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Sexual Precocity in a 16-Month-Old2 E7 @* M& C7 n' ~
Boy Induced by Indirect Topical* A, m. C. @5 ^! d
Exposure to Testosterone* T. m/ O. C2 Q9 r8 J) e
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
x; y' \" b9 E' V4 V! f* L1 Vand Kenneth R. Rettig, MD1
. ?+ Z& U* ]5 {# xClinical Pediatrics
9 V$ h# ^ s: iVolume 46 Number 6
f& ~2 X; z7 U8 x" D u" X) m( O) }July 2007 540-543
; S( J6 Y# e# [6 m5 u, l; p© 2007 Sage Publications( D7 V) T" Z& y1 o5 y6 {; U
10.1177/00099228062966512 R7 k7 T& y7 B/ U
http://clp.sagepub.com5 ~+ [7 W4 `! [9 C% t
hosted at2 f" w9 S7 I$ U" R7 k- {" z7 G7 x5 f# C F
http://online.sagepub.com
. ^. X5 O( E, P1 P4 }& U7 [Precocious puberty in boys, central or peripheral,
4 j* @# }" b, m( ?6 W9 Iis a significant concern for physicians. Central3 k6 W K9 I2 h
precocious puberty (CPP), which is mediated
# m' ?! _. r& n8 V* \# `1 lthrough the hypothalamic pituitary gonadal axis, has
8 }/ }+ n5 M( u! `% |* Na higher incidence of organic central nervous system
/ m8 @ Q+ }: @5 ~lesions in boys.1,2 Virilization in boys, as manifested
- x; l& P! A" n. K7 X6 N9 `by enlargement of the penis, development of pubic
) W; `' ?2 h' Y6 @; Rhair, and facial acne without enlargement of testi-
G5 w$ f" l; M! O) ?cles, suggests peripheral or pseudopuberty.1-3 We& C0 c( P9 n' Z7 O, O
report a 16-month-old boy who presented with the
$ O" @+ R4 c! o* ~enlargement of the phallus and pubic hair develop-
: B/ y+ }. `6 ~" E$ Ument without testicular enlargement, which was due
$ {" O9 i7 }4 z& X0 ~. ~7 Wto the unintentional exposure to androgen gel used by
' Y3 v, ?' p3 c( }9 f1 }the father. The family initially concealed this infor-
! _# d3 @3 Z0 N8 F/ hmation, resulting in an extensive work-up for this R8 o& P1 ^( X: W f( l) i. P
child. Given the widespread and easy availability of
- b4 ~4 s& I" ktestosterone gel and cream, we believe this is proba-. E0 |# w2 w% {) ]* U+ Q6 j
bly more common than the rare case report in the9 ~% P# s" l3 F* |$ v! P' ^
literature.49 x) `( ]* B& g8 {* s+ o y# }
Patient Report! ~ l4 `1 p" |1 i
A 16-month-old white child was referred to the2 d1 n; C6 m! ]8 p( y
endocrine clinic by his pediatrician with the concern
5 B4 \" r& O' r: Y' Z' gof early sexual development. His mother noticed
8 y) M8 C$ y' @3 q( { v6 hlight colored pubic hair development when he was! i, y8 G8 G8 Y. z
From the 1Division of Pediatric Endocrinology, 2University of- V7 {; H5 w: V7 s3 M
South Alabama Medical Center, Mobile, Alabama.
1 n& P/ C- G, M" M/ _- QAddress correspondence to: Samar K. Bhowmick, MD, FACE,
# h2 x9 U, Y% H3 D8 Z: d) ]! Z( A# ]Professor of Pediatrics, University of South Alabama, College of
5 N! L& n" O' _7 \" E2 w, lMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! _* N' X- w" v9 m5 s+ G. Le-mail: [email protected].
