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Sexual Precocity in a 16-Month-Old
0 D' ?* J4 m* Q0 t5 \Boy Induced by Indirect Topical9 J+ G' _9 B( A3 i: S
Exposure to Testosterone% \6 g' |6 Y4 z- B9 [
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 h O& X$ N+ Eand Kenneth R. Rettig, MD1+ g4 i0 z* n; u. |2 B
Clinical Pediatrics; K& v, _+ Q8 e' [, }- W7 @& f# ]
Volume 46 Number 65 Y+ O/ }8 t/ k
July 2007 540-543
: }" d7 _6 s6 M2 Y s6 K% ^0 N© 2007 Sage Publications: ~6 M; t) m3 Q6 V+ s0 j# W
10.1177/0009922806296651
5 U/ A5 v& ]8 R" t% t3 Z# k# X3 Ohttp://clp.sagepub.com* i& I# T3 a5 C2 h' Y' }
hosted at" k+ M' P. G5 y6 U6 J8 [! e
http://online.sagepub.com
5 x# y! Y1 @; u& W( DPrecocious puberty in boys, central or peripheral,
* @' h o# @) Z3 x; c* [is a significant concern for physicians. Central: ]/ A# {( V# I/ {
precocious puberty (CPP), which is mediated5 K; _$ R" x& p+ N( G' P i
through the hypothalamic pituitary gonadal axis, has
' ?* ]/ K: `( |% I# L$ K1 }/ l# Za higher incidence of organic central nervous system
1 d* M# G+ |" [# Ulesions in boys.1,2 Virilization in boys, as manifested
$ q1 x% Y/ v# w. Y K8 kby enlargement of the penis, development of pubic w9 G6 `! r; L0 N) w+ @( n7 E
hair, and facial acne without enlargement of testi-
9 C( H/ B. [! z% [# I8 Rcles, suggests peripheral or pseudopuberty.1-3 We" b# T+ j! j! R3 w; j. y! C
report a 16-month-old boy who presented with the
- e$ U5 v# ?- R/ yenlargement of the phallus and pubic hair develop-3 `: y% p/ V3 o( b7 U# X
ment without testicular enlargement, which was due& f( S% g& Y% d( ^ q! i2 O$ Q4 m
to the unintentional exposure to androgen gel used by' _* C. N% k I6 i& g+ [
the father. The family initially concealed this infor-$ D! s0 b4 O1 Q5 I4 O2 `, x5 z B
mation, resulting in an extensive work-up for this
4 ]* n8 R9 c% Lchild. Given the widespread and easy availability of
9 M# T# \: }4 rtestosterone gel and cream, we believe this is proba-
3 t1 P# j0 e0 e# \; jbly more common than the rare case report in the
9 }6 E7 z7 d8 l1 w0 Jliterature.41 Y" Q4 u% l- l* h7 z* B
Patient Report2 X+ q$ L- L# M. F$ A: J2 r7 @
A 16-month-old white child was referred to the( I) e+ y, h# s/ i
endocrine clinic by his pediatrician with the concern
6 P$ H0 j( C x; Yof early sexual development. His mother noticed
9 D/ x2 f9 i, w8 X1 C+ R6 ]light colored pubic hair development when he was
' R( t( h. }0 I& L. e% hFrom the 1Division of Pediatric Endocrinology, 2University of
. b6 W9 n3 k* j8 rSouth Alabama Medical Center, Mobile, Alabama.
. s6 ?( M' U: T9 tAddress correspondence to: Samar K. Bhowmick, MD, FACE,
: o2 Q3 ]9 i6 J: y( B- p- x0 IProfessor of Pediatrics, University of South Alabama, College of. T6 y. e! Q( o4 b
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;; {/ o/ A; ~8 d- p$ \3 t5 q
e-mail: [email protected].* v) ?6 H+ v- O# X4 O
about 6 to 7 months old, which progressively became0 I+ S* C$ j* ^5 ~/ x0 x% f9 i
darker. She was also concerned about the enlarge-
* Z9 R% L! ]5 x+ }" g/ nment of his penis and frequent erections. The child
7 b3 D8 i q$ T& n; Jwas the product of a full-term normal delivery, with
: e+ R$ i5 a& M, g. ia birth weight of 7 lb 14 oz, and birth length of
5 J' f l" g, j9 J4 b! J# j& l20 inches. He was breast-fed throughout the first year, ?' U. D* W% R0 m5 h) Z
of life and was still receiving breast milk along with, \/ o/ Y$ a' o1 B* H1 b
solid food. He had no hospitalizations or surgery,
4 l7 `' k% a( Y5 |* F8 nand his psychosocial and psychomotor development( y* \' Y2 M: t. T4 D* H
was age appropriate.; }' R: O; H+ V# W! \
The family history was remarkable for the father,
( ?6 S' Z3 r! _2 pwho was diagnosed with hypothyroidism at age 16,
/ D$ @2 v% J! R8 [9 lwhich was treated with thyroxine. The father’s
w7 P1 L' j. @ ~; x h/ C4 J& jheight was 6 feet, and he went through a somewhat
/ b4 @2 W; C* I6 O3 _( J- g' Pearly puberty and had stopped growing by age 14.
