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Sexual Precocity in a 16-Month-Old
) `9 i) S8 F8 S8 T) F J7 ABoy Induced by Indirect Topical
8 ^- u' g& R7 m7 ?2 v3 C. pExposure to Testosterone& K9 P9 ?/ ^2 d% A
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
- K8 c% S9 a+ ^' T- {% Mand Kenneth R. Rettig, MD1$ d( z# M3 i4 b/ O7 @
Clinical Pediatrics2 \$ C0 w/ Z# ?# T0 Q" X
Volume 46 Number 68 \ I# b+ C0 ]/ g1 G& ~
July 2007 540-543
6 ~2 [; U0 b' ~! n© 2007 Sage Publications
2 T* P, U1 {* j$ D' M10.1177/0009922806296651
7 U- r7 \* H9 B2 X5 rhttp://clp.sagepub.com' Z8 X6 A g2 A$ N: v8 T/ m
hosted at
5 L D$ E6 b1 C6 I. K4 Vhttp://online.sagepub.com, g' p/ @- S: b1 A8 C a
Precocious puberty in boys, central or peripheral,5 y1 b) i; C; B+ A2 j
is a significant concern for physicians. Central
- Z1 S8 Q( O. r; [# Jprecocious puberty (CPP), which is mediated( m* `6 v1 @$ q) {/ S% v
through the hypothalamic pituitary gonadal axis, has: y1 P$ y- W; b: d' J
a higher incidence of organic central nervous system
0 X+ _5 b6 U( [# Glesions in boys.1,2 Virilization in boys, as manifested% [) D P( f5 H) k& R
by enlargement of the penis, development of pubic* V$ A" I* o# k7 F2 C
hair, and facial acne without enlargement of testi-
7 E' v9 C' s! l! J _cles, suggests peripheral or pseudopuberty.1-3 We
7 N3 L' K! C& I3 u2 ?* ^report a 16-month-old boy who presented with the
+ T0 W3 p3 O! U; D, s! q7 Lenlargement of the phallus and pubic hair develop-5 j7 H# O) P, A6 \
ment without testicular enlargement, which was due4 q$ d# |* r& ?# K8 L! m2 \3 k2 `' i
to the unintentional exposure to androgen gel used by
1 l* k6 j2 _/ T0 ^# }1 x% ]the father. The family initially concealed this infor-2 E$ e) j6 _' I; C5 y6 b
mation, resulting in an extensive work-up for this8 I4 d8 D. M* M
child. Given the widespread and easy availability of+ ?3 \% z# U# }# y
testosterone gel and cream, we believe this is proba-# `6 o/ X& |! k% Y/ K
bly more common than the rare case report in the0 K$ J& x: p' {- U" W2 T* m
literature.4
3 X2 ^3 ]; w; C1 }) L: OPatient Report3 m% N( g3 I* Y1 {$ o2 Y- n
A 16-month-old white child was referred to the
. _! O( t% t0 K1 Rendocrine clinic by his pediatrician with the concern$ J3 E9 Q4 V' q$ @! A
of early sexual development. His mother noticed
6 C- C" t% e5 \/ wlight colored pubic hair development when he was& ?, g/ o# ]4 l7 t* @
From the 1Division of Pediatric Endocrinology, 2University of* G: d* J7 g0 m2 s
South Alabama Medical Center, Mobile, Alabama.7 A$ I8 {- q+ j
Address correspondence to: Samar K. Bhowmick, MD, FACE,
& N7 D$ Z9 Z5 F2 l' uProfessor of Pediatrics, University of South Alabama, College of9 p+ A5 q: e2 U1 D1 v k
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ D( k1 a+ H/ j+ q w+ le-mail: [email protected].+ e2 [* [0 b i/ {
about 6 to 7 months old, which progressively became
* {$ m' p% ], l6 Idarker. She was also concerned about the enlarge-( g$ f; x2 h: Q, f
ment of his penis and frequent erections. The child
L- \7 H/ r# m# |& t0 p% o+ Kwas the product of a full-term normal delivery, with6 L6 T E2 d9 T6 z- v/ E
a birth weight of 7 lb 14 oz, and birth length of
8 l, q& T+ Y$ p3 h, P" E20 inches. He was breast-fed throughout the first year
3 p# i$ g l. iof life and was still receiving breast milk along with
* V) u9 D1 r/ U- K* ~solid food. He had no hospitalizations or surgery,
9 _. l3 [, P- \. N5 F" Kand his psychosocial and psychomotor development
, f' x* \; b! v& iwas age appropriate.
