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Sexual Precocity in a 16-Month-Old0 ], E& a, _3 w9 I+ r: z5 C# f7 e5 b
Boy Induced by Indirect Topical' D& z" J; v! @2 x4 u! G/ g& g/ J
Exposure to Testosterone
, k& S/ p) W2 E9 JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 i9 b z# Z' O7 z$ W3 G
and Kenneth R. Rettig, MD1
& C* b& ~) R& t0 W6 sClinical Pediatrics% `; j( M6 t% W% h7 J
Volume 46 Number 6
- t9 h) I5 V9 xJuly 2007 540-543+ A8 Z* _7 E% `
© 2007 Sage Publications
( k& M3 W. d5 z$ ~10.1177/0009922806296651: f/ c4 [3 [! ~# d2 \& Y u) L$ e9 @ F
http://clp.sagepub.com4 V! t4 a& J6 }/ s3 n, @; x ~) ~ }
hosted at+ P6 j# k- |# T/ f6 e
http://online.sagepub.com% [- @$ q$ d7 v2 S/ Y
Precocious puberty in boys, central or peripheral,
t. x0 c6 \- R) dis a significant concern for physicians. Central
, F4 h2 p' d4 u4 Q/ q% J8 m% Wprecocious puberty (CPP), which is mediated
4 G+ X' e! d' q9 r" ^through the hypothalamic pituitary gonadal axis, has/ Z' q4 U# T. n' B3 G1 M
a higher incidence of organic central nervous system9 Y) B% ]! A$ z7 g& F- S( v1 i
lesions in boys.1,2 Virilization in boys, as manifested
- N) H d: k0 p4 W# Q; k# L$ ~! p$ lby enlargement of the penis, development of pubic
" u8 I; J o- s- m3 W! j3 yhair, and facial acne without enlargement of testi-
# N! {2 `2 M) d6 ?' D8 Q2 R6 Ncles, suggests peripheral or pseudopuberty.1-3 We
( z* V( P8 _7 rreport a 16-month-old boy who presented with the2 l4 i. ]9 W& c: G* U9 B
enlargement of the phallus and pubic hair develop-) U+ w) \3 t4 N0 `1 F O
ment without testicular enlargement, which was due7 C' J& s7 B. b4 p6 I
to the unintentional exposure to androgen gel used by
0 y D6 }$ V Y- Sthe father. The family initially concealed this infor-
i. I% l. j7 q& B2 Q. v+ x. rmation, resulting in an extensive work-up for this
! x' I* S5 S6 Fchild. Given the widespread and easy availability of3 M+ ?0 ~+ z. J/ ^6 Z8 G
testosterone gel and cream, we believe this is proba-4 c& L' e: m8 r. h6 j
bly more common than the rare case report in the
" n, p+ B$ [6 H1 j/ g. k9 |; Hliterature.4
) e$ w' H3 ], u2 |7 APatient Report
$ ], N( x! }; q6 F; f4 D8 nA 16-month-old white child was referred to the. M& `7 y% F; Y( U6 I! X) M
endocrine clinic by his pediatrician with the concern$ |. d4 [7 d- v" c
of early sexual development. His mother noticed
# I u' g+ T! K$ a9 _. u( Dlight colored pubic hair development when he was
- ]- C, [, O9 p. e, j) WFrom the 1Division of Pediatric Endocrinology, 2University of l7 |9 n; C) c, J+ D
South Alabama Medical Center, Mobile, Alabama.
3 \# M0 \! T9 H! W8 F7 N0 R2 H) WAddress correspondence to: Samar K. Bhowmick, MD, FACE,# o) n. a+ R. s# r8 e9 o' }" z
Professor of Pediatrics, University of South Alabama, College of
6 u, }' e) V' w: h% @- x, NMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
0 r# e @ ]/ _& ]e-mail: [email protected].: c& T m+ q# ?! z7 P5 X
about 6 to 7 months old, which progressively became
% K' p( w y/ ` `darker. She was also concerned about the enlarge-
: D ~. {; _6 G% m3 @% F1 kment of his penis and frequent erections. The child% m% v* i1 E: g' d
was the product of a full-term normal delivery, with
# |$ D" {( `) u ], Z" na birth weight of 7 lb 14 oz, and birth length of2 f' v- Q6 y& s, B Q& j! R4 v
20 inches. He was breast-fed throughout the first year+ a. v! c2 p6 ]! q+ R2 g4 a
of life and was still receiving breast milk along with
, O8 B+ G9 n; K+ K& X( c1 [solid food. He had no hospitalizations or surgery,4 O( J. `! s2 ]3 m5 Q: \2 R& }
and his psychosocial and psychomotor development
7 c/ }# ]$ ~7 C5 V4 q( Y5 t" f/ Bwas age appropriate.
