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Sexual Precocity in a 16-Month-Old
9 f' u2 Q& K3 w8 l! l# T7 \Boy Induced by Indirect Topical1 V& h: U; `. ]1 U7 ^
Exposure to Testosterone* K$ l* s {" R, q& d) E
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 ?0 r! }+ l. b# ]: h# H
and Kenneth R. Rettig, MD1% I7 q7 C# |9 [
Clinical Pediatrics }9 U+ C% q) ^: ?* F
Volume 46 Number 6 O7 r- [2 v/ u9 R+ v2 A$ Q" L
July 2007 540-543) @ v+ J6 U8 a, H
© 2007 Sage Publications
9 Z+ g3 }3 e) J8 H10.1177/0009922806296651
" F( |. J& M; y, L# c4 uhttp://clp.sagepub.com
0 p/ E3 L" \2 H, i3 ]# Ahosted at- V( l) N9 J5 L5 a4 r; j
http://online.sagepub.com
5 n; y: @" @9 k' R" {: R# h' R2 lPrecocious puberty in boys, central or peripheral,
6 C& l) w3 J a1 p! ]2 d0 W' V0 uis a significant concern for physicians. Central
8 V9 l/ a+ V; W k2 X. S6 L$ `precocious puberty (CPP), which is mediated' z/ n$ W4 ^+ s2 W2 \
through the hypothalamic pituitary gonadal axis, has
9 c% f- Y4 z! d1 S \6 ]a higher incidence of organic central nervous system* ^0 k. \5 Z! B* \4 n
lesions in boys.1,2 Virilization in boys, as manifested
. m- q5 f, k: B' @! oby enlargement of the penis, development of pubic
* W. [* r# E% d: Zhair, and facial acne without enlargement of testi-% y; C0 R0 ?% e7 B* D
cles, suggests peripheral or pseudopuberty.1-3 We: b* t$ f& D1 `; h* F* Y" I
report a 16-month-old boy who presented with the
( X o, [' k+ ?% @! N; s9 U" fenlargement of the phallus and pubic hair develop-
, J7 L# v% _( q! Jment without testicular enlargement, which was due& ~" g) F+ E; B2 E6 G
to the unintentional exposure to androgen gel used by3 g5 O' W( o- ^. J4 _/ Q
the father. The family initially concealed this infor-% v- p( }$ R: M: s
mation, resulting in an extensive work-up for this
5 B% N( C: r8 P/ @( X9 `child. Given the widespread and easy availability of
0 X" j" x+ [ D/ Q! g0 a8 Ptestosterone gel and cream, we believe this is proba-
- R, s8 _% f6 X1 z, Hbly more common than the rare case report in the6 f) m1 p' a& X: N
literature.4
2 s w) m/ |7 s# `$ \) v) J/ O! uPatient Report
( w {" H- [4 }! T5 l* rA 16-month-old white child was referred to the
6 ]4 Q( V+ e1 x9 P/ H, oendocrine clinic by his pediatrician with the concern" X3 W' P+ W# L& d t
of early sexual development. His mother noticed' w l8 h) g# Q% @$ r& A0 T! ], `
light colored pubic hair development when he was
( c) y! ~1 k7 P2 Q; W& ^, bFrom the 1Division of Pediatric Endocrinology, 2University of0 Z8 V' `6 M; A/ {% e% e: ~
South Alabama Medical Center, Mobile, Alabama.0 k& e3 J" S0 Y1 t# a* \0 l8 p
Address correspondence to: Samar K. Bhowmick, MD, FACE,( `1 n6 a) A5 _" B" y
Professor of Pediatrics, University of South Alabama, College of
, w. @8 S' b0 i' Z# pMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 j M$ `( b; Q3 t- I1 s6 U/ Y+ |6 D) k
e-mail: [email protected].
