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Sexual Precocity in a 16-Month-Old
; O6 ~9 O; Y# N% @ m# q+ VBoy Induced by Indirect Topical
9 _; ]: e, O: n A. N- VExposure to Testosterone( z8 i& l0 v X$ q; F7 ]
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; ^& ]' y8 A+ V; c, z' T1 o: Pand Kenneth R. Rettig, MD10 S% x. Z3 ], S
Clinical Pediatrics- r% A9 N S' V
Volume 46 Number 6
& D% J7 H6 ^3 R T! YJuly 2007 540-5432 m t G% D. _# }, D
© 2007 Sage Publications
" y! D- L# ]3 }6 ]9 F4 ^10.1177/0009922806296651: ~, ^$ l) J/ l9 ~
http://clp.sagepub.com
" `' I, p. y* I' N K. Jhosted at8 Z% \) [7 @ c* U; Q, i# Q
http://online.sagepub.com0 D d! j' r) H' e- I9 b
Precocious puberty in boys, central or peripheral,1 b: N, I2 M. y
is a significant concern for physicians. Central2 r* B0 h J! N
precocious puberty (CPP), which is mediated; R! @" X! x; }/ I4 n
through the hypothalamic pituitary gonadal axis, has6 I8 S( Y% N, g) t$ ?
a higher incidence of organic central nervous system
* b% Y* ? o$ N& f: glesions in boys.1,2 Virilization in boys, as manifested
5 z* Q, q! o- X7 [3 gby enlargement of the penis, development of pubic$ ?) f7 `: S) S0 q
hair, and facial acne without enlargement of testi-, N/ ^1 V+ u; f N& i& x
cles, suggests peripheral or pseudopuberty.1-3 We
& D) F5 {7 M# H+ A- a2 `& kreport a 16-month-old boy who presented with the( P9 l$ E: M- A( t9 L; ?
enlargement of the phallus and pubic hair develop-5 D9 v: [7 f" e+ ~
ment without testicular enlargement, which was due
# x+ m4 ]" S# Wto the unintentional exposure to androgen gel used by0 Y. p$ n! B9 s; n
the father. The family initially concealed this infor-- J2 ^; x. t6 j! q9 U# f1 d# r
mation, resulting in an extensive work-up for this; o) v9 i2 i8 F) e# C& Z" t- @3 `
child. Given the widespread and easy availability of
- u# {) x& H- z* m1 q6 h5 f& Ttestosterone gel and cream, we believe this is proba-* P6 u! _! y ^# d2 U5 z! B
bly more common than the rare case report in the0 U. X* W9 Y4 t' d: k
literature.4
/ Z3 q; R* E8 k" n N- _* a' q. C. hPatient Report
+ w9 e% ~" n! g$ L( o: }A 16-month-old white child was referred to the( q8 {$ y, `$ t. O
endocrine clinic by his pediatrician with the concern0 Y" t, h# X3 |4 O1 z
of early sexual development. His mother noticed
# w9 A" T: I1 P# P! Y- clight colored pubic hair development when he was2 x- r2 Z3 s u+ K# u; q
From the 1Division of Pediatric Endocrinology, 2University of
" l7 I; i# e/ s0 ^South Alabama Medical Center, Mobile, Alabama.
( T7 R. V i' f1 K: [Address correspondence to: Samar K. Bhowmick, MD, FACE,
' l9 }1 b! J- H* pProfessor of Pediatrics, University of South Alabama, College of
* T% o, o! S; Q, k0 M( ^' q, qMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
" U0 I2 [6 a' he-mail: [email protected].# g. |* z8 m+ @: u$ R0 M- F j0 [
about 6 to 7 months old, which progressively became
' _) D/ f5 F( ~+ odarker. She was also concerned about the enlarge-
4 A {! v! a+ I/ R# Nment of his penis and frequent erections. The child, t+ `! h5 d* H/ _
was the product of a full-term normal delivery, with8 T/ z0 \) ~, u% O
a birth weight of 7 lb 14 oz, and birth length of
. Y' z8 N$ V, i5 ^0 ]20 inches. He was breast-fed throughout the first year9 }0 u- x" k+ } P
of life and was still receiving breast milk along with+ a: j" z8 x! I) V4 r1 Z
solid food. He had no hospitalizations or surgery,1 }0 a5 U# w" N0 ], ^4 y
and his psychosocial and psychomotor development
* k8 U$ o+ t2 A' i$ d1 S8 ~' pwas age appropriate.4 g5 ^$ N% R# z) C0 M
The family history was remarkable for the father,
/ `+ Z! N. H3 d K, {who was diagnosed with hypothyroidism at age 16,8 w( X+ t2 j$ u1 @/ _1 y
which was treated with thyroxine. The father’s
* E ~( K9 t: p1 Z2 ?; _height was 6 feet, and he went through a somewhat6 P6 N) v0 G! h; e6 b
early puberty and had stopped growing by age 14.