; m$ m% c% R/ r, N+ WThe family history was remarkable for the father,
+ J) n' T# g; _, Vwho was diagnosed with hypothyroidism at age 16,
2 [8 \2 K* L3 s s+ }: H3 pwhich was treated with thyroxine. The father’s
# g0 w5 @9 Z8 x. f) f7 a1 M- K! ^height was 6 feet, and he went through a somewhat
, k9 R& u+ P7 f* J, n) iearly puberty and had stopped growing by age 14.- f" Q2 B2 l. {6 ]4 [
The father denied taking any other medication. The
! W; m" v8 F6 Fchild’s mother was in good health. Her menarche
( Y$ [% H: S( hwas at 11 years of age, and her height was at 5 feet
% E8 [/ H2 h0 h0 J( j5 inches. There was no other family history of pre-; [2 E9 e" {* r! y) a
cocious sexual development in the first-degree rela-5 {& g$ B) v |$ ]2 V% `( j
tives. There were no siblings.
( K7 L5 G' a% H% G- V. FPhysical Examination% v# s- t4 f' j& U3 _) F
The physical examination revealed a very active,; v5 F- ]6 ? b: Y& R
playful, and healthy boy. The vital signs documented) Y- r- _0 \9 D
a blood pressure of 85/50 mm Hg, his length was0 m% r u$ h u" N# t& v
90 cm (>97th percentile), and his weight was 14.4 kg5 j0 _ V1 N0 i4 z1 A) }
(also >97th percentile). The observed yearly growth
4 w" l$ X6 L5 {3 h, T6 Mvelocity was 30 cm (12 inches). The examination of7 R4 s- x& N* X8 O4 Z1 {& l
the neck revealed no thyroid enlargement.
K: c4 o- v4 }9 U2 I' cThe genitourinary examination was remarkable for
. u0 q, Y5 X0 t; A0 D v2 Zenlargement of the penis, with a stretched length of& `( O, n3 ?1 R# Y$ ?; u% s0 }
8 cm and a width of 2 cm. The glans penis was very well
5 }# k6 }, }, d y1 v9 O5 Cdeveloped. The pubic hair was Tanner II, mostly around
5 _- ^: u+ P" @4 c1 |. O* q( g540' s, Y6 Q1 D; U
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from n$ g. p) P- z' D% ~7 g- E9 c
the base of the phallus and was dark and curled. The, T4 ?+ `: \# r, p( L! d# r
testicular volume was prepubertal at 2 mL each.
% Q4 m- ~' ^: _8 oThe skin was moist and smooth and somewhat
, ?+ j& Z0 H8 @; n" qoily. No axillary hair was noted. There were no
% K! o3 b. U9 v$ |- B# b' j9 Uabnormal skin pigmentations or café-au-lait spots.0 g6 _+ x6 o( O" p
Neurologic evaluation showed deep tendon reflex 2+
; N) @2 U1 }) l7 [& abilateral and symmetrical. There was no suggestion
, {. u k4 V6 yof papilledema.
" Y' l* R$ j9 p8 QLaboratory Evaluation: t0 N9 i% J* x0 {& |0 h
The bone age was consistent with 28 months by& d( V& a3 H& i- o q% L! {1 n
using the standard of Greulich and Pyle at a chrono-/ W. I6 q0 |" a$ _5 ?; Z! X) O% r
logic age of 16 months (advanced).5 Chromosomal* V4 f4 o, p6 v
karyotype was 46XY. The thyroid function test7 ]1 m5 M$ I& b4 x
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
- a9 O0 p, C/ `+ F8 wlating hormone level was 1.3 µIU/mL (both normal).
