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Sexual Precocity in a 16-Month-Old. u+ _9 b* Z, b3 i$ p
Boy Induced by Indirect Topical
/ d2 ^- L6 Q8 n3 Z. `& |Exposure to Testosterone' J' c$ X* b/ L4 N8 ~9 U
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,22 O2 T. }7 U7 H
and Kenneth R. Rettig, MD1
" W) W# K/ R0 \; O* d' }; [Clinical Pediatrics( G' y. f; p6 t" ]9 @$ c5 g0 M
Volume 46 Number 6
9 f7 D7 j) I. F/ KJuly 2007 540-543
+ }" ~7 X6 \" V© 2007 Sage Publications' I5 g8 m' y' _2 a$ a1 T
10.1177/0009922806296651
" X o' M% O# N; vhttp://clp.sagepub.com8 }; J8 A# f1 g
hosted at
- D/ ^9 C, Q2 B, i1 chttp://online.sagepub.com
; V; U! x( q4 C1 u- zPrecocious puberty in boys, central or peripheral,
" ]4 f5 Y/ N& f! d, X; k7 pis a significant concern for physicians. Central, f+ d: f9 N/ m2 p
precocious puberty (CPP), which is mediated
# c; ^& [ B3 s* W/ _% pthrough the hypothalamic pituitary gonadal axis, has
6 e/ R4 i0 Q/ w% V9 V1 ba higher incidence of organic central nervous system
: L$ N( I- q" Q; m8 Q9 zlesions in boys.1,2 Virilization in boys, as manifested; z. W/ V: S$ k9 ?' w7 K# C( a
by enlargement of the penis, development of pubic+ U5 c: F, S, V" i& Q1 c- s
hair, and facial acne without enlargement of testi-
! p1 |! _6 v( N9 k8 h, R4 ]. O) {2 C! pcles, suggests peripheral or pseudopuberty.1-3 We
1 x! y) W; o4 x3 I% q! |report a 16-month-old boy who presented with the
. v/ X# ?# i+ j6 z8 xenlargement of the phallus and pubic hair develop-% n, `, V; B: Q2 \- P9 [$ C5 m" Y' `
ment without testicular enlargement, which was due; f/ H4 u/ u! q0 U6 m& i9 o( \ e
to the unintentional exposure to androgen gel used by- P! u1 O j( H* S- l, h
the father. The family initially concealed this infor-' h, p/ d) C2 M: S, m! Z- {8 x
mation, resulting in an extensive work-up for this3 b- v! \- h$ e
child. Given the widespread and easy availability of: W9 k4 {. \9 Y, Z
testosterone gel and cream, we believe this is proba-
9 i) j7 _1 F8 p5 ^5 G$ O) ]" U) ybly more common than the rare case report in the
/ L. i8 c. n9 z; Yliterature.4, L) P' o6 X- g' W8 F
Patient Report
; m- k9 D. _+ l2 jA 16-month-old white child was referred to the
! h& J* I+ i! a y( M9 y5 qendocrine clinic by his pediatrician with the concern" [9 k5 i8 D; D8 i. Q! b
of early sexual development. His mother noticed
6 a; Z' s# A8 clight colored pubic hair development when he was5 V) i+ v3 S7 ]( Z3 l5 J% ?" F
From the 1Division of Pediatric Endocrinology, 2University of7 [* j6 w' E4 L, z2 x
South Alabama Medical Center, Mobile, Alabama.; J7 [! _7 h4 D$ I
Address correspondence to: Samar K. Bhowmick, MD, FACE,6 H/ \+ a o/ H% W. G/ F' @& Q, |4 `
Professor of Pediatrics, University of South Alabama, College of
6 w9 a9 d& [: X9 a0 @& U6 X" E2 |Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 O+ Y' z/ F- Q' U. b& h V R4 Te-mail: [email protected].# a/ }1 O7 ^7 p% U% k7 m" Z
about 6 to 7 months old, which progressively became
+ t7 G4 v/ v6 e* j) V$ idarker. She was also concerned about the enlarge-" N- [/ m- v% i
ment of his penis and frequent erections. The child
( f8 \+ j/ z# t/ uwas the product of a full-term normal delivery, with
: M1 c& L; e" ua birth weight of 7 lb 14 oz, and birth length of
- T' A$ ~! i' z; g( R' a20 inches. He was breast-fed throughout the first year$ z; K* P9 V2 @, H; K1 c
of life and was still receiving breast milk along with
8 O5 U3 H% h7 a J$ S9 b7 M8 Psolid food. He had no hospitalizations or surgery,
$ u6 u8 n, N6 R( U* n' Kand his psychosocial and psychomotor development
7 [8 p+ j* m% P- w# I, Owas age appropriate.; D+ o& \% y7 F1 b, o/ h
The family history was remarkable for the father," ?! N* C1 y% j- B, `
who was diagnosed with hypothyroidism at age 16,0 D9 \' V/ n/ c- Y7 d/ t
which was treated with thyroxine. The father’s
/ n5 r, h# L( _5 @( Yheight was 6 feet, and he went through a somewhat
% Q4 ]' ^/ A) _& c0 nearly puberty and had stopped growing by age 14.