# v, S! y9 J$ M. p" ]& ^The father denied taking any other medication. The
$ d; o2 ^' r: s E& H7 O: a ~! ]. }2 mchild’s mother was in good health. Her menarche, ^/ g& x4 _& G- Y) G
was at 11 years of age, and her height was at 5 feet, ~; S) _ S0 j. E! v6 v" d
5 inches. There was no other family history of pre-6 W7 O- T% m$ }
cocious sexual development in the first-degree rela- a7 }. M" U" R9 ?8 t5 V
tives. There were no siblings.
3 d9 z% Y0 H3 ]3 u$ d- yPhysical Examination
+ }: C0 \9 C% {/ U; bThe physical examination revealed a very active,+ |0 b% f2 J! s! F5 W1 l0 a1 S
playful, and healthy boy. The vital signs documented5 x3 X& H- Z* l$ d- ?( Q
a blood pressure of 85/50 mm Hg, his length was
7 V1 v1 D/ J% J' H1 g; h90 cm (>97th percentile), and his weight was 14.4 kg" a5 |) E) `- W4 a
(also >97th percentile). The observed yearly growth
8 G1 p5 H4 g L+ ~# Wvelocity was 30 cm (12 inches). The examination of5 Y: C0 ` t5 e& n
the neck revealed no thyroid enlargement., `2 w0 j% _; F& D8 \
The genitourinary examination was remarkable for9 ~5 ~' y0 `& \( N4 ?- o0 }1 G8 S
enlargement of the penis, with a stretched length of5 ~- [* F$ c1 [/ h9 i9 R/ s
8 cm and a width of 2 cm. The glans penis was very well$ T- V8 ^2 c; [# Y( {: \
developed. The pubic hair was Tanner II, mostly around
8 `" _. z7 Y& R6 p( N540
3 Q9 `9 S( ]* z. C, K: _& z5 Y* [0 D6 Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 k8 `% j* h& w+ P$ R, d+ nthe base of the phallus and was dark and curled. The- W: b% g; p- h, W& `* s# k$ E+ K
testicular volume was prepubertal at 2 mL each.- c; O8 H$ R8 I; {: @6 d
The skin was moist and smooth and somewhat
/ M2 O/ e) {( N' h' H+ x R! moily. No axillary hair was noted. There were no
) u( w4 j" j; d, r! v0 N' babnormal skin pigmentations or café-au-lait spots.
: c( P3 R2 a" U% `- uNeurologic evaluation showed deep tendon reflex 2+
: P/ E. V7 a* U- b6 g; O/ E1 ?bilateral and symmetrical. There was no suggestion
' x- Z: W- E" H' M9 r4 `: ] ?$ Hof papilledema.
7 }' u8 L0 ^" B5 M, |- @& TLaboratory Evaluation
7 V `( V! }7 I* d) Y* i! NThe bone age was consistent with 28 months by
) d# j: w# e: u& |% j0 Zusing the standard of Greulich and Pyle at a chrono-
$ c+ S x" W1 [6 e" m+ V; @logic age of 16 months (advanced).5 Chromosomal" r8 \5 `4 a) Q
karyotype was 46XY. The thyroid function test4 @! h+ u# Z/ N J5 K) |0 ~9 I
showed a free T4 of 1.69 ng/dL, and thyroid stimu-9 L4 d* s( O/ R) B) x/ `6 Q) w
lating hormone level was 1.3 µIU/mL (both normal).