( u" S8 O5 I; U, }4 S) ^about 6 to 7 months old, which progressively became. Y6 S& P4 J! B) w" t
darker. She was also concerned about the enlarge-8 v" o1 Q, f8 Y0 q5 H6 w+ c2 D
ment of his penis and frequent erections. The child
1 n9 A: b5 o$ \- y7 Uwas the product of a full-term normal delivery, with
1 S8 w1 }) o% D8 u7 H) C6 z ja birth weight of 7 lb 14 oz, and birth length of8 A. t% H1 b+ }
20 inches. He was breast-fed throughout the first year: M7 H( I' k5 {" N; Y5 a$ d. I" X h, a1 J
of life and was still receiving breast milk along with0 P* z. T+ W9 Z
solid food. He had no hospitalizations or surgery,
A' ]) ]3 v/ A7 G, Y# r1 [and his psychosocial and psychomotor development
( d& }$ q/ `0 E) ^# u2 G+ W7 Lwas age appropriate.. ~# Q k/ N! h" j& @
The family history was remarkable for the father,5 k) V! n# P7 _# Q' |
who was diagnosed with hypothyroidism at age 16,: z* T( M/ L3 u& g3 y0 R# G! H5 o
which was treated with thyroxine. The father’s+ T1 o0 I! v; R9 B: C5 o
height was 6 feet, and he went through a somewhat
' D" S U' b( E% z) t2 [+ u& aearly puberty and had stopped growing by age 14.; o. Q/ D, P6 _8 C' z" L' A
The father denied taking any other medication. The8 p% T5 g" n# Q3 }, R: k
child’s mother was in good health. Her menarche; K9 w7 q r m: h; Q/ L" q
was at 11 years of age, and her height was at 5 feet2 v; A( o, P4 S7 C9 e% X
5 inches. There was no other family history of pre-
" C( u- [3 i# M: F+ dcocious sexual development in the first-degree rela- \# i1 S$ ~3 ~+ S' N
tives. There were no siblings.
$ d: {% h4 W1 @% c: a$ {) r+ q8 EPhysical Examination9 |+ T$ ~- q- o. z
The physical examination revealed a very active,
: \0 |. A1 O4 v/ V% z( q, wplayful, and healthy boy. The vital signs documented
9 Y8 p( L: [: g9 M2 S5 ta blood pressure of 85/50 mm Hg, his length was
8 D5 h7 S0 e& c- }9 Q( [, N90 cm (>97th percentile), and his weight was 14.4 kg2 W. `+ Y: _ l# D! W' g5 s
(also >97th percentile). The observed yearly growth8 u* Y' U2 O' B( A1 N. T7 I
velocity was 30 cm (12 inches). The examination of
2 p- G- q6 ^1 c8 {5 t) l6 i5 H: P Rthe neck revealed no thyroid enlargement.
; U' f& o& P4 o& oThe genitourinary examination was remarkable for9 M- O" P0 T6 K/ y b
enlargement of the penis, with a stretched length of
3 t# f& N! B d0 `! V8 cm and a width of 2 cm. The glans penis was very well
, U% C* S- V- C( m+ ?+ Pdeveloped. The pubic hair was Tanner II, mostly around1 _' t% W, B2 f* j! w" p5 z) g
540
& y) L5 s, p, J3 t7 Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 {2 R* C0 M! E y" B* g! }
the base of the phallus and was dark and curled. The
% h8 F# o# @+ I; Utesticular volume was prepubertal at 2 mL each.1 C& V. ^+ c8 u
The skin was moist and smooth and somewhat' h* P8 X K$ y! d/ a# m* B
oily. No axillary hair was noted. There were no
: j! R; I/ W- Q# J. Tabnormal skin pigmentations or café-au-lait spots.' O) d7 E u( V
Neurologic evaluation showed deep tendon reflex 2+
( D& o# q1 _$ [7 L: i& M' \) L gbilateral and symmetrical. There was no suggestion
% `, a8 X: f) ?of papilledema.
