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Sexual Precocity in a 16-Month-Old8 q$ J' U2 u! s& \+ U) I
Boy Induced by Indirect Topical
0 u. f% l8 {. _& u- V' I7 f1 dExposure to Testosterone; G7 u6 l4 t1 D
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 N) v! y* l5 u( wand Kenneth R. Rettig, MD1
% D6 e! o0 N3 Y" s! M# aClinical Pediatrics( u; K: I( W @1 q/ N
Volume 46 Number 6
7 p. k8 s7 S$ {$ J. \" FJuly 2007 540-543' [8 N! Y$ S$ Q$ Q9 o# n* H' C. T
© 2007 Sage Publications2 z6 F* h* n& t) a3 ^* q! V' ~
10.1177/0009922806296651
; T. h4 m$ u4 Chttp://clp.sagepub.com
4 g( ^9 d! U: G# {2 t! Jhosted at
# @- M- L& K8 q2 V9 y& S+ L# thttp://online.sagepub.com: L3 H! W8 ?& v' C% x
Precocious puberty in boys, central or peripheral,
5 o; X/ i6 g7 S3 m$ x4 Qis a significant concern for physicians. Central9 Q0 [: N- M) o$ d) u* o
precocious puberty (CPP), which is mediated3 e+ H! m" L9 ]8 `0 \
through the hypothalamic pituitary gonadal axis, has+ M# {! S+ k1 t5 S4 ]1 _; B
a higher incidence of organic central nervous system
4 j) Z0 i+ E0 Ulesions in boys.1,2 Virilization in boys, as manifested$ P4 G/ w, J! Q- l* K+ U5 C
by enlargement of the penis, development of pubic6 [1 h8 ?& z% B$ L, n3 T
hair, and facial acne without enlargement of testi-; @. {( K7 G4 r( |
cles, suggests peripheral or pseudopuberty.1-3 We
- i b% n+ J# @1 [( E& \report a 16-month-old boy who presented with the4 @% ?( Y: c, R
enlargement of the phallus and pubic hair develop-
( p! ~( Z9 \, Z3 o/ N4 Jment without testicular enlargement, which was due" U) J1 G5 X8 G4 n- \
to the unintentional exposure to androgen gel used by
4 H l I/ {6 s/ T' V! g6 cthe father. The family initially concealed this infor-
4 i3 _+ j) q7 T4 P! m; Cmation, resulting in an extensive work-up for this5 Z6 D0 o8 n) s) V' k
child. Given the widespread and easy availability of
! D j% m8 O/ f( [; Z/ q, j% Wtestosterone gel and cream, we believe this is proba-) I; X6 y; O8 e2 N, B
bly more common than the rare case report in the0 H) f3 ]; D0 ~" c
literature.4
% |; u/ f$ t( ~Patient Report
! }* J8 X6 }7 KA 16-month-old white child was referred to the: D' C# }3 L( w
endocrine clinic by his pediatrician with the concern
5 u2 a2 }, k9 v( F6 cof early sexual development. His mother noticed6 f* V2 b3 |% Q3 R- A
light colored pubic hair development when he was
4 o3 t( T# Z+ lFrom the 1Division of Pediatric Endocrinology, 2University of
9 ?! O7 O- x9 D6 @5 tSouth Alabama Medical Center, Mobile, Alabama.! T2 H$ U+ Q8 F' c5 ?4 g
Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 @, T% I- r. SProfessor of Pediatrics, University of South Alabama, College of2 q! \- {2 |3 ^- n( I1 b
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& F* s4 _; q& Z; K8 we-mail: [email protected].% U- ?" L: `/ q3 X
about 6 to 7 months old, which progressively became
' g: N. X R( _" M4 v) D# ~1 \# idarker. She was also concerned about the enlarge-4 c' t( j! d; h2 R& a! m3 o
ment of his penis and frequent erections. The child
7 m+ g- w& c' ]5 _7 J6 ]4 qwas the product of a full-term normal delivery, with
! t2 u# n+ E) y% Qa birth weight of 7 lb 14 oz, and birth length of" j" B! H7 F& V
20 inches. He was breast-fed throughout the first year
4 M. Q0 s: C4 N$ A. M3 W" q5 J1 Dof life and was still receiving breast milk along with$ K6 l# O9 P3 Q1 R; D, @
solid food. He had no hospitalizations or surgery,2 J6 N1 B* O, E* e
and his psychosocial and psychomotor development
# u3 c0 n0 d9 [6 L) zwas age appropriate.- Z$ S/ H0 \( I9 B5 |
The family history was remarkable for the father,8 f- k0 W7 I& f) q* P# t9 T
who was diagnosed with hypothyroidism at age 16,2 i9 `3 Q7 L# _# m4 w8 |6 d
which was treated with thyroxine. The father’s
a: A/ D5 h; B% H1 f: oheight was 6 feet, and he went through a somewhat
- k# X7 ], Q% F- B J! ?early puberty and had stopped growing by age 14.
