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Sexual Precocity in a 16-Month-Old
2 }7 s5 ~; o9 }: oBoy Induced by Indirect Topical
1 }; E$ q: z: _Exposure to Testosterone$ H# q0 v7 l: \3 ` L# x
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 l' m0 K6 G& M, U% ^: Oand Kenneth R. Rettig, MD1, E$ T P/ |2 |# Z2 Z+ r6 T
Clinical Pediatrics
" `, L8 p: N5 }. P; {Volume 46 Number 6
/ |6 E" \$ l4 R# T& I, mJuly 2007 540-543
+ v# L' ^: Y" f' x/ @+ x+ L© 2007 Sage Publications
* A* F M7 y1 ?0 h1 z6 Q10.1177/0009922806296651
: t, i0 S* ?8 p+ r. Chttp://clp.sagepub.com
+ K# Z# g/ c( whosted at
: r6 {2 e2 U3 T1 e9 T$ Jhttp://online.sagepub.com4 O+ U2 T& g& h
Precocious puberty in boys, central or peripheral,! m( W/ n7 j& t, j' q8 s+ C' i+ F
is a significant concern for physicians. Central2 C& W- W" J3 _# i
precocious puberty (CPP), which is mediated# s- N1 Z0 {, X7 R$ a
through the hypothalamic pituitary gonadal axis, has
* l) K7 e( n. ~6 M' V3 Da higher incidence of organic central nervous system1 L, L4 W! Q; _% \$ I8 o% z
lesions in boys.1,2 Virilization in boys, as manifested5 U, U( q$ o7 ~: ?8 c& s( ]% C( O
by enlargement of the penis, development of pubic
1 F3 d L: N* U% V7 vhair, and facial acne without enlargement of testi- k, H8 y/ o; p8 V( G
cles, suggests peripheral or pseudopuberty.1-3 We' t) O4 c$ f$ z5 S1 D0 S
report a 16-month-old boy who presented with the4 u; }6 m2 ?3 t6 ^4 j$ {
enlargement of the phallus and pubic hair develop-# F3 t& X$ p& {) A
ment without testicular enlargement, which was due
2 A+ l5 x) d7 n8 A4 [) m( Mto the unintentional exposure to androgen gel used by
$ ], [# W9 S* m3 p2 \4 T4 Mthe father. The family initially concealed this infor-7 p8 T+ V/ C2 x1 {3 D6 ]1 u
mation, resulting in an extensive work-up for this. M. T. J$ {+ N' i5 }- K% ]
child. Given the widespread and easy availability of
* d0 a/ S7 |$ S; t' N! |testosterone gel and cream, we believe this is proba-
+ ~, k4 B- ^- i1 Gbly more common than the rare case report in the
7 H; O) O2 D6 b K5 e0 @! xliterature.4. I. x. I9 d; b% b+ w
Patient Report A" _* e' z/ y8 b- k
A 16-month-old white child was referred to the
6 t9 H' b' W' X& K: i/ d4 n& O7 zendocrine clinic by his pediatrician with the concern, H' I. {( M, i4 l- o+ A1 o# D
of early sexual development. His mother noticed
; l& M+ ~2 h$ P, Z9 G. U F4 h: \light colored pubic hair development when he was
+ n U3 G! T: S; C( hFrom the 1Division of Pediatric Endocrinology, 2University of
! M# x. [2 ~0 N1 _8 A7 u# TSouth Alabama Medical Center, Mobile, Alabama.
# R3 a' A2 L: M0 _! t; kAddress correspondence to: Samar K. Bhowmick, MD, FACE,- B/ `! Z2 V; F) ]6 P/ C
Professor of Pediatrics, University of South Alabama, College of d2 f, B @! K3 c* G! q- H
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
0 ?! a, n" V& D$ z. Z/ ^8 be-mail: [email protected].) o: D$ W, G) [2 B' B: ~2 ?
