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Sexual Precocity in a 16-Month-Old$ _, J" F" e4 w
Boy Induced by Indirect Topical
2 [7 B0 j3 |* X5 FExposure to Testosterone
' F& S- M# a- PSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2" G- y9 `# L! Z C# N
and Kenneth R. Rettig, MD1
4 Y3 Q% |2 P5 _- A0 _Clinical Pediatrics1 Z; B7 I% R1 L( i% `
Volume 46 Number 6
( [7 Z/ P! F5 a( N: s6 FJuly 2007 540-543
9 f3 a3 X9 R; O7 B© 2007 Sage Publications
* C9 n- I7 b3 Q. g$ C10.1177/00099228062966510 c/ B, I* U- f3 f
http://clp.sagepub.com. }" g# l; L: i4 D" t
hosted at
, K+ J9 S/ D; k% X5 d# Dhttp://online.sagepub.com
; g& M) r) X0 YPrecocious puberty in boys, central or peripheral,
; O/ s# x) ]+ Q& A5 K$ r4 sis a significant concern for physicians. Central2 J. }3 z( i- j; D
precocious puberty (CPP), which is mediated
4 \. o. n6 X; W! Q, bthrough the hypothalamic pituitary gonadal axis, has
; W: G5 B8 L7 g. r4 d8 ra higher incidence of organic central nervous system8 H+ l/ |+ l4 F# b/ P; H L
lesions in boys.1,2 Virilization in boys, as manifested
8 T0 O, J; o3 p8 yby enlargement of the penis, development of pubic
9 N. _& `: ]+ K# S' mhair, and facial acne without enlargement of testi-
9 N) G2 P7 M7 ^. e0 \5 k5 ]* [+ q8 Mcles, suggests peripheral or pseudopuberty.1-3 We! @, g% l; u$ l G9 S
report a 16-month-old boy who presented with the- ] ^& Y' [( X1 `. S
enlargement of the phallus and pubic hair develop-
: n, B" b) ?/ C* m" G3 ]ment without testicular enlargement, which was due9 f- V0 {4 L4 J- E# V
to the unintentional exposure to androgen gel used by
; M, r' r9 o9 W, a. A$ u' Ethe father. The family initially concealed this infor-
4 M( b0 S% e$ g; A% a* Vmation, resulting in an extensive work-up for this& d/ m* l" Q1 S. Q& L( P; n
child. Given the widespread and easy availability of6 v" A: p! M1 G; X
testosterone gel and cream, we believe this is proba-0 h ~& g' {* B/ X9 W4 ]6 i! ?
bly more common than the rare case report in the7 Y6 Z$ G2 d4 f B
literature.43 v& @' ~& k8 O9 V0 _
Patient Report
. [9 U2 t3 x* G. T1 E# NA 16-month-old white child was referred to the% a) p* ?- l$ Q$ H: X
endocrine clinic by his pediatrician with the concern
8 f% I8 h9 w1 Q# @ fof early sexual development. His mother noticed* Y) T" ^. [: c8 C {+ Z+ c9 ~
light colored pubic hair development when he was* B. T, Y# b1 B k' n/ V- _
From the 1Division of Pediatric Endocrinology, 2University of
b& F+ u% x$ F5 f& BSouth Alabama Medical Center, Mobile, Alabama., L4 k* P Z- p# v1 O
Address correspondence to: Samar K. Bhowmick, MD, FACE,0 |) b J: M4 u2 C) O
Professor of Pediatrics, University of South Alabama, College of5 e6 J, `/ }. o! C& Y6 w0 a. i
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 W) ?' _/ b e; K6 q4 i, e, c8 D
e-mail: [email protected].
# m+ M6 j' E, j: C) qabout 6 to 7 months old, which progressively became
; W: e. `' N/ c8 E: g! cdarker. She was also concerned about the enlarge-
- ]. [; ?* F+ q; x. ^ i7 l9 k4 cment of his penis and frequent erections. The child: \7 q: C/ L1 G# A& f
was the product of a full-term normal delivery, with
: S% I$ c# g4 e( T7 C0 ^a birth weight of 7 lb 14 oz, and birth length of
. g4 n. P `$ w20 inches. He was breast-fed throughout the first year
+ f/ u) j# @& N$ L, P+ ~of life and was still receiving breast milk along with
2 o0 |: p+ b7 p' H# V6 isolid food. He had no hospitalizations or surgery,
2 X! h: C P$ c: h3 ?and his psychosocial and psychomotor development, S8 W) `4 x0 u7 K" S
was age appropriate.
