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Sexual Precocity in a 16-Month-Old+ f9 D3 Y6 z1 d0 b; ?, T2 E
Boy Induced by Indirect Topical
' f! w" [- _+ P; w _) eExposure to Testosterone% T3 ~" S9 A. I v# F* g
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: F9 N' T4 s+ B" H) L. k1 J* F
and Kenneth R. Rettig, MD1% S r) M; e2 h9 k% g( d6 ]
Clinical Pediatrics
H: c: Y1 \- kVolume 46 Number 6
+ H9 `6 S. e& R9 _% E" P# m9 l3 FJuly 2007 540-543
9 y- I5 L5 N5 L© 2007 Sage Publications
2 P. p2 @6 k& a0 h" d( C5 j10.1177/0009922806296651+ n" F1 d, q7 Y% f
http://clp.sagepub.com9 S+ I3 ^6 g# e' {
hosted at% f- {/ t5 Q$ D; t- i' y
http://online.sagepub.com
2 H& ~$ b- l% nPrecocious puberty in boys, central or peripheral,& f3 R* r j) J' b x& S7 |5 U
is a significant concern for physicians. Central
0 Q8 m5 S6 A/ o5 i1 K1 ^precocious puberty (CPP), which is mediated. k L5 ]. U. Y% Z
through the hypothalamic pituitary gonadal axis, has
8 s- H9 e0 I. s8 L7 K/ R& D! S& va higher incidence of organic central nervous system
% m$ g( H. y' A' d' h- N+ x+ flesions in boys.1,2 Virilization in boys, as manifested6 \0 @: F6 v9 a& |8 c0 K7 G% D% N- L
by enlargement of the penis, development of pubic& @: ?% H5 u$ W# n
hair, and facial acne without enlargement of testi-' g1 s7 d/ i$ o) i; E: z' s
cles, suggests peripheral or pseudopuberty.1-3 We: Z( e$ k* F, v; |2 C3 ?$ }% L
report a 16-month-old boy who presented with the
5 q' N. k& t' J& E; uenlargement of the phallus and pubic hair develop-
1 H* z1 z( Q& W+ @3 B7 lment without testicular enlargement, which was due
% j) C$ `! i, d1 S5 E9 y* T, p2 ^to the unintentional exposure to androgen gel used by
4 `) Q" Z( u6 E! n0 ?) G: y" Hthe father. The family initially concealed this infor-
6 j$ }& J" \9 I1 j: S5 m! ymation, resulting in an extensive work-up for this
) m4 a* u! S3 a0 z; Lchild. Given the widespread and easy availability of1 V4 o. j+ |2 [7 k
testosterone gel and cream, we believe this is proba-' E7 o9 c3 a/ O9 e; L/ B9 }
bly more common than the rare case report in the0 i [, U& c' w/ m; d6 b
literature.4
1 T3 q# N \0 F( V7 Q& }( rPatient Report' P/ Z1 X$ E3 t' [2 s6 c
A 16-month-old white child was referred to the: W5 I8 }& y0 G7 F6 T
endocrine clinic by his pediatrician with the concern
! s2 F$ C, }8 @of early sexual development. His mother noticed
* @. R0 }* }! @2 P/ F1 a+ d* olight colored pubic hair development when he was5 S6 |. b7 s8 O& W7 {
From the 1Division of Pediatric Endocrinology, 2University of
% f" t. ]+ q& g8 M6 |South Alabama Medical Center, Mobile, Alabama.+ j |3 |0 ]. T2 U c/ K/ e& [5 H- v
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 v# ]* h* f* \ p) }5 oProfessor of Pediatrics, University of South Alabama, College of: }5 T/ q( s/ {3 F
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ @2 v+ G. Q# d( K1 `/ ke-mail: [email protected].
: r, l8 w! z( D9 `/ b6 o* Cabout 6 to 7 months old, which progressively became M7 }& g" ]$ f3 K% S/ u
darker. She was also concerned about the enlarge-
5 l! {. Y- S$ Q vment of his penis and frequent erections. The child3 [7 Z! }* n; h, K3 w# |4 R
was the product of a full-term normal delivery, with
; @. x2 `4 ?/ v% V" {a birth weight of 7 lb 14 oz, and birth length of' z0 r* H) @. @5 |; U+ b" b
20 inches. He was breast-fed throughout the first year" I3 ]. ^1 h. a! q% Q
of life and was still receiving breast milk along with
s- A" Q4 b8 F6 ?3 jsolid food. He had no hospitalizations or surgery,
3 A) _2 \6 D7 p) Y2 Q/ Zand his psychosocial and psychomotor development
4 t/ I8 a; f: M0 i" H$ u, Rwas age appropriate.
