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Sexual Precocity in a 16-Month-Old
|6 E9 {' \2 L: pBoy Induced by Indirect Topical' j C% b8 Y8 O
Exposure to Testosterone
- G& v1 G+ N0 r9 c0 w* vSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
$ q2 k+ S% |( n, Fand Kenneth R. Rettig, MD1
( k! S/ ]& E! L. P5 kClinical Pediatrics
4 F9 B+ K6 j! c3 b) n7 z1 _Volume 46 Number 6
# i6 \$ S' B! _) _! v. |9 QJuly 2007 540-543) G6 s6 s6 r" Z* D1 C w; _5 z9 i
© 2007 Sage Publications8 T. M5 f% V, A! I- T) P; o
10.1177/0009922806296651
4 t0 k" ~* }$ r! Ahttp://clp.sagepub.com
8 L6 i0 E& O1 B' ^3 t P% Chosted at
! Q$ e: p- k0 \3 h5 y" H4 @7 Nhttp://online.sagepub.com' X6 \$ W- Z2 \' P7 f |
Precocious puberty in boys, central or peripheral,
/ ]. y7 ?' I( w) i* b3 mis a significant concern for physicians. Central
3 n7 l5 h( y* a& j9 Iprecocious puberty (CPP), which is mediated' r$ Z3 _8 ~1 S3 ?4 t1 o9 O4 o
through the hypothalamic pituitary gonadal axis, has1 N5 Y0 ?# [2 C ?# e6 f
a higher incidence of organic central nervous system( k5 c2 p2 R2 H
lesions in boys.1,2 Virilization in boys, as manifested- m6 G3 h5 O: b0 I, |8 }$ F
by enlargement of the penis, development of pubic
% L" w# ]+ @3 N1 b/ _8 {/ Phair, and facial acne without enlargement of testi-
. v1 k, K& m, d. R5 H6 \' lcles, suggests peripheral or pseudopuberty.1-3 We/ h6 N8 ]* K Z( H0 \
report a 16-month-old boy who presented with the$ S* E; m, `, n1 L; ?
enlargement of the phallus and pubic hair develop-5 }3 G! C: R, J# ?$ h: P
ment without testicular enlargement, which was due
# V/ q4 q( D. U2 a) m& Ato the unintentional exposure to androgen gel used by/ ]9 Y; I3 A3 P' M5 r3 b5 a- I
the father. The family initially concealed this infor-* }% {* d$ v+ D& o
mation, resulting in an extensive work-up for this
( q0 W6 q- o5 |6 ~* G$ vchild. Given the widespread and easy availability of* t# B& Q: W9 m& v1 g# h* `! Y% `
testosterone gel and cream, we believe this is proba-# c% W: T8 D: {/ @2 ]/ {5 \
bly more common than the rare case report in the* n+ \! h- p' l% J/ t) [
literature.49 w# x2 {- w" |7 X( _
Patient Report7 c' U3 F- v% [. Y
A 16-month-old white child was referred to the6 O% N8 W4 x/ z* }* ^; E. [
endocrine clinic by his pediatrician with the concern
$ @5 |- K6 a) Tof early sexual development. His mother noticed0 D+ c z% r% A& \
light colored pubic hair development when he was
* Y9 O. U0 t" M1 hFrom the 1Division of Pediatric Endocrinology, 2University of: Z& v$ K. W' q$ D# y
South Alabama Medical Center, Mobile, Alabama.
! M/ n: {, d; e% xAddress correspondence to: Samar K. Bhowmick, MD, FACE,3 z9 d( N: L: Y/ T- W$ B: R
Professor of Pediatrics, University of South Alabama, College of7 `1 w5 p. K2 C; A1 o
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 P. n+ g" Q( P
e-mail: [email protected].9 w$ V& q2 d Q8 e" k
about 6 to 7 months old, which progressively became7 h9 n; q$ X- M# y
darker. She was also concerned about the enlarge-
' G" n- ?2 S: M/ j" fment of his penis and frequent erections. The child3 h5 j2 B# [1 i b- q2 v
was the product of a full-term normal delivery, with
- j' j# `& V: K) \% Y2 R( j% M+ Ha birth weight of 7 lb 14 oz, and birth length of
, C: A6 Q2 H+ @% a20 inches. He was breast-fed throughout the first year& B6 f2 H) ^/ v8 F
of life and was still receiving breast milk along with9 ]3 `7 K# @& w4 B
solid food. He had no hospitalizations or surgery,0 K( s. v9 L# R" Y- k! ]0 W+ |
and his psychosocial and psychomotor development
7 \& B6 Z* M& E3 _% K: L; @was age appropriate./ d7 P5 i6 F8 a7 l2 k0 @
The family history was remarkable for the father,5 ~/ w: v4 |* p" \1 l
who was diagnosed with hypothyroidism at age 16,) c( d# {- _. u, m
which was treated with thyroxine. The father’s
9 k6 b& u2 Q l7 J" H- I2 C! Q( Jheight was 6 feet, and he went through a somewhat/ d, h4 b, b3 {3 a" I3 v9 ]
early puberty and had stopped growing by age 14.
