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Sexual Precocity in a 16-Month-Old
3 ]- u0 R7 Q+ w l- TBoy Induced by Indirect Topical; p! o2 l: ~ v+ I; Y
Exposure to Testosterone
. e5 o$ _ t# C1 eSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% f, f) ]9 `4 A1 U
and Kenneth R. Rettig, MD1- v5 P, J7 z7 }; x, d
Clinical Pediatrics/ V+ c8 G2 X# d) E( e `
Volume 46 Number 68 K! }6 S8 @! Y; b- c/ _# z
July 2007 540-543% t2 p' e6 b2 c( \3 Q3 X
© 2007 Sage Publications0 d3 T' g# [+ j3 R7 e, Q; C! G( |
10.1177/0009922806296651
# M7 |0 d: R9 Y4 o! o- _http://clp.sagepub.com
, {8 f1 m" a$ ^4 h% Fhosted at
( a9 m4 g+ a! F- i: Qhttp://online.sagepub.com" |. X0 c, M, C1 n
Precocious puberty in boys, central or peripheral,, R: L+ k# N5 U3 S$ J
is a significant concern for physicians. Central8 o9 O6 x7 F8 D2 s$ \( h7 c& R
precocious puberty (CPP), which is mediated
9 O* ^( m I# M4 H" [) c0 xthrough the hypothalamic pituitary gonadal axis, has
. d# `. `% r* [4 Q8 P( Q6 ya higher incidence of organic central nervous system
) J3 g- M' E7 hlesions in boys.1,2 Virilization in boys, as manifested: \5 q, W7 \$ q
by enlargement of the penis, development of pubic
7 w. r4 r6 V/ }! p1 Uhair, and facial acne without enlargement of testi-4 [8 a3 l2 y" _
cles, suggests peripheral or pseudopuberty.1-3 We" Y% l; p% U% |2 H7 Z
report a 16-month-old boy who presented with the- J w8 u9 w# _% D
enlargement of the phallus and pubic hair develop-1 N8 a' R# r8 z: I" c
ment without testicular enlargement, which was due
B1 K+ l2 s8 l" u' b2 Sto the unintentional exposure to androgen gel used by3 m, d M C3 o4 y* l, g9 Y% [: \
the father. The family initially concealed this infor-$ G% T/ n. w4 d' L2 B& p
mation, resulting in an extensive work-up for this1 E% b9 J- ]. f
child. Given the widespread and easy availability of5 |$ B M8 _# @. q% O
testosterone gel and cream, we believe this is proba-
* b3 M2 G0 C) ~; Bbly more common than the rare case report in the' s& r% e/ A7 D: q; x
literature.4
0 l+ | E6 i$ q8 G( A8 v/ EPatient Report
0 c* V/ K @1 ~+ O7 p5 \( L+ E2 e. fA 16-month-old white child was referred to the( x+ `* `( q9 A( ^! l: P
endocrine clinic by his pediatrician with the concern
0 `% k, z+ L& g8 r8 M9 S: T }of early sexual development. His mother noticed, b+ L/ H8 x. b2 ^: W
light colored pubic hair development when he was
6 ^" p: t" A. q9 O8 J( e! y$ x" _# mFrom the 1Division of Pediatric Endocrinology, 2University of
4 U" v" V8 ~( V# C" F3 n2 u% NSouth Alabama Medical Center, Mobile, Alabama.5 x! }" z. q" p6 ]/ y7 T2 |( ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,7 l/ h1 p$ N: ~2 o. \$ S' d+ j
Professor of Pediatrics, University of South Alabama, College of
1 y2 V. F5 J1 j% EMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ \+ f7 k5 a. \" N I( ge-mail: [email protected]., T7 D' V$ M1 ^0 J: ]
about 6 to 7 months old, which progressively became
9 b/ Y/ I+ \- n" e6 C# Edarker. She was also concerned about the enlarge-. B% O) W6 ^$ Z a" {8 b) b
ment of his penis and frequent erections. The child# E6 R3 }5 W3 U+ A4 s
was the product of a full-term normal delivery, with5 D: W# ]# c) d% A% S3 H4 V. Z6 ]
a birth weight of 7 lb 14 oz, and birth length of
, x$ ?4 I( Z. U# K20 inches. He was breast-fed throughout the first year
+ D3 ^& i+ V0 @of life and was still receiving breast milk along with0 d3 c2 G- @' y ?
solid food. He had no hospitalizations or surgery,
, e/ j2 [ O( i% A: o% ^and his psychosocial and psychomotor development' D+ B6 a4 i" e! V6 c, f- x
was age appropriate.