0 ^/ `/ ~0 Y+ L9 D) ZThe family history was remarkable for the father,
! I9 y, u: z7 M" [+ I2 I, ?/ jwho was diagnosed with hypothyroidism at age 16,
' e7 y& X5 ? D6 W# Z4 E2 `which was treated with thyroxine. The father’s3 ~* d7 H% Z0 _. m3 X: t5 Q/ v+ p
height was 6 feet, and he went through a somewhat
7 O/ `% b4 f. ]6 a" Dearly puberty and had stopped growing by age 14.
3 ~( n$ U: z& f' `! rThe father denied taking any other medication. The1 `* x' q( w( L9 d3 g3 Z1 ?
child’s mother was in good health. Her menarche
& k. d n8 T% rwas at 11 years of age, and her height was at 5 feet1 |# x X+ Y5 O" m3 w1 `% Z
5 inches. There was no other family history of pre-
/ G( m" o7 a" [4 N g% I% Icocious sexual development in the first-degree rela-
: Y: C+ \7 W* L6 E( D2 a" Wtives. There were no siblings.
- C5 _5 j9 M6 Y, APhysical Examination
2 ^# c! m3 c- K7 i! {5 c" W e; R5 f eThe physical examination revealed a very active,4 t0 B" E4 V a6 U1 \6 D( Y; q2 E& L
playful, and healthy boy. The vital signs documented
8 C9 @/ `( n; l3 O! g$ q" ea blood pressure of 85/50 mm Hg, his length was7 ?' n# r! J2 L! z h
90 cm (>97th percentile), and his weight was 14.4 kg
; z' R* U; p% O! d; c! u- p(also >97th percentile). The observed yearly growth) p- }8 Z) S7 Y+ j" X
velocity was 30 cm (12 inches). The examination of8 v4 E/ P1 v0 r
the neck revealed no thyroid enlargement.8 }. z( {( I0 P7 i% ]
The genitourinary examination was remarkable for
% S& w! g$ V* e: D: H N1 V9 Penlargement of the penis, with a stretched length of# _" z+ m0 C3 Z0 `. P: U
8 cm and a width of 2 cm. The glans penis was very well, M) y" w. p; S3 p
developed. The pubic hair was Tanner II, mostly around
$ N7 j" N3 j. k, a540# A$ U$ e* S1 \
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% Z' }, e6 r% Tthe base of the phallus and was dark and curled. The) U0 b7 v: i+ h7 A9 C
testicular volume was prepubertal at 2 mL each.
- P( P' @/ K( a- x6 HThe skin was moist and smooth and somewhat
8 ]+ ~, O, n0 l/ @8 r7 {) n" ooily. No axillary hair was noted. There were no, l8 f$ X0 E7 d' V. ]( ^) z% S
abnormal skin pigmentations or café-au-lait spots.' N2 M/ M4 Y# o/ P& g9 _
Neurologic evaluation showed deep tendon reflex 2+7 a9 Z% s! x) X; }& G
bilateral and symmetrical. There was no suggestion
( ` ^0 O4 x: n+ s/ z4 m+ P; fof papilledema.
; D% g% |8 G( l. b; q0 vLaboratory Evaluation, _1 ?- m0 q( a( \' a: a b
The bone age was consistent with 28 months by+ x5 W- t; }( m6 Z2 t! G2 V
using the standard of Greulich and Pyle at a chrono-( r' z/ U4 T7 U0 ^8 ^9 l
logic age of 16 months (advanced).5 Chromosomal& j/ b1 H' R* }0 _. N# o' Q2 e! ?
