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Sexual Precocity in a 16-Month-Old& i3 g4 n1 l+ D' b E, b
Boy Induced by Indirect Topical
2 m" J) t* U* m1 k# oExposure to Testosterone
6 Y1 J, h3 a, J' }$ ?Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 e( \+ W6 R) j
and Kenneth R. Rettig, MD1; F' v% N$ ~9 z) _5 i
Clinical Pediatrics# G3 o* Z3 m1 d9 H2 A7 l! x6 j
Volume 46 Number 6
! \( T( q& V: [7 c C" I1 c9 ?July 2007 540-543* w; S9 x. O8 s0 \/ N
© 2007 Sage Publications
5 ?/ L8 L; K4 b/ J5 Z8 l8 b( \+ m10.1177/0009922806296651) \1 ?/ K5 ?' R9 r
http://clp.sagepub.com
9 W. g. v D9 C) [5 l* mhosted at. w9 q; i) a- F$ f
http://online.sagepub.com
9 ?) i$ e( S% m5 Q0 nPrecocious puberty in boys, central or peripheral,( s `3 d6 k9 V l6 a/ {: G" T
is a significant concern for physicians. Central4 B: b8 ?; t/ \; B7 N3 o2 \
precocious puberty (CPP), which is mediated% E% z& C- y! Z' _. z; D( ]
through the hypothalamic pituitary gonadal axis, has
8 f, g4 l/ R4 |/ w# ]a higher incidence of organic central nervous system4 e, J- ?4 n6 R9 x0 K* u |8 a
lesions in boys.1,2 Virilization in boys, as manifested/ `' o1 T1 x6 I6 L3 z# _- w J; b
by enlargement of the penis, development of pubic
9 \& h0 x' \2 \1 [. zhair, and facial acne without enlargement of testi-
' d) J9 o4 L, ^7 y2 rcles, suggests peripheral or pseudopuberty.1-3 We7 G+ L! s) o& ]6 H4 n g. ]9 {& V! r
report a 16-month-old boy who presented with the
1 w* _# e" ]0 _' l/ [enlargement of the phallus and pubic hair develop-: d) q0 u( D" l# A1 Y# W
ment without testicular enlargement, which was due, y% e- v- m* n
to the unintentional exposure to androgen gel used by+ f( X9 `: B) M+ H' |
the father. The family initially concealed this infor-
$ U4 Z( k2 H/ C. X6 B4 nmation, resulting in an extensive work-up for this3 I+ K, c' Z' O, i- N y7 s$ u* E
child. Given the widespread and easy availability of S7 J. _) y' M0 x$ b
testosterone gel and cream, we believe this is proba-8 k+ E0 X8 J. Q# k4 `/ y
bly more common than the rare case report in the/ h9 x7 u5 v# Y( [
literature.4" l" O. T" I+ g" @' \
Patient Report% j6 n# ?& l( S& l3 ?2 J
A 16-month-old white child was referred to the3 A% ?# p3 q0 Z, j" ^3 }: ?
endocrine clinic by his pediatrician with the concern( Y, ]# b7 F/ V6 }& B# }
of early sexual development. His mother noticed' A3 b8 Y+ n0 q
light colored pubic hair development when he was, T2 i6 `3 N- d0 D! A7 ]' E. y0 l
From the 1Division of Pediatric Endocrinology, 2University of
3 O+ e1 }. x4 q# x4 h8 N4 Z# q6 L7 ^South Alabama Medical Center, Mobile, Alabama.
0 h+ O& u6 F$ ]- kAddress correspondence to: Samar K. Bhowmick, MD, FACE,
* h$ X, s5 r f, J) o" uProfessor of Pediatrics, University of South Alabama, College of
6 r% s7 l& v/ iMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) I/ }0 }. ]3 X' D! f) z& V' ]e-mail: [email protected].
i) T9 ~: u6 W0 R* Xabout 6 to 7 months old, which progressively became
3 _. l3 z& K5 ]( a, f: W, c4 H5 jdarker. She was also concerned about the enlarge-, @7 k; y) ?* r# i! ]. w
ment of his penis and frequent erections. The child# e6 L- v- V i9 g
was the product of a full-term normal delivery, with
' V% |( V- o6 f: Z& p% Ua birth weight of 7 lb 14 oz, and birth length of* M a7 s% y2 }1 d9 u
20 inches. He was breast-fed throughout the first year( l ~. E: [' v$ \
of life and was still receiving breast milk along with3 v) \7 O; z4 [! L4 U
solid food. He had no hospitalizations or surgery,& v8 P6 |" c/ Q" h
and his psychosocial and psychomotor development& c4 ?# V- o+ H5 L. ]/ T
was age appropriate.