' W. j' b0 t1 Z+ O" Q9 OThe father denied taking any other medication. The. m2 p8 l1 x+ H, t
child’s mother was in good health. Her menarche5 v8 S! L5 n' z& x# P) y
was at 11 years of age, and her height was at 5 feet9 t+ H- u; z; u6 `7 a
5 inches. There was no other family history of pre-
4 @1 J- i- H4 R$ z5 Lcocious sexual development in the first-degree rela-
' Y/ z' |- m% z6 g$ ptives. There were no siblings.- ]2 h% E" [5 B2 O4 t
Physical Examination1 Z2 x: P8 {* H
The physical examination revealed a very active,4 x' \8 h5 D }8 ]) w `
playful, and healthy boy. The vital signs documented; m+ r* C7 A. d. j& ^+ y
a blood pressure of 85/50 mm Hg, his length was
( r- a4 h- Y( D& |5 i$ T4 H90 cm (>97th percentile), and his weight was 14.4 kg# N7 u0 {5 S8 R" G( Y' b" x3 o
(also >97th percentile). The observed yearly growth
/ f6 s7 n% i% M9 V5 Q8 Bvelocity was 30 cm (12 inches). The examination of$ J/ s$ }$ f0 [3 x w0 V
the neck revealed no thyroid enlargement.
8 t$ R* `3 p l2 RThe genitourinary examination was remarkable for
: ?) |8 v- k* n+ I5 W; G8 Benlargement of the penis, with a stretched length of7 F" N( ~% p3 v: R2 E4 W3 U. K x
8 cm and a width of 2 cm. The glans penis was very well
. ~ g5 j K* r* _# O ]" S9 Gdeveloped. The pubic hair was Tanner II, mostly around
/ x" X4 H6 C5 z/ a+ e2 C6 F0 ?- v540
) Z% {1 _' @. t7 R) zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- L- \' K' A p& n. c7 ethe base of the phallus and was dark and curled. The" }8 ]' ]5 N3 O, M6 c
testicular volume was prepubertal at 2 mL each.. q/ r+ z1 H* P- {" F O6 c* @
The skin was moist and smooth and somewhat7 f. { v; a3 b' W
oily. No axillary hair was noted. There were no
$ ?$ H, E! \. l" N) _abnormal skin pigmentations or café-au-lait spots.
' K4 T6 m) p& H7 h, v& Y( K( UNeurologic evaluation showed deep tendon reflex 2+
% q0 l9 g/ r$ `: Y+ O4 Y7 Fbilateral and symmetrical. There was no suggestion
+ T6 z. \* m! s" pof papilledema.6 \ I2 u a- Z' L% V% ?5 I
Laboratory Evaluation$ M: t2 o6 x9 B& D# f G
The bone age was consistent with 28 months by6 ~7 V N8 u1 I" ?, s! `- J
using the standard of Greulich and Pyle at a chrono-
" @" z( C8 V" @8 K; P' _logic age of 16 months (advanced).5 Chromosomal
7 \$ t, @2 I+ o3 `2 K- Q) C: Zkaryotype was 46XY. The thyroid function test
9 D, ]$ s8 \/ E; |) ]) Wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-3 p$ P' i2 g4 J4 y1 z
lating hormone level was 1.3 µIU/mL (both normal).
