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Sexual Precocity in a 16-Month-Old
) q" a. |0 o' n3 }; H' a9 pBoy Induced by Indirect Topical; O: f3 P' V3 }8 g) _, w, ^
Exposure to Testosterone
, i' j! B% p; o+ I4 B1 j% Q3 }; v- MSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,22 e3 }+ A" ^' q. D5 o2 \% o- k+ X9 {
and Kenneth R. Rettig, MD1
6 ~, ?( x% Y% N2 C/ S9 bClinical Pediatrics
4 ]; ~$ D$ A: BVolume 46 Number 6
& b3 R. H& k4 C' Q& I: s$ ^ ^1 wJuly 2007 540-543+ }" O1 h3 S/ w5 n9 Z# f
© 2007 Sage Publications
0 e; }1 W+ _6 }' l10.1177/0009922806296651
$ h; _3 w/ a6 ^/ l. X6 K+ T7 V1 ~http://clp.sagepub.com* K- D! _% o( k! K) _% B, j9 ]( G
hosted at6 U# t5 y: k# S" @
http://online.sagepub.com
U# z" p v5 v \Precocious puberty in boys, central or peripheral,3 F1 j3 P8 A$ U. S: H
is a significant concern for physicians. Central, |+ Q, k ?- t1 A2 c+ s
precocious puberty (CPP), which is mediated6 a% d. {- D0 Y3 [
through the hypothalamic pituitary gonadal axis, has
3 o3 k" \4 I% Q7 N6 c1 ?$ Ma higher incidence of organic central nervous system
' @$ w+ \# G5 B5 q( O& J( mlesions in boys.1,2 Virilization in boys, as manifested- G# X: z( x' T+ u+ V
by enlargement of the penis, development of pubic
( q+ w- C5 t- s- c. c5 k, Uhair, and facial acne without enlargement of testi-
2 i' r ^+ X+ vcles, suggests peripheral or pseudopuberty.1-3 We
: S' V3 S2 @+ b5 @0 Y! Greport a 16-month-old boy who presented with the) x# Z+ O" h! k1 s/ v. l! s
enlargement of the phallus and pubic hair develop-3 w8 x8 X- t$ t. k2 H5 \
ment without testicular enlargement, which was due
0 A; v8 p+ d$ Cto the unintentional exposure to androgen gel used by
1 T$ h6 X# Z c, z, Gthe father. The family initially concealed this infor-
- ^% ~7 Q# @; rmation, resulting in an extensive work-up for this: H( s( p. g" [# P) o% ?5 |- q0 r
child. Given the widespread and easy availability of
( i( M h/ e6 J3 m3 Ttestosterone gel and cream, we believe this is proba-1 \- t$ ]6 v* j% U( ]% D
bly more common than the rare case report in the7 r3 W2 j% r2 M$ v# L
literature.4) M+ M Z% O) n6 n6 L
Patient Report
% x( u$ p' O) ^/ e; [7 B0 ?A 16-month-old white child was referred to the3 N& O! c# o1 l: T3 ?8 K2 ]
endocrine clinic by his pediatrician with the concern
, Y- @1 {1 _+ I6 i7 u- e- zof early sexual development. His mother noticed8 E) G- W% V. I* H( F
light colored pubic hair development when he was) E0 U/ Q) H: O- S2 J
From the 1Division of Pediatric Endocrinology, 2University of$ O) r$ W6 ^4 X3 z& d! \1 V; Y
South Alabama Medical Center, Mobile, Alabama./ M- {: |8 w4 v) s! @/ R. N# v: |2 N
Address correspondence to: Samar K. Bhowmick, MD, FACE,3 e3 |- `4 B) m/ H: A' S
Professor of Pediatrics, University of South Alabama, College of
" d/ O4 h& a' MMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ a! L1 L2 h7 [4 ?# k2 j
e-mail: [email protected].