3 r# |9 R8 K7 V6 }about 6 to 7 months old, which progressively became
0 x4 p1 h$ n$ w, B' ^darker. She was also concerned about the enlarge-. D% t/ A( X. c* W$ R6 t, E
ment of his penis and frequent erections. The child
# F% G" ~ P$ ]5 {; Qwas the product of a full-term normal delivery, with+ _8 v& J6 H1 E9 \+ v# b8 {9 m
a birth weight of 7 lb 14 oz, and birth length of
. b# _! v4 D5 y3 @& ] L0 v+ J+ ?* h! K20 inches. He was breast-fed throughout the first year" Y1 D4 _" ~% z& E
of life and was still receiving breast milk along with. I6 _. q4 h8 E8 ^" z
solid food. He had no hospitalizations or surgery,
c2 x8 E! f' zand his psychosocial and psychomotor development
/ \: p" ]: a, H6 cwas age appropriate./ \5 O, S( W, R7 z' I
The family history was remarkable for the father,
- |) `3 E( W* q$ ?5 u$ {who was diagnosed with hypothyroidism at age 16,' ?+ Q* V5 D/ @; a' C$ I
which was treated with thyroxine. The father’s4 h1 Z9 ~3 T% r$ }* a; F2 [9 }
height was 6 feet, and he went through a somewhat
/ @$ H0 G0 M9 q+ }8 a' oearly puberty and had stopped growing by age 14.
. E$ }. Y* T) l% B! qThe father denied taking any other medication. The
' u2 j- I s' v$ H) n& l- wchild’s mother was in good health. Her menarche
- I- R3 S, t' Y2 }9 fwas at 11 years of age, and her height was at 5 feet
- h6 D9 N- o- }% d" |6 I5 inches. There was no other family history of pre-/ l0 q4 I" Q) V! i: E- j
cocious sexual development in the first-degree rela-
! u% p' {" A c1 j+ R2 ytives. There were no siblings.* e* h: [/ a9 s4 b/ v8 j0 f
Physical Examination
! T( M( m# Q* m; |( VThe physical examination revealed a very active,0 C4 f3 p) |0 c0 p8 ~0 J
playful, and healthy boy. The vital signs documented
[ `6 }9 {2 e2 K" b! i) |a blood pressure of 85/50 mm Hg, his length was
! h! C4 J3 O# ?! Q% p( ?90 cm (>97th percentile), and his weight was 14.4 kg
* j1 y4 G+ ^; T(also >97th percentile). The observed yearly growth
& Z) X! Y. l; Z/ {5 pvelocity was 30 cm (12 inches). The examination of
( Q/ y8 u8 }+ a+ c+ T) M4 fthe neck revealed no thyroid enlargement.
6 h1 X# T/ w+ H. g' T7 f& AThe genitourinary examination was remarkable for; E! Y' Q2 U. V& z+ M4 W
enlargement of the penis, with a stretched length of
3 n3 H1 c: a8 h( V8 L$ Q8 cm and a width of 2 cm. The glans penis was very well' @/ W. E9 `0 U5 U
developed. The pubic hair was Tanner II, mostly around" v4 g9 W0 b2 h/ l F2 p k! j
540( a6 C9 F, D! t) V7 J& m
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 J) s$ R/ Z( a8 N& V
the base of the phallus and was dark and curled. The& K0 m, O( }' f! n# K% F
testicular volume was prepubertal at 2 mL each.
6 Q& n9 b1 p1 G$ h( M2 PThe skin was moist and smooth and somewhat
4 `8 Q" \! L9 R( X7 O- @/ ooily. No axillary hair was noted. There were no
0 u! A9 b) J4 G4 vabnormal skin pigmentations or café-au-lait spots.
4 Z8 d' D' \6 n, B+ y8 ^Neurologic evaluation showed deep tendon reflex 2+
% h, x8 n' o3 J! T; V. N" ybilateral and symmetrical. There was no suggestion
' d) P$ D( y/ j/ }of papilledema.
