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Sexual Precocity in a 16-Month-Old. i+ L, a. U, f# ]) `5 y" k+ d
Boy Induced by Indirect Topical
3 t X6 C, X$ o/ D' A# F# w% X8 bExposure to Testosterone
6 v# k1 |. \; x+ X6 t& I& Q* m7 {Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 O2 D* Y I3 g9 T p0 X- Q+ [
and Kenneth R. Rettig, MD1
$ |/ |& G4 I0 h2 T2 j/ LClinical Pediatrics+ h; m0 D, V/ Y2 L# v! u! J
Volume 46 Number 6" ^4 v$ W, X; D( r) f
July 2007 540-543. d1 ~: z3 `. A5 v8 y+ J
© 2007 Sage Publications
8 i L( D6 g- o7 z; E1 v5 o, p10.1177/0009922806296651
. b# j# E, m9 E. T# ohttp://clp.sagepub.com
8 ^8 g6 N+ m. \6 i8 b0 Shosted at: U" {; i, N: n! A
http://online.sagepub.com
1 L( x q4 ^% |$ t! t& J7 B3 M, ~Precocious puberty in boys, central or peripheral,' e+ d8 w+ b* {$ Q) X7 i
is a significant concern for physicians. Central8 B! y" h0 I7 t2 i- Y( ?! r$ r* B
precocious puberty (CPP), which is mediated. z5 @; f$ g1 I7 J5 P
through the hypothalamic pituitary gonadal axis, has4 n# m5 y$ w, `1 u
a higher incidence of organic central nervous system8 d, Z( S$ k) ^! A8 \
lesions in boys.1,2 Virilization in boys, as manifested% ]9 W$ D& ]0 H0 n( G
by enlargement of the penis, development of pubic
# u4 b* q: D. s/ i- A# K Vhair, and facial acne without enlargement of testi-7 i8 q6 e3 S: U7 x$ U" D* `
cles, suggests peripheral or pseudopuberty.1-3 We& |( I. u( @) n" R
report a 16-month-old boy who presented with the
, I f1 m0 k$ G' H, d+ a& e" ?; {enlargement of the phallus and pubic hair develop-
0 `& G# `4 }( Y1 g2 sment without testicular enlargement, which was due
4 ^- X2 ` A- S, `. ?# k2 |0 kto the unintentional exposure to androgen gel used by
j7 t0 R7 o9 |) f- T* I* Othe father. The family initially concealed this infor-: x4 g5 u. j3 @
mation, resulting in an extensive work-up for this
" s7 J8 M! g/ ^; {child. Given the widespread and easy availability of
# Q+ L; n9 R* S/ p* o( Atestosterone gel and cream, we believe this is proba-
# R: U/ _- L& D8 Rbly more common than the rare case report in the
* w) n2 q) A/ d& c _; H7 Oliterature.4/ r. L+ o0 l4 f
Patient Report
1 X: h; |3 w" z2 M' _3 w' kA 16-month-old white child was referred to the! [$ f" E- Z7 \, g9 }
endocrine clinic by his pediatrician with the concern
; I ?% y# o0 |1 u( @# y3 cof early sexual development. His mother noticed
6 J; z9 }9 ~5 F: _light colored pubic hair development when he was1 h6 J2 c$ F; x @1 S4 M
From the 1Division of Pediatric Endocrinology, 2University of) p9 D4 N9 ]; t3 `* ^: w, a0 \( p
South Alabama Medical Center, Mobile, Alabama.& ] z I) Y* Z% V6 ^2 M3 D" B
Address correspondence to: Samar K. Bhowmick, MD, FACE,
' c6 t) E) X" G" Z' e/ X1 {Professor of Pediatrics, University of South Alabama, College of I' z7 l; B( D7 i( n0 H l
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;& z5 q2 K5 a) u/ Z& R- B
e-mail: [email protected].
- I. I+ O* B- Fabout 6 to 7 months old, which progressively became
# r: Y/ W; y* w4 udarker. She was also concerned about the enlarge-7 x6 P3 w* Y: ~2 x9 v. Q
ment of his penis and frequent erections. The child! y5 z; p% w" C, {7 X5 j
was the product of a full-term normal delivery, with: a, f- q( q' A3 |! W( `
a birth weight of 7 lb 14 oz, and birth length of" q! B. ~1 I( t5 M5 K1 h
20 inches. He was breast-fed throughout the first year% y @ n" P9 {# \9 P+ @: m
of life and was still receiving breast milk along with
3 \7 s3 c5 X5 L6 Ksolid food. He had no hospitalizations or surgery,
/ c8 `. x- z* `1 p) sand his psychosocial and psychomotor development
7 i' I) M& `" [& e5 K' b7 k6 vwas age appropriate.