karyotype was 46XY. The thyroid function test
* S$ R( w# d1 s% b* m( Q5 Q. p$ I( Gshowed a free T4 of 1.69 ng/dL, and thyroid stimu-( Q' X' F' X1 q
lating hormone level was 1.3 µIU/mL (both normal).) R( U7 W! N6 ^. T
The concentrations of serum electrolytes, blood) K$ {# }9 L4 f# e& x
urea nitrogen, creatinine, and calcium all were% q9 ?' ~) ?! L: f* m# C6 e
within normal range for his age. The concentration
1 p; |( b4 S0 ?8 xof serum 17-hydroxyprogesterone was 16 ng/dL3 u+ O; V0 b+ f5 X
(normal, 3 to 90 ng/dL), androstenedione was 20
, l0 M& q# U; eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, O6 L8 b0 J5 T( B) V; R$ ~! Sterone was 38 ng/dL (normal, 50 to 760 ng/dL),: O: X% _- H: E/ ^. \
desoxycorticosterone was 4.3 ng/dL (normal, 7 to7 s4 p8 f5 G& V& N9 m* J
49ng/dL), 11-desoxycortisol (specific compound S)
0 r; X# D0 _# {. C3 @5 Nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ k1 Z$ j7 y7 W2 B* e+ p" ^$ ^4 ^
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) q; E/ Z& w, K5 e
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 y7 A: M0 i0 E% s P
and β-human chorionic gonadotropin was less than
; n. D! V, W; W* T. i! j6 z5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 d7 A- x/ A* C. ^% Ystimulating hormone and leuteinizing hormone2 i+ B; o0 u$ S( `2 B2 Z
concentrations were less than 0.05 mIU/mL2 K2 [3 H' L" k# b. b7 H
(prepubertal).
8 _! p. H9 S$ s$ q; n6 Y1 { |The parents were notified about the laboratory- R3 k$ n3 h; R a) o! g! W% E
results and were informed that all of the tests were. E5 ~1 ?7 Q$ U4 w, j% m4 \/ a* q
normal except the testosterone level was high. The, ^! f+ F& Z2 s2 f' O
follow-up visit was arranged within a few weeks to
7 @# g% D( E- `% G: wobtain testicular and abdominal sonograms; how-
( B9 K6 t4 l F. F, @8 ?( mever, the family did not return for 4 months.
" _1 b+ N6 R5 ?Physical examination at this time revealed that the" X3 T4 \5 [. y% m
child had grown 2.5 cm in 4 months and had gained
0 X9 u7 n1 |! x: |# B1 D2 kg of weight. Physical examination remained7 z# ?% e, E3 A" }
unchanged. Surprisingly, the pubic hair almost com-
+ b6 v& q ?# O9 E/ P0 Zpletely disappeared except for a few vellous hairs at8 `5 l! h4 T$ z" {2 j
the base of the phallus. Testicular volume was still 2
; t$ ]" A" M; J: s# H: imL, and the size of the penis remained unchanged.
9 k* z# ?$ Q! m% t- Z/ WThe mother also said that the boy was no longer hav-
; o W8 X* {; ]; S/ \ing frequent erections.
) W, g h6 ~) T, b& O3 ^Both parents were again questioned about use of1 [) q) d5 K% S1 D
any ointment/creams that they may have applied to+ _: K% Z0 ?& ^) l8 ]+ S$ J
the child’s skin. This time the father admitted the
1 u; [8 z, f, W1 ^+ f& @; _/ {. y: HTopical Testosterone Exposure / Bhowmick et al 541
8 H5 k, u1 x0 a0 g. j8 M wuse of testosterone gel twice daily that he was apply-1 w F b: ?- }: ~+ B" S$ o
ing over his own shoulders, chest, and back area for
3 b$ f- X7 \9 Ba year. The father also revealed he was embarrassed
2 A: b) u* S9 v6 V9 dto disclose that he was using a testosterone gel pre-
; d6 @" X# o0 b( R3 g5 xscribed by his family physician for decreased libido
. `) w* G* ~7 V% S" |+ `& qsecondary to depression.
+ }6 P; q* ~3 q0 fThe child slept in the same bed with parents.
0 C3 ~/ k: d" \2 Y- x0 [. ^The father would hug the baby and hold him on his ~: v: J+ M% \3 a* H: @1 Y
chest for a considerable period of time, causing sig-
, H9 f. Z+ ~' R, T+ C3 d9 ?nificant bare skin contact between baby and father.6 C6 N3 {. o# B7 R/ m
The father also admitted that after the phone call,
+ c5 [9 b6 w) Kwhen he learned the testosterone level in the baby7 ^& S# p3 ^+ n1 Y5 W
was high, he then read the product information
! \9 b% A4 P; z/ J3 n$ g( g4 Lpacket and concluded that it was most likely the rea-
; O1 L. r, h1 S5 W% A+ |, p3 Z5 Zson for the child’s virilization. At that time, they5 Y! Q7 s- _5 w9 d+ y% ^
decided to put the baby in a separate bed, and the
- `# ]) Q7 Z" cfather was not hugging him with bare skin and had
% g' @! d8 w' g4 N/ `3 q# ?been using protective clothing. A repeat testosterone
: X' j/ C5 z! f% f& O$ y3 Stest was ordered, but the family did not go to the
, Y* x7 L6 S. I) S4 e7 z* x7 tlaboratory to obtain the test.