0 Z: @+ A7 K3 Y' J5 t( `0 Y( RThe concentrations of serum electrolytes, blood* a4 Y" }$ O) j
urea nitrogen, creatinine, and calcium all were
' ^) c+ J% B5 Rwithin normal range for his age. The concentration5 N3 e2 z$ `! R' T* `* `6 X
of serum 17-hydroxyprogesterone was 16 ng/dL
" v7 t: O- V1 K& P' {. x(normal, 3 to 90 ng/dL), androstenedione was 20
9 ?7 ~2 T, n# @% p9 Ong/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
% D. Y5 ]$ g! \6 e' B E1 o3 Xterone was 38 ng/dL (normal, 50 to 760 ng/dL),
( y, N, O; p8 @8 p- Z0 X6 qdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ W8 Q" G* n V- D9 R49ng/dL), 11-desoxycortisol (specific compound S)5 g0 o) o9 ~, V9 ?; g! P8 a/ Q6 X2 B
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# F, f) {9 l% n- f- I
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' J4 v( V$ M6 _4 i5 Y G
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, L0 a3 }, A' B& z# W: ^/ @
and β-human chorionic gonadotropin was less than I. K/ t6 L( l# A, J
5 mIU/mL (normal <5 mIU/mL). Serum follicular
; j1 }* q7 N1 v8 \% g0 O' t# vstimulating hormone and leuteinizing hormone6 y% U& o7 U$ I& {& W+ F
concentrations were less than 0.05 mIU/mL
% Q7 F5 [# Y( W/ m2 P& I# F(prepubertal).
& D) c. B) t9 j0 t& R2 S7 m1 p5 gThe parents were notified about the laboratory
. Q4 A. k# _4 t9 l5 }8 V5 ^results and were informed that all of the tests were
$ B! K# ]9 G/ inormal except the testosterone level was high. The
: {. N) H0 H" O/ r3 a/ T( kfollow-up visit was arranged within a few weeks to
X" G! S5 s. fobtain testicular and abdominal sonograms; how-; Q5 ?5 L) ?3 G. Q% @
ever, the family did not return for 4 months.+ N2 o E T6 S% d7 O/ F" N
Physical examination at this time revealed that the& h6 N4 P( f/ w1 [& p' G
child had grown 2.5 cm in 4 months and had gained
% K' z. M1 T" u. _) i1 j+ A! P2 kg of weight. Physical examination remained# k6 n# m: M- e2 [
unchanged. Surprisingly, the pubic hair almost com-1 ~: r8 H7 _1 i, e+ L
pletely disappeared except for a few vellous hairs at, F n$ L0 Y6 P. d6 j5 R
the base of the phallus. Testicular volume was still 2
; J8 s" e: p& \) f# dmL, and the size of the penis remained unchanged.
' [5 i4 F2 c* p4 Q' T& M) fThe mother also said that the boy was no longer hav-- a* |# D8 \ U2 w
ing frequent erections.
* R# y* p4 I) i2 d6 Y4 r, [6 K) vBoth parents were again questioned about use of* B% }4 H, ]1 J6 P# M9 h
any ointment/creams that they may have applied to' E5 ?, G A4 ?
the child’s skin. This time the father admitted the6 Q) Q7 ?5 w8 ^# v
Topical Testosterone Exposure / Bhowmick et al 541
7 P6 B$ M3 k$ e& fuse of testosterone gel twice daily that he was apply-" k. b( n9 [3 J2 c
ing over his own shoulders, chest, and back area for; C9 f# g/ ^/ J8 U! E, W
a year. The father also revealed he was embarrassed
- a# ]* I- y# H) D! mto disclose that he was using a testosterone gel pre-
+ {3 N2 u/ J h: ]: [5 P( Escribed by his family physician for decreased libido/ b1 L$ c3 M. |7 E6 F/ F
secondary to depression.1 e! u. s' v) s3 ?/ a
The child slept in the same bed with parents.! o: w3 R: I( ?/ Q0 u/ j
The father would hug the baby and hold him on his# N6 ]/ g4 t# [& B
chest for a considerable period of time, causing sig-
/ W1 i9 g* T" k' Q0 z4 }% Z* _nificant bare skin contact between baby and father.+ S [* Y& V! h- j1 d" X G' ]: x