! ] w) K- a @' G; |: o2 H+ VThe family history was remarkable for the father,2 y' \1 b, Z2 j4 f+ q2 r2 y+ \
who was diagnosed with hypothyroidism at age 16,/ u! `+ R* P! \% f9 k( [
which was treated with thyroxine. The father’s
% G& Q7 f' b, Yheight was 6 feet, and he went through a somewhat: ~. t3 A( p3 t( L
early puberty and had stopped growing by age 14.
7 C6 }( N1 V# c2 _$ B( ?! aThe father denied taking any other medication. The- ^* h1 u# x0 x7 D* q. Y
child’s mother was in good health. Her menarche
4 n) B V5 K: i- W; Jwas at 11 years of age, and her height was at 5 feet
u0 P# M; L8 ^& X7 c+ w' e5 inches. There was no other family history of pre-; U6 l! T1 S$ h+ i5 P% T
cocious sexual development in the first-degree rela-
1 l' g4 w' m. `tives. There were no siblings.
( |1 `. F9 c) W% F* D9 o! \Physical Examination
" T# X+ E2 E) N. `The physical examination revealed a very active,
6 e) k% }2 h$ z9 k' iplayful, and healthy boy. The vital signs documented
4 K8 x3 s) ]8 `3 G% oa blood pressure of 85/50 mm Hg, his length was: I3 T* B0 F8 u# R/ H
90 cm (>97th percentile), and his weight was 14.4 kg
! G6 F4 ]* H" O; |2 p( Q6 [- C. E8 \(also >97th percentile). The observed yearly growth( m! V4 b' \3 W% `$ d/ i; i
velocity was 30 cm (12 inches). The examination of s, a! u' E9 Q# k: T9 ~- v2 Z& A
the neck revealed no thyroid enlargement.
% c# i6 [! S, w) \3 zThe genitourinary examination was remarkable for
2 x# F, e, ~7 l n& [3 S. ienlargement of the penis, with a stretched length of3 W) T9 L0 p5 R% j# [. l
8 cm and a width of 2 cm. The glans penis was very well5 x, k# Z0 N* }8 O
developed. The pubic hair was Tanner II, mostly around. `8 Q$ @* x9 E; J
540- H8 T9 X2 }1 l" i7 s! E/ Z0 o3 e
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: U4 a4 F! c8 e; Z( [5 P
the base of the phallus and was dark and curled. The
8 I" x* G H; [ Ttesticular volume was prepubertal at 2 mL each.
P% L# @5 \' g$ D0 W3 \3 E- WThe skin was moist and smooth and somewhat
% T' \+ W( D5 G( m. L8 {( j9 P' ?2 Ooily. No axillary hair was noted. There were no
/ \ N9 N }8 C# H- ^" G& Uabnormal skin pigmentations or café-au-lait spots.3 J1 y. a+ c, a/ H$ R4 a# g( j
Neurologic evaluation showed deep tendon reflex 2+" I- s, L- |; t, r$ N
bilateral and symmetrical. There was no suggestion" e# o8 N7 x) q9 y% ~
of papilledema.$ c- Z2 I }6 G" i9 R. l
Laboratory Evaluation
7 o! B) o1 Y2 `* e! |1 g8 D1 cThe bone age was consistent with 28 months by
. F! ] h* i' K& d9 eusing the standard of Greulich and Pyle at a chrono-
, w3 t9 e9 p. Y' H8 K9 E# P l4 Glogic age of 16 months (advanced).5 Chromosomal/ k4 X* Q: b" I0 ^& o9 I) E8 L
karyotype was 46XY. The thyroid function test; c1 U6 N5 Z$ u9 x; y, y) q& L
showed a free T4 of 1.69 ng/dL, and thyroid stimu-2 d) m; R, R5 e1 G% B4 h$ m. c6 i, _
lating hormone level was 1.3 µIU/mL (both normal).. V( q5 Q, o+ K2 i& x( S3 z
The concentrations of serum electrolytes, blood; f5 K( D+ ^* M. }: L9 G# x1 k
urea nitrogen, creatinine, and calcium all were$ r3 @4 t$ E, d7 e
within normal range for his age. The concentration