* C* z! N$ e4 o7 d' a; UThe family history was remarkable for the father,
' Q8 D! e" [5 @/ J1 a" q4 ^" Ywho was diagnosed with hypothyroidism at age 16,0 h {0 ?, p3 o9 p& c( e0 {
which was treated with thyroxine. The father’s# a- ~ B4 k% |9 Z; ]
height was 6 feet, and he went through a somewhat% p9 i' r# a+ c4 H; U( B
early puberty and had stopped growing by age 14.% K, Y; ?" I1 m# E
The father denied taking any other medication. The
5 m- I6 a6 a } ^1 K6 ^3 {+ K- |child’s mother was in good health. Her menarche7 t6 }6 \ r# v- B
was at 11 years of age, and her height was at 5 feet+ M/ y" Y& I* L8 A3 v e% i4 d$ K
5 inches. There was no other family history of pre-
% J% [7 C t& N- ~cocious sexual development in the first-degree rela-' U' A2 e% ]; Y) v3 P8 D5 l
tives. There were no siblings.
1 h) r% @. B% j: T# H7 uPhysical Examination
2 s" G' B8 |& o. l& l! VThe physical examination revealed a very active,+ W' x0 ^- C( M9 [& X
playful, and healthy boy. The vital signs documented& {3 n9 [# x6 s6 E* M2 B* W. S; }
a blood pressure of 85/50 mm Hg, his length was
% X8 x _' o# i: H90 cm (>97th percentile), and his weight was 14.4 kg1 `1 R* A+ k: c+ b3 k- f1 M
(also >97th percentile). The observed yearly growth
- p/ J% u2 r, t' Nvelocity was 30 cm (12 inches). The examination of
. q: V* q+ A; H% q; |+ Uthe neck revealed no thyroid enlargement.
* D* p+ {" l9 o0 J9 P; j" e5 E/ [! T7 fThe genitourinary examination was remarkable for' z: ~/ E6 \- {
enlargement of the penis, with a stretched length of
9 u/ _# p6 F9 [6 ^3 H- d( E- E8 cm and a width of 2 cm. The glans penis was very well
O0 ^% E& p% @5 O6 h6 bdeveloped. The pubic hair was Tanner II, mostly around- T. R9 b; V/ q
540
' i' Q& v% ^( Z. P, A! o) nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ P; n" j& ?2 _, d. m% [7 \the base of the phallus and was dark and curled. The; K1 m0 I7 u* y) F" | Q. F' Y# M
testicular volume was prepubertal at 2 mL each.; @% p/ x, K' h8 T
The skin was moist and smooth and somewhat
6 A6 r7 e& O7 woily. No axillary hair was noted. There were no
) ~) F+ K# }1 h. P& K! D! Q Eabnormal skin pigmentations or café-au-lait spots.
