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Sexual Precocity in a 16-Month-Old; l; {" l5 S9 x3 j4 A
Boy Induced by Indirect Topical O+ X# V) X0 \) z: F- {' L+ c
Exposure to Testosterone8 G2 Z$ j8 e2 _* K m6 b
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ E7 [% ?, A6 w, k+ x
and Kenneth R. Rettig, MD17 T% X9 @% ?' ]7 M
Clinical Pediatrics
# ?# N- C; x5 E9 E3 A1 D' bVolume 46 Number 6
3 A* q9 I, z$ j# SJuly 2007 540-543
( d1 ~ R7 [3 A0 V4 y) r© 2007 Sage Publications4 D0 P9 X# _9 T6 {" d" b
10.1177/00099228062966516 J2 }; c' b7 e: M
http://clp.sagepub.com
* y. w1 B+ |+ k x3 [) Y7 ahosted at6 b0 s$ z" ]3 a1 L! y5 H' I
http://online.sagepub.com
) k) Y3 t; y% f: k/ D9 nPrecocious puberty in boys, central or peripheral,4 t6 U9 T9 y$ V' x0 t
is a significant concern for physicians. Central
# [4 ~$ `; C5 o6 N) e; | ` Qprecocious puberty (CPP), which is mediated
5 v# |% l- y# F! A( R) j0 q7 @through the hypothalamic pituitary gonadal axis, has; h+ g% a; ^0 a5 Z. o4 ]! ~
a higher incidence of organic central nervous system
6 @# O6 P; Y$ Q% vlesions in boys.1,2 Virilization in boys, as manifested1 E; ~" v/ `# G. z( S- P
by enlargement of the penis, development of pubic
. Q, T8 |% D. z0 S& z7 `; }' T3 R$ [# A% Ohair, and facial acne without enlargement of testi-7 H$ `: H0 B {5 O. a
cles, suggests peripheral or pseudopuberty.1-3 We
, K& n1 a2 i( J+ V, F" Ureport a 16-month-old boy who presented with the t7 e _8 l$ A8 u; d6 Z5 s
enlargement of the phallus and pubic hair develop-
$ I& V: S p3 Hment without testicular enlargement, which was due
- ?1 D# W; n% I* O) d+ a7 I" ito the unintentional exposure to androgen gel used by
\) X. D% p" i W% Jthe father. The family initially concealed this infor-
3 j }$ d9 T0 _: J% `# vmation, resulting in an extensive work-up for this
) n, v. d0 m, n/ H' J: fchild. Given the widespread and easy availability of
/ w( X/ W, M2 \0 h5 h3 m' Z qtestosterone gel and cream, we believe this is proba-8 A& I; W* @# m0 g
bly more common than the rare case report in the+ n" h; ?( m3 M# S
literature.4* o0 b' Q5 B) P( ^$ I* }
Patient Report" D7 C ^% @2 U( r% L% x7 m
A 16-month-old white child was referred to the$ L# m; j2 t) z4 ]) T# W
endocrine clinic by his pediatrician with the concern. J) S- @9 ^ r# l+ w
of early sexual development. His mother noticed
1 h7 d$ H, t5 F' Olight colored pubic hair development when he was
+ X3 f! g8 q3 NFrom the 1Division of Pediatric Endocrinology, 2University of$ J, C) R1 r5 z3 S, B3 o1 P( \+ A
South Alabama Medical Center, Mobile, Alabama.( s8 z7 ^; }4 P/ p) \/ k* Z
Address correspondence to: Samar K. Bhowmick, MD, FACE,
4 F, c6 z6 X9 F( j- G, r3 oProfessor of Pediatrics, University of South Alabama, College of
1 ?* T# _8 p- @, bMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;: ]* I% P/ J0 H3 b- q
e-mail: [email protected].
