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Sexual Precocity in a 16-Month-Old
0 S# o" m3 B5 q1 B; k4 FBoy Induced by Indirect Topical
$ S! x: |* {3 M1 T z5 Z3 HExposure to Testosterone' t( x! r' x8 {: R: v5 k6 L
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. \4 p% @8 d/ N" z# N
and Kenneth R. Rettig, MD1! Q2 q7 `& C3 G$ O5 f I+ X
Clinical Pediatrics
+ q& c: ?, K2 E9 l+ F+ G6 J1 ^1 HVolume 46 Number 6
, H/ S7 E8 k8 V' fJuly 2007 540-543$ F0 N3 n9 \, S. z" ]8 S
© 2007 Sage Publications
# y3 s! k; u& _/ q2 g( q- b10.1177/0009922806296651
+ }8 [& E3 R' J2 h1 H9 \http://clp.sagepub.com1 V9 A- r% _$ z9 K% L' N& ^8 M( X
hosted at5 z9 Z; W* d( v
http://online.sagepub.com3 c* T2 V8 h2 X
Precocious puberty in boys, central or peripheral,
& d1 N2 E) |5 i2 Gis a significant concern for physicians. Central
, C/ _! J8 \! ?2 kprecocious puberty (CPP), which is mediated1 t- p G. w! A7 ` f
through the hypothalamic pituitary gonadal axis, has4 X5 p' C# \6 w! E% }5 Z. j2 W
a higher incidence of organic central nervous system# u3 t3 `* n7 i! ~: b2 D1 T
lesions in boys.1,2 Virilization in boys, as manifested1 f* W, N0 W8 }1 [
by enlargement of the penis, development of pubic
5 }; g" v8 A; p( }hair, and facial acne without enlargement of testi-1 X4 r( u0 O: Y' L% C! h" ~; f
cles, suggests peripheral or pseudopuberty.1-3 We" ^6 z6 V! K' _; Q! j
report a 16-month-old boy who presented with the" B0 C c# R _2 p$ Z* A& ~
enlargement of the phallus and pubic hair develop- T6 |: s5 ]- Q/ J4 K. c
ment without testicular enlargement, which was due+ ~( D0 f$ m: o* y- r; ?
to the unintentional exposure to androgen gel used by
, N; ?, p0 P) S1 d+ e6 tthe father. The family initially concealed this infor-2 O" Z1 G% z. r. F s/ x$ \( x
mation, resulting in an extensive work-up for this9 R4 a4 m, k5 a/ K6 M. G6 C+ f
child. Given the widespread and easy availability of
: w- I- a* H* N5 }. |" G6 R/ \testosterone gel and cream, we believe this is proba-; m' @8 C5 T f5 G$ Y" J: U8 M, E
bly more common than the rare case report in the
8 |. L% o3 A" Z% Uliterature.4; N" _7 j- x7 [) n9 a3 g2 g
Patient Report
: h$ e% w( v: \/ C" R$ x3 Y" PA 16-month-old white child was referred to the- L: e; ~+ V3 b x$ V; n" c
endocrine clinic by his pediatrician with the concern
: [+ Y: W% `/ @- S& w; _of early sexual development. His mother noticed( z& s% s& ]( n/ W7 j& S
light colored pubic hair development when he was
) p# M! b, Q+ o! V" ^From the 1Division of Pediatric Endocrinology, 2University of
! ~+ y7 { O1 Q' RSouth Alabama Medical Center, Mobile, Alabama.7 U# [5 y% b* c6 Q& Y( S/ d
Address correspondence to: Samar K. Bhowmick, MD, FACE,
4 J6 w# D; W, ~. _' SProfessor of Pediatrics, University of South Alabama, College of. m4 R% x. u4 J5 ]/ Z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) M4 {+ [' {; z, T
e-mail: [email protected].2 ~2 M+ x) A j6 A
about 6 to 7 months old, which progressively became" U3 X' N8 x5 ^5 @ M7 e/ M
darker. She was also concerned about the enlarge-' J' c; u- P# v4 X5 E' k, [" k
ment of his penis and frequent erections. The child
2 b( c. z. M0 b8 [was the product of a full-term normal delivery, with
' P4 V4 d# H7 S: N i; Va birth weight of 7 lb 14 oz, and birth length of) L- Y3 J& w' F* M1 A
20 inches. He was breast-fed throughout the first year3 r* i; a# Q* V) p+ }' G
of life and was still receiving breast milk along with
# T0 K; _! G: Jsolid food. He had no hospitalizations or surgery,1 f$ P% g1 a: \( R- w: I4 S: r: o
and his psychosocial and psychomotor development
) G! j7 l" K6 L9 _was age appropriate.
