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Sexual Precocity in a 16-Month-Old
4 m# m6 H7 g, C& B, `Boy Induced by Indirect Topical' o' U( F$ }) g
Exposure to Testosterone
* W8 C4 @4 H# m7 M, `Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2# v, G, h) }# C6 H" X7 T$ l# E3 ?) D
and Kenneth R. Rettig, MD1$ v9 M7 x$ ?0 W' g* _; T
Clinical Pediatrics: Y3 N7 ^: F3 j) O2 L- |! J; e; r
Volume 46 Number 6
K$ r& E0 I( i; t EJuly 2007 540-543
! z5 u- }2 U6 W8 _, x© 2007 Sage Publications; w: B) V! \$ `: Y' K ?1 \
10.1177/0009922806296651
0 q$ t& o7 g w& B. T( z& R/ ~http://clp.sagepub.com8 C4 p3 H0 ~' d6 g) K( Z
hosted at
7 x3 D/ D& }% N, x# c' g+ shttp://online.sagepub.com
1 W3 `. F1 |, C# P4 I) |Precocious puberty in boys, central or peripheral,9 P8 w. s! o4 J1 V' {' k# ~8 ^" h& F
is a significant concern for physicians. Central& V: ^4 [9 k; H. N% G) I; R& J2 m# X
precocious puberty (CPP), which is mediated
! W7 f" W, g0 k7 Sthrough the hypothalamic pituitary gonadal axis, has- A' [- u& i9 o" H5 F% ?; u! c& y
a higher incidence of organic central nervous system
, A6 ^# ]$ B) ]0 k2 S; olesions in boys.1,2 Virilization in boys, as manifested
2 s# J6 u( C( W% m3 v$ m3 Gby enlargement of the penis, development of pubic
) C) q2 `( l4 ~0 uhair, and facial acne without enlargement of testi-
$ ?. D7 t1 d# ]. B; Tcles, suggests peripheral or pseudopuberty.1-3 We8 o0 u4 b+ x: y0 E/ ]+ J
report a 16-month-old boy who presented with the) H e3 C" ~* p# x6 p2 j' t- b5 l
enlargement of the phallus and pubic hair develop-
2 _% o5 y' n" d0 o. U; W9 [ment without testicular enlargement, which was due
2 n; H; G4 s, \to the unintentional exposure to androgen gel used by
. X$ J4 E% v( f9 Zthe father. The family initially concealed this infor-
2 T! ^' U6 b4 K5 n. E( e" wmation, resulting in an extensive work-up for this
1 |3 n9 U1 m4 K x! kchild. Given the widespread and easy availability of9 v1 \5 y$ z1 \# a3 [3 j5 D
testosterone gel and cream, we believe this is proba-! Q" }0 ^2 z; Y( x
bly more common than the rare case report in the1 i( L6 u; {% c. N; u, i3 f9 @* s
literature.43 C" q9 n$ t2 Y" w
Patient Report
9 k% {5 ~( D! f6 R# }A 16-month-old white child was referred to the) M+ h- H5 s. w
endocrine clinic by his pediatrician with the concern
' J f: V# d" Y+ A `of early sexual development. His mother noticed- A. b6 j4 n* e
light colored pubic hair development when he was. f; u7 l1 M) p0 i8 j# T. n
From the 1Division of Pediatric Endocrinology, 2University of
- H2 R% q4 G: A, g: |South Alabama Medical Center, Mobile, Alabama.. F8 e2 C: K8 Q- w& c1 [8 f
Address correspondence to: Samar K. Bhowmick, MD, FACE,) J* L/ F( c( p
Professor of Pediatrics, University of South Alabama, College of
: t: l9 S. q; a' h2 sMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: k& \" o' }6 _' Ee-mail: [email protected]., a5 H4 S2 ?1 Y q9 m7 `+ }
about 6 to 7 months old, which progressively became9 M8 t$ A" j) I; W+ g1 \
darker. She was also concerned about the enlarge-" y5 d4 X' w) j8 y) X5 t- V
ment of his penis and frequent erections. The child2 K; b V; m' c1 [, d
was the product of a full-term normal delivery, with5 Y! P& j+ x0 u$ B" I! }% b- s
a birth weight of 7 lb 14 oz, and birth length of
. }, J. K! m, X2 H. f& @3 T/ q4 c20 inches. He was breast-fed throughout the first year
; b3 O& }0 u2 m- uof life and was still receiving breast milk along with
& I: {& Q& z; G. H% Isolid food. He had no hospitalizations or surgery,# O7 M! K* [5 q; e& l" [
and his psychosocial and psychomotor development" @ Q- Q# f7 y' ~
was age appropriate.. }! S4 B& k9 K
The family history was remarkable for the father,
9 p( m& C! t8 x2 D5 lwho was diagnosed with hypothyroidism at age 16,
' L3 G, R7 `1 J2 Fwhich was treated with thyroxine. The father’s, C4 ~$ W) ~! Q( j# M: ]5 d
height was 6 feet, and he went through a somewhat' n$ I/ c- l5 y4 v4 v# S( V) `5 }
early puberty and had stopped growing by age 14.
