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Sexual Precocity in a 16-Month-Old/ x% U& J7 S- E
Boy Induced by Indirect Topical
& q0 p c4 [% ]. l+ i3 eExposure to Testosterone5 F: X& E, |6 D8 G' z7 ^3 z
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 {4 l3 T, U2 O
and Kenneth R. Rettig, MD1 c: u$ O1 X: O1 {+ q
Clinical Pediatrics
1 n! O& Y, j4 Z8 X& \7 }* m: Q0 XVolume 46 Number 6
! V+ U( a/ z, ~0 u! D6 n5 iJuly 2007 540-543/ i3 U) X5 L% U6 p
© 2007 Sage Publications9 p4 r* X+ H# K% ]9 ~$ T
10.1177/00099228062966516 ^& ]# w8 x! C8 O
http://clp.sagepub.com9 `# M+ v2 f7 A7 I4 V2 f2 ?
hosted at
; i! u6 G% J$ @http://online.sagepub.com
) e( v3 u2 r% i% |6 u6 U. NPrecocious puberty in boys, central or peripheral,
' X0 a$ O$ T2 ~0 P: fis a significant concern for physicians. Central
! G* w" h9 O2 I+ R+ F! Iprecocious puberty (CPP), which is mediated
/ r" I; c/ J- i3 U" g- ythrough the hypothalamic pituitary gonadal axis, has
, ]+ Y! n7 Z& T$ r' C# I, Za higher incidence of organic central nervous system5 j4 J- Y8 K# G4 y
lesions in boys.1,2 Virilization in boys, as manifested: ?2 m1 m H3 L/ D% v$ b; n+ [
by enlargement of the penis, development of pubic
5 V7 q2 N5 u0 ehair, and facial acne without enlargement of testi-
0 y5 F! V$ V" R) F( a! p. y% Y* f& u4 i6 [cles, suggests peripheral or pseudopuberty.1-3 We
V2 n: U; D2 d$ s: ^/ Dreport a 16-month-old boy who presented with the3 \1 }% l; f4 Q
enlargement of the phallus and pubic hair develop- g3 H1 b% l: t& A: f
ment without testicular enlargement, which was due
) d, Q5 g* E0 a' ^. {4 W* s( b, @to the unintentional exposure to androgen gel used by% n! Y3 N! W% D9 M+ I
the father. The family initially concealed this infor-
9 J- A; ^* q+ ^' C! C% U/ J1 dmation, resulting in an extensive work-up for this
' l" _ j7 |" w% D/ hchild. Given the widespread and easy availability of
- r. o0 e& b" Z$ N$ C% U4 Ytestosterone gel and cream, we believe this is proba-
( Q5 e; P- Z" w1 K2 o* cbly more common than the rare case report in the
# m( T* N# f& Y' V2 k/ t$ J% Y# uliterature.4" N8 l+ M& J) L+ U( T/ z
Patient Report' I/ L8 y& H. i- [2 X( L
A 16-month-old white child was referred to the/ A; [/ J) @6 ^0 z C
endocrine clinic by his pediatrician with the concern
6 C8 z% }; s$ B9 R+ q% _7 |' `of early sexual development. His mother noticed4 [7 }, v7 P' @6 V
light colored pubic hair development when he was# f/ D$ O' Y( D( v* X, }$ f
From the 1Division of Pediatric Endocrinology, 2University of3 X2 t4 v% M. L& }
South Alabama Medical Center, Mobile, Alabama.* o( J& C( W1 B$ h4 X9 C) ]
Address correspondence to: Samar K. Bhowmick, MD, FACE,' B, [! V7 B: g. X8 a; s5 J1 i
Professor of Pediatrics, University of South Alabama, College of
K) ]# J, k9 f6 g, f# k) M; ZMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
G M5 c/ z [& L5 y4 B: Ve-mail: [email protected].. }) @: L- |: ]8 R) r
about 6 to 7 months old, which progressively became
. C9 ]4 z; \1 [darker. She was also concerned about the enlarge-. A# f5 _ F, _5 O# Y$ O
ment of his penis and frequent erections. The child
+ V/ W* n, m( zwas the product of a full-term normal delivery, with
( c9 m `: `8 j0 M" e; j- ba birth weight of 7 lb 14 oz, and birth length of
& p; K9 _: Y; ]! V! @20 inches. He was breast-fed throughout the first year
, Z8 n( {4 H# a% d* l5 lof life and was still receiving breast milk along with6 |( x3 ?0 _& h( i) R
solid food. He had no hospitalizations or surgery,
9 w% z# s: n$ o* ]and his psychosocial and psychomotor development
$ ]4 E0 @8 Q% w3 O9 ~+ O! \was age appropriate.
