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Sexual Precocity in a 16-Month-Old3 x! G. r3 v9 [ ]4 s0 V& `, _
Boy Induced by Indirect Topical; N5 \2 k9 ~, |" Y
Exposure to Testosterone( g; w6 R( p0 w* C% ]+ `
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' V( I1 N) G. E+ m, ]2 |and Kenneth R. Rettig, MD1' c9 E8 I7 }% X
Clinical Pediatrics" T" r; U v! B
Volume 46 Number 6
* L5 Z. H* w _5 Z+ d% EJuly 2007 540-5434 n& \' I5 E8 z8 [/ {
© 2007 Sage Publications( k% y, c' I% K4 X
10.1177/0009922806296651) w& s% i: f/ P# u t2 x+ `2 r
http://clp.sagepub.com
2 g- D5 w2 \' S; Y% C4 V. ]$ K" Zhosted at ~$ z: v9 H9 s0 z* C* g
http://online.sagepub.com
0 v O, S5 s* W. |& N. IPrecocious puberty in boys, central or peripheral,, `7 b/ B/ y' V) `6 K, n; N
is a significant concern for physicians. Central& k1 b( l9 {: b
precocious puberty (CPP), which is mediated% z+ J* _: o7 ~2 i; b8 Z% N) D
through the hypothalamic pituitary gonadal axis, has
* m4 c0 X& M7 w; ~* ~! ca higher incidence of organic central nervous system# z9 c1 m" F! U' p" H$ V. C3 ^
lesions in boys.1,2 Virilization in boys, as manifested
6 M1 c) t; `- q y9 k( m& F+ [" P+ G2 qby enlargement of the penis, development of pubic! s, q$ {* G B& N+ K+ S% R
hair, and facial acne without enlargement of testi-4 F5 ]0 _' _+ _: S, @
cles, suggests peripheral or pseudopuberty.1-3 We
9 R( n" H, C! K( o$ yreport a 16-month-old boy who presented with the
^ J" K- a( K( u+ o9 x& Kenlargement of the phallus and pubic hair develop-
# n$ [0 V& T" v$ y+ Zment without testicular enlargement, which was due6 S g* D. z! R- ?- h$ e! Z& x
to the unintentional exposure to androgen gel used by! p* H3 m0 B9 h0 Z4 r& Y8 r
the father. The family initially concealed this infor-. k. \1 }/ L3 J' g& N
mation, resulting in an extensive work-up for this, N4 p$ v. B7 D8 U
child. Given the widespread and easy availability of# H. h$ }- b q% A" \: T0 z2 \
testosterone gel and cream, we believe this is proba-
: j+ ^; r0 W2 r, d: _! W& p! ~7 Sbly more common than the rare case report in the& N0 H8 j+ r8 o
literature.4
+ z# h7 \' m: e' gPatient Report
$ z* o- }" h m' v& zA 16-month-old white child was referred to the' _! _8 {: _/ }3 m5 |& l
endocrine clinic by his pediatrician with the concern
5 Q# D8 P5 s! M4 T; N6 [of early sexual development. His mother noticed1 i4 f! O+ u. {$ _, u/ V
light colored pubic hair development when he was
$ r7 v# {7 \/ e5 ^From the 1Division of Pediatric Endocrinology, 2University of# K( r- {9 S" B% H1 }
South Alabama Medical Center, Mobile, Alabama.
5 o7 x2 K( Z% @% c; E% U& p. TAddress correspondence to: Samar K. Bhowmick, MD, FACE,
. a3 K3 ?3 ]& E) k$ XProfessor of Pediatrics, University of South Alabama, College of+ E0 c1 S8 h6 ^- d% y+ L& d
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ q2 H' H0 c2 {3 ^ a, y, s7 K
e-mail: [email protected].