+ q, {: V% } N& `, e- T: uLaboratory Evaluation
& I; e" S5 r: j9 YThe bone age was consistent with 28 months by& y% M* q7 t$ Q* ]
using the standard of Greulich and Pyle at a chrono- h# |5 m) L& k M
logic age of 16 months (advanced).5 Chromosomal
7 }2 f5 c, c! Y+ V- U+ skaryotype was 46XY. The thyroid function test5 b1 A6 _9 V6 E H, x
showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 Y. `: b1 \1 d7 _" i
lating hormone level was 1.3 µIU/mL (both normal).( \2 y/ R3 g9 [1 K' x6 }9 `
The concentrations of serum electrolytes, blood7 s% p5 Z b- H5 q
urea nitrogen, creatinine, and calcium all were8 p3 m" A& R! z3 L3 `3 @
within normal range for his age. The concentration* G6 Y% B5 V5 B" n: i- G
of serum 17-hydroxyprogesterone was 16 ng/dL
$ S- Y# M+ X3 G5 \7 s( T(normal, 3 to 90 ng/dL), androstenedione was 20
4 U7 N' b7 y* t H% Xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# A- O# v. m8 \+ O, W
terone was 38 ng/dL (normal, 50 to 760 ng/dL),; L( g9 ?& `4 q6 J0 F8 v* C
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
% t. c5 D% ^+ Z, u. k* E9 i49ng/dL), 11-desoxycortisol (specific compound S)8 m, a% m( P, W7 O8 O0 H
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-' \8 o9 r" g- B( Z) @/ M! [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, x2 Q4 T+ h# I; ]; g) w' A8 Y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 _. Q1 S+ K9 c0 J8 I0 gand β-human chorionic gonadotropin was less than
# Z/ u. Z& C# L* A5 mIU/mL (normal <5 mIU/mL). Serum follicular+ h, M- F9 y& ~8 }2 P9 {( x7 X
stimulating hormone and leuteinizing hormone
: F; _8 H x- e* ]concentrations were less than 0.05 mIU/mL
( `3 X; F% Q2 y `' t(prepubertal).4 y3 X/ Q7 H- u/ W* b
The parents were notified about the laboratory
; W6 ?: M: Y! xresults and were informed that all of the tests were0 l6 b$ k- a! c2 O. I
normal except the testosterone level was high. The/ ~$ F* ^ [; q% \: i5 w3 I- S
follow-up visit was arranged within a few weeks to( e4 F0 n1 t. v% H% w1 m
obtain testicular and abdominal sonograms; how-) Y+ O1 g& `/ A, N$ U4 B0 d
ever, the family did not return for 4 months.
7 K3 ?9 [5 Y, t+ P9 }! P; zPhysical examination at this time revealed that the2 [, t% K' L2 m' E- @
child had grown 2.5 cm in 4 months and had gained
/ e, i2 H4 ^- v& n) K( z9 ^) l& Y2 kg of weight. Physical examination remained
5 P% J/ ` p0 I4 ^ lunchanged. Surprisingly, the pubic hair almost com-
0 B/ l6 Y. O: D* m/ O; A. h5 H2 Mpletely disappeared except for a few vellous hairs at4 H% h7 T/ R1 u2 t7 @
the base of the phallus. Testicular volume was still 2: y, _ M, ?& k7 m, c. d2 p
mL, and the size of the penis remained unchanged.+ [5 K, F, M" f) Z5 D+ ^+ t! d
The mother also said that the boy was no longer hav-
; m! r3 A/ _2 e+ \4 cing frequent erections.
' S- X2 L2 u3 B% ]* |: m/ vBoth parents were again questioned about use of& {8 t3 r' x) x* `
any ointment/creams that they may have applied to
0 g1 t1 f8 F* M+ ethe child’s skin. This time the father admitted the, h+ C( q+ g6 K7 i- ]4 c- u
Topical Testosterone Exposure / Bhowmick et al 541
2 o7 p; C- i$ j& j4 Juse of testosterone gel twice daily that he was apply-, K3 g- f# q6 j+ s
ing over his own shoulders, chest, and back area for0 {3 K- N |! z8 n
a year. The father also revealed he was embarrassed. K! d3 n) r9 P& v! U( Q# F; j( w
to disclose that he was using a testosterone gel pre-2 X/ }0 Y/ T( j( _/ @: B) F- R
scribed by his family physician for decreased libido
2 O O, \8 p9 Msecondary to depression.8 t2 h H8 E- y+ V. ]/ A- {3 F
The child slept in the same bed with parents.+ K0 Q0 D( I1 F$ |: {# c
The father would hug the baby and hold him on his
( _! O3 e# z* q( U7 Vchest for a considerable period of time, causing sig-
; L5 c1 V0 C3 x1 [" S9 S2 qnificant bare skin contact between baby and father.% H& J' `$ g' U3 ]- T w
The father also admitted that after the phone call,
# X) W- P3 }' _when he learned the testosterone level in the baby
4 R1 S# c' z5 n, n+ I M8 C t) c$ xwas high, he then read the product information
7 c& G$ A P2 F% E& G ypacket and concluded that it was most likely the rea-$ r8 c. A F/ O
son for the child’s virilization. At that time, they
, D; ?1 [, d( i+ i9 B' ?decided to put the baby in a separate bed, and the; \3 C6 ]% S! j0 A8 E4 p0 V+ y
father was not hugging him with bare skin and had
: ^' E. n1 r" i. e* mbeen using protective clothing. A repeat testosterone
4 y+ I$ f; J( z Ktest was ordered, but the family did not go to the
) i/ A' o4 [* z, slaboratory to obtain the test.
