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Sexual Precocity in a 16-Month-Old
/ E3 A% A; X u+ [Boy Induced by Indirect Topical0 i8 _3 v5 \6 F. v0 \
Exposure to Testosterone& U$ o' [; D T$ J# \- b/ M% L
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 V3 r5 g5 a+ r7 t2 Q
and Kenneth R. Rettig, MD14 n. i6 H, V: T
Clinical Pediatrics
5 ^) j1 v$ ~6 d, o" N* L1 g8 S6 kVolume 46 Number 61 k* ^1 ?0 j' g/ `
July 2007 540-543
% U# J ^$ O; j/ e© 2007 Sage Publications
; p! _: K! Z1 a! I10.1177/00099228062966518 |5 Y( n7 p w3 \
http://clp.sagepub.com
1 P6 \5 i, U5 P, T) e a+ ]hosted at' \' \" w9 l4 t7 w6 }# e5 b3 p
http://online.sagepub.com
3 N" f% P# n! b8 v$ LPrecocious puberty in boys, central or peripheral,
4 |) P3 T0 P* \8 G0 a5 l: qis a significant concern for physicians. Central
2 _* G" W' N; sprecocious puberty (CPP), which is mediated9 s; w; {: M( ]( _
through the hypothalamic pituitary gonadal axis, has3 G+ O& m# v$ ~# Y1 A7 e* h
a higher incidence of organic central nervous system. w, s4 Z" C: E& k0 `
lesions in boys.1,2 Virilization in boys, as manifested4 ~& t, d7 A* C" ?. j W8 }9 e4 w
by enlargement of the penis, development of pubic9 ?8 S; @9 J1 z! s( n
hair, and facial acne without enlargement of testi-& U* L: Q" d) h2 X! @5 V
cles, suggests peripheral or pseudopuberty.1-3 We
+ ~* U) {$ o. `& rreport a 16-month-old boy who presented with the$ I' m. Z# Y; R L" Z& x# M: E
enlargement of the phallus and pubic hair develop-( B6 w* D4 A/ t( P5 x3 Y' _2 g
ment without testicular enlargement, which was due2 F, {: W3 h: O; S8 U
to the unintentional exposure to androgen gel used by
( _6 @! r; ^6 }. b0 Qthe father. The family initially concealed this infor-
; P; l5 Q/ V& {& V# W) ?mation, resulting in an extensive work-up for this
. W- Z, L6 n9 G h j# b$ Cchild. Given the widespread and easy availability of; T h) Z/ M7 o x9 Y1 t$ j
testosterone gel and cream, we believe this is proba-% C* _9 Y2 z8 N; r$ B \; f
bly more common than the rare case report in the1 [& i: I+ y0 `
literature.4( X( R- ]$ r+ g2 a
Patient Report) P: A8 O( l0 u- {
A 16-month-old white child was referred to the
! ~0 E+ R2 C. e9 e3 rendocrine clinic by his pediatrician with the concern0 q, I7 o& }; H5 q0 T
of early sexual development. His mother noticed
: W/ ^. D1 Q( e- u vlight colored pubic hair development when he was( { _. |: k# D5 \, a5 V- m
From the 1Division of Pediatric Endocrinology, 2University of [9 \9 n) X3 s" s3 j2 k$ [$ R
South Alabama Medical Center, Mobile, Alabama.
: Z B# F/ q' Q3 h8 B4 PAddress correspondence to: Samar K. Bhowmick, MD, FACE, V4 k9 D6 q1 w8 L
Professor of Pediatrics, University of South Alabama, College of
( x; w+ [- r5 I) [+ T( bMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 ?+ R$ r! p7 z5 G- Ne-mail: [email protected].
. ^% i7 Q, g# [about 6 to 7 months old, which progressively became0 w w& a; ~$ w" R* B" ^! s* W
darker. She was also concerned about the enlarge-6 D% E" X# e+ q6 s- u1 S0 t6 f. R
ment of his penis and frequent erections. The child
- C( `+ x/ N) J# \was the product of a full-term normal delivery, with
$ W; @! a3 D1 Y& ]a birth weight of 7 lb 14 oz, and birth length of
# R3 n5 h4 m1 g0 z1 e20 inches. He was breast-fed throughout the first year
; r2 F! f; V! ~# H2 }7 }: mof life and was still receiving breast milk along with% G: _) P/ \' u4 I
solid food. He had no hospitalizations or surgery,7 V3 o" I7 V& b5 s% g
and his psychosocial and psychomotor development
0 ^0 m6 z: @+ S, A1 T! Jwas age appropriate.