The father also admitted that after the phone call,, [3 s. E# N1 R6 y5 w
when he learned the testosterone level in the baby
# e/ X7 o# }6 y7 U# Q6 N5 \was high, he then read the product information3 K" D) w# J5 @
packet and concluded that it was most likely the rea-0 E' V- b& o: }. W0 ~! Z# e% w
son for the child’s virilization. At that time, they
5 ^0 I+ j& O" h3 {, P0 Bdecided to put the baby in a separate bed, and the
; g7 Z: Q$ }0 v$ S+ r. hfather was not hugging him with bare skin and had* v! r2 @8 z. D* a5 Y7 K( c
been using protective clothing. A repeat testosterone" y) g2 A2 Q! Y
test was ordered, but the family did not go to the
: @7 r" ]" J. b: w1 y! d8 Xlaboratory to obtain the test.- x! e9 P9 `3 ^4 K9 G
Discussion
% B$ a Q8 {4 a0 G# TPrecocious puberty in boys is defined as secondary) U3 B4 E* Z! i9 X9 z+ b8 |
sexual development before 9 years of age.1,4& { R& W" b5 b
Precocious puberty is termed as central (true) when0 V6 X/ F7 ~; b2 G; O2 @ H
it is caused by the premature activation of hypo-
" I3 ]4 N7 B P7 l. W+ Jthalamic pituitary gonadal axis. CPP is more com-2 A* w9 x$ q5 N @
mon in girls than in boys.1,3 Most boys with CPP
0 A1 K- J6 I3 S; D" N! M' Pmay have a central nervous system lesion that is& t4 t' `5 J; |' ^5 D/ J$ P4 d1 j' u: F
responsible for the early activation of the hypothal-
& L% O" d) `/ D7 Gamic pituitary gonadal axis.1-3 Thus, greater empha-' f7 m, q6 p o0 k( P8 s
sis has been given to neuroradiologic imaging in
4 \4 t8 T9 ^/ b! kboys with precocious puberty. In addition to viril-8 s, H3 a1 S8 ~5 m9 z8 e* @
ization, the clinical hallmark of CPP is the symmet-
6 d$ C' Y0 C/ G ^" xrical testicular growth secondary to stimulation by* N; A' t# ~7 G# z/ j, n! f
gonadotropins.1,3# }4 M, ~: q+ p( {
Gonadotropin-independent peripheral preco-
' c+ z* l# v9 `0 `cious puberty in boys also results from inappropriate( I& {5 i! g T1 b! j% w5 T
androgenic stimulation from either endogenous or: _ n7 l6 x/ ^* D1 B
exogenous sources, nonpituitary gonadotropin stim-
- L9 K6 B8 ~ F+ s! ?4 p/ |* Lulation, and rare activating mutations.3 Virilizing8 C, g/ D- E; o' o" y2 t
congenital adrenal hyperplasia producing excessive
) ]; W1 b2 T$ A) F5 Sadrenal androgens is a common cause of precocious1 w4 I( [3 _+ i. o9 }4 ~
puberty in boys.3,4
; Q0 v! r) ^% x# a; FThe most common form of congenital adrenal$ L9 E4 t& \0 m; }
hyperplasia is the 21-hydroxylase enzyme deficiency.
7 I% H# j2 J7 Y! G% Z. z& oThe 11-β hydroxylase deficiency may also result in
% \' e/ ]/ a& N8 Q) E! ]# A6 Mexcessive adrenal androgen production, and rarely,1 s c/ t5 B; x$ ~3 n1 J
an adrenal tumor may also cause adrenal androgen
9 v7 n. H& ]$ s1 zexcess.1,3 O$ m$ C6 K1 t" A7 y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ y7 d5 T: v8 j- n1 S2 F( n. t' B542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; \6 P6 ]* o& C Y. EA unique entity of male-limited gonadotropin-: t; J0 S( I7 h1 n# k3 ~
independent precocious puberty, which is also known; F7 @7 d* V9 r- K0 J3 A/ Z+ J
as testotoxicosis, may cause precocious puberty at a
+ Z2 D! q+ D3 Z* ?0 y. h& l5 Wvery young age. The physical findings in these boys( _6 m& {* R0 x$ }1 S: o! r( e
with this disorder are full pubertal development,
1 X* Q% T& R7 T: d! b$ r# y+ jincluding bilateral testicular growth, similar to boys* Y |% k5 J# ]2 z6 v