about 6 to 7 months old, which progressively became
3 C. g3 P- m3 b% I, zdarker. She was also concerned about the enlarge-! H* a& L- K& L# A) u7 z4 c
ment of his penis and frequent erections. The child
; X: K$ Y1 Y: O4 E( P1 P0 F1 uwas the product of a full-term normal delivery, with. t1 p& k$ g( a
a birth weight of 7 lb 14 oz, and birth length of
6 K' d- U+ N; A# D+ p. g20 inches. He was breast-fed throughout the first year9 s0 X" v6 o6 e' Y8 T
of life and was still receiving breast milk along with- x6 k$ j, J( J
solid food. He had no hospitalizations or surgery,$ Z) ?/ k: {3 x% {
and his psychosocial and psychomotor development( X$ A0 x8 J% V; E3 ~( e9 `! _
was age appropriate.; j/ n) a& M, g1 |$ e& L1 b- z
The family history was remarkable for the father,: ?4 r$ d" m) t; U6 ^& l# f
who was diagnosed with hypothyroidism at age 16,
, Z) Q* g. O; H# Q/ G3 X, [which was treated with thyroxine. The father’s% i' P% X1 R! B: P8 U( ^
height was 6 feet, and he went through a somewhat
% r6 N1 c# M! _/ Q$ H5 \5 Uearly puberty and had stopped growing by age 14./ a2 Z& j7 t3 F' `$ r0 M
The father denied taking any other medication. The
& i! a6 L9 d: b9 _ K9 Fchild’s mother was in good health. Her menarche
5 z. o/ m: X- P! }: C4 Vwas at 11 years of age, and her height was at 5 feet! c# S M' b3 P& B+ K
5 inches. There was no other family history of pre-
% i! ~: s( H( C/ Jcocious sexual development in the first-degree rela-3 H# Y8 {1 r5 B8 k8 j
tives. There were no siblings.$ {2 `! N% d( D% P V3 w2 [! s2 f) x
Physical Examination) X3 r* u' L- H+ _& ^' o# j/ \8 T
The physical examination revealed a very active,2 [- x# I2 i; d1 j8 ^& D% R
playful, and healthy boy. The vital signs documented: E( c) z5 e% s/ r0 ~1 P* u
a blood pressure of 85/50 mm Hg, his length was
$ n% j* J2 w' O8 b" Y5 Y90 cm (>97th percentile), and his weight was 14.4 kg" x8 [4 `; B2 D5 V" N" }( y) H
(also >97th percentile). The observed yearly growth0 d6 n; O6 l6 g! L
velocity was 30 cm (12 inches). The examination of
" x9 M; H; d w0 z! t9 ?% D, K8 ^the neck revealed no thyroid enlargement.: M: ]/ B+ l4 N6 }2 z: {' T
The genitourinary examination was remarkable for1 Y7 I4 f( e6 q; M' A
enlargement of the penis, with a stretched length of1 R% O* B( }% Y/ K* Q/ n; ^ O
8 cm and a width of 2 cm. The glans penis was very well
1 F; M( h" ~" H! B8 [; jdeveloped. The pubic hair was Tanner II, mostly around: ]& s8 U; _+ C4 Y* g
5409 \% n# O2 L# t% q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" d9 C- ~8 B* ]& j2 T
the base of the phallus and was dark and curled. The
2 Z$ ?9 L: Q+ J; ^5 dtesticular volume was prepubertal at 2 mL each.% m8 Q& i' [# U/ K4 f
The skin was moist and smooth and somewhat* o1 H# f; d) X' y6 ^8 Z5 b; z
oily. No axillary hair was noted. There were no
2 W* \ Z! W$ e' K/ I. Tabnormal skin pigmentations or café-au-lait spots.' w5 ?& d% P3 f
Neurologic evaluation showed deep tendon reflex 2+
% X, w( }- Z0 `+ d2 i ibilateral and symmetrical. There was no suggestion
0 j* r A9 t9 D2 S4 n! cof papilledema.
* e9 \* z1 H) y, l ^7 WLaboratory Evaluation3 G) K2 o; G; S% {, e2 {- ]& t7 ~
The bone age was consistent with 28 months by% m( |7 J2 e, G8 [4 B
using the standard of Greulich and Pyle at a chrono-
( `$ R: S M7 Tlogic age of 16 months (advanced).5 Chromosomal; b6 u x* j, M/ n3 ^* u
karyotype was 46XY. The thyroid function test
0 P! d9 X8 R* G# n3 j% @6 _# A: Mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
# s( [) Y+ B1 Slating hormone level was 1.3 µIU/mL (both normal).
) Y( N2 }5 b9 y4 s1 mThe concentrations of serum electrolytes, blood; q' L8 \0 j" V% U
urea nitrogen, creatinine, and calcium all were
9 h& z$ V, `6 f5 k4 `within normal range for his age. The concentration$ P: x+ W9 J9 ?. B5 o
of serum 17-hydroxyprogesterone was 16 ng/dL
; m/ z" x- R9 i) o(normal, 3 to 90 ng/dL), androstenedione was 20 G3 ?1 X$ S1 O! ~" a0 a6 C5 v+ ?
