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Sexual Precocity in a 16-Month-Old* l/ R6 S' n. P) F
Boy Induced by Indirect Topical7 ~* z0 ~$ m/ L0 r
Exposure to Testosterone! g+ ^7 `3 L1 h; a/ I& w$ G
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 I9 v( B3 E3 H
and Kenneth R. Rettig, MD1- V) r: t) e1 o
Clinical Pediatrics, Y; c7 g3 ~; u+ E
Volume 46 Number 60 r- L. W. k3 k4 I
July 2007 540-543# Q9 j3 u, L! a6 E# _
© 2007 Sage Publications; d( x _9 C) u4 N
10.1177/00099228062966516 u, W! v" Y4 L& l( A* Q+ M2 E
http://clp.sagepub.com
0 q) U. v0 o4 c+ }. [- x. c5 X$ z8 Ahosted at3 G' w+ d- J5 @3 Y. r5 J
http://online.sagepub.com& ^* }# Q3 ?+ I. t# n
Precocious puberty in boys, central or peripheral,, ?" N: U0 P0 o. h8 e! {; ]
is a significant concern for physicians. Central8 n! q% g0 M5 D
precocious puberty (CPP), which is mediated
+ z1 K- O7 J$ T3 w+ Dthrough the hypothalamic pituitary gonadal axis, has
8 G' G) D! v' t# k4 e5 R& A3 a# ]a higher incidence of organic central nervous system, E. [, L- ~: X; u- L0 ?
lesions in boys.1,2 Virilization in boys, as manifested6 K- L& F2 x; d+ s! e; {9 z
by enlargement of the penis, development of pubic$ e3 S/ m: e% T( i- }9 d
hair, and facial acne without enlargement of testi-3 v. E* N7 K% ], b' L2 G: f- O. ^
cles, suggests peripheral or pseudopuberty.1-3 We0 U5 [: H( ~7 h& K( C/ ~+ A
report a 16-month-old boy who presented with the, \+ i1 i" z4 g& L8 L# b! ^. i" H2 z
enlargement of the phallus and pubic hair develop-( q/ U) v# L* _
ment without testicular enlargement, which was due- p% n" I8 {+ z" _6 L
to the unintentional exposure to androgen gel used by$ l* }( T: g2 d5 P2 ]! s8 e
the father. The family initially concealed this infor-
' L$ \+ z" B! k: z5 w. b1 J$ Amation, resulting in an extensive work-up for this
, z) ~) N" ^# t. f n+ D# pchild. Given the widespread and easy availability of/ L7 W+ Q* `/ m
testosterone gel and cream, we believe this is proba-
" w; ^, @! L" T; wbly more common than the rare case report in the1 w8 j, b6 F; r3 [2 O ?6 [
literature.42 I+ [0 H( K. e# R/ H" X. S
Patient Report
2 g7 s$ _4 ?; h7 y. F* uA 16-month-old white child was referred to the
8 c- A+ U: R% E Gendocrine clinic by his pediatrician with the concern
8 q# G; F+ Y" _7 T+ r8 J! W; Eof early sexual development. His mother noticed
# v9 r, {6 H( o' h k7 glight colored pubic hair development when he was
4 t+ ~8 l1 G* N: Z. oFrom the 1Division of Pediatric Endocrinology, 2University of
- I: D9 p/ x a0 |/ Y$ _8 uSouth Alabama Medical Center, Mobile, Alabama.
