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Sexual Precocity in a 16-Month-Old
/ j& C% K. D9 e2 nBoy Induced by Indirect Topical
+ t& I* @9 w, h5 \Exposure to Testosterone. {3 S, H O4 H- d# L6 ]1 G: o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: l% e( Z. C- h) z) {and Kenneth R. Rettig, MD14 ~" \! j. w1 V6 P7 n
Clinical Pediatrics
% f3 I: ^% t# DVolume 46 Number 6 a7 y( J4 _0 K
July 2007 540-5433 y' n5 K$ o& o' y3 E7 @4 r
© 2007 Sage Publications2 ^5 K% e. ]. c4 P3 v7 `( m
10.1177/0009922806296651
& e# l# n) [, ohttp://clp.sagepub.com, @% c$ M G q) i3 L8 @
hosted at2 C) R6 q% v. M# V
http://online.sagepub.com
" ]# o s( g3 p/ E- Z7 x* W# hPrecocious puberty in boys, central or peripheral," ]! X. t: P$ a, R; e7 G' |
is a significant concern for physicians. Central
, t. Y" Y$ G8 R9 L7 kprecocious puberty (CPP), which is mediated
" v$ r7 {5 c$ zthrough the hypothalamic pituitary gonadal axis, has8 b' e) X* U5 P
a higher incidence of organic central nervous system
/ F. U1 Z. q( b$ \ Tlesions in boys.1,2 Virilization in boys, as manifested
( i5 T9 \( D- t. M' Qby enlargement of the penis, development of pubic
. E2 X V) T r1 Z" ohair, and facial acne without enlargement of testi-" R/ _8 e( s1 R {6 D# H
cles, suggests peripheral or pseudopuberty.1-3 We: z9 V/ {6 m X
report a 16-month-old boy who presented with the8 m% h9 L" v6 b# I( w2 ?
enlargement of the phallus and pubic hair develop-
$ A( v+ z+ d0 b, e4 [ment without testicular enlargement, which was due) q7 d7 U4 _2 ~5 F2 M9 \# }% y0 a
to the unintentional exposure to androgen gel used by" ?' `$ e( ~$ U# W0 J
the father. The family initially concealed this infor-- f* ]4 j, y G' S% [0 M! b
mation, resulting in an extensive work-up for this
& E2 U3 x! y* R- `child. Given the widespread and easy availability of9 z; n, G: M' V0 ?; ~% N
testosterone gel and cream, we believe this is proba-
4 @% ?' B& J2 V' J$ T: T5 ?bly more common than the rare case report in the: b4 u) f# t( ~5 h- e1 o( o
literature.4
" z8 x; {* \1 Z8 s$ n6 q7 NPatient Report- t1 X( |* f, d6 f
A 16-month-old white child was referred to the; K! y5 C+ D$ q
endocrine clinic by his pediatrician with the concern3 |, m9 S `" p: l3 G6 N( T8 l
of early sexual development. His mother noticed
6 `' r: e( \% H0 Slight colored pubic hair development when he was( S" c1 J6 n- o L; y3 @0 F, P7 L
From the 1Division of Pediatric Endocrinology, 2University of
) Y4 k) A! A& aSouth Alabama Medical Center, Mobile, Alabama.
9 ]3 R- N j. c4 i# x$ `4 H, NAddress correspondence to: Samar K. Bhowmick, MD, FACE,
$ K, N8 t) g/ a: b8 WProfessor of Pediatrics, University of South Alabama, College of
. A9 @" _* z: y- mMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# V$ O! F5 D- m0 h+ b& me-mail: [email protected].
; T- Y2 o4 i) Y0 t( X8 q. Habout 6 to 7 months old, which progressively became
3 q! W# B2 ~" Udarker. She was also concerned about the enlarge-0 y1 B. R, K, N# l6 ?
