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Sexual Precocity in a 16-Month-Old
$ j, O! z9 m! c: `0 k* gBoy Induced by Indirect Topical% h3 i- L6 b Z5 H t/ g
Exposure to Testosterone$ E. O: t$ E; r6 R
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
) A: _" h2 q# U9 M, dand Kenneth R. Rettig, MD1$ P, \2 {5 s, T. s3 g* E/ z
Clinical Pediatrics
* Q! v" k" ]! \Volume 46 Number 6
6 w& V! o" G3 ?" FJuly 2007 540-543' V' j# v4 p8 X7 x+ M5 n2 C- N1 Q
© 2007 Sage Publications/ Q' H. v$ _* o" n6 R
10.1177/0009922806296651
' ~. f3 B3 u- M/ F+ Qhttp://clp.sagepub.com
& ~; Z7 N% {" v' e4 B) Fhosted at
: o1 E- z* Z+ D- y* f% L" m4 jhttp://online.sagepub.com
" x0 T$ _) [7 A) |2 A6 v7 yPrecocious puberty in boys, central or peripheral,
' b: H6 J6 _+ x% R: i- Z5 [is a significant concern for physicians. Central6 j6 V& I$ v' f, A( X b5 L7 c
precocious puberty (CPP), which is mediated0 s( p$ h8 Z3 g7 k+ d
through the hypothalamic pituitary gonadal axis, has
( ~. L7 a) y7 V) T" |* F3 ?. Ya higher incidence of organic central nervous system2 _+ m! R4 Q$ u3 M8 E; `" b
lesions in boys.1,2 Virilization in boys, as manifested
& k, ^' U0 E7 u' o; L* X1 [by enlargement of the penis, development of pubic, W! j y5 r& d8 ?# \3 r3 j# {
hair, and facial acne without enlargement of testi-
+ M" x3 g- a2 A8 I" |cles, suggests peripheral or pseudopuberty.1-3 We
6 B& \9 R) @6 b v/ s+ greport a 16-month-old boy who presented with the
/ B' z+ w K j0 ]$ Oenlargement of the phallus and pubic hair develop-3 Q5 }. U6 M$ G; ?" X
ment without testicular enlargement, which was due
: }9 b$ q8 i. Eto the unintentional exposure to androgen gel used by0 P7 l/ [% a# f
the father. The family initially concealed this infor-
! e3 x4 v% }! Pmation, resulting in an extensive work-up for this4 a, _* s7 R7 g- O, }$ [1 [
child. Given the widespread and easy availability of
8 t2 f; F, b! k8 ]- n! ptestosterone gel and cream, we believe this is proba-
- G5 `# J, \# r2 U3 F% i% E( ]bly more common than the rare case report in the0 C, a9 w- p, X$ h6 T
literature.4
! Y( K% \5 R) t2 hPatient Report& h+ N- x o; V; W- Q" }+ Z8 w
A 16-month-old white child was referred to the0 V) d! _5 [, N0 D- U
endocrine clinic by his pediatrician with the concern
: T9 z6 y4 h+ c8 {, S0 U- dof early sexual development. His mother noticed0 f8 {1 i: j7 L3 y1 K0 M/ a5 i
light colored pubic hair development when he was) O1 Z- _% p$ H& r
From the 1Division of Pediatric Endocrinology, 2University of8 y; s0 w$ P7 x
South Alabama Medical Center, Mobile, Alabama.3 `" _& J5 P8 j0 d/ V
Address correspondence to: Samar K. Bhowmick, MD, FACE,
( K$ g8 l ^6 ^9 A5 u6 I3 ]8 BProfessor of Pediatrics, University of South Alabama, College of
$ b4 H1 ?6 `+ G `* WMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 _, c7 s2 p3 S5 B) R- c, [
e-mail: [email protected]. S% P& V+ E) G2 ], d" L
about 6 to 7 months old, which progressively became
* e0 p; k' R% B2 J* f0 b& bdarker. She was also concerned about the enlarge-1 R. w& p( f4 {- w
ment of his penis and frequent erections. The child' v2 F& y1 P4 y- [
was the product of a full-term normal delivery, with
9 V: A) ~" j0 ^4 ^. ga birth weight of 7 lb 14 oz, and birth length of
: g' i9 O' q r ^0 j q* ^20 inches. He was breast-fed throughout the first year
. g% J) c# g" {. _of life and was still receiving breast milk along with
+ P0 w. I: d2 @solid food. He had no hospitalizations or surgery,5 [5 e* I# o. ?3 `% ~
and his psychosocial and psychomotor development
" n4 G8 N1 ^) w' I' T4 pwas age appropriate.+ U: o$ P! q6 U7 E7 I* s i8 b
The family history was remarkable for the father,0 E$ s$ _* x9 u( L* G \' A2 R9 q" X
who was diagnosed with hypothyroidism at age 16,$ L% W9 O) I+ l2 N% ~; v! s. w- X
which was treated with thyroxine. The father’s
' V/ m3 w4 M* l; {' |9 Z0 Cheight was 6 feet, and he went through a somewhat# G* t! V) ~& K# n. Q8 Q, j& M: W4 E" K
early puberty and had stopped growing by age 14.