6 x% m9 X$ h6 `. ^8 f: F2 X4 uabout 6 to 7 months old, which progressively became+ X+ ^* [( b8 d' g! d
darker. She was also concerned about the enlarge-' p5 N9 P7 l* u! {
ment of his penis and frequent erections. The child0 d4 e% F6 u5 M* G$ X
was the product of a full-term normal delivery, with
7 }' |# P: M1 O' Y: Z- T- u W% Za birth weight of 7 lb 14 oz, and birth length of
3 S, O, u" E8 r4 @( u20 inches. He was breast-fed throughout the first year% D' b5 z: C$ t- s
of life and was still receiving breast milk along with
+ I+ i) U2 j/ A7 N" M/ Tsolid food. He had no hospitalizations or surgery,
' h0 K/ U) J7 D a: X/ Mand his psychosocial and psychomotor development
3 U- J5 x1 {, w+ _was age appropriate.
' n( F% q3 D( j8 q9 g8 W6 w7 WThe family history was remarkable for the father,
/ y: e9 x+ e# ?# M" Q$ ~6 u( Awho was diagnosed with hypothyroidism at age 16,
! Y: @/ g" s5 j9 e8 Vwhich was treated with thyroxine. The father’s7 }+ ?& W! ` M6 W2 u2 e$ F/ C
height was 6 feet, and he went through a somewhat
8 Q3 Y- r, z, O* Hearly puberty and had stopped growing by age 14.
- a, l- ]& e( _# `9 ?9 x% Q! xThe father denied taking any other medication. The
1 L' p, }* p* w, Q0 g0 bchild’s mother was in good health. Her menarche. k: @5 f& I& F8 w: e7 F/ ^8 k% v Z
was at 11 years of age, and her height was at 5 feet
# e: R+ ?/ u! n5 z; l5 inches. There was no other family history of pre-
, J4 Y! H% ]# q5 Jcocious sexual development in the first-degree rela-, ]. K) E" U* i) w* t+ d
tives. There were no siblings.' u" v% _$ n2 L" [
Physical Examination
9 x' g/ O: }: f1 l. j" h5 _ N1 h" WThe physical examination revealed a very active,
% q0 r. H. v- ~$ f+ f" Splayful, and healthy boy. The vital signs documented2 }) C: t, e' j: Z
a blood pressure of 85/50 mm Hg, his length was! h9 f& ^/ b: c8 z" c
90 cm (>97th percentile), and his weight was 14.4 kg& L; g3 e `0 f- r; F& ^& O* }
(also >97th percentile). The observed yearly growth
8 h# a! G% Z4 ^+ O1 ?+ N, ^) d1 Ovelocity was 30 cm (12 inches). The examination of$ _/ C; Y3 H" \: o5 e4 h
the neck revealed no thyroid enlargement.3 F K: n/ E: o5 ]; Z, C
The genitourinary examination was remarkable for- U4 a: R3 S+ l
enlargement of the penis, with a stretched length of- [) O$ k2 D+ J3 \. h* l
8 cm and a width of 2 cm. The glans penis was very well
8 r' Q% o& l! w$ i5 [; mdeveloped. The pubic hair was Tanner II, mostly around/ l( }# z( t& Z& b) l- N6 M
540
( g, y: G3 \4 f4 _at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 Q; H0 v' L1 a( N
the base of the phallus and was dark and curled. The
% o9 f( j: L+ e3 D9 i0 gtesticular volume was prepubertal at 2 mL each.
- T* n3 O: m& I/ UThe skin was moist and smooth and somewhat* |# x; |5 s: v& s+ n4 g
oily. No axillary hair was noted. There were no
: y! t5 M9 _' E9 ~ labnormal skin pigmentations or café-au-lait spots.
0 \: e4 N! w) d8 ONeurologic evaluation showed deep tendon reflex 2+. ?- K; n% g9 `' b9 R! U- k0 o
bilateral and symmetrical. There was no suggestion" M4 B3 s6 h$ r
of papilledema.