; |' B; A- O6 `/ Y DThe family history was remarkable for the father,! B1 a. ?+ |6 o; d }
who was diagnosed with hypothyroidism at age 16,) N2 o# I/ Q2 p- ]; E8 Z
which was treated with thyroxine. The father’s
8 _( ?1 G/ m# [5 J/ d6 Rheight was 6 feet, and he went through a somewhat
* _; f, y4 H* f+ z( Xearly puberty and had stopped growing by age 14.' S p3 X( o0 j$ k
The father denied taking any other medication. The; @: \/ m! ]& }$ f! C3 c3 o3 a7 g$ ~
child’s mother was in good health. Her menarche# v5 W& R# f$ x9 p* N4 W. R7 b; `8 O) ?
was at 11 years of age, and her height was at 5 feet! ?# V @: e/ a" s( G. R
5 inches. There was no other family history of pre- v0 z0 L5 `6 w7 `* {
cocious sexual development in the first-degree rela-
# e% y, F- p0 Q; b- a, q7 y( N. z/ }tives. There were no siblings.2 K6 u0 D- B: t. B& V' M
Physical Examination7 s: z2 c$ [ H- B
The physical examination revealed a very active,
9 n& E" C1 \( U# Dplayful, and healthy boy. The vital signs documented
3 v0 T) q" L9 B9 ha blood pressure of 85/50 mm Hg, his length was
9 ? R, M* Z7 F5 Z0 L- x7 P! E90 cm (>97th percentile), and his weight was 14.4 kg: X1 o& W2 ~( p8 D
(also >97th percentile). The observed yearly growth f' s+ J% B5 u$ b& p9 c% {; ]; }
velocity was 30 cm (12 inches). The examination of. k4 R" O7 }) h( P7 {$ V
the neck revealed no thyroid enlargement.
" K# J: L* g! K4 X/ X" AThe genitourinary examination was remarkable for5 g+ H# X7 Z! n- E5 p
enlargement of the penis, with a stretched length of
9 g' O* ]( t' }6 R$ c8 cm and a width of 2 cm. The glans penis was very well/ U# Z- [; t5 B
developed. The pubic hair was Tanner II, mostly around2 q F' Q- S: y3 P! O" |/ r
540' ^ Q$ z* {# s8 N$ H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 i- q& B0 b* F# m0 h3 k' f& S
the base of the phallus and was dark and curled. The
- w1 x9 d! M/ k- S& B) _* z( J3 ttesticular volume was prepubertal at 2 mL each.8 B: X; t B, m4 {
The skin was moist and smooth and somewhat1 B* o2 p* \& N% Z- Y% t
oily. No axillary hair was noted. There were no9 f3 d v$ F" q, y& |9 a5 h8 m
abnormal skin pigmentations or café-au-lait spots.
6 ~6 V4 V Y4 N: RNeurologic evaluation showed deep tendon reflex 2+1 T& m; E% e- p* ~( a3 V! w; [
bilateral and symmetrical. There was no suggestion- Z2 x; }7 A( B) n+ W7 B T- L
of papilledema.
5 M3 N5 i) `9 G: _3 |5 eLaboratory Evaluation
. `5 K( M- z* D& Z4 E7 D9 t/ ?# yThe bone age was consistent with 28 months by1 N, Z4 R q* ]; k, I/ T i7 D$ g+ P
using the standard of Greulich and Pyle at a chrono-! v3 P# i! n4 `* G9 E
logic age of 16 months (advanced).5 Chromosomal8 m) I9 J, g: `' o9 n! G
karyotype was 46XY. The thyroid function test3 u0 R: O& @: |9 O' w, W3 D
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ Y. P9 Y: m% ]0 b+ Plating hormone level was 1.3 µIU/mL (both normal).2 `: v N F' ?
