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Sexual Precocity in a 16-Month-Old- ?( G- e& `( d @4 J9 t$ w
Boy Induced by Indirect Topical
. \4 X* z4 e3 s ?8 g0 ?. zExposure to Testosterone
6 X% D9 ~: \; C' O( _/ o+ l5 o6 c: USamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. c) D' X1 {) @8 W. A
and Kenneth R. Rettig, MD1 O& l- z; N/ m! p9 G+ E7 x
Clinical Pediatrics
- E3 M$ D- q$ U% _- X# x3 BVolume 46 Number 69 y* r% G8 a' T! Z' r! ^& f
July 2007 540-543+ z# ?. y M5 Q5 ^2 i& I
© 2007 Sage Publications
3 y/ @( x7 h! z, { A3 ?10.1177/0009922806296651
( e ` |# ]& F# X% E& vhttp://clp.sagepub.com! R1 {$ I; b/ ~. L
hosted at
3 g/ b8 O4 D" w, b" I. o0 G; [http://online.sagepub.com
% |( m/ M+ o1 v/ l7 @9 PPrecocious puberty in boys, central or peripheral,- X& d! n% R7 J7 b: |: s( P( Q
is a significant concern for physicians. Central( o* v) K r$ |) f P$ d, L
precocious puberty (CPP), which is mediated6 |: {3 P& t0 w: Y
through the hypothalamic pituitary gonadal axis, has
& I' p) Z. R$ i+ Q3 p1 ~a higher incidence of organic central nervous system
- O! ~; P, u, B) F4 \0 r2 L' Slesions in boys.1,2 Virilization in boys, as manifested
0 S: S3 o s+ t' j) ^$ oby enlargement of the penis, development of pubic
8 K: V x1 h' R1 Q2 l& yhair, and facial acne without enlargement of testi-$ G; G' W- N4 T8 a/ q8 M
cles, suggests peripheral or pseudopuberty.1-3 We3 |' a- G1 b2 `, Z2 _
report a 16-month-old boy who presented with the& o; v" y$ R' Y T
enlargement of the phallus and pubic hair develop-
6 c% L! y$ h8 G" ?! J9 Fment without testicular enlargement, which was due
/ q5 {( o9 x7 T5 pto the unintentional exposure to androgen gel used by/ F: ^: h; [3 w, A1 Y1 n$ A: U/ }
the father. The family initially concealed this infor-
7 V$ t' X+ w3 l- F0 J7 J1 smation, resulting in an extensive work-up for this
) T9 }$ R: F$ B" W' P8 ochild. Given the widespread and easy availability of& P) t) P* ^! x
testosterone gel and cream, we believe this is proba-
; @+ @6 u8 A# R3 n( c1 Z8 [bly more common than the rare case report in the
& V* ?8 P- Y, S4 ]2 dliterature.46 D0 J' @& a9 Z6 ^9 J
Patient Report
5 G- g% ]. b' o6 R1 rA 16-month-old white child was referred to the! _# l) j1 O+ X6 U
endocrine clinic by his pediatrician with the concern7 P# v0 l/ m7 u' T3 Y9 H
of early sexual development. His mother noticed
% _9 g; }& N' ] U! g& f4 j: Glight colored pubic hair development when he was" N6 Q" F- i/ _% d. \
From the 1Division of Pediatric Endocrinology, 2University of
( ~! b" E6 K4 F; v# \South Alabama Medical Center, Mobile, Alabama.' W- L: M9 W0 g! _7 ~2 i& E
Address correspondence to: Samar K. Bhowmick, MD, FACE,
% I: U4 M. S9 j! B- EProfessor of Pediatrics, University of South Alabama, College of
+ Z2 p: s* l+ @; JMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297; Q0 N$ q s& v! Y
e-mail: [email protected].) I7 D+ e- L0 U2 r5 z, h0 l
about 6 to 7 months old, which progressively became
$ s; ?- R" r3 D; Wdarker. She was also concerned about the enlarge-3 g4 z% i0 ^: B$ r" [
ment of his penis and frequent erections. The child
; @. J* ?1 L [/ L3 ]1 |was the product of a full-term normal delivery, with
5 j: d) Q& R1 X. Ea birth weight of 7 lb 14 oz, and birth length of
: g& u7 S. {* @) O20 inches. He was breast-fed throughout the first year
: U& b/ {: r* I# J0 G- |: Z, aof life and was still receiving breast milk along with
, I2 ~9 \) N% t0 f/ O) M+ esolid food. He had no hospitalizations or surgery,1 ]9 R: m/ A/ R0 C$ o, t
and his psychosocial and psychomotor development
7 a0 j5 F/ M, m3 ~- g8 F; dwas age appropriate., \) j: b5 x1 \' o) {7 I( T: [
The family history was remarkable for the father,
9 Y6 S! T& z! S6 Fwho was diagnosed with hypothyroidism at age 16,
; |4 t. A) V4 O0 I, N% @which was treated with thyroxine. The father’s2 q7 u! m+ H- b; E% N& [0 f7 \% |
height was 6 feet, and he went through a somewhat K1 h' C& F0 p1 c
early puberty and had stopped growing by age 14.