( R7 R& }% \1 D& M& n4 YLaboratory Evaluation. J9 O! j9 q6 d# t9 {
The bone age was consistent with 28 months by, f# V1 m9 R* l, B! h) @2 u
using the standard of Greulich and Pyle at a chrono-
6 `, b! r* ^" ^! ~2 q: Zlogic age of 16 months (advanced).5 Chromosomal9 y0 O n7 K: N {9 b4 w' S
karyotype was 46XY. The thyroid function test- L% ~. z" p) ~. [! d) Q& Z
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 ~+ i7 D8 `! W% H9 R( ?lating hormone level was 1.3 µIU/mL (both normal).8 X2 ~9 \. F' x! u/ ~4 A
The concentrations of serum electrolytes, blood
+ G: ~5 \9 x+ S1 Y5 burea nitrogen, creatinine, and calcium all were+ v: _, z/ r$ k( r6 k! c
within normal range for his age. The concentration
$ ^1 Q0 _8 }- _* ` w6 |" `of serum 17-hydroxyprogesterone was 16 ng/dL7 ]+ M4 s) x$ Z8 v2 U( p
(normal, 3 to 90 ng/dL), androstenedione was 204 n1 L% U6 a& m1 ]
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-5 g; k8 V( C& A( r9 @/ b, w
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
+ ~5 `9 K* h8 x2 }. D. mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( P1 V" Z( C5 b1 P; s3 x) [ y49ng/dL), 11-desoxycortisol (specific compound S)
: g \/ L" T9 C% bwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, I( i$ e/ G/ k# I) E* S0 o
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 T, M( C# t& z- M0 jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; z' E# Y( w7 K% M8 Cand β-human chorionic gonadotropin was less than9 q% O( C- F7 _' E# b8 ^9 d! X, B6 l
5 mIU/mL (normal <5 mIU/mL). Serum follicular9 Z6 U' c4 a. ?
stimulating hormone and leuteinizing hormone
* ^2 V, P, \3 Q' S1 Zconcentrations were less than 0.05 mIU/mL
! T, K6 F% p* \* P( G7 k% ^* s(prepubertal).
8 O {. Q8 H8 J+ }3 {The parents were notified about the laboratory' P, Q2 B$ m6 y5 m' L
results and were informed that all of the tests were, Y- P8 S$ W0 g9 p+ N
normal except the testosterone level was high. The: b; ]* s4 a8 k1 z- s5 L6 w q
follow-up visit was arranged within a few weeks to% |- e! q! O/ q4 p3 g
obtain testicular and abdominal sonograms; how-* L% ]/ B' }$ }
ever, the family did not return for 4 months.8 h8 g; N- i' H6 F; }% }1 o8 n4 y
Physical examination at this time revealed that the
8 ^5 T2 d. }2 y9 A2 rchild had grown 2.5 cm in 4 months and had gained) r# d1 q" p" N$ k5 P4 c$ h
2 kg of weight. Physical examination remained
/ u4 B6 p; x7 e# j k3 runchanged. Surprisingly, the pubic hair almost com-
, L8 G F5 O# `6 M3 Dpletely disappeared except for a few vellous hairs at
* j, p& H# {, l* c, F: \2 ~the base of the phallus. Testicular volume was still 2
* @/ L7 I! X+ q" x2 F* R% MmL, and the size of the penis remained unchanged.
- l: y3 G. A0 ?4 XThe mother also said that the boy was no longer hav-3 U* H) `* I' A$ g3 H) O6 y: N, s
ing frequent erections.
% M3 L2 {8 I# L* nBoth parents were again questioned about use of0 i/ ]' b: U M n
any ointment/creams that they may have applied to
- C% H* R9 r8 t7 ?* Gthe child’s skin. This time the father admitted the
* B2 Q, a: Z7 O+ z1 dTopical Testosterone Exposure / Bhowmick et al 541
- V; N6 p$ K2 Luse of testosterone gel twice daily that he was apply-4 V' K+ i+ K5 b( e2 l
ing over his own shoulders, chest, and back area for
_4 O: L9 ^* _+ y& ` }a year. The father also revealed he was embarrassed
3 `- B/ v0 l. X, ]- F, Oto disclose that he was using a testosterone gel pre-; U1 d3 P& N" c" p' P0 T
scribed by his family physician for decreased libido
4 u( @& Y k9 |, n2 r; ?secondary to depression.! ]) G1 O; W9 k; G1 v @
The child slept in the same bed with parents.
7 C) h) t1 g7 l' @( ]% VThe father would hug the baby and hold him on his
1 s. u; q4 K3 a# L8 A/ ]chest for a considerable period of time, causing sig-
) q. ~7 ~$ L% x& Q- n+ @nificant bare skin contact between baby and father.
