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Sexual Precocity in a 16-Month-Old
5 C# m, e6 f8 U4 WBoy Induced by Indirect Topical: t! w4 ? I; d8 ^* z6 ?# h
Exposure to Testosterone
9 N3 e$ y/ t- V+ y' Y/ TSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,27 F& G# w* S7 _+ q3 |+ D5 I# z3 Y
and Kenneth R. Rettig, MD1
/ K& T% H3 ^3 L% {% D |! y$ E2 }Clinical Pediatrics
# q, L2 I) x% E+ o4 fVolume 46 Number 6
: W/ ?0 D# r1 ?- u# U+ f5 bJuly 2007 540-543
: B- l! X5 ]2 }9 T3 o© 2007 Sage Publications
8 Y$ w4 F1 k0 I7 |6 E( B S* q% H10.1177/0009922806296651* a, {) G B; z I( ~
http://clp.sagepub.com
' f0 V2 F* U- A, a1 e$ F" H% ohosted at
9 V. Q3 M, a6 r6 Y& O5 P( \http://online.sagepub.com5 _/ b# V& \5 f$ V/ h6 Q
Precocious puberty in boys, central or peripheral,
0 K; v# M! z% s5 K( s1 l$ \is a significant concern for physicians. Central2 V2 p/ m$ t$ G* I& u8 l/ c' Z
precocious puberty (CPP), which is mediated
3 i2 l ]8 h, X/ f/ A9 q mthrough the hypothalamic pituitary gonadal axis, has8 m" m" ^3 A! J% ^0 ^
a higher incidence of organic central nervous system& i7 Q1 u5 l b" m2 g
lesions in boys.1,2 Virilization in boys, as manifested/ C k; `8 P/ d4 }7 D* Z
by enlargement of the penis, development of pubic; e' l: c( P# ~
hair, and facial acne without enlargement of testi-
: I' _( |' {9 t: l0 E1 ucles, suggests peripheral or pseudopuberty.1-3 We
: E; L; {8 }( oreport a 16-month-old boy who presented with the/ m% d. G9 R1 x/ \' h8 ?
enlargement of the phallus and pubic hair develop-
$ K2 t8 g- t! q8 d# tment without testicular enlargement, which was due: R# Z! P- K9 e! p$ u
to the unintentional exposure to androgen gel used by
. e6 f2 t5 c1 l6 c$ [1 R: Z$ d2 a( Othe father. The family initially concealed this infor-
9 Y9 R8 C9 B; B8 A* S/ ~mation, resulting in an extensive work-up for this% `/ l; |/ L& v T, c: {) @
child. Given the widespread and easy availability of8 b: ?3 D: a( P3 }! O# ?. H7 Y
testosterone gel and cream, we believe this is proba-
' M" o$ z) f" M" ]9 ?9 ?bly more common than the rare case report in the$ ^+ }. `+ \9 x# ^0 M& b! N5 F
literature.4
5 W) x! t* j0 jPatient Report
* F' T% @. z8 F4 i4 i: |/ gA 16-month-old white child was referred to the# J7 _1 b/ ^) l- |
endocrine clinic by his pediatrician with the concern3 ^* d2 U% G* R' Q
of early sexual development. His mother noticed
/ l* X. {( [4 x, u3 elight colored pubic hair development when he was
: s$ ~5 b) Z) e3 p: o; NFrom the 1Division of Pediatric Endocrinology, 2University of$ O, x7 s3 h% y
South Alabama Medical Center, Mobile, Alabama.% |3 O/ C. k/ g8 b
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 m/ F$ J9 M) L. \, F7 W2 oProfessor of Pediatrics, University of South Alabama, College of, h& i5 W3 }/ W3 v4 A4 l8 |
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ p4 y; \6 t( ?1 w' [, T% Z- u% ve-mail: [email protected].8 Y/ i$ K6 G" p- m( ^. }; ?! O
about 6 to 7 months old, which progressively became
* k+ W8 M6 w- f& y- S, e7 idarker. She was also concerned about the enlarge-$ H7 @, q; T+ D. n
ment of his penis and frequent erections. The child) ^. `+ v* o/ d; V
was the product of a full-term normal delivery, with7 d9 H& J+ |' M- i- [9 E+ n
a birth weight of 7 lb 14 oz, and birth length of) ~6 j9 ]. n8 {2 h5 O
20 inches. He was breast-fed throughout the first year2 I* h$ |# N4 v
of life and was still receiving breast milk along with- j2 D. J1 h: w) h/ U
solid food. He had no hospitalizations or surgery,+ f+ u' l! [4 b) }! t+ L0 K5 } ]
and his psychosocial and psychomotor development
. T: M' [( t2 Kwas age appropriate.