: T4 d" F) f" e" p; {+ S3 eThe father denied taking any other medication. The9 Y3 ~" i) S( t7 u$ f
child’s mother was in good health. Her menarche; @. `- ^5 u! p8 v( j
was at 11 years of age, and her height was at 5 feet
9 j7 ~1 l+ W* A# z: m$ g5 inches. There was no other family history of pre-
. K4 Z* r; S6 W7 Q" |7 Xcocious sexual development in the first-degree rela-
6 i% V3 p+ e) X& ^$ t' G0 ptives. There were no siblings.( c9 C; c; D" W
Physical Examination0 ]" t3 d! ?' b5 x
The physical examination revealed a very active,9 r* q2 K: [2 [
playful, and healthy boy. The vital signs documented$ O. k% t4 {6 i5 H
a blood pressure of 85/50 mm Hg, his length was
" v- [; R' A, x9 `& A/ ~, o90 cm (>97th percentile), and his weight was 14.4 kg, C% i% p' p- }. q: v- {1 E' @
(also >97th percentile). The observed yearly growth
- f9 E. i& g" [+ N) Hvelocity was 30 cm (12 inches). The examination of; ~- ?$ y( q0 f; `
the neck revealed no thyroid enlargement.
$ u' Y! }0 [) {The genitourinary examination was remarkable for8 V6 o9 ?8 ^$ H2 I
enlargement of the penis, with a stretched length of7 l' Z9 X- B. L" v, s
8 cm and a width of 2 cm. The glans penis was very well
+ b. }" a2 V/ M) C' r! Edeveloped. The pubic hair was Tanner II, mostly around1 `5 q8 p$ U0 {8 P
540" a9 t( ^& w: c4 r/ D( e t
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 b* H, K) h2 v$ j+ y" Sthe base of the phallus and was dark and curled. The
$ \( V; J, I* Ztesticular volume was prepubertal at 2 mL each.
2 ]& c: v- [" z# n$ d2 z, I" X& qThe skin was moist and smooth and somewhat
) o) E# H* `9 D! b7 @. T3 [* Koily. No axillary hair was noted. There were no
; e. K- m0 u" `3 D% }% labnormal skin pigmentations or café-au-lait spots.+ r+ V, n" ~/ j7 E6 c
Neurologic evaluation showed deep tendon reflex 2+
( U1 f+ E, K: [% H- c; G! {7 _bilateral and symmetrical. There was no suggestion) `) l9 U9 ]! A0 l( X& p2 z8 z
of papilledema.- |( }+ n' y, d
Laboratory Evaluation
) w7 ]( D( F/ B, P, o- wThe bone age was consistent with 28 months by4 A, a2 {& e5 D/ Q3 u% h
using the standard of Greulich and Pyle at a chrono-) u3 r6 U. [* [5 ?' I
logic age of 16 months (advanced).5 Chromosomal# H2 W1 J0 c0 \0 T9 i
karyotype was 46XY. The thyroid function test1 C. @ _- l2 E. U* Y: d0 j
showed a free T4 of 1.69 ng/dL, and thyroid stimu-$ W2 c m9 {8 u2 q% V0 s7 o0 a3 D
lating hormone level was 1.3 µIU/mL (both normal).
