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Sexual Precocity in a 16-Month-Old9 E9 k9 ?% @ A4 q# j" `9 d$ Q
Boy Induced by Indirect Topical
6 I2 ]0 k8 _8 t. ^. JExposure to Testosterone% o2 t) Z% h6 j( O
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
3 ^3 o) O, H7 H3 T9 Uand Kenneth R. Rettig, MD1
% ?8 h. N, t- B7 ~2 Z7 f m* `Clinical Pediatrics0 Q! K* S5 e" l, T" w, y
Volume 46 Number 6
/ r# T" t' Q8 uJuly 2007 540-543% Z/ H6 X6 s# t% ^; n2 [
© 2007 Sage Publications9 o- u4 Z1 v4 v$ Q7 E# {: c7 i" l
10.1177/0009922806296651
, P- ]) t* h' V: r) }# Xhttp://clp.sagepub.com' Q9 P" Y4 b: m M: s
hosted at
' F# T4 _5 N* V7 chttp://online.sagepub.com
% U+ }; h5 M5 {, S" {Precocious puberty in boys, central or peripheral,2 ?: g$ P+ g( r+ g
is a significant concern for physicians. Central; X' `' r8 j( P0 h, t
precocious puberty (CPP), which is mediated
& X0 e( y3 f) @4 t5 Jthrough the hypothalamic pituitary gonadal axis, has" W6 ]; o* \# o6 k" |
a higher incidence of organic central nervous system
0 E( D7 P+ C5 L% nlesions in boys.1,2 Virilization in boys, as manifested& ^' o0 h A# Y
by enlargement of the penis, development of pubic
# n' g0 i: b- q+ Shair, and facial acne without enlargement of testi-
: G8 y$ l" Q6 e! F0 A- bcles, suggests peripheral or pseudopuberty.1-3 We
, H7 F8 C0 F5 ~6 P. [report a 16-month-old boy who presented with the: Q; k8 r' w0 ]8 k9 ~- l6 C
enlargement of the phallus and pubic hair develop-1 O! l+ q) @, L! e! @) A4 ~
ment without testicular enlargement, which was due* t G: `# U; c8 d+ t8 Q
to the unintentional exposure to androgen gel used by
, I6 [4 h- s, f1 l# Sthe father. The family initially concealed this infor-. w( z* U9 ?$ \* }+ Y J
