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Sexual Precocity in a 16-Month-Old
' C4 R0 \5 t7 J1 {2 pBoy Induced by Indirect Topical& O3 F7 P/ \1 v' {1 `% n
Exposure to Testosterone3 ?% S$ h p3 ]) v& W1 A* |, p9 U
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2* n# g; w: ^: d+ L% o5 i1 y+ T
and Kenneth R. Rettig, MD1- h8 M$ Y2 z9 u1 O' n6 p
Clinical Pediatrics* g! \$ |* ]# ~" w
Volume 46 Number 6
8 a* v6 |* i) ?/ r, O* U8 LJuly 2007 540-543* T8 x9 i3 C$ U" u
© 2007 Sage Publications
6 b- {3 ]6 A+ `/ H1 ? g( f4 N10.1177/0009922806296651
) p- n! n! j7 M E7 Qhttp://clp.sagepub.com: b% H. y% r% ~5 _1 I
hosted at$ k, l; z& Q- T3 Z* f
http://online.sagepub.com
8 i" Z9 x: j$ o4 {Precocious puberty in boys, central or peripheral,+ ^7 ?" P2 A5 B# X# L
is a significant concern for physicians. Central
0 n1 j& e6 r- T! ^precocious puberty (CPP), which is mediated
* Y" Y! G; a; ]through the hypothalamic pituitary gonadal axis, has
. }9 L4 I2 Y# I/ \, u. q+ b& ?" Pa higher incidence of organic central nervous system( B& E: ~5 l4 S4 ~- k
lesions in boys.1,2 Virilization in boys, as manifested; k8 f: [) z7 s! p3 d8 u
by enlargement of the penis, development of pubic
( C: V) S8 e- H' d3 S! e, jhair, and facial acne without enlargement of testi-
1 R) M: J- t+ ]cles, suggests peripheral or pseudopuberty.1-3 We9 Y$ C. r" H7 L( y
report a 16-month-old boy who presented with the
; C& ]2 D4 ?. y9 j7 Venlargement of the phallus and pubic hair develop-
3 p7 d6 _- k* A* F5 Iment without testicular enlargement, which was due
' i9 {( q+ O6 N q6 @to the unintentional exposure to androgen gel used by) a& r. W) u" s, z# i8 P
the father. The family initially concealed this infor-: I: g9 o- K* V6 \# l: d7 P- E& H
mation, resulting in an extensive work-up for this# H& H; w& U! G( A# ^8 o
child. Given the widespread and easy availability of
" n: [7 d# k( [/ I+ ~3 w) itestosterone gel and cream, we believe this is proba-' U0 ?$ i/ D! e
bly more common than the rare case report in the# z4 j" h+ A8 \8 v2 X3 Z2 P9 U
literature.42 t6 L+ r" l, K8 @& E
Patient Report
: {2 |# J2 H% a3 zA 16-month-old white child was referred to the; _& g/ w2 K5 m& o7 P; }
endocrine clinic by his pediatrician with the concern+ ] ?6 ~! F" q! \( q
of early sexual development. His mother noticed- |/ ?, F6 [$ w1 Q% ~
light colored pubic hair development when he was1 J& U4 b! P/ H( h1 X, l' n9 p0 k
From the 1Division of Pediatric Endocrinology, 2University of" e* K( G; S6 G7 C9 D
South Alabama Medical Center, Mobile, Alabama.
" I& y/ ^* D% o1 j, Q3 @Address correspondence to: Samar K. Bhowmick, MD, FACE,
* s+ E: M' d0 X- K& v0 x" |/ Q* f! rProfessor of Pediatrics, University of South Alabama, College of
- |- p$ k4 j0 A* C3 q* L, iMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% a; [3 r6 l. e P
e-mail: [email protected].
