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Sexual Precocity in a 16-Month-Old$ s8 D* n8 w3 c( V: o/ e
Boy Induced by Indirect Topical6 \, y/ d8 L9 ?1 W; [* D
Exposure to Testosterone
% J6 P9 j( ?% j+ O7 rSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! Z7 i# z' b; J% v3 J) w( n% Land Kenneth R. Rettig, MD1
: ?+ `& [) W$ m; z! C' B( HClinical Pediatrics. l: F1 i" x- S" k w# T- m# m" j. k
Volume 46 Number 62 y, U+ V* m- _! k }# z5 d4 H
July 2007 540-543
& z8 y/ r1 z, C. f( x© 2007 Sage Publications
" N' ~, W/ Z4 G) h% ?10.1177/0009922806296651
' S% n8 N$ b& C2 g: h+ W9 L8 v5 ]http://clp.sagepub.com0 k' M2 ]) W# J3 n( w( W7 ?* c+ n( I
hosted at/ H9 K/ G; o8 P8 j0 c! K
http://online.sagepub.com' A/ E' [" a% [
Precocious puberty in boys, central or peripheral,
3 ]3 j$ c0 T4 D8 zis a significant concern for physicians. Central/ _4 A. V% O, I* l
precocious puberty (CPP), which is mediated6 h1 U2 `! d+ y' |
through the hypothalamic pituitary gonadal axis, has
# ~5 r& J( }2 ]& \+ Za higher incidence of organic central nervous system
: w. Q0 O% s- K* m( ilesions in boys.1,2 Virilization in boys, as manifested
9 [$ a4 x6 u3 Y3 K% ]2 fby enlargement of the penis, development of pubic2 }* h! y6 } y7 v+ R* j C# u+ d
hair, and facial acne without enlargement of testi-2 t" Z4 ^) z+ c
cles, suggests peripheral or pseudopuberty.1-3 We
& k6 v9 M4 H2 V9 |. _) e) F: m( [7 Mreport a 16-month-old boy who presented with the
; F9 `! y1 X) h* |& oenlargement of the phallus and pubic hair develop-7 D/ W, C3 w! l9 _1 j1 t
ment without testicular enlargement, which was due
% u; j. w9 y% S6 S) wto the unintentional exposure to androgen gel used by
6 ]2 B4 q M" ?the father. The family initially concealed this infor- y5 P! a& I, q# _6 m8 d
mation, resulting in an extensive work-up for this
" ?# ]1 G# y1 t% @! h) }& S+ V) [child. Given the widespread and easy availability of. o" z2 a9 o% {: Y
testosterone gel and cream, we believe this is proba-
0 p1 i4 _5 P. _/ I% w+ Z* Bbly more common than the rare case report in the# ~$ g1 [; Y! B3 o% g9 H9 N
literature.4% r6 r& E: E2 w
Patient Report
% ^, Q+ [4 e; b2 D7 |0 kA 16-month-old white child was referred to the
0 S5 L4 }, B$ Wendocrine clinic by his pediatrician with the concern! U6 x0 T+ h" U$ Q$ ]; T8 h
of early sexual development. His mother noticed n9 T6 j# ~3 x* A
light colored pubic hair development when he was
( A+ ^2 K1 F @* S; v, yFrom the 1Division of Pediatric Endocrinology, 2University of
( q6 V1 h) B- D4 O1 eSouth Alabama Medical Center, Mobile, Alabama.8 v+ G8 R _/ z6 \( X, j; V
Address correspondence to: Samar K. Bhowmick, MD, FACE,! G" x2 r. x; c5 X- L
Professor of Pediatrics, University of South Alabama, College of+ q: q/ q! Z0 t% {
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 O, d% x" {% `" t
e-mail: [email protected]., r# k# \4 ~, V, L4 w$ g8 {6 j# c
about 6 to 7 months old, which progressively became- D2 R N8 L9 y' l2 F' E1 k/ ]
