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Sexual Precocity in a 16-Month-Old
2 t* [+ x/ L* o. N$ l$ G) {8 JBoy Induced by Indirect Topical4 ~7 f$ u# G r$ L) Q' K
Exposure to Testosterone
5 j7 K' Z) k$ U7 @) u# }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
n& J6 [! n9 q4 ]; e; tand Kenneth R. Rettig, MD1, C* ^/ @6 D2 t1 W4 Z
Clinical Pediatrics0 S$ ]! [+ M( ]* r
Volume 46 Number 6: h5 c/ z, f1 _) p' W6 ^0 K
July 2007 540-543
4 S. `! t4 v" N' M/ w© 2007 Sage Publications( D+ Y" G2 s0 D$ \% ]3 w2 e
10.1177/0009922806296651( t, g+ t r0 Z1 Y# H
http://clp.sagepub.com6 d! T* d1 Y" @/ f6 {* K
hosted at5 s, k0 |0 f/ Y6 A' b
http://online.sagepub.com
3 t5 ^( j) Y: f! Q$ i; lPrecocious puberty in boys, central or peripheral,1 A$ w4 B+ U1 g* s
is a significant concern for physicians. Central# X9 N0 Z. A# x1 R' k. W
precocious puberty (CPP), which is mediated; @ |* J! {* \: W) \6 m% L" F. v
through the hypothalamic pituitary gonadal axis, has1 X7 R8 J' w. l" m: d8 ?6 W
a higher incidence of organic central nervous system! B( L4 l4 o5 |% ~& u$ f* K# `3 p8 d
lesions in boys.1,2 Virilization in boys, as manifested8 R4 e. y& J/ c# j& a. M
by enlargement of the penis, development of pubic
0 a; v; {1 l7 ]2 s0 V8 Qhair, and facial acne without enlargement of testi-/ I+ O! V* N2 W
cles, suggests peripheral or pseudopuberty.1-3 We
( h; }# Q; s8 o5 E5 I$ Y8 B8 jreport a 16-month-old boy who presented with the
4 `. h1 E3 i5 U: i# L, \4 Z+ t. ] aenlargement of the phallus and pubic hair develop-
9 U5 C" S8 g% {5 mment without testicular enlargement, which was due
2 Y- |/ U5 w* N4 Y3 Qto the unintentional exposure to androgen gel used by
5 u3 _2 Q# {; w; x# J) Ethe father. The family initially concealed this infor- ?9 z' b! M! L, Z9 |+ ~
mation, resulting in an extensive work-up for this! w0 n" k5 v' G
child. Given the widespread and easy availability of
~/ T) z, [" ~; Y' H: B. m# }" }testosterone gel and cream, we believe this is proba-
! h8 V# z8 M+ n* R' m6 A" u' ably more common than the rare case report in the+ t4 Y+ J: R4 L) Z$ r# \: }; n% _
literature.4
1 F1 u" `& ? HPatient Report$ r% [( D% V) ]
A 16-month-old white child was referred to the- e& I5 K2 n# D8 ?) O- ^6 N
endocrine clinic by his pediatrician with the concern
3 ]$ e4 w; n+ m9 e' H, g- ]of early sexual development. His mother noticed' I5 ]' p0 y6 l: A
light colored pubic hair development when he was, W1 [8 m$ h& x# S" @. L9 O
From the 1Division of Pediatric Endocrinology, 2University of. L' Z7 S1 B+ A, G+ ~" ^; Z8 a" W
South Alabama Medical Center, Mobile, Alabama.( |2 g x* x; ^$ R$ t
Address correspondence to: Samar K. Bhowmick, MD, FACE,1 P7 K. F% R; x0 a2 B' D
Professor of Pediatrics, University of South Alabama, College of
# n" i" L$ z: w+ F* w# J# z3 ~+ UMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) t5 e6 i; z) d; z5 te-mail: [email protected].5 E4 J* i7 ~/ K. |8 y8 G, j
about 6 to 7 months old, which progressively became8 D& s7 I0 u- j0 @
darker. She was also concerned about the enlarge-, m1 |4 {$ u& N, r- [0 A5 p4 C% C
ment of his penis and frequent erections. The child
: `& ^6 ]. [7 ~* A2 [was the product of a full-term normal delivery, with
4 T' X% W, S1 \: T( _) J3 ^- o3 ia birth weight of 7 lb 14 oz, and birth length of
+ h b0 u, L9 y _# j6 Y' [20 inches. He was breast-fed throughout the first year3 M( Z. H0 B, z9 H" y* x
of life and was still receiving breast milk along with' |$ P; S+ Z0 l0 G7 i: f
solid food. He had no hospitalizations or surgery,3 ^3 Z+ y* l# a+ |
and his psychosocial and psychomotor development
% Y6 c: k3 e* m4 @- G, | o! lwas age appropriate.
