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Sexual Precocity in a 16-Month-Old
9 u8 s; M, _; i) J# ~7 l6 jBoy Induced by Indirect Topical! _- ]2 R8 e N& ?8 b7 W
Exposure to Testosterone7 y0 X8 V# p" I( R% ^4 I- z7 f
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2+ @8 P: J. z+ i9 w
and Kenneth R. Rettig, MD1
; A) R0 _& z: I" E3 Z* i2 vClinical Pediatrics/ G3 G/ a0 l* {7 Y
Volume 46 Number 61 q- }: I( D3 m
July 2007 540-543; K( x0 p: J/ X N
© 2007 Sage Publications
( J" o. T! t7 `2 S! e: L7 S10.1177/0009922806296651
% Y& Q! \+ d2 i+ l* h5 g$ h3 Yhttp://clp.sagepub.com& |2 ?, y& V1 ?6 X
hosted at0 q; Y: e2 D5 X; r
http://online.sagepub.com5 S, y- R, C0 ?) y5 z4 e* W
Precocious puberty in boys, central or peripheral,; r, b+ q/ x( h1 V; Y- ~
is a significant concern for physicians. Central
/ s* E& X! `4 Z" j" L' {precocious puberty (CPP), which is mediated
4 `+ j/ l+ }* ~1 l9 `* ?" p3 A4 cthrough the hypothalamic pituitary gonadal axis, has1 X, c3 W9 \. z" Y. ]% M7 u" T5 U0 H+ O
a higher incidence of organic central nervous system
" z* ?3 b# B" K$ U( N/ qlesions in boys.1,2 Virilization in boys, as manifested3 B7 n5 @' m* A8 @ u# L: e5 V& ~
by enlargement of the penis, development of pubic
/ I7 A4 c0 E1 U. [# `) e& E' Z+ fhair, and facial acne without enlargement of testi-7 A* D# @+ x" \. o; n
cles, suggests peripheral or pseudopuberty.1-3 We
, l7 c- a9 `) T: |6 L7 W$ o/ }report a 16-month-old boy who presented with the
8 Q( D- h$ i3 k9 ]8 v0 `5 |4 menlargement of the phallus and pubic hair develop-
6 @6 W0 z" V. g/ h6 oment without testicular enlargement, which was due
/ {& o$ I% l0 X# Z3 @to the unintentional exposure to androgen gel used by' e9 E6 s$ ^1 Y. y( `! ?
the father. The family initially concealed this infor-
! w* [" ^* L7 d- ]$ o% }% o" Gmation, resulting in an extensive work-up for this
# O2 W0 l; ?+ }+ F+ C. xchild. Given the widespread and easy availability of6 ^; V% e0 s5 z/ v
testosterone gel and cream, we believe this is proba-; |! F: A X# S
bly more common than the rare case report in the
9 E' ?. f) _- R3 J# q# tliterature.4( j: K+ M9 A& w, B
Patient Report
% p% \3 J% N- ~A 16-month-old white child was referred to the
; X! A1 W0 R; d, |$ [9 Oendocrine clinic by his pediatrician with the concern
( k! `' y8 F! g$ @& eof early sexual development. His mother noticed8 \* `. |5 k9 l& W. H* U$ T
light colored pubic hair development when he was
# c0 M: k: P* FFrom the 1Division of Pediatric Endocrinology, 2University of; @& ?+ q7 R; w5 a. L. t
South Alabama Medical Center, Mobile, Alabama.3 ^- m+ j9 c1 Z$ F$ v3 A- Y
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* o$ ~8 [$ P: _7 MProfessor of Pediatrics, University of South Alabama, College of
u5 ~% G- o7 e; m7 K+ {4 J+ gMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;& E+ K/ s; w6 [$ Y; {* W
e-mail: [email protected].