* d0 ~+ \3 O! E6 SThe father denied taking any other medication. The
( }& C6 J; E0 x8 \7 tchild’s mother was in good health. Her menarche
( J0 l: D7 _$ r, U3 ewas at 11 years of age, and her height was at 5 feet
; D( h4 g; n5 |0 l5 inches. There was no other family history of pre-
2 k& t$ |5 w9 R: b$ u6 ycocious sexual development in the first-degree rela-) ~4 `+ u9 P) j4 m
tives. There were no siblings.. r( t4 E j0 h" g- f9 C) H% I
Physical Examination
" Z% i4 J& \: TThe physical examination revealed a very active,9 T5 E$ n# Q& ~7 Z4 k3 c8 p9 I
playful, and healthy boy. The vital signs documented8 l. F- ]* h C8 Z
a blood pressure of 85/50 mm Hg, his length was7 k9 k# ~+ e8 Z ?7 C
90 cm (>97th percentile), and his weight was 14.4 kg
9 S& A2 [9 Q7 Y' c$ F$ ~- t; s& r$ U(also >97th percentile). The observed yearly growth* O; Z5 M1 l! _' l8 R
velocity was 30 cm (12 inches). The examination of# y# Z% _0 a8 w5 I
the neck revealed no thyroid enlargement.' e- v1 M: I, w0 Z9 B$ N
The genitourinary examination was remarkable for
# y. S. [+ e( s0 q9 m2 x* zenlargement of the penis, with a stretched length of
% K6 M+ _6 a8 }' m) Z$ m8 cm and a width of 2 cm. The glans penis was very well& } K" i! ?5 @% q
developed. The pubic hair was Tanner II, mostly around
$ F. Z) ?) K+ z# P% x7 x540
0 @. a$ \. @7 J, P' Dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ Q) Q4 T. Y6 A ]the base of the phallus and was dark and curled. The
2 j9 }% ~' {9 ]7 J: H! m7 etesticular volume was prepubertal at 2 mL each.* A. Y+ K; T. n, z |
The skin was moist and smooth and somewhat
( t8 ]6 e$ d3 M. m5 zoily. No axillary hair was noted. There were no
+ S7 y5 B7 x2 |abnormal skin pigmentations or café-au-lait spots.
$ _6 L0 q' _. ~Neurologic evaluation showed deep tendon reflex 2+" d& G4 d$ X( O) Z
bilateral and symmetrical. There was no suggestion) n% d; F: n" z' `7 [6 D9 ]
of papilledema.
