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Sexual Precocity in a 16-Month-Old
; S9 [. ]5 q/ H( X. Y* e) p7 @, |' fBoy Induced by Indirect Topical% y; E; u6 O# d+ k: @4 Q% i* F4 x0 z
Exposure to Testosterone3 _, G2 t0 m8 T$ a) f; t. \
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 N9 m# _! f+ X3 Jand Kenneth R. Rettig, MD1
5 g8 b5 N: a6 yClinical Pediatrics6 Y% J. M. \1 D+ s. f
Volume 46 Number 6
2 r5 O/ S/ v0 p1 hJuly 2007 540-543- `6 ^/ S* U$ R) C1 b
© 2007 Sage Publications9 k6 \0 j7 e+ ~2 y
10.1177/0009922806296651
% z8 a0 s( ^& C3 s- F4 }/ R |http://clp.sagepub.com. F) S' b: n* b# \1 x
hosted at
; d ~) n8 m: C3 S/ k2 W3 xhttp://online.sagepub.com; x; k( J8 F( [: D) o# M
Precocious puberty in boys, central or peripheral,
; e0 D, k$ e9 O R9 I2 Pis a significant concern for physicians. Central
/ M1 R) Y; E" E2 Sprecocious puberty (CPP), which is mediated) O& u" w( ]8 {6 b& K
through the hypothalamic pituitary gonadal axis, has
, [2 `8 _ ]4 y& k, f7 I1 Ca higher incidence of organic central nervous system
: ^. u9 O* }2 W8 ilesions in boys.1,2 Virilization in boys, as manifested
+ q# U# _1 f, u! s/ J5 fby enlargement of the penis, development of pubic G! F5 L" e+ b" E7 ?: l& s9 M
hair, and facial acne without enlargement of testi-$ B0 v U& r6 z) s
cles, suggests peripheral or pseudopuberty.1-3 We
0 O- z3 i; d$ h1 y1 M& P8 a* wreport a 16-month-old boy who presented with the7 F3 r, `) K% U, @4 S
enlargement of the phallus and pubic hair develop-
5 ?9 ^! g7 |+ i3 Pment without testicular enlargement, which was due
/ I s0 K: ]' W0 nto the unintentional exposure to androgen gel used by7 ?- Q+ Z$ U2 a9 R5 U+ K' j( ~; m
the father. The family initially concealed this infor-7 l/ j* u5 B. P' i3 o7 S
mation, resulting in an extensive work-up for this
9 Y/ {7 C/ y3 B+ C- {7 vchild. Given the widespread and easy availability of
2 j& Y n- ]9 {, A L# r1 Ttestosterone gel and cream, we believe this is proba-4 F; Q" Q, D9 c6 T
bly more common than the rare case report in the
4 y: }) K7 J+ c1 b- gliterature.44 }6 n& r: X5 _
Patient Report
) l' M/ n3 b+ ~A 16-month-old white child was referred to the1 o# r4 r# p6 ]5 z. j0 i
endocrine clinic by his pediatrician with the concern! C& W: A% Z' h
of early sexual development. His mother noticed
' }2 C. T! e7 j. w) t3 Rlight colored pubic hair development when he was
& H# b: F+ S4 R8 KFrom the 1Division of Pediatric Endocrinology, 2University of. L7 i7 O! b& R4 m
South Alabama Medical Center, Mobile, Alabama.
- b% [, ~. _& |% UAddress correspondence to: Samar K. Bhowmick, MD, FACE,
0 r' r+ D2 _ X8 kProfessor of Pediatrics, University of South Alabama, College of
4 O3 k, A8 [/ aMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;: x7 T1 N L8 Z. d. l: q; b+ c! P& B
e-mail: [email protected].
