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Sexual Precocity in a 16-Month-Old$ B+ g; q. k0 F9 b' V
Boy Induced by Indirect Topical7 _" G( r2 r. w! P O/ L; n- R
Exposure to Testosterone
7 ?8 A# N; `$ b1 T( W5 _2 uSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& k4 p$ f, {+ A
and Kenneth R. Rettig, MD1
9 ?! _; d+ f( v0 T+ y0 E5 C" FClinical Pediatrics
! l. \( _) x$ `Volume 46 Number 6
7 y3 x" ?# p: D! pJuly 2007 540-543. ~( O2 n& U4 P
© 2007 Sage Publications
% K8 C6 j: k; l. u6 E O& c) L10.1177/0009922806296651& y+ u5 H5 n8 K# Q
http://clp.sagepub.com
+ V- l. s- N. |7 E7 R7 `# Rhosted at
) n: e9 _( ?. j! m$ r# n) Thttp://online.sagepub.com; f5 ]1 `" k7 N) _4 x: \1 h
Precocious puberty in boys, central or peripheral,
C$ \# |; B# t* [8 Wis a significant concern for physicians. Central6 y( ]" n! N6 G/ L; _
precocious puberty (CPP), which is mediated
, F& u9 c6 s0 p2 Bthrough the hypothalamic pituitary gonadal axis, has
& ~7 z. u9 \5 C, ea higher incidence of organic central nervous system
7 _' s4 _; x5 K1 n7 o4 N9 zlesions in boys.1,2 Virilization in boys, as manifested
. W2 J t; f ?# m( Y$ E1 `1 U& p+ jby enlargement of the penis, development of pubic) [4 p: J6 U, \+ X/ q, t% N; }; y
hair, and facial acne without enlargement of testi-
' G" u% k: W2 G0 a- ~% Wcles, suggests peripheral or pseudopuberty.1-3 We/ f5 ?7 C5 ]8 |# a" P- C% Z( L4 s" D M
report a 16-month-old boy who presented with the) i3 |5 @8 }5 q: v L# T
enlargement of the phallus and pubic hair develop-$ d* r4 j* y* M0 ^
ment without testicular enlargement, which was due& E5 o# k% a' q7 S
to the unintentional exposure to androgen gel used by
1 J: O, ~ a6 z8 E& {# Q6 ]) pthe father. The family initially concealed this infor-
1 U, f4 j M# y9 ?8 |# ^+ ymation, resulting in an extensive work-up for this
& s1 O$ ^$ g% i/ I! @2 X* Mchild. Given the widespread and easy availability of Z3 G1 { V' ~" D3 ^
testosterone gel and cream, we believe this is proba-
* Q- H+ {4 X; k1 tbly more common than the rare case report in the
. `* c+ v: ^2 k; b! s V% t# j9 k1 zliterature.4# ^4 _; \$ R- }& y9 E0 j- T
Patient Report
$ |6 o9 Q4 x# w; ~1 f" W; N8 zA 16-month-old white child was referred to the
2 D1 i% R2 J. iendocrine clinic by his pediatrician with the concern/ }+ p7 y! M5 ~: t2 j
of early sexual development. His mother noticed
, E! ]/ {& w. X' D* ^0 Blight colored pubic hair development when he was/ i g2 s) ~; }- k
From the 1Division of Pediatric Endocrinology, 2University of: [1 q5 U( s# |& R
South Alabama Medical Center, Mobile, Alabama.
5 g4 I6 Z. t% y4 [9 f* hAddress correspondence to: Samar K. Bhowmick, MD, FACE,
( G B' d9 E s7 oProfessor of Pediatrics, University of South Alabama, College of
2 @$ d. x s& O# ?: L, gMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;& m. q' r9 z; V7 D8 H" _
e-mail: [email protected].
$ d# ]2 G! S! b6 z6 oabout 6 to 7 months old, which progressively became
6 S- }1 p* b. ?2 T+ D' ?7 Sdarker. She was also concerned about the enlarge-
, L/ b* Z& _" J& U% Mment of his penis and frequent erections. The child8 W, n# y9 L$ _$ d! `: W5 h
was the product of a full-term normal delivery, with5 q3 C) c0 \8 [; I1 h8 K
a birth weight of 7 lb 14 oz, and birth length of( X7 F% T! U% L; D0 `; f& ~
20 inches. He was breast-fed throughout the first year
$ A( T! @6 Z& W. ^of life and was still receiving breast milk along with
$ q v9 e3 Y% R6 nsolid food. He had no hospitalizations or surgery,* ?" k6 o% g" @. v) d
and his psychosocial and psychomotor development. p+ V; p% W, h( J& `" I- Q
was age appropriate.