M9 h5 R5 z7 O& ^% i. K3 ]The family history was remarkable for the father,
2 n9 e4 T! G4 d, H" P o7 m y0 Wwho was diagnosed with hypothyroidism at age 16,
- Y+ {' R* [4 \! G; [which was treated with thyroxine. The father’s6 c3 v( p- v; n# N0 |, g
height was 6 feet, and he went through a somewhat
# G- V" _) D0 h' ]8 i, Fearly puberty and had stopped growing by age 14.# _3 _3 m7 o* O. t5 G$ k( D
The father denied taking any other medication. The$ t+ B& J, [9 ~$ v' N" `5 P
child’s mother was in good health. Her menarche
. @0 x" Q* l6 ?1 A( |: _; ], R$ uwas at 11 years of age, and her height was at 5 feet
$ B b9 X- N) U* O+ T3 I6 O5 inches. There was no other family history of pre-" h# v8 [! c3 Z9 q) o
cocious sexual development in the first-degree rela-
, h- v8 [/ C8 J, h* b Jtives. There were no siblings.1 ]% j. j9 R! y0 f' M/ r
Physical Examination# Z$ [2 v* s) {- @) c
The physical examination revealed a very active,
+ m% o( g! \* @1 Y9 l0 j% iplayful, and healthy boy. The vital signs documented
: D% D- _( a7 j' P: F4 va blood pressure of 85/50 mm Hg, his length was
! k0 u% u: T6 L! R/ v( t3 d90 cm (>97th percentile), and his weight was 14.4 kg, ~/ I, M" O+ o% @
(also >97th percentile). The observed yearly growth% J3 D1 L" b: i9 w; c1 Z
velocity was 30 cm (12 inches). The examination of
2 V1 N) W0 _3 V! I8 E: U( Uthe neck revealed no thyroid enlargement.
6 ^, ?3 j8 u* i# J0 A. M& B$ U, wThe genitourinary examination was remarkable for
; v z. Q, `" h; I& Aenlargement of the penis, with a stretched length of! F' u# E# y( P
8 cm and a width of 2 cm. The glans penis was very well1 |) t8 L5 }- N1 Z" w# Z5 o J" m
developed. The pubic hair was Tanner II, mostly around2 E1 n' B& Y$ S3 ?* c0 E
540
8 D* Z. e5 s/ K. ?0 N6 u! uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) s% u' g) n! T5 L e0 `the base of the phallus and was dark and curled. The$ h3 Z7 D" d7 H. C+ _8 ~* @
testicular volume was prepubertal at 2 mL each.
9 I4 n R0 T$ W2 hThe skin was moist and smooth and somewhat
2 q' x6 `) `! P( M) o- h3 ooily. No axillary hair was noted. There were no, q8 t7 ?8 k6 ?, @2 U# D) J
abnormal skin pigmentations or café-au-lait spots.
( k+ \( P; ?; ]4 H% aNeurologic evaluation showed deep tendon reflex 2+% F, y i. T, _( w5 ^) b
bilateral and symmetrical. There was no suggestion ^; ]/ U# {5 `% x/ K9 S
of papilledema.