8 `. @' t0 f- y7 U* xThe father also admitted that after the phone call,8 [. w6 X2 w# [; J5 O% T2 X8 B& Z: R
when he learned the testosterone level in the baby# h4 ~( L9 r' ^; C- Y6 F6 H
was high, he then read the product information
; w) @0 R `+ S! Apacket and concluded that it was most likely the rea-
! y& _, z7 A$ G8 g4 w# p3 yson for the child’s virilization. At that time, they
+ a1 l& h/ l; e6 udecided to put the baby in a separate bed, and the- x; c! S: K4 x1 y u+ V
father was not hugging him with bare skin and had
\8 u8 x1 V- tbeen using protective clothing. A repeat testosterone& O: U" K0 \% p! g
test was ordered, but the family did not go to the
3 U0 F6 S; f/ d K/ Slaboratory to obtain the test.
/ f# `; {0 K: N2 C1 ?4 n* n7 G% UDiscussion
2 C$ _' A$ v+ q9 p5 IPrecocious puberty in boys is defined as secondary
; O* ]1 @4 }) Bsexual development before 9 years of age.1,4# w4 d- s( E- f. t% B7 h
Precocious puberty is termed as central (true) when
; Q3 U4 Y- i0 q7 q9 M* D: {% E4 Tit is caused by the premature activation of hypo-" z4 A% _6 P; l I: l8 [( U7 ?. Z$ [, L
thalamic pituitary gonadal axis. CPP is more com-
, e- ` ?1 ]4 M) i* c6 Amon in girls than in boys.1,3 Most boys with CPP
* \) e$ Z" V; K& h5 \$ t% jmay have a central nervous system lesion that is
- x; s3 h% k$ ~+ U7 ]8 cresponsible for the early activation of the hypothal- N4 I) w& f/ R' Q# u& ?4 ?
amic pituitary gonadal axis.1-3 Thus, greater empha-
- @' _6 a* [9 tsis has been given to neuroradiologic imaging in
% ^1 E# t* \/ Vboys with precocious puberty. In addition to viril-
# h! s; I+ {1 ]5 K2 S4 H8 l* Sization, the clinical hallmark of CPP is the symmet-
% O- E2 K6 @: |0 arical testicular growth secondary to stimulation by$ N: p" v+ b& m
gonadotropins.1,3# L. b; G' w1 M
Gonadotropin-independent peripheral preco-. }; l" y# S6 ]. a0 x! W" Z& s
cious puberty in boys also results from inappropriate9 Z+ ^8 j$ w) O" J
androgenic stimulation from either endogenous or
, C" Z7 h" E9 u& {5 l: ^) ~. Iexogenous sources, nonpituitary gonadotropin stim-
- b0 e, x8 r& e" D: a3 y7 ?# Xulation, and rare activating mutations.3 Virilizing- h6 ?# c8 Q" b2 K( K
congenital adrenal hyperplasia producing excessive0 S6 u. ^8 x" U% z7 m
adrenal androgens is a common cause of precocious* G( V9 ?% L$ B% m
puberty in boys.3,4
4 f" U, k9 W7 H/ NThe most common form of congenital adrenal
+ G& x& A0 C B' ~4 l9 s4 phyperplasia is the 21-hydroxylase enzyme deficiency.4 r6 ]5 t k+ Q+ C z% U4 s1 s
The 11-β hydroxylase deficiency may also result in8 r( I4 y! y* j9 F5 l6 i
excessive adrenal androgen production, and rarely,
# g# Y6 g, Y; I% O2 G3 Q" m0 Aan adrenal tumor may also cause adrenal androgen( h1 k+ Q% G/ p2 _5 I. i% T
excess.1,3. H% n- o7 E4 G K3 R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- V! }* B1 S! O% N; y$ R: Q! R4 K j
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
/ [: a+ C- B) o0 B% m6 r. wA unique entity of male-limited gonadotropin-
+ Y' D9 `0 F7 a7 K r+ ?independent precocious puberty, which is also known
1 x6 t5 O9 h0 X, t3 P# `as testotoxicosis, may cause precocious puberty at a
& y/ y- P& y$ C Wvery young age. The physical findings in these boys9 }9 Q+ {1 z+ e( R/ |
with this disorder are full pubertal development,
7 Q, R5 R% t8 j4 C3 n' X8 Eincluding bilateral testicular growth, similar to boys, ]! L; e" T& k4 [# K1 S0 y1 P
with CPP. The gonadotropin levels in this disorder
5 S/ V+ c2 u$ e! p: |9 _; }5 iare suppressed to prepubertal levels and do not show
1 J( `! U6 N0 N" T Wpubertal response of gonadotropin after gonadotropin-
6 W# n9 y* H' m) Xreleasing hormone stimulation. This is a sex-linked
' _, Y8 l, ^8 [, k2 P/ j7 M7 _: _' ?autosomal dominant disorder that affects only
2 t3 E, z- c, a+ Fmales; therefore, other male members of the family& m- Q3 Q) }$ L! z2 y- U/ D
may have similar precocious puberty.3
7 N+ i; h! z$ R; PIn our patient, physical examination was incon-# [2 {: z9 e, w