; u {4 _6 h: P; X ]The family history was remarkable for the father,: r: O; M0 S2 g; L
who was diagnosed with hypothyroidism at age 16,9 K) t, q8 R+ x/ E; y2 z' m
which was treated with thyroxine. The father’s
3 d! v& d' X* _! L+ ]height was 6 feet, and he went through a somewhat
9 G$ C* n" j8 U2 Q: Aearly puberty and had stopped growing by age 14.3 r# D _- \7 i# |" t j
The father denied taking any other medication. The+ d+ ]" Z# }! }$ i; }
child’s mother was in good health. Her menarche) O; _) |! O. H% n& G5 Y0 O# K/ s k
was at 11 years of age, and her height was at 5 feet
# f( z7 h; ~2 l! ~3 X( g5 inches. There was no other family history of pre-. Q$ Q0 c1 P7 p
cocious sexual development in the first-degree rela-
# G6 f* ]% Y5 h" M' D2 b7 v4 [+ otives. There were no siblings.
. |, D$ i" p3 _9 m! x# ~7 NPhysical Examination" \2 G x7 y* j8 \
The physical examination revealed a very active,( r2 P6 I& T- A# D
playful, and healthy boy. The vital signs documented
1 ^0 K/ A: A9 N/ h8 b9 O0 c, wa blood pressure of 85/50 mm Hg, his length was
& D6 ?$ K( U) w9 N90 cm (>97th percentile), and his weight was 14.4 kg& G% ^, L4 K- D, e- P3 b
(also >97th percentile). The observed yearly growth; U) W! J5 ~2 u8 @
velocity was 30 cm (12 inches). The examination of
/ C: ]0 J" f9 `+ k5 K, Ethe neck revealed no thyroid enlargement.7 h' `& `( a. k2 l6 r6 h) @. d
The genitourinary examination was remarkable for
( i5 r j9 A2 A, }enlargement of the penis, with a stretched length of* o& q& `' `4 U) b( x D2 m9 [3 J2 g
8 cm and a width of 2 cm. The glans penis was very well
( k [) P- L4 w$ g7 G" W6 kdeveloped. The pubic hair was Tanner II, mostly around2 s8 C9 ~- u1 {4 [: E: T
5405 c+ |2 C q% p; W# [* Y/ N2 y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: x! ]) ~. e0 w. J/ p
the base of the phallus and was dark and curled. The
( p; j4 I2 S! `* htesticular volume was prepubertal at 2 mL each.
7 \7 d4 p5 w- y+ x1 v# UThe skin was moist and smooth and somewhat$ l6 j: a# w7 M$ D
oily. No axillary hair was noted. There were no
- ]0 T4 O; H X, ] Rabnormal skin pigmentations or café-au-lait spots.- ?, q9 I( X5 O8 |3 Q
Neurologic evaluation showed deep tendon reflex 2+
, p7 Z: z; d# p$ p/ e) abilateral and symmetrical. There was no suggestion
1 Z& V7 C# J4 j* [3 v. P- ]' F. Bof papilledema.* e; e, g0 k: z Y( ]
Laboratory Evaluation: c9 g2 c2 z. e, {
The bone age was consistent with 28 months by
, z; c+ m% m, g5 Q$ jusing the standard of Greulich and Pyle at a chrono-4 h; `: ?! w2 d6 q' R
logic age of 16 months (advanced).5 Chromosomal7 `1 R! E* _% N; k2 e
karyotype was 46XY. The thyroid function test
2 S! `* q" W% s5 ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-7 }: {0 n3 J$ `0 ]0 ?5 a/ I
lating hormone level was 1.3 µIU/mL (both normal).: L1 [: A5 e' {7 p
The concentrations of serum electrolytes, blood
) R: m" @) ^3 H Turea nitrogen, creatinine, and calcium all were+ D. c" X' |8 J5 Q$ |
within normal range for his age. The concentration7 \0 g) {% F( p* @& ^
of serum 17-hydroxyprogesterone was 16 ng/dL) s0 H4 ^4 Q$ U! r6 p
(normal, 3 to 90 ng/dL), androstenedione was 20& W0 W" C7 Y- x
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
: U: g4 G& m2 V% Iterone was 38 ng/dL (normal, 50 to 760 ng/dL),. e2 D: H% M. a
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
- m+ B8 ?1 F3 Q! Y" J2 r49ng/dL), 11-desoxycortisol (specific compound S)
