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Sexual Precocity in a 16-Month-Old7 F' H: g5 N( K
Boy Induced by Indirect Topical2 m- b5 U. c% j' r4 |0 R- w, y) u# R* O
Exposure to Testosterone
0 n; p+ `- X- DSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 P# N( T+ n. u% {* a$ m8 W
and Kenneth R. Rettig, MD1* J' [3 w7 m1 w& s
Clinical Pediatrics/ ~$ q6 Y" A$ o
Volume 46 Number 6
. c$ Z+ s8 t" H7 D% h5 w/ t; g2 MJuly 2007 540-5438 i* S; ^1 I* x4 m" O2 G" g% ^
© 2007 Sage Publications
" h2 |" [' D1 [; D10.1177/0009922806296651
; L- @/ ]4 {& H$ [4 Qhttp://clp.sagepub.com6 T6 @/ c- V x+ |3 d
hosted at' a* s: M( }* r+ r) V! @0 D% g
http://online.sagepub.com
9 v$ n; s6 p. B/ Y; {% V" l# ePrecocious puberty in boys, central or peripheral,- V5 N9 r+ u5 Z" E
is a significant concern for physicians. Central- f, t+ P- m; q! p7 d: \
precocious puberty (CPP), which is mediated2 t1 ~$ X7 Z8 r. A4 y/ H- z
through the hypothalamic pituitary gonadal axis, has
0 `& @9 {: l8 m' S! K# `a higher incidence of organic central nervous system) _7 M4 W/ ?+ }1 U: R
lesions in boys.1,2 Virilization in boys, as manifested1 h$ `. c: d8 S
by enlargement of the penis, development of pubic c2 F$ o/ @7 n. u7 q
hair, and facial acne without enlargement of testi-
5 q6 h, {/ l( t+ S9 `6 c% {cles, suggests peripheral or pseudopuberty.1-3 We
! m& {! `/ d- [2 \/ T0 k! ireport a 16-month-old boy who presented with the
6 g6 Y$ M$ s Y% m3 u9 Fenlargement of the phallus and pubic hair develop-8 T' ?: ?5 N8 w9 P3 I
ment without testicular enlargement, which was due% C, ^( G6 ]' a3 I) E4 i
to the unintentional exposure to androgen gel used by
2 n& c9 D2 A! C+ bthe father. The family initially concealed this infor-% l |8 A6 ~, ^0 J
mation, resulting in an extensive work-up for this0 J$ q! l0 l% I m0 c# S
child. Given the widespread and easy availability of
% f+ r' n1 n% i# I* c/ ?testosterone gel and cream, we believe this is proba-
$ `7 {/ Q: k9 |0 E/ F* P5 c5 Xbly more common than the rare case report in the
3 G$ @" Q3 f- Wliterature.4" [# Q0 U8 _ r; \0 \) L
Patient Report
7 g* v( T0 A& C) H [- |, \8 a8 RA 16-month-old white child was referred to the
3 C! \) |% c4 E5 i- Z3 T- Mendocrine clinic by his pediatrician with the concern; W" x/ Z/ r4 N y7 j% j
of early sexual development. His mother noticed
% r7 O m! z5 P4 ~$ M9 J, Zlight colored pubic hair development when he was
: e3 Z0 U+ X" g6 c# R8 w& J# hFrom the 1Division of Pediatric Endocrinology, 2University of/ c. l# j4 R& Q5 y+ {& X* L+ \
South Alabama Medical Center, Mobile, Alabama.
4 S) A; X2 x- ^3 F- @3 h3 Q6 f9 M6 V. BAddress correspondence to: Samar K. Bhowmick, MD, FACE,6 O1 ~- L l* u5 w b" ~
Professor of Pediatrics, University of South Alabama, College of% Y6 I1 r4 C" R6 f9 N) X; x" l+ A
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 O3 [2 k2 T8 n' c
e-mail: [email protected].