; t* t! W( A6 G Y$ n) ]Laboratory Evaluation2 K! D% G1 j* j( A5 J3 w* U, M& n' @
The bone age was consistent with 28 months by
: a% i! ~* A9 ?7 zusing the standard of Greulich and Pyle at a chrono-# h$ L& a6 H' W: Y$ n5 R
logic age of 16 months (advanced).5 Chromosomal
% e0 k, ?$ S" F2 t. Rkaryotype was 46XY. The thyroid function test
' Q, q: b0 q5 ?4 ushowed a free T4 of 1.69 ng/dL, and thyroid stimu-
# O( w' I3 c( `/ ylating hormone level was 1.3 µIU/mL (both normal).5 G- V9 v6 ]9 ^/ y' O( C: U# H7 H
The concentrations of serum electrolytes, blood8 w, X- E! T. W9 s6 P$ Q2 x# k' I
urea nitrogen, creatinine, and calcium all were
3 I0 u! a# B; p Rwithin normal range for his age. The concentration
5 \2 I; T2 M6 X9 i' W7 [of serum 17-hydroxyprogesterone was 16 ng/dL) [+ p0 n) d5 S; N- {6 z
(normal, 3 to 90 ng/dL), androstenedione was 20
: c! j* G0 D0 M4 ~ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 ]* L( G$ _- Y% |, jterone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 l( B( N% d. Edesoxycorticosterone was 4.3 ng/dL (normal, 7 to- G5 {1 F( h0 k* c% t, F0 p" q2 f& U
49ng/dL), 11-desoxycortisol (specific compound S); B' J6 r8 A% [6 }+ W* @" u$ }
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* G( M/ G3 X! L9 B& \& qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total n- x! K! @6 D3 v8 Y7 K
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( M- z. l8 V$ y7 ?: u1 v
and β-human chorionic gonadotropin was less than
4 y( @8 Q0 u2 g) B$ O5 mIU/mL (normal <5 mIU/mL). Serum follicular
) N! C( V1 }- U: s( |: N4 \: Gstimulating hormone and leuteinizing hormone
- O& i. W/ | M5 Pconcentrations were less than 0.05 mIU/mL/ l* h+ z) c6 s/ l# Y% `( n
(prepubertal).
/ e8 h' f8 P( D$ h% JThe parents were notified about the laboratory
, H) h' ^, ]1 lresults and were informed that all of the tests were
$ T0 ~6 C. I5 [- D" i1 b5 \normal except the testosterone level was high. The4 ^ t, {4 R$ I2 C" D; X* [
follow-up visit was arranged within a few weeks to$ i8 k, F7 @8 Z( D$ H
obtain testicular and abdominal sonograms; how-
( _7 e8 Y6 X% ]9 C6 A7 `9 \6 Tever, the family did not return for 4 months.
% {% \5 q( U( l/ [' R, v# PPhysical examination at this time revealed that the
% R" s/ j$ c9 k4 ?! Z" R* S+ qchild had grown 2.5 cm in 4 months and had gained# R" V: Y$ |# s& B7 h9 }
2 kg of weight. Physical examination remained: a# K) e4 k: p
unchanged. Surprisingly, the pubic hair almost com-* J9 J: W! z6 P& o
pletely disappeared except for a few vellous hairs at
1 V, Q/ i: Q$ mthe base of the phallus. Testicular volume was still 2
7 i, B& I( Z4 F/ a [" VmL, and the size of the penis remained unchanged.
: [* V4 \3 p: C H& s. A; SThe mother also said that the boy was no longer hav-" R: U' [- Z, G3 M& m6 ?4 R
ing frequent erections.
" X- M* ^0 u. HBoth parents were again questioned about use of
" k2 M6 \6 S6 b- Q9 n- y S, O5 Eany ointment/creams that they may have applied to
" h* z) Y3 O8 ~( t( C- x9 xthe child’s skin. This time the father admitted the
9 B# \. \- z+ _6 ^4 D( T4 dTopical Testosterone Exposure / Bhowmick et al 541
' R3 c) A8 g9 x5 B9 {1 B5 U2 buse of testosterone gel twice daily that he was apply-% j- A4 N4 t' v1 K' {2 @
ing over his own shoulders, chest, and back area for
( y3 b5 o0 Y$ c/ U" ~) V; ~% G. J Na year. The father also revealed he was embarrassed
* m8 i) e& y. P% W- h6 nto disclose that he was using a testosterone gel pre-. X. {/ e" W9 Q% i
scribed by his family physician for decreased libido
# ]# \8 S1 l. Csecondary to depression.) Y" b, T. j! i1 l: @' Y5 k
The child slept in the same bed with parents.* k3 y& l7 C! V& M$ h( K3 a
The father would hug the baby and hold him on his7 Z9 S C$ w9 ?- M% ]1 T* J8 a
chest for a considerable period of time, causing sig-/ u% v4 N' J+ a" I3 I: D
nificant bare skin contact between baby and father./ m+ r7 @6 E! c
The father also admitted that after the phone call,' [) `3 P) ?' i9 o m
when he learned the testosterone level in the baby$ a5 Q& U J% F
was high, he then read the product information8 s# s( C5 r1 O. J e& s6 y5 Z, @
packet and concluded that it was most likely the rea-( t y- J! ?) z/ r
son for the child’s virilization. At that time, they
9 {7 O) J" O* Z2 C5 V' I" T/ ], Udecided to put the baby in a separate bed, and the6 R$ t0 u( f& F0 y4 t
father was not hugging him with bare skin and had; X; x* e a3 d5 c
been using protective clothing. A repeat testosterone
! S& k" W0 u- \$ F7 v* etest was ordered, but the family did not go to the4 f- ?- g" b1 Y: I& Q2 u/ }6 w
laboratory to obtain the test.