9 G5 O$ I$ D' x9 QThe family history was remarkable for the father,( B. L7 I8 b6 W8 A
who was diagnosed with hypothyroidism at age 16,
/ F' z( E, A/ g% t! A- d5 ]which was treated with thyroxine. The father’s
1 \2 ?5 n- ~6 {5 eheight was 6 feet, and he went through a somewhat
- f5 ~# m! v( l e, a8 B1 rearly puberty and had stopped growing by age 14.
, r: P( A# I% _, ^' i$ zThe father denied taking any other medication. The" v; X, K# W5 k/ s- w% i. S
child’s mother was in good health. Her menarche
# r1 V9 Z! o1 h! s% q4 rwas at 11 years of age, and her height was at 5 feet
' x/ S, h* v. R: o3 S! [9 ^8 b9 g; R5 inches. There was no other family history of pre-9 k1 M; n m/ _' A' Q7 k
cocious sexual development in the first-degree rela-- f+ n0 p7 Y; b
tives. There were no siblings.
) e7 d! x) L! i8 t, dPhysical Examination
, ~2 k7 ]$ W N/ RThe physical examination revealed a very active,
/ F. p3 ]# {5 X# U' H6 m" cplayful, and healthy boy. The vital signs documented4 o% B6 L4 V1 r: V5 N1 N6 A" t
a blood pressure of 85/50 mm Hg, his length was
5 [9 c, f$ h- q' D# k f& L0 W90 cm (>97th percentile), and his weight was 14.4 kg
" Q# w, B, K- Q; ~( ~(also >97th percentile). The observed yearly growth
& B& V; ~. Z3 xvelocity was 30 cm (12 inches). The examination of
2 C5 D7 k L5 J. [6 |* n7 rthe neck revealed no thyroid enlargement.
9 x# }; k8 Z7 \. U h/ m; R [9 }The genitourinary examination was remarkable for
) l0 m! e& X* X: Renlargement of the penis, with a stretched length of$ x: f7 a: p" X1 `
8 cm and a width of 2 cm. The glans penis was very well
: c- P9 M0 n# |" h0 Q+ c$ u8 C8 Hdeveloped. The pubic hair was Tanner II, mostly around1 I9 c) q6 i$ r( X5 H
540
# d' O* q' E9 q) @. E6 N7 d4 ~at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 W: e0 O/ g: T6 @, C, ^9 u8 S
the base of the phallus and was dark and curled. The
m* P% I( k" ]- `: D: f0 W7 Btesticular volume was prepubertal at 2 mL each." H3 w) x5 o0 @' v& j: x. D3 Z
The skin was moist and smooth and somewhat
9 S. u* V( s' ~! r, b% Poily. No axillary hair was noted. There were no
5 B6 a7 G$ K& q2 H5 v, _0 sabnormal skin pigmentations or café-au-lait spots.
) g3 {& {- t l C2 V: o& p- u) ENeurologic evaluation showed deep tendon reflex 2+
" g; x2 Y% E" y! `: U3 x9 C; vbilateral and symmetrical. There was no suggestion
0 K/ C0 r2 |. |9 h% W6 t2 {of papilledema.
' @, l2 U1 C7 q, ]! R* j" K. mLaboratory Evaluation
* F! o' t4 w. P( V- UThe bone age was consistent with 28 months by
# Y5 o& x+ {) `7 h. u8 eusing the standard of Greulich and Pyle at a chrono-' P! L* _, {, f/ V' @+ \. q
logic age of 16 months (advanced).5 Chromosomal8 l9 H! G1 i F- ~
karyotype was 46XY. The thyroid function test
y8 V6 p( S1 @% O. qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
- f: w" i8 }. Q! q, F6 elating hormone level was 1.3 µIU/mL (both normal).