9 x. R3 m P8 `% G" PDiscussion: f" C/ E2 h1 l% M$ O0 a* i; H9 ^
Precocious puberty in boys is defined as secondary" A' T+ a# |6 X. S4 Z9 C
sexual development before 9 years of age.1,4/ Y7 z/ J, w) Q/ D/ S5 K
Precocious puberty is termed as central (true) when3 Q9 v n# t4 r7 D8 [' N
it is caused by the premature activation of hypo-5 |9 q6 B+ Z/ m' U- D4 \
thalamic pituitary gonadal axis. CPP is more com-1 i* h9 r* S7 j/ X* K7 u$ e' `! Q
mon in girls than in boys.1,3 Most boys with CPP
- ]6 V* U1 \- G" Zmay have a central nervous system lesion that is
* [4 e" C: h6 m! jresponsible for the early activation of the hypothal-+ _8 K5 i3 U' v0 ]1 f% D& @
amic pituitary gonadal axis.1-3 Thus, greater empha-
2 G$ I2 U8 ]# _5 M0 X1 hsis has been given to neuroradiologic imaging in
- @ P: S! l* V- h6 S! Uboys with precocious puberty. In addition to viril-
3 }7 O) w% P/ xization, the clinical hallmark of CPP is the symmet-9 { v- S! u+ o6 f9 u6 F- S
rical testicular growth secondary to stimulation by) F8 }" i. U) b A$ _; L/ \* J
gonadotropins.1,3
" c5 ] ?3 \ _0 Y7 Q K$ zGonadotropin-independent peripheral preco-
5 a& `8 k. H0 W% S: Z a3 p$ H* ^cious puberty in boys also results from inappropriate
) U1 Y& g# T; L8 o, ?8 oandrogenic stimulation from either endogenous or
' `/ k$ c9 l8 iexogenous sources, nonpituitary gonadotropin stim-
( D K7 ^7 ~1 e+ j8 ] zulation, and rare activating mutations.3 Virilizing
/ ]2 c; b" \# c- Y' j% D3 Jcongenital adrenal hyperplasia producing excessive
4 m! r* B" L: K0 j5 m3 O$ Z# gadrenal androgens is a common cause of precocious9 p6 h& h8 y6 A( B1 f
puberty in boys.3,40 W, N b( Y7 k M/ O
The most common form of congenital adrenal2 W; S- G6 v* Z$ e; g
hyperplasia is the 21-hydroxylase enzyme deficiency.4 W+ z' y$ e- J5 h$ g! i
The 11-β hydroxylase deficiency may also result in4 P. N, d( l; q$ N( _; p
excessive adrenal androgen production, and rarely,+ [3 ?8 o+ o$ k
an adrenal tumor may also cause adrenal androgen
1 J- Y! j! I& r7 l2 ~# d/ B- W% eexcess.1,3: \( N2 d1 K1 S1 C2 w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! ^9 a- e0 R% i7 R542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 o7 m7 z/ \; Q$ zA unique entity of male-limited gonadotropin-: ]: r# F1 F, v
independent precocious puberty, which is also known z- W1 Y, w$ \( e3 [% y! {# l
as testotoxicosis, may cause precocious puberty at a
/ k" L2 ^+ O* r% `& }- pvery young age. The physical findings in these boys
+ f4 `$ M/ r7 [9 \% O& awith this disorder are full pubertal development,1 P1 n A# I$ a( w1 V
including bilateral testicular growth, similar to boys/ ?8 S( p9 t1 D% H& ^
with CPP. The gonadotropin levels in this disorder! n# y3 d; k3 L* m$ R( d$ |
are suppressed to prepubertal levels and do not show; k8 \0 {8 l8 i: U, q P
pubertal response of gonadotropin after gonadotropin-' L( x& w' f! Z$ X4 w
releasing hormone stimulation. This is a sex-linked8 y4 ^! ]* P& s: ^. C
autosomal dominant disorder that affects only