/ J. Q) q. P# \5 R9 yThe concentrations of serum electrolytes, blood5 A, P) v4 e, ~' P1 S
urea nitrogen, creatinine, and calcium all were
- B7 J- i4 x( A& Qwithin normal range for his age. The concentration
: S/ A5 K; t5 F |) S1 E% Xof serum 17-hydroxyprogesterone was 16 ng/dL! i: N% P" i' q9 X4 D
(normal, 3 to 90 ng/dL), androstenedione was 20% [" W( z& D4 m& A
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-4 O! e9 d) p0 w1 B& U# R
terone was 38 ng/dL (normal, 50 to 760 ng/dL), I6 j2 p/ P$ [+ ]" J
desoxycorticosterone was 4.3 ng/dL (normal, 7 to* I& h3 |: u$ x0 a
49ng/dL), 11-desoxycortisol (specific compound S) y t6 m; u* J1 X+ b- U+ k
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 H$ ^# |8 f/ f4 O Mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 M. S( M# S& |# S: X: Ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),& `! s1 O; \+ g. O2 L% B2 t
and β-human chorionic gonadotropin was less than
: H" v$ w& k8 K8 m+ {" ]& l5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 x3 p2 d3 L% Q2 T% ?stimulating hormone and leuteinizing hormone' Z4 o/ h3 h) R8 H6 ?
concentrations were less than 0.05 mIU/mL
, R9 S# e3 g/ J' B(prepubertal).9 r1 s) v# _2 W+ |% K/ m
The parents were notified about the laboratory
/ }! h/ p( C" z- Y8 u+ D# }8 ?results and were informed that all of the tests were" R' f, N1 v, I* D% o5 p n
normal except the testosterone level was high. The5 p7 s8 Q, A; n4 q
follow-up visit was arranged within a few weeks to; E& R6 L3 N$ o2 L* D
obtain testicular and abdominal sonograms; how-2 L8 n, a+ ?6 V2 i/ H% ]
ever, the family did not return for 4 months.
# M1 c7 f3 u9 K! Q# iPhysical examination at this time revealed that the
. p8 E! r1 b2 x* Achild had grown 2.5 cm in 4 months and had gained: G% h+ u4 \- w
2 kg of weight. Physical examination remained6 y- ]: |. f9 i0 z4 u. r
unchanged. Surprisingly, the pubic hair almost com-
+ t0 Q5 {, `0 F9 R0 }pletely disappeared except for a few vellous hairs at
; b3 w: }/ v" f6 Mthe base of the phallus. Testicular volume was still 2
% O# {1 Q0 D' a9 u2 tmL, and the size of the penis remained unchanged.- E/ u3 b( p( ~" }
The mother also said that the boy was no longer hav-3 h; u0 b) m& i2 Z0 P( f
ing frequent erections.
6 t4 g5 _% t0 L) e- x) ^7 t. MBoth parents were again questioned about use of8 e3 A. }7 S4 c, U' ^% u$ `
any ointment/creams that they may have applied to
! R/ N4 G6 E: d# \ R& E/ z: Jthe child’s skin. This time the father admitted the8 S2 D6 y! Y2 C( Y
Topical Testosterone Exposure / Bhowmick et al 541
) k5 v7 _2 ~- s2 Xuse of testosterone gel twice daily that he was apply-$ E0 ?- `& V l
ing over his own shoulders, chest, and back area for" a' @% _4 E# I6 v9 ?" G
a year. The father also revealed he was embarrassed
' o5 T* z. ^! F! h' tto disclose that he was using a testosterone gel pre-# F1 z; a+ w ^9 M, ?
scribed by his family physician for decreased libido6 |9 J; L8 L0 X# a; ]9 T- W0 Z
secondary to depression.. ^% ^% T/ V) ? W
The child slept in the same bed with parents.