" m2 I6 _1 q+ Q# b- RThe father denied taking any other medication. The
d n4 d: S% T' i: B& Mchild’s mother was in good health. Her menarche3 }! I, M6 Y$ I2 N* `3 X
was at 11 years of age, and her height was at 5 feet
5 w. ?, H, _1 @. Q) F3 K. v5 inches. There was no other family history of pre-
% b) d3 N8 d, {5 p* Fcocious sexual development in the first-degree rela-, x$ W8 A' {( [8 y$ i9 d( j- e( y
tives. There were no siblings.3 g& u, z5 G/ z. i' d+ `* j# K
Physical Examination
2 ], z- K |# g0 FThe physical examination revealed a very active,5 B, N3 @. E7 r; m- o% {
playful, and healthy boy. The vital signs documented; F! a( g- D+ A" a% C6 l. H
a blood pressure of 85/50 mm Hg, his length was
1 R% k0 M* a; M; I5 h! C5 a/ h90 cm (>97th percentile), and his weight was 14.4 kg/ Y% O: G2 r4 C$ T3 ]1 e; j+ W
(also >97th percentile). The observed yearly growth" T# `/ y0 [+ I' N
velocity was 30 cm (12 inches). The examination of
- ^0 g. [4 W( [4 v H1 Ithe neck revealed no thyroid enlargement.
" Q( a/ W- f9 w, rThe genitourinary examination was remarkable for
; ?8 h& p/ M. V, E( Y; f8 w; Henlargement of the penis, with a stretched length of
# D( E8 j3 e, q, O0 t. d8 cm and a width of 2 cm. The glans penis was very well
" C% f' E$ `- t. K8 T- |- Ddeveloped. The pubic hair was Tanner II, mostly around
0 x/ q2 r4 e3 }* z9 q* b( q5400 z9 m0 a* O1 Q7 h- v
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 e/ h2 x7 U) F' p
the base of the phallus and was dark and curled. The
7 C, [1 ?4 ^& s+ vtesticular volume was prepubertal at 2 mL each.+ U0 C, }; y& G0 q
The skin was moist and smooth and somewhat: _ `: x* l& Z+ n
oily. No axillary hair was noted. There were no% i: I' W/ D. [1 ^8 |
abnormal skin pigmentations or café-au-lait spots.