' Q: D9 B5 A" DThe family history was remarkable for the father,! t. D- f6 [# ~
who was diagnosed with hypothyroidism at age 16,
: N2 g0 v7 t: r) Fwhich was treated with thyroxine. The father’s
# {0 m1 w. q# X9 `height was 6 feet, and he went through a somewhat6 P$ J5 z) n. |. i9 T
early puberty and had stopped growing by age 14.1 j) U3 ~! s. c; o; Q
The father denied taking any other medication. The
# m) C1 W: o5 @! I' O2 Gchild’s mother was in good health. Her menarche: f$ i) f0 e4 W. W& l- J$ E" @' O. R
was at 11 years of age, and her height was at 5 feet& K8 T/ ~ \1 J# l1 n2 v
5 inches. There was no other family history of pre-
( H' @( X6 C" D" H& A5 Q5 s/ U8 kcocious sexual development in the first-degree rela-
`) O6 D8 Y, ~; K3 I E7 `) stives. There were no siblings.0 C5 G% O" I& w: I2 ` C" m: K9 j
Physical Examination
! C/ J9 b1 W. tThe physical examination revealed a very active,
+ p- }; J7 p+ x, |2 P( }) tplayful, and healthy boy. The vital signs documented
2 p% j) F! s4 O f8 ~% w- A9 L* ia blood pressure of 85/50 mm Hg, his length was
9 D' ~& V7 R0 o2 F/ [3 G+ @& B, z1 I90 cm (>97th percentile), and his weight was 14.4 kg8 F6 a, c3 ]% e- C) u2 @
(also >97th percentile). The observed yearly growth
3 Z4 P$ T: m2 fvelocity was 30 cm (12 inches). The examination of
7 G6 C: S* r, `8 |# u: ?7 qthe neck revealed no thyroid enlargement.
7 c: \ o& Y" v; N1 K* ^& d! _The genitourinary examination was remarkable for" M$ U: ` M! ~
enlargement of the penis, with a stretched length of
- V6 V5 m8 _- E# a# ~! b1 A8 cm and a width of 2 cm. The glans penis was very well% P. ~) v7 C9 S' w3 k: K& m
developed. The pubic hair was Tanner II, mostly around
8 A9 w; T6 u6 x( v' x4 F" r540
0 ]$ ?6 o" ?! s' z; X0 }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( ~+ G' F; O! R8 L( `
the base of the phallus and was dark and curled. The; C- `. q9 {, O* c
testicular volume was prepubertal at 2 mL each.
8 r' @7 l. L9 ?/ b: D5 k* D p+ | jThe skin was moist and smooth and somewhat
4 L V' _2 r! E( _oily. No axillary hair was noted. There were no/ G7 B8 }) N* [2 A/ w3 I
abnormal skin pigmentations or café-au-lait spots.