! o. q9 M* u) babout 6 to 7 months old, which progressively became+ L$ R/ I( P" Q' \4 E c
darker. She was also concerned about the enlarge-
2 @, D- y5 P: w+ Oment of his penis and frequent erections. The child
* N7 j9 j- y6 R! V& {% C2 iwas the product of a full-term normal delivery, with# R" |3 D% L% x5 b
a birth weight of 7 lb 14 oz, and birth length of) A0 x7 }# k( G- @! H
20 inches. He was breast-fed throughout the first year' B: H$ y# s- R
of life and was still receiving breast milk along with. F5 J( Z$ s& m8 L
solid food. He had no hospitalizations or surgery,
: w+ b. h( r" I0 O& O" A, mand his psychosocial and psychomotor development/ R# y6 ]4 A% D: N: w) F6 O8 Y
was age appropriate." d# Z4 m' r) x; z0 U. ~
The family history was remarkable for the father,
- | {: f+ l% _7 Q X1 C6 R) jwho was diagnosed with hypothyroidism at age 16,
* c N$ |2 y4 O h) J! owhich was treated with thyroxine. The father’s
' V1 y$ s' r) N( qheight was 6 feet, and he went through a somewhat/ D# h Z4 e6 W
early puberty and had stopped growing by age 14.
2 L0 J7 S% o @& I& ], ?0 z( yThe father denied taking any other medication. The
- p# b1 ^0 @ w4 r! Q/ D* N3 `$ cchild’s mother was in good health. Her menarche
. K- p9 Y2 J; y, _+ R& p) Bwas at 11 years of age, and her height was at 5 feet
]& s( v ^- z f7 V5 inches. There was no other family history of pre-
& d! q+ u4 z( S( lcocious sexual development in the first-degree rela-! V8 D2 r- e! }- n. j6 }1 f
tives. There were no siblings.
- x* ^, a) T* W8 H+ T0 p. E- w) G5 ]0 _Physical Examination
! y9 f8 m0 {: Z- \8 }The physical examination revealed a very active,
0 x) Q: b& Z$ B) b% f. \playful, and healthy boy. The vital signs documented
/ Y, d$ ?3 }% K) @ Pa blood pressure of 85/50 mm Hg, his length was
* x7 b& w3 m1 }90 cm (>97th percentile), and his weight was 14.4 kg8 f4 M8 D! |8 _" H
(also >97th percentile). The observed yearly growth0 P8 E |* i C7 ^0 P5 r
velocity was 30 cm (12 inches). The examination of$ Z3 ]5 J, Z1 H
the neck revealed no thyroid enlargement.
. R9 Z) m) s$ m! ^5 A9 wThe genitourinary examination was remarkable for
3 h" U, S7 S" D5 e C2 M7 @& }: benlargement of the penis, with a stretched length of
$ v" m, f4 ? _1 U4 t% ]8 cm and a width of 2 cm. The glans penis was very well+ G! Y4 H- }* z a! A. A
developed. The pubic hair was Tanner II, mostly around
! v9 f4 W5 l, @6 J2 N( ~$ c540
) y U; ~+ ]$ wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, O3 _% z- m8 D6 ~: g6 B6 t
the base of the phallus and was dark and curled. The
; t/ n* o" n+ C& `5 Ttesticular volume was prepubertal at 2 mL each.
1 n9 L) `6 d% `6 M4 H/ `The skin was moist and smooth and somewhat
5 w+ |5 {( o( v" v0 foily. No axillary hair was noted. There were no
7 g7 i# s' z) y- ^abnormal skin pigmentations or café-au-lait spots.( X! H8 w& G5 ?( F& N
Neurologic evaluation showed deep tendon reflex 2+) D( c& T6 K+ j" S/ z6 ?
bilateral and symmetrical. There was no suggestion0 ~, p/ z9 V! d: K8 T, M
of papilledema.
m0 ?- a. o* j, G5 J+ RLaboratory Evaluation, P0 p2 Q1 N9 n, c
The bone age was consistent with 28 months by
9 B. b. D3 C: X: e8 v) C2 ousing the standard of Greulich and Pyle at a chrono-3 `' M8 q/ n6 b( V
logic age of 16 months (advanced).5 Chromosomal( m9 Z; U+ a: j( F4 y( C
karyotype was 46XY. The thyroid function test
$ ?- h3 ~1 {6 O$ w2 |1 Dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
- j/ M/ o2 o% I$ P) K, H% |! q: _lating hormone level was 1.3 µIU/mL (both normal).1 h) P- Y, D! H9 x+ t5 ?