. O8 t' J7 F9 {& D: @2 [9 kThe concentrations of serum electrolytes, blood
4 Y2 y# Q1 C3 |. F! \7 A* P# ]urea nitrogen, creatinine, and calcium all were
3 J0 K+ U9 N9 L! E1 r( _" P( ^within normal range for his age. The concentration
8 v" O5 j @8 h/ Z" p. r; wof serum 17-hydroxyprogesterone was 16 ng/dL3 ]" M; b. C4 p1 W$ u% n
(normal, 3 to 90 ng/dL), androstenedione was 201 v+ I( A! J& ~9 S% g
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
+ o% O- L4 I. Z7 Z' Uterone was 38 ng/dL (normal, 50 to 760 ng/dL),( C* K. G* Q) H$ F0 b. a
desoxycorticosterone was 4.3 ng/dL (normal, 7 to; T& I4 I5 N1 _" |7 w9 Y# P7 i
49ng/dL), 11-desoxycortisol (specific compound S)( H F% [$ |. y8 @1 Y
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
! R. k, a4 u, n* `9 Mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
+ ?. T0 \; j0 s8 U# ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
. l. X& t+ m7 N$ r xand β-human chorionic gonadotropin was less than
$ L1 g" P* r9 y% r5 mIU/mL (normal <5 mIU/mL). Serum follicular# G- e5 F" _4 `2 u, [! S: m
stimulating hormone and leuteinizing hormone
# D( u' g: ]( j* g: \* Y3 qconcentrations were less than 0.05 mIU/mL) b+ r N; a1 j$ N# f
(prepubertal).+ M* e D, L, K' m4 n" c R) G
The parents were notified about the laboratory$ A, _5 H9 e# @ Y: t+ ^
results and were informed that all of the tests were
% P5 O. F6 h3 o% Z" k( Snormal except the testosterone level was high. The
$ q: N7 G4 m) Wfollow-up visit was arranged within a few weeks to9 w( w% Q& V5 Y
obtain testicular and abdominal sonograms; how-' `6 |& P1 O; h0 E
ever, the family did not return for 4 months.
# r- Z% x# q2 n9 U$ g% ]3 cPhysical examination at this time revealed that the
+ x7 Q* f! O" s) n# nchild had grown 2.5 cm in 4 months and had gained& X6 c+ B: o4 D) A: D }$ F) F
2 kg of weight. Physical examination remained+ s6 E4 U4 g# B& [4 K' ^! I
unchanged. Surprisingly, the pubic hair almost com- \6 W' l5 I- i
pletely disappeared except for a few vellous hairs at
4 X& d% ~9 H5 o' Qthe base of the phallus. Testicular volume was still 2
' ~% j. h$ ^8 V. w' M) ?9 z+ Z4 \+ Y* ImL, and the size of the penis remained unchanged. f6 P1 N' o8 V4 V e, [5 N
The mother also said that the boy was no longer hav-
5 [; [: N7 B% f; ring frequent erections.) p7 M. s: w# {; F: [
Both parents were again questioned about use of
& s" v" P9 a' y3 X2 D, M3 u3 k$ ?any ointment/creams that they may have applied to5 ^0 @9 M$ t9 C' ` V7 I
the child’s skin. This time the father admitted the( Z' ]9 J& M+ _, @; [/ N
Topical Testosterone Exposure / Bhowmick et al 5419 e7 i1 |# g: Q }6 s% @0 u; t, V8 t2 _
use of testosterone gel twice daily that he was apply-
4 x/ }! r; H; ?+ K. x7 I- b9 J! n4 Qing over his own shoulders, chest, and back area for" t4 t$ O5 u$ G& ^4 t7 p
a year. The father also revealed he was embarrassed
- t) o; t. ^) k bto disclose that he was using a testosterone gel pre-" K1 \% ^- U, h* K3 g# e% O
scribed by his family physician for decreased libido0 N' w. P5 Y1 g8 R, h. r6 L' o
secondary to depression.1 Y {9 `# d# T$ i g# p
The child slept in the same bed with parents.0 `# w) a8 N9 i1 x4 X. p5 n' n
The father would hug the baby and hold him on his
9 H' X: S7 n# Schest for a considerable period of time, causing sig-
& ^6 c8 S4 @; U- x3 Unificant bare skin contact between baby and father.