sistent with true precocious puberty since his testi-. v, z9 t* k0 {; b
cles were prepubertal in size. However, testotoxicosis3 B! n+ M1 L) U: L" z
was in the differential diagnosis because his father
7 Z1 X& v3 p( estarted puberty somewhat early, and occasionally,2 g% L" B @; G8 ~5 L: }
testicular enlargement is not that evident in the) o% c, F0 F) H1 |5 E
beginning of this process.1 In the absence of a neg-. S$ R1 i6 b) O: x2 r0 W
ative initial history of androgen exposure, our9 b9 _1 q. O- x6 k
biggest concern was virilizing adrenal hyperplasia,
% ~9 L+ I: ]: J; e2 T! N Peither 21-hydroxylase deficiency or 11-β hydroxylase
7 u: e5 k# N8 `3 |4 x- s' ~deficiency. Those diagnoses were excluded by find-2 d7 `! R$ \3 }6 @
ing the normal level of adrenal steroids.# }+ l0 {( v& A9 l4 j- n) Q* B
The diagnosis of exogenous androgens was strongly
) }7 O* y1 M) k' h) _+ q# V2 Fsuspected in a follow-up visit after 4 months because- k( `) ~0 ~/ q7 g- s( V
the physical examination revealed the complete disap-
9 X$ s/ m; S9 K3 L7 p8 n0 h3 {pearance of pubic hair, normal growth velocity, and
% f" Q4 _6 ~- p6 ~/ s7 ydecreased erections. The father admitted using a testos-
$ y n: }2 A# V: ^7 p Y4 h: qterone gel, which he concealed at first visit. He was
4 W! c; D I. f8 Husing it rather frequently, twice a day. The Physicians’# j" \: z, P) Q7 F) {% w! f) o
Desk Reference, or package insert of this product, gel or
4 y+ g% q( z, B" I& g* icream, cautions about dermal testosterone transfer to
4 f" n- _+ V1 ounprotected females through direct skin exposure.
# m* K' m' X7 b0 ISerum testosterone level was found to be 2 times the+ Y2 d7 |5 q: \9 u h1 H0 w
baseline value in those females who were exposed to; P2 J! A5 b/ x9 p/ D# e+ n- H
even 15 minutes of direct skin contact with their male. j+ B- P2 C% |/ m) ?
partners.6 However, when a shirt covered the applica-
% ?, \& m/ f' V! N! ^1 z9 p3 z6 f) Z' ?tion site, this testosterone transfer was prevented.$ R8 c F! L ?8 C
Our patient’s testosterone level was 60 ng/mL,
2 Z0 Z: l) H" L& {) R. S8 m H' @: @3 Mwhich was clearly high. Some studies suggest that
6 x0 ^: y0 h3 u# Vdermal conversion of testosterone to dihydrotestos-/ ^0 r3 T9 h; h0 d8 z4 u
terone, which is a more potent metabolite, is more
) f1 i' T, K. Zactive in young children exposed to testosterone
. A4 m6 Y) ]7 j' v& oexogenously7; however, we did not measure a dihy-
+ B3 u" b4 r; }* {4 N7 F! A* tdrotestosterone level in our patient. In addition to% n4 F$ f/ Z* [4 ~# w" r
virilization, exposure to exogenous testosterone in
/ v0 E$ z: e0 H0 t3 b2 b& E5 zchildren results in an increase in growth velocity and( G5 X7 r% L. U4 |' f" r! {
advanced bone age, as seen in our patient.. y6 \- c" m" Q O, n
The long-term effect of androgen exposure during
( W6 \+ o0 m5 b8 }. s; \; C) {early childhood on pubertal development and final0 t' m+ L2 t$ \( t* H3 s B" E
adult height are not fully known and always remain! F; y. O' t3 l+ }- T) e
a concern. Children treated with short-term testos-
" ]; y) }/ {2 X4 C0 A, cterone injection or topical androgen may exhibit some0 A% e5 u: w6 s# y
acceleration of the skeletal maturation; however, after
. |: {4 R! i4 U8 z0 [% ocessation of treatment, the rate of bone maturation6 B% i/ c) M" u1 o* e: e
decelerates and gradually returns to normal.8,9
8 h9 x( U1 Q& I9 ?7 M. QThere are conflicting reports and controversy8 H! _% W/ N' t0 m, @: b. Z
over the effect of early androgen exposure on adult
0 j# U9 Y1 N& u9 L( w; E, E' } Z5 Lpenile length.10,11 Some reports suggest subnormal
- r4 J% A2 r2 m( r6 ?. t# Madult penile length, apparently because of downreg-" Y7 p/ K# i% ]1 A2 ~) n% D8 e: N
ulation of androgen receptor number.10,12 However,
; w; U2 W& Q. G+ sSutherland et al13 did not find a correlation between
# z9 v; Q% h, o5 ^" I5 `childhood testosterone exposure and reduced adult/ c: y6 g; w2 H
penile length in clinical studies.