! I0 \" \" c- ^8 `Address correspondence to: Samar K. Bhowmick, MD, FACE,$ P+ }. x; L" _6 t
Professor of Pediatrics, University of South Alabama, College of
& z8 L/ K; t" e$ IMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ e3 V, z5 ?; T" u; d8 d Y4 me-mail: [email protected].' }0 ~4 i2 |$ ]4 G. u9 x* o. C
about 6 to 7 months old, which progressively became
* t7 w( X$ W! W$ {; ~6 t' X5 Udarker. She was also concerned about the enlarge-
, h9 C9 v& d( @ment of his penis and frequent erections. The child* N1 o1 J. b& w- W
was the product of a full-term normal delivery, with7 z5 R" N& A0 i5 l) r
a birth weight of 7 lb 14 oz, and birth length of
( `- }4 S7 a6 g! }. r20 inches. He was breast-fed throughout the first year
" Q2 l- f r. c5 yof life and was still receiving breast milk along with
/ j1 N' ?2 D0 P, [+ T( [9 G# Xsolid food. He had no hospitalizations or surgery,
) k! D' D9 h9 j9 Oand his psychosocial and psychomotor development
. B. t9 m5 q* h6 n' O/ D! Y# H& wwas age appropriate., O7 @% m2 b% e% Y9 h
The family history was remarkable for the father,
4 {1 K+ S4 K% B6 r% t9 C/ ]who was diagnosed with hypothyroidism at age 16,
H" s( S) ]- p8 D+ H6 I8 T# Z# s. x" cwhich was treated with thyroxine. The father’s
- r9 G1 C: z3 s) @; ]- ?height was 6 feet, and he went through a somewhat
8 H; ~- M' G% t* `: Z6 yearly puberty and had stopped growing by age 14.
" ^2 n6 e1 k" u. P. O7 }9 dThe father denied taking any other medication. The2 ] F2 q* c5 m2 T& Y1 a
child’s mother was in good health. Her menarche
0 F+ o* n) [+ c8 swas at 11 years of age, and her height was at 5 feet
; m% b* c, e* ^$ k% h* x5 inches. There was no other family history of pre-
* J& b: |" s# Ncocious sexual development in the first-degree rela-
) ^7 L$ f3 B Z4 g' F1 Ntives. There were no siblings.
* f% Z6 L' Y# [+ c% K: OPhysical Examination
* d5 {+ Z0 i7 ~& C: yThe physical examination revealed a very active,; i. _3 Y+ \$ s) d0 S
playful, and healthy boy. The vital signs documented; j" ^) ^6 t0 p, u$ L6 p' m
a blood pressure of 85/50 mm Hg, his length was' X# g1 a; p4 j& T D* ~ i- X
90 cm (>97th percentile), and his weight was 14.4 kg
8 E- j4 Z% F- P7 N& n(also >97th percentile). The observed yearly growth: u0 H4 h% W8 Q/ w0 x
velocity was 30 cm (12 inches). The examination of
" k+ d( n4 Y7 J* D5 kthe neck revealed no thyroid enlargement.
& n0 N& [# `" V* q/ V0 _The genitourinary examination was remarkable for% g" J( L8 T5 }, ]" H
enlargement of the penis, with a stretched length of3 B! H" c1 }7 C7 J
8 cm and a width of 2 cm. The glans penis was very well) O! E0 ]0 E3 X) I. p2 Z7 d' x2 M& _
developed. The pubic hair was Tanner II, mostly around( X: `- c& j7 x @7 j5 N0 I
5402 t2 ?0 K6 X: N6 _
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" i# G0 @3 { Y4 z* ^0 q0 n! M
the base of the phallus and was dark and curled. The. S! \: w1 y% ~) I# v; c1 H P! |
testicular volume was prepubertal at 2 mL each.
% U, v& V' V3 dThe skin was moist and smooth and somewhat/ e( q A7 m0 b% W/ w3 l) T3 z
oily. No axillary hair was noted. There were no. L' \8 m8 o1 |, _. \
abnormal skin pigmentations or café-au-lait spots.# x0 `# ?5 |* {9 E8 b
Neurologic evaluation showed deep tendon reflex 2+
0 O! f7 e- G9 [" s% Xbilateral and symmetrical. There was no suggestion
8 U. O0 g& W7 k0 T8 Jof papilledema.: h2 k* x- u0 l8 s
Laboratory Evaluation3 B/ h, d0 K( ~; @- _9 H1 J' S/ O
The bone age was consistent with 28 months by2 j1 J1 r }' z
using the standard of Greulich and Pyle at a chrono-9 I7 j( n! m+ T+ H3 p4 E* ?5 c8 n
logic age of 16 months (advanced).5 Chromosomal3 y4 O F* b; u+ L E
karyotype was 46XY. The thyroid function test
! h0 I" ^3 f, X* L S# m/ P. y' B; bshowed a free T4 of 1.69 ng/dL, and thyroid stimu-" Q* `8 L$ g* l# P
lating hormone level was 1.3 µIU/mL (both normal)./ N# ~: l7 ]% y2 J: {8 @ d& P6 g
The concentrations of serum electrolytes, blood0 k% @* {) U) ~5 b# b3 ~4 ?