ment of his penis and frequent erections. The child
" C! [8 h. G" k% U5 awas the product of a full-term normal delivery, with0 L c7 C2 B- r* S; ^5 G* B
a birth weight of 7 lb 14 oz, and birth length of- A1 y- g3 F& a/ ]; j1 C
20 inches. He was breast-fed throughout the first year: a7 i7 H" S6 Y# H
of life and was still receiving breast milk along with
$ K* v4 S& k0 p+ Lsolid food. He had no hospitalizations or surgery,
. [2 q9 ~/ ~* O6 M% A8 k4 p( {* nand his psychosocial and psychomotor development
1 \+ C! E, w* K4 d Pwas age appropriate.: _7 V% B$ p) X6 i
The family history was remarkable for the father,
" w6 d- c$ X% e/ wwho was diagnosed with hypothyroidism at age 16,
$ y: k4 o4 x2 h8 F0 T4 k* Q, }which was treated with thyroxine. The father’s
) ?* y! p0 l$ ~6 f/ j6 _- fheight was 6 feet, and he went through a somewhat
( m9 L/ W# `" @( S" D0 _early puberty and had stopped growing by age 14.
/ [- C9 o4 ]/ i3 p' f4 H2 @, SThe father denied taking any other medication. The
: F' P3 w0 l1 W" e ~/ D* L9 `child’s mother was in good health. Her menarche
+ o; ` _1 v* h; R' H" x' |was at 11 years of age, and her height was at 5 feet0 x1 j, R' t C/ {
5 inches. There was no other family history of pre-+ h1 \9 Y( B& F5 \ q9 ^# G9 y0 o) t, N
cocious sexual development in the first-degree rela-: m7 P5 T% Z( e6 n
tives. There were no siblings.
+ J. m5 g* T- X: C! T: z8 DPhysical Examination
) a4 k9 Y' ^/ y( E) \The physical examination revealed a very active,8 \& F: P" P3 r' G3 ?# T2 U
playful, and healthy boy. The vital signs documented# Y6 X$ ?. G7 u4 @9 s
a blood pressure of 85/50 mm Hg, his length was1 E: w4 `$ D* K. Y& K, `0 A( w) e
90 cm (>97th percentile), and his weight was 14.4 kg
/ ^( m: L8 |/ o5 q$ S(also >97th percentile). The observed yearly growth
/ x0 b( o3 ?( @' F- o1 vvelocity was 30 cm (12 inches). The examination of6 F) W6 J7 I( i) l" r+ K1 A8 g
the neck revealed no thyroid enlargement.
# `* h( { ^9 p# T/ L( y- `The genitourinary examination was remarkable for/ d: H: s! _" p( u
enlargement of the penis, with a stretched length of" r6 R0 B) O! N4 p1 M2 g0 [/ C+ v
8 cm and a width of 2 cm. The glans penis was very well6 Y0 p! f# ?# A& r4 a4 R! k2 B
developed. The pubic hair was Tanner II, mostly around% n: r P2 f1 C6 B6 p* \+ A- w
540# u7 `7 F' a3 |$ h2 i
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; l( i4 h2 D9 K6 }: [/ Q
the base of the phallus and was dark and curled. The: J2 ?' V+ U( i4 Y9 D3 n% F
testicular volume was prepubertal at 2 mL each.( @( V- x6 Y) r; e! I% z! c. k
The skin was moist and smooth and somewhat
' g0 s. i; U E" V3 g% ~- xoily. No axillary hair was noted. There were no& S# s6 z, |% {3 a* L' `
abnormal skin pigmentations or café-au-lait spots.' M1 C1 J X5 i8 \/ i( r
Neurologic evaluation showed deep tendon reflex 2+
! |- \: e. Y, ?( V3 |bilateral and symmetrical. There was no suggestion
; e. N) M0 @* u! W" B# T# Q' f4 Dof papilledema.
! Z; q# _0 T- yLaboratory Evaluation
" ~7 B) ~6 ~) F% p& u8 L7 z0 qThe bone age was consistent with 28 months by
& P- }# q" y, S, {using the standard of Greulich and Pyle at a chrono-
" J" \% y8 ~9 xlogic age of 16 months (advanced).5 Chromosomal/ Y q0 q7 n: q% q2 k
karyotype was 46XY. The thyroid function test
( m% w. e6 N& C5 u9 _showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 C* A/ S) y% k7 i& C
lating hormone level was 1.3 µIU/mL (both normal).
