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Sexual Precocity in a 16-Month-Old# m& C T- O3 ~$ N6 t/ L! c: E
Boy Induced by Indirect Topical
3 s F: w8 \! Q. F; Y* ^Exposure to Testosterone
! {1 n+ c1 k t0 YSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& c2 H: S1 {8 B1 d# o
and Kenneth R. Rettig, MD16 e" h. B. q. k" @1 @) X0 C( B/ v
Clinical Pediatrics
! C1 O4 x. c7 \; q4 W& |Volume 46 Number 6
/ _: p, n! q5 y! FJuly 2007 540-543
% J' G# q. z2 U1 R: P© 2007 Sage Publications/ q9 ]3 `) y6 }: t& \
10.1177/00099228062966514 P/ V. C i3 B& p
http://clp.sagepub.com
# I7 _& B$ R% Vhosted at9 `. e, H/ l3 g: s% j
http://online.sagepub.com7 \9 b/ Q3 c. j1 z( l, `: I( {3 k
Precocious puberty in boys, central or peripheral,4 {0 ?/ q2 G8 h) U) v( E/ g
is a significant concern for physicians. Central/ T0 u. e; I! j# K! Q
precocious puberty (CPP), which is mediated
. E3 q4 o* E1 u# S! G# J2 othrough the hypothalamic pituitary gonadal axis, has. G" }" n# `; {* @% r
a higher incidence of organic central nervous system+ J% z1 |0 J8 [) C- m. o" i% j
lesions in boys.1,2 Virilization in boys, as manifested: d& D! ]# Z+ ^# v5 d0 A' q7 A S
by enlargement of the penis, development of pubic
( r3 a, h, _4 `9 w+ W/ x5 i. d* Thair, and facial acne without enlargement of testi-
' ^2 B Q5 a) _% I4 \0 `cles, suggests peripheral or pseudopuberty.1-3 We" I: c6 W" F( l4 j$ K! H5 \
report a 16-month-old boy who presented with the
u4 S# `/ w/ z) d# n2 Renlargement of the phallus and pubic hair develop-' t; N8 d5 B2 @) x. A+ U2 I' x
ment without testicular enlargement, which was due& T' l+ E/ I/ \8 ^" {. x4 H$ m$ w
to the unintentional exposure to androgen gel used by1 ?( k* o5 f5 t6 d5 q6 s+ y; w; n5 t
the father. The family initially concealed this infor- h4 w1 @9 C! z% F+ Q M/ ?& i
mation, resulting in an extensive work-up for this( S% ]) a! \9 k I8 F
child. Given the widespread and easy availability of
) ^! C( ^" A; ~$ t+ `3 ^: Htestosterone gel and cream, we believe this is proba-" d' V& }( x) r0 I! z3 T
bly more common than the rare case report in the
- ]9 p. X, P" p. Z, cliterature.4* c5 Y2 L6 E! e8 A
Patient Report
, r" D- M0 C% a$ GA 16-month-old white child was referred to the
' P; u: b+ I; e% x6 ~. w( z/ {. {endocrine clinic by his pediatrician with the concern
- V- m! e& R7 C+ E8 Fof early sexual development. His mother noticed. ^. l# t9 ~$ y9 m5 \
light colored pubic hair development when he was1 ^4 e* `5 [ N" b8 Q) @- W
From the 1Division of Pediatric Endocrinology, 2University of
4 g& p/ W. E& O$ r. }( YSouth Alabama Medical Center, Mobile, Alabama.