, t8 z3 c- n- }. c3 Sabout 6 to 7 months old, which progressively became( ]) T* E2 B( K; W# E& Z
darker. She was also concerned about the enlarge-. W8 {9 D$ }$ e: O% l7 d
ment of his penis and frequent erections. The child
* X& ~, |$ i2 F* j0 vwas the product of a full-term normal delivery, with
; a. K' B8 |2 } N2 {3 L+ ca birth weight of 7 lb 14 oz, and birth length of
1 {& R. m; M: V; e20 inches. He was breast-fed throughout the first year& v( h! z5 d: `- U$ o1 L, E
of life and was still receiving breast milk along with
% |, e L* q/ Y: B2 ~$ o5 Qsolid food. He had no hospitalizations or surgery," J$ G- B+ `- ]* K
and his psychosocial and psychomotor development( }' p$ o+ f" ?- c5 e# Y: P
was age appropriate.# ~7 c8 C- ^( G) @
The family history was remarkable for the father,
( O9 o) q" B. B: x, {who was diagnosed with hypothyroidism at age 16,
( ?8 Y0 r" W" f/ b& n, D* z0 d; e% Swhich was treated with thyroxine. The father’s
9 ]% J4 S3 p& R- Lheight was 6 feet, and he went through a somewhat
( k$ E* J0 U( {8 M" a5 y+ eearly puberty and had stopped growing by age 14.
Q$ t! h* v( g7 [5 xThe father denied taking any other medication. The
4 v* P+ M) y1 U# K# wchild’s mother was in good health. Her menarche1 X# |/ ^4 R) g) Z
was at 11 years of age, and her height was at 5 feet
! B+ z$ p4 N) A% Y9 e5 inches. There was no other family history of pre-6 `5 z7 H+ m7 c4 }
cocious sexual development in the first-degree rela-
/ @* b/ W! y, Ytives. There were no siblings. w4 g( |; v- c6 |) m) _% x
Physical Examination
6 l9 C9 x% T3 H6 E' ^' XThe physical examination revealed a very active,. q' D" f2 G1 i& ^ s
playful, and healthy boy. The vital signs documented. e1 Z; [/ ^! [* t$ o4 D8 n& n l. h+ [9 X
a blood pressure of 85/50 mm Hg, his length was
5 V" ?8 @* B$ v8 K0 s y+ f90 cm (>97th percentile), and his weight was 14.4 kg, K0 J& T$ l/ U# t V1 _$ L# [( M. ^7 ~
(also >97th percentile). The observed yearly growth
3 a1 ]) m# A4 Z1 i$ I( Kvelocity was 30 cm (12 inches). The examination of1 p# w3 G2 \7 Q1 c
the neck revealed no thyroid enlargement.# b) `: m1 }6 D) ~' y) j. v) l
The genitourinary examination was remarkable for
) D8 g2 V+ X6 f1 [$ Xenlargement of the penis, with a stretched length of
R9 B$ V$ H) e8 cm and a width of 2 cm. The glans penis was very well
! t$ O( g4 h, U. f, e: sdeveloped. The pubic hair was Tanner II, mostly around
# J% z8 v6 B4 b5 j2 I0 m1 P540
2 {" T6 w9 A- O" u: Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* B# y4 w8 }+ x Xthe base of the phallus and was dark and curled. The
9 D, ]1 [0 t/ x5 ?( c4 stesticular volume was prepubertal at 2 mL each.
# a' l: O: m* r2 [) PThe skin was moist and smooth and somewhat
7 a3 Z1 ~4 ^8 Y. A# N) aoily. No axillary hair was noted. There were no
4 e! x& [! n3 ?abnormal skin pigmentations or café-au-lait spots.
- _, G d$ n+ I* V- w5 [Neurologic evaluation showed deep tendon reflex 2+
6 A6 N- j1 h; k/ Y& Qbilateral and symmetrical. There was no suggestion! S3 c) ?/ X+ D( h" ^
of papilledema.
& {. e8 Z8 F6 b sLaboratory Evaluation
; c% M9 Z2 d0 ^3 ^The bone age was consistent with 28 months by; [7 a* x/ e& D
using the standard of Greulich and Pyle at a chrono-
' W) N# H# i$ A2 n5 zlogic age of 16 months (advanced).5 Chromosomal/ J0 Z6 h& [6 z
karyotype was 46XY. The thyroid function test
9 H1 d5 ^$ K. Mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
1 v' \* Q6 q! X( h" ?lating hormone level was 1.3 µIU/mL (both normal).
