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Sexual Precocity in a 16-Month-Old+ M" ?" W, r5 O6 x4 |
Boy Induced by Indirect Topical
: c' y( R( R2 J4 sExposure to Testosterone+ z! k# U- F) R% u) _1 a! [3 ]& K
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. t" |- ] P3 M4 @7 {
and Kenneth R. Rettig, MD13 |7 |) v# o0 N
Clinical Pediatrics9 U% G9 p, P% a9 w
Volume 46 Number 6
9 f2 _! i1 M# KJuly 2007 540-543+ V+ @ s3 m) B8 t% ^; t& w% e/ F
© 2007 Sage Publications7 W( e8 E- n! C0 g9 a' f0 `
10.1177/0009922806296651$ l6 Y. G4 ?9 J- `1 s
http://clp.sagepub.com9 w0 P8 f6 }8 h" ~4 U
hosted at4 J0 ?) s4 o7 S0 n
http://online.sagepub.com
; ^$ i" `% J! \Precocious puberty in boys, central or peripheral,5 S" g& B5 }4 u3 v7 C
is a significant concern for physicians. Central
! W+ R- D6 g4 i2 T2 nprecocious puberty (CPP), which is mediated. @2 R* u B6 O
through the hypothalamic pituitary gonadal axis, has6 q. ^' f3 ~6 H) ~9 m% M, u
a higher incidence of organic central nervous system
& u( n) c0 }! V$ l L: v+ Jlesions in boys.1,2 Virilization in boys, as manifested6 q# L8 m$ x$ b. T0 e, ^
by enlargement of the penis, development of pubic
- P1 J0 x4 o5 o/ O7 u! ?hair, and facial acne without enlargement of testi-* ]# h8 I! a) u) j0 }3 K' N: z/ E
cles, suggests peripheral or pseudopuberty.1-3 We
{/ J. O `! `# e- y6 Q3 A* m2 {report a 16-month-old boy who presented with the& f1 v/ b; |+ \
enlargement of the phallus and pubic hair develop-% Z# E7 T: h8 a9 w+ C
ment without testicular enlargement, which was due
' g e; C8 E% J4 U- y0 Ito the unintentional exposure to androgen gel used by
9 V* {) c) p5 |0 ]0 Jthe father. The family initially concealed this infor-
/ T8 e: c* ?& Rmation, resulting in an extensive work-up for this5 o2 r. V. t1 m- M+ |
child. Given the widespread and easy availability of
; h9 D( I2 i' F a5 k% atestosterone gel and cream, we believe this is proba-% ~0 R6 _ z p* G
bly more common than the rare case report in the
5 M6 n& a& V* o& c& bliterature.40 V* U$ j: G9 S6 _ c
Patient Report) c4 o: q8 t9 y8 Q. ^: g; S+ h9 u4 `, X/ o
A 16-month-old white child was referred to the# u/ h6 d l+ F, t( v, m
endocrine clinic by his pediatrician with the concern, r$ d" c/ O" A/ I; b
of early sexual development. His mother noticed6 a; H. z' z% C" F& f- M5 f. v7 t
light colored pubic hair development when he was" I& |4 J1 D& j# C/ [6 H
From the 1Division of Pediatric Endocrinology, 2University of
6 B: g7 y' f6 p' t/ ~South Alabama Medical Center, Mobile, Alabama.
! m9 D" V1 m! A1 iAddress correspondence to: Samar K. Bhowmick, MD, FACE,& k' w" C. j9 u$ y& \+ _
Professor of Pediatrics, University of South Alabama, College of
& ]+ q! z4 m0 Y- p( q' g' v. VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. q: e2 ~. c1 ~# a8 k
e-mail: [email protected].