3 |% u5 s0 B* _- @Laboratory Evaluation( O7 ~, k( W) f1 g
The bone age was consistent with 28 months by
. [$ a% o: x8 u3 Busing the standard of Greulich and Pyle at a chrono-
5 ^+ f% R' X6 V: P1 N; Flogic age of 16 months (advanced).5 Chromosomal
! Q7 n% m2 {, @* D2 `/ \karyotype was 46XY. The thyroid function test
6 @! V0 s; O _% M3 eshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
4 h1 ^" U' @+ Alating hormone level was 1.3 µIU/mL (both normal).4 D/ N% r5 H5 r& f9 R" I
The concentrations of serum electrolytes, blood
/ l& |$ u3 n1 |3 xurea nitrogen, creatinine, and calcium all were
9 g) `9 _& N: G4 h9 h1 Swithin normal range for his age. The concentration/ b! w7 Z; ?) @" ]# y7 ?0 m
of serum 17-hydroxyprogesterone was 16 ng/dL8 b2 ~# a% J" D, m2 v6 l
(normal, 3 to 90 ng/dL), androstenedione was 20
% C% H$ _$ x" Hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
% o- r8 Q9 e* k; z2 N/ Kterone was 38 ng/dL (normal, 50 to 760 ng/dL),
; g8 n7 o, w8 J- T) f! Xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to+ u2 ]! {' W, | `0 }% L0 p
49ng/dL), 11-desoxycortisol (specific compound S)
; [- h( E" U5 }1 P4 s' G* Zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& D# |# N8 z+ j+ M* Y8 ltisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total& _2 |/ w/ j3 X
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ m7 R3 _8 I+ |; M% i# o
and β-human chorionic gonadotropin was less than
/ F9 k$ G4 @3 @! i7 G) ?, }, I. i% M5 mIU/mL (normal <5 mIU/mL). Serum follicular( e+ Z4 T* H/ s$ z: o6 l
stimulating hormone and leuteinizing hormone" j8 R, [, B1 U6 E$ ]' f& `
concentrations were less than 0.05 mIU/mL
% N" f3 o, L7 p2 u' L L(prepubertal).' G1 s4 S0 p* @. E, V V# k9 J
The parents were notified about the laboratory, }; r/ f7 w3 c3 s! L: y3 H' t+ c
results and were informed that all of the tests were$ k! W9 Z8 j* l! c: x( \
normal except the testosterone level was high. The( e; L: d; [" `) ~8 ^/ U, L
follow-up visit was arranged within a few weeks to
) K2 n" T% @0 I2 wobtain testicular and abdominal sonograms; how-
3 V" V1 A$ [7 N" Rever, the family did not return for 4 months.: G+ r8 ]7 G7 N/ W/ l2 w
Physical examination at this time revealed that the) G- t. {. ?# n# S
child had grown 2.5 cm in 4 months and had gained0 Q3 L* a# k/ s! g
2 kg of weight. Physical examination remained
8 n8 L5 J, L2 f4 E3 H; u" Punchanged. Surprisingly, the pubic hair almost com-
9 r' p- Y( ~7 f5 _, Y* [pletely disappeared except for a few vellous hairs at5 \" A" f( }( C+ L
the base of the phallus. Testicular volume was still 2. h- @" V5 n" a0 X* [7 p8 D
mL, and the size of the penis remained unchanged.
+ ^5 g& P5 ~. b/ x1 {# @+ n# CThe mother also said that the boy was no longer hav-# E* c( V" o+ E
ing frequent erections.
5 y+ S& f C* b$ ?" _! r/ vBoth parents were again questioned about use of
$ j. e! v. T% e8 B6 B& F5 L: \" Many ointment/creams that they may have applied to5 ?; r) y2 B/ P7 G& \4 p% x. Q
the child’s skin. This time the father admitted the
* i M: Z3 C' b$ ETopical Testosterone Exposure / Bhowmick et al 541
r$ h( f$ v1 U; T2 D" Ouse of testosterone gel twice daily that he was apply-( z( k' _/ N, u2 ^ o5 c% W8 Y
ing over his own shoulders, chest, and back area for, G- ]" o: u: u- k4 r3 V! b, H2 y
a year. The father also revealed he was embarrassed1 Z2 d. }/ \9 c# b& Q$ _
to disclose that he was using a testosterone gel pre-# _& {/ l' G! O
scribed by his family physician for decreased libido
) x0 S0 s2 l, xsecondary to depression.; f1 Z( T- k8 m3 y; V& f. r/ T& r
The child slept in the same bed with parents.
7 g5 ]8 I$ t# c* o. q6 _The father would hug the baby and hold him on his, t2 j0 [' F. p h+ N% k7 M! c
chest for a considerable period of time, causing sig-! E% }% H' ~4 Z3 _: g% S3 @9 h
nificant bare skin contact between baby and father.