3 c4 [0 c9 _1 N' nabout 6 to 7 months old, which progressively became$ d! |& H" }% q0 K7 v6 K
darker. She was also concerned about the enlarge-2 q; g% A) N- W
ment of his penis and frequent erections. The child+ l N3 s) n$ ?( R5 m4 I) j# A+ Y
was the product of a full-term normal delivery, with
( p$ |: r% \' q h/ o9 la birth weight of 7 lb 14 oz, and birth length of' C6 T! J4 N+ Y( V" B; q8 I
20 inches. He was breast-fed throughout the first year: Y" N: S& J6 Y7 y2 W! Z) Q
of life and was still receiving breast milk along with
6 k; ~+ h' R8 w6 e1 [solid food. He had no hospitalizations or surgery,
- B. W2 s v9 u/ band his psychosocial and psychomotor development& H5 B% k6 _- }% x: i, W0 _. J
was age appropriate.
4 C/ ]5 s2 S4 d2 Y0 ~The family history was remarkable for the father,4 ^/ I; v q- C3 s. R6 q9 T V# f
who was diagnosed with hypothyroidism at age 16,+ n. v$ ?7 y* G3 `, E E
which was treated with thyroxine. The father’s3 u: r2 r: \0 T
height was 6 feet, and he went through a somewhat
- m& W0 K# |' [) Q; P+ zearly puberty and had stopped growing by age 14.
* V- o& \% a/ r- F6 r" F, nThe father denied taking any other medication. The2 n* B8 y8 }) d4 A
child’s mother was in good health. Her menarche
8 W* M3 [; A2 ewas at 11 years of age, and her height was at 5 feet8 T) X* ?5 \$ G6 L# Z' E
5 inches. There was no other family history of pre-/ N* R% c: D/ k/ {4 D
cocious sexual development in the first-degree rela-$ D9 d! Q1 Q" Z2 `/ {, O; K
tives. There were no siblings.
7 T) O. l8 w9 x: H+ z' |( `Physical Examination
' K7 O, g" {" r4 y; }* C. D: F; hThe physical examination revealed a very active,; l" b; q6 s( s& x1 h* z
playful, and healthy boy. The vital signs documented2 n7 W W' o8 O$ ?4 h+ F. d
a blood pressure of 85/50 mm Hg, his length was5 L3 a- ~- k1 s: q7 K
90 cm (>97th percentile), and his weight was 14.4 kg! U& w. P+ Y5 ?+ U& K% [/ [8 B9 c
(also >97th percentile). The observed yearly growth
3 x ^) t( S# P& F0 r/ Evelocity was 30 cm (12 inches). The examination of; Z9 ^# j, ~0 w/ Z
the neck revealed no thyroid enlargement.
! a7 {% R& f5 R/ K1 [The genitourinary examination was remarkable for/ V' s$ [* Z+ M6 m! G6 s- w h
enlargement of the penis, with a stretched length of
0 V3 M, |2 m' T+ P/ B3 }/ q8 cm and a width of 2 cm. The glans penis was very well
6 `: L1 M @4 m% X5 c0 _developed. The pubic hair was Tanner II, mostly around) B$ h* _) e1 k. Y: T
5406 s) m( \3 @$ n4 S" t$ \
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, e" y" f1 ]0 x- Q8 G- n. p
the base of the phallus and was dark and curled. The
& i' @' [* N6 ]9 otesticular volume was prepubertal at 2 mL each., H; e$ }0 G, r% \7 m
The skin was moist and smooth and somewhat
W- l: t! q0 g% foily. No axillary hair was noted. There were no
8 C0 s5 S5 l9 S7 n' j2 O+ ~abnormal skin pigmentations or café-au-lait spots.
% L* y" m( i z: X% }3 C3 ^8 GNeurologic evaluation showed deep tendon reflex 2+
% j8 t& b0 A6 ~( P3 f' }3 H3 pbilateral and symmetrical. There was no suggestion2 y* P0 X! G3 i9 F1 J$ ~
of papilledema.& ^( o0 g1 ?+ F* Y5 a
Laboratory Evaluation" ~3 X- {' L% b; `. P1 t" o: q
The bone age was consistent with 28 months by% Z) W1 {3 i+ p
using the standard of Greulich and Pyle at a chrono-( w C& d8 O& e, J4 m
logic age of 16 months (advanced).5 Chromosomal. P/ ~5 d1 g1 v
karyotype was 46XY. The thyroid function test1 @$ J, q$ o' d5 c
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
; z0 N. n6 _, ]" l$ m( m; `( klating hormone level was 1.3 µIU/mL (both normal).