with CPP. The gonadotropin levels in this disorder/ K% S: s0 `/ t) f1 u
are suppressed to prepubertal levels and do not show8 A1 F) t3 P! x1 M6 Q
pubertal response of gonadotropin after gonadotropin-" k3 H5 T! h% f9 Z6 D* [
releasing hormone stimulation. This is a sex-linked
! J( R2 Q0 W6 o L" u! zautosomal dominant disorder that affects only
8 o5 w9 D9 q* ~; N1 A. z' m cmales; therefore, other male members of the family# U: b! W2 _, l, ]7 Z) w H" I, H) p4 t
may have similar precocious puberty.3
; D! m: n6 S1 d( P& U Z" ?In our patient, physical examination was incon-0 ?5 d# P, P& _5 j- r$ O3 B
sistent with true precocious puberty since his testi-0 T1 H5 V2 ~* `5 T! ^; U
cles were prepubertal in size. However, testotoxicosis0 U( O1 t5 h! n/ j9 b4 g
was in the differential diagnosis because his father9 y% F0 @) E) R$ G' x
started puberty somewhat early, and occasionally,* c* E& O; ~2 {6 K9 l( l) R
testicular enlargement is not that evident in the
) T6 z6 E3 v7 o5 zbeginning of this process.1 In the absence of a neg-
, v" ?* C1 ~4 S y% j6 B/ zative initial history of androgen exposure, our
2 f# Y) t- f# N) Nbiggest concern was virilizing adrenal hyperplasia,
$ X+ ^$ a" ?, ieither 21-hydroxylase deficiency or 11-β hydroxylase
' |& e* M' v; U0 {& l# Jdeficiency. Those diagnoses were excluded by find-
: P& N+ g0 o ^; H0 q; P5 |ing the normal level of adrenal steroids.
, ^+ n4 } K7 }: bThe diagnosis of exogenous androgens was strongly
3 l; K0 v2 {, ?6 ] L- ?suspected in a follow-up visit after 4 months because" U( ~* X) g* b$ x& c
the physical examination revealed the complete disap-, S$ t' C1 n+ ~4 \: e+ u8 |
pearance of pubic hair, normal growth velocity, and* B. ~4 C3 Y, i2 ^! B. z% i, T6 N
decreased erections. The father admitted using a testos-
- ~2 B4 a6 A! g# v/ e8 ]; g, Wterone gel, which he concealed at first visit. He was
; U$ D |/ R( u/ d+ ~1 Y% lusing it rather frequently, twice a day. The Physicians’+ \! y% [- L9 B( d+ Q
Desk Reference, or package insert of this product, gel or
4 Y9 \- i8 m8 \( Z/ q8 {cream, cautions about dermal testosterone transfer to
# f2 Z, u' ?" V7 A+ junprotected females through direct skin exposure." h) C8 B ?+ \$ x/ W. a
Serum testosterone level was found to be 2 times the3 m N; Q2 t) |# i5 j! l5 j( w
baseline value in those females who were exposed to
1 X4 e2 Z" g8 M1 O1 ceven 15 minutes of direct skin contact with their male
' W# S3 J2 }" w& t$ T0 _partners.6 However, when a shirt covered the applica-
) P0 H& f* N+ M! @8 \! Ztion site, this testosterone transfer was prevented.
: J. }2 ~+ G7 d+ z. EOur patient’s testosterone level was 60 ng/mL,
+ T3 Y! K8 S0 {, v Qwhich was clearly high. Some studies suggest that
. L4 e/ Y: Z. t* C$ k' p1 S9 gdermal conversion of testosterone to dihydrotestos-5 B8 V, |9 T0 n+ Y9 \3 u
terone, which is a more potent metabolite, is more
" _- ] w. l" p* Kactive in young children exposed to testosterone
, m, O; m# q0 c r+ a$ Iexogenously7; however, we did not measure a dihy-/ G3 P9 C7 f5 q- Y
drotestosterone level in our patient. In addition to( A, {1 S+ w" Y8 ~0 A
virilization, exposure to exogenous testosterone in, O" Z% D) D3 v( I5 o, K
children results in an increase in growth velocity and
+ J! D0 P2 A, J5 h; l" tadvanced bone age, as seen in our patient.