- Z$ l Z9 A' \8 {: f. G I/ dThe father also admitted that after the phone call,
2 w. S. B$ \. x$ Y! Twhen he learned the testosterone level in the baby( N* E6 c6 S) i2 K
was high, he then read the product information/ n# E% G3 X8 \& t' z
packet and concluded that it was most likely the rea-
9 o8 p4 D0 K& o6 nson for the child’s virilization. At that time, they1 h) j; m7 S% C& \+ w9 H( ?
decided to put the baby in a separate bed, and the; [8 N7 C! c x2 R
father was not hugging him with bare skin and had8 i9 A1 Q# d2 j1 x; ~
been using protective clothing. A repeat testosterone; G9 B5 U' q( p( i/ v7 j9 {2 W
test was ordered, but the family did not go to the C4 s% C% R6 D) w+ \
laboratory to obtain the test.
) o, \0 k# T! v3 nDiscussion
$ q( |' T6 ]( OPrecocious puberty in boys is defined as secondary9 l- F7 k) o' U9 ?0 M" g+ U
sexual development before 9 years of age.1,4) F# F. w9 V0 C& @& t) l8 [
Precocious puberty is termed as central (true) when% {$ [: \2 v" U2 I0 @- o; G. m
it is caused by the premature activation of hypo-% r7 Q' T: m0 G/ U5 t
thalamic pituitary gonadal axis. CPP is more com-
+ R7 X; d% J" ]5 M: d' l4 ^mon in girls than in boys.1,3 Most boys with CPP( H2 r+ ?$ ^3 M% v& R- N
may have a central nervous system lesion that is F! s, t# r5 | l W# w! q
responsible for the early activation of the hypothal-; P- P& ]; @3 w! g
amic pituitary gonadal axis.1-3 Thus, greater empha-
3 p" z% O, \6 t% k/ H5 w) wsis has been given to neuroradiologic imaging in
( C5 n9 h* Z( v8 p2 f; Qboys with precocious puberty. In addition to viril-. g/ q1 C2 [1 t$ [6 {3 e) _
ization, the clinical hallmark of CPP is the symmet-
$ u N8 p5 ^. Y: x" Q! D3 ]; v( orical testicular growth secondary to stimulation by l. [/ J8 t8 A; X/ R
gonadotropins.1,3
0 j- |7 A. N* ]2 C/ H' Y- gGonadotropin-independent peripheral preco-* V0 `7 j8 \- o2 s& V) r% ?
cious puberty in boys also results from inappropriate
* n2 k( i. e) d t d2 ^5 Qandrogenic stimulation from either endogenous or# h7 k/ K9 S: m* f
exogenous sources, nonpituitary gonadotropin stim-
1 Y2 ?% P0 x# r; u. m: Aulation, and rare activating mutations.3 Virilizing" q* @* C J$ i4 q
congenital adrenal hyperplasia producing excessive
! d& K' h% S: ?6 J# Uadrenal androgens is a common cause of precocious
; ~" B7 u$ E( N: `, }puberty in boys.3,40 i6 p) k M, {/ {$ A$ e
The most common form of congenital adrenal& w9 K3 x! @' P( ~# w: J9 n0 v) B% O
hyperplasia is the 21-hydroxylase enzyme deficiency.0 {" x" T% b% q3 x4 c
The 11-β hydroxylase deficiency may also result in
& v( l& R+ a4 z4 Gexcessive adrenal androgen production, and rarely,
" B/ N! n1 F* o5 Zan adrenal tumor may also cause adrenal androgen
. f l9 r3 M/ u. V7 Lexcess.1,3
* o% U0 k: t4 cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 R# n7 u J4 j* D
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 h+ |) F" Q9 e. |- V- ~A unique entity of male-limited gonadotropin-& S B1 p! Q, `. ^( J u, Z- `' G
independent precocious puberty, which is also known q* O; L' q/ f! R9 ^
as testotoxicosis, may cause precocious puberty at a
- H" Y; Y& z! s" J9 [+ I* Svery young age. The physical findings in these boys
! X( F, z- T8 v7 B) k$ ^* J" F3 Y4 Iwith this disorder are full pubertal development,
D8 Q _ N4 L4 J' ~including bilateral testicular growth, similar to boys
+ k! {7 t4 g D/ p0 O0 ~with CPP. The gonadotropin levels in this disorder