) \& w. B( a( p' B% T" sThe father denied taking any other medication. The" X0 M% o2 G! e7 z
child’s mother was in good health. Her menarche* B+ M/ n( j4 a1 }$ Y$ D1 }
was at 11 years of age, and her height was at 5 feet$ a- S1 P6 r. }* L8 m' R6 U# R9 X2 ?! w
5 inches. There was no other family history of pre-
$ M2 |$ D+ I/ d" q1 _% e; zcocious sexual development in the first-degree rela-$ q- b9 F1 E! T/ i
tives. There were no siblings.# U+ f8 Y8 M' {+ P# d
Physical Examination y4 u7 U( R1 i; W' ^, z7 E7 m6 d. B
The physical examination revealed a very active,3 a4 h' T* B1 ?# b! p. H; l
playful, and healthy boy. The vital signs documented
, _( z _/ L2 ]5 l$ Ca blood pressure of 85/50 mm Hg, his length was P0 U! R. _1 @$ r
90 cm (>97th percentile), and his weight was 14.4 kg; G+ l9 G( v; m0 r. n
(also >97th percentile). The observed yearly growth
( Z9 z+ s5 q% k4 O$ U% {! g8 @- bvelocity was 30 cm (12 inches). The examination of
% u9 Y- a/ r6 D# t) Bthe neck revealed no thyroid enlargement.5 N6 f0 U6 Z/ i
The genitourinary examination was remarkable for
! O- u6 {* P- `% O kenlargement of the penis, with a stretched length of
8 Y) K! L* A/ }& ?1 l( A. _7 S8 cm and a width of 2 cm. The glans penis was very well
; d, }% Q& t! Z$ k1 D( Gdeveloped. The pubic hair was Tanner II, mostly around
# B2 B! r* Y; ~. L540: s+ O" X8 [; E T8 Z* M
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; G7 c0 Q; a/ J) L# o' P0 kthe base of the phallus and was dark and curled. The
; s6 u% {9 @* S5 A& I6 Mtesticular volume was prepubertal at 2 mL each.5 d' `* a( o! C8 Y0 H4 s l& r
The skin was moist and smooth and somewhat2 v# z5 G. y5 T4 ?. f% Z6 e
oily. No axillary hair was noted. There were no
, T; S6 n6 Z9 T7 ]* Jabnormal skin pigmentations or café-au-lait spots.
( h7 N* B# z, k" BNeurologic evaluation showed deep tendon reflex 2+. L5 K1 @, o$ t0 R3 o5 @; {
bilateral and symmetrical. There was no suggestion* ]) O2 N6 i: j; B4 [
of papilledema.
& a Q' s3 |# L: \- MLaboratory Evaluation
) j2 R% H' `- i! Y J2 U' cThe bone age was consistent with 28 months by6 ] E: H$ c6 p8 U4 v
using the standard of Greulich and Pyle at a chrono-
8 g3 ]6 a7 N4 G7 l3 R Y( \) X) Dlogic age of 16 months (advanced).5 Chromosomal1 o/ _0 L8 O. H8 L2 |: a( J. Y7 ~$ x
karyotype was 46XY. The thyroid function test, S# ]! u# y3 o% ?" R' J/ l9 L6 X
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
& q# R, F5 s* O ?' G- B; R, f( qlating hormone level was 1.3 µIU/mL (both normal).