urea nitrogen, creatinine, and calcium all were+ W& N7 w2 B. n
within normal range for his age. The concentration" [$ Y9 v1 q" J2 G3 W4 a$ d1 D. E
of serum 17-hydroxyprogesterone was 16 ng/dL
" p' y! d% v# m# U4 L(normal, 3 to 90 ng/dL), androstenedione was 20& B0 \: E/ k( C1 M' `
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ d4 |/ T- c2 H6 i3 {
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 d$ h$ f! ?* U" b) M) vdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 V# f7 Z) K( c49ng/dL), 11-desoxycortisol (specific compound S)* s0 l; k5 T8 h r% R6 G; w
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& r; d; F7 t) _" ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total b) S5 F( L! G0 N1 H
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
- {/ C# h, o# Y/ [3 n$ m3 zand β-human chorionic gonadotropin was less than
5 |: ~) s0 d+ _5 mIU/mL (normal <5 mIU/mL). Serum follicular9 x6 K/ C; g p$ s4 Z6 u% ~
stimulating hormone and leuteinizing hormone
) D5 e$ T1 M5 }% }% B0 U- Lconcentrations were less than 0.05 mIU/mL3 |3 |: `' y0 j& N A
(prepubertal).
; n/ A6 ~ x3 ]" T, h. ]( FThe parents were notified about the laboratory( w$ w& i* L# Z' _: W- w
results and were informed that all of the tests were- k" J4 A, A6 S$ K% Z
normal except the testosterone level was high. The
( [" i8 A. p: S% Mfollow-up visit was arranged within a few weeks to8 Y& n" E/ G% X( h6 N( T
obtain testicular and abdominal sonograms; how-
+ v, {. {: t9 T/ f5 E+ C: G, w0 gever, the family did not return for 4 months.6 S' ^1 H6 B L7 G7 \
Physical examination at this time revealed that the
& G' T4 a& O/ Q+ S# M+ Zchild had grown 2.5 cm in 4 months and had gained
* r* A7 Q0 [0 F0 X+ \5 s8 [2 kg of weight. Physical examination remained
) y( Y, b6 Q7 l* munchanged. Surprisingly, the pubic hair almost com-
- w7 y# W/ k0 z6 V9 n' |& epletely disappeared except for a few vellous hairs at
, ^$ |& u9 t2 ~6 t2 G9 othe base of the phallus. Testicular volume was still 2
. j( r% _$ ^8 vmL, and the size of the penis remained unchanged.+ N" y$ \. B: G& n: ]6 z. l5 v
The mother also said that the boy was no longer hav-
: F- s6 W0 @9 v6 O. ~0 Ling frequent erections.# s9 z3 l9 C1 e/ S& X8 O
Both parents were again questioned about use of+ P! [" T- o: G
any ointment/creams that they may have applied to
" d" T$ {& c; vthe child’s skin. This time the father admitted the
4 [& y# p; c d+ h1 MTopical Testosterone Exposure / Bhowmick et al 541' u' B) e/ Q" l. k) C
use of testosterone gel twice daily that he was apply-5 F% j( Q8 q/ w" H
ing over his own shoulders, chest, and back area for
& o& v$ A+ p6 O/ ea year. The father also revealed he was embarrassed
\" J! [0 r- H1 ?3 w& Vto disclose that he was using a testosterone gel pre-
* o* ?" s. v+ Xscribed by his family physician for decreased libido
- p* w! M" _- m5 U5 d4 rsecondary to depression.( G2 F- \2 K1 L
The child slept in the same bed with parents.
, g* @7 U5 [. d" f+ E4 [- ?: tThe father would hug the baby and hold him on his
' {; a8 V* p* a. K- F* ]: E+ A h' Xchest for a considerable period of time, causing sig-
2 `6 q* p, x8 P6 K8 I3 }nificant bare skin contact between baby and father.