. H9 W% F* u' M7 v, Z9 tThe concentrations of serum electrolytes, blood0 C- c. H7 q J) d+ a4 u
urea nitrogen, creatinine, and calcium all were* V3 F: t$ z1 f8 W/ K7 O: ~
within normal range for his age. The concentration' |6 p: j2 B. A9 B
of serum 17-hydroxyprogesterone was 16 ng/dL n$ w9 {' \! J
(normal, 3 to 90 ng/dL), androstenedione was 20+ D5 P! d2 O4 A
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# m% ? u# \6 E
terone was 38 ng/dL (normal, 50 to 760 ng/dL),0 M3 l4 S2 x+ t
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
# j" G3 \! H& O1 f$ H6 E1 N49ng/dL), 11-desoxycortisol (specific compound S)
9 j2 f: V3 X2 q [ y, j" o( C/ Dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# \2 R) s A5 k2 o
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
' g0 C, p8 u1 J) w3 itestosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ h2 k: o; F3 B( J+ Y- O; {
and β-human chorionic gonadotropin was less than/ `3 [* o; J7 `/ B, Y
5 mIU/mL (normal <5 mIU/mL). Serum follicular
# F2 F" l" i9 s( K' gstimulating hormone and leuteinizing hormone
/ `) N3 U+ e/ p4 X8 `% ~concentrations were less than 0.05 mIU/mL
* `- t! Y6 p1 s9 K/ v6 Z# L) L(prepubertal).
% m2 q4 g# D/ p/ J. z, a8 G# o# eThe parents were notified about the laboratory
8 \5 Y t2 E& z1 S4 a( H; M" Vresults and were informed that all of the tests were
; R0 b3 X8 @; \) I) w* H5 vnormal except the testosterone level was high. The, H1 ?$ m/ Z; e+ i0 l- x: e
follow-up visit was arranged within a few weeks to$ ^: p6 E3 T- Y- S
obtain testicular and abdominal sonograms; how-
+ n v* ?' F9 W6 Z9 qever, the family did not return for 4 months.0 A9 z+ B) H0 p1 V% J
Physical examination at this time revealed that the
0 R3 u0 _3 x* e* X3 }# X( g" j0 Pchild had grown 2.5 cm in 4 months and had gained4 V4 B; `- I6 _. `. i' u5 f. f9 a
2 kg of weight. Physical examination remained' v9 m$ i) r3 x' b- O9 T
unchanged. Surprisingly, the pubic hair almost com-
; H* k2 R# G- i* [" Jpletely disappeared except for a few vellous hairs at
7 q1 N7 I# r/ R2 Dthe base of the phallus. Testicular volume was still 2$ ?+ @0 { b, A" ^0 R
mL, and the size of the penis remained unchanged.8 ]! v1 W3 ~8 c9 d5 n+ M. k
The mother also said that the boy was no longer hav-
9 m6 F# I7 k+ c8 Y. S# N3 Aing frequent erections.
. a, m* P0 ^) l BBoth parents were again questioned about use of# s( b3 j! J k4 ]- Q1 u' B1 S
any ointment/creams that they may have applied to
+ F. s) l. W: x. G+ gthe child’s skin. This time the father admitted the7 |/ Z( W+ L! y% T
Topical Testosterone Exposure / Bhowmick et al 541 [, q8 \9 \+ ?8 R
use of testosterone gel twice daily that he was apply-
" F0 Z$ _+ }" }# U' `( o1 hing over his own shoulders, chest, and back area for
7 }$ g6 S7 k- l' wa year. The father also revealed he was embarrassed/ @8 }2 u# V, Y. [/ ]
to disclose that he was using a testosterone gel pre-8 z4 }$ D5 |9 L- `* M/ \. f
scribed by his family physician for decreased libido
( |: b" i" J5 |7 Q# ]: hsecondary to depression.