darker. She was also concerned about the enlarge-
, x8 t; F8 ~+ U9 Q; Ement of his penis and frequent erections. The child
& |% `( i0 j1 ~was the product of a full-term normal delivery, with
' @7 C% k4 I6 ?$ F" o; Y# r6 Va birth weight of 7 lb 14 oz, and birth length of
) p2 ^2 j, O4 I; X! N* W9 r2 w8 H20 inches. He was breast-fed throughout the first year
( N7 F* E) V$ Y8 L# Hof life and was still receiving breast milk along with
" n x) ~# g5 X, u. p/ Z1 B. X2 h+ lsolid food. He had no hospitalizations or surgery,+ P% t% d @" ?! \+ A$ ~
and his psychosocial and psychomotor development; c: `7 \+ Q8 F/ h& z& H2 g) Z
was age appropriate., e; d" T3 j5 u; z% T
The family history was remarkable for the father,
/ M4 d( ]1 y# v, ?5 b& [& Qwho was diagnosed with hypothyroidism at age 16,
) |" N: C+ d+ Hwhich was treated with thyroxine. The father’s
! h; E' p, H) l6 w, Cheight was 6 feet, and he went through a somewhat* ]% G' r/ S( q% ]' Z, s3 A
early puberty and had stopped growing by age 14.* K% r+ a0 g+ e' U" f- Z% |
The father denied taking any other medication. The O. y0 s* x+ e
child’s mother was in good health. Her menarche; Y" l$ D; f* [
was at 11 years of age, and her height was at 5 feet, k0 @" E* G# d
5 inches. There was no other family history of pre-
' I1 Z! c- E. lcocious sexual development in the first-degree rela-
" u+ U$ ^$ x! L) ^tives. There were no siblings.. D) T u R' w2 I" G5 y$ h
Physical Examination
) ]( \3 P! }* a5 {7 U; ~ UThe physical examination revealed a very active,5 J# o( d6 f7 l7 j
playful, and healthy boy. The vital signs documented) ]7 {/ d# N& C. f2 H# P
a blood pressure of 85/50 mm Hg, his length was
0 f4 k: w' L, k8 S" m) K' f3 f90 cm (>97th percentile), and his weight was 14.4 kg% {5 M! D+ F/ W9 x& E+ [% D+ Q6 x
(also >97th percentile). The observed yearly growth* Q4 X: Y+ e7 @! ?
velocity was 30 cm (12 inches). The examination of
) A4 }/ J: E5 F$ qthe neck revealed no thyroid enlargement.) h [3 v8 `* {* i: n
The genitourinary examination was remarkable for2 C: q* a1 x, }# E; @( G# l9 a9 ^
enlargement of the penis, with a stretched length of
/ s+ A& N8 S0 \" h* {! F2 }+ M8 cm and a width of 2 cm. The glans penis was very well
: i6 R4 q! k! [6 V8 q* hdeveloped. The pubic hair was Tanner II, mostly around
J( ?* u' ^- {6 Z* M) N540
( p, I; j5 Y. r9 n: H7 Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' a- ?5 x. x' d' T7 m- Q; T/ v) {
the base of the phallus and was dark and curled. The/ \+ |, g7 k Z2 v) Z4 L# T6 o
testicular volume was prepubertal at 2 mL each.
8 {" ?' Q- R1 x- E1 r7 [The skin was moist and smooth and somewhat4 M- Y$ K* |" T2 N
oily. No axillary hair was noted. There were no. @' c$ X2 H( f
abnormal skin pigmentations or café-au-lait spots.9 Z+ @9 p, u6 L9 @! z- N% Q
Neurologic evaluation showed deep tendon reflex 2+6 r' h- t8 \4 \ ]( v
bilateral and symmetrical. There was no suggestion; Z$ h( ?, K8 n4 y! I- V7 G) `
of papilledema.