* S; l. `) x5 g. |The concentrations of serum electrolytes, blood( U9 z7 ~/ \2 ?! t+ M
urea nitrogen, creatinine, and calcium all were+ D% ~8 s6 Y3 o, |" ^% b# C; ~
within normal range for his age. The concentration
# t: G& {' I) O6 W, {of serum 17-hydroxyprogesterone was 16 ng/dL* {2 m: \( W0 n3 n, I
(normal, 3 to 90 ng/dL), androstenedione was 208 L$ |; l% k, v) q' K: j
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros- X# q2 |; B R3 ~
terone was 38 ng/dL (normal, 50 to 760 ng/dL)," r/ f! `4 x% e1 g0 U
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
# H' L. ^& B0 w/ z49ng/dL), 11-desoxycortisol (specific compound S)( g5 B7 _$ ?% q3 r* s
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 |) D3 |6 z' m) Z: s" ]5 [# e: [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- u4 X# a- V# `& w- _
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) ?3 B9 T% W5 W, A! K" rand β-human chorionic gonadotropin was less than
) F' G I3 Y' ~, X( o- r/ m5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 x3 ^/ d# T$ Lstimulating hormone and leuteinizing hormone
4 f4 a8 m8 d, B Q4 A5 Rconcentrations were less than 0.05 mIU/mL; r' c6 H! o% W+ U8 f
(prepubertal).) M3 V! \# E' B2 T) w% p
The parents were notified about the laboratory
, x0 ^% q+ m2 {+ s* `; J# W" T# Sresults and were informed that all of the tests were
# V. Q/ Y, m# k& s9 bnormal except the testosterone level was high. The
( K E7 E2 |6 H. i; j8 ~follow-up visit was arranged within a few weeks to
# S0 j- @3 r: w4 F4 kobtain testicular and abdominal sonograms; how-8 j7 A9 Y7 n6 j* q* i. E/ q, I
ever, the family did not return for 4 months.
% |& J" j! x5 s6 L/ k5 qPhysical examination at this time revealed that the+ J4 P( ]8 V0 `7 K% W9 F
child had grown 2.5 cm in 4 months and had gained
5 [7 D$ J7 y& y6 u' x9 i2 kg of weight. Physical examination remained
5 @ w, l- h5 K1 X+ Q8 R8 K3 g6 Tunchanged. Surprisingly, the pubic hair almost com-
/ I$ r' N7 s1 G( Y$ Dpletely disappeared except for a few vellous hairs at7 J$ `; G% O7 v9 Q+ ?, g- m$ c
the base of the phallus. Testicular volume was still 2$ D. z2 P+ e d; B( ~
mL, and the size of the penis remained unchanged.
4 d7 x$ k+ Q3 [3 x o' [The mother also said that the boy was no longer hav-
! g! O/ j: [9 ]9 |$ P& Xing frequent erections.
" |1 p3 ^6 d2 L: O- e. U' j/ aBoth parents were again questioned about use of
6 K9 I/ V" M/ ]. b0 K& Dany ointment/creams that they may have applied to
7 ?, j4 ^ c1 @the child’s skin. This time the father admitted the
+ P% Q7 T8 N4 A, h5 z8 l* J: N0 iTopical Testosterone Exposure / Bhowmick et al 541/ h: J, n+ D* |: B
use of testosterone gel twice daily that he was apply-2 E9 Q2 \2 m( x) U7 T# x' b
ing over his own shoulders, chest, and back area for$ Q) h9 {4 [' s6 ?* o$ d: \! L. w9 n
a year. The father also revealed he was embarrassed U1 C" C' T# }' v3 r$ a7 |8 v* w
to disclose that he was using a testosterone gel pre-, d" s$ D$ C. ?; V
scribed by his family physician for decreased libido$ W( e6 E. `: a9 c* X
secondary to depression.
- _: g+ z( e! _The child slept in the same bed with parents.
! S& j% y* I4 d, r5 }3 k7 W9 WThe father would hug the baby and hold him on his: K& }+ N& ?: X9 r2 i
chest for a considerable period of time, causing sig-
! `( N c, d9 N/ W3 A, |4 Nnificant bare skin contact between baby and father.