' r6 @* L6 v* dThe father denied taking any other medication. The9 D; |) C* F9 j' \, X" X5 Z
child’s mother was in good health. Her menarche, D5 y9 m" |. O8 T$ u0 b4 N
was at 11 years of age, and her height was at 5 feet
% r7 q+ D* T5 {$ r5 inches. There was no other family history of pre-
$ E4 V- O4 u1 ]" v# ?) r) H. scocious sexual development in the first-degree rela-' j; d7 Y1 A1 |, ]1 m* \! ~( b8 Q
tives. There were no siblings.' P0 w' j$ x4 c) ]8 O5 w
Physical Examination
3 t$ Z" i" |2 TThe physical examination revealed a very active,( Z' R: [: K& H' D0 M2 d
playful, and healthy boy. The vital signs documented" l' q' L& }, X8 {7 |
a blood pressure of 85/50 mm Hg, his length was
T' M+ ^/ `5 s; L& t' k90 cm (>97th percentile), and his weight was 14.4 kg
* h; L5 Q! @; @0 g4 x(also >97th percentile). The observed yearly growth
- i, {5 {3 s; Y; t) x9 ?/ }velocity was 30 cm (12 inches). The examination of
7 e- X( i; p5 G9 \the neck revealed no thyroid enlargement.
$ b7 ~9 W# O! ~1 PThe genitourinary examination was remarkable for
1 j; O6 E6 B+ O# i8 f" S7 [enlargement of the penis, with a stretched length of9 X+ z2 C1 z& Z
8 cm and a width of 2 cm. The glans penis was very well& ~# r+ O& I. Z% O
developed. The pubic hair was Tanner II, mostly around! k ^* h5 F; Y
540* p o* n- s0 {' @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 ~8 P. b$ L! ~5 d/ k
the base of the phallus and was dark and curled. The
& }$ L2 i% ]) e( n& S) ktesticular volume was prepubertal at 2 mL each.
) H+ b: j+ p Z) r) GThe skin was moist and smooth and somewhat
* d: W6 D4 v& q c/ R9 noily. No axillary hair was noted. There were no
. z: L E4 A6 w6 h5 f- Q( f' zabnormal skin pigmentations or café-au-lait spots.
9 d3 G8 }! ?/ [# NNeurologic evaluation showed deep tendon reflex 2+2 p$ B- \( W2 P
bilateral and symmetrical. There was no suggestion
; E" p+ ^, R6 \' I# Eof papilledema.
& b3 m1 d0 v1 Q8 S& sLaboratory Evaluation
8 ^& p* N% U6 J# F! iThe bone age was consistent with 28 months by" ]4 g# T& j* o, D5 s" |! [
using the standard of Greulich and Pyle at a chrono- W# ~" O% \7 n0 n7 E( T1 y X
logic age of 16 months (advanced).5 Chromosomal) `1 ~+ {$ Z9 F9 D4 b. r* u ?( e
karyotype was 46XY. The thyroid function test) P0 [& ]* J: G5 O6 `2 W
showed a free T4 of 1.69 ng/dL, and thyroid stimu-2 {$ m Y- O. ^6 D
lating hormone level was 1.3 µIU/mL (both normal).