4 S8 q# t$ u2 l! V8 d; dabout 6 to 7 months old, which progressively became s. o' S$ B( x( W$ u- o/ W+ C
darker. She was also concerned about the enlarge-
. g8 b2 Q/ J$ E+ m/ r3 ^* kment of his penis and frequent erections. The child
7 m; t* A, K2 S% t2 ~was the product of a full-term normal delivery, with2 L) g2 L! ?* D8 w% c9 }7 G& F
a birth weight of 7 lb 14 oz, and birth length of/ R% l; B3 r& }8 o
20 inches. He was breast-fed throughout the first year
; k: h [- b |; ]+ E9 ^# Oof life and was still receiving breast milk along with7 n/ `7 J; D* q7 u3 E& N/ Q
solid food. He had no hospitalizations or surgery,$ T8 s. a, n: t/ \# r
and his psychosocial and psychomotor development8 o! _ ?! i& m
was age appropriate. ]) O) t" F# D+ l$ v$ I" a
The family history was remarkable for the father,
. L/ `2 k" {' Zwho was diagnosed with hypothyroidism at age 16,
+ z+ b' w; Q! O5 z' Hwhich was treated with thyroxine. The father’s5 o+ _6 e/ P; d8 n7 y7 G* R1 [
height was 6 feet, and he went through a somewhat, Q7 h4 k7 C- _- F
early puberty and had stopped growing by age 14./ J4 M6 U- a# _$ Z' o& v* M
The father denied taking any other medication. The
# i2 e' E( ^' }child’s mother was in good health. Her menarche
/ O( ^. r" E) Ewas at 11 years of age, and her height was at 5 feet
, n6 m3 I& H+ h5 inches. There was no other family history of pre-
2 M- e5 ?) l T3 ^& D9 N& Acocious sexual development in the first-degree rela-
! f+ q2 ]5 O( \& M# `tives. There were no siblings." ^: J* C, D0 C/ d/ l
Physical Examination; f; u, ~. k( p* L
The physical examination revealed a very active,) J( N: k" c) x; q6 h
playful, and healthy boy. The vital signs documented! ~5 i6 U( U8 f2 V: W& j* y
a blood pressure of 85/50 mm Hg, his length was2 E' q+ C/ s8 B" C! T
90 cm (>97th percentile), and his weight was 14.4 kg9 j" j5 t1 _. `* T8 S# q6 f
(also >97th percentile). The observed yearly growth
2 D1 \8 J) D- S0 Q5 Y' D( q6 k8 P% Bvelocity was 30 cm (12 inches). The examination of- b0 @* T/ z& E7 T( g/ q3 G0 U
the neck revealed no thyroid enlargement.
( N5 J: x% d" D6 S& A. I: ^% XThe genitourinary examination was remarkable for
( a& v' Q% s) Y3 V; C) Venlargement of the penis, with a stretched length of
( }5 f* s b' ~# S Y$ X8 cm and a width of 2 cm. The glans penis was very well
# H- X( R8 i; s9 Pdeveloped. The pubic hair was Tanner II, mostly around
+ c8 [ T: s1 [540* ]/ I" i* }$ j! ~3 E' e
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 w1 ?5 V# n, R! Ythe base of the phallus and was dark and curled. The" c4 j" v) P9 h/ H
testicular volume was prepubertal at 2 mL each.: p, m+ B1 v. j7 ~
The skin was moist and smooth and somewhat! i, R4 m$ ?: ]5 Z. W2 b0 [/ f
oily. No axillary hair was noted. There were no! z2 G9 @5 {. c8 `% b
abnormal skin pigmentations or café-au-lait spots.
6 M: T" D3 Q, z1 b5 lNeurologic evaluation showed deep tendon reflex 2+- ?) N% w* {" V9 y5 h. L& x i
bilateral and symmetrical. There was no suggestion
" D* E; {' r3 F2 Jof papilledema.
. R- O" I: m0 Z* I" S9 \8 \Laboratory Evaluation/ p: T, x7 Y* g5 c* [ G$ _
The bone age was consistent with 28 months by
% ]( a* u, @4 j! Tusing the standard of Greulich and Pyle at a chrono-
, i& q: r0 e O; ^* \logic age of 16 months (advanced).5 Chromosomal4 x" I) }! o, f8 q0 o' k4 G" d
karyotype was 46XY. The thyroid function test
" J4 S% T- \+ R {, R2 F& Z) vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
( k; m( L8 z, G' z2 slating hormone level was 1.3 µIU/mL (both normal).0 X2 e: Y- S( q9 }! ?