0 m" m* F1 s" G' l5 M% D" H3 cThe father would hug the baby and hold him on his
4 X# ~- P$ b* R0 d4 T- j8 Qchest for a considerable period of time, causing sig-- Q% [' D# a/ Z9 o% C/ s, v
nificant bare skin contact between baby and father.# T8 j, @, K: O5 }+ l- c
The father also admitted that after the phone call,7 G0 j$ H6 p1 @' Z
when he learned the testosterone level in the baby" ^6 Z, @" u& }1 W. i3 f! O, l7 k8 g5 t
was high, he then read the product information6 ^" L& v, J2 C, x
packet and concluded that it was most likely the rea-
3 M$ m5 _, ?; V/ lson for the child’s virilization. At that time, they A5 I! {3 Q9 e
decided to put the baby in a separate bed, and the! F/ Q9 L: Q2 x* G4 t
father was not hugging him with bare skin and had
' \; h) N. Z- Z. _been using protective clothing. A repeat testosterone
) N: H3 y. Y# O4 @$ @test was ordered, but the family did not go to the W& l# r$ z) Q. k
laboratory to obtain the test.4 i0 S( m- \/ K% W2 j
Discussion
" z0 m9 M8 d0 J) R) z. {' kPrecocious puberty in boys is defined as secondary! ]/ |- O5 ?* v w+ @, [8 O/ E
sexual development before 9 years of age.1,4
; L5 A0 E* R. APrecocious puberty is termed as central (true) when4 w. i4 ~. w' y
it is caused by the premature activation of hypo-3 O5 E+ r" m5 u. u: U: l
thalamic pituitary gonadal axis. CPP is more com-
& |$ E9 o3 G# a4 B6 G- Ymon in girls than in boys.1,3 Most boys with CPP
8 e6 Y, X" ^5 E) `may have a central nervous system lesion that is4 i& ~; A9 t: ~
responsible for the early activation of the hypothal-; G. ~3 Q7 |7 \5 X: G- n
amic pituitary gonadal axis.1-3 Thus, greater empha-
- g' t& L2 A0 k! O! o- d2 dsis has been given to neuroradiologic imaging in8 ?( ^+ X9 ]: L4 |8 d6 y$ ?
boys with precocious puberty. In addition to viril-" m! }# ]: X3 n) ^9 D% D: }
ization, the clinical hallmark of CPP is the symmet-& v2 J* s5 [9 u0 X* V. ^
rical testicular growth secondary to stimulation by
2 A3 D- Y& G/ X. u5 Rgonadotropins.1,3; L# U# b1 i/ }' F" K- O* c+ E
Gonadotropin-independent peripheral preco-
; z6 O4 |! h Q- Hcious puberty in boys also results from inappropriate
& [( [5 M3 }" @4 aandrogenic stimulation from either endogenous or# S' A) [6 W$ P" X4 i
exogenous sources, nonpituitary gonadotropin stim-
+ e8 ~& |0 \1 d( e: ^7 Y( U# Zulation, and rare activating mutations.3 Virilizing
! x% v4 a+ D/ }8 Ccongenital adrenal hyperplasia producing excessive5 r) T- S- ~+ ?6 ~/ A9 \3 d, n9 G
adrenal androgens is a common cause of precocious
! v4 {" h$ P& X2 w) vpuberty in boys.3,4: K6 ^) `9 b8 A/ \
The most common form of congenital adrenal( ^ N) K# d' Z' I9 \
hyperplasia is the 21-hydroxylase enzyme deficiency.
7 L3 p8 T( K' k" _# g; qThe 11-β hydroxylase deficiency may also result in: {7 p" G9 H1 n8 ^, w
excessive adrenal androgen production, and rarely,
3 ?0 W! _( h/ i+ c! x9 x! N/ Van adrenal tumor may also cause adrenal androgen
) l# v$ [& f W! y; }2 Fexcess.1,3& ]7 n9 V+ X( Y/ i: X
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, s" O2 S8 @$ e( R2 o
542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 R0 M1 H2 ?9 h- G8 J2 z8 ]) D
A unique entity of male-limited gonadotropin-
: x. L3 A* N7 B _" }0 m4 b4 N3 H" Hindependent precocious puberty, which is also known* x) e* Q8 n) Y/ `0 s" E% q
as testotoxicosis, may cause precocious puberty at a
9 T/ H! ^) v, }" v8 r/ avery young age. The physical findings in these boys
3 F2 `# s2 J0 ^8 [. uwith this disorder are full pubertal development,
; n5 M6 G: x# p/ `" N0 J" A Oincluding bilateral testicular growth, similar to boys
0 ^6 J3 X2 r. N1 H4 T0 c( M7 Swith CPP. The gonadotropin levels in this disorder4 w5 n& }+ I4 T0 ~
are suppressed to prepubertal levels and do not show4 ~( p( H& U6 `7 d3 Y5 `( ]1 D! [
pubertal response of gonadotropin after gonadotropin-
1 n" o @2 c7 R' O, o+ e0 }releasing hormone stimulation. This is a sex-linked0 _4 h) f* [: |( g( @, f6 a
autosomal dominant disorder that affects only! C% P; p) b. ]6 {
males; therefore, other male members of the family
1 y! x! I! s+ @ M1 n |' X9 {may have similar precocious puberty.3& A; Q0 Y7 c! E6 N% x7 o9 S9 |
In our patient, physical examination was incon-" {; w0 f, M8 G+ f p
sistent with true precocious puberty since his testi-
6 @+ i9 Z$ h$ l# E# A. y8 }: ]5 ^cles were prepubertal in size. However, testotoxicosis2 U; J- Y' n8 o0 p$ ] m, R: ^) I
was in the differential diagnosis because his father) w+ h$ L8 v' `1 ?. }7 R2 ?