" p, e/ k3 S! B" f4 @( [1 xDiscussion: r9 z M/ W5 c, I* v" b
Precocious puberty in boys is defined as secondary" m+ {2 Z3 ?- P" {8 ^- S* S; h
sexual development before 9 years of age.1,4$ s4 ~: k7 y5 t! z
Precocious puberty is termed as central (true) when4 s$ E! U7 }# {# {% E! M- g, J
it is caused by the premature activation of hypo-0 C( o/ g4 ^' y" N+ M
thalamic pituitary gonadal axis. CPP is more com-% P3 |& }4 D. N+ \/ C6 a
mon in girls than in boys.1,3 Most boys with CPP
+ i% E/ p1 ~6 V/ @2 Zmay have a central nervous system lesion that is3 h0 E+ s0 D: B4 L, y5 q9 n
responsible for the early activation of the hypothal-; M7 h p' }; e. W
amic pituitary gonadal axis.1-3 Thus, greater empha-
5 T1 {: ^# |- @: p- A. Ysis has been given to neuroradiologic imaging in
3 [$ R- k/ T' j( e4 {# Iboys with precocious puberty. In addition to viril-
9 j/ n2 a- g0 v0 N' qization, the clinical hallmark of CPP is the symmet-7 s, E1 J/ I) p% S
rical testicular growth secondary to stimulation by
1 e+ z0 K, S7 D; ]- _- vgonadotropins.1,3
# j: l' A a; T, `Gonadotropin-independent peripheral preco-/ E# F5 `* H g' k( e
cious puberty in boys also results from inappropriate
( q `5 I- o0 C+ b$ r0 Z1 O9 jandrogenic stimulation from either endogenous or! ^/ k. O, L9 t' F" A: S6 K
exogenous sources, nonpituitary gonadotropin stim-+ o y. A! Z6 L/ S- v. c* ~, o. w* ~
ulation, and rare activating mutations.3 Virilizing
' }" f& W- N& U M. Ycongenital adrenal hyperplasia producing excessive
" [5 b3 M1 ^9 G1 Y% V3 {/ J! B% ]adrenal androgens is a common cause of precocious
1 b2 d! ^* O% [puberty in boys.3,4! m [) s- C- V) k
The most common form of congenital adrenal- ^; Y9 V0 g) |2 w# j- C8 f$ N
hyperplasia is the 21-hydroxylase enzyme deficiency.- s8 I# h2 z- }/ p) X N& @' ^
The 11-β hydroxylase deficiency may also result in+ W: B' k7 g, k! B1 Y2 R3 J
excessive adrenal androgen production, and rarely,8 G. c1 {& G, d: v5 Q# W
an adrenal tumor may also cause adrenal androgen: d, P3 \' L$ v) T! ]5 m6 a
excess.1,3
3 [& [; v) F; s+ ?$ A8 D. d/ mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ o, S7 g4 ^ @542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
1 _8 o |1 m* v {. q! U8 A0 ]: {A unique entity of male-limited gonadotropin-
/ t- d/ I& E" ]4 o6 ]% lindependent precocious puberty, which is also known! X& x7 q8 V6 K- F( z) _; U
as testotoxicosis, may cause precocious puberty at a) C2 a0 t' w9 _8 W$ Y
very young age. The physical findings in these boys
; k* e0 s9 B' R, x# D, rwith this disorder are full pubertal development,
! w- I9 b7 p$ @4 {$ Fincluding bilateral testicular growth, similar to boys
@9 R |. u4 @0 mwith CPP. The gonadotropin levels in this disorder9 _- T& c1 P, m! k
are suppressed to prepubertal levels and do not show
* u; g3 }0 z& O- E6 Ipubertal response of gonadotropin after gonadotropin-
7 X2 S: @. F# Z" Oreleasing hormone stimulation. This is a sex-linked* B1 e7 x. u" E* M
autosomal dominant disorder that affects only
8 ?8 o& k5 O- z, q' v4 Tmales; therefore, other male members of the family
" i% z) E! W- ~, X! [8 w1 A% L" umay have similar precocious puberty.34 P7 E' S. W5 X2 P c6 e
In our patient, physical examination was incon-
4 t1 \1 S$ [* A4 t! fsistent with true precocious puberty since his testi-
- z" T3 H% _' O* [6 J, V* lcles were prepubertal in size. However, testotoxicosis
6 D7 d, }* ~9 B5 S% Swas in the differential diagnosis because his father
: K7 h$ n/ l8 n9 p! Ustarted puberty somewhat early, and occasionally,
