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Sexual Precocity in a 16-Month-Old
6 ^/ m/ ]% v' y. ^2 J* OBoy Induced by Indirect Topical1 q9 f k3 v, i: S/ Y! p6 b" u
Exposure to Testosterone: E1 Q% p( z8 ~5 e* @; c
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ |3 X9 M2 U+ C/ v4 vand Kenneth R. Rettig, MD1
: }( q" e% E+ o8 P7 H# ~Clinical Pediatrics2 X- K0 r9 ^( E L0 v8 d
Volume 46 Number 62 z/ u% Q( p% K5 Z' n a" a5 S
July 2007 540-543
( M# ^# o. j B" W9 S* F5 t ]© 2007 Sage Publications
: ?, \: d/ I/ N2 o10.1177/0009922806296651; z4 J$ c8 C. _
http://clp.sagepub.com
& P" G6 i1 f2 n1 ^0 {hosted at* X, R( a3 [& R) i' d
http://online.sagepub.com
/ R% @% q9 p# M4 \Precocious puberty in boys, central or peripheral,& E5 \% t4 g% N, y6 S4 ]) ^
is a significant concern for physicians. Central9 ]# |- L7 C2 `
precocious puberty (CPP), which is mediated' g- k+ i- e5 b
through the hypothalamic pituitary gonadal axis, has) Y4 ~/ T$ ] b
a higher incidence of organic central nervous system' y4 }$ |+ o: v4 u7 v# [2 }/ ?
lesions in boys.1,2 Virilization in boys, as manifested
+ A+ K9 [4 m2 fby enlargement of the penis, development of pubic& |& b6 n" r6 D, l
hair, and facial acne without enlargement of testi-
& X% d6 r5 q, G4 g" L, L; I. \cles, suggests peripheral or pseudopuberty.1-3 We( J! ]$ ?- v1 G, [0 d K4 E
report a 16-month-old boy who presented with the$ c$ y. i( _" x/ r+ ]& U: I
enlargement of the phallus and pubic hair develop-
1 S! U; P1 d1 X' y4 m9 Tment without testicular enlargement, which was due
9 }* }( A2 N' v; ^! L P; ?to the unintentional exposure to androgen gel used by
+ y* O# x8 v. I6 T; S1 Fthe father. The family initially concealed this infor-% {. q( Z' A6 a( W0 w/ t, c
mation, resulting in an extensive work-up for this' B2 H1 s! `5 }7 P& Y" S' z
child. Given the widespread and easy availability of0 V% z3 `1 G/ X+ T+ U, w w5 B4 i# y" s
testosterone gel and cream, we believe this is proba-; `) k( e) p3 A0 w5 A# V9 q
bly more common than the rare case report in the& B: K& I6 a" J( b
literature.4) f0 \. h7 _: \# _9 U: D! T
Patient Report
, i- |- Z! _3 X4 p0 e9 O+ fA 16-month-old white child was referred to the) s- }) k0 o3 [1 M* `
endocrine clinic by his pediatrician with the concern6 M$ G6 F( U9 g% u# p- M6 W3 V8 k
of early sexual development. His mother noticed
$ M4 M3 g/ s' w4 Xlight colored pubic hair development when he was6 c+ d! C6 F/ P2 V, Y) U
From the 1Division of Pediatric Endocrinology, 2University of
) O# G, c o. H% I6 n" i( Y) ? ?South Alabama Medical Center, Mobile, Alabama.
9 Y- i. h" I* E$ P6 m& HAddress correspondence to: Samar K. Bhowmick, MD, FACE,% r2 Y3 }# ^% M" k8 R6 j( }
Professor of Pediatrics, University of South Alabama, College of
$ T. b% L Z- \+ QMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. `) [/ [5 |3 D. \- Ee-mail: [email protected].
/ w8 x+ H) {3 A2 @+ c3 K0 a/ k; fabout 6 to 7 months old, which progressively became8 V- [% J5 X) h: Y" R" ~! @& w
darker. She was also concerned about the enlarge-6 w3 ~% P) U2 g: |2 G
ment of his penis and frequent erections. The child
+ ?# f9 S+ ~* G* ywas the product of a full-term normal delivery, with
" R: v2 o: G% A7 za birth weight of 7 lb 14 oz, and birth length of e6 q" j: V5 T7 q0 [5 e8 Q
20 inches. He was breast-fed throughout the first year6 d3 V9 k. z0 `
of life and was still receiving breast milk along with3 y! k; P0 w% b7 f
solid food. He had no hospitalizations or surgery,. i y/ k1 J& q/ Q
and his psychosocial and psychomotor development/ X! O# k* H v/ O0 Q5 G5 @; G f
was age appropriate.