- m8 V- g, U' U# F0 B0 _Neurologic evaluation showed deep tendon reflex 2+* m' O4 b& C! C$ r9 Z. \9 x
bilateral and symmetrical. There was no suggestion
6 U5 [9 E1 |* jof papilledema.2 g( r* p. h7 _; \6 X
Laboratory Evaluation1 K" n2 |) O5 ?3 ?- y6 e
The bone age was consistent with 28 months by
1 U' c4 p# I% s9 P7 b/ e( {using the standard of Greulich and Pyle at a chrono-
2 l4 y8 q3 r- ologic age of 16 months (advanced).5 Chromosomal7 @3 b% T) k0 o+ w/ ^9 y2 X
karyotype was 46XY. The thyroid function test
! F, S: e# |9 a, X- u$ mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-2 `! b0 ?# v3 w- m( v
lating hormone level was 1.3 µIU/mL (both normal).' {% d, O0 a0 ?, {) [
The concentrations of serum electrolytes, blood
' U& R2 m' R. I8 I7 furea nitrogen, creatinine, and calcium all were1 o( R, o( v4 @* _; m& w8 L
within normal range for his age. The concentration' `6 K) S8 i) x9 c, v/ o" l5 r+ G5 x
of serum 17-hydroxyprogesterone was 16 ng/dL
: j6 v1 o( r. z- C: z' T(normal, 3 to 90 ng/dL), androstenedione was 20 \5 S8 Z/ S! G' R
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) v% x" e$ @! [+ X! k% h; d
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 b/ {# Y/ @0 q5 C: wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
! A) y: m, t' I49ng/dL), 11-desoxycortisol (specific compound S); F% i t/ z% a" p8 J4 v$ E- {. h
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, k9 T1 o* b! g, ~- q0 R! }+ ~
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
2 U. Y. P4 z# v4 t- P, C' Jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& s2 ]* Z8 H5 {# |& R% v+ \& @2 Mand β-human chorionic gonadotropin was less than
) e8 {& Z; } u) o5 mIU/mL (normal <5 mIU/mL). Serum follicular
% P; f% ^& l, P4 r9 Estimulating hormone and leuteinizing hormone
2 n. Y, H/ R7 |: }concentrations were less than 0.05 mIU/mL3 b3 q. c( t6 a( f+ a
(prepubertal).& ]( g# T4 o1 W9 t4 L
The parents were notified about the laboratory
. f& H" |0 [. i4 Dresults and were informed that all of the tests were
) Q; p* @( R& {! L8 p' jnormal except the testosterone level was high. The# |4 a% l* P, { u8 C) ?
follow-up visit was arranged within a few weeks to; Y' d" d# a% r# {, S, A
obtain testicular and abdominal sonograms; how-
, K. P" G5 I" ]0 y0 W1 Mever, the family did not return for 4 months.; v* f# S/ P, d( G! d, x. D
Physical examination at this time revealed that the
6 g' ^4 ]4 q* K- Y1 K% `child had grown 2.5 cm in 4 months and had gained
( J) j* `' |' e' X9 I* N) a2 kg of weight. Physical examination remained5 r' w* {4 i" k. H2 N
unchanged. Surprisingly, the pubic hair almost com-5 t, w- ]4 u0 R: z# |) @: ~6 J
pletely disappeared except for a few vellous hairs at
8 ~# n5 ~- U2 z5 r, pthe base of the phallus. Testicular volume was still 2
2 e# \! C8 I& wmL, and the size of the penis remained unchanged.4 L. p) X, D" ?4 ^9 l! O! {
The mother also said that the boy was no longer hav-% o& A4 F! o* e# {, V
ing frequent erections.$ w2 f+ O5 O$ ~6 h# B6 J4 _; x
Both parents were again questioned about use of$ S: w5 V7 ^- |' E: V1 p
any ointment/creams that they may have applied to0 j" l+ \" O/ N$ n6 Z* F `0 b
the child’s skin. This time the father admitted the
$ x2 }' |# A. ^7 |Topical Testosterone Exposure / Bhowmick et al 541
) K- |! v2 |, o0 [& muse of testosterone gel twice daily that he was apply-" v0 O( G5 v4 j% @* T/ h0 {
ing over his own shoulders, chest, and back area for
( P/ ]- T& d! Q9 |8 ua year. The father also revealed he was embarrassed- Y# W1 k2 N! a+ V
to disclose that he was using a testosterone gel pre-
& t! R: l$ l& J0 ?$ T# `scribed by his family physician for decreased libido; k! }+ e% s A6 r, b9 E2 }3 y
secondary to depression.
( D, K: g$ N6 O+ t5 i. gThe child slept in the same bed with parents.
5 i( Q0 s; g) P9 PThe father would hug the baby and hold him on his4 }# X' a( o- A, [1 h: H
chest for a considerable period of time, causing sig-0 e: X9 p% y3 a# a A- u" X
nificant bare skin contact between baby and father.