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) Z( C5 D" w! O
terone was 38 ng/dL (normal, 50 to 760 ng/dL),, O$ Z7 \% b2 K7 X5 j0 _
desoxycorticosterone was 4.3 ng/dL (normal, 7 to1 ^3 w$ U7 n u: y
49ng/dL), 11-desoxycortisol (specific compound S)
3 H% J8 d% D0 _' Cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 A3 J$ @/ h0 T1 b. Atisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; e5 T" \8 O* n5 J2 c" h; Ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),4 k3 M7 E. v9 W
and β-human chorionic gonadotropin was less than: r; E9 M* U, b
5 mIU/mL (normal <5 mIU/mL). Serum follicular7 V* u) P5 o1 D+ e4 d# T
stimulating hormone and leuteinizing hormone& r3 F2 O! i! e6 g
concentrations were less than 0.05 mIU/mL
& a7 X5 R( M9 F2 u- z1 x$ A4 o6 `. a(prepubertal).
$ M7 n. }* ]$ P K. Q0 ]) \The parents were notified about the laboratory
: L$ k* T/ F$ Gresults and were informed that all of the tests were
6 l& `2 f4 O: ]2 ~6 ]normal except the testosterone level was high. The' K6 O# R& e/ V& t" n6 Q. q8 y
follow-up visit was arranged within a few weeks to6 O! J! f7 Y; M# G2 U3 q% f( A
obtain testicular and abdominal sonograms; how-
- @3 o5 }7 |" p8 Hever, the family did not return for 4 months.
% ?3 R! l u$ e$ U8 ^Physical examination at this time revealed that the
7 C6 r) v( ^' K' H* _& Ichild had grown 2.5 cm in 4 months and had gained& m! l7 m/ s' }8 Q. k7 `
2 kg of weight. Physical examination remained9 f0 ^! H- }7 b- p" x8 ]/ x0 C8 Y
unchanged. Surprisingly, the pubic hair almost com-$ |# q4 _: t% R' B9 y/ w3 s
pletely disappeared except for a few vellous hairs at
+ d( ~, I& Y$ M! K; r& [the base of the phallus. Testicular volume was still 2
9 J p: }- |5 Q" g4 h8 K! N3 `mL, and the size of the penis remained unchanged.3 [: Y* O9 V: A9 b' C
The mother also said that the boy was no longer hav-4 ]; j/ H% U# k. E! }9 v9 K
ing frequent erections.
4 p! `! V( t( v( z/ c8 y: b0 {) qBoth parents were again questioned about use of
- E" J {3 J$ Y! S8 Lany ointment/creams that they may have applied to/ { \7 b. K6 ^, h: l0 G
the child’s skin. This time the father admitted the
3 W0 N' b! W- d( STopical Testosterone Exposure / Bhowmick et al 541* }+ |& y* M6 }6 k6 l+ q
use of testosterone gel twice daily that he was apply-6 L, @8 k0 c, A2 E; M( E$ ~$ r
ing over his own shoulders, chest, and back area for4 J; G% G, ^: d. v% q% ^
a year. The father also revealed he was embarrassed
9 {7 {4 g0 j0 `, h4 mto disclose that he was using a testosterone gel pre-( t& M" O6 B- O4 J; [1 O9 ~+ J9 y
scribed by his family physician for decreased libido* M0 O1 R8 k- ^' ~1 R
secondary to depression.2 _# Q2 X/ L& e/ G1 G0 q
The child slept in the same bed with parents.- f' ]; U0 f8 v; S4 s. {
The father would hug the baby and hold him on his
+ s6 t& v; j: e8 \) ]chest for a considerable period of time, causing sig-9 w' C2 |% ^/ k; F$ |* r
nificant bare skin contact between baby and father.