9 e9 W7 E0 \8 C) N2 C2 r( b6 w6 kabout 6 to 7 months old, which progressively became0 N \/ ?; s6 ]; O) Y/ H7 n
darker. She was also concerned about the enlarge-" p: Z! o, w0 C# @
ment of his penis and frequent erections. The child
: r( _/ g& Y+ twas the product of a full-term normal delivery, with( s& |* B, V, y& G
a birth weight of 7 lb 14 oz, and birth length of# r, @7 w9 _( a, h' }
20 inches. He was breast-fed throughout the first year$ L$ H1 B A- J G
of life and was still receiving breast milk along with& M2 e: p* f2 m m! [/ B- F
solid food. He had no hospitalizations or surgery,7 D/ _, r. l. i/ O$ E; ^6 \
and his psychosocial and psychomotor development# L8 M, r6 e4 N" u) @$ C
was age appropriate.8 z, m! J" o8 Q$ m D" o4 N2 L
The family history was remarkable for the father,
3 O. h, x! |3 J- r% q: n, Rwho was diagnosed with hypothyroidism at age 16,5 N+ W1 C& e& p w' Q7 V
which was treated with thyroxine. The father’s! n$ R8 R) a* W6 R# ~: U
height was 6 feet, and he went through a somewhat
A9 `; W7 W0 @early puberty and had stopped growing by age 14.
- D) i8 N: r2 S. W% fThe father denied taking any other medication. The
* l0 Z1 _, G! K. qchild’s mother was in good health. Her menarche1 s' w J* M0 J4 |# N, S8 a. P3 e
was at 11 years of age, and her height was at 5 feet ?5 p) @6 h! P8 l1 P/ k- R& Z4 ]( I
5 inches. There was no other family history of pre-0 h, f* F1 B' ?$ C, g3 K1 h
cocious sexual development in the first-degree rela-. m0 M; N$ s, A+ h6 i
tives. There were no siblings.
3 v3 H# f% i$ g4 d) B+ B9 TPhysical Examination
) u8 h$ j& h$ \; {+ \! }8 `) yThe physical examination revealed a very active,
`3 h3 S" \* O, V* o4 Nplayful, and healthy boy. The vital signs documented
5 Z& m8 Z/ y& ^; t, x$ ^6 y s1 ka blood pressure of 85/50 mm Hg, his length was" d" z2 R6 J- ~5 @
90 cm (>97th percentile), and his weight was 14.4 kg, @# T% f4 ~+ n/ z- c
(also >97th percentile). The observed yearly growth
( W( ^2 V8 B! e e7 Q5 t0 Avelocity was 30 cm (12 inches). The examination of
1 l' t6 ~. J4 b! n, M1 z5 K/ athe neck revealed no thyroid enlargement.5 Q. i; x) l$ b; f0 z
The genitourinary examination was remarkable for
4 i0 Q; n" P, A- G: Henlargement of the penis, with a stretched length of3 x4 ~- U" t. Z" P+ K
8 cm and a width of 2 cm. The glans penis was very well
Y. n M: ^( M7 b9 s; x% [developed. The pubic hair was Tanner II, mostly around
1 q0 \' w( g" a' Y H' j! G540
. E7 g9 i- ~) L4 {. Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 ~) g% D- h9 Q$ T4 w# Qthe base of the phallus and was dark and curled. The- {- g2 {7 o8 g0 p
testicular volume was prepubertal at 2 mL each.
( G8 D! z/ x4 ^$ p4 t3 E* |1 EThe skin was moist and smooth and somewhat
. M, S- f. A% ^1 C) A% uoily. No axillary hair was noted. There were no) @9 c5 ]' X% O9 k. z
abnormal skin pigmentations or café-au-lait spots.
# h) o, @+ G5 Y* SNeurologic evaluation showed deep tendon reflex 2+7 @1 m2 q& J' k1 @5 F* w9 r
bilateral and symmetrical. There was no suggestion; S# W3 c) c$ a1 [/ v4 N
of papilledema.
3 ?3 U+ C8 w/ z! TLaboratory Evaluation- r. l- ]5 \0 s0 D) V! ~9 K7 F+ _
The bone age was consistent with 28 months by9 d- f x7 s9 F# U& k4 e8 ~
using the standard of Greulich and Pyle at a chrono-9 Z" N5 M* E3 f1 w0 E4 W
logic age of 16 months (advanced).5 Chromosomal
7 ?) E7 S5 G- K" a4 S) Pkaryotype was 46XY. The thyroid function test
. a8 f/ ]- O" @showed a free T4 of 1.69 ng/dL, and thyroid stimu-3 K x; {% g: M. s; a
lating hormone level was 1.3 µIU/mL (both normal).
