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Sexual Precocity in a 16-Month-Old, C7 @( q- {1 u- B; t) x/ Y* ?
Boy Induced by Indirect Topical
: H0 {8 Q) A3 AExposure to Testosterone
& g6 p; J' v0 }+ JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
6 c$ e( H; z& k5 m! M# [and Kenneth R. Rettig, MD1/ e) B: W9 X3 x% x; n4 p
Clinical Pediatrics
3 l' b4 m2 X6 q+ TVolume 46 Number 6
- |" t/ t) y, gJuly 2007 540-543- p0 ~6 b4 r8 v
© 2007 Sage Publications- Y$ m5 N! f8 G! V$ ~7 g
10.1177/0009922806296651; C8 ]9 W; t5 q9 m. [
http://clp.sagepub.com
, K9 [+ d5 b! a2 i( }# shosted at0 M# O; `3 X! E) i2 S+ V3 B9 u
http://online.sagepub.com/ m7 n2 |. y2 W
Precocious puberty in boys, central or peripheral,
( {3 ?; r: c8 n% Eis a significant concern for physicians. Central. s( z0 M3 T: d* ~3 I/ {
precocious puberty (CPP), which is mediated; l2 U! u$ ^1 e* M6 f. \& G
through the hypothalamic pituitary gonadal axis, has
2 X8 K5 M+ F: z/ h. ]" ?4 s4 S# W, Sa higher incidence of organic central nervous system
! p2 y3 f2 _+ `$ K! W7 \7 Qlesions in boys.1,2 Virilization in boys, as manifested& d1 ?+ q* g% w: h
by enlargement of the penis, development of pubic
, {% L8 |" M9 o% [7 D/ xhair, and facial acne without enlargement of testi-4 z, _8 W, H3 @4 [1 @* {8 r; t, c5 }- `
cles, suggests peripheral or pseudopuberty.1-3 We
, H; j, R: y& b9 }1 e, a; v* mreport a 16-month-old boy who presented with the# |! |9 h& j0 o+ l9 y4 }5 J2 H
enlargement of the phallus and pubic hair develop-
" V* [8 m: ]7 | Jment without testicular enlargement, which was due" m7 G* u$ f, ~8 J! _; g: T
to the unintentional exposure to androgen gel used by
, {$ m7 H1 n# {, L8 H5 g; Y3 Vthe father. The family initially concealed this infor-
8 v6 s8 |/ h/ d1 f4 Q! f6 Xmation, resulting in an extensive work-up for this6 @& g% y2 Q& M. e% G
child. Given the widespread and easy availability of, t: {0 W. o, t/ S6 R S
testosterone gel and cream, we believe this is proba-8 C! i" Q! ^7 d% T* d
bly more common than the rare case report in the, ^8 {, C2 { I$ `' |. ]
literature.4
1 W; [6 R- x. e- D- UPatient Report$ b" A. J# n! Z# ^
A 16-month-old white child was referred to the
3 N6 ~( y, d% J- A4 A! E/ l3 `endocrine clinic by his pediatrician with the concern2 K" R7 P& N; {
of early sexual development. His mother noticed
5 F& k. `. Q) d# y, Xlight colored pubic hair development when he was
9 ^, X) a; j lFrom the 1Division of Pediatric Endocrinology, 2University of# x. |7 G- s2 s# S) E# ^4 w- J
South Alabama Medical Center, Mobile, Alabama.& ~5 U/ z9 x G* H# u: V: R
Address correspondence to: Samar K. Bhowmick, MD, FACE,
# L; u+ ~* d2 y3 n6 `4 l0 iProfessor of Pediatrics, University of South Alabama, College of2 h0 C3 L* _# J+ [! q Q/ W
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
, V' ^. @+ h) I: a# l' J8 o ue-mail: [email protected].