1 x! N7 Z/ {' i* R7 WThe father also admitted that after the phone call,1 W& I0 c) S0 o [7 w8 ^
when he learned the testosterone level in the baby
8 {3 Y8 i: _1 k2 Z; bwas high, he then read the product information) m$ P' u2 J- _% ]. |8 E
packet and concluded that it was most likely the rea- `- x4 B& e2 u5 y. }* e# T. N- X
son for the child’s virilization. At that time, they2 Q3 `8 U2 Z1 G/ M
decided to put the baby in a separate bed, and the+ X, h0 |' N& [2 S, g7 C/ P4 r
father was not hugging him with bare skin and had
* j u, I& p& ]% Zbeen using protective clothing. A repeat testosterone
! g' ?& d5 B5 H( d6 htest was ordered, but the family did not go to the6 X) Y; W0 _" b
laboratory to obtain the test.
8 H7 N7 }% v& I; q# KDiscussion
* j& c$ V7 c6 V# Y% t/ k8 RPrecocious puberty in boys is defined as secondary
]6 A$ z# W( u1 I xsexual development before 9 years of age.1,4
9 m, G/ _; S) J' W: _! bPrecocious puberty is termed as central (true) when
& O& B2 p( ?, f0 K! S A8 g8 bit is caused by the premature activation of hypo-0 e! ~$ N% `( t4 r, c- Q0 d) S( {
thalamic pituitary gonadal axis. CPP is more com-
8 Q1 b. d5 V; G6 J4 S kmon in girls than in boys.1,3 Most boys with CPP
- i* q- d- e. Smay have a central nervous system lesion that is
- O1 v8 j; l) A* @6 O% B1 K7 Oresponsible for the early activation of the hypothal-3 J, W2 n4 _, n/ i% z, R
amic pituitary gonadal axis.1-3 Thus, greater empha-7 q9 a5 f( `& {
sis has been given to neuroradiologic imaging in, v6 I( H/ V5 T/ w& N* ]+ P
boys with precocious puberty. In addition to viril-$ Z+ P8 n8 y0 w! O/ e% {- g V
ization, the clinical hallmark of CPP is the symmet-
2 @/ m) T0 J+ f' j; j9 N) F% |rical testicular growth secondary to stimulation by
* Q" ]) \$ R; f9 a% fgonadotropins.1,3
& P2 D0 B/ K$ ^% SGonadotropin-independent peripheral preco-: m- w7 T8 K( A4 y6 W' \& x8 L: s
cious puberty in boys also results from inappropriate4 P- t5 H+ P0 h5 K+ J! S: `4 h
androgenic stimulation from either endogenous or6 q( J2 F8 R; |8 P6 c
exogenous sources, nonpituitary gonadotropin stim-
) P$ D3 x% B! F+ @- }" dulation, and rare activating mutations.3 Virilizing2 a7 d0 R. V4 o9 e+ c
congenital adrenal hyperplasia producing excessive
# j8 l. n3 f' M1 xadrenal androgens is a common cause of precocious' l; B$ u7 L& t: Z: r# u
puberty in boys.3,4: O5 y K, W2 ^0 \
The most common form of congenital adrenal: f0 [ @7 ]# Y2 S9 B
hyperplasia is the 21-hydroxylase enzyme deficiency.- \2 M/ C1 A3 c* m1 `
The 11-β hydroxylase deficiency may also result in
. O$ h) ~9 {0 ~) yexcessive adrenal androgen production, and rarely,# ]: s* w+ T* `, K+ S
an adrenal tumor may also cause adrenal androgen$ u F# o% J9 L) D D ]
excess.1,3
9 ]! l5 X& l& _/ U; u! Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' P* d- M3 N! L
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ p1 @. K# P# b! K YA unique entity of male-limited gonadotropin-
$ Z6 M( D9 b. _/ cindependent precocious puberty, which is also known
( O4 m% V. ]0 vas testotoxicosis, may cause precocious puberty at a" Z5 o* @3 L3 ?; c# Q( A2 p+ R+ M. b
very young age. The physical findings in these boys0 \0 J6 Z7 R: Q$ _) M) |9 I4 E1 Z1 ?
