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Sexual Precocity in a 16-Month-Old2 Q s! R0 L! P' d! |
Boy Induced by Indirect Topical, Q9 S7 \ v& j4 N: C: X
Exposure to Testosterone. C0 z4 _, s9 J2 C( K+ K+ b! E4 X
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; ]' t: N: W7 \6 t+ u6 l& Xand Kenneth R. Rettig, MD11 f( Y) C" E. x* k$ C
Clinical Pediatrics
. ^* u5 T) `$ t3 _8 R+ SVolume 46 Number 6- V! h" U' b5 ?+ Q9 a
July 2007 540-543: D0 D6 O8 m C s- Q# Q
© 2007 Sage Publications; }" ]$ L/ j% b
10.1177/0009922806296651, k9 Q: |4 D2 o' Y
http://clp.sagepub.com
, {: ], ]5 {; G3 W0 H7 k; m4 g$ vhosted at* |: A1 b2 u! Y8 w6 I
http://online.sagepub.com4 i E/ p+ d8 @0 c
Precocious puberty in boys, central or peripheral,) n& v5 h0 H# C. ]
is a significant concern for physicians. Central
0 q7 J) ~) y! P+ U3 Tprecocious puberty (CPP), which is mediated H9 D7 t9 B. w2 e; a0 j* Z
through the hypothalamic pituitary gonadal axis, has
2 r2 s* i. B) I! V- l6 B2 Ca higher incidence of organic central nervous system- c1 h* X8 `2 ?2 h( v. O# \
lesions in boys.1,2 Virilization in boys, as manifested
: E8 x8 Q$ @6 H7 x Aby enlargement of the penis, development of pubic; ?* K$ S O% k/ n+ ?
hair, and facial acne without enlargement of testi-
* ^+ i$ B' I5 p! O! ?( ycles, suggests peripheral or pseudopuberty.1-3 We, G' h3 o6 ^% ^3 ~3 \' |6 p7 E
report a 16-month-old boy who presented with the
! o9 u8 a) D2 aenlargement of the phallus and pubic hair develop-3 H- U4 p5 T$ E C6 z: @
ment without testicular enlargement, which was due
0 A, I+ |6 `; u% Vto the unintentional exposure to androgen gel used by5 w a' f5 d8 P9 ?, h
the father. The family initially concealed this infor-
& |& _3 C6 v1 g% W& W7 [( u4 X# amation, resulting in an extensive work-up for this! y9 o) }* N9 |
child. Given the widespread and easy availability of
0 e) i- H+ b6 Z8 t" Rtestosterone gel and cream, we believe this is proba-& d x! E% ]% N7 m4 o4 v# J( u4 h; [
bly more common than the rare case report in the
; Z0 u" L Y+ m$ B$ ?7 D' wliterature.4
) Y$ v: Y; q+ b" _" ^Patient Report
0 C: R+ G. o, c5 qA 16-month-old white child was referred to the
7 d: z6 K R. u2 ~endocrine clinic by his pediatrician with the concern
$ J' T% Y2 k- q4 a# z% y& m6 f0 X' t( jof early sexual development. His mother noticed
" C4 k ~. K z& plight colored pubic hair development when he was2 U1 C6 p) x$ j% W) ^
From the 1Division of Pediatric Endocrinology, 2University of
% A; ^1 R- N5 _( F! ~( ESouth Alabama Medical Center, Mobile, Alabama.
2 \2 _9 q4 I4 f- q6 VAddress correspondence to: Samar K. Bhowmick, MD, FACE,
- F+ a; o2 z' G+ H5 s- b* rProfessor of Pediatrics, University of South Alabama, College of' H. t8 H h, s- b
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; f. `; M8 J: A. P m$ t. re-mail: [email protected].
$ M$ G# B U3 j5 ^about 6 to 7 months old, which progressively became
2 O0 q3 b) B3 d* Jdarker. She was also concerned about the enlarge-2 ?9 T/ l, p; N8 d4 \2 H- w l9 @
ment of his penis and frequent erections. The child+ p8 Z4 C6 w) l
was the product of a full-term normal delivery, with
i; y! I) Q* K" \) b* `a birth weight of 7 lb 14 oz, and birth length of6 h6 u! `% u( X- W. f2 R$ n
20 inches. He was breast-fed throughout the first year6 [) t" e: S, ^$ S% R6 O2 i! H
of life and was still receiving breast milk along with1 F0 N0 ?) w& z: F
solid food. He had no hospitalizations or surgery,
: M4 A' J2 d) ^and his psychosocial and psychomotor development
: Z, M" l, w- P- m' M" {3 owas age appropriate.