& D+ r, `2 f6 d& e- w0 {# w0 Y( sThe concentrations of serum electrolytes, blood
5 {9 J& Z5 n; h" [- N6 q. ourea nitrogen, creatinine, and calcium all were- t9 y. t6 o e( t% \
within normal range for his age. The concentration
3 N; ?1 c/ w9 S1 L5 `* cof serum 17-hydroxyprogesterone was 16 ng/dL \' d) ?% s8 ] L4 u
(normal, 3 to 90 ng/dL), androstenedione was 20
- C- U* U0 @5 N. Y8 Vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ _7 @3 J7 z8 r! j5 Jterone was 38 ng/dL (normal, 50 to 760 ng/dL),
" r+ N! ^8 R4 D7 E, q$ tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
# W% X4 I) w. C- ?49ng/dL), 11-desoxycortisol (specific compound S)6 d0 M& u6 S# w2 i% W9 g
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: B2 e T! z" @7 ? f
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; G4 p- A6 G3 V! j; ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
% D* s" O" g9 m& A2 i, [; C aand β-human chorionic gonadotropin was less than( h& h3 H# h9 G3 U9 D2 \# b" @
5 mIU/mL (normal <5 mIU/mL). Serum follicular% Z* z6 [+ z4 K; [! A6 w6 J
stimulating hormone and leuteinizing hormone
) k5 j" d" J( z" L4 V5 i6 Cconcentrations were less than 0.05 mIU/mL
1 V) r$ C$ O* q(prepubertal).
' U; H; \' p5 SThe parents were notified about the laboratory
* s9 ?# D; x4 c9 M% Vresults and were informed that all of the tests were5 M% \' ?3 a; P# K/ w! o. I% F
normal except the testosterone level was high. The
- N. u8 `. @6 Y" Lfollow-up visit was arranged within a few weeks to
5 D5 }3 {9 V* G' g7 q. p) Oobtain testicular and abdominal sonograms; how-
+ t6 Y: [1 E, \0 x" ^! r9 hever, the family did not return for 4 months.
, h3 T/ B) ]' S; h* O9 lPhysical examination at this time revealed that the
9 a# H9 z0 n) u3 ichild had grown 2.5 cm in 4 months and had gained$ V3 w+ ?: t1 q
2 kg of weight. Physical examination remained3 Y# k1 J6 N% e/ `7 j) }
unchanged. Surprisingly, the pubic hair almost com-
( P6 h0 j9 o: h( Z: C2 z* qpletely disappeared except for a few vellous hairs at/ i; P1 v8 I0 t; p3 b3 [
the base of the phallus. Testicular volume was still 2. l1 V3 {: P( b6 ~: B
mL, and the size of the penis remained unchanged.
! A; U# O& I# t( jThe mother also said that the boy was no longer hav-3 I7 ^. c& X9 g$ Q
ing frequent erections.# ~! d% y( R- O7 f; Q* I
Both parents were again questioned about use of
5 ~( l! ]: |' j' ?4 M6 Pany ointment/creams that they may have applied to- B1 _2 {1 |) J M+ V
the child’s skin. This time the father admitted the; }, z; K1 _0 I2 m( m' u! P
Topical Testosterone Exposure / Bhowmick et al 541% R# R$ L" e$ `# Y5 A r M3 Y
use of testosterone gel twice daily that he was apply-
0 U7 D9 @& B9 r: H* ?3 c" W, Ring over his own shoulders, chest, and back area for, q$ S; V; A$ t% h7 J+ ]
a year. The father also revealed he was embarrassed
0 [; Q, x/ A2 U& f8 V, nto disclose that he was using a testosterone gel pre-/ u1 j. l8 Z4 i7 C2 ^
scribed by his family physician for decreased libido4 T* n- }6 @" x. u5 F
secondary to depression.
}% `% e6 K8 zThe child slept in the same bed with parents.
; D' P6 A. X* k! Y! C$ }8 IThe father would hug the baby and hold him on his* e6 I; X2 U$ f( ?: c6 H9 E
chest for a considerable period of time, causing sig-
7 w% l6 w9 q# U- Wnificant bare skin contact between baby and father.