3 X; P! t$ q u2 T# I+ m8 rThe father also admitted that after the phone call,
8 }. d' h( D' _5 I# P5 ], d4 wwhen he learned the testosterone level in the baby4 y$ W( C* J) v
was high, he then read the product information
' S* g: X7 ~1 r. i+ `packet and concluded that it was most likely the rea-
! q$ i3 F6 K2 M0 m9 @( Xson for the child’s virilization. At that time, they
6 F7 z6 {$ _4 q4 f7 _% V: k8 sdecided to put the baby in a separate bed, and the
3 K& A' n9 O! d) @father was not hugging him with bare skin and had8 z; S @* Z: j
been using protective clothing. A repeat testosterone
8 D/ N& Z# f" Y- B+ I# m& Itest was ordered, but the family did not go to the
' v: x; ]) Y$ i s( T/ N4 I6 klaboratory to obtain the test.
1 J3 o7 q: i w' D, o4 e7 W/ SDiscussion- g4 l6 j4 H" _7 p. O5 M5 T5 q
Precocious puberty in boys is defined as secondary3 \/ P/ H* N. m4 H
sexual development before 9 years of age.1,4
5 ?. G: T! t7 _* a8 h" Z, y2 n6 dPrecocious puberty is termed as central (true) when- H4 K0 F: V( f% l2 T7 U6 ^4 p6 I
it is caused by the premature activation of hypo-
; R& y7 i6 ^3 {, }* K; Wthalamic pituitary gonadal axis. CPP is more com-
/ K# U& s% W% F1 G9 C' ^2 p8 Qmon in girls than in boys.1,3 Most boys with CPP9 G: z# M9 b5 M! Q* ~4 G
may have a central nervous system lesion that is
/ G: Z( L: U2 ?3 C2 eresponsible for the early activation of the hypothal-
, s4 d* E/ Z W6 b* T/ Namic pituitary gonadal axis.1-3 Thus, greater empha-
+ g; d! Y) e! R5 r4 Q& \) n% Lsis has been given to neuroradiologic imaging in, K1 c/ a& n3 [( |; b, O* |* o% D6 j
boys with precocious puberty. In addition to viril-
, J) L! |& g# H( D: J$ I. E3 Dization, the clinical hallmark of CPP is the symmet-
F5 p* F7 W6 t' z/ `rical testicular growth secondary to stimulation by H1 S5 w t4 y, Q9 c
gonadotropins.1,3
6 @2 C! d( U, a6 p; nGonadotropin-independent peripheral preco-
]* X& E7 _( O1 `2 t; B2 s/ Kcious puberty in boys also results from inappropriate+ z& e+ k4 P0 `: M5 m* g
androgenic stimulation from either endogenous or, Y6 x, C' V. ], Z
exogenous sources, nonpituitary gonadotropin stim-2 c3 u6 a5 W, a8 {6 ~# O
ulation, and rare activating mutations.3 Virilizing
2 H9 ~8 ?9 f0 B, Z2 t7 q6 r% fcongenital adrenal hyperplasia producing excessive
\3 o, i& D4 _# nadrenal androgens is a common cause of precocious
8 q) G4 _+ |. L: Q( J/ M9 X) j# Q& W* Qpuberty in boys.3,4" `8 W+ V8 A( f6 K! w: h
The most common form of congenital adrenal6 B3 A9 g; ?% \. R, ~$ h/ @- x
hyperplasia is the 21-hydroxylase enzyme deficiency.( h% E/ X, n$ R% P& B
The 11-β hydroxylase deficiency may also result in: g. @1 D' X5 Y
excessive adrenal androgen production, and rarely,! _' K2 P) V+ q3 ?! ?
an adrenal tumor may also cause adrenal androgen
9 ]9 {3 M( _! y. Z/ G7 V$ @5 I. cexcess.1,3& L2 m; w5 I* _3 B6 M% g* t
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& K. k( l M. P' Y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 r: h; J2 j. bA unique entity of male-limited gonadotropin-
, I7 [6 Q0 C: ], a- |% f( m6 f0 hindependent precocious puberty, which is also known
9 @( t( E: C5 w: Uas testotoxicosis, may cause precocious puberty at a
2 H2 L* e' N( Z- |+ l3 Vvery young age. The physical findings in these boys+ B, u7 F% j4 y) C4 K5 ?
with this disorder are full pubertal development,
+ [- u$ j. w$ @ H& {including bilateral testicular growth, similar to boys! ?% {5 [/ M, M' n5 A q
with CPP. The gonadotropin levels in this disorder
* ?. _0 ~4 p5 f' ?4 f }. iare suppressed to prepubertal levels and do not show" m. e5 t# ~$ L3 F
pubertal response of gonadotropin after gonadotropin-
/ j+ w2 ?5 {# p. ]4 jreleasing hormone stimulation. This is a sex-linked
! q9 [, T, e% f% E/ |1 Jautosomal dominant disorder that affects only( v& W/ E6 Q, E% h3 t- @6 O* M. Y& T. [$ E/ c
males; therefore, other male members of the family' N" s) V; x. L9 Z5 [$ e8 ?6 ?