/ F4 a, ?7 O0 Y5 \) J9 _The family history was remarkable for the father,# B; M3 m/ H- M3 Q6 X0 g9 R
who was diagnosed with hypothyroidism at age 16,
5 M( r, K0 W% b. [# G5 X2 twhich was treated with thyroxine. The father’s
( S' U5 g/ j0 B/ bheight was 6 feet, and he went through a somewhat
9 c+ h. Y) K" v$ Pearly puberty and had stopped growing by age 14.
& q& i, j0 Z: d( p/ KThe father denied taking any other medication. The
& w! [7 r" B5 ^2 N Fchild’s mother was in good health. Her menarche
0 O3 k: j7 c' k: K. r& ?was at 11 years of age, and her height was at 5 feet
5 U. C/ q3 Z, O) p- r6 l' n9 B" ?5 inches. There was no other family history of pre-1 u% D: }" t2 K( |7 w; b0 M
cocious sexual development in the first-degree rela-0 ~, Z8 R$ C P
tives. There were no siblings. `/ k& b" `2 Q& N
Physical Examination+ B1 H: U, \9 L3 j$ Q
The physical examination revealed a very active,
/ Q( ~# V, {- B) N: ]playful, and healthy boy. The vital signs documented
2 d- R8 {; t: {+ q( fa blood pressure of 85/50 mm Hg, his length was
( e" V% a$ T% D/ x' l1 @90 cm (>97th percentile), and his weight was 14.4 kg
% i8 T0 W8 K! q% D7 U(also >97th percentile). The observed yearly growth
0 k! d8 d6 I; d' ?velocity was 30 cm (12 inches). The examination of$ ~' U* t- @6 P1 k) {
the neck revealed no thyroid enlargement.
0 W2 O$ P W% ~6 E' W' V3 q* _7 UThe genitourinary examination was remarkable for# H; O# k! L. W& x( N! e
enlargement of the penis, with a stretched length of: C* ~0 j/ K# D
8 cm and a width of 2 cm. The glans penis was very well
# _6 Q0 c# j _% Cdeveloped. The pubic hair was Tanner II, mostly around
5 D: i5 p( i, _. |8 I4 n540
, A* E$ e7 e3 H& Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, x6 \0 G2 W+ B. x+ Z8 q; hthe base of the phallus and was dark and curled. The
f$ Y" w7 c2 n" Ltesticular volume was prepubertal at 2 mL each.2 _) C1 D, }( E* z
The skin was moist and smooth and somewhat
6 U4 V) Z( ]! k: f6 uoily. No axillary hair was noted. There were no
1 N" E/ u& f: S8 _" F5 Xabnormal skin pigmentations or café-au-lait spots.
5 W$ U' {" t3 R5 \4 `- dNeurologic evaluation showed deep tendon reflex 2+
' J1 K& W1 ?( a3 r% q, ^bilateral and symmetrical. There was no suggestion) i2 X3 Y- [# o4 R; l) x# ~
of papilledema.
# S+ _/ I8 j& w2 j- V1 NLaboratory Evaluation; H. Q! y. Q+ Z8 W1 R# {; ], O# D$ c( P
The bone age was consistent with 28 months by
+ u9 y% i1 }9 t0 Zusing the standard of Greulich and Pyle at a chrono-8 N. A) n6 i2 I& [% O, S1 q
logic age of 16 months (advanced).5 Chromosomal
5 q: C; d; z7 S, R& }, mkaryotype was 46XY. The thyroid function test5 E/ e; a/ `* ~* E" m6 s
showed a free T4 of 1.69 ng/dL, and thyroid stimu- m8 o K% F: N! q* P
lating hormone level was 1.3 µIU/mL (both normal).