, J; K- @; {8 Q3 T4 xabout 6 to 7 months old, which progressively became1 X4 i* i F$ Q4 t. p" V! P& [
darker. She was also concerned about the enlarge-/ r: i3 t+ y5 M/ E
ment of his penis and frequent erections. The child
1 s6 x% ~. f0 H! }- T0 Kwas the product of a full-term normal delivery, with! }) c6 V& u8 y9 a6 q
a birth weight of 7 lb 14 oz, and birth length of
9 g" `& ?" \" h( H, Z2 L20 inches. He was breast-fed throughout the first year! C5 L6 v) M% {3 L, M9 F8 [: q5 d
of life and was still receiving breast milk along with
. r/ N3 X2 G D9 g; k# h4 psolid food. He had no hospitalizations or surgery,
$ b3 U6 N9 j" I( V1 V0 h9 q, Mand his psychosocial and psychomotor development
& r5 Y! M4 I l# Mwas age appropriate.9 a# D% N; s( f/ a+ C. n" x' S; D# z
The family history was remarkable for the father,
% j0 R8 s% {/ w" {# a. U2 nwho was diagnosed with hypothyroidism at age 16,& a% g9 W% K' @
which was treated with thyroxine. The father’s% S- ^' ]/ P/ T
height was 6 feet, and he went through a somewhat% J; d& f1 x, C* n5 }
early puberty and had stopped growing by age 14.' d- w. i, {2 M' L" D m- B3 b: V& M
The father denied taking any other medication. The
, m# ^' }. S* K5 A7 Rchild’s mother was in good health. Her menarche
) _1 x- Z4 M/ P, Mwas at 11 years of age, and her height was at 5 feet
0 J% ^7 K! y8 ~' @. T5 inches. There was no other family history of pre-, F/ g& m4 ]" p! t5 I9 J( S
cocious sexual development in the first-degree rela-/ z( G) ]9 y3 A z+ T
tives. There were no siblings.6 m6 G6 c" [& l' Y" } \# _
Physical Examination
& W2 z( a1 F* P/ _The physical examination revealed a very active,( q) R3 `* c2 Z
playful, and healthy boy. The vital signs documented% T p/ L8 b: F5 |1 K6 Z' \
a blood pressure of 85/50 mm Hg, his length was
+ i" E: l1 O& E7 b# d90 cm (>97th percentile), and his weight was 14.4 kg! S4 B( x( [$ [
(also >97th percentile). The observed yearly growth; K7 Q& u- a. W0 q/ t3 `7 d. O6 K- X
velocity was 30 cm (12 inches). The examination of
) X4 N5 Z( |7 d! g+ x; g3 N* q0 Rthe neck revealed no thyroid enlargement.
9 v. I8 R/ h# B: ^The genitourinary examination was remarkable for5 X6 e* |4 m# c6 H
enlargement of the penis, with a stretched length of
) W# l9 i& N- a9 A2 G7 R0 I. ^* j8 cm and a width of 2 cm. The glans penis was very well
# W( a: V5 O" {* D2 Pdeveloped. The pubic hair was Tanner II, mostly around
: ^/ h0 R+ N, }0 T t540& S4 c1 {& j% P1 G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 h8 c0 H! Y# @$ ?- Nthe base of the phallus and was dark and curled. The2 {' a! _/ [) o/ }! }5 d* F
testicular volume was prepubertal at 2 mL each.
% v4 L$ G n& N H6 _The skin was moist and smooth and somewhat2 o. O8 U# A2 o
oily. No axillary hair was noted. There were no0 t- y' S3 X; _3 H
abnormal skin pigmentations or café-au-lait spots.
: w. d9 B1 `' MNeurologic evaluation showed deep tendon reflex 2+
" y( Z5 M1 t6 m: J% }bilateral and symmetrical. There was no suggestion
1 ~; s+ H! f& f" Wof papilledema.