2 o/ Y/ N0 [! s2 v- a# k* hLaboratory Evaluation
: U( m7 S* [8 T0 f, T" X* cThe bone age was consistent with 28 months by
: {( {# u0 m3 B1 musing the standard of Greulich and Pyle at a chrono-
! E/ A( B( \' r# mlogic age of 16 months (advanced).5 Chromosomal
$ G- C @# [2 e7 @) T3 t% T1 [karyotype was 46XY. The thyroid function test# v0 s- I+ W, I( ^
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 M$ G. x4 _. N& B+ L5 p# ?lating hormone level was 1.3 µIU/mL (both normal).& J* W0 L. m4 j7 D& p6 H
The concentrations of serum electrolytes, blood
6 h4 g: W+ p8 Rurea nitrogen, creatinine, and calcium all were
1 p8 }1 w) x- a7 g- x! @within normal range for his age. The concentration
. L9 O# k: \* J6 @3 A; ~of serum 17-hydroxyprogesterone was 16 ng/dL" _( L- d1 |' f" ?5 A; r$ R& b. s
(normal, 3 to 90 ng/dL), androstenedione was 20
8 w/ S R. U; V3 K4 x: K8 ong/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 G7 {, c, I4 v3 P& Yterone was 38 ng/dL (normal, 50 to 760 ng/dL),
T) f: ~/ z" sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to! b0 c! Q- h2 U
49ng/dL), 11-desoxycortisol (specific compound S)& R1 ] L8 x3 X0 z
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 |. o, ?. S0 ^& ~) ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
! O; C0 g8 v/ _6 Ptestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 D& G& B( D% I7 I8 eand β-human chorionic gonadotropin was less than* a( P, E+ `. j; W
5 mIU/mL (normal <5 mIU/mL). Serum follicular# b# j: \ b3 W. U
stimulating hormone and leuteinizing hormone% H4 v8 B" h X" V6 K; Y
concentrations were less than 0.05 mIU/mL
* z3 `9 O- s: [8 G0 ^6 S3 D1 n: n( S(prepubertal).% f- s: n0 R8 d: D. l# K: g, ?! m. `* b( u; j
The parents were notified about the laboratory) g, y) ?- r& v2 J8 Y: {* l
results and were informed that all of the tests were) ]* |1 _$ F) D% [
normal except the testosterone level was high. The9 ~+ n% p3 @; N) ~
follow-up visit was arranged within a few weeks to
# }$ d8 Q. c6 a9 P/ O3 T; Y: Nobtain testicular and abdominal sonograms; how-
, ]$ V3 U$ o" V8 dever, the family did not return for 4 months.
9 M. Y0 U0 c6 t. Q8 b8 I0 tPhysical examination at this time revealed that the: Y* ~- j8 d% s* C3 E4 r
child had grown 2.5 cm in 4 months and had gained6 U3 ^! D5 L' S' c; Y. o% y7 C
2 kg of weight. Physical examination remained
* ], m( {$ ?( n2 q, p+ nunchanged. Surprisingly, the pubic hair almost com-
0 n! U# D' `, O6 w. u" wpletely disappeared except for a few vellous hairs at
" D8 g* C0 B; a* ]' x2 Ethe base of the phallus. Testicular volume was still 2
- V+ P! Y7 e) G1 J; TmL, and the size of the penis remained unchanged.1 j* G7 J; n H% _1 [
The mother also said that the boy was no longer hav-
) i2 ]7 ~3 P, Ling frequent erections.! D8 X8 O; Q, w, i# l$ t. g4 L+ q
Both parents were again questioned about use of! D d/ K9 N; ?/ `+ u; M) k* ]
any ointment/creams that they may have applied to' p2 m2 |$ k% {5 }
the child’s skin. This time the father admitted the, ?1 M+ g8 Z0 I. i8 n. e. }# m
Topical Testosterone Exposure / Bhowmick et al 541
; A* g! T' E" m0 \0 [use of testosterone gel twice daily that he was apply-
( z4 d+ A3 v eing over his own shoulders, chest, and back area for
& s: S/ d) [% W* H' Q! ja year. The father also revealed he was embarrassed$ D! ?) r, o& V& t; J* h
to disclose that he was using a testosterone gel pre-7 b5 U- v1 P3 W& v6 C/ W, i' \/ P- P
scribed by his family physician for decreased libido/ Z8 T/ `5 J! Q
secondary to depression./ I. n2 k& z- a2 c
The child slept in the same bed with parents.3 H1 q$ K" ?4 O3 H' n9 a, R