; | s( U. O+ ^: \ t( i: b( p/ o/ uNeurologic evaluation showed deep tendon reflex 2+
6 c0 Z( O/ p! Ibilateral and symmetrical. There was no suggestion
3 o" W U1 _% a. Vof papilledema.. u7 [, d. h5 p6 ~8 F
Laboratory Evaluation
( [$ H& B' o4 |The bone age was consistent with 28 months by
- i# Q2 w" D( l% C5 g0 ^2 Qusing the standard of Greulich and Pyle at a chrono-5 A/ N' E& D6 }' p3 J0 b( p
logic age of 16 months (advanced).5 Chromosomal5 W: d3 f0 y2 {: g3 d; ]+ {
karyotype was 46XY. The thyroid function test& C) I! N y) y0 ~
showed a free T4 of 1.69 ng/dL, and thyroid stimu-; h. a& Y+ W' u* u
lating hormone level was 1.3 µIU/mL (both normal).: N) O7 Y" |! b8 G- c. y
The concentrations of serum electrolytes, blood
+ U0 v e1 N( J* A( o9 c; o Ourea nitrogen, creatinine, and calcium all were
: U& O" X- S. U( `/ wwithin normal range for his age. The concentration, e2 ^9 e9 p8 |+ q
of serum 17-hydroxyprogesterone was 16 ng/dL
8 J, p$ j/ q5 l9 O5 [(normal, 3 to 90 ng/dL), androstenedione was 20
2 F: }" e; I& @& {! {ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& k$ E7 }' n) l+ n, L7 x7 l! @terone was 38 ng/dL (normal, 50 to 760 ng/dL),$ t* h9 E& I* s: E: V$ _$ s7 J/ J
desoxycorticosterone was 4.3 ng/dL (normal, 7 to" c% y! f- A: V0 x: N1 Z/ J
49ng/dL), 11-desoxycortisol (specific compound S)6 g) e2 B; C" X, r8 J
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. v& {; H8 s" P1 t0 \9 e; _: Ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" M. g$ P" |' y* E5 _testosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 r( H4 y) b2 ~
and β-human chorionic gonadotropin was less than
& ?) X7 l& o9 Q3 ?" P, q @9 X5 V5 mIU/mL (normal <5 mIU/mL). Serum follicular
! l7 H( ~1 ?1 Z( ~. g, y) Ustimulating hormone and leuteinizing hormone
& ^/ @0 A) ~6 J% N3 y8 G! n0 H- t+ j: Hconcentrations were less than 0.05 mIU/mL
j- o% n7 T) _(prepubertal).
# t$ m: h2 y! P: @9 u, c7 gThe parents were notified about the laboratory# \* F7 Y: M: z6 D+ l. l
results and were informed that all of the tests were
0 q; a( u+ d* B# r7 Nnormal except the testosterone level was high. The# X/ ~. x6 u$ e
follow-up visit was arranged within a few weeks to9 q' t# s# M$ A# V( p3 Y m
obtain testicular and abdominal sonograms; how-
2 p' q( ?3 y3 Y4 p% x5 K; x Eever, the family did not return for 4 months.
* Q* ~9 H" s/ F. i9 K- [Physical examination at this time revealed that the% B Q/ k, d- D9 q% g1 F# l
child had grown 2.5 cm in 4 months and had gained
7 N/ r5 r9 {& U" j$ p2 z Z( E# q2 kg of weight. Physical examination remained$ q% t- x. y& _/ x6 d6 c
unchanged. Surprisingly, the pubic hair almost com-6 @7 E$ r6 d; Z" i4 n0 K
pletely disappeared except for a few vellous hairs at0 e* w* Q q' a X3 I8 b, q
the base of the phallus. Testicular volume was still 2
1 K5 \0 H6 o& e5 @& u( |" ~4 o) TmL, and the size of the penis remained unchanged." }8 ^) O! ], M
The mother also said that the boy was no longer hav-
f7 W) y: r/ S% |ing frequent erections.% L9 ^0 q+ T# }+ \0 a
Both parents were again questioned about use of
$ B$ ?1 h7 ?6 h7 V$ d Qany ointment/creams that they may have applied to
# k3 ~1 A2 ?* Uthe child’s skin. This time the father admitted the
' W! R2 _0 W. a( y. V* GTopical Testosterone Exposure / Bhowmick et al 541
' ]1 i* R" ^" `use of testosterone gel twice daily that he was apply-
1 a% T( V; J& X7 \) ?4 \1 }, Ning over his own shoulders, chest, and back area for
2 b* y+ B4 r* z: d+ H; h, h0 ~3 ^# Ca year. The father also revealed he was embarrassed, @6 b( ?! \. O) H% X! |* V# `
to disclose that he was using a testosterone gel pre-
- u, g0 k& j5 f3 [/ Z$ }& k7 Qscribed by his family physician for decreased libido7 n7 o* |3 \. |! F% i2 |1 x# M
secondary to depression.