& Y) m5 z% t" `2 C% eThe concentrations of serum electrolytes, blood# U, _. |- E: z! w
urea nitrogen, creatinine, and calcium all were% E/ p: x6 q4 \9 t! g
within normal range for his age. The concentration
! N+ E/ X+ s, X1 [: c7 ?, Gof serum 17-hydroxyprogesterone was 16 ng/dL: G; I! a9 } l0 y
(normal, 3 to 90 ng/dL), androstenedione was 20
' z. [$ v; K I) B9 fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 m' i6 D+ `. @: }; i* X+ N: Mterone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ O6 u# N R% t- Q4 w# sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to/ q0 Y3 Q6 B( m
49ng/dL), 11-desoxycortisol (specific compound S)8 m9 j8 W E) V: R# W
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) P0 j1 A. ?2 K- Z% P L
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- C3 T, w8 Z$ w/ F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! B( z6 W1 z* {+ v4 vand β-human chorionic gonadotropin was less than
7 @5 ?; _+ s }& x* ^# E5 mIU/mL (normal <5 mIU/mL). Serum follicular
# X, c: q. Q# r- N" K) ostimulating hormone and leuteinizing hormone3 B. j+ B4 n" N( j4 z+ I7 @6 K, P3 C
concentrations were less than 0.05 mIU/mL
% A" N- G+ R9 j+ l2 I1 H(prepubertal).
" T+ f5 ^" g7 d$ xThe parents were notified about the laboratory
. g! K& ]- r4 f! S2 N$ Aresults and were informed that all of the tests were
* O, l' h3 h' z% k4 Onormal except the testosterone level was high. The
Y0 h% G# e9 T$ T) bfollow-up visit was arranged within a few weeks to
+ Y3 G9 N8 Q# ] Fobtain testicular and abdominal sonograms; how-
+ N; j7 n; b2 J$ o: z! z" Tever, the family did not return for 4 months.
4 q. J2 z" W6 B. t3 }0 M, @. xPhysical examination at this time revealed that the
: Z9 _3 k% H9 \6 [: t, _4 [child had grown 2.5 cm in 4 months and had gained
8 b% z$ W: b* b k1 P2 kg of weight. Physical examination remained9 O E3 b4 t3 E3 q4 M7 ?8 ^9 {
unchanged. Surprisingly, the pubic hair almost com-
+ f9 a+ D4 e- u- p: p* [pletely disappeared except for a few vellous hairs at
6 S7 b1 K4 j/ A' y+ _the base of the phallus. Testicular volume was still 2
6 T/ K' W7 c( z; ]1 y$ V; vmL, and the size of the penis remained unchanged. q; D5 |( y8 o& ]( ]
The mother also said that the boy was no longer hav-
* m# t ]" e2 _; O- sing frequent erections.4 e: B' [" A+ \3 s0 _, ~
Both parents were again questioned about use of
I# ]2 |8 [8 [. A2 b5 Y2 d b+ oany ointment/creams that they may have applied to5 _6 U# u' n* b6 ~3 t. B
the child’s skin. This time the father admitted the
( G* C# L0 P& w6 d1 g; dTopical Testosterone Exposure / Bhowmick et al 541* d- V8 X, \- v. p
use of testosterone gel twice daily that he was apply-3 [$ x1 e/ Q5 p4 h% ~
ing over his own shoulders, chest, and back area for
7 h! H* e' h5 A" d6 A& P# B# a/ aa year. The father also revealed he was embarrassed
9 O1 J! d" _1 F& Zto disclose that he was using a testosterone gel pre-0 L, D( u6 F5 L
scribed by his family physician for decreased libido
$ l! Y$ c' s+ ^$ i1 ysecondary to depression.
# E) B4 c' ? B* @; n# PThe child slept in the same bed with parents.
( B6 K% g& Q' V8 \3 ^! e8 LThe father would hug the baby and hold him on his* G- _3 m7 m p6 Q
chest for a considerable period of time, causing sig-
" z+ J0 Q; M0 T9 ~nificant bare skin contact between baby and father.