' i# g+ Q+ N3 G* X, {The family history was remarkable for the father,0 ?3 P2 {- }7 H! z- e$ v; Y
who was diagnosed with hypothyroidism at age 16,
4 d7 F, Y" k+ N& n3 r( ?# I: Q. cwhich was treated with thyroxine. The father’s) l. t* R3 T2 S7 Y. x. K5 g
height was 6 feet, and he went through a somewhat
1 A+ ^+ W1 z8 {) [6 A0 hearly puberty and had stopped growing by age 14.) m# N5 [4 T+ V. {
The father denied taking any other medication. The1 ?: \8 K- {0 y; ]# g5 i0 q
child’s mother was in good health. Her menarche
( c! Y5 Z# F& H N5 w4 Wwas at 11 years of age, and her height was at 5 feet
. G2 l# G0 q: S" ~ h5 inches. There was no other family history of pre-+ f9 G ?0 l* j
cocious sexual development in the first-degree rela-: h+ I2 N& S- D5 _( ~
tives. There were no siblings. {6 w/ S6 b2 Z7 b6 L2 `9 I% ^
Physical Examination- D ~. ^9 P8 f% R1 h. B
The physical examination revealed a very active,
' _* X3 W# L3 v# Yplayful, and healthy boy. The vital signs documented
" C4 Z/ s8 _, t! k! |! V/ ua blood pressure of 85/50 mm Hg, his length was
6 w* h- s0 D5 P$ d. k! `" d90 cm (>97th percentile), and his weight was 14.4 kg" A) g/ l! d o. q9 w2 U
(also >97th percentile). The observed yearly growth/ X) y0 w3 Z0 r
velocity was 30 cm (12 inches). The examination of
3 k! E2 Q3 x* H/ C6 rthe neck revealed no thyroid enlargement.
' R. u6 j4 i* [+ Z( U9 ]) pThe genitourinary examination was remarkable for6 x2 s9 Q' X5 u! z; U2 Q2 Y
enlargement of the penis, with a stretched length of
& b7 Y$ F2 u8 o) o, I8 cm and a width of 2 cm. The glans penis was very well& X3 p! Z. }1 s% T5 k
developed. The pubic hair was Tanner II, mostly around
; _5 G3 S% T7 M; m7 N+ u540: ?, ?1 t. Q6 [0 y$ t6 |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 y: u. r2 K3 {! ~- B6 C8 D
the base of the phallus and was dark and curled. The
) S1 K( N6 w+ e$ C% Ptesticular volume was prepubertal at 2 mL each.5 A. y0 ?8 z$ d. R# F- D, x7 B0 {
The skin was moist and smooth and somewhat g" a8 Q' G# p B% `7 [7 G
oily. No axillary hair was noted. There were no% A' B' G! {# y+ u7 m7 r$ l
abnormal skin pigmentations or café-au-lait spots.' E5 {" r, |- _$ d6 o' q; Y7 G
Neurologic evaluation showed deep tendon reflex 2+
' q* w3 V# R9 Ebilateral and symmetrical. There was no suggestion% K" j8 g+ h s! n! l# v+ F& Q
of papilledema.% E& e- R& i: K% H6 i1 F/ V2 _
Laboratory Evaluation
; U) E; Z4 D1 c8 G jThe bone age was consistent with 28 months by$ S7 Q) U$ D# V* Q2 T$ v
using the standard of Greulich and Pyle at a chrono-
$ X+ a7 X3 s2 a/ q5 S2 e0 q5 n hlogic age of 16 months (advanced).5 Chromosomal
5 p1 B" y h% V6 lkaryotype was 46XY. The thyroid function test
6 z. M5 Z9 y( K/ Dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-3 }+ S& Q* @5 v( w& y0 G4 T6 e
lating hormone level was 1.3 µIU/mL (both normal).+ e9 z& Q, I- @- N! y4 u+ P
The concentrations of serum electrolytes, blood
8 v+ W: }4 i, f3 y1 x Furea nitrogen, creatinine, and calcium all were
0 G3 b0 U- x0 O0 p& R' B, C2 A; swithin normal range for his age. The concentration# K; M* b- A, m- r2 {& r