) |3 A) C6 l. F2 t) D9 G6 G) Z0 R6 FNeurologic evaluation showed deep tendon reflex 2+. J; O5 F$ Y% y: d, y
bilateral and symmetrical. There was no suggestion, x4 N3 |- _+ Y W4 `
of papilledema. b5 t$ _, L, x; D# r
Laboratory Evaluation2 L" C( }( k/ @8 w3 h
The bone age was consistent with 28 months by
" \& t0 v; i7 v1 P) A! kusing the standard of Greulich and Pyle at a chrono-
* E. F( i* G# Jlogic age of 16 months (advanced).5 Chromosomal3 w8 Z, D, I3 u y: v
karyotype was 46XY. The thyroid function test8 i3 Q0 T7 m9 x0 b" j
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 V2 Y- S+ ]2 O, Alating hormone level was 1.3 µIU/mL (both normal).9 }" Y" C* p- ~# e- O5 X
The concentrations of serum electrolytes, blood% b2 x7 m: ?, `8 E% ]
urea nitrogen, creatinine, and calcium all were
$ h6 c: c. J& U4 U& cwithin normal range for his age. The concentration' V" n8 S8 a9 f: q! [+ n4 X
of serum 17-hydroxyprogesterone was 16 ng/dL
& S( G' p; ^9 o- O3 f# O4 c3 G(normal, 3 to 90 ng/dL), androstenedione was 204 {1 b5 v ^ z4 @! l/ o
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- N' f$ r8 r4 k8 L+ l, m% d0 a
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
# k" G$ ?, D6 F U& ~, qdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
9 c. w. e- z7 e' f3 l* l49ng/dL), 11-desoxycortisol (specific compound S)0 t( {8 V1 x, k- I
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
3 k& N" I- e( i9 A# ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total& J/ E6 v9 [) \4 x* {
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 A2 g6 S; o. i' ~4 W: Z6 `( [and β-human chorionic gonadotropin was less than# H- o' m Y; a- Z9 z
5 mIU/mL (normal <5 mIU/mL). Serum follicular
4 S* M% t4 Y- y6 Q+ @6 u/ H& ]' ustimulating hormone and leuteinizing hormone
* Y- F' G2 h: V& L$ E& Dconcentrations were less than 0.05 mIU/mL, F) S# X1 O/ H( P, q
(prepubertal)." u% p, Y% H0 L7 X) e, q$ w
The parents were notified about the laboratory* f, K# c. q6 r' A5 z+ p
results and were informed that all of the tests were4 [0 L4 T/ I+ t$ x$ q! {2 b
normal except the testosterone level was high. The0 ^1 D" `$ a7 Z [
follow-up visit was arranged within a few weeks to
( X1 K8 w0 h V j0 Fobtain testicular and abdominal sonograms; how-& ?$ V, f t* T$ ?3 n( k/ c/ _
ever, the family did not return for 4 months.
; R* Q% W' \. c1 R2 y5 [- fPhysical examination at this time revealed that the5 u+ X. n% v% w( E; F9 C
child had grown 2.5 cm in 4 months and had gained2 _4 `6 B0 N: Q; \( H3 M
2 kg of weight. Physical examination remained
" X2 S t5 p( C; r0 Lunchanged. Surprisingly, the pubic hair almost com-
3 z5 _) s0 M0 X3 i! w3 p+ npletely disappeared except for a few vellous hairs at
! N; M: w( l8 Lthe base of the phallus. Testicular volume was still 2: O* s4 Z5 K: }- E. k
mL, and the size of the penis remained unchanged.6 a0 t+ G3 i8 a% l6 E9 r; Y
The mother also said that the boy was no longer hav-1 t* [* W: `( o1 T6 s! H" ?3 c+ s& m4 P
ing frequent erections.5 W; D3 `/ O- A" N3 s+ b7 \
Both parents were again questioned about use of! H+ Y+ [7 w' [1 A
any ointment/creams that they may have applied to" I" Z5 t1 {1 K' D
the child’s skin. This time the father admitted the: A7 p6 g2 O1 ~4 I
Topical Testosterone Exposure / Bhowmick et al 541
. y8 p/ F3 L( I b3 U/ wuse of testosterone gel twice daily that he was apply-
4 y! g `. j4 _- y/ n! Bing over his own shoulders, chest, and back area for: `- @" K% Q# j# b3 M3 K
a year. The father also revealed he was embarrassed* r; B( A/ S9 m* D/ V# Y$ l4 U( [1 r
to disclose that he was using a testosterone gel pre-
- ]: C+ t. A3 n: ]5 S; ^0 vscribed by his family physician for decreased libido3 [) a O K& A3 s
secondary to depression.1 m* x* ?7 \! H
The child slept in the same bed with parents.
& S1 |0 o# T2 `- Q$ Z9 p1 C. g& y# oThe father would hug the baby and hold him on his0 }4 o) k! b- N% A% j
chest for a considerable period of time, causing sig-
! O% ~) G3 B* v3 \nificant bare skin contact between baby and father.1 z5 T! E6 _5 @4 }8 y
The father also admitted that after the phone call,
6 }0 l" I( F- C6 l- T6 uwhen he learned the testosterone level in the baby" S# T) |8 R9 p* C
was high, he then read the product information/ W+ B0 K: P+ C
packet and concluded that it was most likely the rea-
; H T: I7 z) m* m E& R& c* p' tson for the child’s virilization. At that time, they
& \8 v, W, K: a% Z4 z$ H6 ydecided to put the baby in a separate bed, and the
$ G2 W# E1 I$ S1 m; H; Ifather was not hugging him with bare skin and had
) ^0 Z2 E- Y9 z b6 O/ q% `been using protective clothing. A repeat testosterone
2 Q \3 _6 F9 f" W! j# s) E* ytest was ordered, but the family did not go to the; b! `9 O/ n! P1 S
laboratory to obtain the test.