with this disorder are full pubertal development," R% j: L8 E) K! s* f b7 E) {, z
including bilateral testicular growth, similar to boys
1 H0 e& ^# f: `( Mwith CPP. The gonadotropin levels in this disorder# O% q, w6 D6 z; U5 A0 t0 N
are suppressed to prepubertal levels and do not show( {! W! J% \6 } K" R
pubertal response of gonadotropin after gonadotropin-
4 C0 H7 `7 ~; p1 p( P1 breleasing hormone stimulation. This is a sex-linked; o; b! b2 \9 w1 W
autosomal dominant disorder that affects only% Z5 V9 \# U- p: m( o
males; therefore, other male members of the family
4 g) ~2 }3 D* _ {may have similar precocious puberty.3" e7 E, z" ]( x$ r7 _/ {
In our patient, physical examination was incon-
: V1 ~; X" X; Q5 I/ J1 p3 ~$ S7 h( `sistent with true precocious puberty since his testi-+ ]7 Y- H: j, S. f" F
cles were prepubertal in size. However, testotoxicosis" f" M1 o$ G# \
was in the differential diagnosis because his father. X S' |! a a8 x1 q
started puberty somewhat early, and occasionally,3 `5 U q3 a! E7 ?+ F+ z. ?
testicular enlargement is not that evident in the' `" E. E. w t" Z" D# D7 L8 M
beginning of this process.1 In the absence of a neg-
0 r3 |! ^- ^6 o' N* }1 ]! Native initial history of androgen exposure, our
( e; f2 Z: C5 F1 |6 m1 F, obiggest concern was virilizing adrenal hyperplasia,% r: P- \1 g7 M+ d. l' q
either 21-hydroxylase deficiency or 11-β hydroxylase
* n7 Y2 |* w; Ydeficiency. Those diagnoses were excluded by find-! m9 |- {* |2 U
ing the normal level of adrenal steroids.) P, Y" k6 y( v: }# z
The diagnosis of exogenous androgens was strongly
2 a# }% ~- X' @5 { nsuspected in a follow-up visit after 4 months because8 F- ^5 }" r! E
the physical examination revealed the complete disap-
# c' m$ k$ J N0 {pearance of pubic hair, normal growth velocity, and/ N- d1 J4 n- F9 ~9 Y* v6 p
decreased erections. The father admitted using a testos-, W. q d3 d1 |* Z! U
terone gel, which he concealed at first visit. He was
7 r/ J/ f8 H( A+ ]using it rather frequently, twice a day. The Physicians’- G, w V+ Q! @: N/ P y
Desk Reference, or package insert of this product, gel or
9 K1 C3 a3 z0 Pcream, cautions about dermal testosterone transfer to
6 o* w! K; l) _4 A, punprotected females through direct skin exposure.: J# T5 T6 T& A9 b- c: t' m/ ^
Serum testosterone level was found to be 2 times the
3 }, F- Q, E$ {+ Y abaseline value in those females who were exposed to$ T9 f1 e1 ]* x% D; E
even 15 minutes of direct skin contact with their male
6 q. s- T3 ?& p* S% {# H8 ?partners.6 However, when a shirt covered the applica-
) L; C; E5 E1 jtion site, this testosterone transfer was prevented.; Y) Q8 f$ [' N8 b4 [$ s. z
Our patient’s testosterone level was 60 ng/mL,
3 ?) R9 g8 M+ T& E% D, q+ W$ M# I, Zwhich was clearly high. Some studies suggest that
5 I9 s8 {% ?4 w' G fdermal conversion of testosterone to dihydrotestos-, r4 q: O5 U6 \) f
terone, which is a more potent metabolite, is more
& [- q7 L3 i, j. B( _active in young children exposed to testosterone
5 e% y2 m: m" q1 v& C2 Sexogenously7; however, we did not measure a dihy-" a P! s, _5 S O9 x- e* {0 k
drotestosterone level in our patient. In addition to$ ~. n; G; v( J4 ]/ f$ d8 K, a
virilization, exposure to exogenous testosterone in! ]4 k8 y3 p9 `* f: U. `( j Z) ~
children results in an increase in growth velocity and
% {( x0 w# I" G+ }) B* |/ s+ P( cadvanced bone age, as seen in our patient.