& g9 Q& ~6 ^( ^% T1 s' h/ B0 q2 qAddress correspondence to: Samar K. Bhowmick, MD, FACE, J6 j) \/ w% h1 D5 z
Professor of Pediatrics, University of South Alabama, College of
/ z: i" w* P/ I5 A) CMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& J1 a7 H5 |" K/ Z& Re-mail: [email protected].9 x R" B) @* s5 e# n& }: ?, L
about 6 to 7 months old, which progressively became
/ e' I9 ^ X' Cdarker. She was also concerned about the enlarge-$ y! W7 q' H1 U. n- d
ment of his penis and frequent erections. The child, r7 c( s6 X" ^! l% T& o7 W7 t& m
was the product of a full-term normal delivery, with
) U, o+ ~2 X7 x6 F" P, oa birth weight of 7 lb 14 oz, and birth length of
R/ E0 C% }9 k+ G7 z+ M, C20 inches. He was breast-fed throughout the first year& g+ i ~! E% J ?* K0 T; H! \
of life and was still receiving breast milk along with2 O# e$ [, H: m, ?5 Q. R/ A
solid food. He had no hospitalizations or surgery,
# Y- N- _* k) M# rand his psychosocial and psychomotor development
; v! P7 h& l% z0 x$ l( _' ]- Swas age appropriate.' h1 d+ y6 R* ]
The family history was remarkable for the father,
7 L7 T+ a7 ~! D4 E! q3 @who was diagnosed with hypothyroidism at age 16,6 c: \- C* ^* @ u3 ~7 v
which was treated with thyroxine. The father’s
& N* W2 K+ Y0 X* n$ Xheight was 6 feet, and he went through a somewhat9 O/ Z3 }9 ?1 l+ `
early puberty and had stopped growing by age 14.
* ]; Z9 P: y/ ?2 K6 o7 k0 NThe father denied taking any other medication. The
3 v' v) A4 ~! m" N& lchild’s mother was in good health. Her menarche& _# m; z P# g( s- N
was at 11 years of age, and her height was at 5 feet6 q# @ K! a* S" d7 @) d
5 inches. There was no other family history of pre-
% a# @& j4 V0 j8 \cocious sexual development in the first-degree rela-
) N) l5 }7 D: L" A; P1 ftives. There were no siblings.
# n# o% C. R5 X! J% A2 A6 P# RPhysical Examination
! ]4 O! I7 Q9 G, j q( t+ p! dThe physical examination revealed a very active,7 l) U8 W+ [5 c8 p+ h& h1 y2 R# U: ?' t
playful, and healthy boy. The vital signs documented8 {3 [; h6 l1 Z3 R; i& a' b' S
a blood pressure of 85/50 mm Hg, his length was
- X5 v8 J3 v& c# x% M90 cm (>97th percentile), and his weight was 14.4 kg
7 Q( @6 B# U, I& g+ G$ h1 q(also >97th percentile). The observed yearly growth
: i/ a9 d$ Z7 Tvelocity was 30 cm (12 inches). The examination of
" D: N' ~: c. kthe neck revealed no thyroid enlargement.
7 c, W8 f+ g7 s, e2 W4 eThe genitourinary examination was remarkable for
" g- M! b9 m/ b4 N; w menlargement of the penis, with a stretched length of
2 B4 N% d2 X" ]( t3 O3 f- Z1 S1 n8 cm and a width of 2 cm. The glans penis was very well
9 _, o/ a4 x' |5 B: ?5 [0 h& \developed. The pubic hair was Tanner II, mostly around
! {, X0 z* ~0 ~540
! x2 F* z) w6 d' K T/ jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" S x, ?# z& ~& Zthe base of the phallus and was dark and curled. The
# a; b# ]1 L4 G; o. M' B; Gtesticular volume was prepubertal at 2 mL each., P# J, ]/ p7 b) @
The skin was moist and smooth and somewhat
# h0 E% E7 c, o* B* Z. a( B p# R# Doily. No axillary hair was noted. There were no# d7 [' X! h- i F% R
abnormal skin pigmentations or café-au-lait spots.% \# n8 ], g# P6 g1 D
Neurologic evaluation showed deep tendon reflex 2+
7 p& _0 P& N- X3 l9 R, V& fbilateral and symmetrical. There was no suggestion
" K# `5 C& H1 t3 yof papilledema.. x( f3 _- S8 D$ p, T ?: I
Laboratory Evaluation
& c7 E& H' s% vThe bone age was consistent with 28 months by
t4 z# D3 W5 d r9 H5 X" Pusing the standard of Greulich and Pyle at a chrono-
; u9 d$ d/ V6 _. ?4 U5 M8 Alogic age of 16 months (advanced).5 Chromosomal) ^8 `% y+ f+ z* r$ ?
karyotype was 46XY. The thyroid function test `! w) B, T$ ^& ?/ |- _1 W
showed a free T4 of 1.69 ng/dL, and thyroid stimu-% U+ i1 L3 {, d2 K* _4 R
lating hormone level was 1.3 µIU/mL (both normal).