* {4 L' a7 o+ \! P5 G1 ?was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
/ p6 B2 Q; I* m; V/ Etisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
# l, E. {; U9 c# }4 `testosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 O' r( d; T( v. U7 @) _3 H6 Y
and β-human chorionic gonadotropin was less than: y+ o+ V+ @% F* {, B. z
5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ ^7 B Y/ t9 W4 Mstimulating hormone and leuteinizing hormone
6 k0 v6 |3 k% E1 |+ J* N+ A1 Yconcentrations were less than 0.05 mIU/mL0 N$ _. S" f; i, j: _
(prepubertal)., @0 X8 S' t0 X2 T3 j& \
The parents were notified about the laboratory' I( h! L+ ^2 u1 e
results and were informed that all of the tests were$ h0 x, n( m7 g
normal except the testosterone level was high. The
7 U. V: x7 }9 e" Y' S$ Vfollow-up visit was arranged within a few weeks to
$ i+ t2 q) L4 \obtain testicular and abdominal sonograms; how-
- f4 I0 k5 c' C9 i& gever, the family did not return for 4 months.3 z# G, M" p1 i- I, ]4 u3 T+ K3 q2 ~
Physical examination at this time revealed that the
/ L* _! ^' G4 M2 ]4 a9 D& }child had grown 2.5 cm in 4 months and had gained
1 o& O) U( b* O: D" x8 k0 e2 kg of weight. Physical examination remained- r% R6 o e# [) t
unchanged. Surprisingly, the pubic hair almost com-# {4 E) H$ B/ ?( S, b
pletely disappeared except for a few vellous hairs at
) H* }" ?2 K' }. b; f3 C9 p9 Xthe base of the phallus. Testicular volume was still 28 [7 j! _ M' q& ]5 R' M
mL, and the size of the penis remained unchanged.) |* Z6 w6 g6 B( |0 w# Z& R1 Q# i
The mother also said that the boy was no longer hav-
7 Z3 j& b# u1 H& Z" q; wing frequent erections.
8 W6 w% q$ w" X- f0 OBoth parents were again questioned about use of& i! O6 n/ ?* r' P' H1 O( y
any ointment/creams that they may have applied to6 z7 a6 F. V& j1 Q) {0 J
the child’s skin. This time the father admitted the
0 m3 H" I+ b( `) c! f4 n/ s3 [# H+ bTopical Testosterone Exposure / Bhowmick et al 541
0 [2 H( O: M; X) Kuse of testosterone gel twice daily that he was apply-1 o) e" Z" M7 I) x# E2 d
ing over his own shoulders, chest, and back area for
) h4 p) Y I' c) t0 D2 Ga year. The father also revealed he was embarrassed
$ d7 |4 {+ p4 F' Pto disclose that he was using a testosterone gel pre-
- a/ ? r- ~. I9 cscribed by his family physician for decreased libido% w9 I% {6 A! ^* a- t7 h" Z
secondary to depression.
# m% t8 B0 G& h$ ]0 E B5 y* [The child slept in the same bed with parents./ U( z0 d3 W( \$ p) l
The father would hug the baby and hold him on his
5 i2 T; e) E+ Q3 dchest for a considerable period of time, causing sig-
1 S2 x/ s1 P& Bnificant bare skin contact between baby and father.7 {& _( I4 F0 h/ T3 ^
The father also admitted that after the phone call,
4 m" c% K R0 D% ~! T2 Awhen he learned the testosterone level in the baby0 {2 O2 D I: Q1 E. z1 Z# I: M
was high, he then read the product information
4 z# T6 w3 Q8 J, w4 H8 Npacket and concluded that it was most likely the rea-
% m- }& V* B! N* W- o! _$ gson for the child’s virilization. At that time, they
S3 H' y* U, C! B% n" f8 ~% ^decided to put the baby in a separate bed, and the8 E( Q* P1 L7 x, n6 Q3 S8 d. Z$ A
father was not hugging him with bare skin and had: r% u) I+ j/ ]8 b! l! z# Q
been using protective clothing. A repeat testosterone
0 F+ x! Z) b5 |1 P. ztest was ordered, but the family did not go to the+ c0 |" z& r, V! E4 g
laboratory to obtain the test.