" e- d5 }5 b a: QLaboratory Evaluation2 K/ D9 h5 x, ?+ C/ G
The bone age was consistent with 28 months by& z" g+ m4 W4 Z1 l
using the standard of Greulich and Pyle at a chrono-, G: W/ s- c" i4 z5 Q0 _* k3 \+ ^! _
logic age of 16 months (advanced).5 Chromosomal0 \1 m9 R5 I' ?# ~
karyotype was 46XY. The thyroid function test6 n8 } }2 }, u/ f7 e. E, M( R
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 D( u! C, }: H# m$ C+ dlating hormone level was 1.3 µIU/mL (both normal).3 j5 s7 _) n# k }3 ^
The concentrations of serum electrolytes, blood4 M5 A2 J( B( i
urea nitrogen, creatinine, and calcium all were9 i7 y) D3 ^6 D3 _$ o" h5 P' C9 E
within normal range for his age. The concentration
% M- m( t1 t* {' O; yof serum 17-hydroxyprogesterone was 16 ng/dL9 g% V4 z T$ @* I* v$ J# \/ M# h
(normal, 3 to 90 ng/dL), androstenedione was 20
+ ~" n5 K5 o) L+ ^ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( D7 G' {! |' R I! ]terone was 38 ng/dL (normal, 50 to 760 ng/dL),4 `5 F. R' t; S d0 W" t9 \
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
# r/ N$ k/ t7 E49ng/dL), 11-desoxycortisol (specific compound S)5 x- [* M# h2 ^' A
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
y4 Q9 d$ g- r9 Mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( d/ J1 J; w5 K7 I$ gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 w7 P$ e) D& u$ X6 i) z1 G
and β-human chorionic gonadotropin was less than
4 d7 w4 D% x1 Z. G/ L, O6 M5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 S7 \9 Y/ C" hstimulating hormone and leuteinizing hormone
* Z3 ?" u" U' c) ^9 Y" Nconcentrations were less than 0.05 mIU/mL
+ f6 @, U- E5 X6 F3 D(prepubertal).
# M9 M- m' m8 u4 T: y* |5 CThe parents were notified about the laboratory$ r1 T+ p( ], [- L6 _+ b% v) C% V% h
results and were informed that all of the tests were
! I/ l0 |' [: Fnormal except the testosterone level was high. The+ ^7 @, H3 b( D3 `) |6 s0 W
follow-up visit was arranged within a few weeks to
/ _9 y6 n- p& L, H. Bobtain testicular and abdominal sonograms; how- G1 _ J9 d( ]; i- y/ j9 V! N5 O
ever, the family did not return for 4 months." d) L. {5 Z& B
Physical examination at this time revealed that the. O: {, U. R$ t: J; _. ^: Y" c9 {' a
child had grown 2.5 cm in 4 months and had gained
8 F+ z$ o! y5 C, c: W3 A2 m% Y2 kg of weight. Physical examination remained L0 V/ v3 b+ W. b3 T
unchanged. Surprisingly, the pubic hair almost com-
' ?3 d l; H2 N |1 a% w6 Hpletely disappeared except for a few vellous hairs at2 H& _& ]" L" y
the base of the phallus. Testicular volume was still 2* x9 Q* \: c0 `, v
mL, and the size of the penis remained unchanged." ?7 y: |8 f' ~3 u% j0 Z0 K
The mother also said that the boy was no longer hav-
; {: ?* r. k" K1 ^9 u$ uing frequent erections.8 F. d8 f% K) ~# A5 F
Both parents were again questioned about use of# G( j- ]" F( T! v( l
any ointment/creams that they may have applied to' ~# x& r$ A. K y: C9 m
the child’s skin. This time the father admitted the' ]* a0 c( }9 ~1 I0 w$ N
Topical Testosterone Exposure / Bhowmick et al 541
! _8 g$ c- J9 k( l4 Nuse of testosterone gel twice daily that he was apply-
4 B' e3 v+ r/ I4 r5 r) { ving over his own shoulders, chest, and back area for
! ]$ H$ D& g3 [2 ua year. The father also revealed he was embarrassed
/ b$ M! z4 _1 N8 j2 v5 ? Wto disclose that he was using a testosterone gel pre-; `1 k/ ]; T; G( o T2 f. B
scribed by his family physician for decreased libido1 n/ \+ [' b, {! W, {; E. @" O
secondary to depression.