2 E5 N& K% D% h! XThe father denied taking any other medication. The3 V5 V1 Q% H: V0 `7 _8 e$ @+ k: Y1 g$ `3 P
child’s mother was in good health. Her menarche3 U& S0 o! e0 ]) w
was at 11 years of age, and her height was at 5 feet3 b8 }3 M3 q2 f- f$ k5 ~+ a4 J
5 inches. There was no other family history of pre-9 z7 l' h0 e. c! H
cocious sexual development in the first-degree rela-5 Q2 R" q% D7 h: `6 F; t
tives. There were no siblings. Z7 x) T% B* x8 X4 K
Physical Examination
2 ^' G( R: }! u1 H) ~5 h4 O. EThe physical examination revealed a very active,
1 h: b% T- Z* U% {, ~/ Q' fplayful, and healthy boy. The vital signs documented
7 _1 J- A/ J4 a2 A2 }% Ba blood pressure of 85/50 mm Hg, his length was" R |/ T- A5 V0 w }
90 cm (>97th percentile), and his weight was 14.4 kg
. p/ G% Z5 w% g* p& ](also >97th percentile). The observed yearly growth
# N2 n' Q) h$ e3 a' ?, r# ~8 W+ \velocity was 30 cm (12 inches). The examination of
& J7 m% m9 I0 m/ G. dthe neck revealed no thyroid enlargement.% I; e" Y. i1 W. @& [
The genitourinary examination was remarkable for: T: P9 t g0 b& w& A3 j, M5 X# ^
enlargement of the penis, with a stretched length of
6 m+ a6 {* W1 m8 ?: {$ \$ [8 cm and a width of 2 cm. The glans penis was very well
" H) |; ~( t( W" b$ g# {* bdeveloped. The pubic hair was Tanner II, mostly around4 A4 v. h" ]+ ~8 H7 ^* c3 H
540/ |" W& _' O% {- A% J
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- q# F0 s5 T: L% t
the base of the phallus and was dark and curled. The
$ o9 p" C0 J# f; qtesticular volume was prepubertal at 2 mL each.
. F/ b# A/ q) _+ B4 m3 ^( Y8 VThe skin was moist and smooth and somewhat
* m6 v9 x' g; b* Boily. No axillary hair was noted. There were no) O, B1 |+ @8 F- R" S3 \
abnormal skin pigmentations or café-au-lait spots.9 l7 g: |( ^1 d' I/ Q* ~7 ~
Neurologic evaluation showed deep tendon reflex 2+
2 c+ h7 V9 i7 T c0 R* @# P; qbilateral and symmetrical. There was no suggestion5 L P# y# Z' Q* ~/ H) e% _
of papilledema.
1 E. W) q" i. g( QLaboratory Evaluation, f- t' p4 T- z: _$ z
The bone age was consistent with 28 months by3 @$ o! [. v/ Z: L6 T+ K4 ?$ S
using the standard of Greulich and Pyle at a chrono-( L5 M0 ?# Z+ f8 ^0 g( v- t! R; w
logic age of 16 months (advanced).5 Chromosomal/ A! t. K1 k9 C. b& r
karyotype was 46XY. The thyroid function test
! [& W P5 T# G! y: g/ ?) wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-' e! p2 H ~1 s% p
lating hormone level was 1.3 µIU/mL (both normal).