The concentrations of serum electrolytes, blood
% i' m4 Y* R: nurea nitrogen, creatinine, and calcium all were
, `7 |( [; V6 r3 lwithin normal range for his age. The concentration- i; i% q! C* t0 Z- J( }
of serum 17-hydroxyprogesterone was 16 ng/dL6 `: V8 h" @8 q3 m7 k3 s* b
(normal, 3 to 90 ng/dL), androstenedione was 20
" Q% G" Y# m0 K8 H; J7 D8 A vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* p% b A$ \( [% s( Z) t& O
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 j# J* J h- O# Mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
& j8 W! Z3 \( f+ w5 j& U49ng/dL), 11-desoxycortisol (specific compound S)( u# @9 t0 {8 N; B* m8 o& ~
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
0 r: z" r3 c: \8 Ytisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
6 P8 P7 V* a: b- etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),: T# ]6 [# f9 K9 w2 T9 x& L
and β-human chorionic gonadotropin was less than
8 }( ~ A0 P% U/ ~6 D: e. @5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 i# Q2 [$ \+ {' S0 D( Dstimulating hormone and leuteinizing hormone
' V, s6 s8 [: }concentrations were less than 0.05 mIU/mL$ B7 Q$ p+ r# }& |$ @( {7 N/ I2 q
(prepubertal).0 M9 u) [, |- _9 x& R6 l: _5 k" ]
The parents were notified about the laboratory
3 W8 G" F$ p3 K/ k6 F% Eresults and were informed that all of the tests were7 t; N6 o+ G, ?" `1 ? ?3 Y
normal except the testosterone level was high. The. Q6 w" V. F" B% Q1 {3 R
follow-up visit was arranged within a few weeks to4 ]* x7 C( P3 ^% N. I# f+ N
obtain testicular and abdominal sonograms; how-; K# ?- h) N4 _+ }% `7 g7 L
ever, the family did not return for 4 months.
& y0 c# z3 \4 f, HPhysical examination at this time revealed that the
$ X$ G: Y7 ]; l/ Q& Ichild had grown 2.5 cm in 4 months and had gained
- y3 j( I, _8 x& ?! N2 kg of weight. Physical examination remained
& [0 D' T9 Q6 O) F, S% w B8 runchanged. Surprisingly, the pubic hair almost com-
. V* @& c3 f' j# f) I8 t0 F$ Zpletely disappeared except for a few vellous hairs at
# z0 A5 t8 v3 R- M' Q+ f4 t) Ethe base of the phallus. Testicular volume was still 2, e( Z: T6 G8 ?; \ M0 s
mL, and the size of the penis remained unchanged.4 ^6 Z' O/ X3 V' I! ?* y
The mother also said that the boy was no longer hav-$ N6 q$ W0 e3 `4 p& r
ing frequent erections.0 U9 R) }1 A8 _
Both parents were again questioned about use of
0 A. f3 Y0 g8 H# V+ m1 Aany ointment/creams that they may have applied to# o7 |! `- _; ?
the child’s skin. This time the father admitted the$ s1 Z$ C& }: I
Topical Testosterone Exposure / Bhowmick et al 541
5 s; x) L+ x3 Z& Q5 A$ {use of testosterone gel twice daily that he was apply-3 ^ a6 B/ C2 p. L
ing over his own shoulders, chest, and back area for
8 g5 s5 @% l6 F+ \a year. The father also revealed he was embarrassed# L0 \' ]7 V( |2 N; `- p
to disclose that he was using a testosterone gel pre-
% x7 ]! v/ G6 yscribed by his family physician for decreased libido
& [- {6 L/ r! W0 A' n, M7 {secondary to depression.
9 l/ t7 {, r) g) {4 B8 Z( O8 DThe child slept in the same bed with parents.7 r0 E* @- h) D. M
The father would hug the baby and hold him on his n0 A& ?* Q) w$ ~8 I" i* J! t
chest for a considerable period of time, causing sig-
% V o$ f9 R4 \& O7 h) Enificant bare skin contact between baby and father.