2 ~( }8 S. O3 a6 n" ~6 M9 g5 UThe child slept in the same bed with parents.+ N6 h/ F! u& V1 ^' X
The father would hug the baby and hold him on his) h; e7 L5 Q, X/ `, o
chest for a considerable period of time, causing sig-6 s, @+ L& Z; Z0 g( a1 v5 Z
nificant bare skin contact between baby and father.# _- Y; S) v9 F0 h
The father also admitted that after the phone call,& Y, s, a' d& t6 i1 S: ]
when he learned the testosterone level in the baby# j m3 n5 |7 X7 @" @
was high, he then read the product information
: u: V4 z/ T7 `packet and concluded that it was most likely the rea-: t3 @- l& ]( V4 }6 ~6 s) g8 j
son for the child’s virilization. At that time, they
; a, ?0 n1 W m3 d2 U$ S' D% S8 T+ _decided to put the baby in a separate bed, and the
1 _& L4 X5 D+ @! Vfather was not hugging him with bare skin and had8 S* Q4 U/ c) m8 s0 t7 Y9 L% b
been using protective clothing. A repeat testosterone' |1 v2 x' H, g! n" o* m% O+ i8 I
test was ordered, but the family did not go to the4 h) Z2 P- j/ r( q- U- H% b7 E
laboratory to obtain the test.# b7 m* g: L4 \) w* x
Discussion$ L, @" @% n0 D3 m r4 x8 \# I: U
Precocious puberty in boys is defined as secondary
& @% p7 u5 a- z4 X ]& |3 P0 P+ _sexual development before 9 years of age.1,49 d; p" {3 ~3 q
Precocious puberty is termed as central (true) when- s0 {9 @5 v4 c2 I, P
it is caused by the premature activation of hypo-4 A; Q% C& ?1 ^+ B$ T' ]
thalamic pituitary gonadal axis. CPP is more com-
7 ]: i% O9 l1 [" \! n2 c4 Vmon in girls than in boys.1,3 Most boys with CPP
, t. t" n2 a' n: `! Jmay have a central nervous system lesion that is; e$ I z* P j1 w
responsible for the early activation of the hypothal-
9 g$ t. F. F- d# t3 Z `, e; gamic pituitary gonadal axis.1-3 Thus, greater empha-5 u! c; _- a% v @0 z2 q" D
sis has been given to neuroradiologic imaging in+ ^6 f3 v3 ^; ]9 e
boys with precocious puberty. In addition to viril-
& s1 L- {/ V6 T6 oization, the clinical hallmark of CPP is the symmet-
; ~" W9 s2 c7 v+ ?rical testicular growth secondary to stimulation by
- R7 B) Z2 A- Z5 k2 Z( Zgonadotropins.1,3$ Y& `4 ~ l; L9 A
Gonadotropin-independent peripheral preco-' C- i* T5 ^* w, f7 x
cious puberty in boys also results from inappropriate
0 h ]& a y2 M$ u+ v7 handrogenic stimulation from either endogenous or7 M2 y% T& q8 h \* b$ K
exogenous sources, nonpituitary gonadotropin stim-9 u- O/ ^, ~: g( z' {5 o
ulation, and rare activating mutations.3 Virilizing
' ]% O" L3 n$ u* q* vcongenital adrenal hyperplasia producing excessive& j2 G, k* A6 t+ p: o
adrenal androgens is a common cause of precocious0 @3 R9 _/ ~7 _; s4 x3 c
puberty in boys.3,4) Z$ ?: a+ x3 O! \- C; A- A
The most common form of congenital adrenal
$ O" u# g* `2 N" k- x# s5 ]8 Ohyperplasia is the 21-hydroxylase enzyme deficiency.
% W& R M4 e3 I1 z: f0 S6 B* YThe 11-β hydroxylase deficiency may also result in* d1 z9 l2 q. ]" F- @
excessive adrenal androgen production, and rarely,
5 ~4 O7 _2 H" Ian adrenal tumor may also cause adrenal androgen
2 J$ e7 U$ t0 x4 F- O! [9 p" Kexcess.1,3. h, @& u$ |. z( I9 C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 H) G( G. z7 z% J7 {1 Y6 q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& ~0 U, l8 i9 E1 i/ wA unique entity of male-limited gonadotropin-
: H/ i$ ^5 S3 u# _ ^* Jindependent precocious puberty, which is also known6 s* b9 _, w; p+ Y7 q- q- k1 h" ~
as testotoxicosis, may cause precocious puberty at a, U3 H( d9 ^3 `& {5 A
very young age. The physical findings in these boys u5 w" q- U( t+ e4 d @3 k