{; K3 O$ D7 A' X$ fThe family history was remarkable for the father,
& w: a1 W# o. V; `4 Lwho was diagnosed with hypothyroidism at age 16,
7 y4 \4 e( `7 e2 w9 B0 O# ^; Xwhich was treated with thyroxine. The father’s
. \) n9 N$ o* k8 theight was 6 feet, and he went through a somewhat
2 w2 O- m6 L# ^# c7 Oearly puberty and had stopped growing by age 14.% C- u. f$ x6 ]/ { T( ]
The father denied taking any other medication. The( w+ U& H0 J5 K
child’s mother was in good health. Her menarche, [! g9 H l* T* a+ n
was at 11 years of age, and her height was at 5 feet
7 C8 b/ t8 b3 w2 c6 L# G$ K4 v5 inches. There was no other family history of pre-8 i7 T$ Z+ ?' U) t" j; w/ f5 b, m
cocious sexual development in the first-degree rela-
+ ^# A" R& H0 k. n3 u' v" z9 xtives. There were no siblings.( j) d2 i0 ^2 c z4 a$ O
Physical Examination
: M8 ]# ~! C w3 s% qThe physical examination revealed a very active,' c8 n& z- d3 S2 d
playful, and healthy boy. The vital signs documented
|( V6 `2 N1 O) Z' Ea blood pressure of 85/50 mm Hg, his length was9 @# M: L0 x: Y- b, B _% F; Z
90 cm (>97th percentile), and his weight was 14.4 kg
5 K- |) Z) S Z1 I: x(also >97th percentile). The observed yearly growth
* A {' Z, m! Q+ k; z% H& {7 O; Avelocity was 30 cm (12 inches). The examination of
' `$ C3 V8 s) M1 Z- x$ V: i1 @6 ithe neck revealed no thyroid enlargement.. `. ^, n& `- }/ n! P4 W# U
The genitourinary examination was remarkable for L, A# n9 ]* Q. O
enlargement of the penis, with a stretched length of, E' R: O! J2 m% _' U
8 cm and a width of 2 cm. The glans penis was very well! q; d2 l' v8 x- \) k5 ?
developed. The pubic hair was Tanner II, mostly around
: H2 x$ r5 V4 I* w' Y540- V. Q3 M) Q$ i0 z$ ?2 V- I" W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
j' j' e: i9 H" ?! I+ n: C) ^; _, o5 zthe base of the phallus and was dark and curled. The% k" M! ~* A+ _2 t5 w
testicular volume was prepubertal at 2 mL each." v9 m+ g9 W+ A, l8 u9 i, z
The skin was moist and smooth and somewhat
4 Z4 u3 h' N+ ^4 R& N) ioily. No axillary hair was noted. There were no
7 s& w ] o0 M" J$ w+ w6 Uabnormal skin pigmentations or café-au-lait spots.
5 X" i {/ X2 v* f; }Neurologic evaluation showed deep tendon reflex 2+
1 M( W0 [# l$ n) _! \bilateral and symmetrical. There was no suggestion, T: }6 F# }9 U5 @
of papilledema., h: x3 Z) g Q1 j* O' q; ^
Laboratory Evaluation
% \' @. H' @3 L5 C& G3 ], C2 I( eThe bone age was consistent with 28 months by- T# o, l8 T( L3 x9 J
using the standard of Greulich and Pyle at a chrono-
% ^, v, N3 G/ ~) l% K7 e5 Slogic age of 16 months (advanced).5 Chromosomal
/ ^5 B+ T; f0 n0 i2 y& B% \* gkaryotype was 46XY. The thyroid function test( e$ m$ E0 w: [ S* q' C7 ^& d: G
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 o( w2 E. b3 C$ @+ {lating hormone level was 1.3 µIU/mL (both normal).