' H: i* B( A/ U4 _ p! bDiscussion
! t" u9 C9 F* t z3 h$ Y! gPrecocious puberty in boys is defined as secondary; \/ X; H+ }; V6 \
sexual development before 9 years of age.1,4
8 f1 M3 P6 N* |9 W% lPrecocious puberty is termed as central (true) when% z8 Y& b* h% d
it is caused by the premature activation of hypo-, r# u# z/ e7 J, r F, M1 R/ p
thalamic pituitary gonadal axis. CPP is more com-, {2 K0 I1 H- C) Q/ m1 `7 L
mon in girls than in boys.1,3 Most boys with CPP
/ ?& C% O3 E! V( q# u: k. rmay have a central nervous system lesion that is# B) c8 i9 o; z; e9 e. j* D
responsible for the early activation of the hypothal-
( P* E! G* J5 e' uamic pituitary gonadal axis.1-3 Thus, greater empha-, B0 |+ B+ l& v0 X
sis has been given to neuroradiologic imaging in) p5 b) W' N* Q" g" ^ I
boys with precocious puberty. In addition to viril-$ G ~# w" ]1 V5 L' x
ization, the clinical hallmark of CPP is the symmet-
& W3 P( E4 ^4 ^- G' zrical testicular growth secondary to stimulation by" `6 j7 K/ X8 H# d( |6 ]
gonadotropins.1,33 k" A* d9 [5 v, [% m
Gonadotropin-independent peripheral preco-
4 u! {( c& i4 ]! a* q4 y/ Ccious puberty in boys also results from inappropriate
2 |6 J1 A; U9 k8 Dandrogenic stimulation from either endogenous or# L% y, R3 c) W+ F, j. P7 B
exogenous sources, nonpituitary gonadotropin stim-/ f! N+ g* F+ _2 @ Q$ B
ulation, and rare activating mutations.3 Virilizing
& p: E! b3 [2 l$ M& j' ~congenital adrenal hyperplasia producing excessive7 l" c A% ~8 A" d! E) |4 e% K
adrenal androgens is a common cause of precocious) J% O. u6 X8 ?) x
puberty in boys.3,4
! Z) E% _ t& h9 TThe most common form of congenital adrenal
! G+ I' Y9 T, B9 d9 P" {: Dhyperplasia is the 21-hydroxylase enzyme deficiency." S _5 v6 r% J! Q" F+ R
The 11-β hydroxylase deficiency may also result in
( r2 O# N9 }" y7 H: ?excessive adrenal androgen production, and rarely, e+ I# g) X5 n1 v6 g
an adrenal tumor may also cause adrenal androgen* j9 s, x+ A8 ^
excess.1,3$ q% o( y8 f% _# l$ A2 D
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' R0 T. ]% I* K: O
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 p3 O, h+ [1 w) i# P2 `: P) [A unique entity of male-limited gonadotropin-* l) V5 {4 _4 m* A: ]
independent precocious puberty, which is also known8 r2 l2 K; ~8 S
as testotoxicosis, may cause precocious puberty at a
8 r( J2 U7 N3 u' Z! B ivery young age. The physical findings in these boys& i. ~; o2 a; a( I
with this disorder are full pubertal development,
9 h5 Q. P5 U6 ]0 a2 {3 y; yincluding bilateral testicular growth, similar to boys$ G9 d# G! `' @9 y3 s( ^
with CPP. The gonadotropin levels in this disorder+ H) n2 o6 P1 e' B2 ^9 Z4 k2 k/ h
are suppressed to prepubertal levels and do not show
7 ]# F+ c/ P5 v6 l9 d' ?# Zpubertal response of gonadotropin after gonadotropin-
% t$ t9 ?5 Q& H3 breleasing hormone stimulation. This is a sex-linked
4 S7 D1 x4 V! O, a2 \) \* _autosomal dominant disorder that affects only