! A8 Q& u! J( pabout 6 to 7 months old, which progressively became
0 v& I7 I8 T! ~$ e4 ?# N. A7 i. Bdarker. She was also concerned about the enlarge-: t w& N! ^+ \, T5 v. K
ment of his penis and frequent erections. The child
& a( q9 b. Q4 A4 Y2 Lwas the product of a full-term normal delivery, with! ~2 K$ D2 C! H- R
a birth weight of 7 lb 14 oz, and birth length of
# ?+ J) c6 I2 F, `3 g20 inches. He was breast-fed throughout the first year
5 l% [: |8 n) D+ N& _2 _ o6 Hof life and was still receiving breast milk along with! r$ Y7 c0 q- C/ ?$ U: N1 f
solid food. He had no hospitalizations or surgery,
& k) x9 H; g; K$ G3 f6 r4 mand his psychosocial and psychomotor development
: u, [" e. f- f1 x. Q3 ~/ twas age appropriate.& `( N3 K; A: V4 {3 d: G' x. d+ l
The family history was remarkable for the father,
0 F, s5 @0 E$ ^1 }& l' `4 rwho was diagnosed with hypothyroidism at age 16,
, \4 _& |0 A" H5 y) Fwhich was treated with thyroxine. The father’s
! j- ^5 j, g E: [* i0 theight was 6 feet, and he went through a somewhat
- J% U) X4 E" g# ?" K3 U0 v# fearly puberty and had stopped growing by age 14.
o0 a" y- P% ]: V% Q" u" k! NThe father denied taking any other medication. The% W4 {1 g) b5 T% g# t% j
child’s mother was in good health. Her menarche
8 F) n" d, S! D$ J" u/ Awas at 11 years of age, and her height was at 5 feet
1 T% U2 n, |8 f$ {5 inches. There was no other family history of pre-) F: w( a' [- v% S p1 f* w
cocious sexual development in the first-degree rela-
4 @5 Z1 P/ B5 Dtives. There were no siblings.. |% @, \6 f, e& M1 C
Physical Examination
7 D+ j/ F9 n- |The physical examination revealed a very active,
* G' r* p( y9 i. E$ ]6 {: N/ Rplayful, and healthy boy. The vital signs documented, u* q4 X2 J# z1 S. K
a blood pressure of 85/50 mm Hg, his length was
, z5 W2 M5 D6 X% P9 P! G/ q8 v0 M- v90 cm (>97th percentile), and his weight was 14.4 kg
: H3 @: g6 B: C% J(also >97th percentile). The observed yearly growth! x1 p* ?$ B( g. c# y0 _
velocity was 30 cm (12 inches). The examination of
/ h" D0 ~* f: r! Pthe neck revealed no thyroid enlargement.- m3 r( F) N6 e F' G! r
The genitourinary examination was remarkable for G( N0 Z& O: u* {) J) n* K) k- z
enlargement of the penis, with a stretched length of
2 v( x5 i6 m# C8 cm and a width of 2 cm. The glans penis was very well% ~' H5 [2 u$ @0 d% [7 |% E
developed. The pubic hair was Tanner II, mostly around4 C, ]$ n# S8 e7 v
5403 @8 \% s3 P" r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- @. x$ t v2 _0 l4 E/ Wthe base of the phallus and was dark and curled. The
& C4 T7 ^" ^/ E7 y u7 ]% S, ?testicular volume was prepubertal at 2 mL each.9 h9 K: W( p4 O' N: s% `% G
The skin was moist and smooth and somewhat
2 c/ @/ [/ u9 S2 ]2 F3 ^oily. No axillary hair was noted. There were no
+ k3 C: D# L: F3 Mabnormal skin pigmentations or café-au-lait spots.
6 E: b5 q. N; h3 R- w8 @Neurologic evaluation showed deep tendon reflex 2+
1 Y4 y3 C% ~4 r- P0 N, Q# Gbilateral and symmetrical. There was no suggestion& ]( }; V q# B% x3 C6 u
of papilledema.
