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Sexual Precocity in a 16-Month-Old
* R3 G5 j3 d+ P; rBoy Induced by Indirect Topical( s1 k, x5 F3 x4 R% B
Exposure to Testosterone5 ] ~7 V9 a0 _6 }! z, v, m
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2; t5 Q8 K8 F& }# M
and Kenneth R. Rettig, MD1" j* K2 H* u" W( c
Clinical Pediatrics6 m: k9 m$ c5 F o- K% q
Volume 46 Number 6
) F; b$ @! `, {; @6 R+ bJuly 2007 540-5436 I' J, ~+ D5 B' ?6 m
© 2007 Sage Publications) Z1 ~* c @; k& \1 w
10.1177/0009922806296651
; o1 ^0 t- s0 U7 ghttp://clp.sagepub.com% j" f, ^ }- m! h/ r
hosted at. Z8 \ J3 @$ x# m. ~. O9 f3 U" b
http://online.sagepub.com
: j% p) p! n2 w* b+ Y* w! A/ SPrecocious puberty in boys, central or peripheral,' l. Z2 Z2 [8 \) b" }
is a significant concern for physicians. Central: E+ L! K) m2 A/ E0 s
precocious puberty (CPP), which is mediated4 ^, u; [) p% v: V; [
through the hypothalamic pituitary gonadal axis, has( l0 V! G: ^4 ^) X! p. f
a higher incidence of organic central nervous system2 U4 s! E- N7 X$ @
lesions in boys.1,2 Virilization in boys, as manifested
& N" e/ y. A: l) t# x3 Sby enlargement of the penis, development of pubic
) V4 j) ~- P, o0 Y3 z6 g- Jhair, and facial acne without enlargement of testi-
* {1 K2 _0 M+ [4 y4 e) D0 p! xcles, suggests peripheral or pseudopuberty.1-3 We% z8 k+ u- d# q h x/ @/ a
report a 16-month-old boy who presented with the
. o5 W. z' _- N$ Fenlargement of the phallus and pubic hair develop-
; U& j' H/ ~1 P# _2 @ment without testicular enlargement, which was due
4 f: i. w9 x! t" Nto the unintentional exposure to androgen gel used by3 ?3 V9 Q. @( b: \
the father. The family initially concealed this infor-+ V8 \# x* z7 E) B0 N
mation, resulting in an extensive work-up for this
; d8 E W( a3 Y0 N4 E# {child. Given the widespread and easy availability of* s, }: ~& Y* m4 l. F, x4 ~4 O
testosterone gel and cream, we believe this is proba-; s: A g+ v) P2 U7 T
bly more common than the rare case report in the1 c( { _. g Y/ w
literature.4/ S. z) U# J) p9 Y: I2 ~# i
Patient Report3 W0 o s6 j8 J8 N( Y' y
A 16-month-old white child was referred to the
1 O8 u7 q0 N& h7 M7 A1 {endocrine clinic by his pediatrician with the concern9 a5 u1 Y" t8 t/ q: f, V5 x, r
of early sexual development. His mother noticed( k$ n! E& h" C" d1 l9 j5 b4 D
light colored pubic hair development when he was& l3 j9 h, K5 W& o* v
From the 1Division of Pediatric Endocrinology, 2University of
( J) E7 B1 Z& P0 `, L3 j2 PSouth Alabama Medical Center, Mobile, Alabama.% [/ N: T5 y# I
Address correspondence to: Samar K. Bhowmick, MD, FACE," Z, d3 c% O9 D) B: R
Professor of Pediatrics, University of South Alabama, College of" S/ y0 l1 G9 \ ~# D4 v2 R" q
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ S- Y8 o9 k% ?2 p# R& o, `e-mail: [email protected].