The concentrations of serum electrolytes, blood
4 e2 y; Y8 P a1 L; b/ turea nitrogen, creatinine, and calcium all were
7 Y, K3 U; {. n L' pwithin normal range for his age. The concentration" N# G+ r6 l) u) k/ U
of serum 17-hydroxyprogesterone was 16 ng/dL& V+ F6 Y1 S3 X6 Y
(normal, 3 to 90 ng/dL), androstenedione was 20
, G- D7 Y$ p% I2 V) c* Xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 u% |6 p$ I, p" x" \" cterone was 38 ng/dL (normal, 50 to 760 ng/dL),: e$ F G9 X/ y% q5 c0 \8 A
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
' b+ d: p- v/ W2 c F% V; D49ng/dL), 11-desoxycortisol (specific compound S)3 [# N; ?: n6 e
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% f$ o7 Q$ Y& D( m6 Ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; [) T) y. e; `$ c$ `% Q# G4 j5 M
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),% R1 r0 C4 ~% W1 @0 B4 Q D
and β-human chorionic gonadotropin was less than' Y9 k" `9 R: T2 y
5 mIU/mL (normal <5 mIU/mL). Serum follicular4 D6 R1 }. Y/ f. a/ u! C0 f
stimulating hormone and leuteinizing hormone% P. D5 q4 T$ P% C* k( g J j7 i9 |
concentrations were less than 0.05 mIU/mL
5 m! s+ E; N! z0 b(prepubertal).9 B: W$ B. `2 D
The parents were notified about the laboratory0 @* F+ v" d2 x: Y' }
results and were informed that all of the tests were
. O: ~" B/ J+ A) _2 w2 h Z- znormal except the testosterone level was high. The
2 Y: |# [+ U X( N. n) R- Ifollow-up visit was arranged within a few weeks to
! L% W1 i1 Y! n" H$ a7 j1 K3 Zobtain testicular and abdominal sonograms; how-: Z( c0 h% S, ?# k6 h/ q
ever, the family did not return for 4 months.
4 f; d. w. H3 j$ n; U# t, q) jPhysical examination at this time revealed that the
, g, V7 _: ]1 d; |. K+ @4 a. E8 Wchild had grown 2.5 cm in 4 months and had gained
8 P" J( E0 T Z$ U! S" \2 kg of weight. Physical examination remained3 v+ X. O9 x: n9 X, v) y) |
unchanged. Surprisingly, the pubic hair almost com-
- k' A X. U0 _' z! s. @! \+ qpletely disappeared except for a few vellous hairs at3 h) X8 C, W. m3 t i4 b5 V
the base of the phallus. Testicular volume was still 2. y3 \" S3 M3 Z2 w
mL, and the size of the penis remained unchanged.( S& k( ~" `( Z/ D9 R' Z4 A
The mother also said that the boy was no longer hav-
4 T" U ~# {4 o/ H1 g# bing frequent erections.. J' `9 h! l) f" A2 ~5 f
Both parents were again questioned about use of
s5 P% H$ u, ]5 @- m% vany ointment/creams that they may have applied to1 R: X3 z5 r* I/ ?! Q1 ~- B
the child’s skin. This time the father admitted the3 D4 S( P; e( q. O9 ~
Topical Testosterone Exposure / Bhowmick et al 541
( k6 {# i+ v" G( xuse of testosterone gel twice daily that he was apply-
, Q1 g/ T8 s5 y# uing over his own shoulders, chest, and back area for
# {5 X E) R; n; H6 T' O1 _4 Sa year. The father also revealed he was embarrassed7 ~) Q7 n. \# k+ _: }, b5 u. m) ]
to disclose that he was using a testosterone gel pre-
- p, d: _' N9 m# j* e& K- s2 n$ {4 Nscribed by his family physician for decreased libido S/ T/ N1 W' \- r
secondary to depression.
3 Q9 t% H, P4 j5 U* L$ H4 H+ VThe child slept in the same bed with parents.# X% Q. p7 d$ {. Y: W
The father would hug the baby and hold him on his) K: o0 X6 E5 i6 a4 m
chest for a considerable period of time, causing sig-
2 m8 g1 l6 V9 q$ f: Unificant bare skin contact between baby and father.