0 y$ E+ p2 n$ z' D% D7 TThe father also admitted that after the phone call,( X& T$ X- u: ~: }2 b6 d H
when he learned the testosterone level in the baby
8 f/ [/ l, q4 E2 z0 ~2 z- V1 ?9 xwas high, he then read the product information
0 M _% p9 m% dpacket and concluded that it was most likely the rea-6 g" D( v9 x( M# L
son for the child’s virilization. At that time, they
. t1 _" @1 L& |& I& N" H# E) mdecided to put the baby in a separate bed, and the b4 f( O8 y) W- g4 M5 @: p; P" V
father was not hugging him with bare skin and had- t8 `" L3 ?, r2 @' n
been using protective clothing. A repeat testosterone
: g2 S' N1 Q8 | B: qtest was ordered, but the family did not go to the; l/ a6 d4 z* x
laboratory to obtain the test.
& h* _$ k) P% _4 t4 G7 sDiscussion
: p2 Z( T" N9 sPrecocious puberty in boys is defined as secondary W$ n' w* R2 t8 t$ f G
sexual development before 9 years of age.1,4
% h4 [" t3 V/ d2 l: qPrecocious puberty is termed as central (true) when
% g9 u7 g2 L# g. D8 I9 |it is caused by the premature activation of hypo-3 `% Z9 e# o# I V! P
thalamic pituitary gonadal axis. CPP is more com-+ ]" W4 d3 P9 z
mon in girls than in boys.1,3 Most boys with CPP1 Y+ F5 Z* z, P# t% ]0 T, L
may have a central nervous system lesion that is
% ^/ Z; _2 v2 n, u4 D6 p2 Zresponsible for the early activation of the hypothal-- N# z7 A! r# t U9 q, ^7 c) g
amic pituitary gonadal axis.1-3 Thus, greater empha-2 T, I; q* R: S8 m2 ~( ?: l4 E
sis has been given to neuroradiologic imaging in
8 n/ K$ C+ K& Tboys with precocious puberty. In addition to viril-
( C6 V8 U l+ l- mization, the clinical hallmark of CPP is the symmet-
7 m$ [; i$ t9 \5 Mrical testicular growth secondary to stimulation by5 z* H' T* d6 h( ]5 R9 e- G
gonadotropins.1,3
7 q, }; I7 K! k3 [6 x. \( GGonadotropin-independent peripheral preco-
; }) |1 E, e9 Q/ q" W5 h6 W! Bcious puberty in boys also results from inappropriate
5 {. U* g7 S* p( e+ C( Sandrogenic stimulation from either endogenous or
* \. i. N3 x# b, bexogenous sources, nonpituitary gonadotropin stim-" G: K g6 W2 ]; X* A3 Z5 A% e: p+ S) ~
ulation, and rare activating mutations.3 Virilizing. z" u1 ]+ h4 Q' j+ G# [+ p
congenital adrenal hyperplasia producing excessive$ M6 l$ p/ l2 x* y$ q
adrenal androgens is a common cause of precocious
, }+ t! X# n: @" {% ^& |puberty in boys.3,4& V2 P) S9 f$ a# M
The most common form of congenital adrenal
0 W5 \# w0 I' S* Zhyperplasia is the 21-hydroxylase enzyme deficiency.
$ @( w2 u+ E3 K" I- M0 X6 k1 y1 MThe 11-β hydroxylase deficiency may also result in
2 t. J- _& j9 Z$ Oexcessive adrenal androgen production, and rarely,
+ a \0 v9 Z: n K% O$ oan adrenal tumor may also cause adrenal androgen
0 ^8 Y( |1 F( s; {, }) q/ L$ Lexcess.1,3
/ E8 }6 w, I; g" O0 c/ Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! N8 ]# T6 d" {8 P542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' x8 n) a/ _6 l& `9 TA unique entity of male-limited gonadotropin-! L2 }6 x9 o E. j+ x
independent precocious puberty, which is also known
8 i4 T7 h& {7 _& X4 H8 Yas testotoxicosis, may cause precocious puberty at a
6 `' R+ y# q/ F1 J+ [very young age. The physical findings in these boys' J( L+ B$ p% U- s/ H* v5 Y1 j" W0 w
with this disorder are full pubertal development," ?6 z% a( C& p- ^8 F, Q
including bilateral testicular growth, similar to boys M" p( v0 ]3 s7 V! T4 R! m7 i: M% O
with CPP. The gonadotropin levels in this disorder
% Q* H. F& B8 P* r0 @are suppressed to prepubertal levels and do not show
8 t9 n- @# B7 M& K% ^- n6 I8 _3 Z: |pubertal response of gonadotropin after gonadotropin-
6 Y" T8 b B2 C- f. U/ Q. w& T2 t& Areleasing hormone stimulation. This is a sex-linked5 v2 s7 }/ ~* x h! V
autosomal dominant disorder that affects only3 C0 Z7 x A, b- D% B8 L j* w6 C) ?