( m( `' j( V# m& W1 \The concentrations of serum electrolytes, blood2 b& _& w) M: {( f/ m$ \$ ~/ h
urea nitrogen, creatinine, and calcium all were
0 e0 @+ h! O: `4 ?9 swithin normal range for his age. The concentration
; z2 E) Q& _- c0 U) k# h- ^3 h! h# Yof serum 17-hydroxyprogesterone was 16 ng/dL. w, R( j6 S! X' ~# X
(normal, 3 to 90 ng/dL), androstenedione was 20
5 {; j5 a2 a) X/ i9 z8 I8 V' [+ lng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 H% z# F ^( G5 p+ rterone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 z5 F! ?6 D! `; ]! ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to6 C( X+ b' I1 [
49ng/dL), 11-desoxycortisol (specific compound S)9 |5 X* I( b9 u0 ^) s) g
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 X2 g0 v8 c( O; v `) Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 p- D0 @, y- B: E" a% ]2 A T" Vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 k% [# Z5 w5 i
and β-human chorionic gonadotropin was less than
% S: Q: X+ {4 L& u- H5 z5 mIU/mL (normal <5 mIU/mL). Serum follicular
" D& R' e8 M I$ U. B: Ystimulating hormone and leuteinizing hormone$ e) X. R( B- d
concentrations were less than 0.05 mIU/mL4 }4 |' @, b. G& A; P1 r x0 f
(prepubertal).( c9 e, S9 N& M7 X1 T! r
The parents were notified about the laboratory
% v; Z" `, C! D8 Yresults and were informed that all of the tests were
1 \- S: Q! S( _8 Q4 K' wnormal except the testosterone level was high. The
5 T3 }8 B" n8 ~) a' p' {' p/ ]follow-up visit was arranged within a few weeks to9 g% ]8 T* O3 x: G& c Q# o0 H
obtain testicular and abdominal sonograms; how-
3 r/ L `( L6 U0 Y( X4 o; S& o( wever, the family did not return for 4 months.
' }# ^5 r6 H7 q9 c& `# ^, _7 QPhysical examination at this time revealed that the
% M3 `! ~& N/ s) `# v- A* _child had grown 2.5 cm in 4 months and had gained2 z; g' X$ k. M) ^, j R
2 kg of weight. Physical examination remained
6 I0 H5 U- M$ r6 w. \0 junchanged. Surprisingly, the pubic hair almost com-
! V6 V- r2 l& [6 A8 b u( zpletely disappeared except for a few vellous hairs at
+ g) w/ \4 g3 Ethe base of the phallus. Testicular volume was still 27 t' S: I, B7 u: I( D6 U5 V
mL, and the size of the penis remained unchanged.
" [3 x% j& N2 x) g1 O0 Q# UThe mother also said that the boy was no longer hav-. Y6 D& `8 j7 A7 U' Z- K0 P
ing frequent erections.
& z4 Z, Z: Z7 h% pBoth parents were again questioned about use of
( |# Z8 s4 e) U3 @9 P! Lany ointment/creams that they may have applied to% V, o+ |' ]8 H/ Q, J V! @
the child’s skin. This time the father admitted the
( x) g$ P. s) RTopical Testosterone Exposure / Bhowmick et al 541
$ h7 v% B3 j" ?2 Fuse of testosterone gel twice daily that he was apply-+ Z0 A9 B3 w1 K7 b8 f
ing over his own shoulders, chest, and back area for
9 d5 g2 [5 u# J3 _; Y n" i5 m: Oa year. The father also revealed he was embarrassed0 Z% z6 r7 N0 w& @( Z v
to disclose that he was using a testosterone gel pre-
# I$ s+ B/ B7 s ~/ P$ gscribed by his family physician for decreased libido+ M! N0 G) w- q' y
secondary to depression.
' ?4 S4 \) G: qThe child slept in the same bed with parents.
* q `5 _1 {" n; {The father would hug the baby and hold him on his
" B$ |$ h9 W$ `, [4 f3 ichest for a considerable period of time, causing sig-- t5 p0 Y( Q, r8 g
nificant bare skin contact between baby and father.