The concentrations of serum electrolytes, blood7 T6 {1 ]; k2 q. v7 b! ]7 g
urea nitrogen, creatinine, and calcium all were: T2 a2 G3 B" k
within normal range for his age. The concentration8 j% v" X+ g. i6 F% k
of serum 17-hydroxyprogesterone was 16 ng/dL4 r% z' o0 [3 A+ a7 z4 K1 K
(normal, 3 to 90 ng/dL), androstenedione was 208 H4 j3 ~# y9 @/ N' K) P
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% I9 @/ Q: v2 e5 v1 o, W
terone was 38 ng/dL (normal, 50 to 760 ng/dL),3 n* @8 d% I2 V1 g: ~
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
; g* s5 G3 p0 M2 f# Z49ng/dL), 11-desoxycortisol (specific compound S)4 m+ Z& F Z# W7 A8 A& \
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- E6 k- z; v- B8 E- A% m
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 {: p. v6 |* _6 r- D& X
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* N2 I, v/ L5 i; mand β-human chorionic gonadotropin was less than
$ D, f9 v8 G; C1 T5 mIU/mL (normal <5 mIU/mL). Serum follicular) W$ K* D' v$ z, x9 y' a
stimulating hormone and leuteinizing hormone$ T- f' y. m/ D9 a2 t. Z, o( e
concentrations were less than 0.05 mIU/mL
4 h( A8 ?, q* m$ d6 t' J(prepubertal).: s& C) Z- f! D# o4 W% H
The parents were notified about the laboratory
: j9 H( t& D2 R- F( x9 ~; q, O4 @results and were informed that all of the tests were
) q7 s4 [4 n9 rnormal except the testosterone level was high. The
8 L5 s5 T, Z. \+ [+ I+ Sfollow-up visit was arranged within a few weeks to' U& u. E1 k- ^; r3 x
obtain testicular and abdominal sonograms; how-9 z) p. S+ F, u; B4 {! v2 n
ever, the family did not return for 4 months.1 z# | p( v) L; A% X
Physical examination at this time revealed that the
5 v$ L. A4 A) L) y! g* L( @+ k* tchild had grown 2.5 cm in 4 months and had gained2 x9 S: W2 D8 {' `
2 kg of weight. Physical examination remained$ \0 k+ @) P% h l3 W0 N
unchanged. Surprisingly, the pubic hair almost com-, W& A' c N, D* i9 q
pletely disappeared except for a few vellous hairs at
3 G: u; m. t! a+ y: cthe base of the phallus. Testicular volume was still 2, N* z4 ^) v' |/ x' o, O: d3 r
mL, and the size of the penis remained unchanged./ H& K% ~* y% Q7 b0 @3 J2 }
The mother also said that the boy was no longer hav-, E9 r$ g$ B2 L! f5 y/ v
ing frequent erections.
; c* k* G t: ~' V- v" ?! Y, ABoth parents were again questioned about use of
9 T/ E! { \/ c" Q) Qany ointment/creams that they may have applied to
3 Z* @$ V0 b. [7 c5 D; Ithe child’s skin. This time the father admitted the
9 ^. e! ?, o9 q4 n- S, \' YTopical Testosterone Exposure / Bhowmick et al 541
) c# y+ g1 H$ A; F- `) Huse of testosterone gel twice daily that he was apply-
7 N$ e) c2 u+ N3 Iing over his own shoulders, chest, and back area for
! h+ s( M2 B0 ya year. The father also revealed he was embarrassed
3 V7 |/ P5 p* k2 L- \% Jto disclose that he was using a testosterone gel pre-& Z5 _! c$ Z( b$ n) @
scribed by his family physician for decreased libido% }/ d+ Z% C( l/ v$ v
secondary to depression.: m) ~% J* A2 W# d$ W
The child slept in the same bed with parents./ Y* X6 M7 |2 k) q3 |+ Z: k
The father would hug the baby and hold him on his
. w c% f M, n. K/ t% jchest for a considerable period of time, causing sig- U0 O- g7 C+ ^9 [
nificant bare skin contact between baby and father.