of serum 17-hydroxyprogesterone was 16 ng/dL
! K+ u1 ]3 N$ P( X(normal, 3 to 90 ng/dL), androstenedione was 20' B- n4 Y, B8 C
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 o4 n; M; i! z1 M* eterone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 d* s' U8 z: @5 q: ]desoxycorticosterone was 4.3 ng/dL (normal, 7 to; J: r& b6 I' e; J. |" E
49ng/dL), 11-desoxycortisol (specific compound S)' b3 b% x7 L3 A$ ]7 j9 s; I
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
5 \$ \7 @/ i$ m& D3 S- I! ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: h7 }" M6 q; F' g7 } F2 G6 D, ?testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, w+ b0 w2 n+ a; u9 g, F$ I, ?" Eand β-human chorionic gonadotropin was less than
1 e# n; Z, r6 y* R2 h5 mIU/mL (normal <5 mIU/mL). Serum follicular( t7 F5 [$ ^. N0 `2 g. p
stimulating hormone and leuteinizing hormone9 u! G3 a0 @& ~7 j( }/ A+ s% ~
concentrations were less than 0.05 mIU/mL9 L9 Y/ T. D3 X- K/ R" n: W9 K
(prepubertal).
; q( F$ g4 N P2 ]The parents were notified about the laboratory! i1 q% H3 q: h8 ~% D' j
results and were informed that all of the tests were
0 C( q }& o' D8 ]( unormal except the testosterone level was high. The
$ `" K* W" h- B( b2 o3 T# zfollow-up visit was arranged within a few weeks to
. t, V. Q e; Z. Nobtain testicular and abdominal sonograms; how-+ L% ?$ Q7 z0 A& D6 _* e' E6 j
ever, the family did not return for 4 months.; s- s2 t, a! |* f
Physical examination at this time revealed that the5 o- ~! ^) o% V7 p
child had grown 2.5 cm in 4 months and had gained
C, K) Y# X6 b: @* M/ R- X$ i' L. G2 kg of weight. Physical examination remained( |" q6 I/ |$ I
unchanged. Surprisingly, the pubic hair almost com-
- M, H# ?$ q; v- I l* z9 b, npletely disappeared except for a few vellous hairs at
$ p# i4 V) h8 b/ vthe base of the phallus. Testicular volume was still 2/ r$ @' t* A \6 \1 G+ H( ]
mL, and the size of the penis remained unchanged.
9 `. e! z& x6 n9 UThe mother also said that the boy was no longer hav-
6 C/ k7 k7 ?( N9 A1 _3 {0 ting frequent erections. t0 F0 c+ Q2 w7 u& {: P, l
Both parents were again questioned about use of& ^1 E8 f% t6 p) G0 W9 N8 x
any ointment/creams that they may have applied to8 R5 s% \/ v1 {& l8 B/ i! K
the child’s skin. This time the father admitted the& C% ]" ] s0 c, |; }0 L3 r
Topical Testosterone Exposure / Bhowmick et al 541( B( b$ X9 p a- S
use of testosterone gel twice daily that he was apply-/ G. x, h0 P' ?6 \, O8 C- u2 J
ing over his own shoulders, chest, and back area for
$ z5 m. }, x# z2 x9 ba year. The father also revealed he was embarrassed( B0 s" h% l: A0 w. I: S
to disclose that he was using a testosterone gel pre-
! |+ D/ T. ^6 y3 ] d6 Mscribed by his family physician for decreased libido g4 R" I# J7 {. u# Z
secondary to depression.& A% h) H. u! s2 o8 E2 f
The child slept in the same bed with parents.
" n @( A. l- R0 a1 I. K. LThe father would hug the baby and hold him on his
% x! w" y* |4 G5 Q1 Vchest for a considerable period of time, causing sig-1 |! x7 w# r1 M# b/ l T
nificant bare skin contact between baby and father.