mation, resulting in an extensive work-up for this& {+ |& P6 n/ D' D) C$ n
child. Given the widespread and easy availability of' K7 ]; g) h, A5 E$ ?8 q
testosterone gel and cream, we believe this is proba-. a2 e* h: D- p2 q- @; c, O
bly more common than the rare case report in the8 {7 w. G" M8 e2 H* ~
literature.49 ^* n! Y- ?) q0 l$ k- I; L* x
Patient Report
3 a" ~( o# p* ~( q+ G: ^7 iA 16-month-old white child was referred to the
|! }% k& I- }- [8 J: Uendocrine clinic by his pediatrician with the concern
* H- D( I# m* G0 F* `8 uof early sexual development. His mother noticed
9 h! |5 r! X3 C$ Y3 j: xlight colored pubic hair development when he was
- h3 X9 K9 ?6 \From the 1Division of Pediatric Endocrinology, 2University of
4 N f7 e$ Y7 J& Z' z3 a. a$ m: w0 ESouth Alabama Medical Center, Mobile, Alabama.
- i% U# h& m( t% P4 x! M- @$ c1 R, ?+ \! wAddress correspondence to: Samar K. Bhowmick, MD, FACE,
# Q' [% ?* f0 a* a( WProfessor of Pediatrics, University of South Alabama, College of9 D# o' [- c( m2 L; x9 E# Z0 ^& A
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ I: }; s! V5 h+ X
e-mail: [email protected].: v/ O- x" x( `8 ]7 f4 l9 H
about 6 to 7 months old, which progressively became5 E! F8 a( q7 p( r. q( X9 |" A
darker. She was also concerned about the enlarge-
! A6 L; ~) k6 ?9 o6 U2 Z* @ment of his penis and frequent erections. The child2 F# }$ f/ t/ I! `9 R2 E1 I; K( U
was the product of a full-term normal delivery, with( a" K6 R" K2 Z! t( s3 Y
a birth weight of 7 lb 14 oz, and birth length of1 ^7 \8 ~" i; c8 K( O& i
20 inches. He was breast-fed throughout the first year
7 V* x7 ~: _+ s" t2 Aof life and was still receiving breast milk along with. e& ^; k. `' |3 Q" M; ?, q
solid food. He had no hospitalizations or surgery,
+ s1 z% _ \* I: m3 kand his psychosocial and psychomotor development
: t4 k9 g' @1 F: N- ^( D3 K6 Qwas age appropriate." ~- X7 O8 V! c; ^ j/ n
The family history was remarkable for the father,
$ s6 Y# d/ N; R6 Owho was diagnosed with hypothyroidism at age 16," h, `& o; \, ]& e* m& n3 D
which was treated with thyroxine. The father’s
/ D# n4 U# R6 |8 x9 Pheight was 6 feet, and he went through a somewhat
$ U9 q6 j6 E( h9 m. ` oearly puberty and had stopped growing by age 14./ |7 T8 f% r' K" S! H/ l4 y
The father denied taking any other medication. The% L8 K& c8 E! j) s9 {
child’s mother was in good health. Her menarche% z0 j) X6 b- c/ o8 N/ U' K9 X, O) P- o M
was at 11 years of age, and her height was at 5 feet
. Y, u3 l. f! O% V5 inches. There was no other family history of pre-4 e! l8 Q. d/ n" j2 r
cocious sexual development in the first-degree rela-7 ^0 L8 @; E4 G/ }! N/ E* z
tives. There were no siblings.3 e( x$ ?9 l; v3 H8 J% j! u m' ]
Physical Examination2 [$ y" C: M Y! t! M
The physical examination revealed a very active,; v; z9 p0 ^5 j, E( Q" {
playful, and healthy boy. The vital signs documented2 o" i* [) M. c9 B5 g$ o0 e4 m5 ]
a blood pressure of 85/50 mm Hg, his length was. g" c6 o" @8 P0 q( ]
90 cm (>97th percentile), and his weight was 14.4 kg
3 Z- O0 E2 G+ W+ ^! j% C+ Z6 A(also >97th percentile). The observed yearly growth" I2 }8 P& T0 l ?# _/ [/ P
velocity was 30 cm (12 inches). The examination of
6 Q7 n: u2 c @ `* athe neck revealed no thyroid enlargement.
8 @2 k7 ?- D j( q4 v! q' }/ YThe genitourinary examination was remarkable for
$ Q' |2 y, R a s, ?- }enlargement of the penis, with a stretched length of
2 B( J [, e* r3 t" X$ c/ m8 cm and a width of 2 cm. The glans penis was very well
) a: L2 p* y8 \developed. The pubic hair was Tanner II, mostly around
6 J* x6 F- K- Q3 `& b1 g) |540
. g& Y! Y. [% Q3 R: \9 [ V! B5 Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 r. w+ G8 [) v8 @- ~8 G
the base of the phallus and was dark and curled. The
1 I! \4 g# |+ m2 `$ H' i7 Etesticular volume was prepubertal at 2 mL each.
/ U& B W* N1 @2 e, i4 `The skin was moist and smooth and somewhat
9 V" Z( V! w( B0 H3 noily. No axillary hair was noted. There were no5 g; v9 t" D2 X4 f$ i
abnormal skin pigmentations or café-au-lait spots.- t$ N: A A7 e, K' h4 B6 o
Neurologic evaluation showed deep tendon reflex 2+ t) i# K( I- d
bilateral and symmetrical. There was no suggestion6 F, S% \6 x' S
of papilledema.