1 k* y" s6 j5 T$ ?- i' `& y1 K: qThe concentrations of serum electrolytes, blood
/ |& C, U* k3 @! N6 Surea nitrogen, creatinine, and calcium all were( ~6 l3 ]% B, ~* P8 Y0 _) E1 z
within normal range for his age. The concentration4 c% K; W6 j( u
of serum 17-hydroxyprogesterone was 16 ng/dL$ o$ [" c9 w& o4 `* ]* Q
(normal, 3 to 90 ng/dL), androstenedione was 20) H1 L+ W9 {$ c( p+ s! U- a
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
% @8 i4 o% V' P6 v7 ]# Dterone was 38 ng/dL (normal, 50 to 760 ng/dL),8 Q1 {7 m- h1 P& @0 \1 Y
desoxycorticosterone was 4.3 ng/dL (normal, 7 to" {4 E5 E- Z, ]
49ng/dL), 11-desoxycortisol (specific compound S)
8 X8 S; ^% ~( r1 `was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 w: X7 w# ~0 _/ ^* Q
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total( s6 n) `) w8 W* [0 x) O
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 ?: E: p# { {9 S) e6 `
and β-human chorionic gonadotropin was less than: S2 {$ l5 w1 [- L
5 mIU/mL (normal <5 mIU/mL). Serum follicular
+ S0 a% A3 ~; h) zstimulating hormone and leuteinizing hormone
+ M" n. K* M/ O: t; s6 Z5 w5 C' }concentrations were less than 0.05 mIU/mL
, [. b" I& p7 X s(prepubertal).( g: x9 n' f5 j5 m4 ~+ R- `; l& m
The parents were notified about the laboratory
0 ]8 n8 ^9 x" e4 lresults and were informed that all of the tests were# I. L, m v6 ]
normal except the testosterone level was high. The4 k8 |7 c& L+ _. |6 c! D7 }, E
follow-up visit was arranged within a few weeks to
% \. j' G& e: e" m% x8 H+ S( Aobtain testicular and abdominal sonograms; how-
7 Q1 r/ M8 N+ ~4 Bever, the family did not return for 4 months.# A3 s/ o! b$ \, q# c
Physical examination at this time revealed that the) ?+ E' M7 g5 |- c% r2 r. V
child had grown 2.5 cm in 4 months and had gained$ R- [/ L# w) Z' b, e
2 kg of weight. Physical examination remained2 Q5 B" g4 Z8 s# ^
unchanged. Surprisingly, the pubic hair almost com-! L1 q2 I. @2 ?1 u7 t
pletely disappeared except for a few vellous hairs at5 w# n0 t$ m7 j+ ]. L
the base of the phallus. Testicular volume was still 2
5 O, f. W# {8 ?, }9 XmL, and the size of the penis remained unchanged.
6 X& z% w% U Q4 Q& n5 |! _+ {6 _The mother also said that the boy was no longer hav-
# p7 D; e4 L1 z+ J. l" o1 f# Z1 _ing frequent erections.! K; }+ _' m c% u8 D, A
Both parents were again questioned about use of
& B0 o5 x# W( tany ointment/creams that they may have applied to
: C% b2 f; `2 [: B+ w( a$ C$ g1 |the child’s skin. This time the father admitted the
2 U& b6 p+ p- c6 ^; G, P5 _4 }$ dTopical Testosterone Exposure / Bhowmick et al 541
' p* c1 v* q* E7 h/ Suse of testosterone gel twice daily that he was apply-
- h5 \$ e+ q& `ing over his own shoulders, chest, and back area for9 A k0 }$ \1 g2 y5 e1 X
a year. The father also revealed he was embarrassed6 u9 j, B& b+ n" {- B8 ~) M
to disclose that he was using a testosterone gel pre-/ B8 k8 n) L# W
scribed by his family physician for decreased libido
9 D; `6 ]& A6 Z1 b' X8 Ysecondary to depression.
u- Y6 Z& T) X5 W$ L* g( aThe child slept in the same bed with parents.
# n3 f( W$ [" g! W* [The father would hug the baby and hold him on his
7 d# P2 L: j; P0 K! y9 Mchest for a considerable period of time, causing sig-. p) z6 E+ K. J- _' S
nificant bare skin contact between baby and father.