4 c/ f0 U: y5 S2 MThe concentrations of serum electrolytes, blood
6 F, h) ^" Z0 w0 d [urea nitrogen, creatinine, and calcium all were
3 M6 K6 j' s; }8 \" |# }4 jwithin normal range for his age. The concentration6 B" ?1 C9 b( l9 [2 i/ Q
of serum 17-hydroxyprogesterone was 16 ng/dL) f$ [2 f4 l5 }5 g& H
(normal, 3 to 90 ng/dL), androstenedione was 20
6 S; _8 ^! E+ T2 D2 ]8 |' Nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- \; t9 k3 [3 y# w& eterone was 38 ng/dL (normal, 50 to 760 ng/dL),
9 ]; @8 g. Q: Xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
* l& ^ z# y' t# ~6 `! f. j; ^$ f49ng/dL), 11-desoxycortisol (specific compound S)
$ k; S3 C. w7 U5 J3 x; Gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
3 k9 ]0 J* E. i, U, K2 `0 ?tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% @! ?6 s, c* X/ N& X) I6 Z& j
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
7 v* Z5 b* |% l: Q/ O- F1 k, iand β-human chorionic gonadotropin was less than
* M. l4 j, ]' o# B& ?3 {5 mIU/mL (normal <5 mIU/mL). Serum follicular0 `2 ]3 |4 U' z0 l: i
stimulating hormone and leuteinizing hormone+ x* b) T: J- L+ h
concentrations were less than 0.05 mIU/mL$ `% W5 L6 F O! g( f5 N8 S
(prepubertal).
3 O) E/ y7 r r9 n% ]1 JThe parents were notified about the laboratory
# w* }0 K3 x/ [5 S* S1 Q1 R ?results and were informed that all of the tests were$ ^% z: ]8 X3 i
normal except the testosterone level was high. The
m/ S! A2 N; [# kfollow-up visit was arranged within a few weeks to
1 k- J+ x5 Y3 x" ]obtain testicular and abdominal sonograms; how-
( t- R; O7 X# E1 ?- ]ever, the family did not return for 4 months.3 Z4 Q# P3 N# ~+ N! F( Z
Physical examination at this time revealed that the. ?: R3 l# |0 X" W* Q. w
child had grown 2.5 cm in 4 months and had gained
6 @* q+ h( b$ v! R( q2 kg of weight. Physical examination remained6 h, _6 y, A: y3 n# }
unchanged. Surprisingly, the pubic hair almost com-. M! _, Y; h* E/ J% a0 f
pletely disappeared except for a few vellous hairs at
6 M. d i' D& k. h4 p$ dthe base of the phallus. Testicular volume was still 2
5 a" r9 q7 b$ N/ C7 @, ~9 v; KmL, and the size of the penis remained unchanged.$ r5 w7 E0 o/ C# D
The mother also said that the boy was no longer hav-
/ s2 A0 D. G& D- _5 ~8 i! i+ y8 Xing frequent erections.
! Y+ U7 Y/ ]- F$ }8 `9 R7 r2 ]Both parents were again questioned about use of4 I8 ?" R) b S: d }7 J7 F
any ointment/creams that they may have applied to
: n! B; ^( m( ?& fthe child’s skin. This time the father admitted the
) g' {: V5 |& T: s: uTopical Testosterone Exposure / Bhowmick et al 541
- ~3 l, I! l8 Q6 ~% e: g7 muse of testosterone gel twice daily that he was apply-
% d" @5 f b8 ?/ Ping over his own shoulders, chest, and back area for6 |# m7 E% F" H# I- ~2 a2 G
a year. The father also revealed he was embarrassed0 [( k* m: j. [: f% Q
to disclose that he was using a testosterone gel pre-; m; n0 g4 ^+ O1 p$ W
scribed by his family physician for decreased libido) b( Z5 d3 `! i, W% u# k
secondary to depression.