2 `* [) e' T; P ]: V9 zThe father also admitted that after the phone call,. ]2 |5 i0 a6 G) m6 Z w6 }
when he learned the testosterone level in the baby
5 X) j* T% o% Q5 m0 N. @ \2 cwas high, he then read the product information+ G5 c. H2 ?* e6 ?9 m
packet and concluded that it was most likely the rea-
/ Z/ I4 r$ m2 n8 n1 g: l$ Qson for the child’s virilization. At that time, they
4 b' k& |7 [, }3 I3 e0 j3 R* Adecided to put the baby in a separate bed, and the
Z: m3 O& d- u: {% z* i3 M' Gfather was not hugging him with bare skin and had
* F8 ^! m9 o; Q% U9 Pbeen using protective clothing. A repeat testosterone8 ?: W. i% i( L) Y1 Z1 p' I! y
test was ordered, but the family did not go to the
* Q3 c8 a, v* L5 z/ P) llaboratory to obtain the test.
1 Z/ t7 l+ y; g/ I9 k( NDiscussion3 n% \( o) k% g" o( ~0 O
Precocious puberty in boys is defined as secondary
+ m7 o/ ]7 g2 H" F8 [/ J: asexual development before 9 years of age.1,4" L. E! ~, [2 I! Z& L+ h0 B
Precocious puberty is termed as central (true) when
4 c+ ^# U% O# o. k# hit is caused by the premature activation of hypo-4 \% ^3 i' z: z7 O8 c
thalamic pituitary gonadal axis. CPP is more com-1 F7 z& _4 R+ ^7 N# R% e
mon in girls than in boys.1,3 Most boys with CPP
7 d: N$ t+ }6 Bmay have a central nervous system lesion that is
# \: g) V: m4 {- Tresponsible for the early activation of the hypothal-
, l( O2 u; R5 \% G9 ~, M0 U% \amic pituitary gonadal axis.1-3 Thus, greater empha-
6 N" ~" L" R* _! Ksis has been given to neuroradiologic imaging in
6 Q/ S" z" r" ^boys with precocious puberty. In addition to viril-- p- a: u3 N$ T6 O) I; \
ization, the clinical hallmark of CPP is the symmet-( n; t- P4 }; I1 q6 B0 |: b
rical testicular growth secondary to stimulation by
+ k) b" w/ c4 agonadotropins.1,3
5 d& j8 J5 }5 W5 w; v4 A' xGonadotropin-independent peripheral preco-+ K+ E$ z$ R( ^: L# g; P5 j9 W+ v
cious puberty in boys also results from inappropriate
8 y/ E' l, j6 t& ~* q- A4 T# ~androgenic stimulation from either endogenous or
/ _$ q& Y) ^! b' |: oexogenous sources, nonpituitary gonadotropin stim-6 r& A* I1 z& a/ L9 n% d; s
ulation, and rare activating mutations.3 Virilizing) z* j C, L! p! p V9 ^- t
congenital adrenal hyperplasia producing excessive
/ g, U6 u5 J! aadrenal androgens is a common cause of precocious
7 @: d8 I) }' D$ @3 Y- L; Ypuberty in boys.3,4' Q2 |; V+ J8 _9 a
The most common form of congenital adrenal- b# Z8 ^) d( N& @) K
hyperplasia is the 21-hydroxylase enzyme deficiency./ m6 G* Q% F& c3 L5 t
The 11-β hydroxylase deficiency may also result in
* h+ @! y) a. D- I0 K- yexcessive adrenal androgen production, and rarely,, e0 Q: N2 s6 g* L
an adrenal tumor may also cause adrenal androgen& v: Q" i8 j5 s' n2 Y X3 ~( f6 _
excess.1,3
/ \: B6 g. m2 M0 aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; v _* h) a6 V9 K" `
542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 c$ g5 D. k3 m/ Z- m
A unique entity of male-limited gonadotropin-* Q ?' W: z5 M* c! B
independent precocious puberty, which is also known. ^! i' Y8 M, z% I9 j
as testotoxicosis, may cause precocious puberty at a2 [1 {' z4 a) _" @
very young age. The physical findings in these boys/ t8 A. Z9 U$ { O+ l( ?