$ ~, Y7 H8 L, i! W7 C" vThe father also admitted that after the phone call,6 b3 h3 F: K0 D& T' o* H7 ~4 Y1 }
when he learned the testosterone level in the baby
9 _! ~3 U5 A9 c# pwas high, he then read the product information$ }- D1 ^9 o) @ t4 B
packet and concluded that it was most likely the rea-
+ a4 @& l+ l( N- Q% o$ ~son for the child’s virilization. At that time, they
4 Z |9 ]' c1 p; `decided to put the baby in a separate bed, and the' N+ d* G+ q9 Z" p
father was not hugging him with bare skin and had1 `4 h1 Y6 [ N2 |, ~' A/ o
been using protective clothing. A repeat testosterone
( ~1 {1 p' W7 `5 q* b+ T8 \test was ordered, but the family did not go to the
5 u9 s# A6 a) k( G6 Ulaboratory to obtain the test.2 {9 M4 F# Z5 V' d" n, g$ ?
Discussion
1 L& c0 S% L* X) m$ v/ `Precocious puberty in boys is defined as secondary
1 ]: X1 m( ?! R1 Dsexual development before 9 years of age.1,4) d$ z# J5 Q! i' [: Y
Precocious puberty is termed as central (true) when
# e9 e! T' M9 O( v+ K+ ^it is caused by the premature activation of hypo-
( b* N, c8 c5 q1 T2 Hthalamic pituitary gonadal axis. CPP is more com-
8 s* Y* b- W7 h% X1 G, Qmon in girls than in boys.1,3 Most boys with CPP( n1 h# \9 R9 d9 g$ y, W" u
may have a central nervous system lesion that is. b9 |1 f8 ?3 }% C
responsible for the early activation of the hypothal-
7 L5 a8 a1 a$ L8 X* S1 s; h: ]amic pituitary gonadal axis.1-3 Thus, greater empha-
8 j+ o* R* j4 t; \6 Asis has been given to neuroradiologic imaging in
$ I: i: d4 w! y3 x7 L5 [boys with precocious puberty. In addition to viril-
! |( f- p s0 j7 y' @ization, the clinical hallmark of CPP is the symmet-
7 C, ]# v5 p: Urical testicular growth secondary to stimulation by$ L% a0 r X5 P! t
gonadotropins.1,3
; o# }6 P& v: {5 \) l' U3 a% JGonadotropin-independent peripheral preco-" w" H1 Y( U8 T" i! m; X
cious puberty in boys also results from inappropriate
/ A7 b4 c0 ]% q s3 q0 q- E! z$ ?( ?androgenic stimulation from either endogenous or) q. r0 W$ t J( f* ?5 z
exogenous sources, nonpituitary gonadotropin stim-
7 L* J7 _5 x4 w# B( dulation, and rare activating mutations.3 Virilizing4 x8 _# X. j* z$ ~
congenital adrenal hyperplasia producing excessive# z* _4 \- Q9 V( Q" q" l
adrenal androgens is a common cause of precocious
e" P f1 x" S9 i# bpuberty in boys.3,4
: F6 L0 a# o; J/ ^/ Z6 oThe most common form of congenital adrenal
7 I: f6 J# W% P/ M( u2 Uhyperplasia is the 21-hydroxylase enzyme deficiency.
7 _) m* x% z' {+ p# G* ?: q- X0 {* N4 `The 11-β hydroxylase deficiency may also result in7 ?5 \# A7 w Q* r, y z8 b2 P
excessive adrenal androgen production, and rarely,4 U, A K! X4 u9 o5 P
an adrenal tumor may also cause adrenal androgen, f/ V2 d% e7 H+ H
excess.1,3
9 U) `' I' \: b, {/ |; @# j$ Tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 u$ m# K% X. {% ~* c' A/ |& U542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- C/ ?9 V0 H3 |4 XA unique entity of male-limited gonadotropin-# W! S1 u# \' o4 p. ~9 c
independent precocious puberty, which is also known; z9 J. k9 h: ], M. _2 t. K
as testotoxicosis, may cause precocious puberty at a
5 N; l+ O7 @7 ]# x$ P w! B4 hvery young age. The physical findings in these boys
0 C# m% b0 I1 Z. f- K$ Hwith this disorder are full pubertal development,
# V9 x# [0 e0 d# i) ^* Qincluding bilateral testicular growth, similar to boys: Y" S8 v8 E3 ^) |" ]
with CPP. The gonadotropin levels in this disorder8 N" l. r' n$ Y. W- s
are suppressed to prepubertal levels and do not show, Z$ l" n( `1 Z
pubertal response of gonadotropin after gonadotropin-& M- L+ P8 H* D$ o3 N
releasing hormone stimulation. This is a sex-linked
( m7 ^4 Y5 O/ y$ p5 t$ F/ i' |; @( ]' Bautosomal dominant disorder that affects only
7 `& V. {/ [# i/ lmales; therefore, other male members of the family
$ W( {' c( e3 M) {# L/ c( Y3 emay have similar precocious puberty.3, u) \$ Y; V6 J, A
In our patient, physical examination was incon-
+ G: K( r/ B r6 G2 v6 Xsistent with true precocious puberty since his testi-
- x2 S$ K/ i% s+ o/ o* e) v9 rcles were prepubertal in size. However, testotoxicosis
* Q4 J* U! e7 ~- y9 d6 [was in the differential diagnosis because his father. D9 w) f( k% X" h
started puberty somewhat early, and occasionally,
. p" g1 t3 O7 p6 [; gtesticular enlargement is not that evident in the8 s# V* {) d5 g- _9 ?