The father would hug the baby and hold him on his
/ A' ~' Z' p# xchest for a considerable period of time, causing sig-, I2 ]; }5 ^$ }& m- Q, R) E$ S: k. M
nificant bare skin contact between baby and father.7 n; H `# }2 W# Q: W) A" S+ c( x' \
The father also admitted that after the phone call,
" B L8 F+ Y [5 F" ewhen he learned the testosterone level in the baby$ |$ X# l$ h2 [ p
was high, he then read the product information, p9 T `- w [: Y* {' t( C
packet and concluded that it was most likely the rea-
. O- A7 Z& ~$ H& M Hson for the child’s virilization. At that time, they' o& y" w [9 p
decided to put the baby in a separate bed, and the
) ?8 C' \' F$ i7 z8 |- ~father was not hugging him with bare skin and had
. f( }' V( a v I3 f+ fbeen using protective clothing. A repeat testosterone, ^0 R+ i+ q. H1 F" z
test was ordered, but the family did not go to the
$ y/ X( O, c: a2 |4 olaboratory to obtain the test. f3 N" e v. R; l; ~4 s) e
Discussion6 m$ P! T: H e3 A/ q
Precocious puberty in boys is defined as secondary8 \7 H& h" u0 c5 G: A( a" ]" W, k% ]
sexual development before 9 years of age.1,4
3 ]& S( A n1 F QPrecocious puberty is termed as central (true) when# q" [2 O" O$ m4 _7 D6 s
it is caused by the premature activation of hypo-
% Y0 _0 K. _8 X6 J3 y7 fthalamic pituitary gonadal axis. CPP is more com-6 E0 G& \* z) P" j P; u2 j8 Z
mon in girls than in boys.1,3 Most boys with CPP
% Y% I( `7 i9 N0 |, ]0 dmay have a central nervous system lesion that is4 o, z) c# O& L8 f
responsible for the early activation of the hypothal-
3 {/ s) W3 f% z1 A* Lamic pituitary gonadal axis.1-3 Thus, greater empha-
6 X& Z6 O: {5 S4 Q" p" {: X6 csis has been given to neuroradiologic imaging in
, D. C/ j2 F9 _. t1 P* s/ l; {( |boys with precocious puberty. In addition to viril-
" W" [- D7 C2 ^+ L- sization, the clinical hallmark of CPP is the symmet-" f3 ~" `. \% [/ r7 ?4 J1 ?3 ~
rical testicular growth secondary to stimulation by) R+ w; h7 S5 a8 G7 F' |# p$ k, T
gonadotropins.1,3
: W, y7 x7 v w7 @5 O HGonadotropin-independent peripheral preco-* g; `: T8 f H0 W Q
cious puberty in boys also results from inappropriate) E' \$ ~* l, f# X# Y
androgenic stimulation from either endogenous or
p) ~) `$ v- n8 O& b8 q3 wexogenous sources, nonpituitary gonadotropin stim-; t* }6 `& U- Y* N2 u5 b* j! |
ulation, and rare activating mutations.3 Virilizing
/ j" n! g: L# k' W- Vcongenital adrenal hyperplasia producing excessive! t& c/ I! r& u) W- J7 I; h
adrenal androgens is a common cause of precocious: z6 Y7 ^$ i1 e6 V* O& S4 z! r
puberty in boys.3,4
& i3 a8 f8 R6 e$ C& Q# l+ {The most common form of congenital adrenal
9 b) ^" {7 d2 b+ S% v" J) g" Mhyperplasia is the 21-hydroxylase enzyme deficiency.
. I; B1 V9 m. H$ j- U: e7 {The 11-β hydroxylase deficiency may also result in; U" @( P- j5 L/ G; P! _/ E
excessive adrenal androgen production, and rarely,
+ X$ `) g5 v) F& m3 Lan adrenal tumor may also cause adrenal androgen
4 F: ]: ^# D8 P2 G7 X, v/ aexcess.1,3
+ h$ O! U! @( M( Hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 Y I1 x" J7 k$ {( \4 ^* Q& C
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 p+ m+ N( r$ J7 IA unique entity of male-limited gonadotropin-
9 x5 R% w7 S- S4 X3 L% ~& p5 qindependent precocious puberty, which is also known
* h* r+ Q1 ^' M, Ras testotoxicosis, may cause precocious puberty at a
; v7 C5 W$ y* ~! y' Q1 mvery young age. The physical findings in these boys
Q% f2 k5 }/ g/ Xwith this disorder are full pubertal development,. l3 g: F- B& J$ J$ z+ N