with this disorder are full pubertal development,9 r$ y$ u0 w' b
including bilateral testicular growth, similar to boys
5 W% ]# f- {8 O+ Xwith CPP. The gonadotropin levels in this disorder: e# Z# v# N% B. `" P0 P0 a2 r
are suppressed to prepubertal levels and do not show/ i, A$ x- |) C: I9 l5 \6 r
pubertal response of gonadotropin after gonadotropin-
& f# T: u4 l( z. u6 X' [+ k& X4 `- i* wreleasing hormone stimulation. This is a sex-linked
% G/ E+ z9 @. J O2 E2 }% h- hautosomal dominant disorder that affects only: ^) p* x& _4 ^& L8 M' Q
males; therefore, other male members of the family
( o4 Z9 `$ }; w# |! }2 h" U1 Kmay have similar precocious puberty.3! }5 A' g, k% _0 |" h C5 l
In our patient, physical examination was incon-1 N! P) n7 b6 `: K1 P$ V6 ~2 W, z
sistent with true precocious puberty since his testi-
/ Y0 Y! u! K" ]7 qcles were prepubertal in size. However, testotoxicosis6 y% g4 {! N% y
was in the differential diagnosis because his father9 g& f3 Z( s& m9 a8 v
started puberty somewhat early, and occasionally,1 N9 }. Z- M7 y
testicular enlargement is not that evident in the# L& u' |4 x+ d; O5 m1 s
beginning of this process.1 In the absence of a neg-
6 v9 T( X1 P) [8 V' I7 I. r0 Cative initial history of androgen exposure, our- n% q$ [2 ]' b1 B- }
biggest concern was virilizing adrenal hyperplasia,
2 P$ H6 M M4 g4 F! i3 beither 21-hydroxylase deficiency or 11-β hydroxylase' v6 b2 ?8 ?9 P% Y; ?" r7 p: d
deficiency. Those diagnoses were excluded by find-+ k! h. J( I, a) K/ f" j
ing the normal level of adrenal steroids.2 J9 f1 ?$ a- ] n
The diagnosis of exogenous androgens was strongly4 }1 ?, |. J$ _+ c( {
suspected in a follow-up visit after 4 months because
: W1 ` k6 a! J; [1 P: Q5 Mthe physical examination revealed the complete disap-, a& h8 E* t4 u4 a5 m$ e/ Z' ]
pearance of pubic hair, normal growth velocity, and9 X0 e( j O* r7 x% Q6 I+ t2 x
decreased erections. The father admitted using a testos-/ t0 H; z0 G3 l
terone gel, which he concealed at first visit. He was
" N6 k" v6 a9 xusing it rather frequently, twice a day. The Physicians’
6 E+ H% g1 N: s# h$ _% i; m$ wDesk Reference, or package insert of this product, gel or1 }' x6 ~" P6 D, r# y, n
cream, cautions about dermal testosterone transfer to1 M& j+ Q7 {2 i# s. ~0 B" ?
unprotected females through direct skin exposure.
+ s+ |9 c8 L/ E* C0 rSerum testosterone level was found to be 2 times the$ O5 l/ a- b! e" e x
baseline value in those females who were exposed to
1 D. `6 M9 h5 I& o0 K: beven 15 minutes of direct skin contact with their male
& L# |8 l _8 u" W7 d ]partners.6 However, when a shirt covered the applica-
; B7 l. V8 A, t% R6 etion site, this testosterone transfer was prevented.+ M6 \- W" l9 d6 E9 d
Our patient’s testosterone level was 60 ng/mL,
# I* ^% I# e2 f. c4 fwhich was clearly high. Some studies suggest that2 T; {9 C( W1 A1 W
dermal conversion of testosterone to dihydrotestos-9 K' i$ L+ @6 e
terone, which is a more potent metabolite, is more
1 U5 B' Z+ ~9 P/ @0 q: O7 {3 d7 H1 Oactive in young children exposed to testosterone3 R' d1 s3 y6 F$ A/ ^8 g( x
exogenously7; however, we did not measure a dihy-
+ N4 V( \9 ?. v7 Ldrotestosterone level in our patient. In addition to
+ D3 E! ~$ ?7 g5 Tvirilization, exposure to exogenous testosterone in
$ a! S. B, I! ?5 {6 _! H$ u7 @children results in an increase in growth velocity and7 m6 z/ ?' v0 {3 q- S! V0 X9 z
advanced bone age, as seen in our patient.' J% ?, z2 b% c, q
The long-term effect of androgen exposure during! k- J. f8 j+ E' [; H' ~5 _$ V6 }
early childhood on pubertal development and final) p8 [3 g- [! y" V