7 q/ r5 ~* n- E* EThe father also admitted that after the phone call,
f; d( W: ]: p" E- j5 _when he learned the testosterone level in the baby
6 x7 V3 O, a" u9 I. X4 b: X8 Fwas high, he then read the product information
4 O$ u: e) m9 [% C1 @4 I- ?, Gpacket and concluded that it was most likely the rea-& J x9 A9 w* a
son for the child’s virilization. At that time, they# n$ |5 ^3 [* v$ C( ^- y
decided to put the baby in a separate bed, and the- ?" u! R# e# ^( A' t# m0 y2 b* v
father was not hugging him with bare skin and had3 U+ k9 z4 I; m6 S0 @
been using protective clothing. A repeat testosterone
7 q- k9 a! P' A! E2 G0 C5 c! vtest was ordered, but the family did not go to the3 s) M1 S# k1 s$ Z- t
laboratory to obtain the test.
. B8 v; n4 }7 d( a# RDiscussion
% \+ m# \0 b3 W; N) X7 F) DPrecocious puberty in boys is defined as secondary& m4 D; J4 O' h* c* A3 C; j& i( Z* W
sexual development before 9 years of age.1,43 ]1 s' g% H0 A! L8 ]& q) N
Precocious puberty is termed as central (true) when ^2 U9 d! ~& q1 H1 J
it is caused by the premature activation of hypo-- d" P* ^. o( F3 z
thalamic pituitary gonadal axis. CPP is more com-
2 k$ \; F0 k4 h# v4 Hmon in girls than in boys.1,3 Most boys with CPP
( \. q/ O/ q1 M0 b& Hmay have a central nervous system lesion that is
/ U: Z( c- Q7 ^% ^$ h4 f2 Eresponsible for the early activation of the hypothal-
0 V( E V7 W4 [: s' gamic pituitary gonadal axis.1-3 Thus, greater empha-
7 x" |2 d4 g. `- Tsis has been given to neuroradiologic imaging in
2 S2 d" P0 ^; F' ]0 r2 Iboys with precocious puberty. In addition to viril-
/ g7 \ G* {5 L4 {ization, the clinical hallmark of CPP is the symmet-
7 T2 `! S9 D4 J" Prical testicular growth secondary to stimulation by
& w9 U. }3 s+ E# k/ \8 wgonadotropins.1,3( p9 V8 F6 j$ O# E% P$ L y
Gonadotropin-independent peripheral preco-
4 W2 i4 d/ R( c. m, _1 z9 D; ]cious puberty in boys also results from inappropriate
8 t- I. W, n1 ^$ b0 ^1 iandrogenic stimulation from either endogenous or; ]0 A: n0 a5 s2 `7 Y
exogenous sources, nonpituitary gonadotropin stim-
/ v& O& Y( D# ^5 p+ z6 julation, and rare activating mutations.3 Virilizing
1 ]# l/ o8 U# y+ fcongenital adrenal hyperplasia producing excessive
, J/ q/ U1 r0 o0 |adrenal androgens is a common cause of precocious# r& m1 s' s2 ^ M
puberty in boys.3,40 z# G) ], M; [+ m. m" O6 \/ |- L: J
The most common form of congenital adrenal0 G. P' }& ~2 _" A# e% ?
hyperplasia is the 21-hydroxylase enzyme deficiency.