8 Z [) i: b- R, lThe father also admitted that after the phone call,
4 ^) [5 X2 C/ W, ~+ V7 Lwhen he learned the testosterone level in the baby5 O% i' c7 R+ j5 C
was high, he then read the product information
& r" ^% p" A) c" V' A6 tpacket and concluded that it was most likely the rea-
7 u7 z1 S4 L7 ?+ R$ {* pson for the child’s virilization. At that time, they- S' W& w6 @1 S; ~, L. I, E$ _/ | e- c& [
decided to put the baby in a separate bed, and the* j6 Q" Z! f5 y# |# ]
father was not hugging him with bare skin and had
7 C7 h$ k- ~1 N4 d4 g0 sbeen using protective clothing. A repeat testosterone
0 d* Z' F4 h$ vtest was ordered, but the family did not go to the
/ D* A: D( V8 u$ V: c; q# a6 Ylaboratory to obtain the test.
6 ^& c1 P. U0 B/ j% n. x. sDiscussion f5 s! t0 `2 i. n* { v
Precocious puberty in boys is defined as secondary1 k- y" a9 N. ]7 L* R
sexual development before 9 years of age.1,4
* y# t0 a8 F* q1 F J% I5 g$ c0 H. YPrecocious puberty is termed as central (true) when
1 h; ?( d0 j% i ^2 t0 O; Kit is caused by the premature activation of hypo-
/ O# I; G. t* D' Jthalamic pituitary gonadal axis. CPP is more com-
2 ~" g) x! B7 n& b# f. g1 {3 \mon in girls than in boys.1,3 Most boys with CPP
3 {0 s# Q( @' i8 v& z/ m5 _5 Qmay have a central nervous system lesion that is
t* y/ x5 C9 t7 rresponsible for the early activation of the hypothal-# B; |( n+ ~0 e
amic pituitary gonadal axis.1-3 Thus, greater empha-
: Y- U' N' k9 X: u0 Z$ Msis has been given to neuroradiologic imaging in
0 c9 L0 c; r8 B9 Oboys with precocious puberty. In addition to viril-
9 B, e( {/ G% b3 V0 l! S/ U+ V! Sization, the clinical hallmark of CPP is the symmet-5 Y. b. x5 [* A; b5 c) z" S
rical testicular growth secondary to stimulation by
+ t' K% q! o5 J' h2 x0 Sgonadotropins.1,3
+ B. m# \: d" f1 b( Q( OGonadotropin-independent peripheral preco-; u" L( `7 U$ ~7 Z# v! x D& n: i
cious puberty in boys also results from inappropriate
* q$ n5 K, z0 D% w# [androgenic stimulation from either endogenous or9 [3 i Q0 L8 J5 |8 U
exogenous sources, nonpituitary gonadotropin stim-
- g3 F5 R2 @: b8 s1 ~9 F @: Sulation, and rare activating mutations.3 Virilizing2 J! g8 Y1 }) A5 n! [- `2 e3 i
congenital adrenal hyperplasia producing excessive
3 y3 ?' `. b/ Z4 x8 F, g8 |' [adrenal androgens is a common cause of precocious% {* A; y, R& @7 j8 s
puberty in boys.3,4
" J7 a) I" ?0 b7 {4 D( qThe most common form of congenital adrenal6 E' y9 C k: d
hyperplasia is the 21-hydroxylase enzyme deficiency.
. P# R0 p! b9 T# H$ M3 m+ WThe 11-β hydroxylase deficiency may also result in. S' _, f; z) }; b
excessive adrenal androgen production, and rarely,& ?$ p/ O: a; ]
an adrenal tumor may also cause adrenal androgen
: @) @2 |( n% ?5 K) hexcess.1,35 l7 R7 ?: f# ~2 [7 _: g, j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 a9 W9 u/ f4 c9 h3 r3 l' A542 Clinical Pediatrics / Vol. 46, No. 6, July 20074 r+ E" F& C2 r: j6 Y2 q2 W
A unique entity of male-limited gonadotropin-- Q% F, C8 a, n% g4 G' i
independent precocious puberty, which is also known# `6 e3 d3 F& a! s0 F
as testotoxicosis, may cause precocious puberty at a
$ [0 s$ i, S4 u5 O8 u* R# K1 Cvery young age. The physical findings in these boys. g8 A g1 ?, N" J" {1 H3 e, F# q, }! w
with this disorder are full pubertal development,1 w+ [( s% n6 J, @$ H1 n