% o$ [( R. @) {0 xDiscussion( ?! B$ z! i* _* o; W: ], W4 _
Precocious puberty in boys is defined as secondary
) H) ]; G9 n; A; ]( i" j% U( ksexual development before 9 years of age.1,41 V$ L6 I6 q" R- Z$ ^
Precocious puberty is termed as central (true) when# ^6 L, r2 d( ]6 v$ P; @
it is caused by the premature activation of hypo-- M7 W) | D. V" k( s1 c4 f: y0 L
thalamic pituitary gonadal axis. CPP is more com-0 [+ w2 P8 R& @, l
mon in girls than in boys.1,3 Most boys with CPP! {2 v0 B# g! X* Y! e) y- |
may have a central nervous system lesion that is
3 Y0 o2 A/ Q' H) Y2 u4 v$ @2 j2 Nresponsible for the early activation of the hypothal-
% T' B0 o7 n4 _4 t0 k; b4 gamic pituitary gonadal axis.1-3 Thus, greater empha-
! z9 Z' d9 Y2 d/ csis has been given to neuroradiologic imaging in
% d, y4 Y8 B! ~% Fboys with precocious puberty. In addition to viril-# e. }1 y4 M6 V* [2 d* M
ization, the clinical hallmark of CPP is the symmet-
7 l( V- f& @4 j! F9 v/ Grical testicular growth secondary to stimulation by2 b; r2 K# a" N$ C3 _! W
gonadotropins.1,3
. \0 t& e3 x1 a' H7 u2 {! GGonadotropin-independent peripheral preco-* `7 f+ K: |5 G* o& p
cious puberty in boys also results from inappropriate1 A* r Q' _2 \; ]. S$ E+ o
androgenic stimulation from either endogenous or: J# `: {, M. x, m/ A
exogenous sources, nonpituitary gonadotropin stim-
- g# o7 w, F7 }ulation, and rare activating mutations.3 Virilizing
$ K. I. u/ w* h( ccongenital adrenal hyperplasia producing excessive& ^( q! h$ k& X. j% M' E! K. I) J: S
adrenal androgens is a common cause of precocious- Z( x4 ], @; f" X- O
puberty in boys.3,4
q9 U- s5 \. Y! F T% |The most common form of congenital adrenal& L6 L1 u# s! C# I& d4 a+ @
hyperplasia is the 21-hydroxylase enzyme deficiency.. g7 ~5 Y4 I( M
The 11-β hydroxylase deficiency may also result in
- M: J* L9 B& d- ^excessive adrenal androgen production, and rarely,
* \( G* O0 _3 L, _9 ran adrenal tumor may also cause adrenal androgen
# ]+ g8 P% {$ }2 yexcess.1,3& ^- W6 J- O" O' F+ ] C0 u
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 Z& F+ r& ]; m542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* f+ k5 `7 A- U
A unique entity of male-limited gonadotropin-
% i, F( n- e. J- Hindependent precocious puberty, which is also known4 g1 [) ?/ b0 T2 Q) l
as testotoxicosis, may cause precocious puberty at a' b6 q& V3 F' b( x$ x4 c" ~, o6 e) U
very young age. The physical findings in these boys& G. q. j; p- o- d% F; a5 X z
with this disorder are full pubertal development,
, D7 o6 w/ ]2 `( B# Xincluding bilateral testicular growth, similar to boys
+ V5 G0 ^ ^$ A: l8 J% x3 Z, ~with CPP. The gonadotropin levels in this disorder
% R9 @( f' b' N% q H6 vare suppressed to prepubertal levels and do not show
6 m+ M6 E' e8 ^. B! \pubertal response of gonadotropin after gonadotropin-: G+ t/ g3 I! t& r" I; L8 {; m# N' m
releasing hormone stimulation. This is a sex-linked
+ |: F3 S- M3 _2 Oautosomal dominant disorder that affects only
, `2 Y# u4 k; l2 Wmales; therefore, other male members of the family
) [9 ~+ ^; n, ^& w2 Q& r3 emay have similar precocious puberty.3
* b+ `% z9 p. U! E& C( CIn our patient, physical examination was incon-# Q! \: L) O# g% t
sistent with true precocious puberty since his testi-3 p6 I9 f" x& \: M3 D. A
cles were prepubertal in size. However, testotoxicosis/ Q5 {4 b. a) }! i5 ^1 ]0 {
was in the differential diagnosis because his father7 u' j2 o S6 z0 M6 f8 d. u
started puberty somewhat early, and occasionally,5 A( i5 x# @. b& g
testicular enlargement is not that evident in the