# p. ]7 Q1 E- B1 U" n; NThe father also admitted that after the phone call,
0 \$ m9 }$ ~1 f% gwhen he learned the testosterone level in the baby
( c2 L2 i5 h, L# O. Bwas high, he then read the product information/ N& k. H( k' }0 \9 J( z. z
packet and concluded that it was most likely the rea-
5 r) V2 G/ x0 Q7 h3 Bson for the child’s virilization. At that time, they
5 X0 q9 Z" U+ x) edecided to put the baby in a separate bed, and the7 U& G8 D, `8 \" R2 O w* E. J0 n0 q
father was not hugging him with bare skin and had) A) h3 X# Z' C
been using protective clothing. A repeat testosterone' X, c! t5 n1 m
test was ordered, but the family did not go to the; h; c" {! ? ~
laboratory to obtain the test.
3 }; ?5 w; r/ K( j0 ^+ N! y0 }5 ADiscussion
8 z2 }2 m5 X0 [ p {$ K9 APrecocious puberty in boys is defined as secondary
) e4 H& `* d6 |sexual development before 9 years of age.1,4
0 E, U7 |: s0 l- q1 pPrecocious puberty is termed as central (true) when
$ D" W; r8 s2 B& Y# Q3 i. ait is caused by the premature activation of hypo-
/ ^! Q' A( M- \$ n% v8 c" s a! Dthalamic pituitary gonadal axis. CPP is more com-& W+ A0 g) E. z9 m$ d, U; v
mon in girls than in boys.1,3 Most boys with CPP
8 ^) b% n. D; ?4 X9 w1 Q2 s% ymay have a central nervous system lesion that is
4 N- }& N* U' f/ Fresponsible for the early activation of the hypothal-2 s6 C& K/ [6 j' R' c8 ^
amic pituitary gonadal axis.1-3 Thus, greater empha-2 e( S' V6 u' T3 c+ ?: w" r
sis has been given to neuroradiologic imaging in1 h2 v0 s. N/ q# \: l5 g: M; W
boys with precocious puberty. In addition to viril-
1 d+ F5 `& Y% R3 Y H" T9 |, j4 `ization, the clinical hallmark of CPP is the symmet-& V6 c {- G4 h% y; D- R0 n
rical testicular growth secondary to stimulation by- h. t, s) T3 L! b
gonadotropins.1,3* e8 j; h( {) |/ y
Gonadotropin-independent peripheral preco-
7 P: r: z# }# K P1 M+ Bcious puberty in boys also results from inappropriate
) q4 o9 |5 {/ \* n5 F- Randrogenic stimulation from either endogenous or
7 U- p8 |9 z; P/ ]# b3 Lexogenous sources, nonpituitary gonadotropin stim-
3 T( J6 O& E- t4 q: Rulation, and rare activating mutations.3 Virilizing
( d3 g5 G2 x* Ocongenital adrenal hyperplasia producing excessive
7 `) K8 K; J# I3 C Z$ j7 G0 iadrenal androgens is a common cause of precocious
+ \1 n5 z/ C! I: I! Jpuberty in boys.3,41 i+ r, D( l, T! Y0 {+ c
The most common form of congenital adrenal
1 B) v7 m9 y; r6 R' Ehyperplasia is the 21-hydroxylase enzyme deficiency.
; q" K8 p$ O" VThe 11-β hydroxylase deficiency may also result in+ u4 C, N1 m7 P& g' P+ G
excessive adrenal androgen production, and rarely,
( ]9 R& o9 Y6 {. \$ |+ aan adrenal tumor may also cause adrenal androgen
3 i( X; i4 w8 h3 w3 k! W2 Iexcess.1,3' u9 O' z2 t$ L$ ]6 M3 D6 `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 v+ N, J, Z; ^6 |6 w ^7 i5 p3 |0 ?