% s2 F+ x; |( L! j2 RThe family history was remarkable for the father,
9 I, P1 b& {, O& l+ ~2 A! |/ O9 v; }who was diagnosed with hypothyroidism at age 16,
' L8 b- A2 T8 s* b/ Hwhich was treated with thyroxine. The father’s8 p) l' a# a0 P9 b$ {% n( {
height was 6 feet, and he went through a somewhat. r% r/ |5 K) q
early puberty and had stopped growing by age 14.- S$ a- A* ~' l, A" K
The father denied taking any other medication. The
( @7 b4 W) c! y+ u/ ochild’s mother was in good health. Her menarche a1 c6 b/ e2 D# D# l
was at 11 years of age, and her height was at 5 feet! g2 c$ H; e7 K; k
5 inches. There was no other family history of pre-
. Z" V# r7 d6 }: ^; i, Y. Ococious sexual development in the first-degree rela-
( G6 J/ Y) C' H# itives. There were no siblings.
; R* ]9 H3 T/ ~) gPhysical Examination
" Z# b( }9 g2 Q9 {The physical examination revealed a very active,
0 G9 N& ~9 a1 K }+ wplayful, and healthy boy. The vital signs documented0 C2 e% {% c6 O. p0 F" x+ y
a blood pressure of 85/50 mm Hg, his length was8 v8 Z$ P7 R3 p0 i/ g+ ~' J" R3 k
90 cm (>97th percentile), and his weight was 14.4 kg2 r4 x: J, v c4 S' K
(also >97th percentile). The observed yearly growth
6 }. h1 ~2 @: r( D& `. Bvelocity was 30 cm (12 inches). The examination of
' Q0 y. b* s' @3 `( nthe neck revealed no thyroid enlargement./ o2 _, x, g! J
The genitourinary examination was remarkable for) H6 g/ B5 l7 u* |+ V/ i3 e. B
enlargement of the penis, with a stretched length of
, V9 u. f, I+ t/ o9 b8 cm and a width of 2 cm. The glans penis was very well7 A) F; l0 R8 D; O/ K
developed. The pubic hair was Tanner II, mostly around4 u5 I4 C! S+ e A, D4 z
5404 W$ J- y( G/ [: X
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# b( M& M* u# uthe base of the phallus and was dark and curled. The- r$ m6 u$ t8 e s$ b
testicular volume was prepubertal at 2 mL each.
/ ^+ [; h# v& X3 R7 M' eThe skin was moist and smooth and somewhat8 D0 N, x; e; {+ n9 [; T/ I
oily. No axillary hair was noted. There were no# C+ C" r# _4 a+ G( m
abnormal skin pigmentations or café-au-lait spots.; ^8 R9 `# t" M
Neurologic evaluation showed deep tendon reflex 2+
, C5 u: A4 S0 T [$ I* v8 S- vbilateral and symmetrical. There was no suggestion9 o2 E9 R: W9 F+ O
of papilledema./ _3 J% A& Y8 z+ i; o5 Q) s
Laboratory Evaluation
9 L9 s7 u$ Q3 u" HThe bone age was consistent with 28 months by
: Z, k. a+ [% U! M# J3 W* Eusing the standard of Greulich and Pyle at a chrono-" i4 \* u7 H" X. n
logic age of 16 months (advanced).5 Chromosomal
3 Z- ?' j$ L- G+ S7 c! ^' z8 Ukaryotype was 46XY. The thyroid function test1 x+ d" Q1 Q) u* C& N
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 ]- u) ?4 M7 N/ O- t1 dlating hormone level was 1.3 µIU/mL (both normal).