; Y* ^; l9 K" ~- k0 }* a4 J+ i" tThe family history was remarkable for the father,& E$ ]6 ^; N( R
who was diagnosed with hypothyroidism at age 16,0 K, E6 m8 m. R$ p P2 E6 E: a
which was treated with thyroxine. The father’s
1 B. }* E$ R- K3 n6 U# ]* a/ H$ Y' Uheight was 6 feet, and he went through a somewhat
% k/ V* E x$ I# s5 P7 d7 a; bearly puberty and had stopped growing by age 14.6 I" z8 ^& [4 D* O
The father denied taking any other medication. The$ M# R- H& ^' i+ L$ z9 t6 A
child’s mother was in good health. Her menarche6 _8 M% U" A( U; V4 r* [
was at 11 years of age, and her height was at 5 feet
$ G( b% d7 h" e) a. H& O5 inches. There was no other family history of pre-6 K7 N6 l) k1 A: t3 o
cocious sexual development in the first-degree rela-
+ ]+ [ b6 G9 ntives. There were no siblings.
4 t! Q) X& T1 l# H0 t+ H+ ^Physical Examination
; r+ N2 c% [2 j C e% X$ BThe physical examination revealed a very active,5 x; t( O6 Z: d5 a. o" D
playful, and healthy boy. The vital signs documented
7 I: U: e6 X7 H. b' }a blood pressure of 85/50 mm Hg, his length was
) {' d& G" O9 d; `+ q. `0 l9 |8 i90 cm (>97th percentile), and his weight was 14.4 kg
1 C5 C- W3 l% J; m2 _. H# t(also >97th percentile). The observed yearly growth
& t, p9 O& z: F( W9 J6 {( \7 zvelocity was 30 cm (12 inches). The examination of
0 |# m8 }9 T# a! E3 mthe neck revealed no thyroid enlargement.6 d, r2 ~9 }) f) s* ~
The genitourinary examination was remarkable for2 I4 p& Q& @# u% K5 ^
enlargement of the penis, with a stretched length of
# n; U" u2 K4 o8 cm and a width of 2 cm. The glans penis was very well+ N2 m- A) F" y# i5 C" x* b
developed. The pubic hair was Tanner II, mostly around
# s0 {% p6 t& z* |6 k, J3 T9 t5409 F; D1 a8 i4 ~5 `1 l5 g G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 v" n z+ }, a0 T/ X8 c! r$ k' A
the base of the phallus and was dark and curled. The' x, M# K8 P4 ?3 M' j6 B8 r% D& S
testicular volume was prepubertal at 2 mL each.: e+ S& l L+ o& V
The skin was moist and smooth and somewhat
5 }) q0 H9 }7 I8 F/ B$ @8 _4 Yoily. No axillary hair was noted. There were no' F1 S! |3 V' `# t2 Y
abnormal skin pigmentations or café-au-lait spots.1 U+ H2 |; O7 W
Neurologic evaluation showed deep tendon reflex 2+3 k" T0 ^0 N' \
bilateral and symmetrical. There was no suggestion
8 h" W" z9 A$ _, e, [of papilledema.
3 I7 J0 q" {: z$ V2 l- G- H1 xLaboratory Evaluation4 t( I0 p2 A3 i, b1 R! t
The bone age was consistent with 28 months by( R8 q7 ]1 V! G, ^ J; Y+ {! p
using the standard of Greulich and Pyle at a chrono-( S. u' y$ L' L' T W# C
logic age of 16 months (advanced).5 Chromosomal. `; I, I. y0 p, a0 P
karyotype was 46XY. The thyroid function test
4 K. n8 ~* P1 }. Mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! ?/ C, k4 {2 W+ L8 k6 Klating hormone level was 1.3 µIU/mL (both normal).