, E. O K) T' Z* {! T: Oof serum 17-hydroxyprogesterone was 16 ng/dL4 c G; a# Z3 U" g. L
(normal, 3 to 90 ng/dL), androstenedione was 20
: }9 c8 d% p6 I* k, W; c- Dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 `" e- M7 f! ]& L1 k) b
terone was 38 ng/dL (normal, 50 to 760 ng/dL),' z" P3 `5 `4 G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to* j N5 g: I+ y5 v+ }2 k5 Q) {% B5 y
49ng/dL), 11-desoxycortisol (specific compound S)
2 X& S6 f9 H. P8 |4 Y2 |. owas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, t0 o* ~) {+ G+ `+ S
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( Q2 V- ^- \7 o6 U, n( A' j7 t" qtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),- r5 O8 x9 }# p# w/ I
and β-human chorionic gonadotropin was less than
( H/ D0 B# h: V5 mIU/mL (normal <5 mIU/mL). Serum follicular" u% P: e. m: X2 s' U
stimulating hormone and leuteinizing hormone
: N' a* W, C$ J$ }( w' |concentrations were less than 0.05 mIU/mL- V7 {4 s9 U! b/ \
(prepubertal).
5 {: n- O" v; D- z, f, I8 ?5 jThe parents were notified about the laboratory, ~2 F' q' d& H2 l. ]3 }' w; L
results and were informed that all of the tests were/ o; c& }. \7 S+ F# G
normal except the testosterone level was high. The
3 A/ B1 L# F+ z& g6 \' R; }* Zfollow-up visit was arranged within a few weeks to$ \! `: J; X/ J- c9 k* A7 E
obtain testicular and abdominal sonograms; how-* z6 m: b2 m: S: J$ v# r7 [) P
ever, the family did not return for 4 months.3 F8 j% f8 b2 R9 U5 E1 E
Physical examination at this time revealed that the
5 [+ L( w; e6 j5 u( I" G; pchild had grown 2.5 cm in 4 months and had gained8 h& d! T1 U3 `3 e
2 kg of weight. Physical examination remained
$ d7 C4 `- A8 U/ |- Cunchanged. Surprisingly, the pubic hair almost com-
0 j. }6 D- k- c8 p& Jpletely disappeared except for a few vellous hairs at
/ ]- b8 l: ^1 \& Wthe base of the phallus. Testicular volume was still 2
. {1 \/ ?, r% M0 S3 `: w0 _: NmL, and the size of the penis remained unchanged.
7 ^5 K9 e. H' u% q% J$ W1 z, U1 y" T5 }The mother also said that the boy was no longer hav-
" ^7 ^8 M- ]. g: B, Aing frequent erections.7 ? \& \& F& E9 ~
Both parents were again questioned about use of( v+ U6 x1 q6 s- i9 T* C0 B
any ointment/creams that they may have applied to- M& G r( }/ [9 W& n+ f
the child’s skin. This time the father admitted the+ e+ m4 k, _8 P' R6 Z" _5 _$ ?
Topical Testosterone Exposure / Bhowmick et al 541
9 X h6 {: I3 R; e+ D& a# z& `use of testosterone gel twice daily that he was apply-3 `2 j! y) F9 V5 S4 \: J+ U" b, H
ing over his own shoulders, chest, and back area for
+ _0 o, [! n& fa year. The father also revealed he was embarrassed
% K6 t, V$ K3 n* S9 T& N) _to disclose that he was using a testosterone gel pre-6 a# r' @0 z& E# v) v/ G" o
scribed by his family physician for decreased libido
2 v! a/ z7 K) D" r- _( [1 bsecondary to depression.
3 `, D ^& [9 W; NThe child slept in the same bed with parents." a1 O' h5 H2 b* p
The father would hug the baby and hold him on his5 }2 X, u8 J4 @6 U* Y
chest for a considerable period of time, causing sig-+ x2 k3 y- z6 W7 V
nificant bare skin contact between baby and father.