- ]4 M. A4 d. G+ T* v3 f1 uThe long-term effect of androgen exposure during& A: N; [9 g% X a$ T
early childhood on pubertal development and final
* s* [+ m2 E2 g* v9 Vadult height are not fully known and always remain7 C9 b4 Z, r) I$ x. S- W
a concern. Children treated with short-term testos-
; W4 T! L; r }5 l' M1 fterone injection or topical androgen may exhibit some i- A4 M U) W7 a5 ]4 {
acceleration of the skeletal maturation; however, after+ d$ N' C0 @3 r" T5 l2 C
cessation of treatment, the rate of bone maturation
2 g9 }7 D- ]1 y7 M% u! g0 Pdecelerates and gradually returns to normal.8,97 B) |: ?' Y* B8 ]: @. X
There are conflicting reports and controversy7 }5 _8 L4 i$ v
over the effect of early androgen exposure on adult% K4 }1 a" M* b; h" R
penile length.10,11 Some reports suggest subnormal
( V8 Z- ]4 H! Jadult penile length, apparently because of downreg-: k3 W: S9 n/ t5 U. J( I
ulation of androgen receptor number.10,12 However,
7 V2 ~! T8 P, b; G. `4 RSutherland et al13 did not find a correlation between3 b! c0 |& T8 _ |) _$ _2 V
childhood testosterone exposure and reduced adult. a1 A5 y4 v3 F' V0 O2 s
penile length in clinical studies.
' `, a" D n- N9 H1 q( W7 fNonetheless, we do not believe our patient is
: K# K7 F" o* S$ A+ Q/ Qgoing to experience any of the untoward effects from+ o" \+ |% S6 K! b1 _$ w5 K
testosterone exposure as mentioned earlier because
% L' S" O2 Y4 z7 F1 e- z9 Cthe exposure was not for a prolonged period of time./ X) ~/ u0 }. U, p1 Y: M! E
Although the bone age was advanced at the time of
* d7 }# ]% b* |2 b- Mdiagnosis, the child had a normal growth velocity at
) s; ^. l+ }3 D& Hthe follow-up visit. It is hoped that his final adult
' k( L4 D- U7 c/ L- P9 D1 Cheight will not be affected.1 D, P: R: H+ R1 Q/ N, s6 R0 M. ~/ A
Although rarely reported, the widespread avail-
( a( M3 L3 _7 F! c: pability of androgen products in our society may* b1 x' d5 U$ m& x/ I- _( V
indeed cause more virilization in male or female
5 R$ b0 A4 ]% nchildren than one would realize. Exposure to andro-/ ~ f9 b$ @" s
gen products must be considered and specific ques-8 M# }9 _4 O0 k/ r5 ^; Y4 [
tioning about the use of a testosterone product or
0 u! w+ l, N: Q% b, ~! Mgel should be asked of the family members during
3 f# T' v6 y. D/ {the evaluation of any children who present with vir-' u( H5 ?$ ^+ X& @
ilization or peripheral precocious puberty. The diag-
/ _4 u- _3 E3 x& |nosis can be established by just a few tests and by2 c: t' R& B. G3 j
appropriate history. The inability to obtain such a6 S f7 i- L2 `# }) C3 M( t' k
history, or failure to ask the specific questions, may
, t9 Z6 {' H! d/ [$ c6 tresult in extensive, unnecessary, and expensive8 {3 i2 y" v4 X1 g# J; r* I
investigation. The primary care physician should be
& ~& m3 y" L7 g- qaware of this fact, because most of these children0 }4 ], X. s4 b& P
may initially present in their practice. The Physicians’, ^ e" O1 e3 T3 J5 k- }0 m) M, i
Desk Reference and package insert should also put a# d% H# a5 k/ [9 f# U+ b
warning about the virilizing effect on a male or" I6 ?! T/ e5 [0 Q3 p) `
female child who might come in contact with some-' v2 n9 K/ B* ]! t! t% M
one using any of these products.* i7 K2 d0 c1 A; q$ {# x
References# z* k# @; P/ b6 M4 z3 D5 T' x5 G
1. Styne DM. The testes: disorder of sexual differentiation- W# j# D0 }2 f* Q$ L3 E" a
and puberty in the male. In: Sperling MA, ed. Pediatric
$ E# Z; R& W! v, f+ E( GEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ _. R/ R4 U0 [/ w! {# a/ f2002: 565-628.5 ~" o" W+ X/ t
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. r7 i. c% J# h8 F" V x% m0 hpuberty in children with tumours of the suprasellar pineal |
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