! `; V2 `8 i B+ E5 i! \about 6 to 7 months old, which progressively became0 M+ S8 ~1 `: Z+ R7 @
darker. She was also concerned about the enlarge-2 @' A3 U' B k! ^9 [$ w" _$ E
ment of his penis and frequent erections. The child
$ J6 s, T" M; S2 ]9 m9 p- L0 G' Lwas the product of a full-term normal delivery, with
2 | |4 y t" x6 l La birth weight of 7 lb 14 oz, and birth length of8 c/ k; O2 D# F
20 inches. He was breast-fed throughout the first year( d9 {1 M8 b* L- K5 r6 S1 c
of life and was still receiving breast milk along with
# |1 t3 z7 n1 l# V* b$ W0 ]. fsolid food. He had no hospitalizations or surgery,, S0 l F4 R1 U$ E# y
and his psychosocial and psychomotor development1 R: w# I. _" r( @1 v$ I' |& k3 Y4 W
was age appropriate.
5 q+ j8 x8 h& l$ \The family history was remarkable for the father,
) [/ g" z- q5 X1 ~' mwho was diagnosed with hypothyroidism at age 16,8 p6 \9 a5 B" r! W, Q
which was treated with thyroxine. The father’s; q6 y- B- S+ s- Z
height was 6 feet, and he went through a somewhat' q+ h/ ^7 K5 L/ H F- Y! }
early puberty and had stopped growing by age 14.
! |* x/ X; R* [' ^The father denied taking any other medication. The
# }- j+ m f4 ?4 B3 N+ t" S/ Z0 Ychild’s mother was in good health. Her menarche
w2 M; p) }% [& i! F" m/ T( N9 r# mwas at 11 years of age, and her height was at 5 feet4 O% o% C9 q! N: v7 [8 l
5 inches. There was no other family history of pre-+ _$ q# |' v( @+ v
cocious sexual development in the first-degree rela-
3 y. _+ @, E8 d% Gtives. There were no siblings.
; Z( P: L$ m( m/ I# V# {* Y PPhysical Examination- X" v, d* X) y
The physical examination revealed a very active,' F' A8 n' l4 O( c; B5 u
playful, and healthy boy. The vital signs documented9 y. a$ j+ S' O) Z' J2 }
a blood pressure of 85/50 mm Hg, his length was: H" n# b0 r% z+ W
90 cm (>97th percentile), and his weight was 14.4 kg
# C. L: m8 x3 Q5 c) _3 p- P2 M$ \5 F1 i(also >97th percentile). The observed yearly growth
! }* l# A6 K% ?0 O1 [9 M8 ]7 [velocity was 30 cm (12 inches). The examination of, ^8 C/ _2 y% Y; A3 L3 o6 E
the neck revealed no thyroid enlargement.
- g5 B2 |# A% Y2 R1 LThe genitourinary examination was remarkable for. ^ F! i& l# r1 l
enlargement of the penis, with a stretched length of
& @: [7 @, d1 |) T% {) l6 j0 q' q8 cm and a width of 2 cm. The glans penis was very well) R4 r8 V4 g- e% J1 F# o8 k
developed. The pubic hair was Tanner II, mostly around) k3 O) _" C5 w2 O: Q6 z+ M
540$ D/ G- ], H3 w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" x! C* f$ p3 e! ?the base of the phallus and was dark and curled. The" q; g1 O5 ^6 r( I K, u
testicular volume was prepubertal at 2 mL each.+ r2 i% G# O/ e+ g" m h
The skin was moist and smooth and somewhat- A: C8 L$ d0 ^2 e
oily. No axillary hair was noted. There were no) A6 n+ m. [ e- b4 p
abnormal skin pigmentations or café-au-lait spots.) o d5 u( I) q) ?3 I( K
Neurologic evaluation showed deep tendon reflex 2+" J+ K0 D# M# Y. Q
bilateral and symmetrical. There was no suggestion
+ V8 U" p- c9 B3 u. E! `) ^4 F2 \of papilledema.( g' E- N8 t7 m% Z9 D
Laboratory Evaluation
: V/ {- P* K( q9 L+ gThe bone age was consistent with 28 months by
5 T+ U ]( |0 ?3 E6 ?* Fusing the standard of Greulich and Pyle at a chrono-0 K, g! v4 Z, H3 d7 P6 Z: |$ R
logic age of 16 months (advanced).5 Chromosomal
$ O2 n: C" d- v3 |# S# b& D- `& ~; N: akaryotype was 46XY. The thyroid function test( k6 t! O- ^( }0 X# z