+ r& j& A. N5 J# _! f- NThe concentrations of serum electrolytes, blood( Y/ x% i" u, G( a9 [
urea nitrogen, creatinine, and calcium all were( G- m( s2 T5 Y( y# w+ n4 v ]
within normal range for his age. The concentration/ A( H. q& O U; ]! w2 D& f+ E
of serum 17-hydroxyprogesterone was 16 ng/dL
% s Z) M) _* N6 X(normal, 3 to 90 ng/dL), androstenedione was 202 ?+ U: j5 |/ X, r3 S
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
P! x3 y) R z. {5 Kterone was 38 ng/dL (normal, 50 to 760 ng/dL),4 {" Q1 F+ s2 U( G" W- V: `
desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ t$ g$ K) O! ?% R
49ng/dL), 11-desoxycortisol (specific compound S)# R* {. }2 b* e3 }' I' i/ a
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, G0 F$ z3 @/ `) V
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ o8 Z6 ~+ e& y7 q; Ftestosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 c9 r' D, C' }9 o9 M
and β-human chorionic gonadotropin was less than
7 i3 N6 P( Y& o8 F4 [5 mIU/mL (normal <5 mIU/mL). Serum follicular
4 w4 C7 L/ I9 O( [stimulating hormone and leuteinizing hormone9 y1 Q+ j: P: o& T& t! L" K! w
concentrations were less than 0.05 mIU/mL% Z$ {& Y Z5 I; R$ e( Z
(prepubertal).7 ^. ~' F ] i( k* p/ q; G/ Y
The parents were notified about the laboratory+ q* p+ j: ?! L. |# R$ t
results and were informed that all of the tests were
2 R7 e7 z+ }/ qnormal except the testosterone level was high. The
2 ]( e" Q' y1 D! zfollow-up visit was arranged within a few weeks to
w7 ]' r2 J! R: q& K9 y( Wobtain testicular and abdominal sonograms; how-
. {, b$ I( C- [. x; d0 Cever, the family did not return for 4 months.
8 @" K3 ~8 n2 M" Z* A8 tPhysical examination at this time revealed that the* t1 s* U1 J7 p1 i0 o. v
child had grown 2.5 cm in 4 months and had gained C$ @% P/ t m1 i2 ?* Y
2 kg of weight. Physical examination remained
, F8 |3 i% C; h) ~: uunchanged. Surprisingly, the pubic hair almost com-
3 L* ~( X6 S4 g( }pletely disappeared except for a few vellous hairs at: ^8 R7 g& x3 J3 ?( |% ~" |
the base of the phallus. Testicular volume was still 27 D7 W- ?9 N7 O) ?
mL, and the size of the penis remained unchanged.
4 u, A% p" n/ o# D, ~The mother also said that the boy was no longer hav-
$ `/ v% y: Q" @. H. _0 ~ing frequent erections.
H1 S' ]8 N4 m3 D+ NBoth parents were again questioned about use of5 r" i% a: b9 u% b$ C! v5 t' D
any ointment/creams that they may have applied to" |6 g" G% B$ ]! n: q& `; P% O
the child’s skin. This time the father admitted the3 u4 C7 s! D& u& J3 }" t
Topical Testosterone Exposure / Bhowmick et al 541
: P# B1 P$ N) L, q/ q3 `' suse of testosterone gel twice daily that he was apply-' e u( t* m2 B7 I' v/ m
ing over his own shoulders, chest, and back area for
9 c* q8 q- L4 ^ @1 X( o! A2 |9 Oa year. The father also revealed he was embarrassed
2 M( }1 [- C5 O/ c I* G; Qto disclose that he was using a testosterone gel pre-5 R, e* M4 n/ v/ w$ @
scribed by his family physician for decreased libido' E9 j2 ^3 Q. w" o6 T
secondary to depression.- I2 p' {8 N: ~- O5 Y M4 y( Q
The child slept in the same bed with parents.) I9 ~: q. X9 R4 D9 b/ |
The father would hug the baby and hold him on his
) ?6 r, i' k3 h; t- [6 nchest for a considerable period of time, causing sig-$ ]$ J7 a/ c0 R3 w$ ?1 J4 Q4 m
nificant bare skin contact between baby and father.