6 Z1 W' Z+ j: u" CLaboratory Evaluation5 c' D: H2 Z* H6 A, Y! z" o. O
The bone age was consistent with 28 months by, R7 u6 O5 w; L
using the standard of Greulich and Pyle at a chrono-0 \( ~+ t; T1 l. b
logic age of 16 months (advanced).5 Chromosomal
$ _6 B9 {! D' {. ?) Q1 c+ nkaryotype was 46XY. The thyroid function test
% Q" _ ?* I0 V- W6 K. Kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-% U4 V# g) T6 W& j2 G, ?2 E
lating hormone level was 1.3 µIU/mL (both normal).7 [( L! ?7 q, z* Q* P$ Z' u
The concentrations of serum electrolytes, blood9 w$ X! X; O' ?; X# N! n
urea nitrogen, creatinine, and calcium all were, R& Y" p+ _1 O5 B' R. O1 d
within normal range for his age. The concentration
! _ [ G& c! }- ^of serum 17-hydroxyprogesterone was 16 ng/dL
: B$ s1 [ _$ l( Q N2 V9 ?(normal, 3 to 90 ng/dL), androstenedione was 20
& l4 T7 g1 f; v8 V+ a: w0 |ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 J! m3 @1 V Y8 I- [9 e& Y( Kterone was 38 ng/dL (normal, 50 to 760 ng/dL),5 i$ ^- t0 L: U9 q, [5 M
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
: M+ P( a4 S5 E' T8 \" N) h49ng/dL), 11-desoxycortisol (specific compound S)
" b! s% l& q0 twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
# Y) x6 h" L* }6 Q Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; a" L1 x3 I6 Y, v5 D e) l' O7 [testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" s* f' f( I. {' ?% X. gand β-human chorionic gonadotropin was less than l0 A6 k& J8 r& b
5 mIU/mL (normal <5 mIU/mL). Serum follicular% _& o7 H- y" H: Y4 M$ [
stimulating hormone and leuteinizing hormone
! r: q& C' M5 q/ T1 T/ U1 c+ Mconcentrations were less than 0.05 mIU/mL0 [2 J6 e, Y7 k1 Z4 Z' Y" m9 Q, X
(prepubertal).
9 n$ K/ c4 X. c$ |' ]The parents were notified about the laboratory
& T" N; P8 ~" h8 e; oresults and were informed that all of the tests were
1 B6 S0 n% x! ~. [! \" {1 enormal except the testosterone level was high. The4 \8 d+ e! p. o& V7 L# a
follow-up visit was arranged within a few weeks to5 ?& d0 I& q* q6 Y1 P* p" `
obtain testicular and abdominal sonograms; how-( f, l8 m' h+ }+ F: V9 c, j
ever, the family did not return for 4 months.
; \. ?( ]0 r5 u8 gPhysical examination at this time revealed that the0 w" J8 V' @; n( P/ E, X
child had grown 2.5 cm in 4 months and had gained7 t8 O8 J. K. p: N! ]/ W7 Z- J
2 kg of weight. Physical examination remained
$ Q/ u4 Z7 |5 }* D% aunchanged. Surprisingly, the pubic hair almost com-: R* C$ C, t# x# I' e
pletely disappeared except for a few vellous hairs at
1 o1 u; l& }9 P' F: t* b. `* Rthe base of the phallus. Testicular volume was still 2
) {2 m3 r8 G- d9 ~# `6 OmL, and the size of the penis remained unchanged.
. \ z6 R* E* W3 t. [) \The mother also said that the boy was no longer hav-* ?( \7 _) H6 d7 b1 D9 ?
ing frequent erections.
# i$ _& J' z* q9 k+ S. cBoth parents were again questioned about use of
: q1 _2 L/ | K) H1 w) E5 `any ointment/creams that they may have applied to4 c( B! W: D7 v- S3 @
the child’s skin. This time the father admitted the6 u6 M* I9 K2 I7 r. j
Topical Testosterone Exposure / Bhowmick et al 5414 u" o! m+ {" {3 \" B
use of testosterone gel twice daily that he was apply-2 k" \4 D7 c0 f1 T+ ~6 K7 P
ing over his own shoulders, chest, and back area for z0 J# |1 Q/ B% q2 x9 v0 w
a year. The father also revealed he was embarrassed, d' r Q$ X8 h1 x# N: `6 G8 s
to disclose that he was using a testosterone gel pre-
|( s3 f. D$ \% u. `( Mscribed by his family physician for decreased libido
) a ^1 g$ U- B. e) d) S3 _) Z3 ?secondary to depression.