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
1 z! c- r4 V1 g) V7 ~% M. Clating hormone level was 1.3 µIU/mL (both normal).# r9 Q( z3 j& C7 I) c
The concentrations of serum electrolytes, blood3 a0 H+ g/ ?) Y" x6 u( I% b
urea nitrogen, creatinine, and calcium all were
8 S4 N( ]9 R: Pwithin normal range for his age. The concentration3 h1 T* A6 q" w, C2 Q
of serum 17-hydroxyprogesterone was 16 ng/dL
% I: M% B3 W/ N(normal, 3 to 90 ng/dL), androstenedione was 203 z, g$ E% p# M
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 A& Y5 T( N6 n
terone was 38 ng/dL (normal, 50 to 760 ng/dL),: S/ g! {' Z' N i
desoxycorticosterone was 4.3 ng/dL (normal, 7 to3 |9 D0 B* D3 J% `6 [
49ng/dL), 11-desoxycortisol (specific compound S)( }( J4 w! r% Q5 ], S4 T
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
7 ^9 x. c, S, wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 ]4 o" U- g6 s! Dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 X5 `2 A% T% U3 ~. P/ E/ H
and β-human chorionic gonadotropin was less than
N( [2 a2 _8 o1 X: p5 mIU/mL (normal <5 mIU/mL). Serum follicular1 h7 W0 j+ M3 }6 j" D6 |
stimulating hormone and leuteinizing hormone8 D# v- t! x3 O; @) ]( K' l% H& Q
concentrations were less than 0.05 mIU/mL
3 j ]2 ?$ Z: O6 W1 Q }0 ~; }(prepubertal)." _: I1 B* B( [$ ]+ y
The parents were notified about the laboratory6 d7 k Q9 [5 m `! u7 U
results and were informed that all of the tests were
5 B; y/ v- w# u+ R$ Z% ~0 snormal except the testosterone level was high. The
* D) D* a M4 y% C& X* vfollow-up visit was arranged within a few weeks to& j5 ~+ {& d' Y7 \* {
obtain testicular and abdominal sonograms; how-
( x; C9 A/ Y- n, i8 j9 ]8 Never, the family did not return for 4 months.* t( ~9 o6 q( G& l9 H- u6 A: C$ H: M
Physical examination at this time revealed that the
; X9 u! D H {0 tchild had grown 2.5 cm in 4 months and had gained* e. p9 ^( x5 q1 F
2 kg of weight. Physical examination remained
6 `( O2 {6 n% S) punchanged. Surprisingly, the pubic hair almost com-
5 \7 e g p1 F0 X' Npletely disappeared except for a few vellous hairs at
! C8 T& i; I6 ^; D2 @# o/ o! Q1 P$ qthe base of the phallus. Testicular volume was still 20 A- M) g0 Z$ |. r% |+ C
mL, and the size of the penis remained unchanged.2 E4 F) i( h7 R5 d+ s
The mother also said that the boy was no longer hav-
' P8 p/ K: Q7 O% X# p0 U8 F Ning frequent erections.
9 @3 U9 n; L0 Q/ rBoth parents were again questioned about use of0 j' U2 k' P; y
any ointment/creams that they may have applied to
, H9 ?( {; A3 L4 q+ S0 {6 Y# ?the child’s skin. This time the father admitted the, ~9 J/ W! Z" X& W$ D7 D* H5 J, A v* Q
Topical Testosterone Exposure / Bhowmick et al 5419 s/ x1 J! `/ h
use of testosterone gel twice daily that he was apply-
, j3 o) E) k- F* L& L: a2 qing over his own shoulders, chest, and back area for
3 \: C$ K4 |/ A0 ?a year. The father also revealed he was embarrassed
! _- L* C: p" p( B: R. f4 Q& Jto disclose that he was using a testosterone gel pre-# o3 R( U" Z% C" m$ J8 T
scribed by his family physician for decreased libido/ X7 T" l5 m2 W" a
secondary to depression.
1 v7 o; b: q9 s6 I) Y$ m ?- }6 wThe child slept in the same bed with parents.1 Z4 W8 m7 X# s
The father would hug the baby and hold him on his
. H2 I/ N4 a9 d$ v& Nchest for a considerable period of time, causing sig-
$ v6 a, a7 q0 u# H. U* dnificant bare skin contact between baby and father.