( ]9 q* E/ ]# u- h# c* `are suppressed to prepubertal levels and do not show
) C8 y) R( a3 a7 G2 _0 |: Vpubertal response of gonadotropin after gonadotropin-
1 s- j8 _3 Y; a% T1 f1 {5 n; R* ^releasing hormone stimulation. This is a sex-linked
/ D* i# A: s, J uautosomal dominant disorder that affects only
5 }2 M9 }/ ]* g, f% p4 V( ?males; therefore, other male members of the family
& }% H V2 H T" |# g! c1 emay have similar precocious puberty.3
( p* H$ S% n7 T! y. L; J# ~In our patient, physical examination was incon-- \/ R4 Z8 e- C) J, }7 N
sistent with true precocious puberty since his testi-
/ F- f3 t8 D0 a7 | l: V5 xcles were prepubertal in size. However, testotoxicosis6 U! j: ~/ W4 Y' R0 d% W0 Z; o
was in the differential diagnosis because his father
* s$ Q+ ^. }# q. g4 R: E& f. ?started puberty somewhat early, and occasionally,( s0 f2 T% ~6 d# e% ]9 _( V6 I% Z6 b
testicular enlargement is not that evident in the
8 o% K; k3 ~8 B4 b5 ?# ybeginning of this process.1 In the absence of a neg-
* s$ Z/ N/ P; m* a; r0 u8 oative initial history of androgen exposure, our
& H0 g4 I( E# ?2 _! m! a2 c7 Z" I# Qbiggest concern was virilizing adrenal hyperplasia,
5 Z0 w1 B W5 S3 Qeither 21-hydroxylase deficiency or 11-β hydroxylase
' b& x8 ]; t: v' t) S- Mdeficiency. Those diagnoses were excluded by find-
: o+ |9 K2 I( R5 S$ `ing the normal level of adrenal steroids.9 Q) N" `* x+ @. N3 Z
The diagnosis of exogenous androgens was strongly8 @" Y! ~" O2 v! [* \1 o
suspected in a follow-up visit after 4 months because1 \# B" |- J0 K. e1 x" E b
the physical examination revealed the complete disap-
% ]6 f( I3 R# f; j$ T# E2 Jpearance of pubic hair, normal growth velocity, and5 O* U) X5 y, b
decreased erections. The father admitted using a testos-- Z/ v. m, N- x. Q
terone gel, which he concealed at first visit. He was* H, b' a( [% M$ Q$ }. z$ s# D
using it rather frequently, twice a day. The Physicians’
- g* K- ^6 I, F/ f o( x9 JDesk Reference, or package insert of this product, gel or( m) t' o/ l! x6 F8 ^* N* `+ d% E
cream, cautions about dermal testosterone transfer to
9 m9 o. q, H' |' wunprotected females through direct skin exposure.
, B: L6 g! k* `0 p5 WSerum testosterone level was found to be 2 times the
4 L/ @- B1 T) I1 T6 T9 K" S( B1 ibaseline value in those females who were exposed to
$ y+ y' i& l: }! t+ M/ Veven 15 minutes of direct skin contact with their male- D8 X" H8 V5 `7 |6 \5 u n
partners.6 However, when a shirt covered the applica-
. {+ ]' i* i* c9 X5 Y9 Ltion site, this testosterone transfer was prevented.
+ Q7 R4 G/ V+ ? q5 \& ] o' XOur patient’s testosterone level was 60 ng/mL,
* y8 t$ D+ k& E( Zwhich was clearly high. Some studies suggest that
9 A- t5 M4 R" n9 J- S3 P* i( Sdermal conversion of testosterone to dihydrotestos-3 J# ^6 C+ w# b# ]: x
terone, which is a more potent metabolite, is more/ D8 R$ K' t. ~ t2 g/ t8 M: V
active in young children exposed to testosterone# N) X) N$ K* Y4 g& ~# T& N8 H
exogenously7; however, we did not measure a dihy-
5 H$ `; Q3 o# e2 }. \ V+ sdrotestosterone level in our patient. In addition to
% ^- h7 q1 I3 r* B4 ~0 Gvirilization, exposure to exogenous testosterone in
2 _) e. y8 d: K- @1 e+ \7 mchildren results in an increase in growth velocity and
; W+ Y0 l( d1 t1 R5 |1 Qadvanced bone age, as seen in our patient.