# g" q! B, W ]: _1 F rDiscussion. Y: ^3 X/ o6 e6 v
Precocious puberty in boys is defined as secondary
0 v$ X) t( Z& F$ ]* e8 {sexual development before 9 years of age.1,4
1 R9 S7 Y* u2 K& c; IPrecocious puberty is termed as central (true) when
5 _; @" P& B) A2 kit is caused by the premature activation of hypo-9 m. I4 C- X$ E& J0 @
thalamic pituitary gonadal axis. CPP is more com-
2 G) y5 S$ `8 ~& s% Qmon in girls than in boys.1,3 Most boys with CPP
- e. q4 s9 c% T$ g. O6 bmay have a central nervous system lesion that is
2 {6 Z- ~, j3 A: J; U( [( Uresponsible for the early activation of the hypothal-
. Y0 j% f$ |( eamic pituitary gonadal axis.1-3 Thus, greater empha-
6 J* t8 f6 ~) Y, k/ V6 |* h/ zsis has been given to neuroradiologic imaging in! `- Z! p5 y5 o7 w# I8 Z
boys with precocious puberty. In addition to viril- t- @8 @. Q; t: ~ ?9 r
ization, the clinical hallmark of CPP is the symmet-
( `" s+ K. l5 [" S- m% zrical testicular growth secondary to stimulation by
4 |0 q1 W" B! A( b( W! r5 Ogonadotropins.1,3
2 |3 K$ X: w1 aGonadotropin-independent peripheral preco-3 [: L* w9 W( m U! N% w
cious puberty in boys also results from inappropriate
% B- _9 E, k R$ C4 \/ V! iandrogenic stimulation from either endogenous or
/ `2 y! C& u: ]. r' l& qexogenous sources, nonpituitary gonadotropin stim-
. b( r' t; ]' i s* p6 A7 Nulation, and rare activating mutations.3 Virilizing+ L5 o* f; H; `" v
congenital adrenal hyperplasia producing excessive
- M# W1 d6 V4 e% a. y: sadrenal androgens is a common cause of precocious
+ r" L$ j' Z c! I; h8 Jpuberty in boys.3,4( @* d6 V! X/ d# I6 J
The most common form of congenital adrenal
% P0 l& E; O8 ?% b! Shyperplasia is the 21-hydroxylase enzyme deficiency.
7 ?, j8 N3 b' W4 Q l- vThe 11-β hydroxylase deficiency may also result in$ ]! ^* s/ K8 M* U
excessive adrenal androgen production, and rarely,( p# \2 n* n l( t
an adrenal tumor may also cause adrenal androgen
* P2 K" |, q( y. N4 Qexcess.1,32 s, S# Z* y1 v# P8 C3 l/ k
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 I+ h: i) D5 z% r: h* a8 p* ^
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
/ ~9 ^: T- m" o" ~$ C6 N5 ]A unique entity of male-limited gonadotropin-
& i: j& p3 `/ [! b! M# O6 Kindependent precocious puberty, which is also known
8 {. n* k; Q, O1 o9 las testotoxicosis, may cause precocious puberty at a
' q2 y+ E! D* {, x, p" gvery young age. The physical findings in these boys
9 I4 H! o& s' G* a! B9 iwith this disorder are full pubertal development,7 _& P. S9 u" f" G3 e' A" {8 r
including bilateral testicular growth, similar to boys
5 M- L5 ?# I1 @9 f/ f& ~' }with CPP. The gonadotropin levels in this disorder+ v' J! I" p4 Q7 S l7 b
are suppressed to prepubertal levels and do not show
5 V+ J) G# p, N5 gpubertal response of gonadotropin after gonadotropin-
3 b ^7 k v# m. Z& X Creleasing hormone stimulation. This is a sex-linked% u0 q+ G0 Y4 E( V; D) t7 q1 k
autosomal dominant disorder that affects only, u: S9 N+ K, j6 [: A
males; therefore, other male members of the family2 S! R' o4 x4 T F5 Q
may have similar precocious puberty.3: K) D2 {% e! X0 F+ b& M6 b: S) v
In our patient, physical examination was incon-2 w5 J* n1 C# }, t! V; ^
sistent with true precocious puberty since his testi-
' b0 E9 O% `9 S8 |6 {" Z. U% xcles were prepubertal in size. However, testotoxicosis
9 D j+ O: C; O! H" qwas in the differential diagnosis because his father/ J3 M5 g& R0 Q* E; {
started puberty somewhat early, and occasionally,
8 R: z. y; n# ^ @8 D: ~2 mtesticular enlargement is not that evident in the