! Y# H; y% m2 i1 NThe father also admitted that after the phone call,
. Y7 B5 \! i$ h, U3 i+ E8 Awhen he learned the testosterone level in the baby" ]' |$ L [) H. V0 L; n: G
was high, he then read the product information
% k. V3 W# ]" S9 Npacket and concluded that it was most likely the rea-
' e$ W6 `% a; X# J& P/ [son for the child’s virilization. At that time, they- a! ^1 H6 x, k X1 M- p( B
decided to put the baby in a separate bed, and the+ H* E' X. j, G. E* F
father was not hugging him with bare skin and had3 I( |4 N$ O; K+ s
been using protective clothing. A repeat testosterone( n7 r5 P5 k) Z4 p& P: B9 v o) N
test was ordered, but the family did not go to the! v$ ]% `6 K. g8 q: L; h5 L5 M* G
laboratory to obtain the test.
5 \ B5 Q$ U3 Q% } B9 z1 Z) \Discussion& y8 K$ l5 t- w
Precocious puberty in boys is defined as secondary& @3 w }$ m- {; u. k4 T
sexual development before 9 years of age.1,4
1 a+ W4 d- p( k* w7 U! |$ g! O: v/ EPrecocious puberty is termed as central (true) when. X, T0 o! W6 Z X! b; P
it is caused by the premature activation of hypo-) W* s# r0 h& F( a$ Q" Y1 q# U
thalamic pituitary gonadal axis. CPP is more com-3 J4 [8 d& m, N3 }( x: O( G
mon in girls than in boys.1,3 Most boys with CPP
1 a7 y# @% |4 ?! Z& f9 lmay have a central nervous system lesion that is
5 w' s! m j- r/ wresponsible for the early activation of the hypothal-5 k: K1 V7 j$ M6 J4 Y" Y7 F! [
amic pituitary gonadal axis.1-3 Thus, greater empha-1 W6 Q1 x) D- g6 J& I
sis has been given to neuroradiologic imaging in
% C/ R' }4 O; o: d* y; {, @boys with precocious puberty. In addition to viril- U4 m) [" U1 j8 Q- m
ization, the clinical hallmark of CPP is the symmet-5 N- e2 t1 Y# m! A, c: w, w
rical testicular growth secondary to stimulation by
8 d( D, _. u4 _/ o# E% q7 j$ }gonadotropins.1,3
% b) l# w8 d5 t: c7 ZGonadotropin-independent peripheral preco-! y" ]" T. h# M& q; W- L# L9 x