3 W8 G6 i ^0 y6 tLaboratory Evaluation
4 k, C0 H0 `5 C/ o/ LThe bone age was consistent with 28 months by1 Y# ]* k/ [- g9 `; r
using the standard of Greulich and Pyle at a chrono-% r4 v4 @- ?. z O: y3 G5 e- Q
logic age of 16 months (advanced).5 Chromosomal" g4 S* G; |: l& e+ p0 f
karyotype was 46XY. The thyroid function test
/ G3 o4 a+ p4 Dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
B% }, f* k4 Zlating hormone level was 1.3 µIU/mL (both normal).% P% [+ r9 P8 C; F/ ]+ X: m/ r1 J
The concentrations of serum electrolytes, blood
k' b" Z8 P8 E* D B6 i: y# A t; y% |urea nitrogen, creatinine, and calcium all were; f! \9 D! r' Z2 y% A
within normal range for his age. The concentration
- C" A- t; z6 U1 ^of serum 17-hydroxyprogesterone was 16 ng/dL
, ?# M/ \2 r6 f5 c Q7 F1 Z(normal, 3 to 90 ng/dL), androstenedione was 20$ M, i' g9 y/ \6 k! c$ C( H
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
" [/ z, t. n3 c6 n2 Yterone was 38 ng/dL (normal, 50 to 760 ng/dL),
( p! V2 _, V0 e+ R! S7 bdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
. t" \$ h' f* S4 x49ng/dL), 11-desoxycortisol (specific compound S)5 r8 ]6 Y6 O: J5 W
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# F7 ^7 _9 v/ S. D1 K
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
! A$ B( i, F2 A' C+ K y- }testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 q4 y+ y" F, ~0 C+ tand β-human chorionic gonadotropin was less than; H/ d- X: `% y% L) p P6 ^7 k
5 mIU/mL (normal <5 mIU/mL). Serum follicular$ n7 m3 d2 n, e& n. o/ V
stimulating hormone and leuteinizing hormone
0 }" }4 W) O" E) d$ gconcentrations were less than 0.05 mIU/mL; O0 G, |9 V5 t) E L% o2 U! u% Y
(prepubertal).( K# R6 d! h7 b# c
The parents were notified about the laboratory
' d0 \! y1 d# v( o+ Z2 _results and were informed that all of the tests were% J: k9 R1 K9 i( M! o
normal except the testosterone level was high. The
- `+ P: E0 D# v% X% h, k, N2 Dfollow-up visit was arranged within a few weeks to3 D) v* T9 v i [% X' \( M6 k
obtain testicular and abdominal sonograms; how-
& A9 w1 z* f9 d9 r$ j9 Bever, the family did not return for 4 months.- _" h; N3 P# Q* {! ?5 R
Physical examination at this time revealed that the4 ^8 @+ ^$ j& w& }- C
child had grown 2.5 cm in 4 months and had gained% P( w$ h t W( ]
2 kg of weight. Physical examination remained
9 ?$ K: z/ n6 G: n( M8 ?* f. Punchanged. Surprisingly, the pubic hair almost com-- ?; e( A7 M% o' c+ l J
pletely disappeared except for a few vellous hairs at2 V' t, L$ S$ ^
the base of the phallus. Testicular volume was still 2
# {1 w: m! n) \' B0 P, k2 CmL, and the size of the penis remained unchanged./ q( C. [6 P M- v0 R5 b
The mother also said that the boy was no longer hav-
# n9 Z% s, q& S& c4 |4 F' Sing frequent erections.9 c+ Y# o, r2 i F0 V% i7 E
Both parents were again questioned about use of. J# }8 I( \% S$ S
any ointment/creams that they may have applied to
$ d- q) Q" z9 r3 A+ s8 ethe child’s skin. This time the father admitted the
& ~# x9 @+ M# A( |) LTopical Testosterone Exposure / Bhowmick et al 541
( i: W2 G5 |' w. ^use of testosterone gel twice daily that he was apply-* f4 s* m7 I- y9 I& F+ K1 @! u
ing over his own shoulders, chest, and back area for" h- M1 u) D8 w2 O& l7 ?+ u
a year. The father also revealed he was embarrassed# l% x$ v6 V) z8 i
to disclose that he was using a testosterone gel pre-
7 ?" M+ x2 x- p# o* ]scribed by his family physician for decreased libido2 t5 i; c. H$ T& |
secondary to depression.
6 ]% b" I$ b4 W$ Y( X. a/ T# Q. y& xThe child slept in the same bed with parents.