started puberty somewhat early, and occasionally,
! Z3 J$ n+ u+ r' w B6 |testicular enlargement is not that evident in the' ]5 C$ y3 S5 D" ]+ b' Y+ b& ^
beginning of this process.1 In the absence of a neg-
# h4 T# {( E0 T# {: a1 Qative initial history of androgen exposure, our" l8 ]6 \. N( M/ E# z$ M( [$ X/ P
biggest concern was virilizing adrenal hyperplasia,
! p6 m0 Z" J; O8 M! r1 j- P2 A1 Beither 21-hydroxylase deficiency or 11-β hydroxylase
/ f6 z4 Z0 C" Mdeficiency. Those diagnoses were excluded by find-& l" c% l. q/ }: y6 _
ing the normal level of adrenal steroids.' q0 E' R' w9 _; i
The diagnosis of exogenous androgens was strongly* j$ l" V& o- l/ F3 e0 Y# w/ \
suspected in a follow-up visit after 4 months because8 t1 L/ B7 y, { j+ Y
the physical examination revealed the complete disap-" q/ r1 @% d; c' Q) U
pearance of pubic hair, normal growth velocity, and9 c9 v$ \4 o+ s: T1 Z( j
decreased erections. The father admitted using a testos-
, L' m1 V% m) V1 y& aterone gel, which he concealed at first visit. He was
* a3 n. F" ?* M' ?1 susing it rather frequently, twice a day. The Physicians’
2 q) U) C# O2 c4 M. LDesk Reference, or package insert of this product, gel or, w$ R ~# b# F3 z% Q7 R. p3 `
cream, cautions about dermal testosterone transfer to
) T4 M( V( |2 j+ M# _- }3 Cunprotected females through direct skin exposure.3 { Q) ^" ]' W+ H, c
Serum testosterone level was found to be 2 times the% u0 w* P7 S8 F( \% D
baseline value in those females who were exposed to) z. \6 i3 ]6 G: d* L0 ]
even 15 minutes of direct skin contact with their male
9 z; d7 h8 E7 n) z$ Ipartners.6 However, when a shirt covered the applica-
( Q- T3 A- ]5 H3 h, R9 G, z& Rtion site, this testosterone transfer was prevented.