cious puberty in boys also results from inappropriate# I7 l1 I$ F8 {0 O% C
androgenic stimulation from either endogenous or; A/ j+ r" N+ C5 H! T" T
exogenous sources, nonpituitary gonadotropin stim-
. _* y/ z* E0 s( ~. uulation, and rare activating mutations.3 Virilizing
! c! b3 F* k( i3 `congenital adrenal hyperplasia producing excessive
* T7 ?( ~- p2 ^( `5 p5 C! Padrenal androgens is a common cause of precocious
# }$ B% e3 A- L3 `. b6 \8 ?puberty in boys.3,4/ S, O$ D" e3 L+ b7 h- ?, a+ m6 C$ ?
The most common form of congenital adrenal
4 _! d* R$ m6 u! `, }1 J& {; dhyperplasia is the 21-hydroxylase enzyme deficiency.; K1 [" ~. D, m9 l1 z
The 11-β hydroxylase deficiency may also result in
* j; d4 N3 p( ^; Pexcessive adrenal androgen production, and rarely,# ~4 x: N: k y2 f) k: e1 a7 q
an adrenal tumor may also cause adrenal androgen. A/ Y6 s7 r! \- B6 z
excess.1,3* R2 P6 W9 @1 U* Q8 z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! l% O! O2 q" j% n542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 D, S1 V6 }2 P" GA unique entity of male-limited gonadotropin-8 X8 d% c! |* K1 `
independent precocious puberty, which is also known
2 ^! z7 y( p9 Fas testotoxicosis, may cause precocious puberty at a
9 B2 V' q. Y, Y* v& |* ?very young age. The physical findings in these boys, u5 _9 S1 j0 e3 T
with this disorder are full pubertal development,$ @7 r% W- L% P/ }6 C z
including bilateral testicular growth, similar to boys1 e1 ?1 r ?0 d$ q k: [
with CPP. The gonadotropin levels in this disorder$ [1 H- C6 Y" N. z' L
are suppressed to prepubertal levels and do not show) A& G# ]# t0 G0 j/ ^: L0 {1 O; p
pubertal response of gonadotropin after gonadotropin-
1 a+ [: a: i* o# r/ R# @releasing hormone stimulation. This is a sex-linked' |; ~: @3 j* f1 \2 g1 i
autosomal dominant disorder that affects only( c& S) o% o C
males; therefore, other male members of the family% g7 w. u( P6 B! {2 R K- U) ~
may have similar precocious puberty.3. Z8 F) C7 r& Z* E4 H6 f
In our patient, physical examination was incon-/ d* n. d5 s( D: d9 J; w, N
sistent with true precocious puberty since his testi-& O; s1 g- m! x% ]7 X, T# h
cles were prepubertal in size. However, testotoxicosis
7 y% v" \! I4 ?2 dwas in the differential diagnosis because his father
' i! l& g' A, V) X: @7 ?2 o: zstarted puberty somewhat early, and occasionally,: }8 p/ r" N: q M2 J7 B1 j
testicular enlargement is not that evident in the
3 I5 z8 I) j8 M6 m. Gbeginning of this process.1 In the absence of a neg-
4 J7 p, [" ?$ n7 T# j8 s, I, ^1 Mative initial history of androgen exposure, our
8 ], X7 x2 C% k6 ^biggest concern was virilizing adrenal hyperplasia,
5 A) J( K' d5 ?. }: v( Aeither 21-hydroxylase deficiency or 11-β hydroxylase
3 M, F. n1 B+ n' mdeficiency. Those diagnoses were excluded by find-
7 O* M8 E* ]% L hing the normal level of adrenal steroids.3 w* X- W. i# s6 i
The diagnosis of exogenous androgens was strongly
, u9 }1 Y2 n$ @. A8 E& t+ l% Ususpected in a follow-up visit after 4 months because) d+ F' j: @( C/ J' |
the physical examination revealed the complete disap-. J9 q4 \. d9 @" R# @3 ~! h
pearance of pubic hair, normal growth velocity, and
4 V3 |2 t2 h. s, S- F9 h! C! g$ `decreased erections. The father admitted using a testos-
* r" G9 L# x) _% G1 h$ q8 Pterone gel, which he concealed at first visit. He was
( {4 i9 v& I0 w( w* Xusing it rather frequently, twice a day. The Physicians’
( F6 c# E( F2 v1 tDesk Reference, or package insert of this product, gel or
3 w8 |0 p# d& I% F4 Tcream, cautions about dermal testosterone transfer to; `! U9 O" E" \1 v" p. G8 ^9 H4 i6 m
unprotected females through direct skin exposure.
1 t h1 H% w* `8 I( |" Y6 e2 fSerum testosterone level was found to be 2 times the
, _1 V1 Y6 T. }- V) W0 _ ], j! wbaseline value in those females who were exposed to
. R4 g( w, w0 t( `% T; w4 jeven 15 minutes of direct skin contact with their male
" x, p- s0 R# l; tpartners.6 However, when a shirt covered the applica-
$ q r9 h7 N9 e! S- ltion site, this testosterone transfer was prevented.# Z* R; i. q& `8 s
Our patient’s testosterone level was 60 ng/mL,6 z8 I0 Y4 e8 z% l- G
which was clearly high. Some studies suggest that7 \: O9 k9 b* _ Q8 u
dermal conversion of testosterone to dihydrotestos-6 F J6 G2 y# g