4 b# q) s6 a) Y \% {0 M. Y6 C+ xThe concentrations of serum electrolytes, blood5 k0 ], h" ~& Z3 d6 ?& s) M5 G7 ?
urea nitrogen, creatinine, and calcium all were& i4 a* ^5 ~7 L2 _2 K, I
within normal range for his age. The concentration" J5 T0 |& {& X: U$ p
of serum 17-hydroxyprogesterone was 16 ng/dL) M" s8 R* @! J) P# O @
(normal, 3 to 90 ng/dL), androstenedione was 204 x) m0 Z7 u$ |; T. M- f4 k
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# W) [4 u4 ? ]& D8 L! F* F' y8 o# b
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
- k1 O" k6 c( ?6 ?3 Ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to
! q8 J" y+ [5 Y! |7 c49ng/dL), 11-desoxycortisol (specific compound S)$ u) M$ [% m. X/ k9 y- t
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
6 `% [/ b A0 E4 v' y/ {2 xtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
# ]& h5 _/ D" }6 _- F! mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 W9 G+ D6 L1 s
and β-human chorionic gonadotropin was less than3 c, t/ z" P# p5 m/ w N3 X
5 mIU/mL (normal <5 mIU/mL). Serum follicular6 i, k) E2 t4 q# D* ]
stimulating hormone and leuteinizing hormone
+ i. |7 f P+ X, j) R, a6 f1 ]6 ^concentrations were less than 0.05 mIU/mL
( o% d, ?5 ~, A* I0 J(prepubertal).
/ J: p7 T5 ]- m0 a# D" |The parents were notified about the laboratory: M6 ^. c+ D$ E3 q9 ]! U8 V8 d
results and were informed that all of the tests were
8 F: y" K; J- z; |; m* [normal except the testosterone level was high. The
4 |. j" w) s9 \+ E3 rfollow-up visit was arranged within a few weeks to
8 y* V( [+ ^! t/ U1 jobtain testicular and abdominal sonograms; how-, O$ \& ^+ G% j% O5 _# O, B) ?
ever, the family did not return for 4 months.
# B3 C0 O( u ^0 [! hPhysical examination at this time revealed that the0 Z3 P+ c! m$ m# O6 E' M6 a
child had grown 2.5 cm in 4 months and had gained! ~; w1 r$ t' U' Y* o6 R r/ L1 o: {
2 kg of weight. Physical examination remained7 U2 J6 I- R& o H6 ?+ t
unchanged. Surprisingly, the pubic hair almost com-3 B" B+ O8 {3 f9 q& Y$ I3 Y; Z
pletely disappeared except for a few vellous hairs at
9 z0 i8 ~0 G) O0 Lthe base of the phallus. Testicular volume was still 24 H H7 E* s: e7 z7 A6 u3 f& z
mL, and the size of the penis remained unchanged.2 I( q/ }! M' B
The mother also said that the boy was no longer hav-3 f5 i- J! Q% P& V, Q, L/ F
ing frequent erections.
3 @( d0 D r) H5 Q! ZBoth parents were again questioned about use of
# K+ l0 M! h d# L f4 R/ _any ointment/creams that they may have applied to1 k- l1 T( _0 T' P
the child’s skin. This time the father admitted the
+ L/ ^) C! W- a0 H9 e. }+ eTopical Testosterone Exposure / Bhowmick et al 541
; E& L7 |9 [ Y9 huse of testosterone gel twice daily that he was apply-; r/ ]6 N1 I$ x# {* k3 R3 F+ [
ing over his own shoulders, chest, and back area for: ~# B: l& I9 w3 a! E$ e& l
a year. The father also revealed he was embarrassed; b* R! R$ Z$ {; f
to disclose that he was using a testosterone gel pre-$ n9 C* g3 V7 e+ E8 @8 [% r4 n
scribed by his family physician for decreased libido
: \& X( A. {$ E, I/ wsecondary to depression.9 _6 M5 j( d4 D! W' \: f: t' Y' I( J
The child slept in the same bed with parents., V& C# @& |! a# d$ }
The father would hug the baby and hold him on his$ Z0 |/ m; S5 S* k; N1 b8 J