8 k: d7 k+ G9 T/ |3 zThe family history was remarkable for the father,
' N. Y: ?7 ]4 B0 a% Rwho was diagnosed with hypothyroidism at age 16,
6 z$ }4 a: m: H( v3 Pwhich was treated with thyroxine. The father’s/ i$ b- ?) _ v" J% o% X3 u5 u
height was 6 feet, and he went through a somewhat1 `' a) Q3 [, `: i8 S. p% v
early puberty and had stopped growing by age 14.
2 s E; u8 U6 ]* ?3 `; u! D9 gThe father denied taking any other medication. The r% u4 M0 {7 Z+ H( V1 r# V
child’s mother was in good health. Her menarche
4 C! _2 E2 |+ W& \, Nwas at 11 years of age, and her height was at 5 feet
2 d% L( F1 r, u, k2 r, F w& \5 inches. There was no other family history of pre-
( P. K* k. ^0 R5 K" b* v! X9 U' _cocious sexual development in the first-degree rela-+ P5 ~9 |% N6 l
tives. There were no siblings.
7 g" X+ `3 B) t4 u; A: CPhysical Examination& I; Y2 { M' K! L
The physical examination revealed a very active," q& v6 i# f& T9 m8 ~
playful, and healthy boy. The vital signs documented0 Y! ?+ _2 y. Y- i; e3 ~
a blood pressure of 85/50 mm Hg, his length was f+ I' i4 n* T( T. Y; _- W( T
90 cm (>97th percentile), and his weight was 14.4 kg- k; o; Q/ U' I a7 G0 I
(also >97th percentile). The observed yearly growth9 J. ?4 M' e- S- a
velocity was 30 cm (12 inches). The examination of" O7 L8 }7 C! M3 w+ y6 ~
the neck revealed no thyroid enlargement.
. _; l* j# l# Q( l; h; z1 n* CThe genitourinary examination was remarkable for+ L1 ]/ i( m% Q% U: e
enlargement of the penis, with a stretched length of
1 {. K7 [0 z1 @$ n k8 cm and a width of 2 cm. The glans penis was very well
( f$ `; ?2 `: Q' I: c* O, \0 W( H8 zdeveloped. The pubic hair was Tanner II, mostly around
5 T' K8 `& o! b/ |6 h+ V! U [540
' x; u2 ^. ~0 }/ [( ?: s, N% d- iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 l. W* _% S, c6 l- y: b2 A5 R* C3 ithe base of the phallus and was dark and curled. The
' y# S! O4 h7 z1 R# L9 itesticular volume was prepubertal at 2 mL each.
8 N7 _$ x" h* \% _ RThe skin was moist and smooth and somewhat
$ O, P1 k7 {5 g5 _& G% Y: Loily. No axillary hair was noted. There were no7 E# D. V- q Q C) P& W. g
abnormal skin pigmentations or café-au-lait spots.
2 Z$ u: q2 Q+ N/ y# a, QNeurologic evaluation showed deep tendon reflex 2+
# C6 d O0 D. M' {. _bilateral and symmetrical. There was no suggestion
: U& y. c3 u$ o4 P: {# _' Mof papilledema.