with this disorder are full pubertal development,
1 @& J& z6 S# E2 Z4 @. sincluding bilateral testicular growth, similar to boys
' Z( I/ c& G# w4 q- C- q; Kwith CPP. The gonadotropin levels in this disorder: I2 |$ B- X1 z. `, H& |, D) ]- k; H
are suppressed to prepubertal levels and do not show
% O0 ~0 z% R9 Gpubertal response of gonadotropin after gonadotropin-( T" ?4 X8 x& X% z) k" N3 M
releasing hormone stimulation. This is a sex-linked0 t4 K ] u0 x; Z. Y. G
autosomal dominant disorder that affects only
8 c& _9 r1 A! ] d" Z+ \) y+ D* ~1 ?& Imales; therefore, other male members of the family3 m- v$ I8 c D# L
may have similar precocious puberty.3
9 E0 N4 e% v' X) N1 ~8 TIn our patient, physical examination was incon- o& H1 z7 U# b! E
sistent with true precocious puberty since his testi-
% o% G8 [' R5 p' @3 r/ ]- |' T- W t3 \cles were prepubertal in size. However, testotoxicosis8 U7 ~& ~. A4 r/ S3 v
was in the differential diagnosis because his father- \8 N" g5 }6 G X |
started puberty somewhat early, and occasionally,8 F4 m: [. o) n: V6 \
testicular enlargement is not that evident in the
' w, r; a9 L4 ]3 I$ d! E+ R/ C1 }* Ibeginning of this process.1 In the absence of a neg-- `* G" s! r9 W+ Y1 @
ative initial history of androgen exposure, our4 E# {7 F& W& p8 w
biggest concern was virilizing adrenal hyperplasia,
( B8 R' m3 T( D% `either 21-hydroxylase deficiency or 11-β hydroxylase
. _* k8 ^$ X* p% V4 B7 B0 vdeficiency. Those diagnoses were excluded by find-
5 c# r! N0 q5 Z0 Y- `ing the normal level of adrenal steroids.: h: l' x6 `! e8 @
The diagnosis of exogenous androgens was strongly
$ }+ p }1 l. g/ H1 u; Ssuspected in a follow-up visit after 4 months because7 ^0 b1 \7 U0 I; N8 `3 a! P1 _
the physical examination revealed the complete disap-
! O4 W# u' i$ q2 \$ { \pearance of pubic hair, normal growth velocity, and6 z8 p# ~. @6 `# Z3 O1 `% x
decreased erections. The father admitted using a testos-
- j" E/ A9 c& V; j4 Vterone gel, which he concealed at first visit. He was7 n; x7 y6 Z# C) E( |# l% D# ^- I1 L/ T
using it rather frequently, twice a day. The Physicians’% m3 E# D0 p* f0 k$ p0 ?" u
Desk Reference, or package insert of this product, gel or1 C8 B& Q) W3 h, X- o' f
cream, cautions about dermal testosterone transfer to
' U; j x7 ? ]1 L/ Uunprotected females through direct skin exposure., H' K* p# X/ O \) O
Serum testosterone level was found to be 2 times the
, s# h/ n0 d# v! c9 Z& Ibaseline value in those females who were exposed to0 ?, }1 _3 z3 H. [ W! Z3 r
even 15 minutes of direct skin contact with their male0 X" Q% ^! T; V; h/ W6 c& ?
partners.6 However, when a shirt covered the applica-1 P& G# m8 o) `. ]8 `7 ^
tion site, this testosterone transfer was prevented.$ _$ h" m7 l$ i6 _
Our patient’s testosterone level was 60 ng/mL,$ m1 ^9 T) B1 J% j9 y% k" s" s) B
which was clearly high. Some studies suggest that
- |4 t8 m* B W1 Qdermal conversion of testosterone to dihydrotestos-
4 v# T) x+ V9 f& Xterone, which is a more potent metabolite, is more7 N$ ?0 A- n3 _+ A# _( p5 }! U
active in young children exposed to testosterone H' S% S( i, ~
exogenously7; however, we did not measure a dihy-- ^8 J7 s% M% w& F5 q% ?
drotestosterone level in our patient. In addition to
0 ^- D M k, `. X# _3 |virilization, exposure to exogenous testosterone in
) F7 S7 R- R6 {) q3 mchildren results in an increase in growth velocity and* F* \/ b) n" k& M
advanced bone age, as seen in our patient.