6 j M' W- Y( O2 r8 o4 UThe concentrations of serum electrolytes, blood
( {+ }3 I2 R9 i, Q2 {urea nitrogen, creatinine, and calcium all were
/ \+ V' d* Z, `1 r/ W4 t( y* F7 _within normal range for his age. The concentration# g$ f' g) s' r$ _
of serum 17-hydroxyprogesterone was 16 ng/dL: s8 o$ y1 W) C7 E( k) Z
(normal, 3 to 90 ng/dL), androstenedione was 20# H- C8 ]) o3 D' [! d. j
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- v1 W3 Y- y. d8 |
terone was 38 ng/dL (normal, 50 to 760 ng/dL),' i, @" J1 k6 d
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ E. P: n( b6 O: E9 t49ng/dL), 11-desoxycortisol (specific compound S)) F) P2 k! z* Q* R% S; W w& E' \
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) D/ R' f- O2 @( B) m' |8 I4 x
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( {( b- L( v: N8 Ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
' W, c' n u% n6 o7 Dand β-human chorionic gonadotropin was less than( d0 M+ u: ~5 G+ ?- `! b# X
5 mIU/mL (normal <5 mIU/mL). Serum follicular0 \- |9 Z6 Q' |: |! v# O& S' X
stimulating hormone and leuteinizing hormone
1 D( Q9 @: Z- e% K' J! M: X0 s% x. nconcentrations were less than 0.05 mIU/mL
' U. h( i2 V J- o* j( R7 }+ p(prepubertal).) {8 J" f' L7 F1 E" X& h
The parents were notified about the laboratory
- ^$ e% u( w$ E; q) `5 S/ [results and were informed that all of the tests were! L- [8 v2 c# ?0 }
normal except the testosterone level was high. The/ ^0 e3 r1 ~: G
follow-up visit was arranged within a few weeks to0 p/ j0 Y" V& O& ~. {3 A
obtain testicular and abdominal sonograms; how-( }- E( y" ^1 T _2 {
ever, the family did not return for 4 months.
* `5 M" D+ j* t7 Q# }+ O2 C, PPhysical examination at this time revealed that the3 h& U( R5 r( E( J$ p
child had grown 2.5 cm in 4 months and had gained
& V a: g7 o, |; b2 kg of weight. Physical examination remained
7 c0 e* P0 Z5 n3 Z8 ?( `6 z& @# @4 punchanged. Surprisingly, the pubic hair almost com-* j( |3 r, u6 g8 a& b) Y' {
pletely disappeared except for a few vellous hairs at
. w I l: G6 W: H/ R+ M' ithe base of the phallus. Testicular volume was still 2# d! b) Y9 f% T5 D1 }& t6 o
mL, and the size of the penis remained unchanged.
3 T' H: J( w' V# s: }; OThe mother also said that the boy was no longer hav-, D' s& P8 p3 l+ U! |* a( D- @4 y: L; V
ing frequent erections.6 ^, ^- p* R' M; X. C8 h, X. [: W
Both parents were again questioned about use of2 M4 A" n; V) v9 K6 Y( [0 L; @
any ointment/creams that they may have applied to
' L; w5 Z$ ^3 R) M: S8 C) Ithe child’s skin. This time the father admitted the0 s% c ^- t, Y+ `7 c5 D
Topical Testosterone Exposure / Bhowmick et al 541
+ D, e" L8 h2 N0 ?6 i) x1 xuse of testosterone gel twice daily that he was apply-7 B v1 f1 f0 c: N7 ]# k, J) r
ing over his own shoulders, chest, and back area for. `1 o2 g( g O
a year. The father also revealed he was embarrassed
8 V+ c) ]* R' ?" a Vto disclose that he was using a testosterone gel pre-
& S' m2 T: K/ g# n0 xscribed by his family physician for decreased libido% u O4 R/ ]& R0 D3 R
secondary to depression.
) z9 z v, d d8 [! c; G2 G$ k4 bThe child slept in the same bed with parents.