6 e+ X! v0 B% E# j3 Q8 e9 C9 \( NLaboratory Evaluation+ m4 e6 @. Q$ V5 t- h N
The bone age was consistent with 28 months by) K/ a4 S) a! V! o/ B
using the standard of Greulich and Pyle at a chrono-$ c" g7 \, `! W9 n% }
logic age of 16 months (advanced).5 Chromosomal
L3 k& z/ X6 b+ l2 M; W2 w# l jkaryotype was 46XY. The thyroid function test
# Z& ?1 d/ g0 I) F$ Z- J8 E& Bshowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 ]! M6 w/ D8 o$ ?/ M' F
lating hormone level was 1.3 µIU/mL (both normal)." s. n0 z6 H7 m4 u& ?# E+ b' K9 V
The concentrations of serum electrolytes, blood
! k: r a8 K; J Z+ k( {urea nitrogen, creatinine, and calcium all were
$ }5 \7 ?+ n/ s% Nwithin normal range for his age. The concentration. E* x+ J* T; b: J& v
of serum 17-hydroxyprogesterone was 16 ng/dL5 [4 R* r9 ~5 {: B2 @- A; X
(normal, 3 to 90 ng/dL), androstenedione was 20) c) i6 x3 r, Y' e
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; ?3 \; p" E. T
terone was 38 ng/dL (normal, 50 to 760 ng/dL),7 d8 ?/ V" I4 m6 E; p# I/ U
desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ v+ C0 U* Y9 d1 ]
49ng/dL), 11-desoxycortisol (specific compound S)9 z) W' K* k/ ^+ h' }. _; D
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
; ?9 J2 w0 H7 Jtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 f, ~' c) j1 \3 Q+ ]
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
7 b% s) V' P) P4 Wand β-human chorionic gonadotropin was less than
/ i+ W2 G2 t7 J6 Z5 J5 mIU/mL (normal <5 mIU/mL). Serum follicular$ ^( Q" [, j% v$ S( R ~1 f
stimulating hormone and leuteinizing hormone
6 F% r- C: |& P: u S2 _) }1 j4 Nconcentrations were less than 0.05 mIU/mL7 K; C7 ]/ R; |/ F9 l
(prepubertal).
7 w2 u* ]6 R. B$ sThe parents were notified about the laboratory3 H" N3 [$ F, f
results and were informed that all of the tests were
- l" V& S: N4 C& m- Inormal except the testosterone level was high. The
5 \' F1 o9 D+ [3 l0 X1 xfollow-up visit was arranged within a few weeks to. f( y1 H, a9 `0 Q) B$ G) c
obtain testicular and abdominal sonograms; how-$ ]0 D2 H7 {; ~* e# _- ?0 ^8 z
ever, the family did not return for 4 months.
U$ v: t# F3 ~( b8 e; bPhysical examination at this time revealed that the
) K7 Z* [" S% _3 S9 Z! K% Ochild had grown 2.5 cm in 4 months and had gained
5 s) ^5 j% a9 f7 e" E- v2 kg of weight. Physical examination remained6 L. M5 r k7 H6 n# V1 V. |, f
unchanged. Surprisingly, the pubic hair almost com-7 o0 l! b5 |% s* B5 x7 E# \+ O% q
pletely disappeared except for a few vellous hairs at8 H4 J1 i! g5 M6 u, d' ]( n
the base of the phallus. Testicular volume was still 2
9 W- z2 E# H" K, V VmL, and the size of the penis remained unchanged.- y0 J; W& F; j) ]; U5 Z
The mother also said that the boy was no longer hav-
6 d* E! D* Q* N3 g' B- ?: Y* z6 eing frequent erections.
9 H5 a7 q. q7 U$ [Both parents were again questioned about use of
7 e" o( _' ]0 x) n* D" V& N, W/ l! \any ointment/creams that they may have applied to
7 V$ g% n/ a/ _the child’s skin. This time the father admitted the
0 H) _; V% e4 F9 KTopical Testosterone Exposure / Bhowmick et al 541% p$ V" K- A* A5 t, ^9 N
use of testosterone gel twice daily that he was apply-
3 B' a; s$ c" cing over his own shoulders, chest, and back area for$ ^$ C* X3 s0 m" r. @2 u0 |5 D/ d
a year. The father also revealed he was embarrassed2 \3 q) ^% ^% ?2 c& Q. F- b _
to disclose that he was using a testosterone gel pre-# |' U9 r! M8 U9 ^7 {; G( [
scribed by his family physician for decreased libido7 S& e& u* {$ M
secondary to depression.