2 n9 i6 |8 s8 ~* r3 V6 x4 f7 I' Jbeginning of this process.1 In the absence of a neg-
8 X9 H8 _# a( N2 M; n3 [ative initial history of androgen exposure, our
7 w6 \1 o; u5 |( C4 L# ^; W' x1 A6 fbiggest concern was virilizing adrenal hyperplasia,
) B* A7 }( s) @; K/ Jeither 21-hydroxylase deficiency or 11-β hydroxylase" M1 ^; o; }% ^, p
deficiency. Those diagnoses were excluded by find-
7 {0 ?8 O$ d4 s: D" Ying the normal level of adrenal steroids.
# B, Q, q& A4 x5 ~* \The diagnosis of exogenous androgens was strongly
2 Z; {, g7 p( W6 c1 X( p! D8 Ususpected in a follow-up visit after 4 months because
# _1 C8 h( |: {* Dthe physical examination revealed the complete disap-0 s9 u+ ~* Y# `2 z# Q, C2 b& D0 V
pearance of pubic hair, normal growth velocity, and2 H) E8 n9 @- r/ V3 e5 W* e8 a
decreased erections. The father admitted using a testos-
# @& K0 W" ?3 h9 F9 {7 G7 B* xterone gel, which he concealed at first visit. He was
; n W# J, Z+ m( X, D& Dusing it rather frequently, twice a day. The Physicians’
, f$ d; |3 Q, H6 xDesk Reference, or package insert of this product, gel or% q. s" ?7 K# A7 L8 L
cream, cautions about dermal testosterone transfer to, f3 Z- g& |: M: N
unprotected females through direct skin exposure. H9 {* E5 K! c2 O
Serum testosterone level was found to be 2 times the4 H2 k9 H K- A" ]8 E2 P) l) O1 T
baseline value in those females who were exposed to
+ N9 j" E' S0 m- q; F7 _even 15 minutes of direct skin contact with their male) X. B3 E$ i3 [; W0 \. \+ ?
partners.6 However, when a shirt covered the applica-
1 p2 t5 Z- l3 k$ I% Ction site, this testosterone transfer was prevented.% h% O0 I& A7 E. `* _( k3 M, \9 c
Our patient’s testosterone level was 60 ng/mL,. e0 }& P" q I9 B- T0 g
which was clearly high. Some studies suggest that( o: T9 N! q& ?% t" D* r; {" s, g
dermal conversion of testosterone to dihydrotestos-
! H- {! _; b% j5 `5 ]- c6 }: _% ~terone, which is a more potent metabolite, is more3 }/ V3 @3 t7 P* M) [. w
active in young children exposed to testosterone
( U; i e# ^; k, \: P" wexogenously7; however, we did not measure a dihy-
; x/ {. z! x4 k* N; u7 mdrotestosterone level in our patient. In addition to; P$ ?+ m- h' y1 r
virilization, exposure to exogenous testosterone in
, J1 E6 ~0 x# y% s5 A6 xchildren results in an increase in growth velocity and; V) E/ u$ W0 B
advanced bone age, as seen in our patient.: U, x' |) e" {7 v- S; I- P: v: w
The long-term effect of androgen exposure during
( \9 @8 N, K4 w7 h7 ?1 p0 ?0 learly childhood on pubertal development and final
, W2 c Z( R0 M$ L$ a" F' b7 Uadult height are not fully known and always remain7 A* f) ^# ]! w8 Y4 M1 k
a concern. Children treated with short-term testos-
8 C6 g* Q1 Z' f9 ?4 X3 q2 h) sterone injection or topical androgen may exhibit some& y! t) }$ E+ c& [" ^7 b
acceleration of the skeletal maturation; however, after
+ }5 T0 O8 _/ }$ `" [cessation of treatment, the rate of bone maturation
* \+ p8 L$ e. w3 v4 m$ h( Tdecelerates and gradually returns to normal.8,90 e U$ `8 d3 ]0 { G, ~
There are conflicting reports and controversy
/ l% F( z0 {: ?/ oover the effect of early androgen exposure on adult
/ D Y7 n. h7 c! k6 k6 cpenile length.10,11 Some reports suggest subnormal0 n! O' G* N: ]; I2 }5 b( p: t
adult penile length, apparently because of downreg-
" X+ K. k$ z: B3 c5 r& H/ hulation of androgen receptor number.10,12 However,
3 j/ G X! r$ N H& S& V% q; cSutherland et al13 did not find a correlation between( X7 ?4 i7 {: a$ @- J+ S4 @/ t! |5 z
childhood testosterone exposure and reduced adult
! U% \) K# n' Fpenile length in clinical studies.