' t+ n/ ~0 |2 r1 N4 W) G( [The child slept in the same bed with parents., u# D6 y# p# X
The father would hug the baby and hold him on his
+ u- u8 K, I% o1 T B3 y. o) [* P: @( qchest for a considerable period of time, causing sig-
5 C( Z- }5 V3 e7 O! K" unificant bare skin contact between baby and father.
5 y% f# n& t0 P9 GThe father also admitted that after the phone call,! K# f9 v% \# A6 |. J) U) u
when he learned the testosterone level in the baby
6 q8 K* m( C1 C, Y) X, Mwas high, he then read the product information
@8 f* [; `& D+ B5 _+ ]packet and concluded that it was most likely the rea-( t5 @: r+ N' i( ?' }+ P6 z
son for the child’s virilization. At that time, they$ A" f1 X" s# b
decided to put the baby in a separate bed, and the
) n6 p# {- R( Wfather was not hugging him with bare skin and had
6 K+ G8 m: v6 e9 U) e* z! \been using protective clothing. A repeat testosterone4 c9 u& h$ ~ o4 V8 O2 ?
test was ordered, but the family did not go to the) ?& d" \; c \/ J
laboratory to obtain the test.
* ]! {& H( b) G9 V3 ?' z# gDiscussion
: e X( a9 T8 B$ @1 CPrecocious puberty in boys is defined as secondary
3 F" K. @" a* \2 f* bsexual development before 9 years of age.1,4 P" u& u, W2 C3 s1 w
Precocious puberty is termed as central (true) when
2 ^" Y9 l* f$ A K0 Y7 E" @( mit is caused by the premature activation of hypo-
8 o) `6 z( S( _- U& A6 l( n' \thalamic pituitary gonadal axis. CPP is more com-
4 ~; j- g( Y, T. C4 T$ Q- ~mon in girls than in boys.1,3 Most boys with CPP
/ F; E9 v! C# d# ^" I- X8 Q1 h$ `may have a central nervous system lesion that is3 L' J L/ S# R. `2 G: Y
responsible for the early activation of the hypothal-
& S8 ?, N+ Y6 e* J$ `, p3 E7 f% lamic pituitary gonadal axis.1-3 Thus, greater empha-- Q/ v7 i# \4 {* Y4 w
sis has been given to neuroradiologic imaging in
" }" ~/ }) x' iboys with precocious puberty. In addition to viril-" k* W. ~2 C! V8 a: d3 `/ m
ization, the clinical hallmark of CPP is the symmet-
. Z! b) c- T0 T+ V; x: `rical testicular growth secondary to stimulation by* @8 N) u5 a9 b, g% H/ Z
gonadotropins.1,33 ~8 k' e9 P J' Y7 J' p( A
Gonadotropin-independent peripheral preco-% ~# Y% l5 r2 k5 Q4 \; n/ I
cious puberty in boys also results from inappropriate* V3 }9 ]2 M: V1 b5 a" D! D
androgenic stimulation from either endogenous or* m' P9 Z- Q3 j5 i3 L2 y0 t7 Z
exogenous sources, nonpituitary gonadotropin stim-
4 e- ]* X! l* G2 b8 [# xulation, and rare activating mutations.3 Virilizing5 }) n1 W1 v7 M( H% ~9 o. J
congenital adrenal hyperplasia producing excessive
) o! H6 L' |) x+ x7 f; o0 d$ Zadrenal androgens is a common cause of precocious/ B. k8 x. Y5 `/ J3 t
puberty in boys.3,4) z8 r+ a: s1 ]& ^
The most common form of congenital adrenal/ F3 w7 S7 D$ @0 k: ]7 I
hyperplasia is the 21-hydroxylase enzyme deficiency. W i( E3 b8 |( ~ A' ]
The 11-β hydroxylase deficiency may also result in
( _" T- S- r7 g+ r/ r' \excessive adrenal androgen production, and rarely,; c. J; {, y b. _) e
an adrenal tumor may also cause adrenal androgen% ]4 m/ l/ Y) F: r/ x. A# {, g
excess.1,3
r! y/ F( d# r/ ^- O1 w7 x" Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from Q" L4 t+ h/ L
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007% V* r! P7 c4 B5 G* e( _9 v+ |9 C
A unique entity of male-limited gonadotropin-
. r) n9 b7 l4 N3 ]8 T, ~1 Gindependent precocious puberty, which is also known; n2 D) Y, K* P- P4 Y3 U: {: G/ O
as testotoxicosis, may cause precocious puberty at a