' \) V% a9 q8 X' I- oLaboratory Evaluation( A S, t6 U3 @3 P" V( h
The bone age was consistent with 28 months by. c3 s3 }5 d2 D$ g! F
using the standard of Greulich and Pyle at a chrono-. o/ R! ~& F5 [+ X: z; S6 J
logic age of 16 months (advanced).5 Chromosomal3 I" `5 z5 g4 s5 ?) _1 j. u n
karyotype was 46XY. The thyroid function test
$ C7 D6 y! X% |4 j5 q# j9 @! Ushowed a free T4 of 1.69 ng/dL, and thyroid stimu-
/ y4 {9 I9 ~/ d8 `lating hormone level was 1.3 µIU/mL (both normal).1 M' o4 r' P9 A& C
The concentrations of serum electrolytes, blood& S/ e& s. g( W3 |% ]# B: C, E
urea nitrogen, creatinine, and calcium all were
. W" _2 L, | n3 J4 W1 \* T4 W4 gwithin normal range for his age. The concentration
z, o9 {1 X, v3 u2 D7 ^* kof serum 17-hydroxyprogesterone was 16 ng/dL
+ ?" [/ R9 I5 i# [0 [2 E(normal, 3 to 90 ng/dL), androstenedione was 20/ k9 O$ t Y9 [8 C0 r6 S
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
: t& H% o m& z. s) z/ Xterone was 38 ng/dL (normal, 50 to 760 ng/dL),7 R5 N9 O$ |. i- M7 R: O' r
desoxycorticosterone was 4.3 ng/dL (normal, 7 to& Z8 L* z7 W' n$ V$ v2 v2 \8 u2 d
49ng/dL), 11-desoxycortisol (specific compound S)5 B8 ^% N0 O& d$ ^8 T
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* B: p1 J% ]5 U; c
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: w. O ?1 K' l% Ftestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 k" d/ n; Q" Sand β-human chorionic gonadotropin was less than
" a. I( Y; n1 M5 mIU/mL (normal <5 mIU/mL). Serum follicular6 @5 d* D2 a( J6 S6 j r1 ?
stimulating hormone and leuteinizing hormone7 T* w: o. ~ n- b, S( Y$ D3 f
concentrations were less than 0.05 mIU/mL
3 m7 }- Q& E2 R0 B( n(prepubertal).
( s: Z9 {# ~# q: ~( EThe parents were notified about the laboratory
+ L% ?; c( X4 n/ x7 M! Xresults and were informed that all of the tests were$ L# i2 v2 n4 O- e. q
normal except the testosterone level was high. The2 O; a& X2 g" B. S2 l8 c8 t
follow-up visit was arranged within a few weeks to
1 w8 D9 K2 s+ |. Oobtain testicular and abdominal sonograms; how-
2 F2 e" ~4 [/ k7 ^$ m# kever, the family did not return for 4 months.- R7 d- Y, W, h }6 A7 @, w
Physical examination at this time revealed that the
5 _6 R8 O2 p" \7 ?. mchild had grown 2.5 cm in 4 months and had gained8 i& \1 D: Y0 `* l. r- Z: _
2 kg of weight. Physical examination remained
0 u# M$ X) z# Z, p! iunchanged. Surprisingly, the pubic hair almost com-
; _# X! v9 n$ M# W- ~pletely disappeared except for a few vellous hairs at V6 A6 x0 R. @: l2 V/ S, }! w8 c
the base of the phallus. Testicular volume was still 2
* A; C( B$ q1 s. |: G j' {mL, and the size of the penis remained unchanged.
9 v2 W- J9 W4 ]; }2 ?% s. FThe mother also said that the boy was no longer hav-
8 Z! I# i8 W2 G4 L, T; Z( c& P% q$ Eing frequent erections.# u: U) S! m$ `1 W7 V- v
Both parents were again questioned about use of
, s( q& E; T0 m7 m7 {9 \. Qany ointment/creams that they may have applied to# Z7 w; c2 q; [ ?7 Q* A
the child’s skin. This time the father admitted the
2 F2 x0 E- O3 t) X3 cTopical Testosterone Exposure / Bhowmick et al 541! ?' R8 P2 M- r9 x) K# Q* L8 m
use of testosterone gel twice daily that he was apply-
* n& `7 U" K2 t$ iing over his own shoulders, chest, and back area for
4 p3 ?0 H1 F9 k; ^0 O f& r& Ua year. The father also revealed he was embarrassed2 o% p& @) y% j. `7 C