1 n$ u* N3 F- X6 V tThe child slept in the same bed with parents.) {, k' O2 k9 v0 z" }- j
The father would hug the baby and hold him on his
; U- [/ a) M/ u6 Ychest for a considerable period of time, causing sig-) @8 z( ?$ M. D4 O9 [9 F) M
nificant bare skin contact between baby and father.4 W2 |4 P m1 ^' ] ^- Y4 ^2 r
The father also admitted that after the phone call,1 @# V4 }) Y% {: I% ^/ x! w
when he learned the testosterone level in the baby
4 E- G$ W$ ^9 \7 X& q* j: |was high, he then read the product information, F. e) f8 {. V
packet and concluded that it was most likely the rea-2 v" V' }4 W5 u0 L7 u, H
son for the child’s virilization. At that time, they
. V8 [+ c% G; Q0 K/ G( q$ C# Sdecided to put the baby in a separate bed, and the0 j, P6 g) p& Y
father was not hugging him with bare skin and had
M# q J) m4 [been using protective clothing. A repeat testosterone
4 O( _& w. w8 e7 P) u1 p/ w& a' Stest was ordered, but the family did not go to the% _+ T4 e: F. I+ L. k. `! k
laboratory to obtain the test.
, d3 m! \& ^# c0 x5 s3 p- FDiscussion# p$ a/ v; \) m, n4 M
Precocious puberty in boys is defined as secondary6 C1 J+ j1 [, V
sexual development before 9 years of age.1,4
3 C4 R0 f) @" X4 `0 |" Y' _Precocious puberty is termed as central (true) when* x, c" X: C/ V0 g) f
it is caused by the premature activation of hypo-
8 y8 d/ i3 B3 Lthalamic pituitary gonadal axis. CPP is more com-! D: v* i; A$ F$ J: ~+ g
mon in girls than in boys.1,3 Most boys with CPP. F* q3 z% `3 ~2 }1 M
may have a central nervous system lesion that is9 X) _2 C' v* R2 g; o
responsible for the early activation of the hypothal-+ v: [6 `3 f5 Y$ k) U
amic pituitary gonadal axis.1-3 Thus, greater empha-( l5 \- S0 z# @8 L# h% {& b: v, }; u
sis has been given to neuroradiologic imaging in
0 d& r. t6 H& gboys with precocious puberty. In addition to viril-
4 O# k4 x3 v* j* j* a& i4 l) r* xization, the clinical hallmark of CPP is the symmet-- F: P, G1 A( ?
rical testicular growth secondary to stimulation by4 s' J' d2 c4 O/ k
gonadotropins.1,3
3 {& p4 X6 F9 D1 k3 j7 FGonadotropin-independent peripheral preco-0 A5 ]) q7 ~: v5 _1 u
cious puberty in boys also results from inappropriate$ g* u! I1 s Z
androgenic stimulation from either endogenous or8 W. K* g; v. l- f9 B2 Y& W. A
exogenous sources, nonpituitary gonadotropin stim-
% Z6 J. S% X" ~ Hulation, and rare activating mutations.3 Virilizing
# b* V& J6 N `* T; ^congenital adrenal hyperplasia producing excessive
4 o0 T' V4 f; p- R: ^$ tadrenal androgens is a common cause of precocious. X# w- ]8 y: \
puberty in boys.3,49 L( _# Z/ [4 X- H8 C6 h% T9 K9 X
The most common form of congenital adrenal
, z' i# t7 {, Q0 A; L* Vhyperplasia is the 21-hydroxylase enzyme deficiency.: C3 l" K/ r7 M; q3 C8 s
The 11-β hydroxylase deficiency may also result in
& Q$ n3 T2 N$ @& B# \. B ^3 dexcessive adrenal androgen production, and rarely,
1 ]- |5 f9 `& d3 [& m2 R) Ian adrenal tumor may also cause adrenal androgen
! z: d. t8 c2 Q5 U+ ^$ }excess.1,3# m# u8 V0 k. I( ]$ Q1 [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# J& l, b' M" Y. x. }542 Clinical Pediatrics / Vol. 46, No. 6, July 2007) \- K2 O! T% j* e
A unique entity of male-limited gonadotropin-
! @9 o t5 _$ R9 Pindependent precocious puberty, which is also known7 c4 j. ?6 I( p# O2 B
as testotoxicosis, may cause precocious puberty at a" M8 p3 }, P# U6 @0 G8 P7 u) v- G
very young age. The physical findings in these boys; c# k4 x+ l- a9 V