chest for a considerable period of time, causing sig-" c1 A. J! D; u0 u4 W
nificant bare skin contact between baby and father.& A3 ~' l& x$ k8 \4 |
The father also admitted that after the phone call,# X( E- x& v6 f3 w3 U% s( V- |; i
when he learned the testosterone level in the baby( Y! I4 v/ H' O* O
was high, he then read the product information( j s2 X' X# R2 g7 ]
packet and concluded that it was most likely the rea-
7 z5 z! i2 s& ~, x) Bson for the child’s virilization. At that time, they
4 D4 {: M' u2 S6 idecided to put the baby in a separate bed, and the
$ {% ?3 `+ Z$ j5 l. Zfather was not hugging him with bare skin and had
1 S9 ]+ I! x- Bbeen using protective clothing. A repeat testosterone
6 L* w7 G8 M& R0 ]: l. {" y/ Ktest was ordered, but the family did not go to the& g1 J* m2 |. u) l3 j Q5 `1 J8 P
laboratory to obtain the test.9 c' ]& F# j$ m) A
Discussion
% x8 v& G: e8 w6 m' G+ e4 kPrecocious puberty in boys is defined as secondary
) v* P8 w) o1 }$ dsexual development before 9 years of age.1,4( }$ H0 Y2 _/ R, H1 n
Precocious puberty is termed as central (true) when
0 O8 c# i B! P9 Lit is caused by the premature activation of hypo-( i8 O; A* `3 @3 [" `( C1 R
thalamic pituitary gonadal axis. CPP is more com-
u* T8 {& M2 _2 a2 X6 @" D! H) kmon in girls than in boys.1,3 Most boys with CPP
3 }. m' c. Q: H Q# P' |may have a central nervous system lesion that is# K1 T! G/ v. ]- Z1 U, i0 w
responsible for the early activation of the hypothal-+ k# j$ }! V9 }0 X4 W4 k
amic pituitary gonadal axis.1-3 Thus, greater empha-# r p& Z# i% w- a9 N
sis has been given to neuroradiologic imaging in! |+ f) K6 ?! c$ a$ L( W
boys with precocious puberty. In addition to viril-9 Z$ m! V9 s- q& z( a/ y
ization, the clinical hallmark of CPP is the symmet-3 p7 ^' N' c* X i, [% S
rical testicular growth secondary to stimulation by+ T) c+ F: c! u! l+ c, [
gonadotropins.1,3- l# J4 T* B% [* [- u1 n
Gonadotropin-independent peripheral preco-
3 ?3 g6 x5 B8 @2 ^8 {/ mcious puberty in boys also results from inappropriate
5 K |# W" O9 {3 sandrogenic stimulation from either endogenous or
0 L* H P z. r( b; Zexogenous sources, nonpituitary gonadotropin stim-, _3 k h/ P1 w2 I; G% v
ulation, and rare activating mutations.3 Virilizing3 [5 `4 W3 ]' Y
congenital adrenal hyperplasia producing excessive
& F* K' k4 }1 ]- ^% Ladrenal androgens is a common cause of precocious
$ E( k6 A3 V w5 W( {! y: Wpuberty in boys.3,44 N/ @ K6 ^8 s1 ? U, D
The most common form of congenital adrenal$ ^. b3 D0 P, I) L1 i' W
hyperplasia is the 21-hydroxylase enzyme deficiency.4 ]3 [, {: y* Z0 y/ X9 T$ T
The 11-β hydroxylase deficiency may also result in
* A6 ~( N8 z! K8 oexcessive adrenal androgen production, and rarely,
+ Z4 w [4 v% D7 kan adrenal tumor may also cause adrenal androgen
: \3 t* J, o- J: z+ o' d! fexcess.1,3
4 S1 p; u: l& s2 Hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# \( J: _3 }3 `$ p
542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 [) R1 f7 k4 ?% [2 c; p
A unique entity of male-limited gonadotropin-$ a+ y \0 X, ?$ t( q' C& U9 P
independent precocious puberty, which is also known9 U8 D3 e, I; M- ~% L" a
as testotoxicosis, may cause precocious puberty at a0 m3 a$ n3 ^8 v! s. A% g
very young age. The physical findings in these boys0 V1 R- W) u7 V2 _7 h0 J5 w9 x8 F9 ?