# Y4 z1 \0 n3 y0 h7 ~3 G2 `/ FNonetheless, we do not believe our patient is; a4 K( b o: c2 {
going to experience any of the untoward effects from
: w4 _9 E7 P" q' U6 B0 T2 Btestosterone exposure as mentioned earlier because
; _* u! x2 C$ e- {# J7 bthe exposure was not for a prolonged period of time.8 L8 e" ^7 a4 a2 v% H# R3 J* S
Although the bone age was advanced at the time of
+ }4 f2 }- M* {- Y' Wdiagnosis, the child had a normal growth velocity at8 R8 u+ P& ^ D' P1 b
the follow-up visit. It is hoped that his final adult
7 S9 E' V' L9 }. u' C( l- theight will not be affected.
/ I6 e/ E, G- t* W8 z; u$ PAlthough rarely reported, the widespread avail-
7 ^/ t2 }) w2 }+ d) pability of androgen products in our society may8 `" y" X7 ~, F" D6 {2 \7 @
indeed cause more virilization in male or female
& q* D1 q+ M4 g7 N! L" }children than one would realize. Exposure to andro-
! c: `1 @& D. e" H3 tgen products must be considered and specific ques-
8 H# _, l* A- ?) H4 g2 a9 Htioning about the use of a testosterone product or: c, i: X1 f( Y9 Q
gel should be asked of the family members during5 |- | Q3 N- H; `
the evaluation of any children who present with vir-7 N6 \3 r7 }' U4 e: j
ilization or peripheral precocious puberty. The diag-; c* i7 C6 J. p! D/ O. ?, ]
nosis can be established by just a few tests and by
- L7 |; M' V7 G% O: f2 bappropriate history. The inability to obtain such a
& s) j* h5 }) R! khistory, or failure to ask the specific questions, may( _$ i9 M# [# b' U
result in extensive, unnecessary, and expensive
/ x2 C, c$ x, n; @$ M) jinvestigation. The primary care physician should be
3 \; e( j; j% Y' Q4 B- Yaware of this fact, because most of these children2 M- Q2 S. v) ^6 X
may initially present in their practice. The Physicians’
" ^' t( |4 c& ?; G- t/ YDesk Reference and package insert should also put a! e, M! N4 W( W7 e$ U
warning about the virilizing effect on a male or
+ L5 i5 G& Q: x4 u3 U& J5 P' gfemale child who might come in contact with some-
# r% ? @# Z1 _8 I# Y3 Zone using any of these products.
# h& T, T, {+ S7 f5 IReferences
) r0 c" Q, s! I1. Styne DM. The testes: disorder of sexual differentiation0 P) Q* F7 U t
and puberty in the male. In: Sperling MA, ed. Pediatric7 L$ O/ W7 w* ^) [# a) v
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& B% O' E/ S0 S2002: 565-628.
6 @% |1 L" [4 _8 s" L, `: y8 `2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 c% P3 h5 z( @8 ~' Upuberty in children with tumours of the suprasellar pineal |
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