may have similar precocious puberty.3: H6 L) k& h' Q& t9 h
In our patient, physical examination was incon-2 ]$ o# X; j/ {6 G, N* ?
sistent with true precocious puberty since his testi-
( a' I% Z! `5 q% x' o& y4 Q% Zcles were prepubertal in size. However, testotoxicosis: I8 B9 {5 Q" T4 v% Y* y4 K) s
was in the differential diagnosis because his father7 i# Y0 N- p2 \. r! a1 F
started puberty somewhat early, and occasionally,
' b7 ^0 v* d5 }0 W- O5 j' v, O3 {6 Xtesticular enlargement is not that evident in the" M8 m' F/ T# c% h+ q- u# t
beginning of this process.1 In the absence of a neg-5 G" ^- o) Q) ^% H7 J' s3 {
ative initial history of androgen exposure, our: i3 v% ~. z) @" A& {5 L
biggest concern was virilizing adrenal hyperplasia,! t T3 F. C' R
either 21-hydroxylase deficiency or 11-β hydroxylase
( e2 }, R4 Z4 o1 q5 {deficiency. Those diagnoses were excluded by find-" \* w. M0 e; Q' o- c: {' _
ing the normal level of adrenal steroids.& V! N" h9 _. b5 W/ a
The diagnosis of exogenous androgens was strongly0 Y( G! d/ q& W' m% t
suspected in a follow-up visit after 4 months because0 y& ]5 _1 b" D" k# r* G
the physical examination revealed the complete disap-& M0 R% C: y* f; B$ _: f
pearance of pubic hair, normal growth velocity, and# `6 w- B9 |" R6 E: n: ^. c+ x* H
decreased erections. The father admitted using a testos-
# r2 W$ m: u$ A8 b% rterone gel, which he concealed at first visit. He was
& s% r; @" L1 u/ p$ c1 Ousing it rather frequently, twice a day. The Physicians’# f6 w6 q: b( H7 y- {. }
Desk Reference, or package insert of this product, gel or
& p) D' o0 Z _4 `, M8 h# P+ Zcream, cautions about dermal testosterone transfer to
) v+ s8 S2 x! z3 N; _% i3 ?unprotected females through direct skin exposure.. d5 O& _% n3 r" v
Serum testosterone level was found to be 2 times the% Z$ K7 h0 A4 a8 s
baseline value in those females who were exposed to
z( n1 L: I, s z3 l2 V( V. ueven 15 minutes of direct skin contact with their male
, q0 V) i) f2 ~0 r- Ipartners.6 However, when a shirt covered the applica-4 q! F7 }7 L5 j% D% n- r/ s0 P
tion site, this testosterone transfer was prevented.
5 B4 p/ Y9 Y6 s8 [2 fOur patient’s testosterone level was 60 ng/mL,3 u- _3 `" D6 R7 p8 P0 `
which was clearly high. Some studies suggest that: t! G+ u% }5 _3 |8 l! c% O
dermal conversion of testosterone to dihydrotestos-
. Z* P/ e% G8 R& Z1 x- Z& [terone, which is a more potent metabolite, is more8 s, q3 t U. H5 e W0 X% W4 \
active in young children exposed to testosterone# ~5 H( N# N( B @1 D4 c! `1 k
exogenously7; however, we did not measure a dihy-
! r0 b/ T/ y T: F+ U4 ~6 _drotestosterone level in our patient. In addition to
- a* a! z& [& `2 A1 y( E0 Hvirilization, exposure to exogenous testosterone in
+ u. J1 B" f) B2 ~' Lchildren results in an increase in growth velocity and
, Z6 l$ S3 B( F* l# Q& eadvanced bone age, as seen in our patient.