including bilateral testicular growth, similar to boys
2 W3 X8 g/ w; d: X H8 |/ xwith CPP. The gonadotropin levels in this disorder
9 `" L& Z, ?7 nare suppressed to prepubertal levels and do not show. @; A# F/ t. a: T
pubertal response of gonadotropin after gonadotropin-
' L0 V9 u2 e% V3 ~releasing hormone stimulation. This is a sex-linked
3 V2 k7 e! V1 S$ z1 Kautosomal dominant disorder that affects only
) X) Y0 }, i( M0 l6 \: qmales; therefore, other male members of the family
M6 Y2 R0 s7 z; h( {2 zmay have similar precocious puberty.3
: B5 D. k0 C& a( A f2 KIn our patient, physical examination was incon-
% o0 i5 D8 |1 b0 Y. Qsistent with true precocious puberty since his testi-( I$ Y/ ]2 J Y% M" b: l
cles were prepubertal in size. However, testotoxicosis) {( a* w9 |; F8 j( O3 h
was in the differential diagnosis because his father2 \6 k$ j6 I8 `# [3 P# {! ?, z2 d( r( n
started puberty somewhat early, and occasionally,: V: N- n* H7 K! l& y. A" b2 T
testicular enlargement is not that evident in the' @. U+ i: p3 X6 x
beginning of this process.1 In the absence of a neg-6 @6 w0 f& p& e5 `+ P3 [8 ~) J
ative initial history of androgen exposure, our+ c: K/ R5 [) g. p/ L, B3 C
biggest concern was virilizing adrenal hyperplasia,- A0 [2 g: _) F i3 ]
either 21-hydroxylase deficiency or 11-β hydroxylase
5 T. N! A" \0 edeficiency. Those diagnoses were excluded by find-
# s' A' g6 S- K0 i; jing the normal level of adrenal steroids.
2 w7 L0 ]; y3 F3 |# n2 N- x$ w4 D/ `) wThe diagnosis of exogenous androgens was strongly) x) a; A2 N5 }( {8 R7 a0 T
suspected in a follow-up visit after 4 months because
+ | F' I& h! {+ [the physical examination revealed the complete disap-
- K6 M3 P( x+ A- \pearance of pubic hair, normal growth velocity, and
5 ^! n* a0 o( e, \2 M9 U/ Pdecreased erections. The father admitted using a testos-, A k, g+ C8 R0 v
terone gel, which he concealed at first visit. He was
; |0 ?8 r D/ uusing it rather frequently, twice a day. The Physicians’7 ]8 P" }2 e! b
Desk Reference, or package insert of this product, gel or
/ W" |2 v, [5 qcream, cautions about dermal testosterone transfer to& I0 G+ ^0 j# L \% N9 M; Q
unprotected females through direct skin exposure.3 V% I0 F5 m" n3 T6 j: G- x( ^( h7 g
Serum testosterone level was found to be 2 times the
+ Y I- Z$ T/ Kbaseline value in those females who were exposed to
" U" v+ b: @: ]+ j' neven 15 minutes of direct skin contact with their male) ~/ H" H: w% x7 B/ w2 [
partners.6 However, when a shirt covered the applica-
i! h! K' `' o$ E0 F; C3 A4 rtion site, this testosterone transfer was prevented.
3 e- n" s8 T2 L g; U8 L5 v1 nOur patient’s testosterone level was 60 ng/mL,# ?3 o" y D/ W* [: c. s3 H2 S# J9 `
which was clearly high. Some studies suggest that
! i' V2 c# W8 l: zdermal conversion of testosterone to dihydrotestos-
$ F e3 w4 t, ^! N& B2 F0 C4 F6 Aterone, which is a more potent metabolite, is more0 T( C# f0 M+ G5 D6 Z3 J, C
active in young children exposed to testosterone4 h5 q" j' J, P- B: A$ u) A+ `5 F
exogenously7; however, we did not measure a dihy-, o9 G. J& ?2 {% [1 Z
drotestosterone level in our patient. In addition to4 e, ?# p! D+ n R' c6 v
virilization, exposure to exogenous testosterone in
2 w; P' p3 r( d& j6 [7 E6 vchildren results in an increase in growth velocity and$ Q0 g/ m: B4 h8 K3 t* y
advanced bone age, as seen in our patient.