" |4 y' r w0 I6 h( H6 wThe father also admitted that after the phone call,
8 a( U9 r1 D# V% f3 Cwhen he learned the testosterone level in the baby
/ U$ d5 n" i2 B5 ]/ P& ?was high, he then read the product information
* [6 ?& I9 `" ~, c4 rpacket and concluded that it was most likely the rea-8 Q8 [) O+ ~9 t+ k2 @0 j. b
son for the child’s virilization. At that time, they
3 g4 M0 K4 y' O) \decided to put the baby in a separate bed, and the" |. `) N7 Z- {" \
father was not hugging him with bare skin and had; H. A: u" h+ l. ^7 J- ?
been using protective clothing. A repeat testosterone
9 Z; d2 E7 h0 xtest was ordered, but the family did not go to the% ^! y# a( P$ P
laboratory to obtain the test.# w% e$ u2 H) q) F8 k
Discussion% F* y$ Q1 A& @" y0 e
Precocious puberty in boys is defined as secondary. c) p% W* S& N/ @ G. T
sexual development before 9 years of age.1,4
% F1 |- D4 l" m3 e) W% F; {4 g$ S) TPrecocious puberty is termed as central (true) when$ W9 X1 B0 I1 E& h2 e' y
it is caused by the premature activation of hypo-
% z p0 P2 u! Gthalamic pituitary gonadal axis. CPP is more com-
0 W* T" d- j3 j) I" Q3 Nmon in girls than in boys.1,3 Most boys with CPP
" A0 \- e$ x, z/ R1 Z4 Kmay have a central nervous system lesion that is
7 A% u# \3 L ?/ U2 ^responsible for the early activation of the hypothal-$ c# B4 } g1 @ X, k( O
amic pituitary gonadal axis.1-3 Thus, greater empha-! k+ r Q) ~0 ~ v2 N
sis has been given to neuroradiologic imaging in
) g: F% r1 g8 Z- v yboys with precocious puberty. In addition to viril-
6 K: _; s- z' q: Y( sization, the clinical hallmark of CPP is the symmet-4 d9 D+ B# g/ T' U. Z
rical testicular growth secondary to stimulation by6 p1 a& a' K1 [" r0 ]
gonadotropins.1,3$ k8 j) d% D C) t1 Y& w
Gonadotropin-independent peripheral preco-- \5 k; U5 q/ Q3 R
cious puberty in boys also results from inappropriate& }& E7 @6 y5 i4 N" k( D1 i
androgenic stimulation from either endogenous or9 D( w2 K# B* U; ~1 O# a
exogenous sources, nonpituitary gonadotropin stim-3 j* o# B8 y+ P1 C2 H$ }
ulation, and rare activating mutations.3 Virilizing
M7 A( D& h, k; n) hcongenital adrenal hyperplasia producing excessive7 @0 a5 |) K- K- J
adrenal androgens is a common cause of precocious+ |; q" \0 g5 \" J) f0 Z2 z' ]' d
puberty in boys.3,47 v7 Y8 [2 j t p, V
The most common form of congenital adrenal
# g8 ~* [9 I" g' R3 ~4 t* v* ~hyperplasia is the 21-hydroxylase enzyme deficiency.
; |" M0 T, t* s: p; {The 11-β hydroxylase deficiency may also result in
* [2 |8 D1 n& h, i5 O8 m' U* F* s1 uexcessive adrenal androgen production, and rarely,) _" z2 \0 C( d- z( E+ ~
an adrenal tumor may also cause adrenal androgen
X j# d' Q9 ~/ R- d7 _* U6 x iexcess.1,3
( L8 @* o, R `5 G8 m; P6 V- vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- N2 M4 I/ W1 H$ ^" a' X+ J2 f542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 S: L5 B1 h2 r9 r/ k: E; Q
A unique entity of male-limited gonadotropin-
9 D: S& \) |& O) K) C. b7 nindependent precocious puberty, which is also known- q7 [7 u* J8 _0 b; M
as testotoxicosis, may cause precocious puberty at a
& B3 A5 q2 q( {9 Q6 Jvery young age. The physical findings in these boys7 P- y3 }9 b3 P# o# |
with this disorder are full pubertal development,
% d6 b9 j. X/ C- f7 B& p$ c0 b5 bincluding bilateral testicular growth, similar to boys
