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Sexual Precocity in a 16-Month-Old
+ v8 k1 J( T& E+ mBoy Induced by Indirect Topical
' I9 a* k# M3 W* X: Q/ q! QExposure to Testosterone
% I+ f5 a3 [# y" tSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 t6 l7 _& F. P& ~$ Gand Kenneth R. Rettig, MD1
7 D/ N' j; n8 s* w \/ t: wClinical Pediatrics
3 v( f5 e5 m: Y, x( I* `4 H& E/ a5 _Volume 46 Number 6
+ O7 r. o* \% R. a9 r5 [July 2007 540-543
* D) A# }: z5 w& J© 2007 Sage Publications
' E1 W1 t' j( C% z0 \- F10.1177/0009922806296651
2 D! V+ n: M) m7 ^( M9 ^) w9 d5 b! m; Phttp://clp.sagepub.com0 n& U% N% y6 k9 _
hosted at
; X& N6 [9 j. g2 F/ jhttp://online.sagepub.com: Z1 n; j1 U; Z0 _4 I9 c: s; q5 d
Precocious puberty in boys, central or peripheral,
9 P q% e S" Y9 L6 a& Cis a significant concern for physicians. Central5 `' s2 x& }" P7 N# Y$ E" }2 }9 O( _; v' {
precocious puberty (CPP), which is mediated
" @$ Z9 z; I5 y" D6 gthrough the hypothalamic pituitary gonadal axis, has) G B; M0 _. G0 c
a higher incidence of organic central nervous system% j) G% J5 i4 _& b8 W
lesions in boys.1,2 Virilization in boys, as manifested
( s: A6 u' Q3 a% qby enlargement of the penis, development of pubic
! Z- x8 F5 o9 F X6 j) T2 Rhair, and facial acne without enlargement of testi-
* Q- |; l) f) e1 Q( w( h# m Pcles, suggests peripheral or pseudopuberty.1-3 We) U( c+ R, s5 P1 K, m2 M: a2 F
report a 16-month-old boy who presented with the
! S* y8 o) _' p8 w5 t0 ~6 T& N* X! tenlargement of the phallus and pubic hair develop-
- T' g4 Y3 b: _3 \3 W8 yment without testicular enlargement, which was due* J8 H% |. ^- L
to the unintentional exposure to androgen gel used by5 ^1 w- z3 |' C9 O
the father. The family initially concealed this infor-
( h6 }6 g% a- ?7 K+ {mation, resulting in an extensive work-up for this1 n1 X& k: b q" q! ?$ \3 a# g Q& s/ X
child. Given the widespread and easy availability of
' R" y1 U7 z1 q( R- ?7 q; [testosterone gel and cream, we believe this is proba-/ Y4 T' v8 p# k& x% F$ _ @
bly more common than the rare case report in the4 c: [' M+ G! P! W
literature.4
+ l F1 a9 e) ]: i+ A- ^$ hPatient Report
0 c1 K' e& _4 ~/ a' o/ ?A 16-month-old white child was referred to the
! b3 W! o: j0 S, a0 e1 pendocrine clinic by his pediatrician with the concern
5 Z& ]5 ~+ O4 Q; R* C% o5 X: e, A4 Pof early sexual development. His mother noticed
3 p! @# b P9 l8 \9 Tlight colored pubic hair development when he was4 q" ?+ A* t' c
From the 1Division of Pediatric Endocrinology, 2University of
5 W( O1 C" t e, J; {1 T0 j( }South Alabama Medical Center, Mobile, Alabama.4 {0 I3 F" R8 p
Address correspondence to: Samar K. Bhowmick, MD, FACE,
. G* u7 }" C- P" ?Professor of Pediatrics, University of South Alabama, College of
$ d; \ q# J8 Q7 OMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 o3 a* x2 p9 ?1 W) o2 |" y
e-mail: [email protected].7 y" Q# Y; Q! F" ]- L
about 6 to 7 months old, which progressively became
; M6 @/ q3 E3 @4 ?darker. She was also concerned about the enlarge-
& L; F7 U5 _- G6 k( |, nment of his penis and frequent erections. The child2 u! p, R( k( X
was the product of a full-term normal delivery, with
: O0 i4 ]/ r; Z6 Oa birth weight of 7 lb 14 oz, and birth length of
) T1 R3 X" K$ z# u8 a+ k+ ]2 R20 inches. He was breast-fed throughout the first year$ \, a( s* H7 p: V7 D$ J6 e
of life and was still receiving breast milk along with
: |6 D' k0 B3 m. k& n$ |' \) Ksolid food. He had no hospitalizations or surgery,
; z, a' W& j* ? iand his psychosocial and psychomotor development
" @8 ^, K8 U" i8 t1 w2 g S1 q4 pwas age appropriate.