9 i D- z4 r: h$ d! o# l5 ^The concentrations of serum electrolytes, blood
+ c2 o) w( o e Furea nitrogen, creatinine, and calcium all were3 N: W" S; s/ K
within normal range for his age. The concentration
# ]8 k% D" D# l/ }- A' w. oof serum 17-hydroxyprogesterone was 16 ng/dL) t/ c% A5 `5 M; p8 V6 H8 B0 {* e
(normal, 3 to 90 ng/dL), androstenedione was 20
# c c. D' q4 n. _ y6 M" F; dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: d2 ?6 d/ C& F1 [3 q
terone was 38 ng/dL (normal, 50 to 760 ng/dL), Z& p' C# r1 _- V& Z! V3 _
desoxycorticosterone was 4.3 ng/dL (normal, 7 to7 k' b: {( r) O1 ^/ b7 X7 p" C
49ng/dL), 11-desoxycortisol (specific compound S)
% x) h( ]$ w7 r9 P8 T. ]4 A1 q5 Qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
/ N* M# N$ h% Ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, ]( l& k! w9 `: U/ k3 n* n0 c
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),4 ~7 _, T- h# z4 l" T
and β-human chorionic gonadotropin was less than" J: Z& }1 x5 ]6 F( u
5 mIU/mL (normal <5 mIU/mL). Serum follicular
, U( u) q# F) Mstimulating hormone and leuteinizing hormone, I# ?5 V& _ U3 ]: @
concentrations were less than 0.05 mIU/mL
I! z1 p( x5 S$ x0 a. P; i(prepubertal).' E: q$ s6 L. h1 J' k5 n. D5 n
The parents were notified about the laboratory, t# o. P {( A: ]
results and were informed that all of the tests were
# r: X6 v0 w$ ?: {8 q6 n6 Anormal except the testosterone level was high. The
& ~& f* r7 H1 Sfollow-up visit was arranged within a few weeks to
' i# Z" h2 V n9 D; b4 yobtain testicular and abdominal sonograms; how-# F% E6 ^2 y+ k0 P7 i, o
ever, the family did not return for 4 months.
6 G; |0 p$ O5 |. l9 t; z- B9 A9 UPhysical examination at this time revealed that the
, H- l( [& a; s; Lchild had grown 2.5 cm in 4 months and had gained
8 }$ N; h' j4 M4 w7 L2 L2 kg of weight. Physical examination remained
- i! |6 \0 _4 zunchanged. Surprisingly, the pubic hair almost com-1 H8 o* {* }* v$ e" z, |, @
pletely disappeared except for a few vellous hairs at1 T) G7 ?4 s% d
the base of the phallus. Testicular volume was still 2: `/ ?9 R$ b3 o
mL, and the size of the penis remained unchanged.
% e6 M- v3 Y& ^7 W- i) o3 C/ O# }The mother also said that the boy was no longer hav-
9 p/ I7 P7 I& R5 [4 {% r0 Ming frequent erections.
# j" I. x9 p+ u; q7 O! ?Both parents were again questioned about use of
- c" k' |7 z5 s3 {0 dany ointment/creams that they may have applied to3 U: f% Q- p- s8 J; y
the child’s skin. This time the father admitted the8 b: Z2 {+ x$ @0 Q
Topical Testosterone Exposure / Bhowmick et al 5416 {* p& y( x8 R! ?: ~8 p
use of testosterone gel twice daily that he was apply-4 V/ ~/ j. T- W! I7 O5 \0 h4 |6 ?
ing over his own shoulders, chest, and back area for% w* x1 `' q$ }8 k+ n! D0 c2 T
a year. The father also revealed he was embarrassed# S+ @7 c9 u5 h9 R8 i
to disclose that he was using a testosterone gel pre-
* I: ^+ [$ ?' j9 R4 H1 I* n" T3 W& ]scribed by his family physician for decreased libido5 S2 d* N! z& [; \
secondary to depression.- X/ _+ T5 J/ z/ `' m
The child slept in the same bed with parents.