# ?. r5 F8 U n# htesticular enlargement is not that evident in the5 r9 \( v* E/ j0 |6 L1 w. u: E
beginning of this process.1 In the absence of a neg-/ ?; U: x4 M+ G8 v4 I0 h
ative initial history of androgen exposure, our
! r6 {8 i/ u, n, e" X, `biggest concern was virilizing adrenal hyperplasia,
2 K" a2 B; o- Z7 x3 g. {, feither 21-hydroxylase deficiency or 11-β hydroxylase, V% Q$ l! y# v# E% u
deficiency. Those diagnoses were excluded by find-
- e' W1 H2 U" ting the normal level of adrenal steroids.
" w1 T6 R4 m! o$ v4 BThe diagnosis of exogenous androgens was strongly0 n4 ~+ v# ?+ M+ z8 T& R
suspected in a follow-up visit after 4 months because, q. Y+ N4 ^; E4 K6 e$ F
the physical examination revealed the complete disap-
& z) H, h$ ]& W; H9 }pearance of pubic hair, normal growth velocity, and: r V( _' `% G: W3 F# F
decreased erections. The father admitted using a testos-) L" D7 j7 K& ~0 v* _* I4 B( E
terone gel, which he concealed at first visit. He was; E3 p P }5 l4 O0 L' g8 O
using it rather frequently, twice a day. The Physicians’/ r& M/ d' w6 E$ L3 h
Desk Reference, or package insert of this product, gel or- b# g( H6 E1 f, I _- ^* ?+ j5 \
cream, cautions about dermal testosterone transfer to
; L5 U$ L2 c w8 q6 O! Iunprotected females through direct skin exposure.
1 \! u3 O4 ?6 b1 e! hSerum testosterone level was found to be 2 times the* P( Z3 q) @5 i4 z" w! ~
baseline value in those females who were exposed to& H) C; q+ K( r3 F) L
even 15 minutes of direct skin contact with their male
" \$ ]: c- P* q6 f3 W% Apartners.6 However, when a shirt covered the applica-; Z% [" J$ f( M7 ~, `
tion site, this testosterone transfer was prevented.
0 r% \ A- L! r. u' r& tOur patient’s testosterone level was 60 ng/mL,2 f4 F* k( B4 Q( i/ e8 x- r
which was clearly high. Some studies suggest that
9 m- a; D9 [$ w. D' j5 d4 l$ Wdermal conversion of testosterone to dihydrotestos-
6 k7 Y! ?: J. b& V* O! ` ~6 tterone, which is a more potent metabolite, is more
' N) i( X- v0 q/ |7 b; u( Y; `2 k" |, z. Vactive in young children exposed to testosterone
* l1 d* x1 O# S Lexogenously7; however, we did not measure a dihy-
+ \0 [8 e" Y3 C: v0 f: h* S( j9 i5 \3 Zdrotestosterone level in our patient. In addition to
/ u! o3 b; m' V: ?& y( m! Rvirilization, exposure to exogenous testosterone in
1 S- j% y: e/ Ichildren results in an increase in growth velocity and+ L7 P9 _7 `3 b2 I$ K2 [/ }# j
advanced bone age, as seen in our patient.8 ~8 A0 M4 H. P7 g& @
The long-term effect of androgen exposure during
4 K# `9 Z5 h! C/ zearly childhood on pubertal development and final
1 Y0 O7 y/ K$ c2 M+ f xadult height are not fully known and always remain4 p6 D+ U( q2 X8 M3 g
a concern. Children treated with short-term testos-
7 m1 o; \. I+ K/ M" `" w8 X5 Mterone injection or topical androgen may exhibit some
) H5 [, J9 z: H& R- W4 W6 iacceleration of the skeletal maturation; however, after. e7 |5 y3 H% {' G
cessation of treatment, the rate of bone maturation: M4 T% J" Q) x
decelerates and gradually returns to normal.8,95 _2 A. q$ P$ b2 M
There are conflicting reports and controversy
' h$ ?2 z3 v$ Vover the effect of early androgen exposure on adult$ \ a+ @" Q6 A/ j. E2 B
penile length.10,11 Some reports suggest subnormal% i) ]- R! _$ Z$ M- d0 e, o7 y
adult penile length, apparently because of downreg-/ b, z1 w+ x0 h1 h: [5 c4 i: M
ulation of androgen receptor number.10,12 However,; h! E% X8 Q$ L7 v# U, [8 T7 r
Sutherland et al13 did not find a correlation between
6 y. W& k1 y5 @; N* V8 ~4 ?childhood testosterone exposure and reduced adult
* u$ D9 A) Y! T7 n7 u. {penile length in clinical studies.