$ @5 e1 i7 t) _* Z# U: nThe concentrations of serum electrolytes, blood- }" T; X3 B& `, x2 f8 W
urea nitrogen, creatinine, and calcium all were* j' G. T1 P/ |" s% V
within normal range for his age. The concentration
0 \3 E2 Y! H, B0 } Vof serum 17-hydroxyprogesterone was 16 ng/dL4 x/ }; p& S: Q- H2 t
(normal, 3 to 90 ng/dL), androstenedione was 20" z: B1 d- Y. H8 L
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-" T7 @3 C$ t; F
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 @) ?" b! Q @" idesoxycorticosterone was 4.3 ng/dL (normal, 7 to
# i& F4 v, L* m% B q3 y49ng/dL), 11-desoxycortisol (specific compound S) d) R' E9 S$ G/ ?1 \) l
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 q1 V( X; k4 H5 I
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: f5 r( l3 N _' Q k. O3 w5 {* J
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),' J4 |7 A, F- B# r+ v* F1 t, N0 d
and β-human chorionic gonadotropin was less than
- J- u' q7 [: I* Y- {( `5 mIU/mL (normal <5 mIU/mL). Serum follicular& B' X% H" a; C" G0 Y. e6 a* u
stimulating hormone and leuteinizing hormone
8 G5 E. b$ s" Jconcentrations were less than 0.05 mIU/mL3 c+ I6 ]6 I" v5 R- _
(prepubertal)./ h3 X: e" } k: v' j8 N
The parents were notified about the laboratory
i) P7 E2 C8 }6 Cresults and were informed that all of the tests were. u, ^5 U. i. _% |" k% h" V0 S: q
normal except the testosterone level was high. The) G5 {1 [6 Y$ u! C3 d
follow-up visit was arranged within a few weeks to
* I6 a* v3 F' D! Q1 |" aobtain testicular and abdominal sonograms; how-
- A: H S% K3 \$ Z" w( Q$ Aever, the family did not return for 4 months.
) U% F; Q2 o4 Z. B, @Physical examination at this time revealed that the
5 W9 V. N' w$ w9 S# Achild had grown 2.5 cm in 4 months and had gained
3 O3 P' h( ~6 j$ v; G: z2 kg of weight. Physical examination remained
1 |1 B/ x( {0 k- ]; \unchanged. Surprisingly, the pubic hair almost com-6 i$ i0 s, T: U. U5 d! }5 l: T
pletely disappeared except for a few vellous hairs at7 j4 i' M1 h) i+ P
the base of the phallus. Testicular volume was still 2
% O2 x/ d5 K$ G5 h( r$ X8 wmL, and the size of the penis remained unchanged./ K4 ?8 s3 f( C" o
The mother also said that the boy was no longer hav-
4 d" i/ A( X" Z9 v( iing frequent erections.
3 j: a' d0 e3 L) L6 ], ~Both parents were again questioned about use of
8 B+ f' t" K C, zany ointment/creams that they may have applied to
, U3 ]( W9 ? H. t! mthe child’s skin. This time the father admitted the6 Y: t2 L1 `9 e( w& {
Topical Testosterone Exposure / Bhowmick et al 541# @+ R, c# A; D" k) T# P
use of testosterone gel twice daily that he was apply-
8 \1 o5 m7 t( G M* J# l1 c# Ming over his own shoulders, chest, and back area for
/ [: w, i. e! r+ |5 x1 q% U7 Da year. The father also revealed he was embarrassed, u0 T5 K5 E$ o4 ?4 S
to disclose that he was using a testosterone gel pre-
0 ~/ h# q {4 O- }# {scribed by his family physician for decreased libido6 f3 j- n! `" G9 b+ v; W
secondary to depression.