8 y0 N- g4 Z' ?3 x6 t8 uThe family history was remarkable for the father,
4 y/ ?, |* K; j* W" m( K5 ywho was diagnosed with hypothyroidism at age 16,
# t% w2 G r$ t1 L9 @8 hwhich was treated with thyroxine. The father’s
' M% x6 C+ |, ~& I5 uheight was 6 feet, and he went through a somewhat
& m0 z) i, U8 t) S _2 y7 B" aearly puberty and had stopped growing by age 14.5 X8 q e: s. ~3 S
The father denied taking any other medication. The- M# }/ J4 S8 D
child’s mother was in good health. Her menarche
% F* [% T$ Z& W. M( ^0 gwas at 11 years of age, and her height was at 5 feet
1 o! N2 ~/ {$ Y' q8 Y, [/ _- E# u$ u5 inches. There was no other family history of pre-
1 V( i/ j9 ^; e% Zcocious sexual development in the first-degree rela-4 b5 ~! t2 Q9 y9 P, O
tives. There were no siblings.
* M+ y; B$ }( R* i' vPhysical Examination2 _# {9 |. n9 W6 f
The physical examination revealed a very active,
) Q' p- c2 g; {" d. I5 Jplayful, and healthy boy. The vital signs documented7 ]3 @- Z1 Q: ~3 Y6 F1 u
a blood pressure of 85/50 mm Hg, his length was
5 A7 r, s1 u" {+ c90 cm (>97th percentile), and his weight was 14.4 kg7 K8 d, j6 W( f2 ~3 ]" d4 b2 {
(also >97th percentile). The observed yearly growth/ {8 {) o* z2 {! o1 p& X6 {
velocity was 30 cm (12 inches). The examination of, Y7 z! s" G9 |) {% _, ^
the neck revealed no thyroid enlargement.5 K F) E$ q1 }9 c
The genitourinary examination was remarkable for$ h( Q" q3 i5 i" h. l! `
enlargement of the penis, with a stretched length of
/ a; }# U/ u& K! U# |$ u$ J8 cm and a width of 2 cm. The glans penis was very well6 f9 m: W; u* H4 b4 V% k
developed. The pubic hair was Tanner II, mostly around
( _+ f7 f- T% G6 J' ^. G3 {( z- X9 j540% H* I1 p( X1 I& Y* p, p* p8 x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 y% m0 j2 n0 H; \9 k8 _2 ethe base of the phallus and was dark and curled. The
& J' b' E2 B& ~" K2 Q" G7 q* ptesticular volume was prepubertal at 2 mL each.; R! |- a2 h% s7 J9 s8 x2 s: u J
The skin was moist and smooth and somewhat3 l ^" B& c5 b2 f1 B
oily. No axillary hair was noted. There were no# R: a, G3 A% e% H
abnormal skin pigmentations or café-au-lait spots.
" D K3 q4 f9 M2 @Neurologic evaluation showed deep tendon reflex 2+
. f" t# q) v- C9 @7 j# V- m" s6 Nbilateral and symmetrical. There was no suggestion
' o0 z2 B" t2 C/ h- P) h) Iof papilledema.
8 Y% p, G* e( t a7 fLaboratory Evaluation
) t4 `) L( \# V# A8 `The bone age was consistent with 28 months by
% m: N! ]0 A. L+ ~0 B5 lusing the standard of Greulich and Pyle at a chrono-
" N! x, e# n( T/ t7 Ologic age of 16 months (advanced).5 Chromosomal) w r: D( R, s! M4 A+ J
karyotype was 46XY. The thyroid function test8 j' X3 z- U# ]
showed a free T4 of 1.69 ng/dL, and thyroid stimu-4 O, J) D0 f% }: Z& M" n
lating hormone level was 1.3 µIU/mL (both normal).