7 E# e1 D( D1 J- o0 ^4 XThe father would hug the baby and hold him on his
7 Z7 G8 y! p5 ~6 p" |chest for a considerable period of time, causing sig-
9 R1 e2 c: h9 f2 knificant bare skin contact between baby and father.
# @) O6 i4 x. D* b1 A) F, }The father also admitted that after the phone call,8 t3 v4 J6 `' A/ r, e |
when he learned the testosterone level in the baby
6 F$ \, b6 D/ h. O9 w6 k" Twas high, he then read the product information+ k" X% Y2 t3 h0 m) S
packet and concluded that it was most likely the rea-! x1 v8 u5 J. T! C6 B
son for the child’s virilization. At that time, they
: V: R7 [ Y. j; u2 p/ e2 K" {2 cdecided to put the baby in a separate bed, and the
$ c- E7 j8 n, R2 M7 Wfather was not hugging him with bare skin and had. S. q) u: |5 R. l @
been using protective clothing. A repeat testosterone
$ {" J; n* \; M7 A" l: `test was ordered, but the family did not go to the
3 w6 ?$ w! D% Rlaboratory to obtain the test.
o% P) ?3 a% S# QDiscussion4 c4 s! L7 A. x7 H
Precocious puberty in boys is defined as secondary/ P+ p! R8 |# {% R' Y/ u
sexual development before 9 years of age.1,4
8 e( o- S5 y7 B, ], C7 H+ e( _; iPrecocious puberty is termed as central (true) when
. K0 v$ P' N% r+ S" Dit is caused by the premature activation of hypo-+ S/ J' n9 I% k' D) v
thalamic pituitary gonadal axis. CPP is more com-$ D* T2 j0 P4 I, f
mon in girls than in boys.1,3 Most boys with CPP: [6 C5 W# W, H2 [( { [8 L. m% X
may have a central nervous system lesion that is. S. q8 |$ D: V, ^# ~$ l
responsible for the early activation of the hypothal-
9 X/ O+ a/ m0 V' s7 ]+ Ramic pituitary gonadal axis.1-3 Thus, greater empha-+ }' F; {% J. J; g
sis has been given to neuroradiologic imaging in+ |5 \! R! M2 [8 I5 ?) L' `9 r
boys with precocious puberty. In addition to viril-
3 b+ i8 ~: R( V- f7 l3 ^0 ^* F1 j2 [4 sization, the clinical hallmark of CPP is the symmet-
) R8 L! q4 Q; z( N$ Grical testicular growth secondary to stimulation by* N* V F; P8 ?( q7 B
gonadotropins.1,3
' g j% e7 Z* V& U& G# H0 o0 PGonadotropin-independent peripheral preco-$ ]+ X% t& N# D, g5 U
cious puberty in boys also results from inappropriate
& }' }. _& k* f" k3 ]androgenic stimulation from either endogenous or
! F! ] n) N+ Cexogenous sources, nonpituitary gonadotropin stim-* Q. f8 N, v6 v+ {+ Q- k, _; P
ulation, and rare activating mutations.3 Virilizing
8 z m4 a3 A' B4 v: E/ hcongenital adrenal hyperplasia producing excessive
2 [# U8 v% s) G( I2 fadrenal androgens is a common cause of precocious6 \5 b" |0 |- h
puberty in boys.3,4
; ^7 p# N5 I# W! p* S5 d0 I+ mThe most common form of congenital adrenal& F- T/ r7 D( o5 h
hyperplasia is the 21-hydroxylase enzyme deficiency.& j9 u6 d( c% t1 t7 i. \3 F
The 11-β hydroxylase deficiency may also result in
# G. O# a3 q+ texcessive adrenal androgen production, and rarely,6 |+ O* C8 {) o2 G O8 ~2 N
an adrenal tumor may also cause adrenal androgen
# }1 E q# I/ Q# wexcess.1,3' ~* P1 U8 q% }" N: ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from i. i4 X/ f) j9 C5 Q/ D$ K0 c9 I
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! r. U+ t4 ]' K0 ]3 `
