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Sexual Precocity in a 16-Month-Old
& | z( J- {3 |$ g/ O+ X6 KBoy Induced by Indirect Topical7 \2 c# Y& A, [% G+ N
Exposure to Testosterone
* r/ W/ I5 p- k( h6 d/ w4 }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. i" e; {- L* ?) D, Z: {5 K' @
and Kenneth R. Rettig, MD1" l/ X1 G) y9 N
Clinical Pediatrics
5 N# e+ M: g% z6 ? G$ y$ Z; ?Volume 46 Number 6, {) R# k' m9 p4 W2 s8 s; y" j
July 2007 540-543
$ f5 J, Z2 s6 Z3 G8 C. N© 2007 Sage Publications
. y- C( z! D' T' ]4 ^# ~* ?10.1177/00099228062966519 Q7 W8 E9 O4 W4 B8 `
http://clp.sagepub.com, e0 v: _) c# G% w
hosted at2 u: a/ \6 ~! ^( k; O" x
http://online.sagepub.com( |; b( q" S9 U
Precocious puberty in boys, central or peripheral,
. ~7 w9 z; P' `- [8 s1 Z; Vis a significant concern for physicians. Central `0 W1 D; ?, E
precocious puberty (CPP), which is mediated
I; }, \9 G$ Y* p9 ythrough the hypothalamic pituitary gonadal axis, has' e- g Z/ p( ~+ Y/ l& G2 w
a higher incidence of organic central nervous system% f _& d/ c* O* r
lesions in boys.1,2 Virilization in boys, as manifested' t. b h+ o* ~' {7 @
by enlargement of the penis, development of pubic8 n5 a1 D# F7 C$ ], e1 ]6 j5 W0 u
hair, and facial acne without enlargement of testi-
0 B- l: k8 T6 S" M8 Xcles, suggests peripheral or pseudopuberty.1-3 We. m. V3 O/ q) j6 b& @4 T
report a 16-month-old boy who presented with the
& W# v: v0 @0 ^3 menlargement of the phallus and pubic hair develop-
* c, D" |3 D' O' U$ pment without testicular enlargement, which was due
/ u6 L" O6 U' E k$ u" G8 c& r' G7 xto the unintentional exposure to androgen gel used by
# a( U. y3 V) Z8 Z) x2 Kthe father. The family initially concealed this infor-
8 N6 C# e2 ^" C5 K2 F( ~$ s4 emation, resulting in an extensive work-up for this
* R. i* q3 `% a( R6 ^7 n) ychild. Given the widespread and easy availability of
2 W; A% d0 p6 ~$ b$ ctestosterone gel and cream, we believe this is proba-; `0 W, n4 r. \
bly more common than the rare case report in the
+ ^0 N* M% Z' _3 Oliterature.4
E3 U5 S. I6 m qPatient Report1 M" X+ _* h4 ?- Z' V) w; Z3 f
A 16-month-old white child was referred to the
: ]: X( L5 \7 `$ ] Rendocrine clinic by his pediatrician with the concern; b; N: H y5 O' E
of early sexual development. His mother noticed
! }/ m L3 V) v" `light colored pubic hair development when he was1 `7 B# r, p6 i( Z3 ^3 ]
From the 1Division of Pediatric Endocrinology, 2University of5 S3 q* P/ z D. h' o
South Alabama Medical Center, Mobile, Alabama./ s8 @- q1 M4 ^" l
Address correspondence to: Samar K. Bhowmick, MD, FACE,
2 D7 P' h- \: IProfessor of Pediatrics, University of South Alabama, College of; O- [$ t: J a1 }: c. X% B
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( N( m9 u) Z1 n! qe-mail: [email protected].
: S* ` E/ H$ N. b5 _about 6 to 7 months old, which progressively became
z, B# }# {' O+ Q3 Q5 v& d Edarker. She was also concerned about the enlarge-3 h2 `7 U: h3 _% W9 t
ment of his penis and frequent erections. The child4 V* `' M0 a8 w1 ?, t
was the product of a full-term normal delivery, with# l' {1 N* g1 U* R2 U" S
a birth weight of 7 lb 14 oz, and birth length of* u+ l- i: w; Y
20 inches. He was breast-fed throughout the first year( Y3 z6 z4 {/ g; X& x/ o4 Z
of life and was still receiving breast milk along with7 w8 X+ F8 c4 R, P( D# U
solid food. He had no hospitalizations or surgery,
4 I/ ?( u3 _9 f& H; Z yand his psychosocial and psychomotor development
4 w% m9 y( K3 o/ m; d0 B( owas age appropriate.