: C, c5 m5 ?7 Y) q: O. Ymales; therefore, other male members of the family A$ C4 _: z2 k& f0 p
may have similar precocious puberty.3: a3 L& g3 I9 m" |7 e* ~$ V
In our patient, physical examination was incon-
! |* O+ S; J. I# [4 @4 C& d' Ksistent with true precocious puberty since his testi-
( V6 b8 z2 r0 Gcles were prepubertal in size. However, testotoxicosis# ~* f4 \ r7 O8 q9 T9 x
was in the differential diagnosis because his father
# P0 g# Q& E5 _$ [6 _started puberty somewhat early, and occasionally,2 ]2 w/ g9 O0 r
testicular enlargement is not that evident in the! f6 G' o3 f# Y7 [& Q! b
beginning of this process.1 In the absence of a neg-
- r1 ~8 F6 Q- A) J/ Z6 u, \3 G. Jative initial history of androgen exposure, our+ b6 A9 T9 R4 Q4 s a3 H) k" S. E1 k
biggest concern was virilizing adrenal hyperplasia,
6 S, ]0 }8 B$ M% h ]7 Heither 21-hydroxylase deficiency or 11-β hydroxylase$ s2 F% c e4 ~+ e- r6 m! _
deficiency. Those diagnoses were excluded by find-
9 Y6 j: _$ x: R8 m) King the normal level of adrenal steroids.
2 x% Q9 U& h( F9 D1 l3 Y9 ^The diagnosis of exogenous androgens was strongly
: y) u5 ]8 M4 @& i4 @suspected in a follow-up visit after 4 months because
6 O' n o7 ]5 othe physical examination revealed the complete disap-
* W/ f5 E: x# t# x( O' qpearance of pubic hair, normal growth velocity, and
1 i4 v0 y" A9 i1 r( q4 U4 O' B: [decreased erections. The father admitted using a testos-$ W9 n0 v L% ^6 q s' y8 k9 A7 s
terone gel, which he concealed at first visit. He was1 Z- E; Q# K+ R' K$ @; Y
using it rather frequently, twice a day. The Physicians’
( e& v+ m8 E5 h* w* QDesk Reference, or package insert of this product, gel or
~. G+ z5 b u$ }2 h. u, Hcream, cautions about dermal testosterone transfer to) s/ b/ Q0 x( v" D* X2 y
unprotected females through direct skin exposure.
" K1 ]* G4 n4 @$ B* q- Y/ K7 iSerum testosterone level was found to be 2 times the
) u' j" K1 V# D% c: e4 Cbaseline value in those females who were exposed to
2 U+ [2 B" F- p2 f" Weven 15 minutes of direct skin contact with their male
& \* f' I' w8 A* ?; ~' mpartners.6 However, when a shirt covered the applica-9 e8 `3 t7 S* k+ p I
tion site, this testosterone transfer was prevented.
6 ~* U3 V9 ?2 ~) \) xOur patient’s testosterone level was 60 ng/mL,1 y& b5 _* V' J! T/ ~
which was clearly high. Some studies suggest that
0 W3 G2 {4 B0 Adermal conversion of testosterone to dihydrotestos-
/ `$ j+ y d/ G: r: p6 pterone, which is a more potent metabolite, is more
- m' V1 w* O5 m$ h& z$ J8 Dactive in young children exposed to testosterone5 b; U- W W! p# o! w+ g
exogenously7; however, we did not measure a dihy-
2 G; D/ l# Q& k, f& U" |2 }1 ndrotestosterone level in our patient. In addition to3 j7 S3 R( T6 ^
virilization, exposure to exogenous testosterone in
% I9 A7 q% c2 Z! y% tchildren results in an increase in growth velocity and
+ w% I& `/ A7 I. Uadvanced bone age, as seen in our patient.