# U+ x2 p6 ^. F) J. T" vwith CPP. The gonadotropin levels in this disorder0 Y" y" ?+ l! e& ]' H
are suppressed to prepubertal levels and do not show
/ J8 u. }$ n' Y/ X3 spubertal response of gonadotropin after gonadotropin-
q+ I$ _0 W0 e9 A3 F3 _8 i; ~releasing hormone stimulation. This is a sex-linked* R1 @3 ?7 V. }5 i( i
autosomal dominant disorder that affects only
% h( @6 z0 Y) q4 S* c+ Vmales; therefore, other male members of the family1 p9 m! h, x/ N4 _' m L6 Z
may have similar precocious puberty.35 v: L m* F, M9 n6 O, v$ z
In our patient, physical examination was incon-
! m0 Z2 X! e% ^3 O2 Xsistent with true precocious puberty since his testi-$ Z0 \2 A6 D/ B, S& A. F! q
cles were prepubertal in size. However, testotoxicosis8 r; C( T7 L/ V
was in the differential diagnosis because his father
5 @9 K o+ L+ V s/ Kstarted puberty somewhat early, and occasionally,
$ i9 Q9 I/ q4 Jtesticular enlargement is not that evident in the
# Z) s5 A8 a Z) Y5 _& |( p6 f: pbeginning of this process.1 In the absence of a neg-" S5 f0 w1 I' g8 x% v
ative initial history of androgen exposure, our4 Y( P; I6 p* X! O
biggest concern was virilizing adrenal hyperplasia,8 N" q7 C1 |8 ^" S9 `: a
either 21-hydroxylase deficiency or 11-β hydroxylase1 h4 n4 d% R; @" y' e- z. q0 W' w/ ?
deficiency. Those diagnoses were excluded by find-' w0 }* p$ U9 ^% n( h5 N, k
ing the normal level of adrenal steroids.$ Y+ m8 r! ]) w, |- H# H
The diagnosis of exogenous androgens was strongly& G* w' E8 r! p) H. {5 n' w
suspected in a follow-up visit after 4 months because
, g" ^" h Z" C |- k; _7 S. {- Xthe physical examination revealed the complete disap-
# C2 Z5 H5 |; T4 Gpearance of pubic hair, normal growth velocity, and
+ b! R8 A) Q7 }decreased erections. The father admitted using a testos- o* t, G4 m* O. d
terone gel, which he concealed at first visit. He was- { g9 C: d- I* o4 l; A1 p
using it rather frequently, twice a day. The Physicians’
2 b& T$ j' e+ x+ MDesk Reference, or package insert of this product, gel or
* d8 l! ^" P, X% L/ ~2 ]+ ?cream, cautions about dermal testosterone transfer to
0 T0 E, C+ {' c, X8 u0 @" uunprotected females through direct skin exposure.5 o# G( S3 N* L( z/ W
Serum testosterone level was found to be 2 times the( }/ O) b2 T* S
baseline value in those females who were exposed to8 c$ [- A, ?7 x/ K' S
even 15 minutes of direct skin contact with their male1 M# ?# d+ ]! Y# y- `7 l3 w! \
partners.6 However, when a shirt covered the applica-% B* a/ K; d6 [, Q3 ^" v6 Y
tion site, this testosterone transfer was prevented.6 Z; _$ W4 c) u# w1 F; H8 D2 ?# e
Our patient’s testosterone level was 60 ng/mL,
! n/ f; ~# c6 K( a% r9 W3 m" z) Fwhich was clearly high. Some studies suggest that/ K/ X7 M2 R9 x, D% T# r7 p
dermal conversion of testosterone to dihydrotestos-
! c5 Z0 P" K4 S. } w: Eterone, which is a more potent metabolite, is more
( C$ c9 [7 r2 a% Z/ bactive in young children exposed to testosterone
0 F( e7 ~. ~1 w2 ?exogenously7; however, we did not measure a dihy-
% Y5 g: e5 ^/ u9 V" X; bdrotestosterone level in our patient. In addition to V& I3 f; S' M7 k, q! S
virilization, exposure to exogenous testosterone in) p$ a' `8 ^- c! G0 u6 L
children results in an increase in growth velocity and
$ U% h( ]3 Z6 x6 d2 G; H$ Wadvanced bone age, as seen in our patient.
