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Sexual Precocity in a 16-Month-Old) _5 U: ^) w9 }! \2 P5 a( R
Boy Induced by Indirect Topical
7 R4 t+ F. x% z5 W3 e. mExposure to Testosterone5 g' x/ _( Q6 e, p' ^
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 k8 a! L" r3 S0 I8 v# h& \: R6 n8 m8 {and Kenneth R. Rettig, MD1
& H* D6 u+ x6 _; }* H+ Y! o" IClinical Pediatrics- k2 y0 v7 j; ? I2 c
Volume 46 Number 6
8 b$ L- K" w; `3 T( RJuly 2007 540-543
2 T. q! v1 }+ J( `9 d% [$ q© 2007 Sage Publications
# g5 p3 J, E. q$ i$ H8 ~/ \: I10.1177/00099228062966518 d% o5 {/ j. j- Q
http://clp.sagepub.com
$ \. F' o; Z7 `+ E0 w) U; n' ?# G% w. Ehosted at/ t( b0 _/ I+ d; r& J1 g4 J( ~
http://online.sagepub.com
; r7 S; {+ E5 }! ^: kPrecocious puberty in boys, central or peripheral,
. O0 g' M+ s) m& M9 |is a significant concern for physicians. Central
- Z/ J, d6 q" v. Q! b* sprecocious puberty (CPP), which is mediated+ B( B3 r Z0 q# x; L8 Y, {# R3 d& r
through the hypothalamic pituitary gonadal axis, has2 z: R5 b2 x& t
a higher incidence of organic central nervous system9 x% p2 {, h s E3 C0 a
lesions in boys.1,2 Virilization in boys, as manifested
p) s: S' s4 W7 i! j" n6 dby enlargement of the penis, development of pubic
' j' H. I9 C9 Y8 q7 u1 Ghair, and facial acne without enlargement of testi-
3 V( r. ]# [( r1 Lcles, suggests peripheral or pseudopuberty.1-3 We
. ^( ]7 U7 r1 L, A( Vreport a 16-month-old boy who presented with the
1 i+ J1 G7 ^! U' nenlargement of the phallus and pubic hair develop-8 W, N& H9 n X/ i: ]9 y
ment without testicular enlargement, which was due
5 k4 U9 `! L) sto the unintentional exposure to androgen gel used by! F# j' M- m( u' C
the father. The family initially concealed this infor-5 J) g. N8 O( M1 _; J/ i0 Q5 s7 a) H
mation, resulting in an extensive work-up for this
" n, f' V) C) I1 r* \child. Given the widespread and easy availability of
8 a" M1 E3 J! T/ K( rtestosterone gel and cream, we believe this is proba-8 Z7 r! L$ C$ M2 O0 y, F
bly more common than the rare case report in the7 j3 A# H) ~) N2 |! W& j
literature.49 z' l7 R, V: b4 p5 i# |6 L
Patient Report$ u6 N; _: {% k
A 16-month-old white child was referred to the7 a! [0 q. b3 H7 X, O$ C
endocrine clinic by his pediatrician with the concern7 @& \, \& N$ d4 d6 D; M
of early sexual development. His mother noticed
* V* ~$ m# |* x+ ~; K4 Nlight colored pubic hair development when he was+ I$ C5 i2 U6 L8 ~8 Y
From the 1Division of Pediatric Endocrinology, 2University of3 j. S& u' O& Y# k
South Alabama Medical Center, Mobile, Alabama.! M6 j; q) ] H r& N' Q4 y
Address correspondence to: Samar K. Bhowmick, MD, FACE,* C/ \$ X! |0 p& g
Professor of Pediatrics, University of South Alabama, College of
% T2 d: e1 m6 ]1 U0 D; b0 t( Z! oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& t" ]; S" b. Y% n$ ]" ~1 ^e-mail: [email protected].4 ~8 o( R& v, l$ g: @+ q, O* O
about 6 to 7 months old, which progressively became
3 P6 a# A" P$ i. cdarker. She was also concerned about the enlarge-
5 w4 ?; ~# `% y5 k( w2 `ment of his penis and frequent erections. The child) }+ R: c9 S% L' Y- i% a- j
was the product of a full-term normal delivery, with7 E8 l* Y+ w. `/ W J0 s
a birth weight of 7 lb 14 oz, and birth length of
% d7 }$ ~, J+ D) S20 inches. He was breast-fed throughout the first year
, @0 Q5 W) y5 tof life and was still receiving breast milk along with
1 C) f; A1 ]3 S! isolid food. He had no hospitalizations or surgery,
S: A" z& q6 T2 L' ~4 ^and his psychosocial and psychomotor development
- [! |; @% x# c, ~# \3 e& c6 p3 ^was age appropriate.