; j, h E8 d" ^* m: ]2 a0 l gabout 6 to 7 months old, which progressively became
' X) d V. `7 i7 A5 k2 L& kdarker. She was also concerned about the enlarge-9 ^. m' k/ E" r' M. H* c
ment of his penis and frequent erections. The child# D* S3 A N" ]! E. u* M( D
was the product of a full-term normal delivery, with' a/ f$ v1 i, Y, { k
a birth weight of 7 lb 14 oz, and birth length of
+ w& b9 d% } y0 f" _$ R% p8 a2 x20 inches. He was breast-fed throughout the first year0 K6 ^5 Q' ]1 I' m
of life and was still receiving breast milk along with1 s* `* a0 b- f6 P
solid food. He had no hospitalizations or surgery,
( R/ P! l' K6 o6 g8 i# T- Nand his psychosocial and psychomotor development6 j- g. F" Z' A' j! G* I0 d/ H
was age appropriate.5 L+ Y# t/ U" ~7 ~* |
The family history was remarkable for the father,
Q- E, |- h' E) ~( Y- }who was diagnosed with hypothyroidism at age 16,* j& ?- E, x' E5 x, C! ?' N/ P
which was treated with thyroxine. The father’s4 V+ o! }# r5 c; P4 M T. X9 L
height was 6 feet, and he went through a somewhat
% `2 j' d) k6 C- a; S" x% Wearly puberty and had stopped growing by age 14., ~: Q0 }( T* u8 m b
The father denied taking any other medication. The5 l+ e( w! i& u( U/ I; a; r% A
child’s mother was in good health. Her menarche, O2 a5 n1 R8 A# s/ D3 O* B, R& v
was at 11 years of age, and her height was at 5 feet% _, y( Z: W" [( t0 J3 W% N* [
5 inches. There was no other family history of pre-
( X L# I. c4 f+ V# Ncocious sexual development in the first-degree rela-1 ~1 v* ^% \$ D- u
tives. There were no siblings.
: _' C; h& V% n% d6 mPhysical Examination
B+ X& n+ F1 _( M3 \The physical examination revealed a very active,6 X6 ~6 p% Z3 M9 X5 V* ]5 x# G! }
playful, and healthy boy. The vital signs documented- v3 n- T) B6 S. w) t" r
a blood pressure of 85/50 mm Hg, his length was) m* s0 v+ H% D' E( ]: I, _
90 cm (>97th percentile), and his weight was 14.4 kg
0 v: B9 b! w( t h(also >97th percentile). The observed yearly growth
% v+ P& A" a1 @" v8 nvelocity was 30 cm (12 inches). The examination of. o8 G: Q! Z$ |/ f* e0 t
the neck revealed no thyroid enlargement.
0 Y1 X5 p2 z4 G( A" B, ]The genitourinary examination was remarkable for2 A1 R3 \) r3 U. a$ y9 q' q2 J' z1 m; ?
enlargement of the penis, with a stretched length of
. o3 U7 }$ @5 z3 a" i5 @8 cm and a width of 2 cm. The glans penis was very well
8 G+ ^) ` j/ F' H; g; f" c; ]6 |7 xdeveloped. The pubic hair was Tanner II, mostly around
% s C* j6 Q" y3 E1 Z540- E* @, m8 Z# B3 p3 b9 G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 K: b9 F6 [- S. m, A! z2 u
the base of the phallus and was dark and curled. The* K3 W$ Z M; _7 X
testicular volume was prepubertal at 2 mL each.
: ^! i7 z8 [, p9 N! JThe skin was moist and smooth and somewhat
8 U5 C5 C# e( v# ~& z. g: |: ^oily. No axillary hair was noted. There were no
! n# O! g7 _2 z+ H; jabnormal skin pigmentations or café-au-lait spots.0 r( t& y0 H& z) I, b6 U0 J) L) @
Neurologic evaluation showed deep tendon reflex 2+, F8 y$ S" c* `* P" @* Y3 [, z
bilateral and symmetrical. There was no suggestion
) S: h: K0 f# ~1 Xof papilledema.
+ o' s' M3 P) ?# n/ c% kLaboratory Evaluation+ n7 x1 A2 G* W3 h
The bone age was consistent with 28 months by2 l7 G1 S, R) [( T
using the standard of Greulich and Pyle at a chrono-9 F- C' t& q2 A* `. Y& i8 o: `
logic age of 16 months (advanced).5 Chromosomal. d$ n; R" Q, k/ G- m q
karyotype was 46XY. The thyroid function test9 V' V) D" U1 y; s7 ~" U
showed a free T4 of 1.69 ng/dL, and thyroid stimu-2 I8 W$ ?4 N7 k @2 z0 }) M& O
lating hormone level was 1.3 µIU/mL (both normal).