5 d! _- V& z1 E4 Y4 {& SThe long-term effect of androgen exposure during
& c: `8 P; {: d; g2 eearly childhood on pubertal development and final: ?) N( V8 p- u4 E
adult height are not fully known and always remain" m+ W* V* N0 K/ R- U
a concern. Children treated with short-term testos-' q' `6 _; r% M2 W
terone injection or topical androgen may exhibit some4 P: G, `' ?' i6 t( Y7 R
acceleration of the skeletal maturation; however, after' v# \7 M5 F2 t! q! a7 g
cessation of treatment, the rate of bone maturation& H9 T8 ~3 d9 X. l) a3 @/ I
decelerates and gradually returns to normal.8,9" p P" L* P$ [0 j) s6 N6 o
There are conflicting reports and controversy, _8 z& @0 d% v$ C7 T
over the effect of early androgen exposure on adult$ E, n$ B) f7 `
penile length.10,11 Some reports suggest subnormal
! W8 D& P6 b {0 q9 G! |9 ^! cadult penile length, apparently because of downreg-
. v p9 U4 E# Uulation of androgen receptor number.10,12 However,
+ i4 o3 v2 T" k+ H) qSutherland et al13 did not find a correlation between
/ o8 w/ v5 E X, u, h' Achildhood testosterone exposure and reduced adult
! x, f; P9 P% W" V; V! Openile length in clinical studies.
( v0 K( U9 D8 w0 ~( t. O6 d" SNonetheless, we do not believe our patient is
$ f# H8 f; K( ]* j/ B' B& y/ j* pgoing to experience any of the untoward effects from
% f% ^4 {( f1 d1 d, W- M$ {4 G- X9 rtestosterone exposure as mentioned earlier because6 ^2 P' L" G; _) ~2 K' V
the exposure was not for a prolonged period of time.
; g" w) `0 d6 _5 Y* J$ C7 P/ PAlthough the bone age was advanced at the time of
/ F) ^4 s7 B! @1 [- o4 cdiagnosis, the child had a normal growth velocity at; W$ p8 G3 k4 G9 i5 f
the follow-up visit. It is hoped that his final adult5 r- r2 c1 e; b. H7 i7 a/ b
height will not be affected.
$ v( C! E2 N) C# WAlthough rarely reported, the widespread avail-
[' F( i. U: d4 x% Lability of androgen products in our society may8 R( L2 ?) K8 o, T- h g
indeed cause more virilization in male or female' j* J* n# c8 {" ?( q& u
children than one would realize. Exposure to andro-
4 }% b7 I0 W& I" h7 H, Vgen products must be considered and specific ques-4 _' L" n4 q# U( G* P. Z
tioning about the use of a testosterone product or
$ Y! p- y+ j8 m% G: ?gel should be asked of the family members during
0 a1 H w) H" Y6 K5 vthe evaluation of any children who present with vir-
+ Y1 q& t3 I, n$ G' z5 X5 R9 `ilization or peripheral precocious puberty. The diag-/ i* h) `- H6 T
nosis can be established by just a few tests and by- n3 m1 |5 f: i3 g
appropriate history. The inability to obtain such a# F1 \6 `" z4 k* U* q$ e) m; V
history, or failure to ask the specific questions, may) M& t& w. J2 X6 ?9 E* V/ A: ]. S
result in extensive, unnecessary, and expensive
: U1 Q( ^4 u/ s! c1 j: T" q# A! k* Yinvestigation. The primary care physician should be" r8 x4 H, e/ c9 W
aware of this fact, because most of these children, R; Q$ x. I2 f! C$ I4 P2 \5 Q
may initially present in their practice. The Physicians’% q7 d% |/ u" u
Desk Reference and package insert should also put a+ n! ?+ z& s3 \: m. l; M% L$ l' R
warning about the virilizing effect on a male or
/ u& T |% m6 y7 ?5 R9 Pfemale child who might come in contact with some-9 x% G' b( v$ ^9 N( v
one using any of these products.2 [$ W7 e/ W4 k: m" `' a
References
A* Y: Z# \7 v1 i+ F1. Styne DM. The testes: disorder of sexual differentiation; I5 l4 y6 l3 d5 T3 {* X7 ]" @
and puberty in the male. In: Sperling MA, ed. Pediatric
+ s7 I6 q$ y6 p! U5 V/ g2 UEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- U) `/ S$ h5 L( U
2002: 565-628.% w& k4 @7 ~9 G* m( L
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ U" G0 m i8 |( G
puberty in children with tumours of the suprasellar pineal |
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