0 V1 k& x$ r- Z( _* \$ h" C e; UThe concentrations of serum electrolytes, blood
t6 U1 X/ G( ^* q& \, Y7 aurea nitrogen, creatinine, and calcium all were# R) Q* \4 m9 R" S1 Z8 J* W2 c
within normal range for his age. The concentration8 m( K. l/ Y9 T# P2 Y" `
of serum 17-hydroxyprogesterone was 16 ng/dL8 h* ~6 {, {! z2 O/ X: V f
(normal, 3 to 90 ng/dL), androstenedione was 20
8 q! b! j$ S: _) z- @/ Ung/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
; A6 _9 i, H2 K4 T7 V0 Q; Yterone was 38 ng/dL (normal, 50 to 760 ng/dL),0 Q8 @6 D9 Z3 o: e" p6 K) B) L
desoxycorticosterone was 4.3 ng/dL (normal, 7 to* i4 ]+ |( D2 k. d6 Q
49ng/dL), 11-desoxycortisol (specific compound S)
! D0 I1 O! V# L X3 h! o; o& jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) L* I+ U/ F" H/ o# U; g, Q q" v" O9 w
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* C, n$ H5 b& d/ h
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( H) `+ c2 Z4 U4 ~& p! y' _$ u( z# `
and β-human chorionic gonadotropin was less than: ^2 i5 _8 r( E; n
5 mIU/mL (normal <5 mIU/mL). Serum follicular
1 m' T8 r# _8 |2 R8 pstimulating hormone and leuteinizing hormone
7 o+ |4 a3 R. x6 i' Sconcentrations were less than 0.05 mIU/mL ^' y( k7 F$ ]
(prepubertal).: m( p) e! O+ r$ x3 C5 _( B; j
The parents were notified about the laboratory' I1 V1 ] _4 E8 ^' z
results and were informed that all of the tests were
/ Q* X6 i+ M0 L1 \normal except the testosterone level was high. The( }. { ~& d+ s* U2 a9 T1 i
follow-up visit was arranged within a few weeks to' o) R, f3 o7 U! \
obtain testicular and abdominal sonograms; how-
* i, p- e( a) Oever, the family did not return for 4 months.
! m5 x: u I8 ?Physical examination at this time revealed that the
) v' Q% S3 `$ C8 {# V( @. l; Zchild had grown 2.5 cm in 4 months and had gained U7 B3 {% G- {2 n0 h" F6 V! _
2 kg of weight. Physical examination remained1 y6 r$ R4 G7 Q# \! \& L* ?: X+ x- h
unchanged. Surprisingly, the pubic hair almost com-
4 @7 _8 Y; V; @pletely disappeared except for a few vellous hairs at. i/ }3 {5 ]$ u) `; F0 b+ o
the base of the phallus. Testicular volume was still 2
2 A3 E& D- W0 T# e# bmL, and the size of the penis remained unchanged.
, T' m( W% \; z) kThe mother also said that the boy was no longer hav-* g( m! O, [6 f7 W9 S# R+ M
ing frequent erections.) N3 ^8 z. o; r8 Z& y
Both parents were again questioned about use of& {5 r4 J& s" F9 X7 Y) o/ l
any ointment/creams that they may have applied to" ~- Z$ m! K; b: T9 D+ q
the child’s skin. This time the father admitted the
* E4 ^& G3 }5 l+ o! \' \! Q# y+ a5 uTopical Testosterone Exposure / Bhowmick et al 5417 N1 {8 N: P0 B# @! T6 N+ D9 b
use of testosterone gel twice daily that he was apply-& v: b3 @2 ~9 g' m6 w
ing over his own shoulders, chest, and back area for
0 \% l- Z, `" A' ]. x6 H2 o' v8 u2 T* Ra year. The father also revealed he was embarrassed
6 k( n0 U% @: e0 o3 ]3 Gto disclose that he was using a testosterone gel pre-$ {; U% I1 j8 [2 Q& Z
scribed by his family physician for decreased libido% j( a$ Q B5 a2 h, E7 X; ~( ~
secondary to depression.