( d" D. D( \2 R) \1 m6 ]The concentrations of serum electrolytes, blood
: z5 V% Q# |4 i1 ?6 Y6 p2 b+ I" M, L/ ?urea nitrogen, creatinine, and calcium all were
* Y) ?: w4 f' a. e! z* A8 _within normal range for his age. The concentration" Q: M& g0 Z8 k9 g
of serum 17-hydroxyprogesterone was 16 ng/dL. z( H! L# F+ o$ t; c& v: f
(normal, 3 to 90 ng/dL), androstenedione was 20$ M1 _* b" f- V: `% C
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 G/ ]7 U' S( T2 x) `
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 S* j2 i1 L' Tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 {" F' A# L: H1 W6 R49ng/dL), 11-desoxycortisol (specific compound S): j$ `7 @4 C4 B0 s$ w
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-' b9 m( q" Y9 A/ y$ ]1 v
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ Q; E, L4 q! ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 }! q. w, h2 W
and β-human chorionic gonadotropin was less than
v6 x8 Q! I$ N! ]1 t5 mIU/mL (normal <5 mIU/mL). Serum follicular) _* j1 H: I, `# @9 Q- }
stimulating hormone and leuteinizing hormone
8 B0 P; G1 ~2 e: zconcentrations were less than 0.05 mIU/mL' y! U o" C3 W G$ t
(prepubertal).
" ~8 i& d+ W4 o8 N! o9 f& J2 pThe parents were notified about the laboratory
6 J: A, _; `2 i- e; \2 Presults and were informed that all of the tests were
8 b7 S* e* }' Q0 nnormal except the testosterone level was high. The
/ |. Z; D& w9 h5 ^" _follow-up visit was arranged within a few weeks to
2 m! t3 x7 m' t% `& ^3 oobtain testicular and abdominal sonograms; how-+ R& u& L% A! W' B' C
ever, the family did not return for 4 months.2 H' R; [! D. x I# c* d/ j( i9 q
Physical examination at this time revealed that the* k$ w& @) m- p/ r9 V
child had grown 2.5 cm in 4 months and had gained
: L+ A [9 k3 ^' ]3 g2 kg of weight. Physical examination remained
p4 \: c7 [/ e1 R. C6 h5 runchanged. Surprisingly, the pubic hair almost com-
1 B( b8 Q( T$ C5 F2 ?8 X, o6 ^ Kpletely disappeared except for a few vellous hairs at9 k3 _5 o) v- s* ~# ^6 e
the base of the phallus. Testicular volume was still 2
' l. _" |! b7 z4 S5 \* [- SmL, and the size of the penis remained unchanged.
6 A2 m) j# Z9 A# BThe mother also said that the boy was no longer hav-
3 O: o' U' t# h0 `' Ying frequent erections.& P/ f& M, T- O3 R( p; b
Both parents were again questioned about use of
5 ~4 X5 @9 A& nany ointment/creams that they may have applied to
. R* W6 ]; l) nthe child’s skin. This time the father admitted the
, f: J2 z+ Q* TTopical Testosterone Exposure / Bhowmick et al 541
6 i% x+ ~5 t6 X* @ _use of testosterone gel twice daily that he was apply-* j. P0 P6 f. }5 U
ing over his own shoulders, chest, and back area for
+ P; k- `* z4 z7 ca year. The father also revealed he was embarrassed1 J' C5 c3 m& X' a. d
to disclose that he was using a testosterone gel pre-7 s$ p. k! b5 g! @: |
scribed by his family physician for decreased libido
; K" d$ |4 x* t3 C6 ^3 k' P+ fsecondary to depression.
; a- j5 P7 w8 m. y% b/ ^The child slept in the same bed with parents.$ @( Q f. J1 Y5 M$ `9 ^5 N- @& e
The father would hug the baby and hold him on his
! W' g: E/ i! R/ l4 n; hchest for a considerable period of time, causing sig-6 k1 e6 m( i9 s2 ^5 N0 `" ]+ F
nificant bare skin contact between baby and father.5 c0 n6 b% A% U& _
The father also admitted that after the phone call,; W4 V% m+ |5 l! g
when he learned the testosterone level in the baby
1 S8 B# A) j1 u: V0 j( Rwas high, he then read the product information0 F6 w. ~9 }( D( [5 H, Z) p! R
packet and concluded that it was most likely the rea-2 ^9 {3 O8 [8 m8 H$ h X
son for the child’s virilization. At that time, they
" ^6 z: X4 G7 U- D" d5 zdecided to put the baby in a separate bed, and the5 o! O. Q; m# i
father was not hugging him with bare skin and had2 C) f* }% g5 k2 ]7 O6 K' l( h
been using protective clothing. A repeat testosterone+ z8 N" _1 Z. C( M' A3 ]; X
test was ordered, but the family did not go to the; O# L8 l) w5 X9 U* ]2 [
laboratory to obtain the test.