7 J, E8 z* g- }& e$ |3 eThe family history was remarkable for the father,$ }3 Q2 }/ {) P) R4 y! S
who was diagnosed with hypothyroidism at age 16,$ {; w0 s' F$ B1 J) B6 W6 v
which was treated with thyroxine. The father’s5 T" F7 w" |8 V7 L/ D0 T
height was 6 feet, and he went through a somewhat
7 Y! E* V7 o' h0 x: Z ]early puberty and had stopped growing by age 14./ L/ v% S+ H2 M2 L$ m4 d9 H
The father denied taking any other medication. The
/ Y: g4 o9 i5 [. X+ Z% }! hchild’s mother was in good health. Her menarche
L( U. X. q- r( I) e/ y* s2 uwas at 11 years of age, and her height was at 5 feet0 i- C* L9 G+ K5 d6 t. `) t
5 inches. There was no other family history of pre-& r' y$ U1 i6 @4 N( v
cocious sexual development in the first-degree rela-4 n0 k" O# m1 j0 H, I
tives. There were no siblings.
& X B2 c7 Z$ m' NPhysical Examination
- ~! \3 y( a5 `8 i1 IThe physical examination revealed a very active,
9 c. T" P& W3 t- dplayful, and healthy boy. The vital signs documented
' L$ Z/ I& t# P. X7 qa blood pressure of 85/50 mm Hg, his length was
6 K2 K" v6 i4 D, F90 cm (>97th percentile), and his weight was 14.4 kg, b* e) p% F {4 R
(also >97th percentile). The observed yearly growth2 ]' J4 O& F4 h( ~
velocity was 30 cm (12 inches). The examination of4 P2 }5 l* b$ H3 y; {! F# u0 x; P8 n j
the neck revealed no thyroid enlargement.+ Q% d! h' x0 u' {3 N! m
The genitourinary examination was remarkable for% M: ^5 v- p' @' E
enlargement of the penis, with a stretched length of
& X- F r* F/ Q6 b1 R7 l8 cm and a width of 2 cm. The glans penis was very well8 W5 p% N) v( |0 i* W4 q
developed. The pubic hair was Tanner II, mostly around
# f: D* \7 c- d- H9 Q( {540" v7 P ^$ V- C1 H: w4 C A! E# \
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: }5 x4 N- V/ O% V) d/ |9 p- lthe base of the phallus and was dark and curled. The6 l3 I0 q, X) k
testicular volume was prepubertal at 2 mL each.
. _! Z- K n8 g. t# C+ PThe skin was moist and smooth and somewhat4 b+ m. L0 y1 z* `1 A
oily. No axillary hair was noted. There were no
" T k" \; @: ~" P( T0 \! G; Sabnormal skin pigmentations or café-au-lait spots.4 @. z. A1 K& x% E
Neurologic evaluation showed deep tendon reflex 2+* {. |& a. f1 ~7 s+ B5 j7 j1 X
bilateral and symmetrical. There was no suggestion# A$ h" g. I6 I; d
of papilledema.
* H% q8 V% N( K- vLaboratory Evaluation; w" D% M: t7 l2 N
The bone age was consistent with 28 months by' I$ `/ r9 ~" w, Z& k1 K8 {6 W
using the standard of Greulich and Pyle at a chrono-% f" N! Y' w2 `$ O# C# o+ }& k$ s
logic age of 16 months (advanced).5 Chromosomal
- G+ } b! `8 Akaryotype was 46XY. The thyroid function test
4 V+ D$ {4 d: D" w( x3 ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-7 n8 K, G3 [, _/ E" y
lating hormone level was 1.3 µIU/mL (both normal).7 n3 h: {- v- s6 i" {+ \. Q2 N P
The concentrations of serum electrolytes, blood
L7 i) x+ ?+ b! U) R* burea nitrogen, creatinine, and calcium all were
% m& I% D4 C w6 B- j, z, d9 iwithin normal range for his age. The concentration
D$ `: g2 h' q8 Dof serum 17-hydroxyprogesterone was 16 ng/dL" r* P/ }% Q& m# c1 W j/ V
(normal, 3 to 90 ng/dL), androstenedione was 20$ t( f; S! t1 l+ Q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, w2 e4 v( Q/ C* g" C
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 g4 `" Y( D; r5 c1 K; xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to" i5 t3 Z$ [) P% G- p0 W! ?