/ a% k' ~# X& d5 }& eThe child slept in the same bed with parents.: \( e/ _+ j% d9 X b
The father would hug the baby and hold him on his
4 w' y- h, U, @/ {chest for a considerable period of time, causing sig- n! d0 i) }4 m% _3 M. D; b! s6 N- z
nificant bare skin contact between baby and father.2 Z* D: u$ \$ Y4 K1 \4 {
The father also admitted that after the phone call,% o; }6 e! y! t, \' _( w
when he learned the testosterone level in the baby& C f5 ^6 L9 U$ b* l# I& [
was high, he then read the product information5 V- L& N8 D# H
packet and concluded that it was most likely the rea-
8 O1 o4 I8 y; ison for the child’s virilization. At that time, they- Q8 c' H' l4 Z. |+ G
decided to put the baby in a separate bed, and the" O+ A9 K; x2 o9 ?. ~6 Z
father was not hugging him with bare skin and had
7 L2 @2 s5 f) O* l9 [/ Wbeen using protective clothing. A repeat testosterone0 N$ W0 B/ e. I/ P( f! O9 q
test was ordered, but the family did not go to the( [8 r: m8 t5 v* n8 n- G
laboratory to obtain the test., p/ f8 t* {9 H
Discussion
* ]6 `1 F# `: `4 q/ C. I% m. RPrecocious puberty in boys is defined as secondary7 L' u, x) n c* J, P
sexual development before 9 years of age.1,43 k% X# _1 w- ?8 N" D3 B6 Y* a# f+ Y
Precocious puberty is termed as central (true) when
2 u: X; t+ L$ P3 }* E4 eit is caused by the premature activation of hypo-5 S( L5 H0 m7 a' ~" O( ^- |
thalamic pituitary gonadal axis. CPP is more com-$ r/ d7 k/ i" F2 \3 c
mon in girls than in boys.1,3 Most boys with CPP+ \! m9 w/ R$ g( _
may have a central nervous system lesion that is# s( P$ j$ K* q, u0 W! L! t
responsible for the early activation of the hypothal-
! Y# V, i8 k( S9 Bamic pituitary gonadal axis.1-3 Thus, greater empha-
/ g/ c: E8 W! N7 E. i/ Nsis has been given to neuroradiologic imaging in6 |! m& F( z! b( ^& x% W$ ^) L
boys with precocious puberty. In addition to viril-
3 j% x0 X, S D+ X1 Y1 Mization, the clinical hallmark of CPP is the symmet-
' }9 f9 q! f' D2 }- Mrical testicular growth secondary to stimulation by: W& R/ J7 x) e/ h
gonadotropins.1,3$ A2 c; F1 F; u- j5 v0 H
Gonadotropin-independent peripheral preco-
6 U- K8 b1 S, P( ]cious puberty in boys also results from inappropriate% s/ z( L. d; Y
androgenic stimulation from either endogenous or+ N: z4 `6 C1 U. |5 J
exogenous sources, nonpituitary gonadotropin stim-" b2 Z6 s4 j, \9 D- p, b1 S
ulation, and rare activating mutations.3 Virilizing
' t. \5 i6 o3 J* fcongenital adrenal hyperplasia producing excessive. |/ _4 }0 ^. ?. ~3 r; m
adrenal androgens is a common cause of precocious
, V8 g) c) ^# n; \/ j9 bpuberty in boys.3,4& H# [% v/ X7 L
The most common form of congenital adrenal) x9 W }! F/ p0 ~" S% H- [
hyperplasia is the 21-hydroxylase enzyme deficiency.
! W9 I3 O9 `# w7 N" b3 x5 |8 Q FThe 11-β hydroxylase deficiency may also result in
+ [: x" y; f) D& E* _1 Dexcessive adrenal androgen production, and rarely,8 u# B% p) j9 T3 w
an adrenal tumor may also cause adrenal androgen$ g" D( s1 a% h4 N
excess.1,3
' J; W2 z' D3 I: ]. B0 `. dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" g0 U, D) d/ u3 [* U, U) V
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 `( L1 L, J, d# q2 Z# yA unique entity of male-limited gonadotropin-* F; ]: {6 N2 d; ]5 H8 a& I, D1 |
independent precocious puberty, which is also known1 k, C% }# Q9 B. @
as testotoxicosis, may cause precocious puberty at a
; z* }5 M# ]8 c3 t" Y7 a5 D: ]very young age. The physical findings in these boys7 ^4 W7 B) U- w$ I @