, r& W4 n! Z* I- iThe concentrations of serum electrolytes, blood- z. G. E& ?+ i+ q" k+ W
urea nitrogen, creatinine, and calcium all were5 Q2 N) q/ T+ a2 X" K2 ]& v+ t
within normal range for his age. The concentration( @! I5 b J' Y7 ~$ s! E5 Y9 t' Q
of serum 17-hydroxyprogesterone was 16 ng/dL: d* ?! w! P3 z% ~# W% t
(normal, 3 to 90 ng/dL), androstenedione was 20
2 v" v( {5 h9 l6 z! S% _ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 Y6 u' T& K+ `+ qterone was 38 ng/dL (normal, 50 to 760 ng/dL),& `3 w4 L. Y( W
desoxycorticosterone was 4.3 ng/dL (normal, 7 to4 J' N2 Z5 h& i- D# H
49ng/dL), 11-desoxycortisol (specific compound S)1 L" y+ _( }8 B
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-& L2 P( N. i; D
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. R7 R) b0 j. ^. U9 C1 U0 Utestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
U3 g, a. K. y' ~, xand β-human chorionic gonadotropin was less than
; e5 n4 ^# ?4 W5 mIU/mL (normal <5 mIU/mL). Serum follicular
: \0 }: S, P0 e* [: Fstimulating hormone and leuteinizing hormone2 t* x5 H3 F& s$ ]
concentrations were less than 0.05 mIU/mL
1 @4 q/ `2 q. v$ G! G(prepubertal).
* u" E) F, u, z, r5 jThe parents were notified about the laboratory8 {; T, l5 l' e& J' w
results and were informed that all of the tests were
I$ R8 T" s: m- D) G8 x5 inormal except the testosterone level was high. The/ f! u5 ^& m$ A7 D+ e0 g, c
follow-up visit was arranged within a few weeks to% U# p' x3 o0 y( H, i4 `0 U5 x
obtain testicular and abdominal sonograms; how-# k7 \' |- i5 ?/ R: D- ?
ever, the family did not return for 4 months., x# }7 ?( e- [+ p
Physical examination at this time revealed that the
8 K! u1 j6 h& f2 ~5 n0 }, Rchild had grown 2.5 cm in 4 months and had gained0 f- z0 C# [6 W+ t% l" r
2 kg of weight. Physical examination remained) j! Q; |9 d9 E- l8 i& n
unchanged. Surprisingly, the pubic hair almost com-
* Y8 c4 z" ^& A, Upletely disappeared except for a few vellous hairs at
2 V$ T7 v3 {: Z8 P4 A" ithe base of the phallus. Testicular volume was still 2
M3 g8 X/ }/ k! u7 x& \1 }) D& cmL, and the size of the penis remained unchanged.
6 }3 }' i* w( eThe mother also said that the boy was no longer hav-8 e- q6 B# D$ Y' d, Z7 r
ing frequent erections.
0 W, G4 _2 h% TBoth parents were again questioned about use of3 E2 ]1 S, C6 x/ y- v' W
any ointment/creams that they may have applied to! r `* |8 h9 {& c
the child’s skin. This time the father admitted the
6 X7 w* ]0 ^, {Topical Testosterone Exposure / Bhowmick et al 541
- G( c/ K* J V4 Cuse of testosterone gel twice daily that he was apply-
# t6 }+ W4 Y K6 U- Ning over his own shoulders, chest, and back area for3 N6 `" d$ C6 c3 [& n+ B
a year. The father also revealed he was embarrassed
8 o: V) n# i+ U( B2 v$ pto disclose that he was using a testosterone gel pre-7 G b" t% S- C8 G2 h+ _4 T0 ?
scribed by his family physician for decreased libido
7 A& j. W" S( `. r5 d$ x l& s0 Zsecondary to depression.- a6 C" v+ {+ a) x/ e5 x
The child slept in the same bed with parents.