' M- x& D5 {" eThe family history was remarkable for the father,
* k' _. M- \6 _7 |who was diagnosed with hypothyroidism at age 16,
- A2 B1 q: M) E1 V7 W( R6 j2 Dwhich was treated with thyroxine. The father’s
" w i2 w F7 N1 ]7 ?0 I& fheight was 6 feet, and he went through a somewhat; P1 L5 ^ D! Q7 m6 f4 e
early puberty and had stopped growing by age 14.
" ~6 ^: ~; {* N6 I DThe father denied taking any other medication. The
$ D7 a! \. h1 _1 A0 [2 S9 e$ Zchild’s mother was in good health. Her menarche; V7 X: m! e# g& w' f# O$ x
was at 11 years of age, and her height was at 5 feet) s) ^& E4 R9 X6 K h1 O3 U
5 inches. There was no other family history of pre-4 v& c$ ^" Q3 o \4 H/ |0 K/ `
cocious sexual development in the first-degree rela-
3 S3 w% Z- I4 M: C' W4 Etives. There were no siblings.: h" S' \8 J4 \; R% h' ^4 r* J
Physical Examination9 O; m) U2 N" Z0 G6 [" ~
The physical examination revealed a very active,
$ Y2 q1 ~7 h, Tplayful, and healthy boy. The vital signs documented
2 \2 b! q1 O, W9 Ca blood pressure of 85/50 mm Hg, his length was* y$ K1 J1 b) J4 u! r0 a0 i# B
90 cm (>97th percentile), and his weight was 14.4 kg
6 X/ ?' a& X k# A2 q6 P' v; n: b$ G(also >97th percentile). The observed yearly growth6 `) Z; _+ y% _; C% }6 `& k
velocity was 30 cm (12 inches). The examination of* Y4 _! C# y' m' z- q
the neck revealed no thyroid enlargement.( O& p' Y0 ^5 Y( B& Q7 A
The genitourinary examination was remarkable for
( Z: g& ?" E* z, ]' [ \7 M2 @enlargement of the penis, with a stretched length of
( B! M+ r5 G# P# J% z3 m, v8 cm and a width of 2 cm. The glans penis was very well# Q6 h' `" I% u _3 A; Y
developed. The pubic hair was Tanner II, mostly around
3 w7 {; w f6 Z2 i2 V# z' O/ A540
/ p8 Z; D+ [7 o7 m( N1 ^4 j* {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( q' F* Y1 ~8 D9 x7 k7 othe base of the phallus and was dark and curled. The( l% X" r& u, j c$ ^) r( n
testicular volume was prepubertal at 2 mL each.
! p6 \* O# l( x* I' P5 BThe skin was moist and smooth and somewhat F# w3 S# T' V3 L
oily. No axillary hair was noted. There were no
1 g% {" I) E. ^5 |- d2 W8 D; iabnormal skin pigmentations or café-au-lait spots.) V. v' U7 b0 e
Neurologic evaluation showed deep tendon reflex 2+
' ~, A) U/ Q5 M% {. Q% Lbilateral and symmetrical. There was no suggestion0 j) c: e5 d; A4 u7 r, X
of papilledema.( ~6 g: m) g% j# R. ]. b: m2 ~
Laboratory Evaluation+ J0 k* F( R. v2 z" Z! _& m
The bone age was consistent with 28 months by
% h' H2 V0 g! Tusing the standard of Greulich and Pyle at a chrono-+ p2 Q( Y7 w9 i) J& p
logic age of 16 months (advanced).5 Chromosomal+ @. W% R2 v- H* J# H
karyotype was 46XY. The thyroid function test
* O3 @# U! u$ K1 c# x$ ^4 d9 W* U) Yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-. i( X& `& E& ^7 ~
lating hormone level was 1.3 µIU/mL (both normal).