: l" P; `# L; y. BThe father would hug the baby and hold him on his- q$ d$ A- _4 K: j& Y' u
chest for a considerable period of time, causing sig-
" M& h% C( O" F. _: Pnificant bare skin contact between baby and father.& ?# J6 b/ r& X% i0 E, p5 y
The father also admitted that after the phone call,
t+ @5 }9 u( O. S$ o% awhen he learned the testosterone level in the baby* `8 v5 I2 e& q, e0 I6 Y A. T2 x
was high, he then read the product information
5 {% R- B* a$ C8 c: O# Z1 tpacket and concluded that it was most likely the rea-. M9 R$ P- j1 `6 T
son for the child’s virilization. At that time, they
% D8 C$ i& v! q0 [) rdecided to put the baby in a separate bed, and the+ g/ Y+ U) |: F& F: @8 J
father was not hugging him with bare skin and had
# \/ L7 f2 U7 h; N+ A `9 C: G) }$ P! Z5 nbeen using protective clothing. A repeat testosterone
. i7 _, r) w7 j" itest was ordered, but the family did not go to the: b, V% g( Q ?* j0 w9 L: L' p
laboratory to obtain the test.
3 T8 N! Q3 A2 J/ [/ W! E' p |$ H+ o. WDiscussion
2 e: [6 F2 C- |/ DPrecocious puberty in boys is defined as secondary
) F5 F- ]4 ?; }! z/ Y; ^4 N; s) J' Zsexual development before 9 years of age.1,41 @* X9 s/ {+ W' t6 p4 N$ `; T- _
Precocious puberty is termed as central (true) when
7 O8 |& n2 M/ D4 `it is caused by the premature activation of hypo-
5 v- L* K3 J+ D+ x6 a# h S1 Othalamic pituitary gonadal axis. CPP is more com-3 g* x2 H% c) |; v: u8 h" ~
mon in girls than in boys.1,3 Most boys with CPP
- V+ F7 o/ |6 o# smay have a central nervous system lesion that is0 K7 ^4 g" B. A* N B- I
responsible for the early activation of the hypothal-
. F6 W/ N& z# T7 ^$ Bamic pituitary gonadal axis.1-3 Thus, greater empha-- G+ M( o: k( y+ [
sis has been given to neuroradiologic imaging in
! I: y% m4 f# ?3 ^; r$ \, d2 {boys with precocious puberty. In addition to viril-# @+ F4 a7 \. M, G* M E1 {3 @8 k
ization, the clinical hallmark of CPP is the symmet-* i2 l$ Z# m8 w4 O. u% m+ Q
rical testicular growth secondary to stimulation by F; w# h. j3 l
gonadotropins.1,39 y" d0 g( ]. o! ?+ K1 I
Gonadotropin-independent peripheral preco-
* q- c4 r: N* u. ?cious puberty in boys also results from inappropriate, B+ A$ z! a1 U" R2 r4 ?6 x
androgenic stimulation from either endogenous or
" x, k( X1 W g/ cexogenous sources, nonpituitary gonadotropin stim-0 [3 m( E% f! j+ S- i