3 v$ |1 Q0 H: Z6 E/ _# o, Q* HThe child slept in the same bed with parents.( a& `/ |4 X' d+ {; a
The father would hug the baby and hold him on his0 d* [- }, @# h, B( I3 W6 U
chest for a considerable period of time, causing sig-% n# [$ O x! [" e& S1 N% I" a
nificant bare skin contact between baby and father./ `( E5 |1 m s" u+ n4 o, y
The father also admitted that after the phone call,& c0 \: [8 y. C+ I& N) [
when he learned the testosterone level in the baby
) W8 j# [6 ^) N6 G$ e F' ^2 C( bwas high, he then read the product information$ {- I; M5 u r0 t# f
packet and concluded that it was most likely the rea-+ a2 f# A# J3 f% W, _7 c
son for the child’s virilization. At that time, they
+ p- W: t) p' K* r, ?9 Mdecided to put the baby in a separate bed, and the( @2 n1 ]+ V1 l3 ~% X
father was not hugging him with bare skin and had0 j9 e: ~1 O" Y$ o; Y' t
been using protective clothing. A repeat testosterone
8 h7 U8 O6 g9 E* `test was ordered, but the family did not go to the
! D6 m; Y( T0 l9 K5 Jlaboratory to obtain the test.. f3 \3 b, |& C3 K* v
Discussion7 I8 G. B. I1 \% N9 _# X
Precocious puberty in boys is defined as secondary
7 c% R& C5 P) B( Q5 l! Xsexual development before 9 years of age.1,4' e6 X# D. c: n& ^2 J; K, s3 Z6 _
Precocious puberty is termed as central (true) when
3 t* q0 S; C: nit is caused by the premature activation of hypo-, Y$ ^% L& C; Z* M% F
thalamic pituitary gonadal axis. CPP is more com-
( p& U* ]/ l0 ?* A" `' x: Hmon in girls than in boys.1,3 Most boys with CPP7 r8 P$ i c4 I% p
may have a central nervous system lesion that is' I N/ p! O2 z( L* e
responsible for the early activation of the hypothal-
6 J" T$ f: I2 yamic pituitary gonadal axis.1-3 Thus, greater empha-
8 f% Z' ?4 w% u0 j& H; ?3 {sis has been given to neuroradiologic imaging in
+ }3 @' Q6 x1 fboys with precocious puberty. In addition to viril-, P4 G" ]* U% c/ Y8 X: K" }, {
ization, the clinical hallmark of CPP is the symmet-& h; D# L2 I+ g8 b
rical testicular growth secondary to stimulation by
; q; L8 ?, J8 x+ d$ Pgonadotropins.1,3
: k9 V4 i& \& A( T. zGonadotropin-independent peripheral preco-& y4 K P% H5 E3 ]
cious puberty in boys also results from inappropriate
2 \3 |. M1 R$ U* p3 handrogenic stimulation from either endogenous or
g; ^8 |& C0 t2 J d; U6 Mexogenous sources, nonpituitary gonadotropin stim-
2 k5 C* v4 a1 `4 b) I9 |2 ^ulation, and rare activating mutations.3 Virilizing3 H( V6 y$ S* Z
congenital adrenal hyperplasia producing excessive. X& \5 e0 F4 W4 I" Q- ]/ O9 j+ N
adrenal androgens is a common cause of precocious' K E: b4 ]1 X) u+ r( Y4 h
puberty in boys.3,44 T1 L1 R* V9 {- r9 Z7 H4 w5 V0 w
The most common form of congenital adrenal
: K( F( x6 A8 w! |" C% zhyperplasia is the 21-hydroxylase enzyme deficiency.