to disclose that he was using a testosterone gel pre-
( T5 E ^" Z) Xscribed by his family physician for decreased libido
0 H1 e0 @% H, \1 E6 ~) `9 bsecondary to depression.
( ~5 o9 ]7 L d9 e l" |The child slept in the same bed with parents.! v! O) H- R1 l- n# c) ?( g Z0 }
The father would hug the baby and hold him on his1 ~ H( K; d* y
chest for a considerable period of time, causing sig-% o; F S& w0 g4 }1 l; J7 U
nificant bare skin contact between baby and father.) \. K5 O$ f& x+ J
The father also admitted that after the phone call,
% b b! @) E: uwhen he learned the testosterone level in the baby" E; b# O6 f; X* O2 t" ?+ S
was high, he then read the product information
h3 @ X; [, l# W' Kpacket and concluded that it was most likely the rea-
Z# A! I$ S4 J e" ]son for the child’s virilization. At that time, they
. G8 c1 _0 P/ V/ A) Xdecided to put the baby in a separate bed, and the
+ l4 c5 z8 ^: _9 h9 z6 {father was not hugging him with bare skin and had4 t6 m& G7 X& Y9 ^6 l
been using protective clothing. A repeat testosterone
. d# }$ g5 g9 T2 e+ Ttest was ordered, but the family did not go to the' U6 E- m. u* J1 K) a) _
laboratory to obtain the test.$ S N0 S, i- V" D/ K7 E
Discussion) l) L, U& |$ ]/ |- V
Precocious puberty in boys is defined as secondary! n, y6 a8 Q( E# N& }# s$ S) I
sexual development before 9 years of age.1,4) m1 V% E/ R. M- z6 E
Precocious puberty is termed as central (true) when9 l1 {8 z W$ |9 ^: p
it is caused by the premature activation of hypo-( u+ \7 s) S2 J1 i- R
thalamic pituitary gonadal axis. CPP is more com-8 I* }$ j4 M* n8 r4 P
mon in girls than in boys.1,3 Most boys with CPP3 W) ^. ? `7 l9 F7 T6 x7 O2 Q& U; s" s2 A
may have a central nervous system lesion that is8 ?' g5 b# d& S7 b# W1 `
responsible for the early activation of the hypothal-
+ j( {4 r- K- b: r3 }3 Q7 namic pituitary gonadal axis.1-3 Thus, greater empha-! ]7 V/ o& ?, d A, M/ s
sis has been given to neuroradiologic imaging in" o1 x, {# C" n. r* k# L5 F: @' C
boys with precocious puberty. In addition to viril-( B, |8 ?9 A- t3 F- P9 v3 }
ization, the clinical hallmark of CPP is the symmet-' X0 ]/ F7 D4 D7 f
rical testicular growth secondary to stimulation by
0 z+ F" o) A1 H1 K0 \$ ]: h& U" Vgonadotropins.1,3 j0 }8 o5 q' c5 k& C, g5 q
Gonadotropin-independent peripheral preco-& }' t2 {5 B1 S, }
cious puberty in boys also results from inappropriate
, q- u. Z3 I8 v9 f& T# c* Handrogenic stimulation from either endogenous or3 a7 C) G8 F- W$ w* k
exogenous sources, nonpituitary gonadotropin stim-
: L8 z: I# K7 @/ W% `ulation, and rare activating mutations.3 Virilizing
* k# O# y9 q- |. A m+ x! ccongenital adrenal hyperplasia producing excessive" b3 P& `1 B, N4 ^5 \
adrenal androgens is a common cause of precocious/ I* e0 E: P- c
puberty in boys.3,4
! s$ \+ _) U: cThe most common form of congenital adrenal. j% B. q* I& g8 j% R* N; {
hyperplasia is the 21-hydroxylase enzyme deficiency.
% P6 l! {6 P3 l4 m, G0 w+ _, a8 l% hThe 11-β hydroxylase deficiency may also result in
c8 F; u8 I( l+ L* _excessive adrenal androgen production, and rarely, x+ X& L/ X I" c! \$ ^
an adrenal tumor may also cause adrenal androgen
& Y8 j4 p6 h6 r0 V5 K' B! S# m/ Hexcess.1,3
/ i8 x% R8 z8 [ v$ K2 Sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: c& l; _! s; j* }0 Z- B542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( i! ]6 X% {$ k% V$ ^6 }: ^
A unique entity of male-limited gonadotropin-
$ r `+ s! w4 P0 |independent precocious puberty, which is also known% f7 ~; x* X {, @( I! Q, `
as testotoxicosis, may cause precocious puberty at a' z# i" p& K$ m3 _8 [