males; therefore, other male members of the family0 l3 i& B3 N a/ u7 p' W# C' T2 K3 [
may have similar precocious puberty.39 x5 D# R* M4 k+ d, [/ \7 g$ @5 @6 k
In our patient, physical examination was incon-
! T" }) ?' }% I/ }6 g) b% s; G; _6 Hsistent with true precocious puberty since his testi-
; E) K2 c' X! A8 O5 ucles were prepubertal in size. However, testotoxicosis5 C- U. N+ o; t! G! l# j0 n8 N
was in the differential diagnosis because his father
9 |. J O" J7 p8 cstarted puberty somewhat early, and occasionally,
' D2 p7 D) X; F: l* m4 B0 ?' ?" etesticular enlargement is not that evident in the
- ]! i; ?8 m6 k3 c5 ybeginning of this process.1 In the absence of a neg-
- E) C* j# Y: F/ o3 f7 Wative initial history of androgen exposure, our
- l+ s/ l6 v3 J! e$ qbiggest concern was virilizing adrenal hyperplasia,
% w1 { U1 }1 D5 f+ I: I/ \either 21-hydroxylase deficiency or 11-β hydroxylase
+ W, t! ~ f; Z0 Ddeficiency. Those diagnoses were excluded by find-
- Q! ]) P4 ^* `( u* y, v4 k9 Ving the normal level of adrenal steroids.% m$ j1 p9 v# D0 N
The diagnosis of exogenous androgens was strongly
3 W& f& f. v6 k! G" ?- z: xsuspected in a follow-up visit after 4 months because6 V6 | b E- {/ U! W' D
the physical examination revealed the complete disap-
7 Q9 F# l! u; H* x" q- Zpearance of pubic hair, normal growth velocity, and* {# C$ q7 Q& I$ _6 X& i7 m. Z
decreased erections. The father admitted using a testos-' U1 `% r# z, `3 u1 V
terone gel, which he concealed at first visit. He was
. V# ]# Y' [/ S/ k9 T% `* dusing it rather frequently, twice a day. The Physicians’$ m3 f+ k. i8 B( C9 C! z" e( T
Desk Reference, or package insert of this product, gel or
) W7 x: N9 f( t1 j! \1 s' Ecream, cautions about dermal testosterone transfer to' Y. C5 h+ q0 g$ a0 [
unprotected females through direct skin exposure.
7 a# o+ ?8 h6 |$ x ]+ CSerum testosterone level was found to be 2 times the
% G; V) {; s3 G2 C- H0 ]+ |baseline value in those females who were exposed to, ?0 E% i. Q' c
even 15 minutes of direct skin contact with their male
$ P" t* \( W6 p+ t, t) F. Mpartners.6 However, when a shirt covered the applica-
6 n, w* u6 w# p& xtion site, this testosterone transfer was prevented.
4 [, k9 `9 h9 cOur patient’s testosterone level was 60 ng/mL,$ B9 c( K, b& W! H
which was clearly high. Some studies suggest that
$ W/ s2 B) R* C6 Fdermal conversion of testosterone to dihydrotestos-
' e/ i& L8 m. [! cterone, which is a more potent metabolite, is more. \3 u3 z$ r4 Z( i3 ^& S
active in young children exposed to testosterone% ~5 b8 H8 i# z* ]" K
exogenously7; however, we did not measure a dihy-& G) ?. J; D' O1 |1 U
drotestosterone level in our patient. In addition to
2 ^0 X$ Z+ x* m+ a- F. Ovirilization, exposure to exogenous testosterone in
* p6 F2 t+ j! N8 ~- Vchildren results in an increase in growth velocity and% i6 h n# W o& |/ ?