. F" U5 Y4 A8 `; O3 wThe father would hug the baby and hold him on his6 ]' b" y, j/ ~; G8 @3 \. z2 o
chest for a considerable period of time, causing sig-
+ Y& h5 b* d, {6 c' tnificant bare skin contact between baby and father.7 M5 T1 p/ s& U9 H4 q; I- I( f
The father also admitted that after the phone call,
}! D) d8 F# |3 F3 l2 Jwhen he learned the testosterone level in the baby! t8 W" J; z; T* }3 t
was high, he then read the product information5 l( K9 d ?- M" @ G x
packet and concluded that it was most likely the rea-
$ ~2 V. |1 L/ s9 ^5 F& oson for the child’s virilization. At that time, they
- T- x' m! Y% Mdecided to put the baby in a separate bed, and the
' ]2 j5 B! \% Z( f# E; Rfather was not hugging him with bare skin and had$ t& a2 ]5 {# Z- \" V
been using protective clothing. A repeat testosterone j+ h+ S8 R) |4 A' O3 Y. N' R( H U: R
test was ordered, but the family did not go to the
, o$ A3 L: ~4 L' T- Nlaboratory to obtain the test.
. q7 ?# |* f# J8 s/ v6 c3 [Discussion5 B9 f9 P& j8 u
Precocious puberty in boys is defined as secondary; l) W6 M! b6 x6 o) U
sexual development before 9 years of age.1,4. N6 t% q; H" h$ ^2 Z
Precocious puberty is termed as central (true) when+ |" h1 k) D4 u3 D
it is caused by the premature activation of hypo-
0 h6 M6 ~4 {5 z7 E# ethalamic pituitary gonadal axis. CPP is more com-
& }" c; i! k* S2 Xmon in girls than in boys.1,3 Most boys with CPP
% _, }% l; V& j* |" Mmay have a central nervous system lesion that is
" z+ r! a- `, S- J0 cresponsible for the early activation of the hypothal-$ K- r$ i+ _+ H5 ^
amic pituitary gonadal axis.1-3 Thus, greater empha-
+ T3 v: e( |9 K1 t: k$ @sis has been given to neuroradiologic imaging in ?! T/ ], S$ b) q/ `/ B1 a
boys with precocious puberty. In addition to viril-
% L0 j" ]+ H; o& g2 Z. fization, the clinical hallmark of CPP is the symmet-8 @) @$ [; R2 w! t. f
rical testicular growth secondary to stimulation by5 y& P/ }. k- m; ~% h9 u: S, Z6 J) p
gonadotropins.1,3
* O: |6 p3 |3 `' U9 H7 n% D4 M* ~Gonadotropin-independent peripheral preco-
2 r6 q, W8 F+ x+ d! E8 ^cious puberty in boys also results from inappropriate
6 y+ f" ^, [1 v& [, candrogenic stimulation from either endogenous or
/ P2 r# o0 L8 G i7 kexogenous sources, nonpituitary gonadotropin stim-! [. `" r, }: E, O
ulation, and rare activating mutations.3 Virilizing
: }( P- J6 K8 Dcongenital adrenal hyperplasia producing excessive, F$ C4 _3 W* X/ `
adrenal androgens is a common cause of precocious
8 M, Y) y4 Y/ B. v9 gpuberty in boys.3,4
3 @3 Q8 F5 L. L7 [6 a& J+ b9 ZThe most common form of congenital adrenal+ B! c+ {# p' X# K( V# I0 N8 U
hyperplasia is the 21-hydroxylase enzyme deficiency.% y0 O+ p# ~; V9 |' C5 U
The 11-β hydroxylase deficiency may also result in7 G; w) U% a& b: a1 g* T: S
excessive adrenal androgen production, and rarely,
8 B0 C2 r- k% x( \# ian adrenal tumor may also cause adrenal androgen
, w1 F; @9 O2 o' k# T, `excess.1,34 [) e) A3 ]8 G% M7 h/ k0 |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 q; J( ^: I6 `
542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 V4 w0 H5 {, D6 Q d
A unique entity of male-limited gonadotropin-* S: Z' K# P# h' z+ c) p4 T+ X
independent precocious puberty, which is also known6 i* Y. [: C( t/ _: r
as testotoxicosis, may cause precocious puberty at a
: m' k# ~3 U! \( y# w8 H3 rvery young age. The physical findings in these boys; ~3 ?+ a/ N0 I% T7 @6 L
with this disorder are full pubertal development,
: ?; A$ W* {" [' Yincluding bilateral testicular growth, similar to boys