: e8 e8 J; V& D1 X7 F- nThe concentrations of serum electrolytes, blood# u% n0 m+ }. s1 C
urea nitrogen, creatinine, and calcium all were0 A& ~( R# [' J
within normal range for his age. The concentration! q8 g( u; J1 W/ d- |' [& _8 d6 D
of serum 17-hydroxyprogesterone was 16 ng/dL6 w. D- A4 y; G# S. g
(normal, 3 to 90 ng/dL), androstenedione was 20; W: d+ o0 x, D8 e% }
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( n2 K( ?" T! [* o9 gterone was 38 ng/dL (normal, 50 to 760 ng/dL),
' _7 N( H, g, b2 c7 i* Kdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ M% U+ {$ X V" u49ng/dL), 11-desoxycortisol (specific compound S)1 R# O/ k; g; I( E: x8 V
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: y+ K ^, z! M# B& Btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 C! c3 t- U& E3 o7 ttestosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 E2 O- o5 l& T. `
and β-human chorionic gonadotropin was less than
) a- I9 v& ]/ G8 m! k9 u5 mIU/mL (normal <5 mIU/mL). Serum follicular
! y4 o0 D# p+ nstimulating hormone and leuteinizing hormone
- C% E P6 y$ S+ |. nconcentrations were less than 0.05 mIU/mL
. b$ K' f" N/ x- E* x(prepubertal).( _; w5 p/ C! M( r' S
The parents were notified about the laboratory( G; V7 l! w5 b1 P: O& M
results and were informed that all of the tests were# ]$ e* W3 i6 w2 ~
normal except the testosterone level was high. The: R0 ^' r. Y @% r5 ]
follow-up visit was arranged within a few weeks to
+ i; R; J I3 s& |8 ?obtain testicular and abdominal sonograms; how-
# ]8 a, V5 u& f( ]1 pever, the family did not return for 4 months.
# s# O# F! m3 V$ I: DPhysical examination at this time revealed that the* Q8 A. [, e. N) ?1 n! G, G/ L5 s
child had grown 2.5 cm in 4 months and had gained
- z# w: `/ C" y% K0 _2 N: B/ [3 ^2 kg of weight. Physical examination remained+ M* c6 _6 \, s+ Z) d' Z: {5 m
unchanged. Surprisingly, the pubic hair almost com-
: ]1 G' Y8 E/ n- U1 \2 Q& K/ lpletely disappeared except for a few vellous hairs at
3 V0 W+ m+ B: s& |. r9 v1 Y( M) n. j# Bthe base of the phallus. Testicular volume was still 2: _7 e. [3 L. d" B+ J w
mL, and the size of the penis remained unchanged.
7 o. ]( W8 k; W4 D1 N' GThe mother also said that the boy was no longer hav-
f5 f6 |6 k' I" q) F0 Uing frequent erections.
7 `( t# f! q; i6 Y) C1 P& kBoth parents were again questioned about use of
! H6 W% V- q( z k- Rany ointment/creams that they may have applied to" M; B5 v9 _$ e* J
the child’s skin. This time the father admitted the
9 q' o) W0 G: oTopical Testosterone Exposure / Bhowmick et al 541( Q1 M: [- }. ^6 | O! Z$ t
use of testosterone gel twice daily that he was apply-
/ b& k! i% W9 D: M! a! S6 ging over his own shoulders, chest, and back area for( s$ A; k# i; Z/ \' }: i
a year. The father also revealed he was embarrassed) I& J# X+ e! R( b5 L
to disclose that he was using a testosterone gel pre-
. y4 t9 H! w2 @0 }scribed by his family physician for decreased libido3 _( ^4 E. Z1 }9 n3 B' R' _: S
secondary to depression.4 c- [# x: S9 ^1 ~; Y, x* g3 @' P& y
The child slept in the same bed with parents. _0 w) M" R0 v: d# ]
The father would hug the baby and hold him on his
- O: E. @7 b+ J- ?3 S, r3 E- L5 rchest for a considerable period of time, causing sig-; Q$ g2 m9 C% }5 I
nificant bare skin contact between baby and father.