4 z; z' S9 ]! F4 @! ^% I% c6 FThe 11-β hydroxylase deficiency may also result in
g( s) ~& s! @- nexcessive adrenal androgen production, and rarely,
( C0 N) c1 |# Z; B) S" a# han adrenal tumor may also cause adrenal androgen5 M2 M2 w' L/ E; R& d' ^1 n; }
excess.1,3+ o# l( j+ U" `! Q5 i( A3 o. s C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* W# J. b ^) C/ ~ O1 u542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% c2 H& R& n+ \4 d% h/ U- dA unique entity of male-limited gonadotropin-
5 Y; ~, X) p! E8 a2 |independent precocious puberty, which is also known
9 R, ]+ i9 s( {8 V: Sas testotoxicosis, may cause precocious puberty at a: _! M$ O- n( X( }$ m$ `0 j/ s
very young age. The physical findings in these boys
/ [ t2 ]3 _; q5 @7 ^with this disorder are full pubertal development,
( Q; S. |4 B! qincluding bilateral testicular growth, similar to boys. T) T* A( w. a9 ^% f1 k6 C* c
with CPP. The gonadotropin levels in this disorder; |8 \5 `: m7 Q, K0 [1 Q
are suppressed to prepubertal levels and do not show
& m" t7 i3 F; V+ w* o- tpubertal response of gonadotropin after gonadotropin-) \$ m$ f7 \( f# l
releasing hormone stimulation. This is a sex-linked0 W. r' t/ U" L: a* o1 D! W
autosomal dominant disorder that affects only/ V: x2 p) G/ _% d' W, L: g
males; therefore, other male members of the family
$ l. V8 a7 O7 t% T: U' Vmay have similar precocious puberty.3
1 \0 I6 c9 v: E. J- M: N1 ?In our patient, physical examination was incon-
6 H5 }. p/ i" t, }( c/ u6 Lsistent with true precocious puberty since his testi-9 | `9 f ~) R `7 O$ _
cles were prepubertal in size. However, testotoxicosis
6 d/ b( q- _' G/ [3 Bwas in the differential diagnosis because his father
: [7 F4 v8 W8 N/ @! ~started puberty somewhat early, and occasionally,
; N1 f" A- X2 e. C/ |) w0 t2 Htesticular enlargement is not that evident in the. J6 f0 I: A) t8 `
beginning of this process.1 In the absence of a neg-
% k& F" D, W, Y( @1 m" Xative initial history of androgen exposure, our
. I. l5 ~& Q5 b" \biggest concern was virilizing adrenal hyperplasia,
" w/ r+ P: N) A) `1 meither 21-hydroxylase deficiency or 11-β hydroxylase
0 G6 y6 S. h+ ?( U. }3 `deficiency. Those diagnoses were excluded by find-
' x( ]/ H6 t% ?/ ming the normal level of adrenal steroids., j8 w6 m' Q2 {" o' R
The diagnosis of exogenous androgens was strongly
: q, y& O2 c& ^suspected in a follow-up visit after 4 months because
) M/ f b- ]6 Lthe physical examination revealed the complete disap-
; @1 ^7 T" F9 z$ mpearance of pubic hair, normal growth velocity, and: L4 l, e Z8 e) Y/ P9 \8 a
decreased erections. The father admitted using a testos-7 i0 x# l/ x: S; u# {
terone gel, which he concealed at first visit. He was
! [ _- z+ B! {8 Gusing it rather frequently, twice a day. The Physicians’ R z$ Y g1 F3 ^
Desk Reference, or package insert of this product, gel or
J5 y, y* a3 Z9 f5 Mcream, cautions about dermal testosterone transfer to$ ]" s; T7 C, I5 T4 P4 r
unprotected females through direct skin exposure.
7 v, e$ T* M# C: p/ jSerum testosterone level was found to be 2 times the
5 c) q( {5 f$ z, U' Dbaseline value in those females who were exposed to6 B8 G) E' ^3 l. a
even 15 minutes of direct skin contact with their male
3 G6 a4 ^& { V7 [; X# ^7 K' qpartners.6 However, when a shirt covered the applica-
0 r @! p* A. O0 B0 N. Ktion site, this testosterone transfer was prevented.
1 N# f" `. g# c. }( H7 n$ q# }Our patient’s testosterone level was 60 ng/mL,- M4 \% K, ~6 ~' S& R
which was clearly high. Some studies suggest that
6 ~/ H1 I- C6 h. V' Gdermal conversion of testosterone to dihydrotestos-! |# I' b; `* a
terone, which is a more potent metabolite, is more; L! L% H+ O0 D( d4 L/ {
active in young children exposed to testosterone
* O/ ]7 s9 M& U% w: Y3 X& N0 U' T3 Gexogenously7; however, we did not measure a dihy-' m' v, ^( @( C
drotestosterone level in our patient. In addition to0 T0 y7 ~: H- B1 {, V
virilization, exposure to exogenous testosterone in+ k8 f9 C3 c' ?6 d( z: a B. A
children results in an increase in growth velocity and/ d& _5 d4 `+ |2 e
advanced bone age, as seen in our patient.