& E1 X5 B* M3 L! _" E7 d( \The child slept in the same bed with parents.# u' U7 V3 s9 H
The father would hug the baby and hold him on his
6 U0 L( i' }, h& gchest for a considerable period of time, causing sig-
% T' W! _7 J. c% A! `nificant bare skin contact between baby and father.% y6 h! M0 J7 w9 r4 F- b+ t
The father also admitted that after the phone call,
1 C8 A. l/ [1 c# g/ i8 p y. k. S" xwhen he learned the testosterone level in the baby6 M+ }0 @7 l) ^. ]9 w1 E" a( n- x
was high, he then read the product information% y, \7 q+ Y4 M- ^* @5 o
packet and concluded that it was most likely the rea-1 |* S2 ]& P" L
son for the child’s virilization. At that time, they8 t2 X( B( z. m. i# K
decided to put the baby in a separate bed, and the
9 L8 ?5 a- B3 X( mfather was not hugging him with bare skin and had
! R3 N9 R, s, t/ @8 pbeen using protective clothing. A repeat testosterone. y; D9 D. ~. j9 W: b/ ?
test was ordered, but the family did not go to the6 `; K7 P3 q! m% o! j- Z% o
laboratory to obtain the test.% \# k# x& A7 D1 W6 g( G
Discussion& t. W2 ^4 `9 \# @+ m: f) ?5 U
Precocious puberty in boys is defined as secondary
) R3 c2 h: Z* ?7 i* dsexual development before 9 years of age.1,4; j' P( r1 U- X6 l
Precocious puberty is termed as central (true) when2 b' _6 n, q; ^- v, ^" e
it is caused by the premature activation of hypo-
2 @1 R! V$ ~) A1 Cthalamic pituitary gonadal axis. CPP is more com-
: R9 [7 o/ r: W( X; Xmon in girls than in boys.1,3 Most boys with CPP- i! z: T9 W0 T
may have a central nervous system lesion that is7 K: M; e7 a K1 N4 X* l1 e( G
responsible for the early activation of the hypothal-( \2 K) @4 J, h+ @
amic pituitary gonadal axis.1-3 Thus, greater empha-
9 C4 F# f+ }5 k- D l5 A- xsis has been given to neuroradiologic imaging in
8 g P, N8 {. R" t q. q( cboys with precocious puberty. In addition to viril-
. ~1 B0 P. R( f% k, P: U1 V0 [ization, the clinical hallmark of CPP is the symmet-8 r3 @" F3 q; `
rical testicular growth secondary to stimulation by# I' K9 s" ~" z2 O
gonadotropins.1,3
/ L" H% u [) i. r' v; Q8 g3 GGonadotropin-independent peripheral preco-
: _) C, T0 e4 U7 ^: Zcious puberty in boys also results from inappropriate
- V2 b6 ]) m0 G' |& ]androgenic stimulation from either endogenous or4 H; o% Q9 }' d/ m# }0 j5 `
exogenous sources, nonpituitary gonadotropin stim-# t; P* z: n2 N, u$ W
ulation, and rare activating mutations.3 Virilizing; m; o( C3 Y8 k, Y0 E2 j* _
congenital adrenal hyperplasia producing excessive
7 i c, h8 m( padrenal androgens is a common cause of precocious
) _3 J/ E& ]1 ?8 \1 q6 G( ?: Lpuberty in boys.3,4
\4 N! g! l+ l% c# J5 bThe most common form of congenital adrenal* V# }% z1 I- {! v2 P1 E
hyperplasia is the 21-hydroxylase enzyme deficiency./ J3 }& |: r2 {6 b& V7 s C5 Z
The 11-β hydroxylase deficiency may also result in
5 ^5 ~, i" H8 P* o& Bexcessive adrenal androgen production, and rarely,( V/ n6 s, [* v/ q/ T6 O% W$ ~; T9 j
an adrenal tumor may also cause adrenal androgen7 T* O1 v# _( L3 V% k
excess.1,3
1 q( U* i) E+ L7 |/ j! Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ O6 X3 v0 F8 Y7 u542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ B/ i4 b" p( |, D) kA unique entity of male-limited gonadotropin-8 \" b$ Z$ y& ?! X* `; a( i- S
independent precocious puberty, which is also known
1 [' y; H( ^, r( Eas testotoxicosis, may cause precocious puberty at a& e9 |; k' ?- X: O# H
very young age. The physical findings in these boys