6 e# q9 {) E0 I) D; m* BThe child slept in the same bed with parents., M( ^$ F2 C* o5 P v$ s* a0 `/ J2 G9 p
The father would hug the baby and hold him on his
# y2 V( T+ Y) S1 {: p3 schest for a considerable period of time, causing sig-4 X( W8 {! h! {, y1 Q2 {3 k
nificant bare skin contact between baby and father.* M4 N2 g z+ E% a, u
The father also admitted that after the phone call,5 g8 H9 h2 B" W' s/ u
when he learned the testosterone level in the baby
$ {' y! w- K: V$ x6 cwas high, he then read the product information
$ k5 H, e6 Q! o/ z5 Cpacket and concluded that it was most likely the rea-6 k4 O' ]+ S! P" q
son for the child’s virilization. At that time, they
: ~8 \# E7 P5 b! w- T& S, wdecided to put the baby in a separate bed, and the* z2 |+ h7 U& I: i
father was not hugging him with bare skin and had( z4 g3 b7 Q' s- U8 M9 t3 M( e7 ?. C
been using protective clothing. A repeat testosterone
: E) G- c! c1 L0 Itest was ordered, but the family did not go to the( H6 _) E$ n7 Y0 Z/ I& |+ z
laboratory to obtain the test.
# I p3 c( @1 p% d$ [; F' EDiscussion
. S4 q& b; J) k2 l) A/ r2 t) ]9 {Precocious puberty in boys is defined as secondary, V1 \) _' v e. `
sexual development before 9 years of age.1,4( N$ B8 e. \2 o0 O L
Precocious puberty is termed as central (true) when
' }: b# Q9 _/ I; `% E1 T* Rit is caused by the premature activation of hypo-& s5 i2 n" ?! \" v
thalamic pituitary gonadal axis. CPP is more com-- q# D) M Q3 |8 ~+ F
mon in girls than in boys.1,3 Most boys with CPP
: j3 Q% q6 t' j6 p( T% ymay have a central nervous system lesion that is( Y- G7 q: [, Q/ Z: T/ G# ]
responsible for the early activation of the hypothal-( T* f) c. e" L' q- S9 D1 l
amic pituitary gonadal axis.1-3 Thus, greater empha-9 l/ }3 r v' y7 J8 B2 f
sis has been given to neuroradiologic imaging in
; ^/ \" F1 y& g8 d3 h% U% z$ {/ Rboys with precocious puberty. In addition to viril-
3 O5 k8 ~1 N. ~ n* xization, the clinical hallmark of CPP is the symmet-) M! ?; {+ s" {& A3 i# l% p7 E) j; C
rical testicular growth secondary to stimulation by
1 F; {/ J- S; Q, }, g+ R4 x. u+ zgonadotropins.1,31 f4 g/ n' z% o# E0 c$ m. U( O
Gonadotropin-independent peripheral preco- A% |- T" q! x
cious puberty in boys also results from inappropriate* X; K1 f# N( L+ c$ p
androgenic stimulation from either endogenous or
) g' W4 ?8 \7 k! xexogenous sources, nonpituitary gonadotropin stim-( q8 H% M* w: m3 k& B3 X' w" |
ulation, and rare activating mutations.3 Virilizing- W1 w9 Z: w I* h, b
congenital adrenal hyperplasia producing excessive
: {3 e0 Y( E/ ?4 I# U1 E1 Hadrenal androgens is a common cause of precocious5 s. J* J# r$ G
puberty in boys.3,40 |- }! O; r% |* J* I; Q3 k
The most common form of congenital adrenal
; j: V. o6 C8 A$ X [: y7 l j# o% ~* dhyperplasia is the 21-hydroxylase enzyme deficiency.