4 b& e( @- Y- G- NThe concentrations of serum electrolytes, blood
( e7 L3 }+ M, P+ S% L- Curea nitrogen, creatinine, and calcium all were& j/ o* [! I4 p
within normal range for his age. The concentration, G: e- r# S! @) u+ ~( b5 L
of serum 17-hydroxyprogesterone was 16 ng/dL
* v- d m. I5 |5 M3 F(normal, 3 to 90 ng/dL), androstenedione was 20' q8 d: [' {) F0 e( x1 i4 n6 O
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
+ f* Y9 Y5 b, ?terone was 38 ng/dL (normal, 50 to 760 ng/dL),
( ~5 t4 _ M1 r) x! E( t S6 ?2 Qdesoxycorticosterone was 4.3 ng/dL (normal, 7 to0 u) ~- V3 v' x4 ?- z6 ^/ A
49ng/dL), 11-desoxycortisol (specific compound S)
) z; e) i3 O- o; `3 v6 Q% |was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
# Z3 B% h0 R# v+ A% [7 D" Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
! l! \* z* H* K6 stestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) I0 [: V9 g9 A" ~7 m$ h' h/ Kand β-human chorionic gonadotropin was less than8 M/ R: g, b$ w
5 mIU/mL (normal <5 mIU/mL). Serum follicular l) G: ]5 V! M1 x; p
stimulating hormone and leuteinizing hormone: b# R( w9 \5 E+ g6 B/ b
concentrations were less than 0.05 mIU/mL
; x, \* d! `! i$ f- C(prepubertal).
: @9 r: A3 Y3 D U) F0 A- e8 E/ yThe parents were notified about the laboratory% O/ q2 r# Y A/ N8 V8 h
results and were informed that all of the tests were) J; D1 b( @4 _1 U% u. ~
normal except the testosterone level was high. The
( M& v t3 z; D2 yfollow-up visit was arranged within a few weeks to
+ ~1 j: h' K8 Qobtain testicular and abdominal sonograms; how-1 G; Y, ?, x" L+ Y4 q2 p: G. h. m7 _
ever, the family did not return for 4 months.. a; Q- B7 q9 L) l A# C, @
Physical examination at this time revealed that the
! {+ X/ Z% e) \' K4 P# {child had grown 2.5 cm in 4 months and had gained
) I- S6 z2 n# E2 kg of weight. Physical examination remained4 z5 T# z; p7 G! ^
unchanged. Surprisingly, the pubic hair almost com-
3 h. X# f9 o: p2 |pletely disappeared except for a few vellous hairs at
( N; B2 d5 O: }& c# S1 V/ T3 ^$ A& Vthe base of the phallus. Testicular volume was still 2
* q: t, P9 q. f$ N2 i: p! W; Y; mmL, and the size of the penis remained unchanged.1 o' F! J6 o$ b# i; M& j i N: A* V
The mother also said that the boy was no longer hav-3 H3 b5 Z; `; X D; e
ing frequent erections.
p- h$ i7 t. K* P$ h7 } r& Y* W* f! WBoth parents were again questioned about use of
, Q" {: G8 }6 |any ointment/creams that they may have applied to. H; n3 I e6 B) ~+ ^2 o3 I
the child’s skin. This time the father admitted the8 B# P1 q0 H, h/ q
Topical Testosterone Exposure / Bhowmick et al 541. y9 G# M+ F7 k$ m' y
use of testosterone gel twice daily that he was apply-
/ v: O+ I* z8 _6 h- P! j6 a7 O" g7 Bing over his own shoulders, chest, and back area for& @0 s, O4 A4 b& G4 @
a year. The father also revealed he was embarrassed: s9 M: p1 f* K8 O
to disclose that he was using a testosterone gel pre-( F6 i+ V Y. O" J% f; O5 A
scribed by his family physician for decreased libido- J1 m7 d; g; H1 Y1 B, e
secondary to depression.- E4 `% Y; j) u/ X7 f" y4 h
The child slept in the same bed with parents.
- D. h! V! I* [: D0 FThe father would hug the baby and hold him on his2 T4 C. Z8 x6 ^3 l4 |
chest for a considerable period of time, causing sig-
) ?# V5 h E6 ~( dnificant bare skin contact between baby and father.