4 J8 y7 ~7 {0 I- oNonetheless, we do not believe our patient is+ L& w$ E; q, I9 b. h; q' O) r: L
going to experience any of the untoward effects from
5 |, ^8 K- t+ q/ _testosterone exposure as mentioned earlier because
1 C: V3 V# `6 q- @8 w3 qthe exposure was not for a prolonged period of time.% r: ~6 }8 F7 e- S( j' K
Although the bone age was advanced at the time of! W% r! T) `4 m: i/ w' r9 s" ?
diagnosis, the child had a normal growth velocity at6 v2 p' P% S& M
the follow-up visit. It is hoped that his final adult5 n" V0 v% G( Y6 k2 Q
height will not be affected.9 j$ g( E& ?9 Y- p1 [
Although rarely reported, the widespread avail-% |7 L$ u8 U: }% W5 E( V' T
ability of androgen products in our society may. z' W& H/ E$ b. ?' x) f
indeed cause more virilization in male or female
) V% n/ c1 }2 ^7 V2 h5 |children than one would realize. Exposure to andro-' A! u7 U. s$ y' s" A' n
gen products must be considered and specific ques-
4 H. T8 s$ c0 Y( ]/ R3 Xtioning about the use of a testosterone product or
$ x% |9 A+ G4 }: M* M, Rgel should be asked of the family members during( X6 |5 |2 K( F1 U- [+ _
the evaluation of any children who present with vir-
, c+ I/ \* f, d$ U Gilization or peripheral precocious puberty. The diag-: |. K4 M* L4 {5 W
nosis can be established by just a few tests and by
/ {9 k4 _: O2 j6 X X, U4 A. b2 tappropriate history. The inability to obtain such a
- T7 E" x) |9 m+ g2 h6 O: zhistory, or failure to ask the specific questions, may
R+ O2 W/ \* X ~9 t* Presult in extensive, unnecessary, and expensive
; f6 u( l0 F" m5 K- V7 o+ U# Qinvestigation. The primary care physician should be
, u- o, {5 m+ S" E/ f, raware of this fact, because most of these children
x# o6 w/ z4 Kmay initially present in their practice. The Physicians’
U! a! a; i8 {" j4 @; g* PDesk Reference and package insert should also put a8 ^5 Y$ o/ P# L* ], K* j; t2 C
warning about the virilizing effect on a male or
; i8 h2 P! |" P' Jfemale child who might come in contact with some-& i$ B8 d D: W9 O& W7 r9 p- t
one using any of these products.
6 Y4 C+ r: b) `& F9 MReferences; I* C5 S) k+ c- d! H$ b
1. Styne DM. The testes: disorder of sexual differentiation
3 _3 Z' p# j+ E5 a! gand puberty in the male. In: Sperling MA, ed. Pediatric
) t& X" p/ N+ l! z$ }9 lEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) s' K( z6 j' q3 c8 b
2002: 565-628.
7 |( h& X. n) B* g4 o1 ^. _ a2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 ~% L: B0 o5 J8 Z* V0 Y! jpuberty in children with tumours of the suprasellar pineal |
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