, z+ x5 i' V# I* NThe father also admitted that after the phone call,
- w' ]- \" `. Wwhen he learned the testosterone level in the baby' @" B: W- ^) r
was high, he then read the product information5 S3 y5 G6 ?! V6 L, x8 E O1 g4 O
packet and concluded that it was most likely the rea-, t" m' ^+ @4 {
son for the child’s virilization. At that time, they
+ c$ Q2 w/ I; A% f8 f% V7 N9 Xdecided to put the baby in a separate bed, and the
5 [1 i( j& N( kfather was not hugging him with bare skin and had0 ]" n& e+ ~; L$ }) v+ ^
been using protective clothing. A repeat testosterone
+ z4 n1 w. J1 J, v3 @ v, h$ Q' Z7 Gtest was ordered, but the family did not go to the |6 O3 i. F" Y* r5 y# F& ^
laboratory to obtain the test.
$ Z; P8 ]' J- _3 d- EDiscussion6 y0 h. B: @+ F) x4 R# c
Precocious puberty in boys is defined as secondary, m' k/ S; k3 L2 V+ X7 {
sexual development before 9 years of age.1,4
; b; Z" J( ?$ A2 YPrecocious puberty is termed as central (true) when
5 l5 k0 S9 i% M6 P" Git is caused by the premature activation of hypo-: }3 M! {4 v& Z* M3 r' i& ~, g6 V
thalamic pituitary gonadal axis. CPP is more com-+ b( J J7 d0 W3 a' J) f2 s
mon in girls than in boys.1,3 Most boys with CPP3 Y' S$ _( c- y+ {' E+ H
may have a central nervous system lesion that is
X0 A0 d) N/ x- o2 Eresponsible for the early activation of the hypothal-! T# o4 d( \8 C: e- B: _2 n" w3 M
amic pituitary gonadal axis.1-3 Thus, greater empha-
: [' l9 h1 z3 N! u& u4 \sis has been given to neuroradiologic imaging in
7 ~. W: B" G7 y% O. a$ y1 X7 ~" lboys with precocious puberty. In addition to viril-; ^5 }( Q4 f: K! P: f
ization, the clinical hallmark of CPP is the symmet-
3 R2 [, L3 c4 t; ^9 b* i, v2 I: }rical testicular growth secondary to stimulation by) f' g4 Q1 R/ B( F
gonadotropins.1,3
! ~9 W" X& D1 V% BGonadotropin-independent peripheral preco-1 i! v% P* Z p0 n+ F7 z
cious puberty in boys also results from inappropriate
: u0 ~* B# y! V/ J& v, T% |9 }androgenic stimulation from either endogenous or
% p1 C1 A) x# r% _+ G8 z# [- _exogenous sources, nonpituitary gonadotropin stim-5 Y: k4 N7 j2 D; y1 d8 k
ulation, and rare activating mutations.3 Virilizing
5 h y. o" _# B3 E/ ccongenital adrenal hyperplasia producing excessive0 j, s8 I" d" N& o
adrenal androgens is a common cause of precocious/ Y; j% C( I9 N% j8 {
puberty in boys.3,4+ L" ^$ s- d: i' ^' T
The most common form of congenital adrenal9 y! r q5 {( |2 S }
hyperplasia is the 21-hydroxylase enzyme deficiency.
- z+ K$ y! f' K* H0 {0 I, xThe 11-β hydroxylase deficiency may also result in1 Q, Q/ m: q k4 N" i( t \. i' u
excessive adrenal androgen production, and rarely,8 p& a9 k, J9 c: _( |9 F" ]
an adrenal tumor may also cause adrenal androgen
# W8 d8 c0 x) u4 |# {; Mexcess.1,3' a5 q; A0 Y( h* ` r# ?
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ u+ N5 c& K, N# [$ ~ g* s% Q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
}4 s" P/ g% j" i! y# G+ WA unique entity of male-limited gonadotropin-( q$ t0 L" j/ C! I+ d/ v8 p
independent precocious puberty, which is also known) }( |( S v! B1 t
as testotoxicosis, may cause precocious puberty at a
R4 O* Q, |( Y- Dvery young age. The physical findings in these boys
4 ~2 N/ b& ^! W: z/ ]with this disorder are full pubertal development,
: w& c2 b" ? ~5 jincluding bilateral testicular growth, similar to boys
0 I$ v ?: L* p1 hwith CPP. The gonadotropin levels in this disorder
6 w9 M/ i5 t" `5 I& X" `/ mare suppressed to prepubertal levels and do not show
3 q* S# G. ?2 R+ Z% L" f! E& Mpubertal response of gonadotropin after gonadotropin-- w }( n- h, a& [
releasing hormone stimulation. This is a sex-linked- ?2 y" g# @+ M% J+ m
autosomal dominant disorder that affects only: P* [- D) n9 a7 R! b* E
males; therefore, other male members of the family, E ]" ~5 a$ [ ?