% B9 A2 i3 y7 z( LThe father also admitted that after the phone call,! K- S5 u9 N4 {6 N. V/ ^: g( W# N
when he learned the testosterone level in the baby) i9 j5 p5 U7 s8 |/ B& r% \: V
was high, he then read the product information
) ~# z% P8 c& D8 c, Mpacket and concluded that it was most likely the rea-
5 C7 z7 E) H5 y- j' u s) D, ~( }8 `son for the child’s virilization. At that time, they
. [5 s6 V8 X7 w- V& p, f* a9 pdecided to put the baby in a separate bed, and the. D( K# u* J' f% A
father was not hugging him with bare skin and had
, R; X- Q6 \1 M+ e3 Q1 }9 O: }0 ?been using protective clothing. A repeat testosterone
, n3 D" [- I8 w l0 x0 _test was ordered, but the family did not go to the
b8 h |) z: o: ilaboratory to obtain the test.1 I$ Z, Y% z- o5 m9 n$ t0 w% ~+ x
Discussion
8 i# h# J# d u: u9 `- TPrecocious puberty in boys is defined as secondary2 n5 O- p9 o. b
sexual development before 9 years of age.1,4" G' h @9 Z) o) H
Precocious puberty is termed as central (true) when; s; B6 \- Z( C4 G
it is caused by the premature activation of hypo-
* T) M( d1 V+ g }- X2 Lthalamic pituitary gonadal axis. CPP is more com-7 T2 Y6 F2 a3 c) r0 Y
mon in girls than in boys.1,3 Most boys with CPP
/ @- t# ^1 E# G$ {" mmay have a central nervous system lesion that is# ]. h3 q: Y2 P) Z
responsible for the early activation of the hypothal-
% y V( ]0 u8 ^& Eamic pituitary gonadal axis.1-3 Thus, greater empha-: Q! ^: D5 Z1 d, s" U/ a
sis has been given to neuroradiologic imaging in, O/ g4 D" y: g* J3 Q/ I
boys with precocious puberty. In addition to viril-7 ?& }& q; v- l) V
ization, the clinical hallmark of CPP is the symmet-
; Q6 N% d& T) l% z% ^- Frical testicular growth secondary to stimulation by/ O& D0 b# T! r% v7 q
gonadotropins.1,3
9 V- [+ ~& p3 d3 S ?Gonadotropin-independent peripheral preco-9 I8 z. t5 p3 n! X; q2 W
cious puberty in boys also results from inappropriate# o: \; m3 Q: r( {( J7 H' q9 D
androgenic stimulation from either endogenous or6 q3 u4 z: z- T3 ~' K6 [
exogenous sources, nonpituitary gonadotropin stim-3 K" N$ P8 ?; C r3 x' Q6 [0 k
ulation, and rare activating mutations.3 Virilizing. I; s. l% q) A% b$ } O& g) ]/ b9 ~' v7 s
congenital adrenal hyperplasia producing excessive: Z" r: I: F$ K$ ]' n1 {
adrenal androgens is a common cause of precocious
/ p+ ?1 w. c8 O0 S( E- w( spuberty in boys.3,4
4 s% V" z$ N4 X0 O+ T% vThe most common form of congenital adrenal, V8 H6 M5 a) a2 G6 c" }, a
hyperplasia is the 21-hydroxylase enzyme deficiency.