' _9 f6 |6 O) |3 j+ b: ?The long-term effect of androgen exposure during* G9 I& w ] }$ s D
early childhood on pubertal development and final
6 U; Z @; }2 u' Q: |adult height are not fully known and always remain7 D+ [. f; d3 u
a concern. Children treated with short-term testos-
& E, [3 F2 o( u3 n& X$ Oterone injection or topical androgen may exhibit some
! B8 ^% ^+ i0 I+ b, Z5 X! }; Oacceleration of the skeletal maturation; however, after2 u; K, L, @" Q3 }
cessation of treatment, the rate of bone maturation
7 |6 I7 e( [) I4 W: i X! k/ bdecelerates and gradually returns to normal.8,9
. k/ H, X1 m: b, x; j* o, ]There are conflicting reports and controversy
$ @' @) Z5 F4 f7 x) f* A( zover the effect of early androgen exposure on adult
2 w* t/ p8 ^+ W8 fpenile length.10,11 Some reports suggest subnormal
: V- D# K% t" k. ]6 Iadult penile length, apparently because of downreg-1 u7 X. F- l# @. E- M2 R
ulation of androgen receptor number.10,12 However,
$ d* L2 z% F0 W$ x- i' ySutherland et al13 did not find a correlation between/ i: P2 m: _$ E1 u0 V
childhood testosterone exposure and reduced adult
% @, r: u# {' T( ` E5 fpenile length in clinical studies.
: D3 p9 s0 R1 m& j, X3 m: qNonetheless, we do not believe our patient is2 Y% z8 j6 O! X6 I8 B
going to experience any of the untoward effects from2 m! _9 L( t# e
testosterone exposure as mentioned earlier because
1 Z, M6 E0 Z! W, o) c% f7 n9 @$ \the exposure was not for a prolonged period of time.
! O) O/ u3 K6 j! y- N3 eAlthough the bone age was advanced at the time of
+ A; g+ ^( Y$ f& cdiagnosis, the child had a normal growth velocity at; @/ j0 a. G! o
the follow-up visit. It is hoped that his final adult
3 s: {0 n/ ^3 b* G; c9 {2 \height will not be affected.' a. C5 V$ W: ?" c" I/ }0 {
Although rarely reported, the widespread avail-; b+ G1 Z! l s$ b7 k6 w% ?& ^: [
ability of androgen products in our society may U( T8 A$ i0 t
indeed cause more virilization in male or female. y. Q6 z$ Z2 V- I/ p
children than one would realize. Exposure to andro-( u$ e2 K8 d) |! O
gen products must be considered and specific ques-$ r& z, W! ]: X7 `# p3 z" g1 Z# K4 ]
tioning about the use of a testosterone product or
: x; u# Y; R% _2 vgel should be asked of the family members during& r6 O8 H' V, }4 j- i4 ]8 F! Y
the evaluation of any children who present with vir-' N# E& G! L5 m' M/ {" C+ _
ilization or peripheral precocious puberty. The diag-
# O3 D9 ?! a* T3 @4 ~$ M0 {' X2 ]; Qnosis can be established by just a few tests and by
7 s+ q, k& |% F( Fappropriate history. The inability to obtain such a
3 \, V2 g- X: s" p: n7 ]4 uhistory, or failure to ask the specific questions, may
0 ~3 D0 x4 O" D4 D2 c: r- @result in extensive, unnecessary, and expensive7 Z; l9 Q+ r) ]( b7 h
investigation. The primary care physician should be& i( K# r# T! ~- \
aware of this fact, because most of these children! Q5 d7 N, D5 W9 w( l
may initially present in their practice. The Physicians’
# Z# g! `& j5 R8 Z; v* C. ~% wDesk Reference and package insert should also put a
! d' A2 `7 C) l7 |; Gwarning about the virilizing effect on a male or8 g# Q8 p1 B+ v' k, J$ H9 k2 N* j
female child who might come in contact with some- z: q2 J) C+ R3 M3 K
one using any of these products.; |* i+ u) w5 ~4 O# h$ f
References( z6 s' p+ U. V5 O/ f
1. Styne DM. The testes: disorder of sexual differentiation; N2 v) f5 d9 X5 _, g: j s
and puberty in the male. In: Sperling MA, ed. Pediatric" X+ f) z _2 b0 a5 L1 S% t# u
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;% g4 X& U( I# Z" `3 V) N) _3 w/ |
2002: 565-628.* E, i. I* V0 ?0 g% L
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 S* K2 B' P1 ^/ l7 \puberty in children with tumours of the suprasellar pineal |
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