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; u/ e( q5 q/ mA unique entity of male-limited gonadotropin-
/ R; T: P( O/ w aindependent precocious puberty, which is also known
5 A5 `$ }3 A) sas testotoxicosis, may cause precocious puberty at a
9 G. n( L; U+ d: i3 \: {% Jvery young age. The physical findings in these boys
. l) o$ [+ l ?* c) Swith this disorder are full pubertal development,2 r: `7 j3 j8 [0 J" ?+ `2 D& o
including bilateral testicular growth, similar to boys; w2 B1 q' I+ j0 Q0 q8 [/ @" m
with CPP. The gonadotropin levels in this disorder5 f- _0 K+ Z, I- z0 T3 L# |% v
are suppressed to prepubertal levels and do not show( x) c$ C! _# p5 L: A |% y+ J, U- k
pubertal response of gonadotropin after gonadotropin-- @' K9 `+ Z- O( @9 m1 ^
releasing hormone stimulation. This is a sex-linked6 j, `' \. ?5 I4 V2 J
autosomal dominant disorder that affects only, d$ A: M1 e, g5 Q- v+ i
males; therefore, other male members of the family" t5 j7 k- ]# ]7 Y) ?! {/ [
may have similar precocious puberty.3
1 w1 Z6 O, x3 e& n+ vIn our patient, physical examination was incon-- z1 ]* r# `* L* N! }/ ~4 Z6 B i
sistent with true precocious puberty since his testi-
[$ F) H1 U% u, U6 B6 v( z) {cles were prepubertal in size. However, testotoxicosis& t' c( I4 x. i$ ~* k2 Q
was in the differential diagnosis because his father
9 Y# d4 b% g; C1 \started puberty somewhat early, and occasionally,# ~" T1 ^* B3 t. ^3 \1 p5 ^0 n
testicular enlargement is not that evident in the
/ N2 ?. z# V9 S; w- \3 [beginning of this process.1 In the absence of a neg-
% X+ _! D, H6 Q9 T6 J1 R% v& ?$ Tative initial history of androgen exposure, our
U p8 T" }/ q# i. U. Wbiggest concern was virilizing adrenal hyperplasia,
+ `8 m' G0 ?$ @6 ?- veither 21-hydroxylase deficiency or 11-β hydroxylase
! s O" i) E4 n) v( `3 _8 Adeficiency. Those diagnoses were excluded by find-2 T* w6 |2 w: S+ T
ing the normal level of adrenal steroids./ y% S- F% h) A( w. S
The diagnosis of exogenous androgens was strongly9 f+ S6 r8 O/ _, t; }
suspected in a follow-up visit after 4 months because
' W; N' h* X( W3 r8 Sthe physical examination revealed the complete disap-+ r1 A5 f# W! d/ R
pearance of pubic hair, normal growth velocity, and
/ `) @) S1 d* z( U5 k {decreased erections. The father admitted using a testos-, Y0 H8 C) x( ?2 q' k/ Y/ S% D
terone gel, which he concealed at first visit. He was- `- a) i/ r/ L3 }8 C/ g
using it rather frequently, twice a day. The Physicians’$ Z* F8 Y0 D7 Z! F
Desk Reference, or package insert of this product, gel or
$ C( u* m- c' }cream, cautions about dermal testosterone transfer to* G# d/ R3 _/ R% Q2 U7 N
unprotected females through direct skin exposure.$ ~. |* @# {2 Z) ?
Serum testosterone level was found to be 2 times the
% P! Y0 J# r: C& Obaseline value in those females who were exposed to
- m1 L- _9 q0 K. n5 M1 peven 15 minutes of direct skin contact with their male
$ ^* V) i5 h& @, h* v& hpartners.6 However, when a shirt covered the applica-
4 m. e9 G5 R$ U3 Vtion site, this testosterone transfer was prevented.
7 A" O8 o L# F4 p( W/ h9 O9 V4 v3 |Our patient’s testosterone level was 60 ng/mL,! b$ o' j2 V- }, k/ d
which was clearly high. Some studies suggest that
* l& p. p# h+ Ldermal conversion of testosterone to dihydrotestos-1 F; f7 ]: M* w' z
terone, which is a more potent metabolite, is more
* M+ n; v. m, f9 vactive in young children exposed to testosterone
! T5 h& s& v3 M X, Q3 m7 I* nexogenously7; however, we did not measure a dihy-; S3 F/ J( B( I8 m( O8 b5 n
drotestosterone level in our patient. In addition to
0 {/ c! j0 J8 y5 `3 L5 b- Nvirilization, exposure to exogenous testosterone in
9 u# r, Z5 [6 r+ e& G! s" V# mchildren results in an increase in growth velocity and, f, N4 }# U1 J' }# a6 \+ o0 \
advanced bone age, as seen in our patient.