including bilateral testicular growth, similar to boys1 b9 p$ ~/ |- M
with CPP. The gonadotropin levels in this disorder
! D7 L) F. Y0 s: n: k& }& C! Iare suppressed to prepubertal levels and do not show/ _6 A) Y& l! H- i
pubertal response of gonadotropin after gonadotropin-
1 s1 D! ] u! b% Vreleasing hormone stimulation. This is a sex-linked
K+ r+ M$ ^" h0 Aautosomal dominant disorder that affects only% I( U+ V! I: b# w% @! L" E
males; therefore, other male members of the family
~5 H* H" U/ O" p& ]' b% gmay have similar precocious puberty.3
6 _) _8 y+ O. @4 sIn our patient, physical examination was incon-
; z7 X) N; A1 ~+ W; |" U0 ?sistent with true precocious puberty since his testi-
. {; B8 S2 D$ k- x/ E, F' zcles were prepubertal in size. However, testotoxicosis
) V" F( g1 D& ^) Swas in the differential diagnosis because his father
( U# c) |/ k; `# W8 g* Fstarted puberty somewhat early, and occasionally,1 X6 }8 ?' G# ^+ M7 k& f! z+ ]
testicular enlargement is not that evident in the6 J7 K2 O3 w- U' Y( _$ A' m6 G
beginning of this process.1 In the absence of a neg-
- x8 {( w& w8 l/ Y2 y& b- F+ d1 Tative initial history of androgen exposure, our
' o2 {- M/ Y. j1 v b; g! `biggest concern was virilizing adrenal hyperplasia,
. ~7 v) D, K) r! Y$ y6 ueither 21-hydroxylase deficiency or 11-β hydroxylase& I G+ i8 p) c. ^5 G# x1 B0 a. i
deficiency. Those diagnoses were excluded by find-
' x7 G) ?( [! i: l9 ging the normal level of adrenal steroids." p( j) ?7 J3 M" ]9 y
The diagnosis of exogenous androgens was strongly* |0 c' L( y* F9 ^2 I
suspected in a follow-up visit after 4 months because
, q `4 O) B4 i9 t5 Tthe physical examination revealed the complete disap-
1 w; \+ ]( W0 h% @- k. mpearance of pubic hair, normal growth velocity, and J9 { w5 P% p& {; y
decreased erections. The father admitted using a testos-5 K( e! v6 l5 m# l& i$ | ?" R
terone gel, which he concealed at first visit. He was) g6 P0 F2 d1 a1 n
using it rather frequently, twice a day. The Physicians’# x; z; d/ |3 q0 l9 U7 t: G1 K3 a
Desk Reference, or package insert of this product, gel or
, H9 T8 _- P2 _0 x' _cream, cautions about dermal testosterone transfer to* v, ^9 I. C* C: W% `: r
unprotected females through direct skin exposure.. n$ S2 F1 E7 f9 J {: l$ O! Y
Serum testosterone level was found to be 2 times the, c- W) x; `9 c, O! J
baseline value in those females who were exposed to$ S8 ^4 R$ n) x' W, u
even 15 minutes of direct skin contact with their male( I( @0 Q1 b" G E7 e/ n
partners.6 However, when a shirt covered the applica-, R" {+ Y: D8 j% U
tion site, this testosterone transfer was prevented.6 Z/ ]! U/ c" d3 s% ]3 }
Our patient’s testosterone level was 60 ng/mL,
( J" p7 B0 ^+ |8 U6 V0 \$ ~which was clearly high. Some studies suggest that
/ s: z: k( @" k8 X# g+ Ddermal conversion of testosterone to dihydrotestos-9 F/ e, |2 ~$ f
terone, which is a more potent metabolite, is more
* o% u/ D! C( |1 o! ]. tactive in young children exposed to testosterone+ p7 i" C. q' ]- J- D
exogenously7; however, we did not measure a dihy-; B+ P" z* P( ]5 V: @
drotestosterone level in our patient. In addition to
0 L6 m2 H8 ~" hvirilization, exposure to exogenous testosterone in8 ^) R# c+ k& k% x- ^! o
children results in an increase in growth velocity and' |- S8 D, W# S" }, F/ W9 H/ C
advanced bone age, as seen in our patient.6 v8 H! @+ a: G2 V' _1 P
The long-term effect of androgen exposure during
' `3 q# ^! y4 O$ C9 r% f% [9 Iearly childhood on pubertal development and final6 ?" |9 n: L1 T( v
adult height are not fully known and always remain