' Y) U/ v( T8 nThe 11-β hydroxylase deficiency may also result in
- \( l1 n- N: t7 j3 J3 t/ Rexcessive adrenal androgen production, and rarely,5 L$ H9 ]2 l8 r [' ~
an adrenal tumor may also cause adrenal androgen4 }. S' Z3 O4 `) x
excess.1,3
/ m( u3 j! I$ y' pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 X' {3 v% K% b9 x, C4 ^9 `8 @: U, U
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
) X- C4 v7 p6 Y& VA unique entity of male-limited gonadotropin-5 N& {4 a y# d2 d
independent precocious puberty, which is also known- r1 z( V2 w& H$ r1 p
as testotoxicosis, may cause precocious puberty at a
7 x+ q2 B! v5 Tvery young age. The physical findings in these boys
/ Y3 l5 N M3 W& zwith this disorder are full pubertal development,; t- |) I9 v# c* f
including bilateral testicular growth, similar to boys5 v0 A4 \% H; Q7 Y, l& U
with CPP. The gonadotropin levels in this disorder
0 [5 u+ w; H6 ]: V" Ware suppressed to prepubertal levels and do not show
/ J3 v; k, h- a5 R4 {+ ipubertal response of gonadotropin after gonadotropin-
) B8 p0 @% X* o! Q. w, zreleasing hormone stimulation. This is a sex-linked( R$ V/ z2 [4 y- z* T# F. c1 F5 V5 w
autosomal dominant disorder that affects only$ c/ C6 w8 \. `! V% p
males; therefore, other male members of the family6 r/ J+ V n( C1 |6 G8 E; J
may have similar precocious puberty.3
5 a# x" s" U7 l$ dIn our patient, physical examination was incon-: [. c, P. `! r6 u
sistent with true precocious puberty since his testi-
' ~( b' \2 c- tcles were prepubertal in size. However, testotoxicosis
q& B& b5 [/ q2 @: _5 M, N9 Kwas in the differential diagnosis because his father
# E( h0 w( R$ pstarted puberty somewhat early, and occasionally,- ~. D& H, c# j; c6 X( A7 V R
testicular enlargement is not that evident in the
% D/ `/ i, B, J+ ~1 rbeginning of this process.1 In the absence of a neg-
k: Y( o& a. R; h% A( j" ?) N. ^ative initial history of androgen exposure, our
7 U% {$ s5 k, b. L- [1 p* W- Mbiggest concern was virilizing adrenal hyperplasia, S+ N2 d: l9 R9 r; m
either 21-hydroxylase deficiency or 11-β hydroxylase5 `$ A2 }4 H2 E( ]# k& J9 s- e
deficiency. Those diagnoses were excluded by find-
: \6 R- k) V* r# ^4 H+ Ring the normal level of adrenal steroids.
# y4 c1 g, U. p. k! I! ^8 aThe diagnosis of exogenous androgens was strongly1 D, g, e2 P, k' x0 J6 J
suspected in a follow-up visit after 4 months because9 V/ N( }3 b( F2 K8 F
the physical examination revealed the complete disap-
# p* R5 q' |+ [8 f) M+ {- E$ ppearance of pubic hair, normal growth velocity, and1 n) ^0 @+ W) c1 M
decreased erections. The father admitted using a testos-
( \$ Z# d- H5 q) T* Dterone gel, which he concealed at first visit. He was- R2 o; l; {% R* U5 c0 l$ }
using it rather frequently, twice a day. The Physicians’
3 N* E1 @& j5 q9 s+ L7 W" CDesk Reference, or package insert of this product, gel or
c) \- q }$ s: i" Q0 a( tcream, cautions about dermal testosterone transfer to
- D" \0 L6 |, M$ Uunprotected females through direct skin exposure.5 U; B% H) q" d& V; i; p
Serum testosterone level was found to be 2 times the
0 ~6 s5 j" P- _6 Z2 Ebaseline value in those females who were exposed to
6 |4 H( o4 [: y3 e2 H3 _even 15 minutes of direct skin contact with their male
8 G F& R& E+ p0 R- qpartners.6 However, when a shirt covered the applica-# c F. O+ F8 f; ^7 `. ]- Q+ s
tion site, this testosterone transfer was prevented.
9 X5 J5 B T$ x. `6 a" ^ e* NOur patient’s testosterone level was 60 ng/mL,
" X2 e* ^8 J2 z$ l9 y% s8 t0 c$ ?which was clearly high. Some studies suggest that/ L7 M1 V2 j! k0 @
dermal conversion of testosterone to dihydrotestos-
# V) H9 o5 z- T1 R" J0 v5 |terone, which is a more potent metabolite, is more
# k e4 _+ Y: N; @& w. X) lactive in young children exposed to testosterone
2 I7 o' {* V8 A7 M: G8 y& Gexogenously7; however, we did not measure a dihy-
3 i$ o( L* n5 ~) x" Z& Qdrotestosterone level in our patient. In addition to8 i% q. B2 p7 @ `) S* d
virilization, exposure to exogenous testosterone in
+ x7 B8 @2 g8 R' ]. _! j1 tchildren results in an increase in growth velocity and