adult height are not fully known and always remain
6 O+ ?4 e" a3 S' s, Fa concern. Children treated with short-term testos-1 i; H* v: Y4 H- o+ p0 [) L
terone injection or topical androgen may exhibit some! }( {. ~) _+ F- _9 b: \
acceleration of the skeletal maturation; however, after
2 u* H2 P' F& v0 V+ K" ]cessation of treatment, the rate of bone maturation6 }, {: K' P9 F
decelerates and gradually returns to normal.8,9 k' ]1 R% P- E3 A" E
There are conflicting reports and controversy2 _9 W! Q, x( a J" _
over the effect of early androgen exposure on adult
/ o: C* u3 i% G! \) |penile length.10,11 Some reports suggest subnormal
% s- S$ ^ W2 t" N3 hadult penile length, apparently because of downreg-( a# d) Z3 {) v0 \! [ N0 }
ulation of androgen receptor number.10,12 However,
' u9 c0 a! l' _! ?& ~. C, L' hSutherland et al13 did not find a correlation between3 r' p+ r: X# v' E0 J
childhood testosterone exposure and reduced adult
' q& @( i0 n7 Y! ^: b. ipenile length in clinical studies.6 P! P+ k7 t* W- i7 v! t
Nonetheless, we do not believe our patient is& w6 A, Y' t: n1 M5 v
going to experience any of the untoward effects from4 L6 A0 t/ }9 ~) W9 K5 b: o. p o
testosterone exposure as mentioned earlier because
1 d! _7 |, \/ C2 R: l% dthe exposure was not for a prolonged period of time.3 r3 z# a$ p' f
Although the bone age was advanced at the time of
) V2 m6 D# a, Y" }3 K' Q3 fdiagnosis, the child had a normal growth velocity at/ W$ i: R3 c1 r% _( W6 G- [7 Y: Q
the follow-up visit. It is hoped that his final adult8 T. D: R4 g2 j/ K* V) T6 i) h
height will not be affected.
h' E8 Q9 L4 D$ B/ f5 Q, @Although rarely reported, the widespread avail-1 F! z4 {4 G# A g$ o' B; _
ability of androgen products in our society may
* l5 @* U+ \0 Z X% a$ _$ [9 vindeed cause more virilization in male or female2 l- K" ^8 B' I! {! V0 i
children than one would realize. Exposure to andro-
4 i0 B8 m$ d; M' E8 agen products must be considered and specific ques-
7 i& e; _# s5 w% Ytioning about the use of a testosterone product or
: Y2 ^/ _/ d3 {! {3 Wgel should be asked of the family members during
; h P8 C! Z. q# x1 Uthe evaluation of any children who present with vir-8 z% b* y# l7 v, M" M
ilization or peripheral precocious puberty. The diag-
" n" a( d5 M* E. |" nnosis can be established by just a few tests and by
7 R" P- ~, f A6 s* jappropriate history. The inability to obtain such a
' [& K: @, o; f) Hhistory, or failure to ask the specific questions, may% B5 a# }4 x8 H* {. e
result in extensive, unnecessary, and expensive
" e: y' w3 x' Q5 H# Winvestigation. The primary care physician should be
: x( L6 x5 X+ g! k" S* d) Paware of this fact, because most of these children3 @2 u9 R8 j; v4 g- v
may initially present in their practice. The Physicians’( G D0 i7 u- n; S# p
Desk Reference and package insert should also put a
3 m1 J. ]' I F, t; T4 d6 Mwarning about the virilizing effect on a male or6 \+ N$ o5 C2 S; G: \3 i- `
female child who might come in contact with some-
9 j3 Q0 y8 i) g1 A/ k) zone using any of these products. z9 d2 N4 L2 W2 W
References
2 x3 ^8 A3 d% m4 K1. Styne DM. The testes: disorder of sexual differentiation
* B3 n9 A& W- c) R# c& E' sand puberty in the male. In: Sperling MA, ed. Pediatric0 [) K1 I" a9 L. k! U6 w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 r+ z e w) I, [ H9 C2002: 565-628.
' _0 k0 W" ]+ v/ E: ?0 V2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' q) k. c. h, t! w4 ]! Npuberty in children with tumours of the suprasellar pineal |
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