49ng/dL), 11-desoxycortisol (specific compound S)& T1 K! H5 j. R! O: J) [
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 R3 P3 H5 m& A' |tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
9 L, a% z! ?2 Jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL), V% S! C2 ?! {$ ]! c, m" T* u
and β-human chorionic gonadotropin was less than" S! c" w9 l0 b
5 mIU/mL (normal <5 mIU/mL). Serum follicular3 n( s% o2 X f6 i( Y- K
stimulating hormone and leuteinizing hormone g: j# Z2 Z: e) f% j+ H* l8 _
concentrations were less than 0.05 mIU/mL
1 P; P- l# c u% t) h(prepubertal)./ s# j7 u" }6 W ?
The parents were notified about the laboratory' E* T/ D2 V% s+ y0 z [' ~
results and were informed that all of the tests were2 ?% S# z7 @5 z# \$ k5 o# K! L
normal except the testosterone level was high. The
( Q1 u v9 `/ e. B! ]* H7 mfollow-up visit was arranged within a few weeks to9 n# Q% y' r1 c) n0 o2 k
obtain testicular and abdominal sonograms; how-) D" D6 ^/ Z% O+ t! i" M* B
ever, the family did not return for 4 months.
7 _3 S# p" x) RPhysical examination at this time revealed that the/ _: c5 h' j2 o2 W! w# ]- \, t2 X- z
child had grown 2.5 cm in 4 months and had gained0 ]3 \+ p V; l8 y1 ?( J# s
2 kg of weight. Physical examination remained; J' v( E2 c# `) n0 t, Q) [
unchanged. Surprisingly, the pubic hair almost com-
6 X( N( ~- f# @2 k) `+ z! Npletely disappeared except for a few vellous hairs at$ S' P9 P, r& z% [5 n
the base of the phallus. Testicular volume was still 2
- O* \" L$ Y" \ c* DmL, and the size of the penis remained unchanged.
1 G! o5 Z z3 z& ^The mother also said that the boy was no longer hav-
" s& X3 i1 [- l$ ?9 @' Ring frequent erections." I* S0 c9 w0 ~3 `
Both parents were again questioned about use of
8 `* ~6 S6 m0 J( m4 d3 Qany ointment/creams that they may have applied to
/ E8 ^$ f: c; E' \( ~$ }* Fthe child’s skin. This time the father admitted the( s3 N2 E3 C* |2 z' S% X3 h
Topical Testosterone Exposure / Bhowmick et al 5416 ]( K& S# L" E* J! n- h9 U% \$ Q
use of testosterone gel twice daily that he was apply-$ o) E/ B0 L4 k6 A) c7 i
ing over his own shoulders, chest, and back area for
9 h3 _* a9 j* [3 Q$ d. b( ya year. The father also revealed he was embarrassed9 K) z* Q1 U* c; K# H, d7 ^
to disclose that he was using a testosterone gel pre-% q1 d% w* h, j1 \
scribed by his family physician for decreased libido
% B( Z% u, d$ l9 t# u5 A8 Z7 Lsecondary to depression.
0 ]1 L! U! r( k8 q5 g$ a0 ?* h# PThe child slept in the same bed with parents.
2 x- y( [ q0 w5 V& GThe father would hug the baby and hold him on his) d1 }- J. ?+ i7 ]
chest for a considerable period of time, causing sig-
4 ?+ r5 W" [! P3 E) W1 ?# wnificant bare skin contact between baby and father.
2 [9 E3 |- E! ~+ f; o! I4 p5 [The father also admitted that after the phone call,; g1 C4 c- I: o$ y# C% @% V2 q! e
when he learned the testosterone level in the baby% C' a$ w2 C' w0 v" l) W( S+ Z
was high, he then read the product information. c' D) W$ }; B0 ]* W& H
packet and concluded that it was most likely the rea-
% I0 w0 O/ R' o! B( A- h& e. d" u! Dson for the child’s virilization. At that time, they
1 ?* ^! ^* Y8 T" h, ~2 B+ A Jdecided to put the baby in a separate bed, and the0 }; M Y- F: k5 a+ {: q6 _$ Y
father was not hugging him with bare skin and had
# X% K2 k! v, p. Q3 Vbeen using protective clothing. A repeat testosterone- N5 E) m5 ]6 [/ X, j
test was ordered, but the family did not go to the
7 b5 a1 C" `" Q, G: B/ dlaboratory to obtain the test.