% i9 J3 n% O& e4 P$ F- y. Y" [The father also admitted that after the phone call,
) ]* h6 v5 `& E% `0 Fwhen he learned the testosterone level in the baby
" q) V3 V# _7 ^& Q0 O5 Lwas high, he then read the product information
/ U) z0 z' a) r+ ^packet and concluded that it was most likely the rea-# s- G% q( H N2 u9 k9 z. p0 _3 q
son for the child’s virilization. At that time, they5 N _: N# x9 e# {5 u: N
decided to put the baby in a separate bed, and the
! G4 Q, ^9 C+ a6 h! Efather was not hugging him with bare skin and had& R! [( [. l& e0 O& G4 h
been using protective clothing. A repeat testosterone# y+ [, _9 {; t6 Z
test was ordered, but the family did not go to the. j% @# p- J$ z9 h" K* t) H
laboratory to obtain the test.
7 X6 G5 Q. D4 |. m: @! ?- A" `Discussion
. T. B1 Z8 s! a3 Z! Q1 r7 kPrecocious puberty in boys is defined as secondary' x7 z. `+ W/ c+ z3 s
sexual development before 9 years of age.1,4% x$ T# {. f5 B) e7 }7 c8 {; m
Precocious puberty is termed as central (true) when! Q& o" O1 k9 A. C' g$ d1 M
it is caused by the premature activation of hypo-
5 r( f7 H* m$ t4 @& C ythalamic pituitary gonadal axis. CPP is more com-2 j6 ^* I6 ^( _/ b# z' H
mon in girls than in boys.1,3 Most boys with CPP7 j8 g/ F* p9 I
may have a central nervous system lesion that is% |) v$ r$ t7 R/ x1 ]
responsible for the early activation of the hypothal-# y2 [3 G+ `5 I4 u6 j* X
amic pituitary gonadal axis.1-3 Thus, greater empha-0 p! K( O2 R0 s% o* Y% a) x
sis has been given to neuroradiologic imaging in# x7 L2 Q. r6 b, \. K% ` ^
boys with precocious puberty. In addition to viril-
7 k, ^+ e5 c! v, |0 W% r4 kization, the clinical hallmark of CPP is the symmet-
+ n9 ~9 q6 M" Mrical testicular growth secondary to stimulation by
) K, f) I! [. h& D9 Ugonadotropins.1,3
# A! p0 Z& g: i# p( oGonadotropin-independent peripheral preco-* v3 m2 L+ C3 k* G. G
cious puberty in boys also results from inappropriate
1 w- b8 t- D+ K; E% Bandrogenic stimulation from either endogenous or
4 r0 ^( j- ? ]# v! Z& |/ w" Uexogenous sources, nonpituitary gonadotropin stim-
7 j! E* K/ U Fulation, and rare activating mutations.3 Virilizing
/ ^2 C, g! z- e: R7 k; \" a Ycongenital adrenal hyperplasia producing excessive# }( @+ O1 o& ~( i
adrenal androgens is a common cause of precocious8 p i# ^0 x2 n* q
puberty in boys.3,4
$ n( f5 m7 u4 E( `5 n( f+ o1 }; w+ \* S- uThe most common form of congenital adrenal
6 L: M: V4 F7 } x! {hyperplasia is the 21-hydroxylase enzyme deficiency.+ f' i7 a* w. w2 C6 |6 y% D% j* D
The 11-β hydroxylase deficiency may also result in
1 J* I+ v* }; M" h, `& F% q, |excessive adrenal androgen production, and rarely,2 K1 A' o) j8 {) J
an adrenal tumor may also cause adrenal androgen% n' Z" Y1 y+ X9 u; g" Y0 O
excess.1,3
+ v, X) Z, L0 uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 z3 R; S1 X0 E$ c% C: a+ v542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, r7 z+ o! D; Y aA unique entity of male-limited gonadotropin-
+ \+ r- |7 R8 `0 Y/ l2 Y6 `6 s3 t$ d1 Zindependent precocious puberty, which is also known7 f/ d9 N4 [ ^% S* S, a6 ?