; s5 v' }0 r2 t5 r1 A# nThe long-term effect of androgen exposure during
3 o( W3 k5 R. rearly childhood on pubertal development and final$ e* [$ V- z* G+ S
adult height are not fully known and always remain
8 b: R5 I7 z+ ga concern. Children treated with short-term testos-& }# \6 N1 U5 x' y4 k
terone injection or topical androgen may exhibit some& M: N3 {- e* V! o5 K2 A
acceleration of the skeletal maturation; however, after5 p# O$ x5 d. {1 ~4 M1 V
cessation of treatment, the rate of bone maturation
# P* m$ F: t' N) D! k5 p7 j6 I+ udecelerates and gradually returns to normal.8,9
7 _! j! M* _( k; [- ]2 kThere are conflicting reports and controversy
5 V& P2 M ?+ uover the effect of early androgen exposure on adult+ R& G/ I+ q( k
penile length.10,11 Some reports suggest subnormal
/ }; l5 o! Y' ~/ Dadult penile length, apparently because of downreg-
! E) e; q( H% {6 D: ]ulation of androgen receptor number.10,12 However,4 C- \0 O+ E/ F4 @, M! ]% g# k
Sutherland et al13 did not find a correlation between
! c& E5 t/ d/ m% l" ]childhood testosterone exposure and reduced adult5 l6 W( s8 u; h5 T' [4 L. p
penile length in clinical studies.
- J' J) e! D- s1 e% D+ XNonetheless, we do not believe our patient is- T/ I7 u, @ C1 K. e' S
going to experience any of the untoward effects from
) P4 A* G( x1 d+ D, y6 ?% Ntestosterone exposure as mentioned earlier because3 l& ~4 U2 j' D/ b3 |% E
the exposure was not for a prolonged period of time.1 a3 A' i1 F7 h' ^5 W6 }& I
Although the bone age was advanced at the time of+ z: i W7 p3 m- c% V
diagnosis, the child had a normal growth velocity at' P" s0 ~% A3 H
the follow-up visit. It is hoped that his final adult
* @7 l+ M; c+ hheight will not be affected.
; [( U1 y/ ~1 o: q% m1 _6 RAlthough rarely reported, the widespread avail- o4 S( _' N2 t+ {! o
ability of androgen products in our society may' X. h- k0 x* O9 w* f
indeed cause more virilization in male or female& e8 y# L2 h" k% E5 a0 s
children than one would realize. Exposure to andro-
! a" M2 w: D: p0 F5 W: d* @; rgen products must be considered and specific ques-
+ \2 N7 n9 w/ `tioning about the use of a testosterone product or, v: S2 {. j8 f, R8 A& p6 C
gel should be asked of the family members during- w# k9 b3 M# @+ ~! }( `2 z
the evaluation of any children who present with vir-0 K: J& @/ `; H8 }/ O
ilization or peripheral precocious puberty. The diag-
& A; a5 S4 G- e/ S( N/ v4 `, ?2 bnosis can be established by just a few tests and by8 T: D {! T4 i8 I: y, a8 Q
appropriate history. The inability to obtain such a
# N l6 x! K/ J/ J- r. A) Thistory, or failure to ask the specific questions, may8 S0 h6 B, f7 o9 f; d
result in extensive, unnecessary, and expensive) ~( @2 R+ @' M3 ?
investigation. The primary care physician should be
1 F7 n* K8 D4 \% `% _0 Caware of this fact, because most of these children
2 P+ n3 p K( E8 K1 emay initially present in their practice. The Physicians’
/ t7 J1 H$ T/ a; KDesk Reference and package insert should also put a
1 \9 g3 O( a1 K" iwarning about the virilizing effect on a male or8 _5 l7 e( j1 V; c7 z* x+ N7 S
female child who might come in contact with some-4 a9 t% t8 D! j& d& B
one using any of these products.
3 v6 M2 i. g6 i# W) ~9 O! C) x* w' dReferences5 J5 H3 w4 ~- e
1. Styne DM. The testes: disorder of sexual differentiation
" n7 O6 D0 S! Yand puberty in the male. In: Sperling MA, ed. Pediatric
. D2 ^# F" w* r6 kEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. m, K$ @$ { U5 W% g
2002: 565-628.
( K# f, E! j+ K& l+ B2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- H& G( v# q* V7 }9 K7 spuberty in children with tumours of the suprasellar pineal |
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