" B5 U& P4 _/ o/ LThe father also admitted that after the phone call,
" N' i2 a/ y& Swhen he learned the testosterone level in the baby7 C7 L6 J( R4 J! e2 m& y
was high, he then read the product information
z3 H X/ H3 v) B" B4 g6 npacket and concluded that it was most likely the rea-
3 z" C( g) c5 Y) n2 cson for the child’s virilization. At that time, they
: s' r$ m; f- n( J, Gdecided to put the baby in a separate bed, and the
3 p( x* H* w' Afather was not hugging him with bare skin and had
# d4 N8 {* h" H& mbeen using protective clothing. A repeat testosterone% M+ f2 P, |8 R/ b' I6 V
test was ordered, but the family did not go to the0 w! e+ ^/ M/ u2 j( O) C9 o
laboratory to obtain the test.
7 _5 o' `. V6 s2 n* jDiscussion; o. y& [( J' R% _
Precocious puberty in boys is defined as secondary7 Z0 I4 B) {! c' @5 L! i/ S
sexual development before 9 years of age.1,4
& `* T/ G9 V7 P6 ^Precocious puberty is termed as central (true) when
6 L+ C9 _! K" M0 v6 `it is caused by the premature activation of hypo-4 F5 \8 h$ H6 L, _
thalamic pituitary gonadal axis. CPP is more com-9 ?& G2 J7 H) J& x c7 N: c
mon in girls than in boys.1,3 Most boys with CPP
; ^5 ?# b* u& j9 g, G4 X2 Dmay have a central nervous system lesion that is
3 I2 ^. ]8 D0 k1 W! \9 K$ Eresponsible for the early activation of the hypothal-2 W: j" h1 b, }
amic pituitary gonadal axis.1-3 Thus, greater empha-& ]& v' ?2 {" @8 G4 f
sis has been given to neuroradiologic imaging in
, x/ N0 k3 P. Hboys with precocious puberty. In addition to viril-7 b4 ], l9 H! p
ization, the clinical hallmark of CPP is the symmet-7 ~( K9 u! W* Y3 R1 w, J' U1 Z
rical testicular growth secondary to stimulation by: e/ X# T0 o- }6 z
gonadotropins.1,32 n3 P( y4 s: m/ ]/ T# q
Gonadotropin-independent peripheral preco-! [0 K2 n( w1 {& L9 s! ]
cious puberty in boys also results from inappropriate7 Y/ s# ~. k7 ~1 ^
androgenic stimulation from either endogenous or H6 r- I, m3 Z& L% s Z) ~4 ^1 l
exogenous sources, nonpituitary gonadotropin stim-
$ ?! ~0 q+ Q1 e7 U6 Uulation, and rare activating mutations.3 Virilizing
/ @' w O# E9 g% @. W5 }congenital adrenal hyperplasia producing excessive& e) d3 c0 Q7 O8 A
adrenal androgens is a common cause of precocious9 _1 [) S T# o; x* l
puberty in boys.3,4
8 ~1 w' z8 q5 C2 |( H! g% ZThe most common form of congenital adrenal8 D. R* a" [# R& I; U2 m9 l
hyperplasia is the 21-hydroxylase enzyme deficiency.
# ~- i- ]; l! m. RThe 11-β hydroxylase deficiency may also result in+ F. g: K& N- o0 @# R8 K
excessive adrenal androgen production, and rarely,4 z6 B5 d- S, Q0 g
an adrenal tumor may also cause adrenal androgen/ T5 n) k* Z& D8 C; i# B
excess.1,3
+ {- a, o5 w4 hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* F! g U1 w6 ~' }$ S
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! n7 M \' ~6 y8 c8 Q% [$ y+ c- zA unique entity of male-limited gonadotropin-! ^3 r- U) w' F9 J- ~
independent precocious puberty, which is also known
& M4 U/ V( l* K1 l$ x2 \% Aas testotoxicosis, may cause precocious puberty at a) K; q4 g8 U0 e2 D# n
very young age. The physical findings in these boys( T( E5 U' k2 e+ ?6 V
with this disorder are full pubertal development,2 O+ @: ]( _) `
including bilateral testicular growth, similar to boys