with this disorder are full pubertal development,
+ [4 K# k) T& n) \" ^including bilateral testicular growth, similar to boys3 ^9 ]; L# v, s9 O# Z4 k) J$ \
with CPP. The gonadotropin levels in this disorder
+ f3 H9 W+ ]/ t7 _" Lare suppressed to prepubertal levels and do not show
( c" Z: K" [) F+ Fpubertal response of gonadotropin after gonadotropin-! x! Q4 w- b3 h6 \. M) p: r
releasing hormone stimulation. This is a sex-linked
" c* M# J! B" }$ M* t8 _4 u$ Jautosomal dominant disorder that affects only
( q7 U" P+ d. P' vmales; therefore, other male members of the family9 q6 g5 [3 P8 c& w5 t( e
may have similar precocious puberty.3# ~& x& a( F6 t- h3 Q3 c* O
In our patient, physical examination was incon-
" ^! J/ z" e3 o3 z5 a xsistent with true precocious puberty since his testi-
6 l% B* V1 R$ y. _cles were prepubertal in size. However, testotoxicosis
, o; G' m+ D/ C6 ?$ Y& T" Iwas in the differential diagnosis because his father: W9 g7 b( }- B) b9 v" [0 i9 h
started puberty somewhat early, and occasionally,+ P; R6 ]; g( F) ]: X
testicular enlargement is not that evident in the3 i& Q; ?" o% D% p) H! S, n |: P
beginning of this process.1 In the absence of a neg-* R! g' q1 T3 j
ative initial history of androgen exposure, our; A Q% N5 i6 ~2 T* C" N+ T3 m/ L
biggest concern was virilizing adrenal hyperplasia,# A8 g9 g2 X* D) Z! _" L% f
either 21-hydroxylase deficiency or 11-β hydroxylase
' S( N) j( n* o0 _deficiency. Those diagnoses were excluded by find-" {* R& ] J, a5 U2 Z& w2 y. r
ing the normal level of adrenal steroids.
. E+ s% l4 y: `) A0 W/ n( g8 QThe diagnosis of exogenous androgens was strongly3 j6 Q3 C0 j7 L- V+ B0 v( J
suspected in a follow-up visit after 4 months because
# u2 ~& I! B* f: t! C% rthe physical examination revealed the complete disap-
# ~" W4 B% x% @1 |8 m0 kpearance of pubic hair, normal growth velocity, and8 _" p: z. `2 C3 `, ]1 B- M, E2 e
decreased erections. The father admitted using a testos-
2 `" |+ Q% x( u9 d; `3 K1 k/ x+ Zterone gel, which he concealed at first visit. He was: o+ T; R* M; y( ^9 n/ R/ C
using it rather frequently, twice a day. The Physicians’/ T( I2 X! T. h
Desk Reference, or package insert of this product, gel or
, V3 c- N' \) }9 s! A4 Fcream, cautions about dermal testosterone transfer to
5 P& P, D9 z1 E, Sunprotected females through direct skin exposure.) g, x) S& J, j) u& q o
Serum testosterone level was found to be 2 times the
) Z7 E! s6 g6 R- f3 }. r9 Ibaseline value in those females who were exposed to
% v6 I* E1 q4 j7 J1 _. _even 15 minutes of direct skin contact with their male9 W5 S; d* q7 y
partners.6 However, when a shirt covered the applica-
8 r6 ]) j* v6 E* g) Ation site, this testosterone transfer was prevented., p; L& O2 d6 L: _: @3 W+ q8 v2 o
Our patient’s testosterone level was 60 ng/mL,% B4 |5 [* Y6 w% } {. t
which was clearly high. Some studies suggest that5 L: J9 M4 D5 ~5 g" g" S% K% J
dermal conversion of testosterone to dihydrotestos-
% k: Y/ A( Z3 N# M7 @, B& Jterone, which is a more potent metabolite, is more: A) A4 s3 w2 x
active in young children exposed to testosterone3 R% ?& g- C' d* q& f# ]
exogenously7; however, we did not measure a dihy-
: ~0 e/ m# P0 t' g4 @! hdrotestosterone level in our patient. In addition to: x8 [4 G5 W; G3 }: J& N3 Z
virilization, exposure to exogenous testosterone in
3 _& j( W9 ?' E: o( J6 \0 e; A8 C; Tchildren results in an increase in growth velocity and