may have similar precocious puberty.3
" M: {1 g9 _/ O) g+ L1 ?In our patient, physical examination was incon-
; E( W" i0 j; E8 z, k, v- K( vsistent with true precocious puberty since his testi-
+ N I3 P1 I. i( }: _8 scles were prepubertal in size. However, testotoxicosis
5 e, ^, k4 C8 K, M4 u! bwas in the differential diagnosis because his father" Y8 V7 Q2 s* n w
started puberty somewhat early, and occasionally,0 x7 N7 m: J' @+ \
testicular enlargement is not that evident in the% Y- b$ u+ K) l) t
beginning of this process.1 In the absence of a neg-
' h( H7 R/ x4 e, e' w. b/ d/ j1 t, Eative initial history of androgen exposure, our
5 v- q9 w3 V3 i+ m0 Ibiggest concern was virilizing adrenal hyperplasia,
) T$ x5 v* g/ u# u0 ^ x" Reither 21-hydroxylase deficiency or 11-β hydroxylase
8 ^) K0 i% p1 N* T0 sdeficiency. Those diagnoses were excluded by find-
* w: u% H# V$ S$ |$ K0 J+ d$ D4 Ning the normal level of adrenal steroids.6 N) `1 U9 a8 ~' V, |
The diagnosis of exogenous androgens was strongly. [+ z) N# U, U& d9 `8 G
suspected in a follow-up visit after 4 months because( [5 P- w1 C3 m) D/ E
the physical examination revealed the complete disap-
( `' Z3 q" {. G4 @2 @, Ppearance of pubic hair, normal growth velocity, and% o7 o1 {7 c6 t) n5 S
decreased erections. The father admitted using a testos-) w+ V9 l( e* |
terone gel, which he concealed at first visit. He was
! Z; N. B* [ x" E1 rusing it rather frequently, twice a day. The Physicians’
) |+ q% K7 A( X( V4 E' R; d" xDesk Reference, or package insert of this product, gel or
, Q6 j2 v# @8 Q2 v4 Rcream, cautions about dermal testosterone transfer to
/ o4 F1 B) O! I4 U2 ounprotected females through direct skin exposure.
: J6 v! J1 @/ d4 o- P. fSerum testosterone level was found to be 2 times the
l. v8 N5 j- k& }& abaseline value in those females who were exposed to C; d5 f& X+ e$ p3 s9 l7 W5 \8 {: J
even 15 minutes of direct skin contact with their male
3 x( {3 M+ B/ [ n' v3 I) J9 e! j, Xpartners.6 However, when a shirt covered the applica-! W/ e) F1 Z# ?; l
tion site, this testosterone transfer was prevented.: J2 Q) N: p7 z' m
Our patient’s testosterone level was 60 ng/mL,
' V, p' J, S7 }; x' Iwhich was clearly high. Some studies suggest that" [( M8 G9 j$ t; F0 y# C& ~- `+ M
dermal conversion of testosterone to dihydrotestos-
! d1 e7 @& p& c3 G) d. i) Fterone, which is a more potent metabolite, is more( h o- }1 T/ H
active in young children exposed to testosterone
, b6 g: L$ ]: _% A! S7 y* Q0 @exogenously7; however, we did not measure a dihy-( o7 v& F! n+ @5 {8 R% ]
drotestosterone level in our patient. In addition to
. J0 V4 ^! R* e/ i& Dvirilization, exposure to exogenous testosterone in
. Y2 o) }' }' O: ~0 ?* _1 e0 @; }children results in an increase in growth velocity and0 w. ~) S; f. H( ~ Z
advanced bone age, as seen in our patient.$ { ]( s6 o6 |4 [$ p
The long-term effect of androgen exposure during
: f- I/ ]3 f5 E9 F$ Rearly childhood on pubertal development and final- z& c+ y1 ?4 k o/ V# U
adult height are not fully known and always remain" A: [( Y- W) r7 A8 U0 [& j
a concern. Children treated with short-term testos-% g/ n/ u+ p: {- i! d+ i, d0 y' Q
terone injection or topical androgen may exhibit some* R9 k4 q \" \- |' `
acceleration of the skeletal maturation; however, after0 }4 D6 ^% |. N5 c+ b
cessation of treatment, the rate of bone maturation
% I/ O2 q* H" s' v, N; kdecelerates and gradually returns to normal.8,9
9 U1 q y: Y! @There are conflicting reports and controversy L' }5 ~# R/ S5 U% S! | U3 h& U
over the effect of early androgen exposure on adult
* j% x; h, G7 H; w$ d& y; Dpenile length.10,11 Some reports suggest subnormal2 ^/ f5 k* M7 p: t) I
adult penile length, apparently because of downreg-
# r `6 O s. {) D" p7 O7 o1 nulation of androgen receptor number.10,12 However,
1 g; x* g! a: S6 f- D" ^0 ASutherland et al13 did not find a correlation between T6 X' Y$ f5 D: i0 I8 g4 J
childhood testosterone exposure and reduced adult
) S. p6 @" T. G+ Vpenile length in clinical studies.