! D' i1 B# b: Y3 RThe father also admitted that after the phone call,# @: J, L( s- A. Z
when he learned the testosterone level in the baby# Z) n% s6 `1 ?
was high, he then read the product information8 ?: A7 S) O! o6 w3 p8 b
packet and concluded that it was most likely the rea-
# Q/ D$ |' G" n5 [! I" F4 cson for the child’s virilization. At that time, they
3 V4 X9 {# }; b R$ \4 c: _5 Jdecided to put the baby in a separate bed, and the8 y8 `0 y" o' S; E! ^) ]
father was not hugging him with bare skin and had' N6 b& q1 X* v& s, _
been using protective clothing. A repeat testosterone
% ~8 U0 J' C- n1 {% Dtest was ordered, but the family did not go to the
9 z$ c4 g. i) P1 g% k1 q; ilaboratory to obtain the test.5 z) S% r1 c% q/ i
Discussion$ J, R3 O- o9 N" E5 M9 c t& W/ u
Precocious puberty in boys is defined as secondary
F% s# q/ v2 x, @) D. C4 vsexual development before 9 years of age.1,4+ y5 i% i% X! E5 ~% Y
Precocious puberty is termed as central (true) when
2 a) ^; F p9 cit is caused by the premature activation of hypo-( x; S9 k* `& {9 l6 {
thalamic pituitary gonadal axis. CPP is more com-6 e$ K* B" B: n& n7 L3 V1 j4 ^
mon in girls than in boys.1,3 Most boys with CPP
# t: }0 N8 }9 O# A" D3 v' imay have a central nervous system lesion that is
) I) \7 I/ n4 k9 e% @0 Eresponsible for the early activation of the hypothal-
" e- } J" f- W E" kamic pituitary gonadal axis.1-3 Thus, greater empha-
7 b% g( \/ f' T. I, h& u, gsis has been given to neuroradiologic imaging in) Z7 Q# p7 j: r8 L6 Q+ l
boys with precocious puberty. In addition to viril-: z3 e8 U7 o2 X( g% V& z) p$ t7 g, s
ization, the clinical hallmark of CPP is the symmet-* i* y6 n! r$ }- I& s4 b
rical testicular growth secondary to stimulation by; I( F2 q7 L6 B8 Z
gonadotropins.1,3# B; C2 J4 r! c, D, ^! H* R1 W
Gonadotropin-independent peripheral preco-
5 x9 H4 p% \- n( V; m) ]* |cious puberty in boys also results from inappropriate$ g! g( v: T! U( v
androgenic stimulation from either endogenous or1 k4 V9 ]$ k& V5 ^4 q V8 l# r/ c
exogenous sources, nonpituitary gonadotropin stim-
; [4 H2 n2 d# z6 p) xulation, and rare activating mutations.3 Virilizing. {& Z ?# t* A% r0 G3 h. v) ?
congenital adrenal hyperplasia producing excessive
1 E* |: W. S8 |2 F8 |adrenal androgens is a common cause of precocious
- A9 h, d/ x r" f6 w+ ] U: xpuberty in boys.3,47 V g4 N* E+ J$ \
The most common form of congenital adrenal
9 N: S( I$ M$ Q8 E+ e; w) ~5 jhyperplasia is the 21-hydroxylase enzyme deficiency. k5 A* A2 @! \1 x7 Q7 k; `5 I
The 11-β hydroxylase deficiency may also result in& H+ c5 t# {: x2 y
excessive adrenal androgen production, and rarely,7 r/ l. c$ R% A$ t w) s- X
an adrenal tumor may also cause adrenal androgen ^6 E( l+ V4 y$ E7 J
excess.1,3- t+ \3 @7 N) I' p7 d; }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 I7 K K: O' I E5 l6 V( I) D X% J7 M542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& A q1 L) {" n$ ~! U, {A unique entity of male-limited gonadotropin-3 E( ?+ [* K. N: C: Y; i6 ], G! o
independent precocious puberty, which is also known
" M5 A! g! g& j7 h9 oas testotoxicosis, may cause precocious puberty at a
) ]$ G5 z+ J9 R6 {, h7 Tvery young age. The physical findings in these boys
+ A0 t( ^' |3 H/ f) M Ewith this disorder are full pubertal development,