9 d" H7 |) ^- ]! }Discussion* {$ D/ O. `1 J' K+ b+ B
Precocious puberty in boys is defined as secondary
@+ O) E- X" j, Msexual development before 9 years of age.1,4
3 R" G" y( A, K; _Precocious puberty is termed as central (true) when
' W. W* S& f* C7 e+ u/ ~; d: w1 uit is caused by the premature activation of hypo-
: B0 v" n; i ]0 P2 Q Othalamic pituitary gonadal axis. CPP is more com-
% s7 q* c) f( J' y0 n7 p2 Zmon in girls than in boys.1,3 Most boys with CPP
) o% p8 M2 L3 y8 u @, ~8 wmay have a central nervous system lesion that is
- P" E0 R& _/ \% i1 \: yresponsible for the early activation of the hypothal-: v4 M- G, r: }; Z4 w- o8 c
amic pituitary gonadal axis.1-3 Thus, greater empha-
]7 Y( a, J# v! Isis has been given to neuroradiologic imaging in+ j% U# r9 f3 L! H
boys with precocious puberty. In addition to viril-
& z% n5 n$ x( u3 B3 [* Sization, the clinical hallmark of CPP is the symmet-
3 y6 Q6 N5 R0 f( _4 H& Frical testicular growth secondary to stimulation by
- T0 ?# z2 z$ j3 [! ~- ~6 X% Y. c0 vgonadotropins.1,3
|4 _5 ^/ V, j% O+ [! Q: |" xGonadotropin-independent peripheral preco-8 y) v0 a# o2 b' x0 ]) R
cious puberty in boys also results from inappropriate
0 ~% H2 @6 V% l& G. k1 Handrogenic stimulation from either endogenous or
2 T8 r% v$ n( Sexogenous sources, nonpituitary gonadotropin stim-
2 R b5 ?) V' I( fulation, and rare activating mutations.3 Virilizing
$ [3 Z1 ~* z# c- Gcongenital adrenal hyperplasia producing excessive
# q. m4 m" h. M5 u8 L, H2 cadrenal androgens is a common cause of precocious
: D- I5 O4 r. o' ?) zpuberty in boys.3,4
- z" p5 v1 @- @. N. W% e$ WThe most common form of congenital adrenal0 E/ D0 J3 V& V, ]; D. N/ f6 v6 R
hyperplasia is the 21-hydroxylase enzyme deficiency.1 Y% m; Z5 @ z* A: ^$ r U% J4 S0 v
The 11-β hydroxylase deficiency may also result in
3 M8 |7 X( Q6 r# [8 Vexcessive adrenal androgen production, and rarely,% Y2 Q7 I7 j8 C$ d8 j0 L9 y
an adrenal tumor may also cause adrenal androgen* r S, P4 S. W2 p1 Z9 z+ Y- S
excess.1,3
5 P& M+ s8 Z5 |; ~' `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% G2 R/ K( y5 Q: ?& q7 A' X
542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 A' [, W M# _8 t3 _" \" G/ l' K
A unique entity of male-limited gonadotropin-
# T2 v' G9 q% |independent precocious puberty, which is also known
; B, A1 B1 p" n7 Jas testotoxicosis, may cause precocious puberty at a/ `0 p9 m$ \2 g" t+ `7 Z
very young age. The physical findings in these boys; n) t" T- L+ i. w2 K0 l/ l2 f$ J; a \
with this disorder are full pubertal development,
3 m6 {/ S N3 Z- |6 z' s, dincluding bilateral testicular growth, similar to boys3 b4 }5 _6 P( u
with CPP. The gonadotropin levels in this disorder& {. w% h& B# b0 K ^3 C6 E$ O
are suppressed to prepubertal levels and do not show0 H( m) N/ K5 e/ i$ P) o' U
pubertal response of gonadotropin after gonadotropin-8 t% v: C, e6 e
releasing hormone stimulation. This is a sex-linked! g" a k K" y9 u V. ]( w+ I4 ]1 j$ }" Z