4 T! [# |; U9 o3 ]2 Q* L+ I: JThe long-term effect of androgen exposure during4 d: a1 g* {) l8 ^" c
early childhood on pubertal development and final& l6 D8 [* b9 J# B
adult height are not fully known and always remain+ K9 z& |' T* M. w! @+ l3 [
a concern. Children treated with short-term testos-4 e0 S" a, i9 R# m' i
terone injection or topical androgen may exhibit some
4 ~# G$ A; B$ |, x$ P! yacceleration of the skeletal maturation; however, after$ b* o4 f9 |, \5 x- E2 p
cessation of treatment, the rate of bone maturation
8 y: {$ B) w) s/ `: C- Pdecelerates and gradually returns to normal.8,9
- f, Q: |+ N1 {7 eThere are conflicting reports and controversy
8 i# D; w0 U% C' e+ q2 k; \2 nover the effect of early androgen exposure on adult7 Z7 C# I2 g; N3 l
penile length.10,11 Some reports suggest subnormal" B1 t' @1 P" q- j+ [! g4 l
adult penile length, apparently because of downreg-
' `, m: L% }6 G7 X7 j4 k- _ulation of androgen receptor number.10,12 However,6 G( ^' s4 x! X' @' I* u, H1 r
Sutherland et al13 did not find a correlation between$ U6 L# r: U+ K- U2 E& q
childhood testosterone exposure and reduced adult) M# O0 e/ p/ Q1 U3 |+ ~+ D3 f
penile length in clinical studies.
1 j; P' g' `7 |Nonetheless, we do not believe our patient is
- E) n% F. D# b, Zgoing to experience any of the untoward effects from" k6 ?9 t: R3 L8 W0 [+ s3 Y
testosterone exposure as mentioned earlier because
5 j9 z2 w6 T( n. h/ Fthe exposure was not for a prolonged period of time.; F6 i0 P+ K- n$ g, _
Although the bone age was advanced at the time of
" e# E3 O) V: _diagnosis, the child had a normal growth velocity at p7 W3 M7 {% \% b; \, g# _
the follow-up visit. It is hoped that his final adult" i4 @% Q, F9 P7 h4 X
height will not be affected.
$ K2 ^& V! p- `Although rarely reported, the widespread avail-
8 A' y1 T3 G4 N5 R$ b' v1 H2 Aability of androgen products in our society may
2 Y$ }* `. `" sindeed cause more virilization in male or female
) W' b6 l' `) H. |' P$ F4 N4 _5 Kchildren than one would realize. Exposure to andro-
$ A! |" B* X: S9 y. u8 G# fgen products must be considered and specific ques-
5 v8 X% S; M& d3 I- } n1 j4 B4 J. stioning about the use of a testosterone product or
5 C1 t; J, t2 B" ]4 b& j. agel should be asked of the family members during1 }# W4 e+ K: g/ P* a0 ]
the evaluation of any children who present with vir-
) W0 r% O7 y& r( oilization or peripheral precocious puberty. The diag-, \: B- ^1 V( u. v0 A* W
nosis can be established by just a few tests and by, X6 w+ h7 r9 x
appropriate history. The inability to obtain such a
% i0 y: M% b8 h3 u( x9 Y- lhistory, or failure to ask the specific questions, may
" B5 k! z1 w0 d9 u1 N6 lresult in extensive, unnecessary, and expensive" t1 O4 l6 E- }5 W. C
investigation. The primary care physician should be
2 M) K) X0 A4 F4 y& }aware of this fact, because most of these children6 z5 @, H) c( ~+ M$ x# @: Q0 Y
may initially present in their practice. The Physicians’
- J: h$ w+ z# d r/ BDesk Reference and package insert should also put a
8 H) n1 m9 l/ A8 I9 j$ Y. a/ Gwarning about the virilizing effect on a male or
) h y. O( _8 k( ^. Vfemale child who might come in contact with some-
; K; T( y4 V3 |+ a) Q, sone using any of these products.
) J& b7 m0 u+ R8 x2 uReferences! o1 s0 b$ b% @4 l0 S; x
1. Styne DM. The testes: disorder of sexual differentiation" G% u# F( u0 ]
and puberty in the male. In: Sperling MA, ed. Pediatric
0 Y- x* s- Y6 V/ eEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% O* ~: F* ~7 x9 I2002: 565-628., l8 e3 a2 B7 a6 l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ `: X- \- r2 S" U9 \puberty in children with tumours of the suprasellar pineal |
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