" L4 H5 N. G* W% [; e6 b: K8 Fincluding bilateral testicular growth, similar to boys
! C1 u1 b j! Q6 gwith CPP. The gonadotropin levels in this disorder
5 S: h2 Z2 X# r8 Y) c) F/ C4 Uare suppressed to prepubertal levels and do not show0 h4 u3 y) O$ c/ d+ r! G
pubertal response of gonadotropin after gonadotropin-2 e r% d' M3 G) H
releasing hormone stimulation. This is a sex-linked6 M6 M3 A! z7 c3 p, Z
autosomal dominant disorder that affects only
3 ?. o# P& @; v" n3 U( c. l' ]males; therefore, other male members of the family
6 U/ X5 j- F; V% I- e) }" Xmay have similar precocious puberty.3* S O4 g3 `" h: L6 ]8 w9 h
In our patient, physical examination was incon-
) s; a$ j3 C. m5 i# p+ N8 _sistent with true precocious puberty since his testi-
, N8 v, i9 \; n$ Q/ g+ H) _cles were prepubertal in size. However, testotoxicosis# o5 S+ m* D& G& K( v/ {5 w( r) T
was in the differential diagnosis because his father2 u* w X9 v- \/ S
started puberty somewhat early, and occasionally,3 i3 H- w; `' W1 O2 k+ f; U. s
testicular enlargement is not that evident in the
k3 d" `% O" k4 s0 d5 O6 @beginning of this process.1 In the absence of a neg-
4 ]5 j& H4 `& [6 r( v: r, uative initial history of androgen exposure, our: v Q Q7 A t: R" _
biggest concern was virilizing adrenal hyperplasia,8 g/ D8 q1 h% M! o9 ?
either 21-hydroxylase deficiency or 11-β hydroxylase5 s o# y+ |( N' v0 T
deficiency. Those diagnoses were excluded by find-
" P% v: H% c* `ing the normal level of adrenal steroids.
7 V X6 [1 L" y5 n# tThe diagnosis of exogenous androgens was strongly: K& @) ] E2 n8 A9 F
suspected in a follow-up visit after 4 months because
. H8 V" ?/ X. E9 d* Hthe physical examination revealed the complete disap-
4 s8 f$ M, K* h9 ]9 E- P, Rpearance of pubic hair, normal growth velocity, and ^+ g( A0 F" A# f; C8 L- M
decreased erections. The father admitted using a testos-
0 s3 ] j; h) R/ Z lterone gel, which he concealed at first visit. He was; c& C& `! L/ ]7 T( ^2 Z- c
using it rather frequently, twice a day. The Physicians’& r+ ]9 e7 Y6 j1 h5 S- K
Desk Reference, or package insert of this product, gel or, C* f0 G/ y. i+ U) u
cream, cautions about dermal testosterone transfer to2 P' Z; D6 D. J0 r
unprotected females through direct skin exposure.7 X( l5 x0 ]6 T* o" [# k, d! A
Serum testosterone level was found to be 2 times the
" u5 {7 L% F( cbaseline value in those females who were exposed to
8 ~' k& k0 G2 l' x/ leven 15 minutes of direct skin contact with their male
" m" d% k/ S. I! ~8 ]partners.6 However, when a shirt covered the applica-
& P' z$ v2 M7 q* Vtion site, this testosterone transfer was prevented.
C, k$ O8 A5 D; m$ Z4 z: OOur patient’s testosterone level was 60 ng/mL,
1 M2 y, P3 `) R7 d+ {9 X% Owhich was clearly high. Some studies suggest that
l" t m* _3 p& @4 {dermal conversion of testosterone to dihydrotestos-
2 a) w( b* r9 G' I9 Y: E, @terone, which is a more potent metabolite, is more
/ P( N ^* ~2 `+ T4 mactive in young children exposed to testosterone: w; y5 t- v5 X/ a% ?
exogenously7; however, we did not measure a dihy-9 ], J2 I/ i! F3 N; c
drotestosterone level in our patient. In addition to
! v4 u; ]7 e$ I. jvirilization, exposure to exogenous testosterone in
3 n5 |) p: l n% {children results in an increase in growth velocity and0 Y8 Z+ x0 x! @- Y$ _# i( s/ G
advanced bone age, as seen in our patient.