) X7 {0 @: ^4 Z/ y8 g- j$ P0 @5 Z0 Ebeginning of this process.1 In the absence of a neg-
2 |; |8 x6 f& j" u! m3 Pative initial history of androgen exposure, our
8 s' U% J: p! D7 T$ M; x% W1 ^8 ebiggest concern was virilizing adrenal hyperplasia,: M; G+ _/ T0 i- r& f9 ]1 R0 W9 z6 q
either 21-hydroxylase deficiency or 11-β hydroxylase% }5 |9 j8 A4 E8 b; h2 Y4 x% r
deficiency. Those diagnoses were excluded by find-" _+ ~0 F; P$ i
ing the normal level of adrenal steroids.5 y( s$ Y/ f6 X0 q* B- d7 R
The diagnosis of exogenous androgens was strongly
; U. S2 u, R0 L0 e7 @suspected in a follow-up visit after 4 months because
7 G: s1 V9 O& o% s& Rthe physical examination revealed the complete disap-) k9 w5 _) o6 i. t
pearance of pubic hair, normal growth velocity, and% H, G1 f; _4 ]) W' `
decreased erections. The father admitted using a testos-
$ q) M4 w# v. O0 w+ n5 gterone gel, which he concealed at first visit. He was b7 b3 H! K/ C3 L" d. D% q9 H
using it rather frequently, twice a day. The Physicians’) D" e& D1 }' F, { J$ Y: M8 T" F0 x, p
Desk Reference, or package insert of this product, gel or" L( I) }8 M4 G* r4 o7 V5 [
cream, cautions about dermal testosterone transfer to
0 h: ?5 c, |& L* K( u( `( U/ l( vunprotected females through direct skin exposure.
# F( n) w4 x9 Y. m7 Z* g6 x* kSerum testosterone level was found to be 2 times the
$ x/ ^- k, T! X5 y7 h. fbaseline value in those females who were exposed to( p# g2 ^3 R5 }* {# z( ] Q
even 15 minutes of direct skin contact with their male
6 j. [2 ]: Q& r0 T Fpartners.6 However, when a shirt covered the applica-: Q+ v) Z8 [3 [4 T' l: B
tion site, this testosterone transfer was prevented.
, u# _$ |/ |1 Q' O% O( i" W- pOur patient’s testosterone level was 60 ng/mL,
8 X H8 d; q' {5 O! zwhich was clearly high. Some studies suggest that
# |! V4 S. S$ _" L' n1 Tdermal conversion of testosterone to dihydrotestos-4 k$ ]; F9 z0 H% q( \3 }: O
terone, which is a more potent metabolite, is more
6 k# w; J6 Y3 P& a `active in young children exposed to testosterone
, J0 J! s5 R+ B) C X u0 A* Bexogenously7; however, we did not measure a dihy-( f8 \( N4 C, m4 w" `) {0 P
drotestosterone level in our patient. In addition to/ m! [: H' M8 k/ U) M
virilization, exposure to exogenous testosterone in
' e" {! |' {$ \: i/ Qchildren results in an increase in growth velocity and7 ]! e5 I% v# W0 {' {
advanced bone age, as seen in our patient.6 E( H* h7 j* v4 H0 E$ l
The long-term effect of androgen exposure during
+ W4 P; R9 Z: Hearly childhood on pubertal development and final$ {$ @' A4 ^5 ]1 m. E7 U2 N
adult height are not fully known and always remain
8 }7 o- \( G k+ ga concern. Children treated with short-term testos-7 g, s, t' B( o3 h" M7 M
terone injection or topical androgen may exhibit some
/ I+ e# H' {+ M! \acceleration of the skeletal maturation; however, after/ Y& [) F/ b" n+ R
cessation of treatment, the rate of bone maturation
# j$ I% m, R: @decelerates and gradually returns to normal.8,9+ g* c1 G! Y0 {+ b+ g" r
There are conflicting reports and controversy2 J. U; L* l, M& ]+ h+ L, ]
over the effect of early androgen exposure on adult2 g1 R) ] z8 L8 I# ]
penile length.10,11 Some reports suggest subnormal
+ r: N& |* d) h$ ?adult penile length, apparently because of downreg-
: Z4 m* o9 {0 q/ R7 Qulation of androgen receptor number.10,12 However,
- [1 b5 f8 |. ?) q$ w; Y( g, jSutherland et al13 did not find a correlation between8 A% a9 s% i8 X2 h& T# {
childhood testosterone exposure and reduced adult+ P) K+ O& b/ j5 L1 t# M; K) [( |
penile length in clinical studies.