" Y: |5 e+ n |The long-term effect of androgen exposure during
7 X- U, G2 `- \8 m/ a8 Eearly childhood on pubertal development and final2 t) l, F& c6 j4 V4 }$ v
adult height are not fully known and always remain
$ C# }; S8 L) v8 v4 m' Ma concern. Children treated with short-term testos-
) `# j' R) b: H7 kterone injection or topical androgen may exhibit some
* {0 ^' y# j5 i. v* Dacceleration of the skeletal maturation; however, after
3 _3 N" ^- D6 Z8 ^3 b; |- Lcessation of treatment, the rate of bone maturation; U( n2 c0 E5 {* ?( @
decelerates and gradually returns to normal.8,9
; g9 C0 T g7 X- S/ ~There are conflicting reports and controversy, C* \1 x+ v Q- _7 f# O8 I3 _
over the effect of early androgen exposure on adult, y. r8 X) \, P$ A7 s/ ?
penile length.10,11 Some reports suggest subnormal
% H1 c& M3 `7 F+ C- N, ]6 jadult penile length, apparently because of downreg-
/ ?# r" R9 A4 G9 h4 \9 gulation of androgen receptor number.10,12 However," U1 h9 M* E* H
Sutherland et al13 did not find a correlation between
4 ~4 }8 A( c6 M* M) m- }& fchildhood testosterone exposure and reduced adult) O5 [! o# a3 N, }# J w$ S- L
penile length in clinical studies.
: a: q- e" [ d1 E. n7 a* |$ T6 I5 U" |; LNonetheless, we do not believe our patient is
8 H3 V2 l. {2 L( Zgoing to experience any of the untoward effects from8 [' d% Z5 Y6 }
testosterone exposure as mentioned earlier because
, h5 e6 U F9 o5 e" Tthe exposure was not for a prolonged period of time.+ S9 h' k: m1 p( O3 r3 e
Although the bone age was advanced at the time of
# |- U, y+ @3 V4 h4 X9 udiagnosis, the child had a normal growth velocity at
6 ~1 R A+ {, U p- o# lthe follow-up visit. It is hoped that his final adult
" K1 g0 `; O U) G6 l: u" ^2 T. Q8 jheight will not be affected.
9 B$ q+ d$ {& q1 K( Y! Q' j$ GAlthough rarely reported, the widespread avail- x& b" [: X7 |, ?8 I' C' s. h4 K
ability of androgen products in our society may
+ m! [1 @, {2 v7 v! S0 V' Nindeed cause more virilization in male or female: G' Y$ ~& q$ E! q
children than one would realize. Exposure to andro-
! }3 J& [; h; c) ]% _gen products must be considered and specific ques-
( _9 d( S" h5 c9 d" `" Ftioning about the use of a testosterone product or8 s4 L5 H! E1 ^ k, b1 i/ Y8 c( ?
gel should be asked of the family members during# L+ H4 E0 u d0 o% k
the evaluation of any children who present with vir- V9 x" J3 A3 r, K$ W
ilization or peripheral precocious puberty. The diag-
( t+ m0 O1 t+ ~ t onosis can be established by just a few tests and by
$ H7 i/ `* O4 L5 o0 Oappropriate history. The inability to obtain such a
. I/ c, F# D S5 c9 ihistory, or failure to ask the specific questions, may
. {) i/ S+ G* C6 O0 Xresult in extensive, unnecessary, and expensive
# {# o; ~- Q' pinvestigation. The primary care physician should be7 G' ^: t) W- q/ l& \( l
aware of this fact, because most of these children
/ O, I. w* f' g M% c" l3 ]4 [7 Nmay initially present in their practice. The Physicians’% F5 H# E1 a$ a4 j* U4 }
Desk Reference and package insert should also put a
' t! t6 {5 x7 v9 o) awarning about the virilizing effect on a male or; e l; s+ G! c$ V8 R. Q6 d
female child who might come in contact with some-
% ^6 S1 {( t7 None using any of these products.0 q% \! F1 j/ f( \% _% f5 x
References
9 C" ~% A. _6 j1 F, j% p% [. r1. Styne DM. The testes: disorder of sexual differentiation
% w' Y$ a3 L" s6 {+ P- Y0 Q9 J) ]and puberty in the male. In: Sperling MA, ed. Pediatric
4 U& r* g6 p; T* [, B8 eEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
e; t/ z J2 K3 c' f+ G2002: 565-628.) C1 x2 g( f9 y; r; r7 b) c- L
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 M$ C7 D+ o6 X9 T5 vpuberty in children with tumours of the suprasellar pineal |
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