with this disorder are full pubertal development,$ k5 H1 D' q- E' T, Y
including bilateral testicular growth, similar to boys
! P7 R4 [* Q+ e9 i% qwith CPP. The gonadotropin levels in this disorder: l+ [ v) B, |. _, o
are suppressed to prepubertal levels and do not show$ N: V/ U: b# V
pubertal response of gonadotropin after gonadotropin-
0 U. \* e1 ^) j. s: e9 ]9 l+ v+ Areleasing hormone stimulation. This is a sex-linked
3 b1 w. C) Y6 Q) _autosomal dominant disorder that affects only
' |! G" J/ C, s' V+ g3 m. i3 K* Nmales; therefore, other male members of the family- V, ]: z4 a0 t7 ~# L0 D
may have similar precocious puberty.3
& d, j8 Z0 }6 G& P4 S3 \In our patient, physical examination was incon-# I C+ z0 j: P6 x0 X' Q# |
sistent with true precocious puberty since his testi-" O6 }6 a6 f6 ?4 q2 {0 i
cles were prepubertal in size. However, testotoxicosis
# d3 s% g. N! T- b _8 _5 xwas in the differential diagnosis because his father V5 M/ Y% Z+ p
started puberty somewhat early, and occasionally,
# J! v# `& c1 Z, o9 P; |- |8 Ltesticular enlargement is not that evident in the q/ Q2 h7 B) J
beginning of this process.1 In the absence of a neg-1 w: @/ C9 @8 {0 R2 {3 j' }
ative initial history of androgen exposure, our% O- s) |4 ~$ a+ }
biggest concern was virilizing adrenal hyperplasia,- ]* m1 E# Q, W! }. G, j" Y% i* Q$ I# \7 [
either 21-hydroxylase deficiency or 11-β hydroxylase
% Z5 [ F6 [3 d5 a! Kdeficiency. Those diagnoses were excluded by find-
- g' ]5 c2 K7 ]( E* d5 z/ @4 _ing the normal level of adrenal steroids.
% {0 m: R- z( j1 J" ]( E" x9 CThe diagnosis of exogenous androgens was strongly$ a9 ?2 f K+ r1 u) Z2 y& o
suspected in a follow-up visit after 4 months because
1 u1 s- _' d* tthe physical examination revealed the complete disap-* R/ L$ \- q9 x: X5 ~
pearance of pubic hair, normal growth velocity, and
: @9 X! F) O# }- |& `& Q" Qdecreased erections. The father admitted using a testos-& P4 d: j: h4 Q1 ^1 y
terone gel, which he concealed at first visit. He was
6 ]2 c: j% @0 s4 c" iusing it rather frequently, twice a day. The Physicians’
x* H" Q' o: j. K) KDesk Reference, or package insert of this product, gel or
. _; e3 j' Z& S$ C% N) o2 Hcream, cautions about dermal testosterone transfer to% B5 c! i% \1 x7 E% r
unprotected females through direct skin exposure.
* e8 R6 K8 t ]( D: O6 d# KSerum testosterone level was found to be 2 times the- N1 e7 |9 V6 [; P0 u
baseline value in those females who were exposed to
" K t( H/ F4 N9 veven 15 minutes of direct skin contact with their male2 @0 d4 ]) {# C9 X- O
partners.6 However, when a shirt covered the applica-
2 G: U7 r7 g* ?, ^$ \. \tion site, this testosterone transfer was prevented.9 d& n. P% B- b5 R" u" ^
Our patient’s testosterone level was 60 ng/mL,
5 O5 G7 N. _& X, _+ j/ pwhich was clearly high. Some studies suggest that! |$ f2 ^% @- \! s
dermal conversion of testosterone to dihydrotestos-& D1 v( t' A: U. _) b% s
terone, which is a more potent metabolite, is more
S8 `; z# U. @: a) Z/ Eactive in young children exposed to testosterone1 S1 {+ P5 u5 Z# t
exogenously7; however, we did not measure a dihy-
% Y7 [7 _$ c' t! ]) [drotestosterone level in our patient. In addition to
- u; Y: k$ |9 Z* svirilization, exposure to exogenous testosterone in' x; z. G2 C Z1 _
children results in an increase in growth velocity and( {+ ~; v6 Q; I! j( d N0 T
advanced bone age, as seen in our patient.