& s- z, l! J' q+ y3 H- zThe father also admitted that after the phone call,7 K! n h1 {# {. r3 w6 L
when he learned the testosterone level in the baby
5 V5 _2 C+ V6 {: Y: v, gwas high, he then read the product information
2 O: _' n+ Y, R$ Q( W. i; C# dpacket and concluded that it was most likely the rea-
; P' i: P0 g2 e( c7 U) b. }+ v; y# ason for the child’s virilization. At that time, they
~4 u. M* }9 B9 \decided to put the baby in a separate bed, and the
: @6 N9 r+ `* l, afather was not hugging him with bare skin and had- C1 f7 u7 P( b- B& k
been using protective clothing. A repeat testosterone
: m7 c# u+ M' ztest was ordered, but the family did not go to the
2 W5 k# T6 T% T! t' a3 C5 nlaboratory to obtain the test.
3 i0 I% ^# {* ^Discussion* I* r, W3 {/ X- S1 }! R/ q
Precocious puberty in boys is defined as secondary& ~# E3 |% u1 s$ A8 Y" `/ v; \ l+ t
sexual development before 9 years of age.1,4
8 S5 ?& X4 @! l- R9 C, [( y4 OPrecocious puberty is termed as central (true) when
6 a' J' J+ i# k! a0 @& |. Kit is caused by the premature activation of hypo-/ v: a7 S6 v+ i J! f
thalamic pituitary gonadal axis. CPP is more com-) o0 ]) _9 {5 g2 C2 \. B
mon in girls than in boys.1,3 Most boys with CPP! _+ {6 o8 v0 f
may have a central nervous system lesion that is
+ R$ `7 J& ~4 t8 \" Xresponsible for the early activation of the hypothal-
c) t$ G. s& c- Namic pituitary gonadal axis.1-3 Thus, greater empha-, G" }& c8 ^! F6 \& H% d
sis has been given to neuroradiologic imaging in+ J* v: ]& M7 `4 M' X. y) D) v
boys with precocious puberty. In addition to viril-3 J2 ~8 ~, E# ~+ u$ n2 B7 T
ization, the clinical hallmark of CPP is the symmet-
! u6 m8 U6 \% J! jrical testicular growth secondary to stimulation by
" d5 h" i8 S# Z I/ D- x6 Cgonadotropins.1,3) C' E0 V# ?. I' ~! m$ c
Gonadotropin-independent peripheral preco-
* d$ ~- j* h) }1 ?! ?( rcious puberty in boys also results from inappropriate# J7 _3 T% Q ]8 l
androgenic stimulation from either endogenous or
) }' f' s6 y9 }) nexogenous sources, nonpituitary gonadotropin stim-
3 ?% D+ Q' D& ?+ F* ]2 A5 julation, and rare activating mutations.3 Virilizing' `2 Y m1 Z. P, r4 B/ m1 I) X
congenital adrenal hyperplasia producing excessive7 ^$ i8 x0 B! N O. b: ?8 x! L1 J5 M
adrenal androgens is a common cause of precocious
5 r# O+ ]/ j8 C5 w' } F+ |, jpuberty in boys.3,43 T% q- g: g4 a3 u% S6 m8 @4 I
The most common form of congenital adrenal1 H0 q! n. d+ R3 D, x
hyperplasia is the 21-hydroxylase enzyme deficiency.
5 [, v8 B+ M* Z! N! C& I8 ]The 11-β hydroxylase deficiency may also result in
6 E3 r3 g6 j _4 T1 Y; W; \excessive adrenal androgen production, and rarely,0 r W& c. }8 N0 P
an adrenal tumor may also cause adrenal androgen2 S9 a. T& ? h! R' T& W
excess.1,3
& ]3 {& ^ W. A$ ~at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from h ~) J, c' l& L+ I4 P$ `( u$ O3 ]
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007% Y, G: |! ~$ s' L5 P0 f
A unique entity of male-limited gonadotropin-
* l, N% y3 p/ m) r5 z% J: _independent precocious puberty, which is also known
. U) n1 W. W6 E) s( T6 zas testotoxicosis, may cause precocious puberty at a
8 W5 K2 }/ _9 @/ fvery young age. The physical findings in these boys W, U0 g1 L; z J; A9 U3 I1 h7 f
with this disorder are full pubertal development,
' t: B; L; ~# G& _" O# Hincluding bilateral testicular growth, similar to boys$ ` _* ^. s! ]# ^% n. F
with CPP. The gonadotropin levels in this disorder
2 H( O, X( Z0 _* Ware suppressed to prepubertal levels and do not show3 l4 T J! ~- }7 d* r7 C