2 q7 d) f2 Q$ |" Z" uThe 11-β hydroxylase deficiency may also result in
1 n g% V. _( {; bexcessive adrenal androgen production, and rarely,
; x! P+ A3 Z- d0 yan adrenal tumor may also cause adrenal androgen) E# [( F' T6 i$ A5 e
excess.1,3
9 q* m; N- ?, d+ Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: N2 }/ x& n9 D$ h& V9 R, N3 T542 Clinical Pediatrics / Vol. 46, No. 6, July 2007 L) M: f2 h; c. z( x H: d
A unique entity of male-limited gonadotropin- d, x, L. ]- ~& r
independent precocious puberty, which is also known
1 E# P9 S- i$ Aas testotoxicosis, may cause precocious puberty at a
6 q- N0 g* \+ M2 Z3 ?: n2 Mvery young age. The physical findings in these boys
1 U. e; r6 o4 S6 z5 K6 s4 nwith this disorder are full pubertal development, ^9 P) y( q& p3 ^+ I
including bilateral testicular growth, similar to boys
- c* e' g9 s4 z0 q/ [with CPP. The gonadotropin levels in this disorder
+ f% Q7 n, Q# @$ o7 c' @% nare suppressed to prepubertal levels and do not show! X( r4 }0 m' e/ M6 u
pubertal response of gonadotropin after gonadotropin-
4 i1 r0 C% W! h% ~4 A2 |9 xreleasing hormone stimulation. This is a sex-linked
- j) x0 Y' m: O% D2 Oautosomal dominant disorder that affects only0 N3 C. E6 z; p: ~# |, X$ h" z
males; therefore, other male members of the family" x r( V% J! O% y
may have similar precocious puberty.3
2 }8 i! S! q* U l9 d# a; r; ]9 wIn our patient, physical examination was incon-- k& Z5 S8 J5 @
sistent with true precocious puberty since his testi-
, S O: U' R3 L+ S7 Lcles were prepubertal in size. However, testotoxicosis
# l, b5 t( s+ W% Y+ iwas in the differential diagnosis because his father
/ D* }2 d" Y3 ~ V6 Astarted puberty somewhat early, and occasionally,
* P, [/ M- ?: L* }4 \( `! z! V" u) Ttesticular enlargement is not that evident in the
4 l) O2 K/ c( b: pbeginning of this process.1 In the absence of a neg-6 k9 @5 X$ U/ I0 M5 y- d
ative initial history of androgen exposure, our
) a E7 b) W% l8 Dbiggest concern was virilizing adrenal hyperplasia,
# w; ~$ v1 H3 F- `- v/ teither 21-hydroxylase deficiency or 11-β hydroxylase& W/ ^5 z4 T1 E& j
deficiency. Those diagnoses were excluded by find-8 U( ?# T: Q/ E5 Z( W, Z( A
ing the normal level of adrenal steroids.
0 y2 Q4 W5 K- F1 qThe diagnosis of exogenous androgens was strongly
& Y! G5 K7 D# K2 g- \; c% msuspected in a follow-up visit after 4 months because: Z) X8 t5 y; z; u" e$ L% j1 L& u* O
the physical examination revealed the complete disap-
5 i6 x1 ^6 i ~9 f! dpearance of pubic hair, normal growth velocity, and, N. {& `7 j$ j# m
decreased erections. The father admitted using a testos-* x6 C6 I" k" [7 t5 v' _! i
terone gel, which he concealed at first visit. He was) b+ c% b* u$ t: R& k+ p
using it rather frequently, twice a day. The Physicians’
9 r/ p, n/ k* L0 HDesk Reference, or package insert of this product, gel or% \1 @1 P" p0 N2 [0 u
cream, cautions about dermal testosterone transfer to, @9 m. p4 {) p0 j
unprotected females through direct skin exposure.1 h5 M. V8 O- I( K: p S8 j
Serum testosterone level was found to be 2 times the
0 v8 X: W4 O% o+ W7 b; c+ l/ Y* b2 pbaseline value in those females who were exposed to
/ z- g2 N6 l; keven 15 minutes of direct skin contact with their male0 P$ i. T A- W9 |- Z ?) J9 k
partners.6 However, when a shirt covered the applica-6 h; c) Z) h; B% i* m( Y2 [- u
tion site, this testosterone transfer was prevented.
* i+ E F, K3 M8 POur patient’s testosterone level was 60 ng/mL,5 _3 L/ b9 p1 G; k/ ~
which was clearly high. Some studies suggest that
9 O4 U( u. g6 F+ e0 pdermal conversion of testosterone to dihydrotestos-
4 X3 ]. m+ K- c7 mterone, which is a more potent metabolite, is more
4 F% R7 R5 [- f5 G; t* j8 _" kactive in young children exposed to testosterone4 o6 k7 R; F# C, E
exogenously7; however, we did not measure a dihy-- P4 C) i& } e; {5 S, @
drotestosterone level in our patient. In addition to
! n% n u& R" B3 o! `+ uvirilization, exposure to exogenous testosterone in
- c- w* w3 E4 [children results in an increase in growth velocity and9 v5 m9 m" D F% x( u
advanced bone age, as seen in our patient.