- \4 h- A2 a, c; g' P0 Pwith this disorder are full pubertal development,+ X' B8 F! ]7 r5 n
including bilateral testicular growth, similar to boys! v B5 ~" y1 V. J- s9 v
with CPP. The gonadotropin levels in this disorder5 n2 u/ ]2 A: E2 I3 d( a9 y5 g
are suppressed to prepubertal levels and do not show
; r/ I' ]# j) f5 Y e% S9 O: lpubertal response of gonadotropin after gonadotropin-
7 i; ^( a h# A3 U) J7 A! |" oreleasing hormone stimulation. This is a sex-linked4 B# c+ @; ~2 {2 j0 b. ]
autosomal dominant disorder that affects only
' _) T& R) o9 _males; therefore, other male members of the family2 v! B5 @* \" [6 O; ]2 w
may have similar precocious puberty.3& f8 P( b- ]- e% Z: J- r
In our patient, physical examination was incon-
* }1 R2 y8 ?" M7 X% \! q6 a7 ~9 T5 qsistent with true precocious puberty since his testi-
" W) W D6 q9 z6 R. a+ b) Z4 lcles were prepubertal in size. However, testotoxicosis" @/ a6 t/ [" _: \: @1 v2 R
was in the differential diagnosis because his father
; B# o- g3 H7 A: T9 d) Zstarted puberty somewhat early, and occasionally,
B1 e" l! z) G, \8 `) k. ptesticular enlargement is not that evident in the5 z# }2 \: x6 |
beginning of this process.1 In the absence of a neg-
+ `+ e \5 M+ K/ ]ative initial history of androgen exposure, our" b2 C4 h; W' J7 ]3 R
biggest concern was virilizing adrenal hyperplasia,
2 F! a4 d: r) T3 M/ |& |+ @either 21-hydroxylase deficiency or 11-β hydroxylase
2 m- q+ }# E- b, Fdeficiency. Those diagnoses were excluded by find-. h) N U2 ~4 J7 J" P! M
ing the normal level of adrenal steroids.
0 Q8 `- A1 W1 {8 V* T% LThe diagnosis of exogenous androgens was strongly! @1 K% t& K# n% w' d9 A' P$ s
suspected in a follow-up visit after 4 months because+ n6 w- K1 Q# _% T% ~" x
the physical examination revealed the complete disap-
' E9 i1 u% C- _ Y- kpearance of pubic hair, normal growth velocity, and3 m! j; R$ w" B& ^
decreased erections. The father admitted using a testos-0 Z7 s1 g: H. J- z5 |
terone gel, which he concealed at first visit. He was" v+ ?1 [3 e+ |# p7 u6 L& E
using it rather frequently, twice a day. The Physicians’; S) Z: h: Y6 W. r7 e2 X! Y; ]1 m
Desk Reference, or package insert of this product, gel or7 h# n+ x& Q# y! a
cream, cautions about dermal testosterone transfer to0 J/ U+ q( O' \2 }, P+ Y
unprotected females through direct skin exposure.
! f/ O" ^/ E3 k# R1 }! g' v, iSerum testosterone level was found to be 2 times the
* F, u8 m% \- K; g2 Ubaseline value in those females who were exposed to2 n, f$ o" S4 o3 [: {4 V# Y5 N, m
even 15 minutes of direct skin contact with their male0 z( \6 K4 `- n& k$ p
partners.6 However, when a shirt covered the applica-
' A' l$ R1 i4 O n5 U% [: ition site, this testosterone transfer was prevented.
$ h, J8 C. q% K- b8 P3 K9 w- n6 w1 gOur patient’s testosterone level was 60 ng/mL,$ \8 b' P8 U# @8 m$ J
which was clearly high. Some studies suggest that7 n, Y3 u% T* W6 S, R* e
dermal conversion of testosterone to dihydrotestos-0 g, h& ], k7 \! T# q2 `3 C
terone, which is a more potent metabolite, is more
; M3 m* ^5 @) K$ u: jactive in young children exposed to testosterone
) m& e$ J% O/ z: o; \/ h, A5 Pexogenously7; however, we did not measure a dihy-
: e3 s+ m# |- h# x2 O* Qdrotestosterone level in our patient. In addition to& e- @. @( G6 Q1 U# ~5 M' X# }
virilization, exposure to exogenous testosterone in
: B; X8 o, ?' @9 z9 {& a T$ Ichildren results in an increase in growth velocity and
; g! }# g, p& b5 r/ Iadvanced bone age, as seen in our patient.