; ]+ `& p( o4 q/ Ywith CPP. The gonadotropin levels in this disorder
y i s: q# q; y8 Jare suppressed to prepubertal levels and do not show
5 ^. s" K+ k6 P1 [# M8 Vpubertal response of gonadotropin after gonadotropin-9 a" l3 b4 m8 J6 K
releasing hormone stimulation. This is a sex-linked* Z+ f9 n& d7 X( T% P5 N
autosomal dominant disorder that affects only
, a: i; k$ c. G, rmales; therefore, other male members of the family
c' U! I" h6 Z/ ~' ~may have similar precocious puberty.3* K8 [3 c+ r: R' F5 `/ v( z
In our patient, physical examination was incon-
; E" U* A5 Z- ?, c: psistent with true precocious puberty since his testi-
9 }$ R! d" H' E8 ^& m5 icles were prepubertal in size. However, testotoxicosis
4 j' u% |. G8 @* E( cwas in the differential diagnosis because his father
; n9 Q: C) \4 _. g7 |started puberty somewhat early, and occasionally,( h; J0 V# l+ G9 ^+ W: T9 F6 F- n
testicular enlargement is not that evident in the2 e: |" ?: U! X0 W, @" M k1 B
beginning of this process.1 In the absence of a neg-* w$ P6 P* H; q& _$ V& C
ative initial history of androgen exposure, our2 m4 N* `, N5 r
biggest concern was virilizing adrenal hyperplasia,6 w% i1 G" s, x; g5 W
either 21-hydroxylase deficiency or 11-β hydroxylase7 W8 T. K0 j/ t7 m P" l2 r
deficiency. Those diagnoses were excluded by find-
4 \ Z! ^6 G! j2 D" g' C* ~. @ing the normal level of adrenal steroids.6 Z. h1 n9 |8 `/ P+ B3 D
The diagnosis of exogenous androgens was strongly6 m9 Y$ \5 v* p3 L! ^$ a
suspected in a follow-up visit after 4 months because
2 ]* e" a0 B& g1 j5 `the physical examination revealed the complete disap-) J, v6 A8 D9 g6 Z$ l
pearance of pubic hair, normal growth velocity, and
7 u1 U( V' S* P! X2 qdecreased erections. The father admitted using a testos-0 b3 M; R @% n- J' A3 f
terone gel, which he concealed at first visit. He was
+ ^! ~# W4 l) |+ zusing it rather frequently, twice a day. The Physicians’
" w7 S: m* o6 w+ C3 c: [Desk Reference, or package insert of this product, gel or
. z( C4 s& Q$ h. Z5 ?4 S# Vcream, cautions about dermal testosterone transfer to
% ?! I% z+ W. l9 X' Ounprotected females through direct skin exposure.
- |; d( q* W" OSerum testosterone level was found to be 2 times the) d9 r8 Z, I# F' n1 p
baseline value in those females who were exposed to
1 |. u* \+ @) o- }3 _+ v4 qeven 15 minutes of direct skin contact with their male
% R. {# `0 N- A% |+ }8 B! zpartners.6 However, when a shirt covered the applica-4 b* m0 t! q* P3 M% i x
tion site, this testosterone transfer was prevented." A H6 ]- R4 k; U4 F
Our patient’s testosterone level was 60 ng/mL,
* z2 |2 O7 q' v7 N8 gwhich was clearly high. Some studies suggest that2 o, v3 S; ^+ l, v
dermal conversion of testosterone to dihydrotestos-" C2 b, O% u# B& S4 M
terone, which is a more potent metabolite, is more
( ^. `0 c' L& Y2 O8 B$ Cactive in young children exposed to testosterone. d. \/ L4 k# D& u/ L% q
exogenously7; however, we did not measure a dihy-
- X5 p B' E9 f: p: k4 P* Rdrotestosterone level in our patient. In addition to8 H# |& e4 U+ V/ H4 T. n; T4 j
virilization, exposure to exogenous testosterone in
' [! o% K) p1 R8 w5 s7 a% Rchildren results in an increase in growth velocity and
5 D6 o6 W( R4 S: o5 b- D! sadvanced bone age, as seen in our patient.$ ?; I+ V( P: H& X
The long-term effect of androgen exposure during' G, I; {! m1 |! Z/ Y
early childhood on pubertal development and final
5 z: M! ?2 q& m: @& u ]4 c" Fadult height are not fully known and always remain
& z0 n! ~9 y/ x% ?+ v1 C ma concern. Children treated with short-term testos-