pubertal response of gonadotropin after gonadotropin-
% s! P& u6 I+ F8 _! n1 b( Vreleasing hormone stimulation. This is a sex-linked
: Z* H0 q7 x; W' }2 o* Jautosomal dominant disorder that affects only
3 C& j- ? i4 @' J8 ?! Z1 X; T7 e) J1 U Rmales; therefore, other male members of the family
: h1 d3 X( j+ Y' y% a A0 [+ m6 bmay have similar precocious puberty.3
2 D: b9 T5 _( P) c% @4 d2 KIn our patient, physical examination was incon-- H1 t+ A6 @) ^; s5 j+ \# f' Y
sistent with true precocious puberty since his testi-
/ J' ~2 T9 u4 L& ?- Wcles were prepubertal in size. However, testotoxicosis" v3 O! o! a+ N# @/ G3 f
was in the differential diagnosis because his father+ G. h8 n: Q/ h5 G( e7 f
started puberty somewhat early, and occasionally,
& G: O" T' w f( ^testicular enlargement is not that evident in the
9 w8 g1 J# w- V! B( Ybeginning of this process.1 In the absence of a neg-
+ v- \9 X/ i. r- T3 [& ^( _ative initial history of androgen exposure, our
: p) Q3 N. Q- Bbiggest concern was virilizing adrenal hyperplasia,
8 s3 X H) B) L4 s/ k* @- ueither 21-hydroxylase deficiency or 11-β hydroxylase; [9 C* R2 I8 S( h; i3 z
deficiency. Those diagnoses were excluded by find-
) K, d& y# W1 v# b& A3 v; U3 ring the normal level of adrenal steroids.% C6 B D" n" t' v
The diagnosis of exogenous androgens was strongly
p( b' L4 x# ^4 {suspected in a follow-up visit after 4 months because
! ^7 E- T$ E3 Q7 C+ ]the physical examination revealed the complete disap-) ^7 l4 W g" G' D) k6 {! s
pearance of pubic hair, normal growth velocity, and- C3 C& S' [) W, A! q5 }( A# G
decreased erections. The father admitted using a testos-0 p+ \! A/ w2 }' j5 j
terone gel, which he concealed at first visit. He was
: |" f7 S7 _( L8 ~+ Fusing it rather frequently, twice a day. The Physicians’
- L! V8 r/ Q' X |2 S' gDesk Reference, or package insert of this product, gel or6 Z8 J9 d* B" w5 g% D5 m" x H' {6 m
cream, cautions about dermal testosterone transfer to
$ B% O( F% p' V! ^. F8 Y3 S* punprotected females through direct skin exposure.1 F0 L# M* t5 X) \, { f; E
Serum testosterone level was found to be 2 times the
6 z: d. d! t( O$ |& P( tbaseline value in those females who were exposed to4 z1 z$ \$ _2 y1 M' ~/ ]" P
even 15 minutes of direct skin contact with their male* ^" a6 T. F2 T5 r6 H" m0 U. d( @4 d
partners.6 However, when a shirt covered the applica-+ h6 j% e& M0 I% C
tion site, this testosterone transfer was prevented.5 Y( _" }1 Z: \' D n
Our patient’s testosterone level was 60 ng/mL,
2 A$ _7 a. s3 p& Q: o$ q0 h; z# [6 }2 kwhich was clearly high. Some studies suggest that
L, B+ Z+ V; V6 t" [3 o, adermal conversion of testosterone to dihydrotestos-
( X6 {1 b1 Q! `* _3 u# A6 l: Jterone, which is a more potent metabolite, is more
7 P4 |# @! a/ _2 Vactive in young children exposed to testosterone& J$ H) W; ^# a* P7 l
exogenously7; however, we did not measure a dihy-; P$ u# L9 F1 r+ Q! _+ v
drotestosterone level in our patient. In addition to
: P1 s: Z5 ]' W L+ lvirilization, exposure to exogenous testosterone in
/ p" a8 ^/ z4 Xchildren results in an increase in growth velocity and, x* J; u' {% z6 j
advanced bone age, as seen in our patient.& H. v3 a0 L5 B% R3 ~/ o! n, t
The long-term effect of androgen exposure during# `0 y. {. L; F& I/ F7 @
early childhood on pubertal development and final
. ~' Y* c5 X; s$ R+ b; Cadult height are not fully known and always remain- F" O# k+ X* K. Z1 a
a concern. Children treated with short-term testos-# T$ r/ I. ?. e; U7 V2 [% A( h4 J9 u' [