5 I- \. \9 S6 ~* l0 H8 A4 @6 cadvanced bone age, as seen in our patient.
; U# c+ A. i& @/ K H+ o6 L0 W, P2 Y$ iThe long-term effect of androgen exposure during
9 J) V0 `3 f' [early childhood on pubertal development and final
' C& K" o& L$ `# N' E" Madult height are not fully known and always remain
5 l, u$ M) q7 B& g+ ~- Sa concern. Children treated with short-term testos-" c7 J Y* l9 T6 O8 r+ s+ W# g
terone injection or topical androgen may exhibit some0 d ?: R0 ]( E; H- J' c8 D9 b2 R& }
acceleration of the skeletal maturation; however, after
. \+ d* t3 V( @$ [; I/ xcessation of treatment, the rate of bone maturation. b' d3 `* T" V+ e, e2 z
decelerates and gradually returns to normal.8,9( K l6 u3 [! H/ [% j
There are conflicting reports and controversy5 Q4 N' O N( [6 F
over the effect of early androgen exposure on adult
' O! i& k) _5 Xpenile length.10,11 Some reports suggest subnormal
( s9 Z+ s6 [7 y9 A$ B$ p% P! G+ V, p7 `adult penile length, apparently because of downreg-
2 m- W: y1 F, A- Z G) tulation of androgen receptor number.10,12 However," G' q8 A: w7 p; l! B5 X
Sutherland et al13 did not find a correlation between
- _+ d! H; S1 x) L V& W+ l; n1 r3 e0 Fchildhood testosterone exposure and reduced adult8 |# o6 U% ]9 f- s' O9 |! ~
penile length in clinical studies.
* z; T8 t/ J `6 C/ ^) |( m; x7 Q$ NNonetheless, we do not believe our patient is
5 ?1 k( s0 F% V' Qgoing to experience any of the untoward effects from
9 x. T) Y3 U9 B6 ]5 h7 f1 ntestosterone exposure as mentioned earlier because2 ~" A3 x% E6 V+ M& r# M
the exposure was not for a prolonged period of time.3 U- n% D8 j8 ?
Although the bone age was advanced at the time of+ W7 [# {) l) Z" k5 D: ~
diagnosis, the child had a normal growth velocity at
) v' O5 ?% j; rthe follow-up visit. It is hoped that his final adult2 U1 f2 v V$ n1 {7 a! \5 s
height will not be affected.- n+ u% i, o+ @" U( ]
Although rarely reported, the widespread avail-
- f) J4 a4 I! V7 E. i! ^/ _ability of androgen products in our society may. B$ L' X# Y* c* Z7 o
indeed cause more virilization in male or female
6 J/ I4 l2 `. l. ]children than one would realize. Exposure to andro-# }. y3 S3 `7 z' [+ s. }, h' x
gen products must be considered and specific ques-
1 p. @0 V# p7 k5 G4 A) |' otioning about the use of a testosterone product or
. {" K0 D# l2 ]) i; T" E% Vgel should be asked of the family members during* q( k- A" \4 j% _) }# l/ ?
the evaluation of any children who present with vir-
" }: i; Q+ n" s" Qilization or peripheral precocious puberty. The diag-
; I! V9 R% e8 _5 H& D& P7 W" Snosis can be established by just a few tests and by
5 K% [* ^9 Q- F* y* h9 W2 aappropriate history. The inability to obtain such a
5 f* @0 l* ^0 g: ~; N: ?/ Ohistory, or failure to ask the specific questions, may* G3 a) Z% ]* {7 S4 L
result in extensive, unnecessary, and expensive
! t1 V$ o& B/ W; K; linvestigation. The primary care physician should be
. ]9 u6 Y1 o5 s, k% Aaware of this fact, because most of these children( {* c, m1 D2 o* U5 m+ F
may initially present in their practice. The Physicians’
8 x4 A6 ^4 S# u8 wDesk Reference and package insert should also put a& }( U' }; D) V# g$ v
warning about the virilizing effect on a male or
8 z) ]+ z+ d! ?+ e8 _female child who might come in contact with some-& K# K( q3 u/ x* U7 j; e/ N; H! f
one using any of these products.
8 X* C1 V4 w L7 J/ y7 B6 vReferences
+ G% K# |7 Q0 ]0 d6 C1. Styne DM. The testes: disorder of sexual differentiation
. j" R6 G# X5 Z- ]and puberty in the male. In: Sperling MA, ed. Pediatric( h- l& I# @( e5 N# |; Q' h
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 f& B& h5 r: |$ H; G) K2002: 565-628.
`$ }" x) [- x, u. |! o2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, L: V3 {' r6 g6 g% z- S9 K" ppuberty in children with tumours of the suprasellar pineal |
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