. y& |. A2 \4 E J& l) ?The father also admitted that after the phone call,& v/ ~+ I; E- k9 c2 _/ m/ j. A
when he learned the testosterone level in the baby
4 D8 i+ I Z7 L" z$ Dwas high, he then read the product information
* L' c- m! `6 M* k* Jpacket and concluded that it was most likely the rea-2 u" @! }% d4 r* D! f C
son for the child’s virilization. At that time, they
8 E. R4 U; |: X' ~1 Ndecided to put the baby in a separate bed, and the/ ^8 ]( p& \1 ~; V' I
father was not hugging him with bare skin and had
* W% B. c# Y- N, P: ?0 Ybeen using protective clothing. A repeat testosterone
# F$ V( s0 G- V- S8 m+ etest was ordered, but the family did not go to the; n& d* s! m1 n9 C0 C0 X( F! F
laboratory to obtain the test.# J& z ]) h4 d2 ^) @2 t
Discussion# X. q( g! h7 y. {4 U9 v
Precocious puberty in boys is defined as secondary
# M( `/ L6 [" D) ~4 i% e' A0 v# A$ Osexual development before 9 years of age.1,4' M* r: t5 A. z1 R9 x
Precocious puberty is termed as central (true) when9 S# N# {! R4 A' T/ E
it is caused by the premature activation of hypo-
4 s. ?! O; d8 u0 l9 bthalamic pituitary gonadal axis. CPP is more com-* T8 y1 K1 f+ d4 w) [" u
mon in girls than in boys.1,3 Most boys with CPP7 J2 M& c7 j0 [4 f7 ]
may have a central nervous system lesion that is
% R: |; Q' K4 A3 ?) g; C% H9 e% hresponsible for the early activation of the hypothal-
# Z! ~, u8 K i& P U! A$ Lamic pituitary gonadal axis.1-3 Thus, greater empha-
1 W2 p& b4 V9 x- z1 w: Gsis has been given to neuroradiologic imaging in
0 e) ~" h2 J6 aboys with precocious puberty. In addition to viril-* x. B5 K6 ^" \/ d( B9 ~- ~, T
ization, the clinical hallmark of CPP is the symmet-
0 Z, H* i) ]8 c' p r5 C# srical testicular growth secondary to stimulation by
4 @0 \' W l5 Q e2 A( D1 h0 Igonadotropins.1,3# \* C! }& d+ G& s4 S. L4 |: B( ~
Gonadotropin-independent peripheral preco-$ J7 q! C' j8 F0 I% A+ P3 u
cious puberty in boys also results from inappropriate
5 p- z3 E1 z& q4 o3 mandrogenic stimulation from either endogenous or# G* n! Q# s3 f
exogenous sources, nonpituitary gonadotropin stim- H! ]- l, ?* v! J1 T
ulation, and rare activating mutations.3 Virilizing; G- v; \ ]# p& G% I+ C. ~' _1 g
congenital adrenal hyperplasia producing excessive& G! `2 U' T. U
adrenal androgens is a common cause of precocious
: f n5 t; m* v1 }- S3 [" i. }puberty in boys.3,4
( w% W9 | X5 q9 n: j8 bThe most common form of congenital adrenal
; o* Z: O: x D3 f8 [7 _1 ?0 {) Z' ~hyperplasia is the 21-hydroxylase enzyme deficiency.* z% D; y' H5 ~6 e# a0 O# u
The 11-β hydroxylase deficiency may also result in7 o* @) Q& ^0 N' {5 V* a0 H& Z6 U
excessive adrenal androgen production, and rarely,
2 r0 [5 I/ u% ~& S3 f3 Nan adrenal tumor may also cause adrenal androgen
% i5 o/ ~* d, d% b5 g2 Aexcess.1,3! | d0 A4 L. ~. Q( U
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from q8 F- Q h8 E
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 t+ p' P0 _7 j9 Q4 `( e, [A unique entity of male-limited gonadotropin- l$ g6 w* ` @# J9 S: o4 P1 Z
independent precocious puberty, which is also known! J0 z, t0 |; m6 U/ m( c+ o
as testotoxicosis, may cause precocious puberty at a7 T5 q' y: ~) `3 j: B. S' U: Y& n
very young age. The physical findings in these boys
( u, q5 d1 m( ]# u# Qwith this disorder are full pubertal development,
% V1 G- h. ` K5 b l& e) tincluding bilateral testicular growth, similar to boys( S( @! D4 w2 J/ U
with CPP. The gonadotropin levels in this disorder- K. \7 Q+ e2 K. V