with this disorder are full pubertal development,
" t3 z; z3 W* ?including bilateral testicular growth, similar to boys- p$ t- U' ^# x' r
with CPP. The gonadotropin levels in this disorder: l' t X. _; @* Q, I' L: @5 j
are suppressed to prepubertal levels and do not show% N5 \9 C: @; U6 }) G! z u" n# @
pubertal response of gonadotropin after gonadotropin-
7 M3 h2 V$ s! E1 o. |, e) T3 z* b9 `) Zreleasing hormone stimulation. This is a sex-linked
3 x7 m G s- Y5 j! Mautosomal dominant disorder that affects only
- I5 V# J6 V) w2 E- _. E% ~males; therefore, other male members of the family# H* _ W/ v0 t) h- T
may have similar precocious puberty.3" `: v+ z0 _3 v. o! m9 [ R
In our patient, physical examination was incon-
5 s5 j& M! N) t, A0 d6 N: d/ ?sistent with true precocious puberty since his testi-( B7 U+ `/ |! N7 T* h
cles were prepubertal in size. However, testotoxicosis7 J" F E2 J7 r- I5 g: T
was in the differential diagnosis because his father
5 P' I% v- A# a# X& }6 X6 Ustarted puberty somewhat early, and occasionally,
x. M( }; a8 U- Gtesticular enlargement is not that evident in the
, G4 W; k' m7 ibeginning of this process.1 In the absence of a neg-
! ^. G4 @& W- |/ Y: P4 @' iative initial history of androgen exposure, our2 v8 W! p$ K$ e5 N& L7 a: B4 f
biggest concern was virilizing adrenal hyperplasia,! A& d6 j0 \" l" D- \; h5 Z
either 21-hydroxylase deficiency or 11-β hydroxylase
2 T" V$ R# o7 O2 W- X _- Bdeficiency. Those diagnoses were excluded by find-
) a) ]- I& T; c: Y1 T% V. v3 Aing the normal level of adrenal steroids.
, o$ E+ w3 g' k8 |The diagnosis of exogenous androgens was strongly
' S- k% ?( [9 P. H% z7 {suspected in a follow-up visit after 4 months because4 E$ s. w; U9 T" B1 l
the physical examination revealed the complete disap-
% Y3 U0 B/ e4 Q3 W: O3 |( ?+ u2 ^pearance of pubic hair, normal growth velocity, and
. i3 ~* h$ T' e& }decreased erections. The father admitted using a testos-* v3 O+ V9 z1 V$ x0 F6 O* Q4 Q
terone gel, which he concealed at first visit. He was! l2 B7 O: y7 w* ~4 y5 Q- M$ u
using it rather frequently, twice a day. The Physicians’
' }. Z% G. t! N: }Desk Reference, or package insert of this product, gel or
5 j) Q8 X4 a: e; A; K/ G' B5 Mcream, cautions about dermal testosterone transfer to' O' q7 a h/ w# P( J
unprotected females through direct skin exposure.
5 Y+ H# `, {9 B& oSerum testosterone level was found to be 2 times the( L) G) |" m4 D
baseline value in those females who were exposed to: @. n5 E! K! n5 j/ b
even 15 minutes of direct skin contact with their male
* P- J2 |9 J4 r/ i0 a3 E4 y$ R* tpartners.6 However, when a shirt covered the applica-
$ P% F. c) v& m! j6 Qtion site, this testosterone transfer was prevented.. {4 \& U1 r" U+ I
Our patient’s testosterone level was 60 ng/mL,* H& v; d; D! X. ?
which was clearly high. Some studies suggest that
; f- s# K1 }6 _4 W& k! N, cdermal conversion of testosterone to dihydrotestos-
) Y6 J! M# j0 J; e4 m, mterone, which is a more potent metabolite, is more# i4 A; h% X# j# ~
active in young children exposed to testosterone( O! _# j6 G1 O3 b0 u4 A8 m/ T
exogenously7; however, we did not measure a dihy-
5 D- B: J5 Z( y3 K6 jdrotestosterone level in our patient. In addition to; ], \& N! e U6 U# A
virilization, exposure to exogenous testosterone in
" |3 a9 n4 ?: }$ schildren results in an increase in growth velocity and. f; {. H5 a1 \' P# _3 H
advanced bone age, as seen in our patient.