ulation, and rare activating mutations.3 Virilizing
, t! z# k# J/ a/ L; z6 \8 hcongenital adrenal hyperplasia producing excessive
, Z, d! Z6 ~; Dadrenal androgens is a common cause of precocious
# _, y: @9 j, J2 \& S& Z& w, Mpuberty in boys.3,40 J5 k6 C6 S2 F: s3 ]
The most common form of congenital adrenal
1 E L* ^) ]6 f3 H' }) k" Lhyperplasia is the 21-hydroxylase enzyme deficiency.
% Y# k _- u4 nThe 11-β hydroxylase deficiency may also result in& O) F. R0 @: w" {2 A: B N
excessive adrenal androgen production, and rarely,# J3 N& G- m* J$ T4 y
an adrenal tumor may also cause adrenal androgen, Z' k- S S2 n0 q
excess.1,3
4 {! H0 y' i/ F$ L; tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 O) ^) k+ O. C) v1 F& X9 T542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- M- H5 a; ?' f7 E/ A1 W2 b8 \
A unique entity of male-limited gonadotropin-0 \8 x' q3 y. ^! m4 f6 G# o& ~
independent precocious puberty, which is also known
- @6 `- r0 a O8 j9 Fas testotoxicosis, may cause precocious puberty at a
6 L# Y& \, C9 x+ k- q# hvery young age. The physical findings in these boys
5 o, i4 F$ ?. w- ~with this disorder are full pubertal development,
h( z% w g1 h& @. r2 P ~including bilateral testicular growth, similar to boys, |: x a- k; `" y) z2 p/ ^/ w
with CPP. The gonadotropin levels in this disorder
/ \& M4 G& j* Z' z: ]are suppressed to prepubertal levels and do not show
( E- Q- T! y% e1 j. I. y t2 ^2 Epubertal response of gonadotropin after gonadotropin-+ F( L5 b5 u, b
releasing hormone stimulation. This is a sex-linked
9 \ x1 n, ?: S7 D P) ^autosomal dominant disorder that affects only: H1 c' r' x1 C6 z: @* [6 d
males; therefore, other male members of the family# p6 j2 ~' {: K8 n: n# n
may have similar precocious puberty.3
/ i, Z' P4 W, l; N8 bIn our patient, physical examination was incon-, T, }7 X' J+ e7 N9 z
sistent with true precocious puberty since his testi-
8 L" d- }1 l. A- L3 ecles were prepubertal in size. However, testotoxicosis
) u+ |+ [0 E8 q/ l( Kwas in the differential diagnosis because his father
+ Q& }( p, ]- k4 {4 ~started puberty somewhat early, and occasionally,/ B, i# |' P8 S' F* f
testicular enlargement is not that evident in the
2 Q t! a5 Z6 p! _beginning of this process.1 In the absence of a neg-
# T4 X' T3 d7 `6 X( eative initial history of androgen exposure, our
5 M; q5 z6 F/ `biggest concern was virilizing adrenal hyperplasia,5 F4 ]+ G3 @' f% X& `6 M
either 21-hydroxylase deficiency or 11-β hydroxylase
6 S; u2 v7 m ydeficiency. Those diagnoses were excluded by find-
# C! S- e- D* A+ \ing the normal level of adrenal steroids.
! U1 O6 i1 V$ o+ T# B" gThe diagnosis of exogenous androgens was strongly
2 Q7 N3 K, j. u% V- ^2 d% ususpected in a follow-up visit after 4 months because
# h5 G) C5 _" Q8 a) k1 g, I4 ~, Gthe physical examination revealed the complete disap-& h& ]9 K u( p
pearance of pubic hair, normal growth velocity, and4 V9 ?: [. ~/ N0 V9 |
decreased erections. The father admitted using a testos-; `" F6 Y! H; f& i
terone gel, which he concealed at first visit. He was
9 L: H3 ~- y& m7 B1 lusing it rather frequently, twice a day. The Physicians’
" x% h3 n3 v! ^" w9 e: c1 @Desk Reference, or package insert of this product, gel or
% o7 W; P8 F+ a. q& O4 i% d/ ucream, cautions about dermal testosterone transfer to: j1 c& Q* E* |6 P( t. b4 Y
unprotected females through direct skin exposure., Y' Y5 R, h( ~. f6 n0 {/ Y# D
Serum testosterone level was found to be 2 times the
3 K) x3 k4 H0 pbaseline value in those females who were exposed to
& s6 X/ d+ k) \5 j& jeven 15 minutes of direct skin contact with their male
' W# A9 Q: h s! r3 j7 {5 Xpartners.6 However, when a shirt covered the applica-8 X2 W( Q7 n7 v4 ]* m
tion site, this testosterone transfer was prevented.
3 E9 G" H2 k |# M1 x" k* b' gOur patient’s testosterone level was 60 ng/mL,
: X7 X, J, i. H# Q8 swhich was clearly high. Some studies suggest that, Q' j8 W0 ?* u) r, s
dermal conversion of testosterone to dihydrotestos-
5 t: `% \2 C) q0 o: gterone, which is a more potent metabolite, is more
7 Q+ r5 X3 @! B* p3 N; d Zactive in young children exposed to testosterone `/ w# j, j' P. ^6 K* v6 I
exogenously7; however, we did not measure a dihy-
, a4 {# ?: `8 [9 I1 `: rdrotestosterone level in our patient. In addition to" Q4 o# k& X3 N! q$ @
virilization, exposure to exogenous testosterone in/ ~2 }7 z; u ]0 q% M: r% u* C" Y; {: h
children results in an increase in growth velocity and
" ]8 J4 ~2 ]' W) r% Madvanced bone age, as seen in our patient.