very young age. The physical findings in these boys
% I% A. f$ R9 o' t) D! ?) swith this disorder are full pubertal development,
- C5 G1 Q6 U v7 X; tincluding bilateral testicular growth, similar to boys& ]4 X$ q1 m$ A x6 s# }! x
with CPP. The gonadotropin levels in this disorder
3 k" P; e: U" b" X$ g/ Z/ D; w% Bare suppressed to prepubertal levels and do not show
' w# t& `8 G1 p0 ?pubertal response of gonadotropin after gonadotropin-" J. u, ?( q/ m1 q& }8 P
releasing hormone stimulation. This is a sex-linked
+ {2 c @0 n% V, z* S d0 S0 xautosomal dominant disorder that affects only0 ?; S" v2 x8 J F. I0 `4 @
males; therefore, other male members of the family( W9 j( \" g/ _! v
may have similar precocious puberty.3
+ X' V8 k, g7 O: T6 aIn our patient, physical examination was incon-+ i* i9 ~4 D+ B3 Z
sistent with true precocious puberty since his testi-5 u; n( U& I+ f( A$ L
cles were prepubertal in size. However, testotoxicosis3 Q: r0 e( Q K# a7 B
was in the differential diagnosis because his father
, b5 T5 |- J7 Tstarted puberty somewhat early, and occasionally,
9 L2 J( q9 d& s _testicular enlargement is not that evident in the
5 C, h2 Y$ M' p8 o2 [beginning of this process.1 In the absence of a neg-
6 e0 q8 S( b. }) } ]ative initial history of androgen exposure, our" P; P$ s* D* D7 ~2 C4 ` X
biggest concern was virilizing adrenal hyperplasia,
+ Z, [& u: K$ F3 Heither 21-hydroxylase deficiency or 11-β hydroxylase7 R+ A: M2 I6 t% y; P! L! w, o
deficiency. Those diagnoses were excluded by find-9 n; E# O; ?. c, D# @* D' R
ing the normal level of adrenal steroids.
8 S5 x' U( I' DThe diagnosis of exogenous androgens was strongly- x: T ^" \9 |3 H3 L _! P( y
suspected in a follow-up visit after 4 months because
+ h3 h) b1 M" a! j# I/ ^, Vthe physical examination revealed the complete disap-
7 U5 g! l4 T; ~! S. |$ \' o2 ~pearance of pubic hair, normal growth velocity, and- U w1 h. i' p2 g% P$ I
decreased erections. The father admitted using a testos-( X, n' C/ I& f; w; o
terone gel, which he concealed at first visit. He was" [' h: R* k! c
using it rather frequently, twice a day. The Physicians’
% G# l; l* ~' ~; t# ]9 b$ pDesk Reference, or package insert of this product, gel or# x- G7 \- M- X# {; j# g
cream, cautions about dermal testosterone transfer to
) y0 r2 A' B8 z0 ?7 tunprotected females through direct skin exposure.. a) L, l2 r1 b6 F4 J) C/ p
Serum testosterone level was found to be 2 times the1 u1 T5 r! ~* o0 w3 F
baseline value in those females who were exposed to
8 M, M' U0 V, E- I% Geven 15 minutes of direct skin contact with their male7 p/ B. I! K9 |8 e: `; S( ^( K
partners.6 However, when a shirt covered the applica-- J& y8 {; e: O% j4 D, s8 _9 p- H) M
tion site, this testosterone transfer was prevented.. G7 f* Y, I1 r2 a1 R! g6 `- w
Our patient’s testosterone level was 60 ng/mL,
4 P# N1 v$ T a/ e/ i( _% e: E; zwhich was clearly high. Some studies suggest that
9 X) r# ~9 L* g2 Qdermal conversion of testosterone to dihydrotestos-
; M+ o; p7 S3 }0 K/ vterone, which is a more potent metabolite, is more
/ ` G& R, S! F, |active in young children exposed to testosterone! p( ~9 K9 ?: V7 \/ E* _/ |
exogenously7; however, we did not measure a dihy-8 K: w Y7 ?! \" Y- J* W7 k# r6 w
drotestosterone level in our patient. In addition to: b2 ?% W# k. F0 ?: u8 w
virilization, exposure to exogenous testosterone in& S9 ?) e/ h! a7 S% s- o7 W8 P, s6 X
children results in an increase in growth velocity and) d6 {4 H* J% O4 w, E/ c
advanced bone age, as seen in our patient.