/ | t( k1 R6 J. h, f) k( xterone injection or topical androgen may exhibit some
- k6 x" o. \1 }/ \& v# a: j* Iacceleration of the skeletal maturation; however, after
' x- z% Y( t" [ Y& ncessation of treatment, the rate of bone maturation
4 r& i3 {; N k8 `1 V6 J$ c5 J0 kdecelerates and gradually returns to normal.8,9
3 Q1 a9 P0 L! z ] P# {There are conflicting reports and controversy
) _" B$ K$ `* L8 U$ m. ?over the effect of early androgen exposure on adult( I6 b, z4 L! D& C& P& ]
penile length.10,11 Some reports suggest subnormal
: U" `' j$ s$ [3 n1 {9 g" T. Madult penile length, apparently because of downreg-7 B1 h; E p2 K/ `) a3 {
ulation of androgen receptor number.10,12 However,
$ z$ w4 H# Z# `; B% \Sutherland et al13 did not find a correlation between
$ s4 o" P& Y+ ~# Wchildhood testosterone exposure and reduced adult
- Z1 ?/ J' q! `8 ?6 c9 o0 mpenile length in clinical studies.' d4 u+ O4 {; @# ?8 D
Nonetheless, we do not believe our patient is
9 _1 M. k9 j- q1 i, L# \# N3 Mgoing to experience any of the untoward effects from
6 Q; t" r( D7 v, I u0 u% Ttestosterone exposure as mentioned earlier because
: l4 A0 L/ V; W% d0 n+ q" W& u) qthe exposure was not for a prolonged period of time. O/ Y# Y0 D6 C) F7 f1 u, x$ @6 n
Although the bone age was advanced at the time of( X; Q! P+ ?1 i! z6 L# g6 @
diagnosis, the child had a normal growth velocity at
& k# g8 H& x1 E+ o, `4 sthe follow-up visit. It is hoped that his final adult2 r* a1 t9 r0 E3 |+ [) A
height will not be affected.
5 a: T+ C, f3 H* M8 y9 @Although rarely reported, the widespread avail-# }. i& x3 c/ j, L1 G
ability of androgen products in our society may
9 H2 t% p' j. F+ \% ?3 zindeed cause more virilization in male or female
0 s4 }6 Z) ^1 @ R' U9 @( }children than one would realize. Exposure to andro-& z' M9 e7 l. ^' p5 _
gen products must be considered and specific ques-
. d* _, J7 [2 m' I+ ?* I4 n# itioning about the use of a testosterone product or
- w2 K# L8 ]0 y5 ?; R: [. G" Lgel should be asked of the family members during# G. h5 X) ]" z6 y) Z. k5 W
the evaluation of any children who present with vir-+ c9 b: h9 d# I/ E& w
ilization or peripheral precocious puberty. The diag-8 V: k" d5 _! C4 [3 p3 V% c
nosis can be established by just a few tests and by1 {4 k8 k" |8 W8 B. X) U3 G- ~
appropriate history. The inability to obtain such a* H! S- Y% f J7 r3 _
history, or failure to ask the specific questions, may
# c8 Y0 r) }8 t- R% g" iresult in extensive, unnecessary, and expensive
3 Z B& B" `3 L3 c5 o5 _3 |0 finvestigation. The primary care physician should be
+ l, W9 X4 d0 R" X( Naware of this fact, because most of these children, M* L3 ?) |# a$ Q$ k: g
may initially present in their practice. The Physicians’3 D# V2 a1 l/ q
Desk Reference and package insert should also put a8 @+ N _( ]$ v g0 z/ N z9 w$ c
warning about the virilizing effect on a male or
: A5 h' q5 e1 B' j2 j3 j+ Vfemale child who might come in contact with some-4 z. @) o% I7 f4 B' z+ v6 E, I
one using any of these products.9 A2 V8 L6 N: A' D8 _7 d) a. l0 s" [
References
2 @2 ?+ `& o2 S' R6 e8 h1. Styne DM. The testes: disorder of sexual differentiation0 ^* m" I# Z6 j7 ~( y; z
and puberty in the male. In: Sperling MA, ed. Pediatric" @2 ]- J4 ^$ ?
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 ]: U, A/ u' U( J/ y, ]7 b+ Q2002: 565-628.
2 y4 e2 l7 d3 w! p" I7 C2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 u# S9 Q* V1 t Jpuberty in children with tumours of the suprasellar pineal |
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