A unique entity of male-limited gonadotropin-' D! `+ c9 y. G4 _ T
independent precocious puberty, which is also known0 Y0 q+ ^: ?1 T: \9 X' P
as testotoxicosis, may cause precocious puberty at a
$ ^* ^9 c& b8 B v! Zvery young age. The physical findings in these boys5 ^2 N# ?, {$ r! o7 o6 R
with this disorder are full pubertal development,+ h4 S" I C; }0 _1 G
including bilateral testicular growth, similar to boys
) i% U6 t/ q0 n6 ?2 _) A' cwith CPP. The gonadotropin levels in this disorder2 Q7 n) n* W3 D" F) V) }
are suppressed to prepubertal levels and do not show8 {4 n8 S) X. H N$ D0 q7 O
pubertal response of gonadotropin after gonadotropin-
' m) j; o7 F% Q% k* t0 P" [7 K: oreleasing hormone stimulation. This is a sex-linked
' b0 [0 L5 M: X& ^$ [8 ]autosomal dominant disorder that affects only& x/ O/ h) K: J9 r2 k8 T1 U
males; therefore, other male members of the family
: k$ O* Q8 A+ p. w) }! z" ?& I2 Umay have similar precocious puberty.3
! Q6 T; b K) p6 P6 h1 }In our patient, physical examination was incon-. `. j1 L9 g3 H: |2 @( B
sistent with true precocious puberty since his testi-
* G% ~/ q7 Z7 Bcles were prepubertal in size. However, testotoxicosis& X2 L# O1 d+ }
was in the differential diagnosis because his father$ u: a1 [' _. u3 t6 U
started puberty somewhat early, and occasionally,
+ F7 g% m8 N/ ntesticular enlargement is not that evident in the. x% p# c' z! Y6 L3 Z
beginning of this process.1 In the absence of a neg-
; D7 @$ z7 B* }& V* k6 mative initial history of androgen exposure, our
. M2 L8 I) I" l5 c! Q5 p# v9 |biggest concern was virilizing adrenal hyperplasia,4 e/ k) W- f0 `2 Y g
either 21-hydroxylase deficiency or 11-β hydroxylase
+ r( i# f* o5 F+ v* jdeficiency. Those diagnoses were excluded by find-
$ h9 W& C t% q+ e5 A1 ~& Y+ u8 Iing the normal level of adrenal steroids.# T) e; l5 ~& V8 z% g; Q
The diagnosis of exogenous androgens was strongly
; n# J. V0 `# Esuspected in a follow-up visit after 4 months because
4 R3 X$ B: x' Ithe physical examination revealed the complete disap-
) J: t. _" R- o2 E7 Y( o" Dpearance of pubic hair, normal growth velocity, and8 V4 j7 d8 j# _, `# U5 Z
decreased erections. The father admitted using a testos-$ Z/ T% X9 x& B! t+ m0 y4 F
terone gel, which he concealed at first visit. He was$ A% H/ ^$ v" b1 v3 |: z
using it rather frequently, twice a day. The Physicians’( J* V% z0 K* k* q1 I( y% w
Desk Reference, or package insert of this product, gel or* @1 C. O: G. l2 o: f5 ^: g
cream, cautions about dermal testosterone transfer to3 r) q7 L1 F, m( ]9 g' f
unprotected females through direct skin exposure.
3 L' d* F3 j" J8 ~% W9 ESerum testosterone level was found to be 2 times the
4 o4 f2 k2 Q5 e2 O* j: D& ~" q* Z( Nbaseline value in those females who were exposed to
; ^0 A) y# D+ Qeven 15 minutes of direct skin contact with their male
% x' v' h7 |0 {, ~' opartners.6 However, when a shirt covered the applica-) p& _9 L) w3 n2 V7 u
tion site, this testosterone transfer was prevented.