terone injection or topical androgen may exhibit some
1 M8 a. x5 A% @) `0 o, a9 qacceleration of the skeletal maturation; however, after8 Q: `/ v3 R2 j9 Q
cessation of treatment, the rate of bone maturation f7 z6 B7 E1 q- @1 G
decelerates and gradually returns to normal.8,9; o" H; [9 g$ g4 `
There are conflicting reports and controversy
& B$ M9 P' k k+ ]7 q5 e( oover the effect of early androgen exposure on adult( x' h& k% U' p0 y4 w; Y' @
penile length.10,11 Some reports suggest subnormal
) e7 K5 ? ^, `, j0 madult penile length, apparently because of downreg-
8 }9 ~+ B# j+ T- [0 h: ~' Lulation of androgen receptor number.10,12 However,
, C* ^. y5 N. l/ q. I5 u' ZSutherland et al13 did not find a correlation between
- G1 d, f j! I; h4 G6 } }childhood testosterone exposure and reduced adult
6 J: V2 \* f$ J: }5 j2 }4 Upenile length in clinical studies.4 E, d6 I1 r6 R; |- F: p/ c3 m f
Nonetheless, we do not believe our patient is: N5 B. A. T6 @4 ?7 R8 [" T
going to experience any of the untoward effects from
& s/ [/ X: X3 I7 l# @9 X1 {testosterone exposure as mentioned earlier because$ w# h9 V7 c& `7 y; N
the exposure was not for a prolonged period of time.8 ~1 k' K" A) h. g
Although the bone age was advanced at the time of B8 t9 P! r1 C8 X
diagnosis, the child had a normal growth velocity at1 I, A# @) v' I* |: L7 X( U
the follow-up visit. It is hoped that his final adult
1 k1 m1 H6 `0 Wheight will not be affected.) V% Q. f: H" o7 N* I
Although rarely reported, the widespread avail-
3 ?9 I6 P$ q3 C O) \+ t- e0 ~/ vability of androgen products in our society may
2 ^2 o' e% ~) Z( j c- }indeed cause more virilization in male or female- M& c- P. X! U$ X2 `
children than one would realize. Exposure to andro-
6 U& c5 V& |3 Z9 n4 q$ D6 }1 ]gen products must be considered and specific ques-
* V5 n* `3 T ^% E) m6 O& A! W$ Ttioning about the use of a testosterone product or: h+ H, Y+ `, @ \) a) c# A
gel should be asked of the family members during
( g& L3 c; X6 _/ bthe evaluation of any children who present with vir-
: E- S" u U- v8 L4 K& y# \% x) bilization or peripheral precocious puberty. The diag-
* H E0 C7 O6 G3 Znosis can be established by just a few tests and by% j* O9 K: O; D9 y; }0 e6 f
appropriate history. The inability to obtain such a
3 h* L, r/ n* S/ b. R! r/ a3 Xhistory, or failure to ask the specific questions, may8 G/ h/ o# G* _, l4 B0 ~% L7 T
result in extensive, unnecessary, and expensive
5 x$ D- m+ ]; Z3 ]investigation. The primary care physician should be9 x) e8 L8 Q. I5 z6 A g( l9 l7 W
aware of this fact, because most of these children- z6 d) T( U6 t+ i' |8 _
may initially present in their practice. The Physicians’8 k. }3 }6 ], d ^; Y; A
Desk Reference and package insert should also put a
' i" c1 g! ^- Z- e" @+ Lwarning about the virilizing effect on a male or- G* ^/ o' K8 x) o: ]: D" x
female child who might come in contact with some-$ b! g* M( v" ~: \3 }
one using any of these products." J) a7 b" V' l- x2 V( k
References4 a, ]$ C) `- v6 N' ^
1. Styne DM. The testes: disorder of sexual differentiation1 {/ e' h! v8 s8 W8 V# `
and puberty in the male. In: Sperling MA, ed. Pediatric
7 Z: ~' Q, y9 M9 b1 f! [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. G Q6 E3 r/ `, s" x
2002: 565-628.- @( `; X f* j4 Y2 x, y* s8 _
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! j: w; C) \0 O- i2 apuberty in children with tumours of the suprasellar pineal |
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