[, c) T0 {: @/ i7 a+ k8 H7 X5 TThe long-term effect of androgen exposure during
! t( z+ ^: ?& w7 y2 @) y' v3 U' w/ Nearly childhood on pubertal development and final+ V" }4 ]* J5 v( T! S
adult height are not fully known and always remain
5 O `7 H0 l0 n$ l2 {a concern. Children treated with short-term testos-
( S! N" P* F. Q# ?9 b, ?terone injection or topical androgen may exhibit some
2 \: g" x) A# G/ S$ E1 u3 V) K" }+ i2 tacceleration of the skeletal maturation; however, after
- \* I- H/ }9 W: Ncessation of treatment, the rate of bone maturation! {: p1 k. X$ E* W! |% e
decelerates and gradually returns to normal.8,9$ _7 L. E% V6 m$ m% r2 z
There are conflicting reports and controversy" b7 J% w% M3 U% y, Q
over the effect of early androgen exposure on adult
) v2 y9 l3 X5 m' H; d; e3 ^) g Ipenile length.10,11 Some reports suggest subnormal U, t- L5 y- l) U
adult penile length, apparently because of downreg-
2 ~2 t% ~$ Z2 P8 a( z/ Kulation of androgen receptor number.10,12 However,
; _/ N: k' ~9 x( A3 ASutherland et al13 did not find a correlation between2 S/ N% ?" n: }+ ^5 s" o
childhood testosterone exposure and reduced adult( d/ o3 x- o8 C$ c
penile length in clinical studies.4 k' l/ T! q- g' s: E* N
Nonetheless, we do not believe our patient is
$ _4 G# M% _/ e& ~' ?* y5 {9 Zgoing to experience any of the untoward effects from
# @0 c+ ]0 V) m: ~) W, [3 k9 n3 ?testosterone exposure as mentioned earlier because
' j/ M- p' x' v) Sthe exposure was not for a prolonged period of time.
5 K2 w2 D( L* w1 ?3 O3 v; T9 H9 vAlthough the bone age was advanced at the time of
1 a3 F( T- A3 S1 N/ O) c4 }0 Idiagnosis, the child had a normal growth velocity at
4 W% `0 ~$ k, X4 `/ F; D% Lthe follow-up visit. It is hoped that his final adult7 K+ _# X* [! @* h: P$ X5 h
height will not be affected.4 R) X' L+ [% r
Although rarely reported, the widespread avail-
: }1 Z1 X8 B/ X) q; `( p5 z, Vability of androgen products in our society may8 j1 {( X2 Y' x
indeed cause more virilization in male or female' K# o5 v& G* Q/ _0 g- m; c, d
children than one would realize. Exposure to andro-
) b9 _ U7 ?% {# C c% `gen products must be considered and specific ques-9 a: ]% D/ [( W5 ?: P
tioning about the use of a testosterone product or, _+ ^2 [' o/ ]9 ~3 Z% Z
gel should be asked of the family members during# K% C9 |, u# O1 Y; y
the evaluation of any children who present with vir-
9 u+ {) D+ @9 h0 e4 Bilization or peripheral precocious puberty. The diag-
% I# }( r6 k, w' fnosis can be established by just a few tests and by
) H1 _6 u& _4 i% lappropriate history. The inability to obtain such a
; j& R/ C; N B! r# ~" Uhistory, or failure to ask the specific questions, may8 K% y0 J9 P1 y. R
result in extensive, unnecessary, and expensive+ Y8 n O9 | x
investigation. The primary care physician should be- E+ z( ]7 j2 V/ |0 T
aware of this fact, because most of these children
6 A: C* b2 b9 ^* Y* W$ Qmay initially present in their practice. The Physicians’6 L: ~4 H$ t( I* m6 Y5 e: F
Desk Reference and package insert should also put a' z/ g0 J1 e- y
warning about the virilizing effect on a male or& }! x6 G1 ~2 M+ W. @- G
female child who might come in contact with some-
1 d" j3 o5 r+ F Ione using any of these products./ W0 y+ d% K' d0 F- o
References7 N1 W1 A5 l" Y2 K, b! d/ P. A0 ^
1. Styne DM. The testes: disorder of sexual differentiation
7 t7 B0 r# ~/ F& M" Nand puberty in the male. In: Sperling MA, ed. Pediatric: S$ ]6 f% X9 @7 Q4 `* I- H, Y
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 K! W" D5 x( V7 q4 v8 E2002: 565-628.
4 L2 H) a1 Q A. }( y( i# J2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
# k% `5 J) T/ V1 Z) f3 v' u8 Xpuberty in children with tumours of the suprasellar pineal |
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