5 w+ b4 p( A. P: N& KThe father also admitted that after the phone call,* c# w6 K( w: C" u4 D7 `
when he learned the testosterone level in the baby
7 M" y( ?* z) M( R& uwas high, he then read the product information
+ o/ F+ ^0 M- X" ]packet and concluded that it was most likely the rea-) ~7 D; R7 h. Z0 S) B# D" l
son for the child’s virilization. At that time, they
8 u1 [& b5 w9 a& T2 ]decided to put the baby in a separate bed, and the m. A. T- l% M( s) w: ~
father was not hugging him with bare skin and had
( M0 }) }7 H) v4 b4 S+ {; wbeen using protective clothing. A repeat testosterone y! s* l: Q, ?0 U
test was ordered, but the family did not go to the
3 q! r+ J9 p" ?2 C& j6 R' Mlaboratory to obtain the test.
+ s1 }$ q2 q% M1 e% k! rDiscussion
5 S0 z, W* W% _- F% E' LPrecocious puberty in boys is defined as secondary
: W; j5 J: y9 e7 k6 |. X2 S( ?sexual development before 9 years of age.1,4" L! S. A# p' _1 G: t( M# r# p
Precocious puberty is termed as central (true) when" r. D0 K$ C+ W5 B/ x- T
it is caused by the premature activation of hypo-; x2 T# o0 t3 s/ Z3 S' O
thalamic pituitary gonadal axis. CPP is more com-% E7 n* U5 W. x$ M" k. }; e. {
mon in girls than in boys.1,3 Most boys with CPP
; W$ n- q0 d( [, q) y/ hmay have a central nervous system lesion that is
" u A0 N6 F' P, zresponsible for the early activation of the hypothal-; }( z( @* o4 Y/ ]& o) G
amic pituitary gonadal axis.1-3 Thus, greater empha-$ L6 g8 Q2 l* W5 v* E. O
sis has been given to neuroradiologic imaging in7 K O2 V3 @1 m- t/ E; N7 T
boys with precocious puberty. In addition to viril-4 l' ]/ G& i! N* l
ization, the clinical hallmark of CPP is the symmet-
3 ~0 a( |( `/ C% ~rical testicular growth secondary to stimulation by
; K) M; T m- B' m- E$ igonadotropins.1,3, l$ y4 i2 @' R, P9 k# r
Gonadotropin-independent peripheral preco-% H% E5 m7 _0 W) g2 q; q; F
cious puberty in boys also results from inappropriate# o/ i% v- L0 [- _4 @5 d% z
androgenic stimulation from either endogenous or
% f5 H. u# G4 N9 p* Gexogenous sources, nonpituitary gonadotropin stim-
, \7 C$ T0 [- j) bulation, and rare activating mutations.3 Virilizing- o; B. b5 F; P4 V6 j0 j$ ` z" P
congenital adrenal hyperplasia producing excessive' c/ }& L! P; \( i
adrenal androgens is a common cause of precocious( \( N; ~/ C# i# j0 W- h
puberty in boys.3,4
" [8 b+ s, p2 a9 a9 bThe most common form of congenital adrenal
! D) [7 C- t/ v# _+ Z8 w9 ]hyperplasia is the 21-hydroxylase enzyme deficiency.
; f* P. H* U( SThe 11-β hydroxylase deficiency may also result in/ \1 V7 U" e0 V! j2 l' ]
excessive adrenal androgen production, and rarely,: Q1 x+ S" H( V( Y( D" S+ y. i
an adrenal tumor may also cause adrenal androgen, x5 U! X' `8 g
excess.1,3
0 f/ c. w" r, L7 E" iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 Y9 ~6 I/ A: g6 y- d1 f7 Q: ]542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 S; l: x p7 q' K5 n! XA unique entity of male-limited gonadotropin-1 e3 p1 K# m' n5 [& _
independent precocious puberty, which is also known/ [$ o# \1 d4 p0 O4 ]" X8 h
as testotoxicosis, may cause precocious puberty at a k& H# O' t9 x" Q3 \: E2 R
very young age. The physical findings in these boys
1 u% g% Z) n) ]$ j' {6 u3 N* Ywith this disorder are full pubertal development,) P1 p: e M' e) w+ ~6 Y
including bilateral testicular growth, similar to boys
6 C m* l# z6 ?& @, E0 i5 s/ uwith CPP. The gonadotropin levels in this disorder& }0 _4 G5 b( k. B
are suppressed to prepubertal levels and do not show- @7 k; G! ]' A& R5 B
