mentioned earlier because
0 q" P2 o" I& M& O: L4 qthe exposure was not for a prolonged period of time. D, a2 d1 ?, ?5 q% z) n- n
Although the bone age was advanced at the time of! ~3 ~# L: k9 E- F9 ^, s
diagnosis, the child had a normal growth velocity at s7 r3 s( v1 K- B" c9 y- O
the follow-up visit. It is hoped that his final adult+ M$ ]0 @2 x. J% I( L
height will not be affected.% I2 v$ ~+ M+ E# q' j* S% `
Although rarely reported, the widespread avail-6 i) W, {4 h8 k8 {
ability of androgen products in our society may
' Z1 g3 x. ?8 B7 q, h4 jindeed cause more virilization in male or female
- b! Q& x4 @4 ?+ s' \/ I( I9 lchildren than one would realize. Exposure to andro-
0 ]# Q8 k$ ]5 r! M( f( pgen products must be considered and specific ques-
% F8 w& E* o% F5 k0 [$ R' Y; N+ \& d) Ltioning about the use of a testosterone product or
( i( w7 ^/ ^' g) k9 |8 _gel should be asked of the family members during
) n9 V5 r2 w) M7 [+ H- i, uthe evaluation of any children who present with vir-
. e% U7 I f* q7 a- S# u- r, L: b# C! dilization or peripheral precocious puberty. The diag-
+ S q/ N0 m8 t" }% p$ A! E/ v7 jnosis can be established by just a few tests and by
7 k: a, ~ n; n. p. Yappropriate history. The inability to obtain such a$ d" [5 m, B8 @6 h3 v
history, or failure to ask the specific questions, may: T" s+ r& W5 {, g% \8 f
result in extensive, unnecessary, and expensive+ S, I: K! r- o R
investigation. The primary care physician should be
$ x9 B0 ^( k/ _' t& k) J" uaware of this fact, because most of these children: J% m: C( t& h4 P0 Q# H3 ?
may initially present in their practice. The Physicians’
% s. K5 O$ \+ t6 cDesk Reference and package insert should also put a* N0 p8 \4 [# y& B! |4 ^# f
warning about the virilizing effect on a male or( L, X2 K4 D4 X& |8 n6 @
female child who might come in contact with some-! I* G" g: M8 b
one using any of these products.6 `# k! X6 J4 r% u7 N# M
References6 S* v- X$ i( D
1. Styne DM. The testes: disorder of sexual differentiation6 \. ?+ j0 {8 `( W% m* b* b
and puberty in the male. In: Sperling MA, ed. Pediatric! X. V4 b: B: c; z4 g8 \$ S
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, f9 P3 ~: {4 i, d$ o8 ~# S
2002: 565-628.; G. B0 @( E# `* D! U5 J
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious7 V1 O+ f8 `9 u; t( Y
puberty in children with tumours of the suprasellar pineal |
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