. A: f: p* @3 L, }" X0 GDiscussion
" A- k# v2 e3 M8 V: R; [Precocious puberty in boys is defined as secondary
- g4 y; i. Z3 ~sexual development before 9 years of age.1,48 H ^- W/ s1 t8 Z i* g
Precocious puberty is termed as central (true) when0 D: e9 ?# c6 `7 k v5 M
it is caused by the premature activation of hypo-& Y& U% t# U9 T" |3 k
thalamic pituitary gonadal axis. CPP is more com-
% T% X, A3 g: r+ G0 b* G `- Zmon in girls than in boys.1,3 Most boys with CPP
6 K, j' L7 K, Emay have a central nervous system lesion that is
9 e& |! R/ W! D1 Lresponsible for the early activation of the hypothal-
2 K$ ^1 W+ r. `) a9 h7 [, oamic pituitary gonadal axis.1-3 Thus, greater empha-$ B" V0 A# `6 O" C$ C
sis has been given to neuroradiologic imaging in
6 t/ C* F5 }2 Y# wboys with precocious puberty. In addition to viril-! o' S3 T0 \4 L: y3 x3 |) |/ H
ization, the clinical hallmark of CPP is the symmet-. L% Y; H, @6 D
rical testicular growth secondary to stimulation by6 j; V3 u: g, U& V6 {5 @. |/ G
gonadotropins.1,3
8 o3 b# ` {+ Z# d6 @" uGonadotropin-independent peripheral preco- V( F1 D# j4 }% |
cious puberty in boys also results from inappropriate3 o3 G" H4 ~5 @5 V( h' P
androgenic stimulation from either endogenous or
2 K' H% ?2 A3 Q2 S( \exogenous sources, nonpituitary gonadotropin stim- S+ `6 k' u) S- P2 n* P- u
ulation, and rare activating mutations.3 Virilizing
: _# A \$ w! @" w+ I5 l9 x, qcongenital adrenal hyperplasia producing excessive
- z( t5 b8 k7 h8 Cadrenal androgens is a common cause of precocious4 J5 e" @0 _+ [& ]9 S
puberty in boys.3,49 R; a& C \) i: s
The most common form of congenital adrenal, N+ f3 f# w/ A; R2 j5 N
hyperplasia is the 21-hydroxylase enzyme deficiency.
3 _; O( a2 A9 J& i7 S+ r' ZThe 11-β hydroxylase deficiency may also result in
$ A- F5 I3 w5 B0 o% T6 T. Texcessive adrenal androgen production, and rarely,
" P' ]0 X/ i, Dan adrenal tumor may also cause adrenal androgen/ N z. T+ ]- Z9 Z O" m
excess.1,38 h! k/ D" v2 r7 D; r3 E
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& g9 z/ X6 \+ ~% |) N5 F6 i
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
) c' L7 b: N3 W/ M0 X# yA unique entity of male-limited gonadotropin-! |. k$ Q1 r& c3 U% g8 _1 Z* ]$ s
independent precocious puberty, which is also known" f$ n7 O- G, H
as testotoxicosis, may cause precocious puberty at a
) O ?. N+ s* c8 B# h1 X1 cvery young age. The physical findings in these boys1 s5 ~2 H1 k7 [' G- E
with this disorder are full pubertal development,3 d, B8 g+ N2 B. o# j! P0 V# y
including bilateral testicular growth, similar to boys
g0 R/ ?/ E$ Owith CPP. The gonadotropin levels in this disorder& k, s1 k/ G% ]2 ?) K; R
are suppressed to prepubertal levels and do not show
7 p8 Y/ b4 {: s# ppubertal response of gonadotropin after gonadotropin-
! h5 _( y0 P' c* O) Hreleasing hormone stimulation. This is a sex-linked
T6 r% p2 Q7 ~# {autosomal dominant disorder that affects only
/ a3 @: C( ^4 E) \males; therefore, other male members of the family" [( d1 B0 d* ]* G
may have similar precocious puberty.3: ?7 c, T6 Q$ A6 W6 j) E( g8 W) Z
In our patient, physical examination was incon-
R. j+ n! \/ i% R( Ssistent with true precocious puberty since his testi-