are suppressed to prepubertal levels and do not show# {: \0 S; A1 t* [+ ]- h1 c9 X7 G: J
pubertal response of gonadotropin after gonadotropin-
- Y! W9 K/ B0 _6 P8 h4 yreleasing hormone stimulation. This is a sex-linked% B$ M* o" w( B4 D: S+ X6 s& W8 R H9 _
autosomal dominant disorder that affects only% S! w H6 U- ^! P% D% Q( ^" p3 \
males; therefore, other male members of the family
0 l( ^" ?$ Z5 \7 _8 z* F1 ~ omay have similar precocious puberty.3
3 G# _; ]6 ~. V6 _: _+ qIn our patient, physical examination was incon-& y$ a+ v. z/ E( o+ d
sistent with true precocious puberty since his testi-, Q/ f4 s7 u) u7 k4 m% w. l' r
cles were prepubertal in size. However, testotoxicosis
- F. r. `$ `5 p+ ]) M: A Owas in the differential diagnosis because his father" y' a" f7 h2 _: Q' x' A: f( j
started puberty somewhat early, and occasionally,
+ G! U* E `8 c3 Ltesticular enlargement is not that evident in the
- \1 s# ?& H7 C& e# j: v) q {beginning of this process.1 In the absence of a neg-2 }) I: i, f# s- O4 N, u
ative initial history of androgen exposure, our
# \' {: h* {% o, kbiggest concern was virilizing adrenal hyperplasia,
$ [; x- d/ X1 C: ?either 21-hydroxylase deficiency or 11-β hydroxylase
! }: C; Z$ _$ f% @; ^deficiency. Those diagnoses were excluded by find-
2 E6 {6 _7 J" ning the normal level of adrenal steroids.# p0 Z# ]# S* A* S5 L' x& P9 ?/ ^+ U
The diagnosis of exogenous androgens was strongly3 g5 `) y9 `2 Q, w s
suspected in a follow-up visit after 4 months because
* z. {1 h% r( |5 X# athe physical examination revealed the complete disap-
, H. S, p E, Y1 g, Gpearance of pubic hair, normal growth velocity, and- M2 `. b+ U6 V) i
decreased erections. The father admitted using a testos-+ a! @0 p& a8 T5 h5 ~1 X' X4 O
terone gel, which he concealed at first visit. He was1 L4 B( l6 O2 i3 P# f
using it rather frequently, twice a day. The Physicians’( l# n. ?- @2 Z& X! U" X8 L, G
Desk Reference, or package insert of this product, gel or! O! B# y8 c m* s2 I( v! q
cream, cautions about dermal testosterone transfer to
! f8 K4 v. t( _4 J6 [7 b) vunprotected females through direct skin exposure.
+ ]& v" p5 A( d, c4 {% s7 h3 MSerum testosterone level was found to be 2 times the) D5 R! j$ D; U7 @3 o u9 b- D
baseline value in those females who were exposed to
n/ ]8 j9 R( W8 ^even 15 minutes of direct skin contact with their male7 l" p" x |# l0 Z& V" k
partners.6 However, when a shirt covered the applica-
! X& P% A ^4 A! u1 z( Otion site, this testosterone transfer was prevented.; r) c+ f$ \5 I9 ]3 K: [1 O9 K3 H( Q
Our patient’s testosterone level was 60 ng/mL,
6 G& D) y4 O; fwhich was clearly high. Some studies suggest that
; e* i! m5 _' b/ t6 A. }: [( `% Tdermal conversion of testosterone to dihydrotestos-
( |6 h- y. m$ ]+ F: P5 Q' M' p! p- Pterone, which is a more potent metabolite, is more) t9 }- Y4 M( ^* B/ k; C- P
active in young children exposed to testosterone
3 v9 x* o; t* m& @1 Y$ U' dexogenously7; however, we did not measure a dihy-; v/ H. [" |' ^- R9 i; E
drotestosterone level in our patient. In addition to9 i& }% ~$ i7 Z; \: N
virilization, exposure to exogenous testosterone in# n6 `5 F6 s: { I
children results in an increase in growth velocity and
; z v5 w* d/ Y. ~advanced bone age, as seen in our patient., b3 ^, u5 p" D) E) D
The long-term effect of androgen exposure during
- D& o! [. K3 C( X& Oearly childhood on pubertal development and final
$ u/ A$ b3 D: _$ u5 a9 badult height are not fully known and always remain