8 U/ R `3 B2 V, C: `The long-term effect of androgen exposure during
' v3 A& _: `, _9 J0 e9 s9 ]early childhood on pubertal development and final" [3 v8 ?4 c( V# K. V% F% T
adult height are not fully known and always remain5 Y1 C3 ^& }: t' R" m1 W$ J
a concern. Children treated with short-term testos-& t% P' X2 C% X8 X/ Y: o
terone injection or topical androgen may exhibit some8 W0 M$ l3 B2 m1 C0 Q4 H7 }5 y
acceleration of the skeletal maturation; however, after
$ X# M# A7 T5 l0 x: Zcessation of treatment, the rate of bone maturation
1 M8 ?. _2 r9 E, Mdecelerates and gradually returns to normal.8,9
" S) C6 v. m" E7 v0 h* k5 V8 MThere are conflicting reports and controversy3 i/ H& \/ `8 f. f& |2 |+ ?; H
over the effect of early androgen exposure on adult
1 l7 }. A, k7 P& Y+ W- L, wpenile length.10,11 Some reports suggest subnormal
" W4 U- B( G: Y' P8 g% \0 }adult penile length, apparently because of downreg-( ?" W1 Y& j! w2 [3 j
ulation of androgen receptor number.10,12 However,1 j: G" }2 w! S& ~! Q x1 k8 M
Sutherland et al13 did not find a correlation between
- t+ n# R0 m. k K* Jchildhood testosterone exposure and reduced adult3 n: {( }3 ^1 T2 Z' _6 v6 z
penile length in clinical studies.
- F4 p- v; S' Y2 N2 PNonetheless, we do not believe our patient is
& o* _; n _' y dgoing to experience any of the untoward effects from/ M$ @1 H1 A2 v8 d2 H
testosterone exposure as mentioned earlier because
8 \* N6 x0 @, p Z1 w/ athe exposure was not for a prolonged period of time.. B+ W4 E. R5 X7 l
Although the bone age was advanced at the time of
2 U U: A4 V3 {. udiagnosis, the child had a normal growth velocity at1 x: B1 e1 D- p, n
the follow-up visit. It is hoped that his final adult, s+ D; t/ ], Q
height will not be affected.
9 H0 A' P2 {2 {9 d5 }Although rarely reported, the widespread avail-
! i/ O) v( X) L7 S' Lability of androgen products in our society may1 t1 g/ f1 _7 p9 D3 M/ L) _
indeed cause more virilization in male or female9 a) C. c2 A/ n
children than one would realize. Exposure to andro-
0 u8 I- f6 }2 g% Lgen products must be considered and specific ques-; U! r: Y i! L6 ~
tioning about the use of a testosterone product or
! l6 I" `2 Q4 g. `( w2 egel should be asked of the family members during7 [0 X. a3 ` v9 Y: K4 X: {
the evaluation of any children who present with vir-
* G( E% W O: I G6 E# p, R+ _ilization or peripheral precocious puberty. The diag-
3 b' q4 _2 ^; y# | Ynosis can be established by just a few tests and by3 y; R- P7 f0 w+ s5 W
appropriate history. The inability to obtain such a( |% z. f z& i( W* D
history, or failure to ask the specific questions, may, R. Z" U& R0 s ~- j9 G
result in extensive, unnecessary, and expensive _8 o, a: e5 x9 z: K5 g& h; n
investigation. The primary care physician should be
, ]5 k( [. r7 j- Laware of this fact, because most of these children: G: H0 @" K5 L. i' g8 l) P
may initially present in their practice. The Physicians’
- z# g- f$ C7 g1 N3 v L% }2 T( fDesk Reference and package insert should also put a: S; S% H' E6 l8 e0 A( X, C+ S
warning about the virilizing effect on a male or2 v2 e' z. x" y( h: c0 E4 y( p
female child who might come in contact with some-
8 C7 y, K0 d' z0 H4 l- done using any of these products.
6 w- k8 d \* S1 Z2 D9 n' gReferences
- y" Y7 d3 D% b6 ?1. Styne DM. The testes: disorder of sexual differentiation
) `# j) M1 M2 N, iand puberty in the male. In: Sperling MA, ed. Pediatric- U9 {! m) ~0 ]6 X: M
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 D! t: J: E" l6 U2 u
2002: 565-628.
3 i0 w) L# {) s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 K( Y5 e( T( B$ A' m% H+ m8 ipuberty in children with tumours of the suprasellar pineal |
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