pubertal response of gonadotropin after gonadotropin- J1 H0 ]; K2 B1 c3 j7 N/ e
releasing hormone stimulation. This is a sex-linked1 E$ c+ \) U* T" G
autosomal dominant disorder that affects only+ R/ v0 C6 }7 m' q5 ~, W3 s5 z
males; therefore, other male members of the family
# }) J$ G, ]: U! h- qmay have similar precocious puberty.3
" k+ k& U( p' B3 \: M `/ Y* iIn our patient, physical examination was incon-8 B5 N) a, c; z, ]; W N* T
sistent with true precocious puberty since his testi-1 q s( G6 |9 i4 G/ X
cles were prepubertal in size. However, testotoxicosis
1 B9 J/ P- C, H$ r( A2 `( Bwas in the differential diagnosis because his father
/ l2 j3 f6 g! a3 M6 T7 `1 q5 S' d. o" }started puberty somewhat early, and occasionally,$ G) F9 N3 f3 a
testicular enlargement is not that evident in the* e9 y4 G3 B* V& Y$ L3 ~
beginning of this process.1 In the absence of a neg-
" ^* @" b& t( ]% Q1 c% Y* fative initial history of androgen exposure, our5 q' ?: A9 q" k+ c+ w/ i" l$ e0 s
biggest concern was virilizing adrenal hyperplasia,; D: D; _3 |" _0 H* v
either 21-hydroxylase deficiency or 11-β hydroxylase
2 y& O# S9 t [ g2 rdeficiency. Those diagnoses were excluded by find-
) W/ c) Q/ E% M hing the normal level of adrenal steroids.( B+ Y+ J- v+ w5 U; H% @
The diagnosis of exogenous androgens was strongly) C& {' p, r; D. g& j# y4 _' r7 B
suspected in a follow-up visit after 4 months because
2 k6 _* x4 i6 u1 O4 @the physical examination revealed the complete disap-: p* s! b- i+ j) W2 p
pearance of pubic hair, normal growth velocity, and& \& q2 |; _9 z- k6 v
decreased erections. The father admitted using a testos-
: r L% |9 C6 s. k. ~7 Nterone gel, which he concealed at first visit. He was/ J+ v, ^' t( w$ l) {# G" W
using it rather frequently, twice a day. The Physicians’1 c$ L: I5 W* G5 y9 }
Desk Reference, or package insert of this product, gel or. c* Z2 i/ g" B6 l: A8 M( H5 P8 K
cream, cautions about dermal testosterone transfer to& w' a: J' k6 b+ a- F) F; e
unprotected females through direct skin exposure./ ]* s( C! z8 `
Serum testosterone level was found to be 2 times the1 c# F/ A' s1 L' ^
baseline value in those females who were exposed to( ?0 F* o1 [0 a: T1 }% j
even 15 minutes of direct skin contact with their male
1 u) p1 M' N: q) F% l) V" B2 Bpartners.6 However, when a shirt covered the applica-
& ] w, e6 x# [, X2 v1 Ttion site, this testosterone transfer was prevented.
2 f; }+ q- O$ ^" X5 I$ O5 [Our patient’s testosterone level was 60 ng/mL,4 u5 v: A0 u9 N2 v* f; u0 c! g2 b
which was clearly high. Some studies suggest that( d3 n. w5 c9 b9 C' P
dermal conversion of testosterone to dihydrotestos-+ I" O# P* [* |# d( f1 J
terone, which is a more potent metabolite, is more9 p0 T1 {$ E; Q2 ?( v/ P
active in young children exposed to testosterone5 _9 k0 C2 r& ~* d
exogenously7; however, we did not measure a dihy-6 f8 V4 ~9 [$ k$ w w
drotestosterone level in our patient. In addition to
- C* t+ w, o% Y& ^. Hvirilization, exposure to exogenous testosterone in
7 y1 |% R* H/ b3 K) b* K$ Ychildren results in an increase in growth velocity and' ~% O! s, i' W3 ~% Q/ P
advanced bone age, as seen in our patient., V; ?& i3 G+ w4 W) Y M' v: G4 R
The long-term effect of androgen exposure during
6 ~+ B6 ?$ i- ~2 h% C% p7 \- S! A( Qearly childhood on pubertal development and final
! w* b2 x$ L2 ~7 {0 r ?( {+ }adult height are not fully known and always remain& J) ^- @" U4 h" q% s% t6 Y
a concern. Children treated with short-term testos-