- L, K1 ^" v% V/ r. c$ z/ \The 11-β hydroxylase deficiency may also result in
" d$ `8 @6 U7 B: F( _excessive adrenal androgen production, and rarely,
+ \4 h }2 q. Oan adrenal tumor may also cause adrenal androgen
; [/ ~5 Q. T% b6 h- e7 d: y; s# m2 O, iexcess.1,3; h/ w0 u0 V0 w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 @+ o: W, h9 _2 \8 ~6 _. w
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; c0 L$ {' t9 s* }9 c3 h$ H2 vA unique entity of male-limited gonadotropin-6 x' J8 B1 S6 P: b2 c
independent precocious puberty, which is also known
0 t5 Y% ^7 k! M- p5 b, r6 N) K8 oas testotoxicosis, may cause precocious puberty at a
" r7 P% x' F, ?( J ^very young age. The physical findings in these boys
l8 k$ |* v2 E3 Y+ A# M0 Xwith this disorder are full pubertal development,0 @& ~- p! m+ H" F
including bilateral testicular growth, similar to boys. ^) D" l4 p3 |. s
with CPP. The gonadotropin levels in this disorder
0 g( s; C* u' N* Zare suppressed to prepubertal levels and do not show5 r; `; Q9 `) L4 [6 h7 b* W
pubertal response of gonadotropin after gonadotropin-
6 b' {- v4 V5 s0 r8 Qreleasing hormone stimulation. This is a sex-linked
6 m& _% A, y" E9 ]* \% o) gautosomal dominant disorder that affects only
8 o7 J" y; X0 G3 y# `6 `: K5 kmales; therefore, other male members of the family
' u3 ], K E0 I" Y# _: Emay have similar precocious puberty.3% ]* M, o& `) p2 ?0 D
In our patient, physical examination was incon- i$ l* ^3 {' [% r/ ~, h# x
sistent with true precocious puberty since his testi-
1 B* ?7 {0 A% t+ Q' Jcles were prepubertal in size. However, testotoxicosis
! ?: Y3 q6 }% l& _% hwas in the differential diagnosis because his father. U1 K5 G5 m: V) f3 m: d/ N7 k
started puberty somewhat early, and occasionally,3 |- O" [& \, L% B5 r
testicular enlargement is not that evident in the
! f9 v8 {: b; A& {6 s: i/ pbeginning of this process.1 In the absence of a neg-
( {6 d5 T8 A9 Mative initial history of androgen exposure, our: f( ^% V" ~- u
biggest concern was virilizing adrenal hyperplasia,
. O% A c/ H, a4 z- j, D$ Xeither 21-hydroxylase deficiency or 11-β hydroxylase2 P( i* a7 j& @# X3 q
deficiency. Those diagnoses were excluded by find-
" ]2 \' ?( S( uing the normal level of adrenal steroids.
E; v }( L1 ]4 k: z3 K3 UThe diagnosis of exogenous androgens was strongly
0 w; Z/ D6 M" y7 {& @; k* v# rsuspected in a follow-up visit after 4 months because% \8 D' n8 C! Q3 j9 y( d7 ~# `
the physical examination revealed the complete disap-8 I9 O( H- D* f. T
pearance of pubic hair, normal growth velocity, and
3 i6 G) ^$ p3 @& j% \, H1 S3 Q! Rdecreased erections. The father admitted using a testos-% g5 O3 I# c% q% X6 v, w
terone gel, which he concealed at first visit. He was- `& x. x: E5 q9 }
using it rather frequently, twice a day. The Physicians’
. ?5 g% x- A* ] h7 kDesk Reference, or package insert of this product, gel or; S3 n) a1 y- v0 F: ~
cream, cautions about dermal testosterone transfer to
% @, U3 n2 n8 g$ h- l) N# Z: [; f+ Hunprotected females through direct skin exposure.
; U/ a3 |5 P5 }- F/ ~: F) y. Y: }# x( {Serum testosterone level was found to be 2 times the' y1 R+ d* a. ?1 u9 y% S7 v
baseline value in those females who were exposed to
( R8 H2 m6 i' H* N1 G8 ~2 oeven 15 minutes of direct skin contact with their male& E' _1 o3 `( ]! B, f' |
partners.6 However, when a shirt covered the applica-) d: Z% M5 R( @9 o
tion site, this testosterone transfer was prevented.
9 e5 W9 r- z! Z; M4 `* ^Our patient’s testosterone level was 60 ng/mL,# P/ f1 ?% I5 W8 d
which was clearly high. Some studies suggest that. u9 J; d6 |: ^6 k6 j
dermal conversion of testosterone to dihydrotestos-
& _) w" M$ K( E `- H, yterone, which is a more potent metabolite, is more
! I3 L7 I1 e# R4 o7 g0 Hactive in young children exposed to testosterone
0 B; a* ^ C; ^3 n& kexogenously7; however, we did not measure a dihy-" }; f6 ^ q5 z+ }9 u1 ?3 q
drotestosterone level in our patient. In addition to0 y! F$ N# C5 H) p
virilization, exposure to exogenous testosterone in
5 t# w% ?+ B& A W/ j- Pchildren results in an increase in growth velocity and, F2 F; B* R: D: ]! |( A. t
advanced bone age, as seen in our patient.