terone, which is a more potent metabolite, is more) C& n# M8 d* y
active in young children exposed to testosterone
" `2 n7 `$ @: H& Aexogenously7; however, we did not measure a dihy-
5 O/ Z8 g/ t# {9 `: U; Xdrotestosterone level in our patient. In addition to
8 Y" i+ F; x- d% M6 e1 Vvirilization, exposure to exogenous testosterone in7 b8 ?. j, {$ I9 b
children results in an increase in growth velocity and
: G5 N P3 b2 h, Jadvanced bone age, as seen in our patient.6 ?3 N5 G7 r* |! `0 V P
The long-term effect of androgen exposure during4 X+ ^+ I0 `- k D1 K
early childhood on pubertal development and final; e) D+ c# o: n" v* }* V
adult height are not fully known and always remain
% o+ F, k# Z9 F) G* Ua concern. Children treated with short-term testos-
0 v) i4 H, f D* P/ rterone injection or topical androgen may exhibit some1 K/ H" r2 J; A6 o
acceleration of the skeletal maturation; however, after
* g: ^1 r3 }: N' }# Q6 ]cessation of treatment, the rate of bone maturation3 D! B9 i5 w" K* y n* z- W/ B
decelerates and gradually returns to normal.8,9
" U2 i Z0 D' W+ c3 S# S& s* NThere are conflicting reports and controversy
6 K& f/ y6 |7 j. J0 M, y! kover the effect of early androgen exposure on adult
' [) x/ d* B+ d! q. Qpenile length.10,11 Some reports suggest subnormal5 X7 F3 w7 K; ^0 L% A9 j: f# |. I E
adult penile length, apparently because of downreg-& i. \: k0 X: h+ V
ulation of androgen receptor number.10,12 However,7 ^2 a" Z Z, Q; |& b' u; x
Sutherland et al13 did not find a correlation between9 E9 c5 [" g, d: V$ i
childhood testosterone exposure and reduced adult
, c( g: B3 {$ G7 w8 U0 D+ r( Qpenile length in clinical studies.' Z1 O7 J3 K* V' X' n4 s* U
Nonetheless, we do not believe our patient is& N ], [6 k* @6 ?+ {# K
going to experience any of the untoward effects from* e, n1 V$ j# _9 _5 D) W, c6 @
testosterone exposure as mentioned earlier because
; [: O/ K! ^0 x' M* Nthe exposure was not for a prolonged period of time.
5 t7 h3 y, J2 ~0 b" TAlthough the bone age was advanced at the time of
: }! y/ [$ l0 ediagnosis, the child had a normal growth velocity at
$ E4 A- V( Y$ O* I: e( |# o( c, H7 H: Cthe follow-up visit. It is hoped that his final adult
$ P6 n. F/ U& k. k/ R! C% d. _ pheight will not be affected.4 V. v; z3 r' [6 w1 e
Although rarely reported, the widespread avail-
- u% D8 H6 w* [5 L4 S: Wability of androgen products in our society may* u T9 y9 ^% D
indeed cause more virilization in male or female
$ `/ O4 H; a* N" }+ |9 k0 c! qchildren than one would realize. Exposure to andro-
+ ] F1 M! D, u2 Qgen products must be considered and specific ques-6 d0 D8 M! A# g8 U( c
tioning about the use of a testosterone product or
% m8 P7 J% ?7 Q. x" \$ V8 ^1 kgel should be asked of the family members during v( E( m6 H8 e- Q5 ?" Y) C
the evaluation of any children who present with vir-0 |! C3 S$ U1 f9 A: A$ A x M
ilization or peripheral precocious puberty. The diag-! s8 r0 S U% q+ n% |
nosis can be established by just a few tests and by
( f; t( N7 D! S6 n, Fappropriate history. The inability to obtain such a8 E( T' |- C+ P/ g4 U
history, or failure to ask the specific questions, may9 d4 Z6 Y( ]! O3 I' P
result in extensive, unnecessary, and expensive
O; {/ u7 g1 Y" f! Kinvestigation. The primary care physician should be
" X; c7 o/ p3 L, t$ _aware of this fact, because most of these children3 @% H* H& ?' P/ r- u# R: K( I
may initially present in their practice. The Physicians’" E$ C8 X1 A+ n# F' e- a b3 ?
Desk Reference and package insert should also put a
/ h$ ]1 @- ?& W; _3 T( {warning about the virilizing effect on a male or
" N! H2 Y: W9 n3 \female child who might come in contact with some-
" ^) u1 R7 P5 B* Eone using any of these products.4 Z( Q- M# X5 W) Q6 d* c! Z
References
- v: _# F8 N1 R& m8 k4 D1. Styne DM. The testes: disorder of sexual differentiation
4 H. p3 Q3 P: dand puberty in the male. In: Sperling MA, ed. Pediatric. F* M$ V7 Y* V! {! o7 E
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; h2 o9 }; M+ @/ D o/ z+ g2002: 565-628.5 } X% e9 M) K7 p+ B
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" E- ?6 l7 t0 R- G; B# o, u. k- I9 d
puberty in children with tumours of the suprasellar pineal |
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