5 F3 h+ u& y1 U9 x) \The father would hug the baby and hold him on his3 p; i" N) H# D- G# A2 C# i" ~$ _
chest for a considerable period of time, causing sig-- V h$ v+ C0 A9 } `8 ?! F
nificant bare skin contact between baby and father., f/ o" k, `3 O7 h' x: G
The father also admitted that after the phone call,
) S7 c" d9 {$ W1 g2 Iwhen he learned the testosterone level in the baby) p* b* Q# `3 |6 \$ C5 D/ }. Q5 } H
was high, he then read the product information
: v; }6 n6 `' F8 {7 w! wpacket and concluded that it was most likely the rea-
8 j- `( S/ n* o: x$ V2 mson for the child’s virilization. At that time, they3 @( B \; i! `5 j# Z0 j
decided to put the baby in a separate bed, and the
" T. Y, O, r P1 \9 J' M- q# i* N$ qfather was not hugging him with bare skin and had
' T1 \! l' u! k7 f$ ?* lbeen using protective clothing. A repeat testosterone/ [5 V5 n- K6 s* ?) S
test was ordered, but the family did not go to the
6 A9 ]& l, K: N, e3 F1 ^. C& Ulaboratory to obtain the test.
# x, x. O( e; ^; |4 F0 p& g# eDiscussion1 {7 ]0 D& r- o- v% c. W" M* n1 Y# ]$ a
Precocious puberty in boys is defined as secondary
9 V2 U6 Y- R3 z/ ksexual development before 9 years of age.1,4/ B8 i% l' R3 ?7 y- M4 i' J
Precocious puberty is termed as central (true) when
; z9 G' m' p: b+ T1 Git is caused by the premature activation of hypo-* ~8 s! v+ q" z2 L- [) N4 \; ]
thalamic pituitary gonadal axis. CPP is more com-$ @( ]0 j' ?; F% Q' r
mon in girls than in boys.1,3 Most boys with CPP
5 W4 k/ n' ?0 n3 g# L5 Q! Qmay have a central nervous system lesion that is) O+ ?% C0 c0 N; C, v8 `
responsible for the early activation of the hypothal-+ D& _3 f* {8 a: |6 O$ U) Y; J4 o
amic pituitary gonadal axis.1-3 Thus, greater empha-8 }( |: \" k, w/ F6 j
sis has been given to neuroradiologic imaging in7 E( s2 _6 A8 V9 W) ]8 e/ u& c
boys with precocious puberty. In addition to viril-2 ^7 t$ ^# } L& s
ization, the clinical hallmark of CPP is the symmet-
( i6 y G# J& m8 l2 h( `, Vrical testicular growth secondary to stimulation by6 Q. R1 J3 C# A
gonadotropins.1,3+ e! d, k3 P9 I/ I$ P
Gonadotropin-independent peripheral preco-$ a6 n' \6 r* l5 t
cious puberty in boys also results from inappropriate6 s" A$ P o# ]
androgenic stimulation from either endogenous or2 o/ a8 ^# S5 L d
exogenous sources, nonpituitary gonadotropin stim-: c% R& k r! Z; Z# E
ulation, and rare activating mutations.3 Virilizing
3 M( W( i& L: K; a. Z9 [congenital adrenal hyperplasia producing excessive3 `4 ~# j% w H4 ~
adrenal androgens is a common cause of precocious X$ D2 Z- P- l% O8 _7 t
puberty in boys.3,45 e6 z% s0 E# o* Q0 X8 ^$ Z! i: g! D
The most common form of congenital adrenal
1 N' i+ j4 n1 Z$ T7 Hhyperplasia is the 21-hydroxylase enzyme deficiency. d& H$ t& r4 \) ^7 n
The 11-β hydroxylase deficiency may also result in3 A& z+ r v- `! }- u% x# Q G
excessive adrenal androgen production, and rarely,/ i. P6 }! w' u" x7 \1 G
an adrenal tumor may also cause adrenal androgen
' K7 L, C0 B* `. P& ^4 \# _4 h5 |excess.1,3
; [& B1 o; L& eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) y! t: z4 L$ A% h) l- L: a1 g