8 n) ~- k7 B. c7 AThe child slept in the same bed with parents.* @' F% ?/ u. p9 w& n8 i
The father would hug the baby and hold him on his% n7 D5 g' J# e2 r" j: X( v4 V
chest for a considerable period of time, causing sig-7 D% P4 Y$ c* E
nificant bare skin contact between baby and father.+ r( M9 g ^( M; H
The father also admitted that after the phone call," Z6 W: H3 i ~( r: n. Z. U0 A i
when he learned the testosterone level in the baby& z( C# R& v3 u! ?1 o, m3 Y! {
was high, he then read the product information# |/ C# B5 i, b4 W* f8 A" o7 E
packet and concluded that it was most likely the rea-
' M; V! C# l, v `son for the child’s virilization. At that time, they
- ~. J4 D& c3 M, M; ?8 Wdecided to put the baby in a separate bed, and the
: S5 }# M. j. G' J, r) [( q$ Wfather was not hugging him with bare skin and had
$ ]# q% w( w: k. A* M% M- u1 T, fbeen using protective clothing. A repeat testosterone& t9 `, B/ g- n% _
test was ordered, but the family did not go to the
0 R# B. v. G, M' ]# {laboratory to obtain the test.
V2 O" ?6 U& A. {Discussion
& L- s6 |1 G! i8 ^Precocious puberty in boys is defined as secondary8 ^& b9 m4 K) F7 O
sexual development before 9 years of age.1,4
9 n; R8 ~, ]% v$ Z8 Q* {( r( e& JPrecocious puberty is termed as central (true) when9 k8 d- Q/ l' L P* p
it is caused by the premature activation of hypo-2 G( n2 x& ]& c! b, Z7 F
thalamic pituitary gonadal axis. CPP is more com-4 [ A3 y% W0 J3 F/ P% l; n
mon in girls than in boys.1,3 Most boys with CPP. B8 S1 z, H% H" W
may have a central nervous system lesion that is
4 n( t) L8 j2 a" T- f3 f$ r! G" i/ zresponsible for the early activation of the hypothal-) I1 Z% M7 y; S
amic pituitary gonadal axis.1-3 Thus, greater empha-
% B. X+ s. c' e! qsis has been given to neuroradiologic imaging in
m! {3 f. |5 v% j& P8 m& b$ Gboys with precocious puberty. In addition to viril-. z1 ^, D/ o: N! s ]! J
ization, the clinical hallmark of CPP is the symmet-) T8 J6 [+ D1 U; ^2 k
rical testicular growth secondary to stimulation by
" ~! D% a1 ?# \1 i# Jgonadotropins.1,3
, t$ `0 S& _* q' X7 KGonadotropin-independent peripheral preco-
5 |; J3 \' @) g1 qcious puberty in boys also results from inappropriate& {$ Z4 l8 t1 I
androgenic stimulation from either endogenous or8 }% b6 L; Q+ o3 S1 G
exogenous sources, nonpituitary gonadotropin stim-# ~0 A4 P7 a& Y2 Z) J
ulation, and rare activating mutations.3 Virilizing+ T+ Y; S4 u8 }4 V0 v
congenital adrenal hyperplasia producing excessive1 R( q1 T: q% ?% J7 X/ V
adrenal androgens is a common cause of precocious
9 t/ q& l, F1 ]5 Wpuberty in boys.3,4
4 o9 P; \: q' Z8 Y3 S9 jThe most common form of congenital adrenal* E; J7 `9 s0 h$ z# l& p0 z2 q
hyperplasia is the 21-hydroxylase enzyme deficiency.