. w6 Z$ b% Y9 H, T; U4 f* Gcles were prepubertal in size. However, testotoxicosis
# h* ^% J$ `+ [/ L7 U( qwas in the differential diagnosis because his father
' u( W8 k; s+ ?: c6 y1 Nstarted puberty somewhat early, and occasionally,
7 ?& e6 o) U& S$ }/ _. ?& [testicular enlargement is not that evident in the
9 Y S* G7 [8 t1 k2 C% {& f, R8 O) xbeginning of this process.1 In the absence of a neg-
! ]$ L8 K7 _+ {$ i4 Q) l- Rative initial history of androgen exposure, our
7 K/ J8 X( M) h9 A2 c5 Z9 Obiggest concern was virilizing adrenal hyperplasia,1 ? T: ?' p, z
either 21-hydroxylase deficiency or 11-β hydroxylase$ }1 r) O; e7 S9 ]
deficiency. Those diagnoses were excluded by find-* @: U, u) R& e! k4 S
ing the normal level of adrenal steroids.4 d9 e: J& @( S" c& T
The diagnosis of exogenous androgens was strongly# z$ G+ V' R4 S6 i# ^. ]! W! K
suspected in a follow-up visit after 4 months because: d* q1 B9 X) n b4 o2 c1 ^* J6 r# m
the physical examination revealed the complete disap-1 ~0 M, j% e% j4 Z* ~, w
pearance of pubic hair, normal growth velocity, and
6 }& |. R; e" {$ Ddecreased erections. The father admitted using a testos-) ~% T* Y( l" P# u3 \$ F1 _6 H
terone gel, which he concealed at first visit. He was
0 x# p" O m7 f& a8 {* ^% b9 cusing it rather frequently, twice a day. The Physicians’
! O, B0 Q0 b6 r/ RDesk Reference, or package insert of this product, gel or
, F R# U N9 q2 s4 Kcream, cautions about dermal testosterone transfer to
1 P$ F+ M: j X) u- Y+ I5 C( Funprotected females through direct skin exposure., s9 E( k; W y( I7 x) C2 V1 K
Serum testosterone level was found to be 2 times the
* D3 {8 ]$ R! f8 `, Cbaseline value in those females who were exposed to, ]2 D' n/ K6 Z) t4 `3 _( A
even 15 minutes of direct skin contact with their male
2 G1 `. W; S$ C5 Y6 ?& kpartners.6 However, when a shirt covered the applica-' W3 F; r, s3 B
tion site, this testosterone transfer was prevented.. {( c: ^* Z3 r( Q' r2 T! L: ]! p
Our patient’s testosterone level was 60 ng/mL,$ Y! W2 @% B* b# C
which was clearly high. Some studies suggest that7 o( S7 |: A Z/ w" T' s1 w! I
dermal conversion of testosterone to dihydrotestos-2 P3 o! e: X* ~6 ^- u% n) k
terone, which is a more potent metabolite, is more
7 O1 b- E1 e) h/ ]active in young children exposed to testosterone4 O! A4 e: Y( }+ ~0 ]* a
exogenously7; however, we did not measure a dihy-7 E6 c: Y, n" [/ z# l1 y# r
drotestosterone level in our patient. In addition to6 L# }' Q [3 T8 S. j
virilization, exposure to exogenous testosterone in
9 c6 B- F U. k8 F; e; H5 tchildren results in an increase in growth velocity and
4 ^) g9 w, M ?& O; v, m; F2 ~advanced bone age, as seen in our patient.7 [: M6 ?; z2 u" m3 Q
The long-term effect of androgen exposure during
0 |5 i9 C6 D& Gearly childhood on pubertal development and final# }/ b+ l- Q* E4 n( ~0 a
adult height are not fully known and always remain0 P# ^1 x9 `4 Z$ u" [& W5 {
a concern. Children treated with short-term testos-
# f9 w! q0 c- b% T1 `terone injection or topical androgen may exhibit some
$ m" F, ~1 W/ q: e$ m/ [* _. ]6 eacceleration of the skeletal maturation; however, after
& ~! }: W( z# R) e X" f0 Mcessation of treatment, the rate of bone maturation