5 B( z0 r' x+ Madvanced bone age, as seen in our patient.
_9 d+ z$ S1 ?2 \3 D. yThe long-term effect of androgen exposure during& U5 l& z0 c4 Q% u' \. g
early childhood on pubertal development and final
9 U8 c0 _9 a. D$ x& I$ O. G8 c" F; Sadult height are not fully known and always remain* f U7 ^- f: T. f6 R
a concern. Children treated with short-term testos-) j$ t( y- F( V L9 b
terone injection or topical androgen may exhibit some1 u0 P- l6 g4 J( E: A/ t& w2 x$ T
acceleration of the skeletal maturation; however, after
+ n* u7 S; c% S xcessation of treatment, the rate of bone maturation
; i% m! f9 \5 L# i7 ~. k& w. Xdecelerates and gradually returns to normal.8,99 K9 H0 l+ F0 D& r$ u5 t5 E
There are conflicting reports and controversy
# Q; n! M% G) @over the effect of early androgen exposure on adult
7 V) `" h/ n1 q$ A) O) i b+ apenile length.10,11 Some reports suggest subnormal- B2 a3 c, B4 }$ \6 ~
adult penile length, apparently because of downreg-
6 B3 U/ T \- g# M4 u# |ulation of androgen receptor number.10,12 However,
* W4 I7 t! e+ o- rSutherland et al13 did not find a correlation between$ b1 Y1 ~* a3 w3 `; W0 G! X, U
childhood testosterone exposure and reduced adult
* ^$ C# E' O9 f# _1 _: y( _6 ~penile length in clinical studies.
W e A4 E# G g! Z" q3 aNonetheless, we do not believe our patient is- m; j4 }3 T" e1 T3 c7 E8 @# e4 w
going to experience any of the untoward effects from" ` \' P3 Q9 A6 a8 A* E& }3 q
testosterone exposure as mentioned earlier because
' i+ q6 a7 o$ f7 h( ~the exposure was not for a prolonged period of time.
% Y# U- }/ z% eAlthough the bone age was advanced at the time of
4 B% q1 [% k# f q* D! ?3 {# w/ l( ydiagnosis, the child had a normal growth velocity at0 z! [. L w% R8 R) s: c8 M
the follow-up visit. It is hoped that his final adult$ R0 l" a1 E* M: f
height will not be affected.
$ R% y: }4 g+ e: O$ b* EAlthough rarely reported, the widespread avail-
2 p( R3 E( W8 z$ Tability of androgen products in our society may* {5 _/ Q+ S O4 [5 r( [
indeed cause more virilization in male or female
' z6 @/ }5 Z/ x5 Q. gchildren than one would realize. Exposure to andro-( s& O p. D: J
gen products must be considered and specific ques- n6 Z6 y! J- L
tioning about the use of a testosterone product or
! Z" {( |6 U/ i8 N) Ggel should be asked of the family members during
$ o/ w1 T; K% [' d' Nthe evaluation of any children who present with vir-
" S- ]2 t8 {) dilization or peripheral precocious puberty. The diag-( h* u1 f' n* u8 I; w" {
nosis can be established by just a few tests and by" E5 F4 o, F" D T. m
appropriate history. The inability to obtain such a; q9 {" d8 V- i3 w5 b" {
history, or failure to ask the specific questions, may
|$ Y" R3 s7 `# i: ~7 u3 Kresult in extensive, unnecessary, and expensive4 o/ \- s9 u' e5 K$ i1 L$ B6 n
investigation. The primary care physician should be5 x8 e% C5 r5 |7 M
aware of this fact, because most of these children
+ \( j/ x h, f- `) |may initially present in their practice. The Physicians’
+ ^7 q' X( Q. Y% g0 MDesk Reference and package insert should also put a
( r: e; D$ s- }- X4 s' lwarning about the virilizing effect on a male or
. r# k- u+ l2 q* xfemale child who might come in contact with some-
: |# N* q7 X' Y& o% {" Sone using any of these products.
9 f8 W7 M6 s8 o3 s* QReferences
) T7 e. J8 K* o5 l u9 ?1. Styne DM. The testes: disorder of sexual differentiation
' B6 e" Y, H& K9 ]- N5 nand puberty in the male. In: Sperling MA, ed. Pediatric
y: |7 w; ]5 c! Q, nEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
0 o2 e v' ? L# E4 J2002: 565-628.' p' G& x Q# T# J: \
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! _* z3 i. L b, Tpuberty in children with tumours of the suprasellar pineal |
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