, \ `6 P1 J7 s7 u% x5 C: H5 M7 m; PThe 11-β hydroxylase deficiency may also result in
7 j2 c, {6 P7 m+ aexcessive adrenal androgen production, and rarely,1 v4 z# }. n" I) o5 E& a* k0 Z
an adrenal tumor may also cause adrenal androgen
( E. K- O7 x, `! D( c: Cexcess.1,3! J. G9 V4 G, u7 ~/ {- j9 E
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 F. K6 U; o4 A0 X6 w, I
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
) x# W! T7 K% p- N% ~( V8 H% iA unique entity of male-limited gonadotropin-0 ]. {8 C0 a7 n+ i; ~: Q, |
independent precocious puberty, which is also known
% z; Q) Z7 c1 F! m! U7 H: Gas testotoxicosis, may cause precocious puberty at a7 o& J% {4 R) n, g+ W( O
very young age. The physical findings in these boys8 v; }( t0 X l
with this disorder are full pubertal development,
9 N9 Q9 |: p+ {! Sincluding bilateral testicular growth, similar to boys
. d3 _3 |; o% s9 z3 z7 Z& J q+ gwith CPP. The gonadotropin levels in this disorder& Y9 a6 ^; R3 _' T% q' Q0 E2 Z& A
are suppressed to prepubertal levels and do not show) n9 X: a- W+ F6 |( O
pubertal response of gonadotropin after gonadotropin-
2 c% @ X/ n- v5 [! ^; H7 H* jreleasing hormone stimulation. This is a sex-linked
" `2 [9 Q( n3 p% F% Sautosomal dominant disorder that affects only" u4 }9 E2 a; z- K
males; therefore, other male members of the family
: q& v6 M+ F: M4 ]8 E2 hmay have similar precocious puberty.3" I$ R1 G9 V* ?5 z3 p
In our patient, physical examination was incon-% b) m4 L G. |) _& L3 g
sistent with true precocious puberty since his testi-
E% q9 T ]- `4 f6 @1 r' A0 Ycles were prepubertal in size. However, testotoxicosis: P+ D. t3 X! M" {+ \5 J
was in the differential diagnosis because his father
. d8 s2 Y3 j7 ~' Ustarted puberty somewhat early, and occasionally,
; W+ V8 ?, B9 c) ltesticular enlargement is not that evident in the
) R; c7 `, A: @9 `5 Ubeginning of this process.1 In the absence of a neg-
' v2 i( s+ \+ p; j2 T1 Dative initial history of androgen exposure, our
( i% ^' w; \- s5 m$ r/ Ibiggest concern was virilizing adrenal hyperplasia,2 {; \! R, W! @) l$ S) O) w+ O
either 21-hydroxylase deficiency or 11-β hydroxylase, @( M( _# t. X
deficiency. Those diagnoses were excluded by find-
8 X0 Z* i# `5 } Fing the normal level of adrenal steroids.6 X" h0 [# G8 T- Z% r# t
The diagnosis of exogenous androgens was strongly2 ]$ u( R- H( P, z) c, G
suspected in a follow-up visit after 4 months because
. g6 `; h) l# v( t5 l; I% Sthe physical examination revealed the complete disap-7 v$ |8 d2 b1 v( a* o, ]% c- W
pearance of pubic hair, normal growth velocity, and( D9 B& A. E5 z Y+ {
decreased erections. The father admitted using a testos-
. x5 q$ L. r C' sterone gel, which he concealed at first visit. He was
3 N, e0 m* t7 V' m' X6 q& i6 K2 |0 p" fusing it rather frequently, twice a day. The Physicians’; m3 j8 n8 _0 t$ }. q' ^# n, N
Desk Reference, or package insert of this product, gel or0 E5 ^: b- N" O1 k
cream, cautions about dermal testosterone transfer to- v$ @# w* u( K2 c7 o
unprotected females through direct skin exposure.0 h. D; e; Y+ k6 {# j4 l" H5 M
Serum testosterone level was found to be 2 times the
% Y' l; q. X) k M$ m+ S% H( Qbaseline value in those females who were exposed to
9 ^; T% m3 x4 Y+ j) deven 15 minutes of direct skin contact with their male! C) R( _" e9 Q% w
partners.6 However, when a shirt covered the applica-" d- @8 T, X: d* B
tion site, this testosterone transfer was prevented.8 w! }2 p- b" ~2 O
Our patient’s testosterone level was 60 ng/mL,
: m& M" j$ w& y9 D" W; U9 q- Jwhich was clearly high. Some studies suggest that' a$ R2 z' I" d, {5 e5 w
dermal conversion of testosterone to dihydrotestos-& ~! x5 |% u2 l, V0 `9 R# e
terone, which is a more potent metabolite, is more
. @0 B1 V8 {* U' O# iactive in young children exposed to testosterone9 g$ D" g7 G3 |8 j7 f" {* n
exogenously7; however, we did not measure a dihy-9 x2 d! o" v6 W! z
drotestosterone level in our patient. In addition to3 a3 c/ F) M- O; g; U1 M