N) h& L, J% f+ Q& swith CPP. The gonadotropin levels in this disorder1 l, n+ f( ]/ q0 S2 E4 I3 u
are suppressed to prepubertal levels and do not show
; |/ L8 X" E( _pubertal response of gonadotropin after gonadotropin-
' X) U/ I% J7 \9 g/ s" treleasing hormone stimulation. This is a sex-linked9 Q; C( i. S7 c: _1 g% n+ s- L: k
autosomal dominant disorder that affects only
+ k! |) ~% a1 M6 j4 Nmales; therefore, other male members of the family3 G. F. v! Q( } z! Q
may have similar precocious puberty.3
( _! }8 k7 N W: a0 t* y) VIn our patient, physical examination was incon-
a: P5 i4 n. U4 c* C: e$ F% Tsistent with true precocious puberty since his testi-
~( W4 m0 X4 a. E% P& _# K) Lcles were prepubertal in size. However, testotoxicosis3 o! [( F5 ]+ A. ~9 V: a3 r
was in the differential diagnosis because his father+ O( s$ \& R9 R( k; h4 q2 n
started puberty somewhat early, and occasionally,
+ L( I) X! l8 Q& F- s8 ltesticular enlargement is not that evident in the
+ {% A k7 E9 \: p/ tbeginning of this process.1 In the absence of a neg-
: y! b* @% x5 H7 I% W* h& wative initial history of androgen exposure, our
" L/ o/ |, g; V6 k xbiggest concern was virilizing adrenal hyperplasia,* V; X$ k$ X' s; U
either 21-hydroxylase deficiency or 11-β hydroxylase, V& V# i) k# k8 o% B3 }: `, R
deficiency. Those diagnoses were excluded by find-. A& O6 \, @5 x" Q- a0 {
ing the normal level of adrenal steroids.
" n j2 Y6 C3 h c" h: D! xThe diagnosis of exogenous androgens was strongly
1 v; T( V; w+ }2 F3 Vsuspected in a follow-up visit after 4 months because2 r6 `9 H0 D) ^- \$ u4 \1 U
the physical examination revealed the complete disap-
, z$ ?- s" L9 e) l4 b( }# l3 Jpearance of pubic hair, normal growth velocity, and
% k, Z+ |# X/ ]decreased erections. The father admitted using a testos-8 I: R! i7 s8 j. l# o% s8 r
terone gel, which he concealed at first visit. He was
! m6 A0 V/ K( I; jusing it rather frequently, twice a day. The Physicians’: g9 t5 T9 x) ?; }8 u
Desk Reference, or package insert of this product, gel or& y$ ~# L% Z) u+ |
cream, cautions about dermal testosterone transfer to
2 d2 l9 D- M+ p& T9 m2 Y3 ?% Cunprotected females through direct skin exposure.
4 n; f0 `" s$ C9 [6 vSerum testosterone level was found to be 2 times the
. Y4 Z t0 w; K& G8 E8 F5 i/ Abaseline value in those females who were exposed to, W2 ^3 b1 k* V
even 15 minutes of direct skin contact with their male
8 q# R' Y# ~$ Cpartners.6 However, when a shirt covered the applica-
( P; z9 z7 `+ ption site, this testosterone transfer was prevented.
. r A+ y2 T) X- mOur patient’s testosterone level was 60 ng/mL,
* l# b2 R1 u5 T0 e/ ywhich was clearly high. Some studies suggest that: m9 g. U2 ~3 z6 K4 v
dermal conversion of testosterone to dihydrotestos-
3 t' E D$ h/ [. V- pterone, which is a more potent metabolite, is more$ [$ b4 \: ]3 D. m8 Z8 v# S
active in young children exposed to testosterone
/ Z" E6 O) N) V% F7 Pexogenously7; however, we did not measure a dihy-
# v$ ]0 M& u+ N \1 V8 Y4 jdrotestosterone level in our patient. In addition to- i6 r+ K% `: l5 w P, _( ]
virilization, exposure to exogenous testosterone in5 S+ @0 h& V; Q& U# Q6 _/ s
children results in an increase in growth velocity and8 _( C0 O% p+ |+ Z% j2 v: K( s
advanced bone age, as seen in our patient.