% N- z4 u: k+ Aa concern. Children treated with short-term testos-
7 Y2 V/ y% @! m$ r3 \terone injection or topical androgen may exhibit some
, v( f" C& `1 x* m- j" facceleration of the skeletal maturation; however, after! f- y, M) N- k$ n; C# v- M
cessation of treatment, the rate of bone maturation- |1 J' |0 r6 A9 w* Y& N: r( j
decelerates and gradually returns to normal.8,9
|! {+ k1 N) nThere are conflicting reports and controversy
- J1 ^0 q7 k# R5 |* ~2 ?over the effect of early androgen exposure on adult
0 n: Y1 X8 z& B9 P5 i0 n8 Ipenile length.10,11 Some reports suggest subnormal* d' T) ?. Y5 q3 q$ j, V7 i, u
adult penile length, apparently because of downreg-
5 Y% M# Q) s$ W% z1 e2 S) e8 ~+ Dulation of androgen receptor number.10,12 However,; W3 N) F7 r4 b j8 v$ k$ _
Sutherland et al13 did not find a correlation between
# M- E7 f& n* c$ t$ ~4 rchildhood testosterone exposure and reduced adult
5 _2 M& U. q2 ^penile length in clinical studies.% i0 h6 S6 s; b) u2 S1 Q
Nonetheless, we do not believe our patient is
- d! {% m( e$ y& Agoing to experience any of the untoward effects from
V- n# M8 {8 i' btestosterone exposure as mentioned earlier because$ b2 w9 D+ J, Y# e
the exposure was not for a prolonged period of time.
' S3 v+ Q3 \7 }* P" tAlthough the bone age was advanced at the time of
0 i7 ?" E/ n, H+ k; p1 ~ ^diagnosis, the child had a normal growth velocity at
( ~7 O- \% i( ~/ n7 ?* v: Bthe follow-up visit. It is hoped that his final adult0 U5 G: e( s, A
height will not be affected.
- M' K4 c2 _% ~2 t4 p0 {Although rarely reported, the widespread avail-
- z2 ]/ {3 Y6 J7 D# v9 W1 ^7 r, hability of androgen products in our society may
0 Y1 w' }$ N$ L% xindeed cause more virilization in male or female
' q1 M. l. ]! G8 D$ D3 a8 n; w2 Zchildren than one would realize. Exposure to andro-) I* {* z5 Y3 ~9 N& i
gen products must be considered and specific ques-
: Q+ u3 g3 X& F* i" e" F6 htioning about the use of a testosterone product or' _3 n& Z3 i6 s! S* u R
gel should be asked of the family members during) X- W6 C* z6 v( V& X# g0 h, s
the evaluation of any children who present with vir-) C/ F, V/ C7 i
ilization or peripheral precocious puberty. The diag-
3 @, o. S6 U* fnosis can be established by just a few tests and by: d7 j# X1 K, v' X
appropriate history. The inability to obtain such a; M- R7 T# A( X& \
history, or failure to ask the specific questions, may0 a1 Z! D+ p* h& v
result in extensive, unnecessary, and expensive
) J5 Q7 g8 P; c; E9 V( B4 Binvestigation. The primary care physician should be
( T5 ^/ W7 s5 ?( q8 ]6 Caware of this fact, because most of these children- {* V1 O& K! d1 S: p7 X6 G/ B
may initially present in their practice. The Physicians’2 c! s' M1 \4 o
Desk Reference and package insert should also put a
, D& s. G3 A( Y- @3 O8 hwarning about the virilizing effect on a male or
0 D, ^, x2 `1 n7 v7 ufemale child who might come in contact with some-: I: R7 P6 W& M y1 a
one using any of these products.! m5 |* x/ q8 L3 w- V
References2 v% |& n+ W) d+ y
1. Styne DM. The testes: disorder of sexual differentiation9 J5 s1 o: z" |0 L
and puberty in the male. In: Sperling MA, ed. Pediatric
4 v* M5 V3 `; ]. l4 }Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: X! ]& g0 k5 L! s
2002: 565-628.
8 `) Z0 J% q7 H' \! i" w2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% h3 c, j7 b8 K! `2 K
puberty in children with tumours of the suprasellar pineal |
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