9 u c# ^" [: x9 tNonetheless, we do not believe our patient is
% W% |/ @7 n; V; S* ~going to experience any of the untoward effects from
2 H$ r$ U3 w: }& O. ^# W' Htestosterone exposure as mentioned earlier because
# \# A) Q) `/ lthe exposure was not for a prolonged period of time.
7 ^8 {3 r$ D: p! `! \4 y" jAlthough the bone age was advanced at the time of, A4 l, F' K2 p
diagnosis, the child had a normal growth velocity at% a' D2 |( u7 x3 V5 z
the follow-up visit. It is hoped that his final adult8 U) b$ v' ]4 {' N" ~2 P
height will not be affected.
# B& f1 q8 D9 S( T* {Although rarely reported, the widespread avail-4 m) C2 n1 A |: O0 }2 Q
ability of androgen products in our society may9 [2 Z R9 A' b; ], z
indeed cause more virilization in male or female6 _1 [6 Q% l- I" }; j8 ]6 w
children than one would realize. Exposure to andro-( T- K1 P$ B7 T/ J
gen products must be considered and specific ques-7 ~4 k/ z% @, ?
tioning about the use of a testosterone product or
3 [: C1 T2 F( b4 h5 J) Agel should be asked of the family members during# T D. O' H2 P- F0 P8 x# Z
the evaluation of any children who present with vir-
7 X/ u% ^% d; @0 ? G& ~ilization or peripheral precocious puberty. The diag-1 H+ B# | c7 |( X d
nosis can be established by just a few tests and by
% L, ^9 O9 v9 r2 u9 B1 }, lappropriate history. The inability to obtain such a
0 e7 m5 z2 N9 P) d3 _- phistory, or failure to ask the specific questions, may3 C0 Q- g* G0 R7 M' P0 s' w
result in extensive, unnecessary, and expensive
, H- b( ^' d9 x% `investigation. The primary care physician should be
. ]* N' u; C; O0 U1 Maware of this fact, because most of these children3 V% q' h+ ?+ d; `& w5 ]. g
may initially present in their practice. The Physicians’4 K! L7 J9 f" F# Z/ T/ Y& Y
Desk Reference and package insert should also put a# D& p" M0 ^2 `+ o7 P5 \' q- S5 e
warning about the virilizing effect on a male or
1 Y( c$ q+ [0 U# V9 ]female child who might come in contact with some-/ _( F8 z& J: C* @2 F+ }+ F
one using any of these products.8 o0 O7 P3 ^+ @, V
References
( n+ B2 L7 ]+ a- @) J3 z1. Styne DM. The testes: disorder of sexual differentiation! ^6 O2 T! d y; X8 v# d
and puberty in the male. In: Sperling MA, ed. Pediatric- T X6 i/ R% D3 E$ h' ?$ l. H
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 |* j2 {' Q3 [! H; F2002: 565-628.
7 {3 L A6 E' o2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 a' U( K4 q! s$ C$ }
puberty in children with tumours of the suprasellar pineal |
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