beginning of this process.1 In the absence of a neg-7 r+ a4 v4 W- L2 `
ative initial history of androgen exposure, our8 D6 ~1 A# _7 D/ o) F/ l5 q
biggest concern was virilizing adrenal hyperplasia,/ ~! B& G2 W1 `) B
either 21-hydroxylase deficiency or 11-β hydroxylase
1 F" R D' l5 T2 L0 q& `deficiency. Those diagnoses were excluded by find-
* Y/ |; d& v% c5 ?5 R% D$ Ming the normal level of adrenal steroids.
7 F$ @& u6 M. m$ E+ O3 @# M5 vThe diagnosis of exogenous androgens was strongly# ?0 t7 B! x* k. P
suspected in a follow-up visit after 4 months because! v6 z& j5 h2 q! t$ Q) T6 w0 e
the physical examination revealed the complete disap-
( V/ k, T5 `1 V7 Q% C4 Opearance of pubic hair, normal growth velocity, and& e8 @( A+ d% X- E5 b# ]0 R: O
decreased erections. The father admitted using a testos-
! V) o3 I) o% ~, Y' R5 }3 h/ |terone gel, which he concealed at first visit. He was
0 n2 I; w6 L+ E$ F* }: Musing it rather frequently, twice a day. The Physicians’6 L! f0 `& R7 `
Desk Reference, or package insert of this product, gel or
u+ C* R& D5 R2 Wcream, cautions about dermal testosterone transfer to8 q- M$ N. {1 M; N6 M
unprotected females through direct skin exposure.' X1 I" p3 j! b6 a+ T; P
Serum testosterone level was found to be 2 times the4 x( S' g! W+ f* e" Q
baseline value in those females who were exposed to/ U; ~9 b) t7 U/ n4 ?* R* c& {
even 15 minutes of direct skin contact with their male
}+ U9 {" O2 D/ ^& [; T" l& Mpartners.6 However, when a shirt covered the applica-
+ r0 ^7 A) ? c% W& }tion site, this testosterone transfer was prevented.0 b* r8 |: K0 E/ C+ X) _; t8 K
Our patient’s testosterone level was 60 ng/mL,
1 T: G! q, d ]2 p* N* }6 Bwhich was clearly high. Some studies suggest that9 m: v9 ?* b7 B% ^ o5 [5 H# H. z% I
dermal conversion of testosterone to dihydrotestos-3 e: M" q7 A+ q- {& L q! @
terone, which is a more potent metabolite, is more$ h/ j& \8 K7 n
active in young children exposed to testosterone
! h; _; ^7 l: T+ L! ^exogenously7; however, we did not measure a dihy-2 \$ q! x% \$ a. I
drotestosterone level in our patient. In addition to
" b, @9 a3 N) {: I+ ?# Dvirilization, exposure to exogenous testosterone in4 Z: t( E3 J7 I/ l0 |% w* f4 A7 y
children results in an increase in growth velocity and
$ I. W: C, @( E& |# f, S+ nadvanced bone age, as seen in our patient.