as testotoxicosis, may cause precocious puberty at a
* M( S/ K5 d zvery young age. The physical findings in these boys/ B) z+ @5 F' z3 D1 q
with this disorder are full pubertal development,
# g# c/ f& I2 x) cincluding bilateral testicular growth, similar to boys
8 j8 b6 |7 _6 N$ A" Hwith CPP. The gonadotropin levels in this disorder
; T+ }5 {1 H9 l! e: mare suppressed to prepubertal levels and do not show
! \2 e& T; ~/ e' H; Dpubertal response of gonadotropin after gonadotropin-
V' z* Y, ~" U. A; E6 Preleasing hormone stimulation. This is a sex-linked
, Y, c) t9 D$ ~) X* mautosomal dominant disorder that affects only
) H, K- T2 T! y$ v' k& w* i! _- V5 Tmales; therefore, other male members of the family1 h/ Y0 V" s4 q! ^0 W( j+ b
may have similar precocious puberty.3
) c6 N5 F$ d/ y8 k* p( b& t( hIn our patient, physical examination was incon-
9 X, R9 q1 m4 L4 l: m; Y \sistent with true precocious puberty since his testi-
/ y/ \1 q/ Z) Z: ~3 V! o& O8 ecles were prepubertal in size. However, testotoxicosis T- w1 M; h3 f* J! @( E
was in the differential diagnosis because his father+ C3 a8 A0 H& t4 l7 `; f& n* b
started puberty somewhat early, and occasionally,
% i! I* n( l* _' i! \$ G5 Rtesticular enlargement is not that evident in the" l/ x/ _2 C3 ^) C
beginning of this process.1 In the absence of a neg-% m+ y& D. k1 k
ative initial history of androgen exposure, our$ w2 \0 l$ ?* i F6 {
biggest concern was virilizing adrenal hyperplasia,0 H/ V8 M6 t P4 k4 r2 \0 S
either 21-hydroxylase deficiency or 11-β hydroxylase
8 X8 f1 ^0 ]. A+ ~deficiency. Those diagnoses were excluded by find-
, b* v: @9 B1 z( c/ K- E ming the normal level of adrenal steroids.
. c z+ |$ g& rThe diagnosis of exogenous androgens was strongly- g+ f3 |( V% r, f
suspected in a follow-up visit after 4 months because8 B) ~% s4 L1 W( K& S1 m
the physical examination revealed the complete disap-5 r. ]* ~$ u& |0 d" z
pearance of pubic hair, normal growth velocity, and" L, d: A1 P( X6 E7 o$ r; R; ]5 m$ x
decreased erections. The father admitted using a testos-) X( R2 W" Z! Q/ D
terone gel, which he concealed at first visit. He was
8 Y- r. J. i9 v' h; t5 W4 ausing it rather frequently, twice a day. The Physicians’; N- v( X6 e/ M& j7 ~
Desk Reference, or package insert of this product, gel or& G. h- M7 V/ W. a+ d4 D% r8 j
cream, cautions about dermal testosterone transfer to
E9 T% [8 \) g) |! F- }unprotected females through direct skin exposure.
# m: A1 m" {& E4 e/ ~% RSerum testosterone level was found to be 2 times the; U6 ^. m0 M k! {
baseline value in those females who were exposed to
3 Y! p& g- t0 [# G% feven 15 minutes of direct skin contact with their male
7 J6 r) p) I p9 {+ m: Gpartners.6 However, when a shirt covered the applica-
& |" z5 f' ^, P0 i% ~4 t" Ction site, this testosterone transfer was prevented.& z# a* z1 F: X0 s+ T
Our patient’s testosterone level was 60 ng/mL,3 K" Q4 }. I6 P
which was clearly high. Some studies suggest that
9 C$ {5 ]! X9 j( odermal conversion of testosterone to dihydrotestos-* P1 O/ H8 Z/ v. h, Z
terone, which is a more potent metabolite, is more
& x% j8 A7 e$ B% K& sactive in young children exposed to testosterone6 Q- d5 O& v% s
exogenously7; however, we did not measure a dihy-) K: ]7 b) i- i8 x4 E
drotestosterone level in our patient. In addition to) r+ ]* d* V5 m, v. S0 W
virilization, exposure to exogenous testosterone in, f; Z% J! A" t
children results in an increase in growth velocity and
8 \* F) h- ~3 g* j0 Badvanced bone age, as seen in our patient.% y4 j: @6 d/ k
The long-term effect of androgen exposure during
4 A" a5 I C9 I9 a1 T* Cearly childhood on pubertal development and final; G" |( B1 I3 C5 O9 C+ T
adult height are not fully known and always remain
8 y% G9 c6 y: n9 X) ka concern. Children treated with short-term testos-
' p7 D' E7 k, v* V7 K! T& @terone injection or topical androgen may exhibit some
, O5 @' h7 B- vacceleration of the skeletal maturation; however, after
1 a) e E$ q/ m) l) e9 d+ _" Ncessation of treatment, the rate of bone maturation
" |) {8 F6 ?' @+ C) Sdecelerates and gradually returns to normal.8,9
' d) R" f/ j' G/ @; r( N$ `) A& p( JThere are conflicting reports and controversy8 t9 @( R) e5 p! C4 x" z
over the effect of early androgen exposure on adult
0 x, `: Y+ I! p+ j/ wpenile length.10,11 Some reports suggest subnormal
$ R G$ b- Z) Y( r4 ]* `; A3 qadult penile length, apparently because of downreg-
- ^. Z, V+ A& }' h6 X. |. {% W, v' }ulation of androgen receptor number.10,12 However,
. L* Z. W: I: h- h" }3 X4 e0 w( XSutherland et al13 did not find a correlation between2 K& z% m% M% u6 {/ u6 S Y
childhood testosterone exposure and reduced adult2 C, ~4 B e/ g$ g
penile length in clinical studies.