: e: y9 d3 d) @; {males; therefore, other male members of the family, O+ D" h" E8 X8 T6 q
may have similar precocious puberty.3- g# T4 g( q! g% m( `$ ~7 C
In our patient, physical examination was incon-
r9 a8 ]; \ ]7 `" h9 L5 {( Z2 r" c' T9 lsistent with true precocious puberty since his testi-* l7 {1 \4 U4 ]# B, i ~
cles were prepubertal in size. However, testotoxicosis
5 b9 \5 E' A; B0 K: _9 V( Cwas in the differential diagnosis because his father) Z: C' M1 W' S0 B0 y# p
started puberty somewhat early, and occasionally,
- q$ p) \9 w# L( Z7 j9 j7 |testicular enlargement is not that evident in the0 H% }( v* ?) q+ t @- x' L. V
beginning of this process.1 In the absence of a neg-
8 P5 h% `: Q6 U0 w7 A! J. V8 O/ kative initial history of androgen exposure, our
6 q8 {. ?. Q/ U+ n$ mbiggest concern was virilizing adrenal hyperplasia,6 j, q, k6 G6 D$ f& b
either 21-hydroxylase deficiency or 11-β hydroxylase
& h* |, [ Q+ m& edeficiency. Those diagnoses were excluded by find-
" F0 ]* Q! ^( Sing the normal level of adrenal steroids.
- l9 ~# b/ V; CThe diagnosis of exogenous androgens was strongly6 ?6 E N; H& _. [6 O- ~9 S% {# ]
suspected in a follow-up visit after 4 months because: i8 @# x6 O. B; v+ Z
the physical examination revealed the complete disap-5 R5 N9 x6 s1 N+ O
pearance of pubic hair, normal growth velocity, and
4 s# F: [& @( X! p6 R, L( edecreased erections. The father admitted using a testos-; o+ j$ z5 L7 s" X
terone gel, which he concealed at first visit. He was- ^; m) F+ ?. T8 ^2 a# L# Y
using it rather frequently, twice a day. The Physicians’$ ^5 A3 q) F A6 |5 H) [4 l
Desk Reference, or package insert of this product, gel or
* x' [; z) x& n! C8 z5 R8 R3 ucream, cautions about dermal testosterone transfer to; B) Z- d) [! b# P
unprotected females through direct skin exposure.
( \$ F5 \" Q# ~1 |4 w: ESerum testosterone level was found to be 2 times the0 q- ?2 m+ }' M( y! _& o
baseline value in those females who were exposed to
) j" |/ F& J6 L/ L2 |. V/ W/ geven 15 minutes of direct skin contact with their male
" q1 ^( B T5 H. w: t5 B; k0 epartners.6 However, when a shirt covered the applica-
4 C! k' I9 i$ g, k i9 ltion site, this testosterone transfer was prevented.
' y% ^- Q- b8 ^0 K% sOur patient’s testosterone level was 60 ng/mL,
% [+ ^. b1 R5 `6 }. [which was clearly high. Some studies suggest that# _3 m h1 T& Z, C$ U
dermal conversion of testosterone to dihydrotestos-1 `% x! z, }0 Q) {8 w
terone, which is a more potent metabolite, is more
5 N. B; W1 d; N& P) ]2 ractive in young children exposed to testosterone& D0 |% M/ ]0 J; M
exogenously7; however, we did not measure a dihy-+ A& q- ^; z; s" d5 i* n
drotestosterone level in our patient. In addition to5 F P' t5 \1 b+ v2 W0 |7 v
virilization, exposure to exogenous testosterone in
6 L+ K) E9 a$ G/ e8 E5 s lchildren results in an increase in growth velocity and
( Z5 Q; m4 X5 m" |2 }) M0 E: uadvanced bone age, as seen in our patient.