, C+ D0 k8 F! ~" n- s- l1 g/ N4 A" RThe long-term effect of androgen exposure during
7 G9 N0 g1 ?3 ~* H( `1 |9 x) Searly childhood on pubertal development and final' v6 F1 T' o8 Y9 n( u0 ?
adult height are not fully known and always remain
1 i* i5 {6 W3 |7 N$ y/ Z8 r4 K0 ya concern. Children treated with short-term testos-
) ?1 r9 v$ a8 z. qterone injection or topical androgen may exhibit some
8 L$ m% o: F Iacceleration of the skeletal maturation; however, after
+ ]; C, u! `" I% R! ucessation of treatment, the rate of bone maturation. N* H* C0 J( e3 H/ L& B- X# I" b
decelerates and gradually returns to normal.8,9) @6 e) I5 K1 |3 D# }( p
There are conflicting reports and controversy) T# D% `) l* B+ y4 ~5 S
over the effect of early androgen exposure on adult
5 `( R9 k1 G' u2 u) P$ Ipenile length.10,11 Some reports suggest subnormal
s; [: r9 L+ l N1 A* Iadult penile length, apparently because of downreg-8 K* t/ W" j: @! B5 r/ }
ulation of androgen receptor number.10,12 However,
" @2 |' c) `1 J3 r6 c0 \Sutherland et al13 did not find a correlation between6 j" P4 c q9 n
childhood testosterone exposure and reduced adult( M$ x+ K, t) C' M* R `
penile length in clinical studies.% i' n+ {8 Y, _$ M; C N" I
Nonetheless, we do not believe our patient is/ E8 v# R/ g: S: a
going to experience any of the untoward effects from* r; w5 R$ @& {) L7 e2 H. `; c
testosterone exposure as mentioned earlier because5 b; E2 d: N% g) c. v8 C
the exposure was not for a prolonged period of time.' q9 i( I% i* ~3 W
Although the bone age was advanced at the time of7 R6 q! Q0 x" D, L' k% }
diagnosis, the child had a normal growth velocity at8 p9 E& @& g7 @& S% j- ~+ `$ Q
the follow-up visit. It is hoped that his final adult! |9 L B8 A. l+ I, k; a
height will not be affected.
, M8 i, |5 e' m3 |% z4 f# }Although rarely reported, the widespread avail-
# k# l: o; \% Z% {/ pability of androgen products in our society may# t# Z, c: I4 i* o
indeed cause more virilization in male or female
9 y5 ]. p! S$ P: k0 Cchildren than one would realize. Exposure to andro-
0 K' @& B% g3 ~1 B7 Bgen products must be considered and specific ques-
/ [* c$ ]2 ?, D3 ` N( L8 T+ ttioning about the use of a testosterone product or
9 K7 p& N. _. N5 E* P5 ugel should be asked of the family members during# J. k! }& `4 m' F% }; g5 _
the evaluation of any children who present with vir-$ y+ N$ f1 j+ L0 x& ` @) V& d
ilization or peripheral precocious puberty. The diag-2 J4 j& u% `7 R) f& M# o/ I
nosis can be established by just a few tests and by
0 `* A! Z: a; i$ }+ _: Pappropriate history. The inability to obtain such a0 C) _( G) z% f& B1 e
history, or failure to ask the specific questions, may
, S# l6 q: }% kresult in extensive, unnecessary, and expensive
' {, a f% [4 `) g4 L" b9 pinvestigation. The primary care physician should be
`: i+ O) G5 Z1 o5 J2 H W9 \aware of this fact, because most of these children Q4 s6 N) x$ S, D0 z$ u* d! p
may initially present in their practice. The Physicians’
8 c7 J: e7 W' h8 \Desk Reference and package insert should also put a
" H# A: H% D$ L: K' Q8 `4 K. W' iwarning about the virilizing effect on a male or$ j$ |5 H+ Z: v3 _
female child who might come in contact with some-
6 K% `; `/ c9 `* V8 _one using any of these products.& I& W7 D% [7 g% M6 u$ ?
References
9 l" s3 ^/ \- i% m& d) t: H! ~1. Styne DM. The testes: disorder of sexual differentiation- n: a& W# ?7 V5 @/ s
and puberty in the male. In: Sperling MA, ed. Pediatric* h( E7 L$ \. [. e
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;; {" C1 U+ ?) h, E2 I- ^
2002: 565-628.7 A* d. T; J4 `
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ S& V7 c; j3 o/ u* h7 t( o
puberty in children with tumours of the suprasellar pineal |
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