/ q" P! N2 x2 a$ f" S4 t. VThe long-term effect of androgen exposure during
( y% P \8 Z: z' I, E+ \7 j0 jearly childhood on pubertal development and final
0 q$ d; i3 O9 O0 nadult height are not fully known and always remain2 W: n. w) N8 h! w. G! }
a concern. Children treated with short-term testos-
# h1 ?4 G+ F" Bterone injection or topical androgen may exhibit some9 J: e% I/ z) l+ |3 a
acceleration of the skeletal maturation; however, after& y+ z" O. o: T: V5 ] W6 u
cessation of treatment, the rate of bone maturation; }/ A: F( }* L z& w: C1 c5 e1 `
decelerates and gradually returns to normal.8,9
1 B8 I7 E/ z2 Z6 c nThere are conflicting reports and controversy
$ Q3 o% B5 W' _! S M& L/ T. J4 Cover the effect of early androgen exposure on adult: Q* d# j7 z4 f; S
penile length.10,11 Some reports suggest subnormal' ?4 G3 @) }8 ?1 q O
adult penile length, apparently because of downreg-6 m8 {$ A( G9 h: z
ulation of androgen receptor number.10,12 However,
) Q! E% @) r9 MSutherland et al13 did not find a correlation between
, D4 N* ~0 N9 [' O+ Y2 y- l+ b: t! L& Pchildhood testosterone exposure and reduced adult, i7 f5 t" \$ X+ B, Z! D5 l( G
penile length in clinical studies.
9 P" z5 j( k5 `2 l1 qNonetheless, we do not believe our patient is
o! ~2 `0 h5 V5 M9 [going to experience any of the untoward effects from
0 C1 j) c4 h5 Y7 R% `" Ctestosterone exposure as mentioned earlier because! ]- _/ W7 j0 ^& A/ I3 R6 x
the exposure was not for a prolonged period of time.2 c c4 {. T; f, S8 b
Although the bone age was advanced at the time of
+ S# f% d5 x* a( G; ]6 b' Sdiagnosis, the child had a normal growth velocity at
3 Y- m3 c6 L# t2 K3 {7 \! |the follow-up visit. It is hoped that his final adult
) ?. i5 M" ^& e6 h0 Mheight will not be affected.3 M7 f4 _" j# y- n
Although rarely reported, the widespread avail-
5 Z8 c5 s1 ^1 b' I7 T* @* o$ Kability of androgen products in our society may
L/ s$ C3 R% f+ E' q; Cindeed cause more virilization in male or female
8 q A' |8 [4 Z3 i+ hchildren than one would realize. Exposure to andro-
: V) {( J! I, `' ]4 w( O6 u" Fgen products must be considered and specific ques-
% j- ]. n5 x% stioning about the use of a testosterone product or8 ]! a* E# x- V+ S! Y* R
gel should be asked of the family members during2 o, i& ?& s) {& k2 X
the evaluation of any children who present with vir-4 ^5 u: E' L0 Q* T( k
ilization or peripheral precocious puberty. The diag-
+ M9 r z: e3 E V, ~1 r6 dnosis can be established by just a few tests and by
7 p7 ?" t7 a9 x! U: vappropriate history. The inability to obtain such a% U4 u0 j2 S( `, d8 Q7 J
history, or failure to ask the specific questions, may
2 e M& i5 l: B0 l1 ~8 N' `result in extensive, unnecessary, and expensive* @, [( Z5 u; C
investigation. The primary care physician should be! ?& M( n" @& _) s
aware of this fact, because most of these children% x4 C% p, v; q8 U6 V- X( j' y2 t; L
may initially present in their practice. The Physicians’: A! F8 F7 f/ C/ t5 R: s
Desk Reference and package insert should also put a
8 I% y% X7 A1 Q: S1 \warning about the virilizing effect on a male or
m' Q; X; Y7 g- u: z- efemale child who might come in contact with some-; L% \( v' ~6 w+ C* u# P& a
one using any of these products.: Z# W, o+ A( G4 ?
References. y* ~! z; Z9 `1 l0 u
1. Styne DM. The testes: disorder of sexual differentiation
. F) {, U N i2 \3 Wand puberty in the male. In: Sperling MA, ed. Pediatric9 ^" f( K! L2 _: n+ r4 [
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" _. i {6 {0 m- g+ `; I% ]
2002: 565-628.7 o5 g/ P- g" ?6 T8 \# L) o' y
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( I6 l. E( s) h, O" k' Jpuberty in children with tumours of the suprasellar pineal |
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