& k4 D3 d( }8 ]9 b# m9 z4 cThe long-term effect of androgen exposure during& c/ o/ V. Q6 O6 n- E, u
early childhood on pubertal development and final
% R) o) Z5 i1 q. s1 _adult height are not fully known and always remain
+ y2 [( v+ g6 wa concern. Children treated with short-term testos-
% c! M# `- i# h* l+ X3 u4 ^terone injection or topical androgen may exhibit some
7 A% d0 ^7 v1 o) U* ?acceleration of the skeletal maturation; however, after
/ g/ @9 X1 g J+ ?0 Qcessation of treatment, the rate of bone maturation
. M# g1 x: `0 J8 X7 P, F; Y2 M- {decelerates and gradually returns to normal.8,9
, K( Z e5 `& ^6 w fThere are conflicting reports and controversy, H" M) h/ ]$ W4 e, m
over the effect of early androgen exposure on adult3 o5 P% B( R+ {6 T
penile length.10,11 Some reports suggest subnormal
! E; x9 Y/ n6 @. U! Sadult penile length, apparently because of downreg-
* K) P f7 I' B' V/ Iulation of androgen receptor number.10,12 However,9 D; I9 N. }* W9 z r, n
Sutherland et al13 did not find a correlation between+ V& P I5 t' S# t4 ]- q
childhood testosterone exposure and reduced adult, m3 H( X% b' Y
penile length in clinical studies.
- r3 ]; E. Y# F0 V, sNonetheless, we do not believe our patient is
- f$ t9 x2 w: B* Pgoing to experience any of the untoward effects from
6 @% t0 t% O W' K) e2 Z" W( E4 J2 `testosterone exposure as mentioned earlier because
/ l7 n/ |. W$ h+ cthe exposure was not for a prolonged period of time." m+ v; ?5 r0 e ~1 }; q
Although the bone age was advanced at the time of5 K& l, D% M' r# z" u& L) C
diagnosis, the child had a normal growth velocity at
3 V0 i# v1 N. X# C0 pthe follow-up visit. It is hoped that his final adult
, @2 _8 \, [7 Cheight will not be affected.
8 E& X3 J$ v# ]/ cAlthough rarely reported, the widespread avail-
. ?) ~) d" ~ b) Bability of androgen products in our society may
7 v* y$ v& C# U5 Yindeed cause more virilization in male or female8 J) e7 x+ P; a
children than one would realize. Exposure to andro-
+ j" v1 I0 ~/ |( B7 g& wgen products must be considered and specific ques-% K; Y" o# P- L" h1 n
tioning about the use of a testosterone product or S. [" h5 |) R! a7 j8 H0 z" j0 a
gel should be asked of the family members during1 j0 T; [" X0 F
the evaluation of any children who present with vir-
2 J" ]; Y0 {: W* F6 y3 d8 pilization or peripheral precocious puberty. The diag-& |. |( c, Y) ~& q1 P/ R
nosis can be established by just a few tests and by2 I# k6 A/ x2 R5 X3 h k2 W$ p
appropriate history. The inability to obtain such a( n3 N* F! e& Y+ I2 R7 |0 P3 p% ?
history, or failure to ask the specific questions, may
- _" Z9 {( ?1 S9 J1 W) r# @result in extensive, unnecessary, and expensive5 ?2 l5 W- \# {% ~6 P
investigation. The primary care physician should be
- |( t7 O6 x$ J6 ?% _6 J& w! g4 Qaware of this fact, because most of these children! j8 N- L6 s# z* k8 k6 i I
may initially present in their practice. The Physicians’
/ N/ [3 G1 u" ^Desk Reference and package insert should also put a
& d D6 P/ C* `warning about the virilizing effect on a male or1 e8 t" s) g3 L2 p/ K; g
female child who might come in contact with some-6 ~# S; J3 ~7 k
one using any of these products.
q- h g* d9 ]/ H" o' v3 Q- g& {References
- E/ z4 f. _+ S4 L; o% q1. Styne DM. The testes: disorder of sexual differentiation
2 v- N( E# R0 K9 g/ \! hand puberty in the male. In: Sperling MA, ed. Pediatric g0 ]- y8 Y) R7 I) o1 {8 I+ n
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;% h3 H4 N+ n! g' G- V0 Q
2002: 565-628.
2 H; U+ s% q* v& b" V+ D' Y' d% N& Z2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( q7 U/ f, x) J% a7 ]# gpuberty in children with tumours of the suprasellar pineal |
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