- ?- ]# D! ?! `1 H, \The long-term effect of androgen exposure during% d+ a- t v) n5 E4 q
early childhood on pubertal development and final
( y9 Y N1 i$ J9 ^0 ~adult height are not fully known and always remain
7 D* W6 R. }( J* G' Ma concern. Children treated with short-term testos-$ h) F9 b4 N: f
terone injection or topical androgen may exhibit some( |# I; X9 ^) q, P2 Y
acceleration of the skeletal maturation; however, after
9 m' ^9 O# T) c5 h1 `+ Kcessation of treatment, the rate of bone maturation5 F8 U1 }* _ q/ r6 x1 J
decelerates and gradually returns to normal.8,9& o0 B5 J% u9 D3 ^, v, [
There are conflicting reports and controversy
9 b- T6 e+ m% @3 P# T5 L& cover the effect of early androgen exposure on adult8 D' R+ I# t7 i0 j/ `* }: M0 y* |# B1 p
penile length.10,11 Some reports suggest subnormal) d; q1 R) m% @( C8 z, i# \ j. B6 D
adult penile length, apparently because of downreg-7 l5 i7 F- z! S5 X4 m% G
ulation of androgen receptor number.10,12 However,
" r; U0 T7 n t3 bSutherland et al13 did not find a correlation between$ Z3 G9 {6 j1 _- _) ]
childhood testosterone exposure and reduced adult* _2 H- s7 r' }9 a, o% G0 x
penile length in clinical studies.
. P0 `, S0 ?. [ E6 l( A3 yNonetheless, we do not believe our patient is5 V1 f* T) R& u5 P8 O0 s* K
going to experience any of the untoward effects from
* k4 r1 N2 b- s8 ]* p9 P7 Ttestosterone exposure as mentioned earlier because$ E! X- M& r' x4 \
the exposure was not for a prolonged period of time./ K7 O9 Q& t6 d/ u8 g+ m
Although the bone age was advanced at the time of" Y7 f& x4 }: J2 n' e; n
diagnosis, the child had a normal growth velocity at9 l: o# o/ I, G7 G, A/ v, ]$ @; O
the follow-up visit. It is hoped that his final adult' t0 P2 ~& e3 `
height will not be affected.
" y: F/ `% y6 X; |5 b( y+ o+ B- N5 ZAlthough rarely reported, the widespread avail-
) _$ |( Q; s, B6 b: B* B3 iability of androgen products in our society may+ b) M: Y8 r" G! P# H9 ]' o g
indeed cause more virilization in male or female: r/ x. p9 {1 n
children than one would realize. Exposure to andro-
' f' }6 {4 i p+ i4 g5 n, M- ]gen products must be considered and specific ques-6 K4 A( |) G% }0 V
tioning about the use of a testosterone product or) W- W9 m+ @, W5 ]- c
gel should be asked of the family members during- e/ j @1 B9 l4 k
the evaluation of any children who present with vir-
* z, y: q2 E7 C' R! B5 tilization or peripheral precocious puberty. The diag-6 n- @$ m- `$ [2 e) x
nosis can be established by just a few tests and by- O$ ~+ C) S' o9 H1 r0 H( N" D
appropriate history. The inability to obtain such a
" z! d; Q( q% z' B; Lhistory, or failure to ask the specific questions, may: Y9 C) e! O# m" D3 I5 h) L
result in extensive, unnecessary, and expensive
& F6 o. Y, O3 \# K& yinvestigation. The primary care physician should be
3 V+ g* j( y- F$ f Oaware of this fact, because most of these children- i+ y/ O. K; b4 }! g$ R) k
may initially present in their practice. The Physicians’
& J' _# Y8 G- q5 O( LDesk Reference and package insert should also put a6 H, O; K6 x$ Q Q- S' \
warning about the virilizing effect on a male or
# e |5 ~+ G* s( C+ Bfemale child who might come in contact with some-
6 s+ W! \6 a1 done using any of these products.
1 P/ y; U0 f8 w- ~0 d2 pReferences
3 D! F- K! v4 Z+ d/ r7 C7 U/ `1. Styne DM. The testes: disorder of sexual differentiation
- q8 ?' g" [5 @5 J( B! r6 ^2 D9 Mand puberty in the male. In: Sperling MA, ed. Pediatric
$ I0 i; p& Y0 o; B: YEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 a! ^& g* r9 |/ `, w2002: 565-628.
4 o5 e, B: O: @' h1 n9 x+ O$ Z5 f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
; Y9 M- {0 [( r H7 ~; A* H' Fpuberty in children with tumours of the suprasellar pineal |
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