2 t8 v6 |6 {* R" L4 T" L, U7 S% _5 bThe long-term effect of androgen exposure during, O0 z( i; S: Z$ w J
early childhood on pubertal development and final0 Z) k+ h( h d
adult height are not fully known and always remain
1 M" y. p8 m# u- u* F+ c3 Pa concern. Children treated with short-term testos-
; x, f ]% f) r3 K8 a) [# Cterone injection or topical androgen may exhibit some
/ Q% K6 N+ u3 m" [; P6 {acceleration of the skeletal maturation; however, after
3 ^2 M7 y+ N$ ~7 F9 {+ Q# c, Gcessation of treatment, the rate of bone maturation
$ U9 |! z% n5 S' }' ndecelerates and gradually returns to normal.8,9
+ M( _$ |% T3 ]. L; @& |; _ C% MThere are conflicting reports and controversy
6 v* J; s& B4 R0 S4 _over the effect of early androgen exposure on adult g3 ] E$ q- H# G4 c% w/ G
penile length.10,11 Some reports suggest subnormal
$ v& i" n3 J& C* t! `, s! ?6 Dadult penile length, apparently because of downreg-1 k8 K/ I$ [$ d( q
ulation of androgen receptor number.10,12 However,
% y: m# S1 d! s1 \% u0 _/ O2 iSutherland et al13 did not find a correlation between& j; Y, z' R, b, P1 e3 B8 W% t) `' o
childhood testosterone exposure and reduced adult W7 ]: ]3 j$ {- J# X5 q/ c) J/ m
penile length in clinical studies.
" ] l M2 h. s5 |& bNonetheless, we do not believe our patient is/ S/ _. F. d/ q* i$ y$ {1 ]
going to experience any of the untoward effects from
9 }# \6 b- g/ k/ }# S* g* ktestosterone exposure as mentioned earlier because
8 G+ s5 q# i- Q& `! Y5 a f& vthe exposure was not for a prolonged period of time.
7 l8 M% v7 C! N! D$ PAlthough the bone age was advanced at the time of
$ U6 n8 |/ |1 V# D Zdiagnosis, the child had a normal growth velocity at6 L8 r/ _% E7 k2 m" J, T' j4 l" U
the follow-up visit. It is hoped that his final adult# o, f* c# ^3 Q7 J! ?2 Q% h
height will not be affected.
* M4 E) s, E$ a9 T7 a. TAlthough rarely reported, the widespread avail-1 z* H3 t( A. t0 f8 U
ability of androgen products in our society may A& ^! ~5 B2 p/ w7 q& U, H& R
indeed cause more virilization in male or female# Z8 \) @8 I9 j* s }
children than one would realize. Exposure to andro-( V9 S+ _( v- V) [! T0 V9 ]
gen products must be considered and specific ques-/ ?0 l& K9 e! Y& O4 Q8 U
tioning about the use of a testosterone product or% h* b- V9 l: w0 F* {6 H
gel should be asked of the family members during
% {) ?" _: l# b' ~3 e9 P5 vthe evaluation of any children who present with vir-
* Q0 E: F; H# \7 T8 x) K8 Qilization or peripheral precocious puberty. The diag-4 k0 V' t1 w: d1 t
nosis can be established by just a few tests and by
V- o/ R9 s, _7 f: ]appropriate history. The inability to obtain such a% ?# s& O# g/ d- d) O
history, or failure to ask the specific questions, may
! a% {" o6 j l/ Fresult in extensive, unnecessary, and expensive
, S1 O# n" t8 ?3 sinvestigation. The primary care physician should be
2 c+ r. q. s1 l* h; V& laware of this fact, because most of these children' e% I4 S$ R4 u5 S0 Y
may initially present in their practice. The Physicians’" M( V) I, U2 ^8 x1 X
Desk Reference and package insert should also put a
- }3 Y2 {6 m, C6 A2 I3 bwarning about the virilizing effect on a male or! h9 T3 J" _4 Q4 b* m
female child who might come in contact with some-
; v9 a$ I% G8 m! M8 ]9 Wone using any of these products.' n! w* @$ N" `% }) q8 Q1 P5 c
References+ T% h' v* `! J
1. Styne DM. The testes: disorder of sexual differentiation" V) I# ]/ n7 \ `6 {! N4 g# ^* x
and puberty in the male. In: Sperling MA, ed. Pediatric
- v$ R1 ~0 o" t2 tEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; v9 N6 n( ?) C2002: 565-628.; `9 q9 A! I2 d4 L0 y1 l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
) e( a3 d" `0 I, Rpuberty in children with tumours of the suprasellar pineal |
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