/ O) V$ H- o/ d1 ?4 jNonetheless, we do not believe our patient is
; q6 L7 x- Q- Z. O& ?8 _: g' i+ _+ Ogoing to experience any of the untoward effects from
; R7 G! K3 U1 ~5 vtestosterone exposure as mentioned earlier because9 W) b" ]: s- j: ?; Q+ m- A. `7 p [
the exposure was not for a prolonged period of time.% j O0 P0 y8 g$ p6 G
Although the bone age was advanced at the time of
+ I5 n& F" o/ k- J. D: s5 Mdiagnosis, the child had a normal growth velocity at
9 g: q5 e3 o4 Fthe follow-up visit. It is hoped that his final adult/ N/ [# V3 d' p
height will not be affected.
# k9 B8 ]3 {: h: jAlthough rarely reported, the widespread avail-
( s0 q* R2 e7 l, [, L1 `ability of androgen products in our society may
- R! ]7 A8 j2 V2 yindeed cause more virilization in male or female
% Q: w# J# F8 T: P# l1 |) e0 R& [% Achildren than one would realize. Exposure to andro-
" y. d# z& E: G1 Rgen products must be considered and specific ques-
8 I' j3 k7 s; p6 etioning about the use of a testosterone product or
4 g& u# f! \: C, f4 l Dgel should be asked of the family members during/ O( a9 V% A+ Z d! ~
the evaluation of any children who present with vir-2 x' n/ ~* l' p6 j3 e2 P3 |: J% M
ilization or peripheral precocious puberty. The diag-4 T8 `; m# B+ B
nosis can be established by just a few tests and by7 w, K: s2 S. @. p! ^5 ?: l
appropriate history. The inability to obtain such a9 T8 K5 V" q- v; p' T) q
history, or failure to ask the specific questions, may
9 v+ |& z1 Z) z# \; e1 T& h# y8 x2 Qresult in extensive, unnecessary, and expensive
% ^5 q0 b" y8 `investigation. The primary care physician should be+ O# S: J0 b9 A) C
aware of this fact, because most of these children+ T& w$ h1 _ Z& _
may initially present in their practice. The Physicians’5 D: Q/ ~) \$ H* @, G
Desk Reference and package insert should also put a, r0 w$ @9 O' N/ r3 j& D9 g
warning about the virilizing effect on a male or
* [. {0 e9 Q& t/ B5 N% {! wfemale child who might come in contact with some-6 x! D) ^* _: l) I
one using any of these products.
+ Y2 ~7 [' n- L0 C4 o; ~References
0 E& P% t; d6 W# {+ ~ p4 ^, A1. Styne DM. The testes: disorder of sexual differentiation8 J* b& v/ _& F) ], }2 o
and puberty in the male. In: Sperling MA, ed. Pediatric r3 y' h5 c& m8 E
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. T/ B0 i2 n$ k' T6 V) [8 p- v9 {' @2002: 565-628.
6 B& g' I* F# i# F2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 `) ^+ F+ w2 p, x4 m4 t- mpuberty in children with tumours of the suprasellar pineal |
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