3 e& ~9 v" l3 y( {5 ]( s! XThe long-term effect of androgen exposure during
1 M! t7 P8 t& \3 ]* M. _" uearly childhood on pubertal development and final0 m! }. g+ L* N# _
adult height are not fully known and always remain9 ]$ V; Y2 [% u- _( }
a concern. Children treated with short-term testos-
1 _, e1 E' F1 A, l, Y1 _7 Nterone injection or topical androgen may exhibit some
- Y y, L" P( Y( h% S2 ^2 j9 \acceleration of the skeletal maturation; however, after+ ]3 x! P% h9 a p5 }( B" u2 A- F! p
cessation of treatment, the rate of bone maturation
- \# c4 M# R. n, ~- d4 mdecelerates and gradually returns to normal.8,9
- _9 w: O! n u; l' m1 Q; A# H1 z3 ~5 HThere are conflicting reports and controversy+ }9 l9 R, [. u4 t4 P
over the effect of early androgen exposure on adult
1 k0 U# h6 E4 v4 Ypenile length.10,11 Some reports suggest subnormal
6 J! m# ^$ A, h$ P5 G( n8 h g: f0 ~adult penile length, apparently because of downreg-8 L8 J! d1 f! D! T6 G
ulation of androgen receptor number.10,12 However,$ ?1 ~6 }3 ~2 P6 i9 {3 R6 W
Sutherland et al13 did not find a correlation between4 x: I( M& A4 ~. V6 ~( C0 d- I
childhood testosterone exposure and reduced adult
8 _0 d# p8 f! w% A# {3 w2 y% P1 m, ^penile length in clinical studies.
+ }1 ?* c$ D; Q6 V% f2 Z! o+ aNonetheless, we do not believe our patient is
- c0 X) d( [7 v1 Q2 B; k Zgoing to experience any of the untoward effects from
& F H! R# r3 q8 itestosterone exposure as mentioned earlier because7 P- b0 j% ~5 G
the exposure was not for a prolonged period of time.0 _) z& ~$ D) ?" I! e7 h
Although the bone age was advanced at the time of
! Q' }9 e9 c& S0 m7 ^1 Ydiagnosis, the child had a normal growth velocity at4 C1 Z2 j' G5 G; e( `/ k, b
the follow-up visit. It is hoped that his final adult
. b- T$ o; y# Uheight will not be affected.
" g4 A4 }* [' Y0 r. t& p" fAlthough rarely reported, the widespread avail-
- A" p H# E4 V0 Z" @3 ~ability of androgen products in our society may/ ?; |& n! f* i5 G5 ]
indeed cause more virilization in male or female0 f7 J# A6 Z; r8 m' @$ x
children than one would realize. Exposure to andro-" s% @3 M3 J& {1 g* F* B5 I
gen products must be considered and specific ques-
, P' E- O$ e' M0 Ktioning about the use of a testosterone product or
4 V- y; y1 T2 }4 L- Sgel should be asked of the family members during% M9 y# Q4 ?; \' t; ~2 L
the evaluation of any children who present with vir-6 K, e; V7 ~- [) ^6 a! Q r. Y
ilization or peripheral precocious puberty. The diag-
( A! o: ?& L7 L' p4 @: d. K& tnosis can be established by just a few tests and by3 C$ g( ~7 j0 U8 C& e
appropriate history. The inability to obtain such a
. p0 I5 \5 z9 Z) r6 Nhistory, or failure to ask the specific questions, may$ N* d8 c2 k7 k8 {0 @. T8 e- ~
result in extensive, unnecessary, and expensive
6 d A G/ o' F, ~investigation. The primary care physician should be; l) \' V% f {" ?6 Q7 c& P' J' M1 o
aware of this fact, because most of these children- r% e# N4 x6 w
may initially present in their practice. The Physicians’: D2 d' B5 A% G3 j& d
Desk Reference and package insert should also put a
2 P, E2 }( X, I6 i) n4 f5 swarning about the virilizing effect on a male or
* R- P1 B. l3 [. nfemale child who might come in contact with some-( ~: p2 S9 q) H% }7 v+ d l
one using any of these products.
, {7 c' R1 X0 d: m n) E/ }References1 H/ x! s* F! ~" l. E* j1 Y
1. Styne DM. The testes: disorder of sexual differentiation
# o: E; b3 b! `1 {and puberty in the male. In: Sperling MA, ed. Pediatric6 y5 A" J2 M- M7 z6 r D
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) W) n( W* L* e9 V! N. \ [ l
2002: 565-628.
/ _6 k" H6 z$ }( w2 M2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
5 N9 v1 g( o1 e# T0 l- A7 Cpuberty in children with tumours of the suprasellar pineal |
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