5 b% x+ l# l8 f5 u. cThe long-term effect of androgen exposure during# K+ J: Q+ @- ]+ O% L; a0 y
early childhood on pubertal development and final8 [* k+ X: S; { m4 q: Y; t4 y4 @
adult height are not fully known and always remain/ V0 O+ }: X" c- {. u L$ I
a concern. Children treated with short-term testos-
) W1 s$ y+ [: g9 P/ K* [: dterone injection or topical androgen may exhibit some0 }; S' l1 b/ m( g9 R' A
acceleration of the skeletal maturation; however, after
. |+ r7 X6 [- X, Y! i: I9 fcessation of treatment, the rate of bone maturation) {; d2 G( q# ?/ p! @( F7 z
decelerates and gradually returns to normal.8,9! J6 ^% @: o- Y( h! t
There are conflicting reports and controversy% E+ |2 [* B3 \
over the effect of early androgen exposure on adult
8 F" i% u1 Z: e: I0 mpenile length.10,11 Some reports suggest subnormal
5 I5 i# L5 C( Ladult penile length, apparently because of downreg-
0 c9 z& D: y- A" m- Q% z/ m2 N, @ulation of androgen receptor number.10,12 However,( J ~+ y" h$ q) I7 S* l) q; \8 S
Sutherland et al13 did not find a correlation between4 i9 P: R. z, R% A% n
childhood testosterone exposure and reduced adult, I6 d% B% \6 M) P- k' L
penile length in clinical studies.
/ C7 n# e9 v+ P) d9 X0 \+ C: u. ?Nonetheless, we do not believe our patient is
* R. y; j7 V0 r3 Xgoing to experience any of the untoward effects from1 t; w8 ^9 @( p- s9 b
testosterone exposure as mentioned earlier because& d C0 h: \5 h. p
the exposure was not for a prolonged period of time.
7 A0 A/ l% N5 C2 {' hAlthough the bone age was advanced at the time of9 K- U7 Q: l' P. m" {# X: T6 b+ t
diagnosis, the child had a normal growth velocity at. G2 H6 D: n! [: N3 J3 _+ \
the follow-up visit. It is hoped that his final adult
7 w( C& S' j; _0 Hheight will not be affected.% j$ K, t* O% {: w; P
Although rarely reported, the widespread avail-& _2 `# A# m$ t; K3 u$ V
ability of androgen products in our society may
0 Z# o+ ` F# N5 f* b1 u& Pindeed cause more virilization in male or female
" Y+ l. Q( O; U5 Cchildren than one would realize. Exposure to andro-
* F6 l) x! V F4 n. Jgen products must be considered and specific ques-- J5 c. i8 g- J$ `) ]/ o3 J
tioning about the use of a testosterone product or
1 b! w8 [4 ~' h! i+ Z5 Ngel should be asked of the family members during
) O( [( h3 V7 C5 } zthe evaluation of any children who present with vir-1 \: u3 j$ o4 U) j) I) E4 E
ilization or peripheral precocious puberty. The diag-" B( z* U: \( I) ]- u3 `
nosis can be established by just a few tests and by% P+ Q q6 t* D3 b" |% `3 u d
appropriate history. The inability to obtain such a4 V5 ]7 H# c! }
history, or failure to ask the specific questions, may! D, d$ c. d7 O
result in extensive, unnecessary, and expensive
7 A4 b+ V) S0 vinvestigation. The primary care physician should be& ?1 @) } V5 p0 ?0 V! F+ U/ s
aware of this fact, because most of these children3 d) M- l- h# U, d7 z, E
may initially present in their practice. The Physicians’: Z+ n! ~7 u% x
Desk Reference and package insert should also put a
4 p2 z1 O0 I; O0 n1 Jwarning about the virilizing effect on a male or
, Y% T0 }5 s. p7 b9 a. xfemale child who might come in contact with some-0 M) G. i6 a' B2 b q' ^6 ?
one using any of these products.6 v- y( z5 v/ t" a7 C
References, G& _6 w# Q8 k. o9 g* A
1. Styne DM. The testes: disorder of sexual differentiation F) |3 K. g9 `
and puberty in the male. In: Sperling MA, ed. Pediatric# M9 ~5 b4 f/ `& B) m
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ o* C7 @' \# [+ `* Y. s5 L2002: 565-628.* W' K& |3 ?1 J1 A) L* e- |
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& ~ x1 Y8 ]+ a3 B' x% o7 q! q2 spuberty in children with tumours of the suprasellar pineal |
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