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 c6 g& J3 l& A& dA unique entity of male-limited gonadotropin-
) q- }+ v. ^. Q1 @! @5 `4 [, h% Nindependent precocious puberty, which is also known
]. Z! @! [4 Das testotoxicosis, may cause precocious puberty at a: G P8 b0 |3 _3 w8 F
very young age. The physical findings in these boys
' E% m5 T- Q! t2 Awith this disorder are full pubertal development,) C% K& N5 D0 f4 [
including bilateral testicular growth, similar to boys
9 \! L- f! K" u# E% swith CPP. The gonadotropin levels in this disorder4 F8 J- G0 _6 W, v
are suppressed to prepubertal levels and do not show
# e6 a6 o3 \' u3 upubertal response of gonadotropin after gonadotropin-0 H5 [% o2 r7 \1 @/ f
releasing hormone stimulation. This is a sex-linked
( x0 ^# i4 ]9 _! y; Hautosomal dominant disorder that affects only
7 S w8 w8 Y8 o! B* cmales; therefore, other male members of the family
- Z3 n9 w+ |+ f+ a3 l" p9 hmay have similar precocious puberty.3
7 {$ ]. t- T3 Z/ c% TIn our patient, physical examination was incon-+ r) ~4 O5 b$ F0 g6 t
sistent with true precocious puberty since his testi-& C( u4 Y7 J$ T( k/ p; U. g3 J
cles were prepubertal in size. However, testotoxicosis+ F% o9 Q) U3 l6 ?9 f9 @& [9 H0 Z3 }
was in the differential diagnosis because his father
+ \+ @, @* K9 ]9 R8 Y9 |started puberty somewhat early, and occasionally,
( J) A2 j* y4 t, q1 w* S* Xtesticular enlargement is not that evident in the& z* Y( m# F" L- g9 Z# d
beginning of this process.1 In the absence of a neg-
1 u+ |7 k, j3 l/ O: Xative initial history of androgen exposure, our
- P/ Y8 q" B0 P. Gbiggest concern was virilizing adrenal hyperplasia,5 ?! M" M! F/ p; V. R
either 21-hydroxylase deficiency or 11-β hydroxylase/ c) G) E& ]7 y
deficiency. Those diagnoses were excluded by find-" r+ X: ~1 S Q: L* p8 o/ Y* ~1 f4 w
ing the normal level of adrenal steroids.4 [* _8 I+ g/ V3 L( t; f
The diagnosis of exogenous androgens was strongly
5 P' R5 o3 [6 ]: Z! Csuspected in a follow-up visit after 4 months because
) N& A: L9 |! x' z( `- `the physical examination revealed the complete disap-( `# X0 w7 l$ T; v5 q! F
pearance of pubic hair, normal growth velocity, and p( z# O; y5 B3 z7 g# V
decreased erections. The father admitted using a testos-, p( m% }4 ?+ v7 `8 r
terone gel, which he concealed at first visit. He was. j4 f, D* F4 d
using it rather frequently, twice a day. The Physicians’
5 H: K0 U4 @7 G4 dDesk Reference, or package insert of this product, gel or; W' `6 V8 h7 V& }
cream, cautions about dermal testosterone transfer to' s) y+ U2 `- X i5 ]
unprotected females through direct skin exposure.
9 p3 S: }- {7 f* K, {Serum testosterone level was found to be 2 times the
% ~/ L, C/ J- i e6 N, Ebaseline value in those females who were exposed to5 q/ y0 V2 x# F& U
even 15 minutes of direct skin contact with their male9 i |& r* w. z/ P! w6 p
partners.6 However, when a shirt covered the applica-; K7 [ D$ Z2 M/ ~" c1 H$ z. J
tion site, this testosterone transfer was prevented.