autosomal dominant disorder that affects only0 Q( N2 r9 S* ^. A) L6 ]' s0 f2 [
males; therefore, other male members of the family
5 t; d# a( w6 O; Ymay have similar precocious puberty.3
) u3 ~7 `0 n" W5 b a' N1 wIn our patient, physical examination was incon-
: X9 `: N5 f- `" F9 |1 P L- Zsistent with true precocious puberty since his testi-- q% P1 A, J7 \9 E6 C
cles were prepubertal in size. However, testotoxicosis3 f' G- @6 I$ A8 p: ?+ A
was in the differential diagnosis because his father: u3 j2 T# k( K" @' d
started puberty somewhat early, and occasionally,
5 M' _& `' w2 J. Y4 n7 D; ]testicular enlargement is not that evident in the
* l; [3 Z6 ^# b& t% Ubeginning of this process.1 In the absence of a neg-8 _ A2 v. ~4 X" Q( I9 X8 v: e+ F
ative initial history of androgen exposure, our8 H4 w3 |. Z* K+ h1 c
biggest concern was virilizing adrenal hyperplasia,9 J) H/ \5 H5 t/ N
either 21-hydroxylase deficiency or 11-β hydroxylase
Y5 q& J G2 u H5 |* K2 odeficiency. Those diagnoses were excluded by find-
: F$ L* K! b4 }ing the normal level of adrenal steroids.
3 j1 g" g V) B1 v: K% AThe diagnosis of exogenous androgens was strongly
& d! ~# j/ L! b+ gsuspected in a follow-up visit after 4 months because7 a( m- f7 H# \+ }4 ^; F9 Q, v5 q( l
the physical examination revealed the complete disap-
9 D9 F9 e9 K( |" ~: @5 Jpearance of pubic hair, normal growth velocity, and# ]7 F4 F' u4 N5 M1 v! k4 W, h
decreased erections. The father admitted using a testos-
' E; v C' V; q/ w3 d0 hterone gel, which he concealed at first visit. He was
/ L5 E1 ^% g: A( F* x1 Gusing it rather frequently, twice a day. The Physicians’% U2 ]% W2 u- K% t& I0 i$ p/ z
Desk Reference, or package insert of this product, gel or
4 f" G$ I: q, w2 v7 k5 jcream, cautions about dermal testosterone transfer to H; q" W( a. {- q
unprotected females through direct skin exposure.
; |" [# Q# E0 [6 X+ fSerum testosterone level was found to be 2 times the
. _9 B5 y. T5 g, |6 w4 Qbaseline value in those females who were exposed to; u# P- X c* {9 [: D, y8 T( q# s
even 15 minutes of direct skin contact with their male' |) _3 n+ A, T0 D3 G8 u2 e. K
partners.6 However, when a shirt covered the applica-
- K4 }' u+ @( ^ P: [( ttion site, this testosterone transfer was prevented.$ L; y$ N# m8 `: Y8 G" C
Our patient’s testosterone level was 60 ng/mL,
/ l# d/ k( i/ w+ u v) V! Ywhich was clearly high. Some studies suggest that& a7 J$ y3 z7 `/ L
dermal conversion of testosterone to dihydrotestos-
* m, ]) ?' [' I8 i, D- Rterone, which is a more potent metabolite, is more, W" z/ G3 K* G2 L) h9 r
active in young children exposed to testosterone" `5 S$ _ O! H4 \& a$ k; ~
exogenously7; however, we did not measure a dihy-) ~' L; v0 W! t: X
drotestosterone level in our patient. In addition to/ r2 Z0 g" S$ q* f3 w
virilization, exposure to exogenous testosterone in! F- I3 @) C9 `; j$ i
children results in an increase in growth velocity and: U9 F0 a! q& O9 o6 r
advanced bone age, as seen in our patient.