virilization, exposure to exogenous testosterone in
2 M/ ?5 H; }1 q. @ b" uchildren results in an increase in growth velocity and
7 u7 L: c- q6 D) Q6 v% P- cadvanced bone age, as seen in our patient.: T; T9 e+ L( }) {7 C
The long-term effect of androgen exposure during3 j9 u C' ]+ t, M8 l
early childhood on pubertal development and final8 ^: @0 n0 R3 G' ]. Y
adult height are not fully known and always remain$ I* u& G: m+ Y/ k
a concern. Children treated with short-term testos-
$ U! E; x' ^9 U2 O+ B Uterone injection or topical androgen may exhibit some
; z! G* a9 {+ z7 \acceleration of the skeletal maturation; however, after, [6 f) i1 b2 P6 J: o5 n# J
cessation of treatment, the rate of bone maturation* ^* l5 _5 j# `9 _4 Z6 m
decelerates and gradually returns to normal.8,99 W. D' I& k- W( h6 t$ a9 S4 w) u
There are conflicting reports and controversy0 X5 ~8 H4 w s5 z$ V
over the effect of early androgen exposure on adult
: B% P6 Y6 Y% U% A9 H, Z- U' Npenile length.10,11 Some reports suggest subnormal7 M9 n/ d) z- L, `/ W
adult penile length, apparently because of downreg-7 h6 Z4 ~, x2 v
ulation of androgen receptor number.10,12 However,
* v/ }/ ^" ~) h9 sSutherland et al13 did not find a correlation between7 r( L8 L1 x8 [
childhood testosterone exposure and reduced adult
; G" Z% Y- }9 Dpenile length in clinical studies." ^1 r- {& \0 O9 D, V4 D% H
Nonetheless, we do not believe our patient is: `/ [& |/ }- V/ N2 U
going to experience any of the untoward effects from
- B: \) S) ?% J; e$ P+ x N3 a& ^2 ktestosterone exposure as mentioned earlier because7 g( _. |7 W. K# J4 w
the exposure was not for a prolonged period of time.
4 ?" M" ]% f; J# p$ d3 o9 E4 mAlthough the bone age was advanced at the time of
* n# m# E8 A+ y; \5 q8 hdiagnosis, the child had a normal growth velocity at
: A# r! K; J9 T. B0 }$ Othe follow-up visit. It is hoped that his final adult
6 T" t+ o t4 ]3 C; Gheight will not be affected.; l) ` q4 x4 h
Although rarely reported, the widespread avail-" _! Q, M8 x `
ability of androgen products in our society may' C0 _1 f! I; Q4 F( J
indeed cause more virilization in male or female) F' M1 ^' v3 o4 c
children than one would realize. Exposure to andro-2 J! x" k, ?, J. U( l1 ^
gen products must be considered and specific ques-, ?- t) p, b' b8 D
tioning about the use of a testosterone product or
- G" E7 }/ q( J! V- O6 ]7 igel should be asked of the family members during$ Y6 G$ f S) a% b8 L! q
the evaluation of any children who present with vir-! m8 H4 p9 w6 G6 N
ilization or peripheral precocious puberty. The diag-
' w v/ N K8 X% Knosis can be established by just a few tests and by
. t5 b$ C& C6 h# T. B$ d# ?/ ~appropriate history. The inability to obtain such a
$ i8 g5 H* f7 t/ _( Dhistory, or failure to ask the specific questions, may
/ B0 q; @. F/ }* J/ D& nresult in extensive, unnecessary, and expensive) k7 [4 b! d$ \. s5 n
investigation. The primary care physician should be
; N" d$ f: V/ P# Waware of this fact, because most of these children
, X2 Y2 l0 N, ]$ Q/ s6 y; rmay initially present in their practice. The Physicians’
& h+ z4 O7 L% GDesk Reference and package insert should also put a
4 ^! P' I$ j" o2 v& C2 h+ ~warning about the virilizing effect on a male or
$ l4 C9 d/ Z u' C/ f7 C! d3 M1 qfemale child who might come in contact with some-
9 T. F/ _. O, W' ]2 ]8 l* yone using any of these products.1 Z/ j0 x4 G4 o5 H4 Z* b1 I
References
0 l: m& a2 d4 X1. Styne DM. The testes: disorder of sexual differentiation9 b, s% f3 v! ]5 v! D! U. m$ v
and puberty in the male. In: Sperling MA, ed. Pediatric
( A& M- d3 I* o, N' Z8 T( SEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; W* \+ w' X# Y1 U2002: 565-628.; E0 V% o/ j+ N! |2 j6 ]3 Z' e. k
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* t0 Y+ p1 i" P1 Y8 ]/ E' mpuberty in children with tumours of the suprasellar pineal |
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