$ Y2 v4 S$ X! mOur patient’s testosterone level was 60 ng/mL,/ K! ^ U6 ]3 H1 W9 x+ x
which was clearly high. Some studies suggest that4 y' h" e1 Q& @: C1 h0 H" Q" H
dermal conversion of testosterone to dihydrotestos-9 L6 P1 s1 E' d0 \1 R: `, B0 I
terone, which is a more potent metabolite, is more
$ ~4 D# M* t) Cactive in young children exposed to testosterone
. z2 x) b @3 i% T2 T- dexogenously7; however, we did not measure a dihy-
& i! W/ b: m+ g0 X6 L0 T0 Pdrotestosterone level in our patient. In addition to
! s5 f! g& G& a6 J9 k Q' x( N, zvirilization, exposure to exogenous testosterone in v/ N+ q3 l9 T( Z5 J. x
children results in an increase in growth velocity and2 X2 x! v5 D( `& s& a, P* b# m
advanced bone age, as seen in our patient.6 M' I- H: M9 N2 U8 F7 j
The long-term effect of androgen exposure during
% d& \, U/ g" L# P9 [5 j( t. ?early childhood on pubertal development and final
, b: R& y) X D4 a! Dadult height are not fully known and always remain% Z D/ j' I. i- N4 W: W; j* |, H3 y& x
a concern. Children treated with short-term testos-4 Z! L" q& N" s( Q& e
terone injection or topical androgen may exhibit some
) @# x; Q( S$ k7 \7 u; Eacceleration of the skeletal maturation; however, after) p' c+ f+ `3 @/ T4 \7 d
cessation of treatment, the rate of bone maturation
1 |5 Q9 ]4 t2 s+ p! z6 h$ ~decelerates and gradually returns to normal.8,9
% r1 N: l" j. ^# y6 YThere are conflicting reports and controversy
1 F: j5 Q- s# e& d, Hover the effect of early androgen exposure on adult
6 `- q% N; q( @* n% ppenile length.10,11 Some reports suggest subnormal# u# Z6 Z$ o' N4 S6 K7 ]
adult penile length, apparently because of downreg-
" n, {' p% q1 F/ Y' I& O \ulation of androgen receptor number.10,12 However,1 A' b5 Y/ E9 \6 f8 w4 `+ t
Sutherland et al13 did not find a correlation between
0 t- X! ]. q5 H2 E4 wchildhood testosterone exposure and reduced adult
+ r, T, ^" p' X9 D" Cpenile length in clinical studies.6 J; C, Q# i$ s' \ @* s( S- I
Nonetheless, we do not believe our patient is
& ?# ?0 T( i3 ~# \% L; v' mgoing to experience any of the untoward effects from z% \$ S8 q+ ]) |
testosterone exposure as mentioned earlier because0 Y. ~, ^ O+ f2 }' V/ }
the exposure was not for a prolonged period of time.
0 i9 T% j# L }7 {2 F1 z1 X: UAlthough the bone age was advanced at the time of3 }! s% @- T( k) R% K
diagnosis, the child had a normal growth velocity at! T! z: p/ [4 S' x h( @! G
the follow-up visit. It is hoped that his final adult' w' F. u4 W; g" H
height will not be affected.: @" @& l+ {* |% Q
Although rarely reported, the widespread avail-
* ~ v1 S/ ~) |2 o, hability of androgen products in our society may
' A) w# H ]0 A- r4 lindeed cause more virilization in male or female
+ @5 q" r3 l$ ochildren than one would realize. Exposure to andro-' u: u% E' u+ _! i. y" f" ]0 h
gen products must be considered and specific ques-
! n" F' m' @3 C( ~4 _8 Mtioning about the use of a testosterone product or. B4 U6 o9 g4 B: h. i6 b
gel should be asked of the family members during
, Z( T& S6 u( l# x) ~, c+ Athe evaluation of any children who present with vir-2 h9 P/ C: r, v* s7 Y
ilization or peripheral precocious puberty. The diag-, m( y/ z% Y" t2 P
nosis can be established by just a few tests and by( c# s3 L& B) \- z1 T
appropriate history. The inability to obtain such a
, D9 j3 T4 H6 D$ C) K& N* Jhistory, or failure to ask the specific questions, may
; B+ p0 `$ b4 k. yresult in extensive, unnecessary, and expensive& l! q% e$ n8 {, Q: e1 T" \) N
investigation. The primary care physician should be
8 h, R; \/ G3 z' V' saware of this fact, because most of these children
, K$ I: w0 C9 L4 |may initially present in their practice. The Physicians’
# c/ P# ], Q# kDesk Reference and package insert should also put a' q7 m% s! R( K0 ~0 h! K2 M
warning about the virilizing effect on a male or. L$ e7 o! K. k v# _
female child who might come in contact with some-
; T. H& |& G& N C' y1 Lone using any of these products.
4 B' y4 V$ S UReferences
% B. b* a5 o) F1. Styne DM. The testes: disorder of sexual differentiation1 ^" Y- d0 t; a7 r, o
and puberty in the male. In: Sperling MA, ed. Pediatric3 G0 y" y9 I5 q& N9 M
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ R+ W( T' q9 p2002: 565-628.: I: H2 c i- I$ z, [, e
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 q* J6 J; V- R# d
puberty in children with tumours of the suprasellar pineal |
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