, V& Q! T3 D" Y+ l" R4 y- C: X6 [a concern. Children treated with short-term testos-
% b" E5 w0 J- D: o: Y( ? Sterone injection or topical androgen may exhibit some
+ d) V o7 M8 h# s2 hacceleration of the skeletal maturation; however, after" f# c, Y8 F2 [* {3 a$ X$ h
cessation of treatment, the rate of bone maturation
6 C/ m1 t( i6 x9 G3 Q! vdecelerates and gradually returns to normal.8,9+ D+ s( ^! V2 Z! M4 Z9 F o
There are conflicting reports and controversy
: D' W, l4 g. X* N4 eover the effect of early androgen exposure on adult
: |; u8 U& k7 N" H, |! M* upenile length.10,11 Some reports suggest subnormal% y4 W0 G4 D, u8 g, w; T
adult penile length, apparently because of downreg- O7 H& |" l, ^8 c
ulation of androgen receptor number.10,12 However,' ]3 Y& L) a1 R0 v1 v
Sutherland et al13 did not find a correlation between
1 d G' j, v- E/ k; Nchildhood testosterone exposure and reduced adult
, l2 C( x: F4 i4 Z+ ~ Lpenile length in clinical studies.& z& D2 c3 s0 P% F& x; E1 T8 t
Nonetheless, we do not believe our patient is% p' |; d7 n8 q/ I
going to experience any of the untoward effects from
$ `1 L- S0 t) R) l8 X" n0 Ktestosterone exposure as mentioned earlier because5 ^2 o. f' ~! _* ~
the exposure was not for a prolonged period of time.6 s( K1 {6 D2 z2 @8 {/ @
Although the bone age was advanced at the time of$ a8 k, Q; |# ] b8 g8 b
diagnosis, the child had a normal growth velocity at
/ p Z- D; h! ?' L# ?+ xthe follow-up visit. It is hoped that his final adult2 }) h0 a4 H; j1 Y7 K
height will not be affected.
" Z0 B) E6 I# Y9 p6 ?0 }Although rarely reported, the widespread avail-7 ~) Y" o+ x. h, O5 }7 s
ability of androgen products in our society may' `. z6 u7 ~6 P# n* D: d
indeed cause more virilization in male or female, e0 g2 g3 K$ s! ~0 X( `& ~0 Y! c' e
children than one would realize. Exposure to andro-
% R0 b/ t9 H" L7 P" l/ K. w- Sgen products must be considered and specific ques-
- q V& N; p* `) L1 O0 i. M* ftioning about the use of a testosterone product or
' L9 N" T$ c7 l5 z r6 L9 E7 S* ~gel should be asked of the family members during
: N& R- L; h0 X9 T& P1 P. @4 dthe evaluation of any children who present with vir- h- H. P7 \2 b. k
ilization or peripheral precocious puberty. The diag-! q# ]; r+ @ X4 m' Q9 I
nosis can be established by just a few tests and by
( R' c8 Y# i' A1 J& {appropriate history. The inability to obtain such a
- O; g% t& @6 Y) V Xhistory, or failure to ask the specific questions, may# B" {3 ]* {0 d6 I* L1 E3 [
result in extensive, unnecessary, and expensive4 Q3 v* t# @# h' E' [2 w- k% t
investigation. The primary care physician should be7 I1 r# w1 J# [" ~2 B
aware of this fact, because most of these children
* r' W1 r/ C( F6 E) C- y$ \may initially present in their practice. The Physicians’
3 \" n; d: L2 Z! sDesk Reference and package insert should also put a
2 F5 O$ g4 ~# p2 [% k( Owarning about the virilizing effect on a male or2 ?, b! Z1 w5 A
female child who might come in contact with some-
: D7 v, @' Z% @0 D6 }one using any of these products.
- A7 d( J+ y5 H1 `6 {1 PReferences
3 c8 P7 ^: W, g. G1. Styne DM. The testes: disorder of sexual differentiation) z) K6 N" w5 C6 S8 c! j
and puberty in the male. In: Sperling MA, ed. Pediatric( v4 o. b2 T: y4 s! e
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; s" _8 g! m7 B* s6 J7 h5 S2002: 565-628.
) O% k, i- U( ?4 Z% l& V2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious7 ]2 [4 S4 J* s1 \, b/ {, b! c
puberty in children with tumours of the suprasellar pineal |
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