9 {$ `5 V! L( w' ~The long-term effect of androgen exposure during
, f$ U% K' x8 G$ c& c. ]% D4 iearly childhood on pubertal development and final
, Q$ W4 Y6 y! [7 \adult height are not fully known and always remain
! s6 w! O8 y: h8 Q3 y; Ma concern. Children treated with short-term testos-
9 m4 o! _1 t- y, g1 T' {8 gterone injection or topical androgen may exhibit some4 l( }- v; X' X) y: }% M$ J
acceleration of the skeletal maturation; however, after! K; [# E, h, l* _8 T
cessation of treatment, the rate of bone maturation2 J* Z, H# p" y& m" s$ D, `
decelerates and gradually returns to normal.8,9+ l2 J8 k$ I9 G6 C" a% y
There are conflicting reports and controversy) V3 d: d4 r8 L$ O
over the effect of early androgen exposure on adult
! L+ b% ~2 n, Wpenile length.10,11 Some reports suggest subnormal+ h) v& U1 V+ O4 d; G* Z; p
adult penile length, apparently because of downreg-
; w9 h$ `9 ~" g& r% I5 julation of androgen receptor number.10,12 However,
1 Y! R \( k+ y9 i) QSutherland et al13 did not find a correlation between
6 v1 i% S: F/ Z* m Qchildhood testosterone exposure and reduced adult8 @/ `1 i7 y2 }; t+ z2 |
penile length in clinical studies.0 W" u9 W5 J, R5 K- w$ l+ t0 W
Nonetheless, we do not believe our patient is+ I2 ?$ T, G8 g, k5 G& X
going to experience any of the untoward effects from1 V/ A3 b( R* q
testosterone exposure as mentioned earlier because0 c3 p3 }$ [ N ^" k& ?% H. G* X. ~
the exposure was not for a prolonged period of time.( W5 o* E, i2 w+ o" \7 s: M
Although the bone age was advanced at the time of
( z8 V4 r+ l9 \9 o1 vdiagnosis, the child had a normal growth velocity at8 e8 _7 i \/ L$ \/ x5 ]
the follow-up visit. It is hoped that his final adult
7 D! |0 c3 }: k+ dheight will not be affected.
. {$ N8 I" A5 `9 @ C8 A+ [Although rarely reported, the widespread avail-
" a( q7 C* C& {* w+ c. z' _ability of androgen products in our society may
* [. I$ J$ k+ V6 ?& _7 W$ f$ a7 Dindeed cause more virilization in male or female
0 \ `' s$ i: x$ k5 v: Ichildren than one would realize. Exposure to andro-
9 P3 t$ Z, W8 d% b$ Y! w9 mgen products must be considered and specific ques-
; w F# p. }: S1 T) P, R( etioning about the use of a testosterone product or6 l+ [+ G" P5 f' w( G
gel should be asked of the family members during
6 o. I$ D3 G7 h: |4 r/ {' kthe evaluation of any children who present with vir-
! S7 r7 r9 w5 o# L; bilization or peripheral precocious puberty. The diag-2 c' Z; Z# {* f' a
nosis can be established by just a few tests and by
" M0 o3 f' ~" v# d; R5 Zappropriate history. The inability to obtain such a
0 F ^7 F1 x; R# T# ? Y/ X( r# F$ ihistory, or failure to ask the specific questions, may8 o( J# Q2 c; [ Z
result in extensive, unnecessary, and expensive
/ W0 R* H$ s f& Ninvestigation. The primary care physician should be8 H2 Z# Y8 I- \* c! N" Y$ t6 r5 C
aware of this fact, because most of these children1 `" _1 f0 z6 V3 w! B* K
may initially present in their practice. The Physicians’
: q# F" E& P# [0 ~- \$ S: z8 fDesk Reference and package insert should also put a" ~2 [& }" M, D8 u! ]7 u/ u
warning about the virilizing effect on a male or$ V& s' }- L7 M0 u, N
female child who might come in contact with some-6 {7 r* n' k" y7 ~, W' d9 w
one using any of these products.* L! O; a" d' Q) m
References
& U2 J* w& b; P9 U* Z( A1. Styne DM. The testes: disorder of sexual differentiation
5 R+ a# d5 o" \( d2 R* land puberty in the male. In: Sperling MA, ed. Pediatric
3 ]3 y' o( b# [$ WEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 h( C5 X# x+ N1 K% }+ s: Q" @2002: 565-628.9 ^" h6 N ^+ Z. p2 m3 u' P0 ]
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& h- b2 D! j& P1 @& ]9 _) ppuberty in children with tumours of the suprasellar pineal |
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