4 S- A4 F; \+ k \0 u0 cNonetheless, we do not believe our patient is$ J, {- j& Q# S8 H8 T, V9 m, l# Z
going to experience any of the untoward effects from
5 e3 D8 M* {4 F- Btestosterone exposure as mentioned earlier because
" f! y; I* y! z Mthe exposure was not for a prolonged period of time.
4 H) @( n, g5 S% \- O) H( z0 qAlthough the bone age was advanced at the time of9 H- w. @8 z' E& Y2 B. L) R" e
diagnosis, the child had a normal growth velocity at1 \6 y t1 }, ?) H, N
the follow-up visit. It is hoped that his final adult% j3 I. {# H2 i! q4 Z9 p G
height will not be affected.
% j. G/ t, m/ o4 m2 x0 dAlthough rarely reported, the widespread avail- f$ h; L. l# i' B8 l7 n$ |. |
ability of androgen products in our society may* V- d' I' u' z Z5 z: @
indeed cause more virilization in male or female
! {/ D6 a1 n/ h! g, ?children than one would realize. Exposure to andro-
, }. A* G+ X5 W2 P" s/ zgen products must be considered and specific ques-
2 f) Q2 k- U% L! O* g/ j6 A& Ztioning about the use of a testosterone product or
8 E! n# o8 C" xgel should be asked of the family members during
. B: |( ~2 q$ T8 mthe evaluation of any children who present with vir-
8 G1 M0 Q0 j! f( t- A+ U) Qilization or peripheral precocious puberty. The diag-) ^/ l2 [: q6 L H2 d) }
nosis can be established by just a few tests and by$ i7 B ]/ z$ x# y3 p! a
appropriate history. The inability to obtain such a
% G, \9 H0 h6 E( T; s! thistory, or failure to ask the specific questions, may
4 r4 `+ y* H4 u: vresult in extensive, unnecessary, and expensive
1 h8 o; M' `$ B6 B; Oinvestigation. The primary care physician should be/ Q/ v. h& q- E/ ^2 s* i* P
aware of this fact, because most of these children0 }0 j: r9 `5 a) D% r5 x' |
may initially present in their practice. The Physicians’5 j( l x1 H6 a# h8 q. q7 ~* W
Desk Reference and package insert should also put a
- S3 S: f* d( a1 d4 s! \warning about the virilizing effect on a male or
8 W: C& Z* z* f/ ]* e1 }- Q+ Cfemale child who might come in contact with some-
+ r# U$ T% |- ]0 c, zone using any of these products.
" k3 m7 |7 F: a# WReferences
$ H5 [1 _4 s. E7 i1. Styne DM. The testes: disorder of sexual differentiation
7 q$ _3 J9 i; A$ O2 A- m. G* ~: m5 s# B cand puberty in the male. In: Sperling MA, ed. Pediatric: i! Z, `! U8 x
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" y, m: M& @; p( ~3 [1 l& X3 X& c* y
2002: 565-628., C6 d2 j% D6 z ^; a
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 T# t9 t( H: B. x+ f) Mpuberty in children with tumours of the suprasellar pineal |
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