advanced bone age, as seen in our patient.. w6 L) ^: X: v9 s: ]
The long-term effect of androgen exposure during4 R( T- i5 r1 p
early childhood on pubertal development and final
9 d. ?+ A8 ]' L/ w0 X5 K8 h1 W! Vadult height are not fully known and always remain. F9 C* s; r) i2 n& D
a concern. Children treated with short-term testos-
6 ^; U6 `; W& Z. P8 ~& dterone injection or topical androgen may exhibit some* C: J" C: z8 g9 _* m
acceleration of the skeletal maturation; however, after
/ Z! `9 H! {, I+ [8 W3 rcessation of treatment, the rate of bone maturation$ y$ E& w1 u, H& m3 Y- Y0 _1 `
decelerates and gradually returns to normal.8,9. ?7 W/ ^/ F% E; j" j* j4 s2 A4 M; c
There are conflicting reports and controversy
% {. p: ?* c8 \: K8 yover the effect of early androgen exposure on adult. | V# h7 z. P( l' n6 r/ I2 W2 H
penile length.10,11 Some reports suggest subnormal# p+ R& a' N0 L: z6 C- C
adult penile length, apparently because of downreg-
' h" m0 g# {* U0 L* [+ R# Gulation of androgen receptor number.10,12 However,5 `) A0 Z2 A3 i" k g% ?% d" V
Sutherland et al13 did not find a correlation between
* C/ W3 S% {5 |' `; f+ }$ ]childhood testosterone exposure and reduced adult
; ?) Y& V) ?" V& epenile length in clinical studies.
m5 r* n3 ], [0 r3 N6 _. W% [9 qNonetheless, we do not believe our patient is
5 ~6 n7 a/ r( ]' o. Ggoing to experience any of the untoward effects from: e4 p& j. l4 q% z. @; P6 C( T
testosterone exposure as mentioned earlier because
4 G2 [( r g a8 @& }the exposure was not for a prolonged period of time.% r' i6 |! }! `' v6 I2 Y
Although the bone age was advanced at the time of
: m/ \; g5 i. D( w$ B* ldiagnosis, the child had a normal growth velocity at' F/ ^* K$ P* j7 W: @" ^. k$ z
the follow-up visit. It is hoped that his final adult% @0 C7 {6 N: W- t" S
height will not be affected.
# B- v6 ]' D6 {, \3 B) ~Although rarely reported, the widespread avail-/ h7 \" a+ ] m \
ability of androgen products in our society may! t8 {+ U; T$ y. M
indeed cause more virilization in male or female
4 C8 G( K" L- ~0 t( Tchildren than one would realize. Exposure to andro-
( K! l! e3 b! Y9 Agen products must be considered and specific ques-" ]# a# V/ Y8 h+ \, G* ]4 F* N# |1 c
tioning about the use of a testosterone product or+ ` @$ E9 q( a3 R& V' c
gel should be asked of the family members during3 |2 I) V0 l5 a8 C' n
the evaluation of any children who present with vir-
- i# }, Q8 e B: L7 \1 Nilization or peripheral precocious puberty. The diag-0 M) R! a6 x6 G
nosis can be established by just a few tests and by$ G5 O) E6 Q8 `8 W% o
appropriate history. The inability to obtain such a
* E0 H8 N* E5 Lhistory, or failure to ask the specific questions, may
( x# X O) O7 v w' N' ?( ?) Zresult in extensive, unnecessary, and expensive
3 U$ C, ]' U$ e2 Qinvestigation. The primary care physician should be
) c8 W) O' w2 }. V6 t/ vaware of this fact, because most of these children- h% N: U) s' g {9 C
may initially present in their practice. The Physicians’' r8 T- I9 A8 ^3 }) U/ C
Desk Reference and package insert should also put a7 ?8 G; }5 N, C; x6 a
warning about the virilizing effect on a male or
$ E) N, }8 [! f3 i' Lfemale child who might come in contact with some-
* K$ M% q B0 f# G$ H8 @4 }one using any of these products. _1 ~ h u: Z# w2 U8 m
References
( W ?6 u/ W: h6 K1. Styne DM. The testes: disorder of sexual differentiation2 q M) h& J+ X% k, J7 c
and puberty in the male. In: Sperling MA, ed. Pediatric
" K) @3 c# k4 h- [3 yEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;# j }% w* O0 }5 z* R
2002: 565-628.7 P9 K+ v/ t2 c. T1 ^% H& s
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 s# g' @- }1 X4 V5 G
puberty in children with tumours of the suprasellar pineal |
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