. O, j. e# x. H, B7 ]0 nThe long-term effect of androgen exposure during
& b( e' ^+ L* g- p) H, j5 _- `early childhood on pubertal development and final
5 M2 F. @. e) _2 n3 w2 r$ Aadult height are not fully known and always remain t* f2 m9 r+ ~' `, c
a concern. Children treated with short-term testos-
; o; i {# c& C, E: K- Aterone injection or topical androgen may exhibit some" N: Y$ ^( k( [! i0 h
acceleration of the skeletal maturation; however, after
2 ~* `+ Z3 p. q$ y+ p3 Ccessation of treatment, the rate of bone maturation
/ @5 E" @3 f. }% @7 j" Bdecelerates and gradually returns to normal.8,90 V/ e' S! i& g0 r
There are conflicting reports and controversy
! T; t& D2 m8 `) r# m7 x- iover the effect of early androgen exposure on adult
- |/ z ~! \: Rpenile length.10,11 Some reports suggest subnormal" w u( y/ Q" \: f) K
adult penile length, apparently because of downreg-
: f f0 }9 |. n: w) ?6 N" y( lulation of androgen receptor number.10,12 However,
8 L$ p \+ V8 f' ?6 c! [Sutherland et al13 did not find a correlation between. P* u: b+ G' x" N k0 a9 H. B
childhood testosterone exposure and reduced adult& z0 U& ]# y( @2 M2 p! o4 {; `
penile length in clinical studies./ M. i* A- t1 t; ` A6 x
Nonetheless, we do not believe our patient is( h! @' R4 i! m: k3 c
going to experience any of the untoward effects from
5 b1 F9 o0 Y' a9 J+ [testosterone exposure as mentioned earlier because4 b6 L! w5 t5 x+ ~ Q% w
the exposure was not for a prolonged period of time.
q. p3 T n$ V2 K: ?Although the bone age was advanced at the time of
2 w) p1 A3 o) x4 U1 y ndiagnosis, the child had a normal growth velocity at4 t. s, Y: b: ?7 }+ K
the follow-up visit. It is hoped that his final adult
; s! o8 M& Q; ^+ f7 vheight will not be affected.
4 ^ P0 x5 H* d+ ?3 k8 A5 y6 _Although rarely reported, the widespread avail-% ^8 j; G' q; R# _# B
ability of androgen products in our society may
; M4 j( Q$ m7 c# ^1 I' Iindeed cause more virilization in male or female
' F( P$ o: f, z. q0 echildren than one would realize. Exposure to andro-
[$ z2 d- I* b( h8 wgen products must be considered and specific ques-4 ~$ y6 S3 x0 P4 m" A# m! x
tioning about the use of a testosterone product or
# R4 m* F5 ?- ggel should be asked of the family members during
) p! R3 X( R3 D( G7 T9 [the evaluation of any children who present with vir-( D1 n) R; C; z- x ^4 \
ilization or peripheral precocious puberty. The diag-* ?) W5 w0 _3 H0 O' C
nosis can be established by just a few tests and by, T* d. M' Q' \& i M X. `2 p
appropriate history. The inability to obtain such a% _) ]5 I& S. M9 {0 n* U3 Z y
history, or failure to ask the specific questions, may
& j6 ]$ c; u0 y {; i# iresult in extensive, unnecessary, and expensive9 i/ ^; \2 H) E9 u
investigation. The primary care physician should be t1 G. ?3 M" [- u- s
aware of this fact, because most of these children
) L' O# u# r0 N) l$ {- x3 d) I5 R6 Zmay initially present in their practice. The Physicians’
' f, t- Y! D" T4 GDesk Reference and package insert should also put a6 l" r5 D3 {6 I# v; O0 Z2 {
warning about the virilizing effect on a male or, D' b% w9 U4 @2 ?
female child who might come in contact with some-5 ^2 I- R. y+ {, ]4 x
one using any of these products.0 l; M( g! f$ G) K
References; b3 u8 s9 N/ g: B% R
1. Styne DM. The testes: disorder of sexual differentiation2 D; E' P- b4 h* L0 {$ d
and puberty in the male. In: Sperling MA, ed. Pediatric
: q4 j* V1 G) ^8 F: AEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) _) D2 O: y# r$ k# F
2002: 565-628.6 r) m/ d6 a2 N. f8 `5 b
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 A; f: @, N+ s6 Y" y- S% W9 o5 Q+ dpuberty in children with tumours of the suprasellar pineal |
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