) a# ^" [# I2 C' k4 |The long-term effect of androgen exposure during
9 Z' K4 K: H1 e+ C( wearly childhood on pubertal development and final& b& [ d# ?2 D
adult height are not fully known and always remain
9 W4 O, {/ Z, @6 Va concern. Children treated with short-term testos-) y( S# B( v, _7 j
terone injection or topical androgen may exhibit some
) ~$ a9 X: ?5 f# { l: H" c, `9 b# Xacceleration of the skeletal maturation; however, after, z1 t7 l$ ]' t9 V9 f
cessation of treatment, the rate of bone maturation
7 c: `) | C) a( P! |/ [decelerates and gradually returns to normal.8,9, E% b: k. i5 r/ T% U( B
There are conflicting reports and controversy4 B5 k5 W$ j% I- X3 {" a* e- K
over the effect of early androgen exposure on adult w/ N' j. m) H: P0 x4 u' b
penile length.10,11 Some reports suggest subnormal3 S) x7 ?0 E. j& a+ _: k: ^
adult penile length, apparently because of downreg-
. A, _. U, R* ^* n5 Lulation of androgen receptor number.10,12 However,) l: W6 q6 c/ m9 A: H
Sutherland et al13 did not find a correlation between
9 S3 h9 m6 y- V; J( W/ k0 u' rchildhood testosterone exposure and reduced adult
* K9 X7 C. g$ B. u) D7 q" Vpenile length in clinical studies.
0 z3 i( u g- d& [, {; v8 LNonetheless, we do not believe our patient is
3 a, V% v. |: ygoing to experience any of the untoward effects from8 z$ q# y; ?2 z; \' C( w% \
testosterone exposure as mentioned earlier because# _6 N& v9 l) m; f6 B, z: ?
the exposure was not for a prolonged period of time.
2 E1 M1 C; m7 B% _4 |* l! ]4 _Although the bone age was advanced at the time of. e+ ~! f1 @" {
diagnosis, the child had a normal growth velocity at, i+ _( x k% H
the follow-up visit. It is hoped that his final adult* v% ~* J+ M& G$ g, }
height will not be affected.2 a6 }( s' r) D! ^
Although rarely reported, the widespread avail-: [' x' `: R; {. n9 k
ability of androgen products in our society may
) E& V4 Q5 S3 R) {) l' t; l; Iindeed cause more virilization in male or female, p& R2 H- o9 L# |, x- r8 q+ ?
children than one would realize. Exposure to andro-8 i# _ V! z3 ^1 H- H# X r5 F$ l
gen products must be considered and specific ques-
}' f2 p" v! z* Z5 {tioning about the use of a testosterone product or
" o# K6 a, R# a/ u1 sgel should be asked of the family members during
4 z/ i0 Z6 w* o& A3 I3 I# [+ Ithe evaluation of any children who present with vir-: n- U4 l3 W; q3 A+ P2 p1 N
ilization or peripheral precocious puberty. The diag-
- _3 v) w/ o& s1 N' enosis can be established by just a few tests and by: R' r6 ?4 n+ l6 u# ~% e! f4 W
appropriate history. The inability to obtain such a: H, n2 F# v6 G! K# h5 _
history, or failure to ask the specific questions, may# K' @+ j9 {6 u
result in extensive, unnecessary, and expensive
% t: N+ D( `* g3 S$ T h; c/ `investigation. The primary care physician should be
# X, s2 s0 Z5 O n, k; O" g0 R8 haware of this fact, because most of these children; }, O# e2 h5 G/ i: R7 y( x# `
may initially present in their practice. The Physicians’
6 T0 u. T) Y( P# p* @Desk Reference and package insert should also put a5 N( R" `! j' N, p' D2 t9 y7 T
warning about the virilizing effect on a male or
. V5 h! l. v; rfemale child who might come in contact with some-+ U% J) {2 g+ {3 n+ E( a
one using any of these products.8 S d# c6 u$ M2 L, z& p% f
References
7 a3 E# h) ]# ?2 L5 z/ H6 W2 x1. Styne DM. The testes: disorder of sexual differentiation, r, Y: b! @# k% p
and puberty in the male. In: Sperling MA, ed. Pediatric. r0 ~9 w9 j8 `0 j
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- H- y: Z) @. N5 `. J/ ]' ~8 m2002: 565-628.4 ~2 x7 C' u6 L) ]! G
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
5 N6 S3 {; P2 Qpuberty in children with tumours of the suprasellar pineal |
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