3 p; Y& q. I% t( v3 xvery young age. The physical findings in these boys
9 A* n+ |* o, u: h$ W Cwith this disorder are full pubertal development,+ @) c/ L1 l: A: J& Y' L
including bilateral testicular growth, similar to boys' [1 E4 O6 d4 _ ]+ B3 g, L" o" h
with CPP. The gonadotropin levels in this disorder) i1 n4 W7 x% C" ]* m
are suppressed to prepubertal levels and do not show# s. ^$ O4 H _
pubertal response of gonadotropin after gonadotropin-' c% l) U5 L ~; W
releasing hormone stimulation. This is a sex-linked# L$ X. E; a% ^2 ^8 a
autosomal dominant disorder that affects only# p8 g. x. v5 J! U
males; therefore, other male members of the family7 g ]" K1 O# u/ D D4 u! O+ Y
may have similar precocious puberty.3" c( v) g$ A- y @
In our patient, physical examination was incon-$ E6 l9 x6 X8 f$ L: Z: M8 Z+ w
sistent with true precocious puberty since his testi-
9 q5 M0 s' A0 _- fcles were prepubertal in size. However, testotoxicosis
- I9 l: X. F( x: Dwas in the differential diagnosis because his father; l" r0 B! S( A/ o) ^2 I9 a
started puberty somewhat early, and occasionally,
9 P8 H# [3 g' \8 B7 I. b4 Ytesticular enlargement is not that evident in the4 h' H6 z0 L' z/ R+ s- s
beginning of this process.1 In the absence of a neg-
- {0 d) @0 ]9 E3 c* }9 e9 Iative initial history of androgen exposure, our
/ `$ [/ s/ l; _, k2 g+ }" ubiggest concern was virilizing adrenal hyperplasia,
3 P3 I% l8 x, \" ]& e8 reither 21-hydroxylase deficiency or 11-β hydroxylase+ S0 e/ y3 v6 c4 `2 x
deficiency. Those diagnoses were excluded by find-$ G9 C1 q. ]. s8 G8 c
ing the normal level of adrenal steroids.& D- ^/ V- Q9 R2 p4 Y$ l
The diagnosis of exogenous androgens was strongly
@: Y: W* l4 s% x' W6 [/ q$ wsuspected in a follow-up visit after 4 months because/ A! K. ] `2 x- s1 ]' Z9 u
the physical examination revealed the complete disap-
( d3 p7 r5 r1 F9 p! ]. R, y1 jpearance of pubic hair, normal growth velocity, and; q; _3 N0 L1 \7 A. O" Q' c
decreased erections. The father admitted using a testos-3 H7 c4 o7 R7 q2 W" p! v1 l3 F
terone gel, which he concealed at first visit. He was& n R) x9 g- L- B
using it rather frequently, twice a day. The Physicians’7 Y S" Q1 @- U5 E& l
Desk Reference, or package insert of this product, gel or
$ H1 B, G1 e( \cream, cautions about dermal testosterone transfer to
5 @ k7 c* u, D6 A: Ounprotected females through direct skin exposure.
) p- O7 {3 Y, C& N) q$ ZSerum testosterone level was found to be 2 times the" Y" ?. `4 [$ _
baseline value in those females who were exposed to
8 d6 J" [' n: ]even 15 minutes of direct skin contact with their male) w c# J; `, V# e4 B" ~ L& a
partners.6 However, when a shirt covered the applica-5 s% c( V. U' p' Z! C
tion site, this testosterone transfer was prevented. x& K+ F" N+ b" `6 B) g+ J9 d0 _
Our patient’s testosterone level was 60 ng/mL,( l N2 r2 _8 { {4 c. V. y# x6 g
which was clearly high. Some studies suggest that
" z+ o2 a5 i, c- H9 @5 r0 K* S" zdermal conversion of testosterone to dihydrotestos-
: m/ e, q- g7 u3 `terone, which is a more potent metabolite, is more7 e6 J; r) o) i p4 X3 f! s: b& }
active in young children exposed to testosterone
7 N- [/ O ?5 l- f/ Uexogenously7; however, we did not measure a dihy-
4 ]/ _2 c8 d& Y+ h [drotestosterone level in our patient. In addition to# |! k% B2 s7 m
virilization, exposure to exogenous testosterone in
- d( r6 i# _0 |, d. ~# \1 E# tchildren results in an increase in growth velocity and0 v; I9 }' ~' W; z6 ]6 y9 b, K1 U
advanced bone age, as seen in our patient.