' W0 K+ D4 n! z2 `$ Rdecelerates and gradually returns to normal.8,9
2 M8 D+ E# ~7 O6 [- uThere are conflicting reports and controversy3 |+ Q. h3 W, O* z+ C/ k
over the effect of early androgen exposure on adult) J8 U1 x+ ?) o6 ~# ^# t( ^- j& h% j
penile length.10,11 Some reports suggest subnormal
' A8 D0 |) F( \4 n9 }9 y7 [2 l7 ladult penile length, apparently because of downreg-1 K8 |+ e7 @$ |
ulation of androgen receptor number.10,12 However,
`8 s7 K0 g: A! mSutherland et al13 did not find a correlation between, F, t' _, E# O& F' o7 ^2 y! ^; y
childhood testosterone exposure and reduced adult
- [, n4 Q! U, X' z3 z, q- I; _penile length in clinical studies.
1 V8 A/ p2 [: ^- l3 _# \# `& PNonetheless, we do not believe our patient is
0 a0 |1 O- n+ @' egoing to experience any of the untoward effects from4 K7 X0 z, F8 ~; w
testosterone exposure as mentioned earlier because
8 }6 N; k% m0 F/ nthe exposure was not for a prolonged period of time.% F- d8 b F3 i( x0 e
Although the bone age was advanced at the time of
% k. J6 J! z6 m$ K) O$ |/ Ldiagnosis, the child had a normal growth velocity at8 z% ?' m3 q; p
the follow-up visit. It is hoped that his final adult j( g1 o5 A9 O7 O# i9 X! b/ v# e
height will not be affected.! G+ }1 v# s6 [" Z2 M# P
Although rarely reported, the widespread avail-5 v- K$ W I4 W- K* Q
ability of androgen products in our society may- H. o( j$ [* d% c! G4 [* y. ]3 m( Z3 `
indeed cause more virilization in male or female
* ^: p- Q9 e C1 [children than one would realize. Exposure to andro-0 ]$ l5 ]) ~# u( A2 U! Y
gen products must be considered and specific ques-
: ?8 F3 j4 u8 q( m* ~tioning about the use of a testosterone product or5 D; j2 W( A1 Z, L2 Y6 e1 R1 E
gel should be asked of the family members during1 l8 |) N$ h, |7 ~
the evaluation of any children who present with vir-
: a5 S# p8 R/ S0 h+ k- c! E5 ailization or peripheral precocious puberty. The diag-
2 j( V# K' G6 n- q. V; Qnosis can be established by just a few tests and by8 i4 [& H5 z; |: X) g. s/ @" [
appropriate history. The inability to obtain such a+ |% L. s! e6 y4 U! N9 m" v
history, or failure to ask the specific questions, may0 Y# r; F5 C6 @& w0 w: X
result in extensive, unnecessary, and expensive
- x ^' s* z' {investigation. The primary care physician should be
0 Q( u1 i3 S8 e2 k6 Caware of this fact, because most of these children8 `/ c. g( F6 j& J
may initially present in their practice. The Physicians’
' P5 S% s% ^; }Desk Reference and package insert should also put a+ D7 y8 J7 m5 [. K& S5 j+ Y
warning about the virilizing effect on a male or4 R- ^& m) q' ~2 Z
female child who might come in contact with some-
# w Y, O8 w; @9 c4 L+ eone using any of these products.; Y: ^1 T+ P4 j5 z9 T
References2 p) {/ i4 g8 l4 o5 \4 Z
1. Styne DM. The testes: disorder of sexual differentiation
p6 D4 l3 U4 aand puberty in the male. In: Sperling MA, ed. Pediatric
- ~* T) n+ z5 \8 eEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" X) }' U6 R, s8 G2002: 565-628.) M$ O" h* y' X
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 ]: s: V L* P9 r* [& }9 Fpuberty in children with tumours of the suprasellar pineal |
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