6 O5 R0 k0 J) KThe long-term effect of androgen exposure during, Z' y9 n7 V1 d; b
early childhood on pubertal development and final* q) Z0 J2 \# S+ D6 ]
adult height are not fully known and always remain
7 f8 `3 D+ `9 D! h9 [a concern. Children treated with short-term testos-
" C- ?) Z! ~* F, e' X3 f: `, X) `$ nterone injection or topical androgen may exhibit some1 {* ~; C' G) T* I N; `
acceleration of the skeletal maturation; however, after, k- G$ Z# ]: |. \1 T+ C
cessation of treatment, the rate of bone maturation
7 t t2 \, Y; [! {3 w9 g3 s) pdecelerates and gradually returns to normal.8,9
2 S: N1 i! f3 g4 U, nThere are conflicting reports and controversy
5 I: j/ ~& x$ T# g$ j# j/ M) G: Oover the effect of early androgen exposure on adult
4 x. @ _+ _0 L% q8 h0 y; q0 I qpenile length.10,11 Some reports suggest subnormal
& o& h6 e& L# \6 R, ?, I/ E$ ^adult penile length, apparently because of downreg-
9 Q0 n& k+ ^( W5 _0 ~ulation of androgen receptor number.10,12 However,
; q2 t4 d7 }6 E* ?Sutherland et al13 did not find a correlation between
! F# o) d, b% }! p& Uchildhood testosterone exposure and reduced adult
# u6 V; g, J: A2 w1 ~penile length in clinical studies.) \) V5 m3 X5 O% R, ]' k* }% E
Nonetheless, we do not believe our patient is
0 r& N9 G# k. D5 Z2 lgoing to experience any of the untoward effects from
0 j9 |) ^5 ]* v& t vtestosterone exposure as mentioned earlier because9 w C0 P7 u/ i
the exposure was not for a prolonged period of time. p! c. h3 u2 |) T
Although the bone age was advanced at the time of
4 Z2 R, {+ t/ H, j( L; y* Ydiagnosis, the child had a normal growth velocity at
6 C; Q" W+ Y! G9 p) }the follow-up visit. It is hoped that his final adult
6 p" l3 k" H. I7 K& I' }height will not be affected.
: M4 x& U) S6 r5 {( `Although rarely reported, the widespread avail-1 M; V. x2 c+ Y- `4 b. }
ability of androgen products in our society may
* \* R* ^8 o* w2 Q# i, _- q1 m3 mindeed cause more virilization in male or female: R. `$ K# T1 p% |4 x; P+ j
children than one would realize. Exposure to andro-" d% \1 a* w" H
gen products must be considered and specific ques-
& [3 v, j0 M! W' G: a( vtioning about the use of a testosterone product or
" n- N7 _% Z5 w! |gel should be asked of the family members during
% y' q& I( M: W9 sthe evaluation of any children who present with vir-' ~0 S6 r! `% a1 p* X, V
ilization or peripheral precocious puberty. The diag-$ q* o4 z' y2 F# s) d' A
nosis can be established by just a few tests and by t, O" d% g" z
appropriate history. The inability to obtain such a
0 m/ x1 E5 b! @! j! P) X7 R$ Yhistory, or failure to ask the specific questions, may
4 k; l, l5 ]5 qresult in extensive, unnecessary, and expensive
2 ~0 ~0 x" o% B2 Ginvestigation. The primary care physician should be5 V1 L+ u7 t( _" _( b& x* Z6 B
aware of this fact, because most of these children
. u. l& B6 A* g% q% y0 R! ymay initially present in their practice. The Physicians’ Y% U% S7 ]) |, ]
Desk Reference and package insert should also put a/ _# S9 t8 \5 D- b$ X) B" @ F
warning about the virilizing effect on a male or
* [" s. E% ^, z4 |; `' s* `female child who might come in contact with some-
) }" z/ O% \8 ^! o, b6 e5 mone using any of these products.8 p6 |7 N q7 N7 Q/ Z
References( I6 y- w( w7 ^8 \) J7 g5 L
1. Styne DM. The testes: disorder of sexual differentiation9 Y, j" E- w3 X. o, O
and puberty in the male. In: Sperling MA, ed. Pediatric
8 F5 y/ t# t6 G$ x8 KEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 V3 x1 D! J0 U2 r$ U9 j5 N2002: 565-628.
% U _* p0 w8 y- N( B2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ f" [, B/ ?* B6 n$ x: i: I; Apuberty in children with tumours of the suprasellar pineal |
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