7 d4 z4 @9 h/ [0 B8 p; aThe long-term effect of androgen exposure during0 S! L) u( b% P" w
early childhood on pubertal development and final
0 q! e% K" O6 l( Qadult height are not fully known and always remain9 u/ J' R8 [+ w Y& \$ w- ^
a concern. Children treated with short-term testos-. f: d' T' Q; F5 l% n
terone injection or topical androgen may exhibit some
1 _! x* f2 m- ^3 v* l/ ~& ?acceleration of the skeletal maturation; however, after
; d7 K( E8 m6 C" p; E/ Xcessation of treatment, the rate of bone maturation
6 e4 m5 k* w g. Wdecelerates and gradually returns to normal.8,9* d) [- k& L1 h2 m6 _
There are conflicting reports and controversy- @3 j) Y$ [( H8 ~" P/ M
over the effect of early androgen exposure on adult
6 p, p1 s: p+ B2 y2 |( X& [9 apenile length.10,11 Some reports suggest subnormal
- M$ P: V4 B# B% X7 X% J9 eadult penile length, apparently because of downreg-
9 I8 p" g1 Y4 D, yulation of androgen receptor number.10,12 However,- X6 g' i6 U4 Z/ ], K& f
Sutherland et al13 did not find a correlation between
1 }8 p3 L" ~ z a% o3 m* A1 ~ Gchildhood testosterone exposure and reduced adult) t% F% B! x& }! g4 ]' I$ z: }8 E
penile length in clinical studies.
; i$ j8 W* a$ t9 k" dNonetheless, we do not believe our patient is9 x& w- A$ o% n) S3 R
going to experience any of the untoward effects from
, t' G W, g N- R: Etestosterone exposure as mentioned earlier because+ z: F K3 Z+ @4 j
the exposure was not for a prolonged period of time.
" C4 @8 H1 j* x5 q& ^7 ~Although the bone age was advanced at the time of
6 {' V4 w. S$ T% V1 k# s6 Ndiagnosis, the child had a normal growth velocity at
8 S8 K$ E/ g0 Othe follow-up visit. It is hoped that his final adult
: w' ~( B! n: ?/ i( Bheight will not be affected.
' A% V4 }' V$ y8 t5 C/ _Although rarely reported, the widespread avail-
5 F' G) L2 _/ k# Bability of androgen products in our society may
/ s2 D! @1 U2 I$ iindeed cause more virilization in male or female: K) U* C4 v. s$ w# R r/ c
children than one would realize. Exposure to andro-' _+ Q/ q* T r6 ]
gen products must be considered and specific ques-9 _, O( x& k( N. D+ Z* m9 ]- H
tioning about the use of a testosterone product or) |1 c2 D+ \- y/ k* v' [8 G3 h
gel should be asked of the family members during
1 @% x7 s2 z7 Y9 g, i" ~, H0 Dthe evaluation of any children who present with vir-$ D1 o/ q0 i) \
ilization or peripheral precocious puberty. The diag-
! s5 m y7 }# W0 I1 ]* Q, Snosis can be established by just a few tests and by8 `& X7 p, X0 D! R
appropriate history. The inability to obtain such a: \2 h3 s- M/ n4 X; q9 X
history, or failure to ask the specific questions, may
! O- s% j. |- s, g1 mresult in extensive, unnecessary, and expensive
/ o% m |/ l- I1 L: oinvestigation. The primary care physician should be: l, d8 N$ P2 E
aware of this fact, because most of these children
% b0 Z: L) J) Q6 ?3 Emay initially present in their practice. The Physicians’
& g* b5 U0 {/ V9 n; rDesk Reference and package insert should also put a: Z" [1 K' O8 K$ ~2 m/ R9 f
warning about the virilizing effect on a male or% d! S. m/ l9 s3 z- L' D
female child who might come in contact with some- X; L9 K( C* h; e- v
one using any of these products.
' X6 ?! i7 P7 D4 _3 O+ \8 U IReferences) _ s2 ^" D) | P% q1 [* q
1. Styne DM. The testes: disorder of sexual differentiation7 G5 k$ }, M" N0 H# o9 U1 ?! e3 p
and puberty in the male. In: Sperling MA, ed. Pediatric
0 i( Z7 k( _( F# REndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 F$ h, _8 Y7 ^+ s. N# c2002: 565-628.% M9 Q8 C% P* r
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# b9 ^$ @1 Q$ e' L6 u5 U
puberty in children with tumours of the suprasellar pineal |
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