, D) }! v% R6 z0 b: ~- |terone injection or topical androgen may exhibit some
7 s/ r& I2 l) S4 D2 Y) w: o u yacceleration of the skeletal maturation; however, after
( A: ]7 S- ]) z! D$ q$ \( acessation of treatment, the rate of bone maturation2 ^9 Z/ u6 {* R' C1 L. `
decelerates and gradually returns to normal.8,96 z$ ~8 S$ |6 `% T, c D7 C8 L
There are conflicting reports and controversy
- u8 U: H( {, C2 @over the effect of early androgen exposure on adult
4 j ~, r- N* A9 f* Jpenile length.10,11 Some reports suggest subnormal5 T( P g( v& z5 c# y1 v' T: d
adult penile length, apparently because of downreg-
# E |6 ?$ Z# M# a/ H3 d% ]ulation of androgen receptor number.10,12 However,+ T. p" j8 [. O1 |/ |- r
Sutherland et al13 did not find a correlation between
2 D( {/ a! x: {9 G3 ochildhood testosterone exposure and reduced adult
: B7 e- a9 w; |7 o6 i6 L. Q! U! Apenile length in clinical studies.& f* z( \! N1 Z! ]
Nonetheless, we do not believe our patient is
) Q4 U5 H" ~" `going to experience any of the untoward effects from
( o! A5 Q% W6 c# e# y8 n, f1 Ktestosterone exposure as mentioned earlier because t2 u: U, E/ z2 w4 @& a6 K; H- j
the exposure was not for a prolonged period of time.
9 w* g& ?" o$ V+ DAlthough the bone age was advanced at the time of( N4 w, ~, \4 ]
diagnosis, the child had a normal growth velocity at
7 ~! F" \' w0 ^/ a8 l6 Xthe follow-up visit. It is hoped that his final adult, l/ {9 U: W8 o; `. k5 i7 ~
height will not be affected.' i l1 \, h% a' H) h* q a5 S, r
Although rarely reported, the widespread avail-4 d9 ]' j7 R1 }% ]
ability of androgen products in our society may
* B" M6 i6 [' d# u% y* Z- K; Eindeed cause more virilization in male or female% y ?: I) T8 b$ U1 r4 u8 H
children than one would realize. Exposure to andro-$ ?* r; ^/ E5 x
gen products must be considered and specific ques-
# L1 S) [4 ?0 D- e# a; f2 Wtioning about the use of a testosterone product or
" W# [! H4 D. Y- r! Ygel should be asked of the family members during' ^: q) `( c# f! q
the evaluation of any children who present with vir-
& k* |* F" x6 Q- ?: M" V9 Pilization or peripheral precocious puberty. The diag-
c# b5 c+ _9 v! q2 C1 W9 D2 h8 qnosis can be established by just a few tests and by7 {$ }: A" d1 r) N1 m8 x$ \
appropriate history. The inability to obtain such a8 n p. z" J$ a# i$ @4 |
history, or failure to ask the specific questions, may
4 G2 r( }0 E/ r- k0 @& ~result in extensive, unnecessary, and expensive
/ V2 C( u; D1 a G4 r. l5 u% {investigation. The primary care physician should be
* }9 l |' c0 e( A, saware of this fact, because most of these children, O5 @( g% }. D( x, O& O' i1 a
may initially present in their practice. The Physicians’
! o" }' q8 {+ ~# t2 fDesk Reference and package insert should also put a8 e* q K4 r3 s/ }4 p# k
warning about the virilizing effect on a male or& n( O! E% U( g3 n
female child who might come in contact with some-
4 U, |1 o, O6 _one using any of these products.
& g$ W0 }2 v6 U$ j% g# wReferences$ p8 W+ C* p" O) u
1. Styne DM. The testes: disorder of sexual differentiation. ^. q2 j+ `3 I* e$ O7 \' C9 c: ~
and puberty in the male. In: Sperling MA, ed. Pediatric4 Q* J& s% H# f2 h1 C5 z4 {
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* C0 v4 r8 o% ]3 p8 h! M* B2002: 565-628.
. M i- v/ p1 G3 V2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 U, Q+ { k: g- Spuberty in children with tumours of the suprasellar pineal |
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