/ Y7 J2 P# k9 }# eThe long-term effect of androgen exposure during
9 |( Z |5 }5 v$ C7 Qearly childhood on pubertal development and final4 ~. Y0 w5 m- Q* {9 [: y
adult height are not fully known and always remain
" ~& _0 S. k5 Q( Q! Q0 }# Ya concern. Children treated with short-term testos-# q; A7 P( L' H
terone injection or topical androgen may exhibit some
5 r8 e" G9 V& z B) h) S" I4 V, Cacceleration of the skeletal maturation; however, after
7 H0 D# J, K" Gcessation of treatment, the rate of bone maturation/ {! l: V% ?: L5 o/ Z5 W6 M: y
decelerates and gradually returns to normal.8,9
: L6 I* B9 ]* } VThere are conflicting reports and controversy
& [8 @& Q5 u2 O& u# x) ^over the effect of early androgen exposure on adult) o, c# j I* G" b! }/ G) ?
penile length.10,11 Some reports suggest subnormal+ N4 s0 W- ?0 D, R5 f( t1 o2 V* P
adult penile length, apparently because of downreg-
! m, p* |$ e8 P, Oulation of androgen receptor number.10,12 However,+ R( W5 E5 N/ Q+ p- f* S, L
Sutherland et al13 did not find a correlation between1 i6 J( V9 h4 E Z, Z- @: C5 p
childhood testosterone exposure and reduced adult; H2 ?8 N+ z t$ r- Q$ \% ]
penile length in clinical studies.1 b) b- z6 F1 S3 l# n: ^
Nonetheless, we do not believe our patient is
' M* t$ ^- ~8 Wgoing to experience any of the untoward effects from
' q5 t4 B! K. ~% G) M$ btestosterone exposure as mentioned earlier because4 z& g/ Y- K' h7 v
the exposure was not for a prolonged period of time.. c3 p: j. S/ S5 ?4 }3 y! o5 Z, `# i
Although the bone age was advanced at the time of
& }, F& H9 r. q+ W. F$ g3 y2 gdiagnosis, the child had a normal growth velocity at
% \9 p+ d7 W$ P" J, D1 I! S! xthe follow-up visit. It is hoped that his final adult
6 P( z: n# P C2 r" `8 Fheight will not be affected.4 H1 Q, F) z1 O( I+ q# G& \& L
Although rarely reported, the widespread avail-
4 ^! _8 T3 {% U3 k5 s1 C9 g uability of androgen products in our society may# [! n2 u- T; ?
indeed cause more virilization in male or female& ?0 r# s. \% V3 }) s' Z9 d
children than one would realize. Exposure to andro-8 ^0 f6 j" u* V- r. ~' i1 ^. [
gen products must be considered and specific ques-- e7 d, i6 E+ s
tioning about the use of a testosterone product or7 i' Q- S. q$ @; Z5 D9 J* [
gel should be asked of the family members during
3 ]1 T- ~& X3 ]6 e8 ~ W, dthe evaluation of any children who present with vir-
. Y) a! Z: m. `. T9 [ilization or peripheral precocious puberty. The diag-
3 T- R, R2 w; d+ i/ Znosis can be established by just a few tests and by- Y# N, n" g; b( |/ Y
appropriate history. The inability to obtain such a
5 p' w) i) u0 hhistory, or failure to ask the specific questions, may' B2 v* X2 s1 ?: q
result in extensive, unnecessary, and expensive0 W3 @7 k$ d1 R& R" U- Z* L
investigation. The primary care physician should be
% ]& u, l9 g# T, @aware of this fact, because most of these children0 L0 o, W3 p% @) L4 u3 |, W' c
may initially present in their practice. The Physicians’
, H7 h; K. r9 a+ kDesk Reference and package insert should also put a
8 U, _. h W2 h, ~) l! p; |( R- J) owarning about the virilizing effect on a male or
4 r5 M0 H/ [ X8 E1 J$ [female child who might come in contact with some-
% _5 l# S8 j. r& f) ]& T5 R- a; Rone using any of these products. |* f1 i+ v* d, M
References) G# ]7 v; ~& A
1. Styne DM. The testes: disorder of sexual differentiation& p& }4 L" l/ i* _0 \/ w3 J: M
and puberty in the male. In: Sperling MA, ed. Pediatric
. U8 {3 ?/ F3 ]) {# \% XEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;0 p# a) P6 T/ S1 s: m# V; Z. I" T
2002: 565-628., ~) ~3 @9 j5 w% a, l2 w
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, o6 R; [- a" k" B4 A% `
puberty in children with tumours of the suprasellar pineal |
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