- t, f4 l A* s9 p& Q- ^Our patient’s testosterone level was 60 ng/mL,
" I, g$ d6 H$ P" f$ k1 d* q C/ Uwhich was clearly high. Some studies suggest that7 j5 Q2 P" g* C m7 a+ g
dermal conversion of testosterone to dihydrotestos-
! b. z5 R: L7 ^% b+ Fterone, which is a more potent metabolite, is more
( j! O x; o' Factive in young children exposed to testosterone
6 T6 @4 Q, t' a+ ?( V. oexogenously7; however, we did not measure a dihy-; n2 M" v# k2 Z! Z* O8 S
drotestosterone level in our patient. In addition to5 E( M5 c* c3 s6 ^; Q& D3 ^
virilization, exposure to exogenous testosterone in
: Y$ l. c' d$ Xchildren results in an increase in growth velocity and2 w6 {, l2 K5 C2 f( [6 H
advanced bone age, as seen in our patient.- F8 P0 |! G" E g7 r6 u/ h9 z
The long-term effect of androgen exposure during, w2 |, J% i: d7 f+ i& h4 F6 M3 [
early childhood on pubertal development and final
2 f+ V$ C6 q5 R- y& v3 aadult height are not fully known and always remain) j. E! p+ G e( r6 x4 f
a concern. Children treated with short-term testos-# G. m2 V4 g9 O5 C% I
terone injection or topical androgen may exhibit some6 y# A9 Y6 ]) Q) t2 y& M9 w
acceleration of the skeletal maturation; however, after
( n8 A7 g/ Y, D4 X, l& fcessation of treatment, the rate of bone maturation
, g; `4 s3 M3 L) F0 s7 n( ~. l6 Vdecelerates and gradually returns to normal.8,9% Y0 _- w( B8 w W6 F- v
There are conflicting reports and controversy; g. ^$ O" K3 A6 k% v) X. ~
over the effect of early androgen exposure on adult, ]3 _5 n8 ?( R1 A; F
penile length.10,11 Some reports suggest subnormal- x4 Q! P; E1 {* C) P
adult penile length, apparently because of downreg-/ Q! f7 J: C6 ^. J
ulation of androgen receptor number.10,12 However,
) a3 z7 P: P. J8 K* gSutherland et al13 did not find a correlation between; R5 g+ J' m+ `& _/ p! f
childhood testosterone exposure and reduced adult$ ~+ f8 r) i1 }7 N( ?) d1 v
penile length in clinical studies.) M" Z7 D% n& X/ |$ L9 F
Nonetheless, we do not believe our patient is6 h" |. f# I; W$ \. c
going to experience any of the untoward effects from
3 p: o& d0 p' S+ d% Etestosterone exposure as mentioned earlier because) }' c) u+ Z5 U% r
the exposure was not for a prolonged period of time.9 u/ ~! }" e) d1 Y
Although the bone age was advanced at the time of
, ~- ^& X8 u# f+ Z$ a' G4 V3 cdiagnosis, the child had a normal growth velocity at
, W7 V/ ]! g/ Q, `0 t1 vthe follow-up visit. It is hoped that his final adult4 p. x4 g% `1 x; g) c
height will not be affected.
& Y" v# k( U8 h0 i! `( @: OAlthough rarely reported, the widespread avail-1 |* X! g0 v9 P) H8 _% a
ability of androgen products in our society may2 F r. i+ x d/ ^- Q
indeed cause more virilization in male or female
2 C' B* Z. M2 D3 s' Y( l: s" Vchildren than one would realize. Exposure to andro-
1 Y- r! f0 p6 F- cgen products must be considered and specific ques-$ q5 e% f b- \$ u* k
tioning about the use of a testosterone product or2 e) B- L% B/ W6 d
gel should be asked of the family members during0 Q( a# d7 i( J0 C5 f" E6 y/ ^
the evaluation of any children who present with vir-
4 V0 K9 Z$ c+ [5 Y0 kilization or peripheral precocious puberty. The diag-) W! O9 o- l% L7 M7 r
nosis can be established by just a few tests and by
0 w4 V4 W5 k) W! x& T: |appropriate history. The inability to obtain such a( q U i6 T: M2 @$ t
history, or failure to ask the specific questions, may; M, j5 ~6 m9 R& I0 v) V
result in extensive, unnecessary, and expensive6 @4 U( F5 u$ A. v
investigation. The primary care physician should be/ z i3 A6 O" v# N7 N6 E8 h1 r e
aware of this fact, because most of these children& D. G: O, B7 m5 a$ Z+ r% p
may initially present in their practice. The Physicians’$ o( R* J& h& D4 P
Desk Reference and package insert should also put a
1 ] K! h7 p% H- o+ Y2 n' R( wwarning about the virilizing effect on a male or
2 z2 B1 Q0 j; j- n0 c5 ufemale child who might come in contact with some-: ~' z" A }" d1 O
one using any of these products.
3 U) T2 S' f4 b* q/ Q9 P+ fReferences
U: u- l& ?$ X7 f/ ^1. Styne DM. The testes: disorder of sexual differentiation8 s9 Y9 H1 [( ^ r0 S* \! U
and puberty in the male. In: Sperling MA, ed. Pediatric8 M3 {/ n% I w7 F+ H! I
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 ?! p: I: K8 y6 i& n3 y: D! d2002: 565-628., F' P( f+ x" ~2 x" h( H
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. i5 {; F9 s3 ^# k" m/ dpuberty in children with tumours of the suprasellar pineal |
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