K! h8 U1 f+ [3 \0 N$ E c% yNonetheless, we do not believe our patient is
6 ?+ Z9 O) Z! N- n( J, ?: Bgoing to experience any of the untoward effects from' E7 h+ B3 o' v& H l, K
testosterone exposure as mentioned earlier because
5 `9 c: G" {/ @- athe exposure was not for a prolonged period of time.4 |. ]& b6 A( ?3 F- n3 T
Although the bone age was advanced at the time of
% F8 F) |7 F2 K9 ^9 _! Ldiagnosis, the child had a normal growth velocity at5 Z( ~5 @8 p7 {* v
the follow-up visit. It is hoped that his final adult' R+ B/ R- Z5 H) A
height will not be affected.
6 R5 n: `0 ^0 n! X8 n! H( \% YAlthough rarely reported, the widespread avail-6 n6 ^0 R, T7 o2 D
ability of androgen products in our society may
M% ?$ ]5 G+ B: zindeed cause more virilization in male or female
8 h9 t; e/ s: `" y8 q0 `, ], ?children than one would realize. Exposure to andro-4 ^3 \! t7 \9 U7 K6 ^
gen products must be considered and specific ques-/ s* X$ K9 k: r
tioning about the use of a testosterone product or
7 x: \: D' M3 y6 a( o* y$ Dgel should be asked of the family members during9 X# E$ ~4 u5 `
the evaluation of any children who present with vir-. v( f" ?4 A7 B' D" u
ilization or peripheral precocious puberty. The diag-
; h5 D- h# i4 u1 f; e! Y2 Lnosis can be established by just a few tests and by
+ I( b! T7 t8 C% ?appropriate history. The inability to obtain such a
. ?# @4 G1 m/ z" z! L4 W+ o* Zhistory, or failure to ask the specific questions, may
8 o H" }3 Z5 |5 b# ?result in extensive, unnecessary, and expensive% ]: \1 d8 |3 X7 N
investigation. The primary care physician should be
7 M. `& I9 A: A/ `$ u6 haware of this fact, because most of these children
5 g U: e! v8 a% M, Imay initially present in their practice. The Physicians’% A* \1 S5 d, K" L$ n9 o- d* P
Desk Reference and package insert should also put a
g4 H% f1 K3 n9 ^" @warning about the virilizing effect on a male or
2 t/ [! i. i" [) w; O) r e4 A' sfemale child who might come in contact with some- F% J3 P( K; y$ H
one using any of these products.
! r+ \7 ^- b# w* K% B/ {% eReferences% ^) M, k% H9 Z0 D& z, D, D* `" @
1. Styne DM. The testes: disorder of sexual differentiation
- {6 W: K: _" H) Z' h9 Vand puberty in the male. In: Sperling MA, ed. Pediatric
0 Z& v" q% q6 _- WEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* D+ @- e9 {3 C7 o! R* f) o8 r b i2002: 565-628.
$ X4 f* }5 G) j/ _2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: c3 M% N0 x7 V b1 e8 B# X6 t: Z/ k
puberty in children with tumours of the suprasellar pineal |
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