7 _, c/ [3 f3 c+ FOur patient’s testosterone level was 60 ng/mL,
0 e2 N% ]2 e2 zwhich was clearly high. Some studies suggest that
; `0 c) d5 p, u( Gdermal conversion of testosterone to dihydrotestos-
" i; W" I% G1 J5 C8 Qterone, which is a more potent metabolite, is more
1 G c8 _$ H0 ]' W& \active in young children exposed to testosterone) K9 i7 B# `# e) c2 t: g9 s
exogenously7; however, we did not measure a dihy- i. e* O* |, J9 k) y" N' Q
drotestosterone level in our patient. In addition to' u( c6 n* x! u: b( e
virilization, exposure to exogenous testosterone in
4 w/ B1 v0 O+ x: schildren results in an increase in growth velocity and
7 a$ ]# G B: `# N* k* Oadvanced bone age, as seen in our patient.1 Z a0 i" S3 w( G8 C
The long-term effect of androgen exposure during1 P7 W: B9 ]1 a$ N+ K
early childhood on pubertal development and final
/ j4 x7 b U- g5 yadult height are not fully known and always remain
0 {7 @( ~# Q3 i$ d1 R) f$ Ma concern. Children treated with short-term testos-
* L% _, s- k/ U, L# kterone injection or topical androgen may exhibit some
- f3 V" g4 Q$ ~ o7 f) ?acceleration of the skeletal maturation; however, after: U+ a9 j. ] v6 O
cessation of treatment, the rate of bone maturation
) o9 _) ~7 D5 k6 ]6 xdecelerates and gradually returns to normal.8,9- k3 A: q' U9 ?) g
There are conflicting reports and controversy
5 d8 ?) M- h: D- z8 @, Q3 hover the effect of early androgen exposure on adult, P1 _' r- [( W" C$ K& j5 ~
penile length.10,11 Some reports suggest subnormal! Y- Y+ I A4 q8 N. S) Q
adult penile length, apparently because of downreg-
9 R# w9 k# `/ C% u8 Y. Rulation of androgen receptor number.10,12 However," U% A9 @3 C& a
Sutherland et al13 did not find a correlation between# g" ^$ ?) T- \0 [: D
childhood testosterone exposure and reduced adult
: C1 b: o! }( Z3 r+ w5 S6 ^, mpenile length in clinical studies.$ U* A. e: v8 _8 z( [, e: r+ H
Nonetheless, we do not believe our patient is
8 f4 M0 E4 N! H! Z* z% x+ |going to experience any of the untoward effects from
. G1 T! r* Y$ n3 f% Stestosterone exposure as mentioned earlier because
) P! M- T( L8 M4 i4 Jthe exposure was not for a prolonged period of time.# }. g6 T7 R7 U8 ~0 l$ P' k
Although the bone age was advanced at the time of
3 m2 ^: H. e4 Z# cdiagnosis, the child had a normal growth velocity at
; P% Z* x! j9 o3 A8 wthe follow-up visit. It is hoped that his final adult
& b6 p Y; \0 F* g( Uheight will not be affected.% t) F% Y4 C/ `
Although rarely reported, the widespread avail-
7 b! P3 m% r6 ?6 f6 g% vability of androgen products in our society may. E2 n. x' N2 ^6 ~6 l/ e% O3 j2 j0 q/ m; A# D
indeed cause more virilization in male or female
/ d7 {4 ?, s$ Q: _/ p" E! Y$ uchildren than one would realize. Exposure to andro-
( W+ z5 z) D. m8 k' Pgen products must be considered and specific ques-
/ @4 I' O( e8 [+ L% Vtioning about the use of a testosterone product or
- s( g- v3 o) `8 X8 E# Ngel should be asked of the family members during
* X3 v& s" _* b' c: o4 ^! W( ~the evaluation of any children who present with vir-
5 V% J$ ~7 |9 }ilization or peripheral precocious puberty. The diag-
r# W8 |( P* t/ V: Q$ }% Xnosis can be established by just a few tests and by
8 L4 Y6 \6 [# X7 A. |; K/ Sappropriate history. The inability to obtain such a
. p7 v. \' {8 \2 mhistory, or failure to ask the specific questions, may
! T \. Q4 l' v0 H" F1 l* a+ {- ^result in extensive, unnecessary, and expensive* Z4 ?3 J1 S' M0 `7 d& {) o
investigation. The primary care physician should be
# F8 R1 |9 T P; I, Vaware of this fact, because most of these children
0 E1 J& H# z! o1 T( j$ T( Jmay initially present in their practice. The Physicians’
. Z8 \! |* l& hDesk Reference and package insert should also put a
& h8 a0 w- L ^/ X/ [" f& Y+ Vwarning about the virilizing effect on a male or
9 P* o9 F+ ]$ o/ W0 g( tfemale child who might come in contact with some-
" O! N# G3 ?/ v* B fone using any of these products., J; H" k8 ?. T* T4 T' q- }
References+ P' E, M) Q; h/ E
1. Styne DM. The testes: disorder of sexual differentiation3 ]) j3 q6 v% y" C
and puberty in the male. In: Sperling MA, ed. Pediatric
' p, g; r" E0 z% D- }6 e9 @Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 ]" d1 U, x* j8 t' P
2002: 565-628.
: s( \% H- \! y1 y b! M/ D% ?2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 b, c: R! u- _+ [puberty in children with tumours of the suprasellar pineal |
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