' z/ ?( w- {2 m7 n% V0 KThe long-term effect of androgen exposure during
( F5 _6 O$ Z" E' @, learly childhood on pubertal development and final
2 {* u) n) ]5 x- \ yadult height are not fully known and always remain
* j! M' i8 C: z( ~/ A5 D$ |% Ya concern. Children treated with short-term testos-
5 ^# E) f4 A/ W9 jterone injection or topical androgen may exhibit some
* l& {% ]1 y7 W# Z) ?acceleration of the skeletal maturation; however, after1 [. V* f p, l* _
cessation of treatment, the rate of bone maturation! |- P! F0 U, f. v* f
decelerates and gradually returns to normal.8,9
$ k, \2 H K! w1 F) z# `There are conflicting reports and controversy
3 ^* m0 t0 q$ a" @& X, M- Nover the effect of early androgen exposure on adult
! _% {5 m' n* X8 T9 C2 F0 O$ L g2 ppenile length.10,11 Some reports suggest subnormal
3 p3 I) t) e% z6 A$ M- ?adult penile length, apparently because of downreg-
" O+ t% n6 u: K( l3 dulation of androgen receptor number.10,12 However,9 l8 v5 [$ V4 [; S0 e5 ^! O% D
Sutherland et al13 did not find a correlation between+ W% U8 k- W Q/ V$ F( s5 i) M6 P' B: E
childhood testosterone exposure and reduced adult+ \! k' ^. W6 Q N
penile length in clinical studies.# T, _+ t6 V. M2 l* O# S' ^9 S
Nonetheless, we do not believe our patient is
+ u" ?" W7 [. O9 T( [/ i2 Ugoing to experience any of the untoward effects from7 h' q1 o4 `- B7 T0 k; n& v/ I; M
testosterone exposure as mentioned earlier because
/ F: Y% T2 c* Fthe exposure was not for a prolonged period of time.
0 R6 R, P7 v% BAlthough the bone age was advanced at the time of/ Y- y, R: V4 B
diagnosis, the child had a normal growth velocity at
3 c S5 v s9 z" D0 w1 u: jthe follow-up visit. It is hoped that his final adult
1 X0 O3 b O0 y' Y3 | D L$ Kheight will not be affected.
& v H m* F5 R, e b. q! I3 NAlthough rarely reported, the widespread avail-
# l% E$ d/ a$ m5 p2 T3 \ability of androgen products in our society may& G( v" U" N9 S0 P9 k
indeed cause more virilization in male or female6 w) h" @ p( g( k) B4 ]5 z. J9 c
children than one would realize. Exposure to andro-
/ a. G# P7 ^6 d+ ^ g4 w& ~$ l' sgen products must be considered and specific ques-
* _! N& W3 w$ V+ S9 Ttioning about the use of a testosterone product or
8 t* W; e1 G9 H2 ~3 h; pgel should be asked of the family members during
( I9 ^% H! h3 K" {the evaluation of any children who present with vir-3 C0 G/ ~% }' k7 e& l. c
ilization or peripheral precocious puberty. The diag-
8 O* Z2 ^: A7 b# n/ N3 gnosis can be established by just a few tests and by
" C T! A% |0 j! B i, Sappropriate history. The inability to obtain such a% z1 ^2 S1 }0 _
history, or failure to ask the specific questions, may
5 S$ k8 ~2 i: O$ J. Cresult in extensive, unnecessary, and expensive9 M6 F7 b( C3 J
investigation. The primary care physician should be$ \$ V6 [& [ a
aware of this fact, because most of these children- X/ c$ f" O9 x5 r1 U2 N
may initially present in their practice. The Physicians’; ?( x( m( Y. l9 e# e6 q: t6 L1 M: v
Desk Reference and package insert should also put a
; l0 ^3 y& j, c4 T4 N" d: m( Lwarning about the virilizing effect on a male or
/ s: C9 \, V2 ?. O$ N+ ofemale child who might come in contact with some-
& i* w/ O0 O$ K% a" g1 G/ ]) v7 h" none using any of these products.
$ |* k3 _3 t6 C. u) |References
+ Y- M9 \+ s# I5 u, r1. Styne DM. The testes: disorder of sexual differentiation: l$ ]1 N# @ n* i9 r* y
and puberty in the male. In: Sperling MA, ed. Pediatric
/ R" E5 V1 G* R4 p! {; qEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, B1 L) ~6 Z0 O/ l7 o
2002: 565-628.; @( R5 e" a+ U& _' z2 d
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 g3 q; t) Y" [% i
puberty in children with tumours of the suprasellar pineal |
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