9 f1 y: H$ s V% q6 `' i( _! zThe long-term effect of androgen exposure during8 E1 o+ _1 J& ~6 u
early childhood on pubertal development and final
* m$ l- k) g! G9 m$ @1 `adult height are not fully known and always remain! L- M! U n) P2 T/ K
a concern. Children treated with short-term testos-9 Q( M% e9 `4 _4 U& ?9 \3 }
terone injection or topical androgen may exhibit some
2 L6 S7 O% z; R& T! Aacceleration of the skeletal maturation; however, after q* @# r- B- d$ U3 u5 e# i2 J# `( r
cessation of treatment, the rate of bone maturation" x" C \% b/ |+ x
decelerates and gradually returns to normal.8,9
: a8 J! V7 Q& RThere are conflicting reports and controversy
0 p/ Q2 J8 u2 J; B0 B* j: c8 W* Z$ ~. i6 jover the effect of early androgen exposure on adult+ @$ g* W& Q$ x% m
penile length.10,11 Some reports suggest subnormal
" D( r+ t7 t/ H6 jadult penile length, apparently because of downreg-1 {- l/ ?8 \6 M& O" u3 F6 K3 H( k
ulation of androgen receptor number.10,12 However," @9 F$ A4 Q- p4 ?1 G; S6 v
Sutherland et al13 did not find a correlation between
" S3 F# A5 y: V% v1 t; P3 g6 r {% jchildhood testosterone exposure and reduced adult$ g' ?' h3 d) l, o
penile length in clinical studies.2 o/ \: B2 C1 r0 U c
Nonetheless, we do not believe our patient is, B$ t$ k$ n4 F- _* ]! B
going to experience any of the untoward effects from
/ P% ~" H6 D `- h) E+ G& m1 m! Gtestosterone exposure as mentioned earlier because6 Z c& v; K( p( G8 s& z
the exposure was not for a prolonged period of time.8 y! N" z) J, ]: K0 _
Although the bone age was advanced at the time of
- e& E# ]: Y% i" cdiagnosis, the child had a normal growth velocity at+ @) }- |7 G# z# ^+ c8 a7 k5 x# |
the follow-up visit. It is hoped that his final adult
+ n4 \ x" M+ F' R9 u; v9 Nheight will not be affected.
( K4 F r% I* I; H5 @9 zAlthough rarely reported, the widespread avail-
6 `6 n1 F) l. ]0 |0 g% sability of androgen products in our society may
/ ?. g: F# [$ ^4 F2 Sindeed cause more virilization in male or female5 ~- E; c# l- M& w
children than one would realize. Exposure to andro-
, x/ L1 N8 b& G) f8 W+ u# }0 l) W# lgen products must be considered and specific ques-
5 s: m, S' E4 s6 N$ `9 |tioning about the use of a testosterone product or/ i7 f2 b% B l' T0 E5 y
gel should be asked of the family members during# m) t$ M) _# f& L& t( i
the evaluation of any children who present with vir-
: [1 }: ]5 P! T* z) oilization or peripheral precocious puberty. The diag-
/ T9 ?' @* e. m) n9 L. X4 K" qnosis can be established by just a few tests and by
& B# F- G. Q2 E$ Z$ ]) f# lappropriate history. The inability to obtain such a
G5 s" }2 r; K2 P" S6 I2 V8 ?( ~6 Jhistory, or failure to ask the specific questions, may
) G0 h$ q* l7 G- F" C: aresult in extensive, unnecessary, and expensive
: ?! r% n+ V. W% Q8 Pinvestigation. The primary care physician should be% z z6 a9 G: K1 \6 o" \) K) i
aware of this fact, because most of these children
( s1 j% B- L9 k% H. n8 X# Ymay initially present in their practice. The Physicians’
/ e H! e5 Z" e9 f5 V, f) IDesk Reference and package insert should also put a4 Q! b% _" |( G
warning about the virilizing effect on a male or
9 M: M6 }6 R( Z( i- T6 h$ Ffemale child who might come in contact with some-$ @4 f. K0 F% r: C) o
one using any of these products.
7 H" g8 V" W, `, zReferences
1 i: ?3 P( P# O" K7 d+ G- ^1. Styne DM. The testes: disorder of sexual differentiation
4 V) X! A$ N. }) [ v$ N) Hand puberty in the male. In: Sperling MA, ed. Pediatric
* X p1 O$ M) |, q4 @Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 u4 c0 e& ]& h8 W- ~9 i2002: 565-628., C+ E! s7 \1 _6 @4 \6 w0 \
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 n% v+ @0 r( e+ Epuberty in children with tumours of the suprasellar pineal |
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