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Sexual Precocity in a 16-Month-Old9 J# r; k5 n$ ?8 i: p
Boy Induced by Indirect Topical5 I3 F& b: Z; f8 x& U
Exposure to Testosterone
0 k l; [6 [3 D' y# vSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
6 f9 s7 l; f4 S& h$ q& u. sand Kenneth R. Rettig, MD10 a4 E8 M* ]& j- P) W8 Z
Clinical Pediatrics
% [5 ~' B) { oVolume 46 Number 6
6 ~7 ], h8 j6 x; t" ?+ u+ v" z$ QJuly 2007 540-543
# N, c/ c; n, Y& x$ S R- V© 2007 Sage Publications, A$ S; ?0 {( T7 g) f
10.1177/00099228062966511 N4 _7 Z2 O f5 M
http://clp.sagepub.com4 o# y( O5 S/ u9 A+ k+ B
hosted at' Y/ a" T6 m2 G( i' h& X
http://online.sagepub.com, o& |+ M5 y) Z0 L
Precocious puberty in boys, central or peripheral,
5 ]) ]9 O- V j1 @6 sis a significant concern for physicians. Central: e& [3 [9 D, m4 s# n( \
precocious puberty (CPP), which is mediated3 E0 W& O: O+ s
through the hypothalamic pituitary gonadal axis, has
/ R9 H9 {$ r/ v6 W+ [a higher incidence of organic central nervous system
4 Y% W7 r5 T% [& llesions in boys.1,2 Virilization in boys, as manifested( m5 j( v( u7 h( \
by enlargement of the penis, development of pubic3 n5 i# G+ c4 W; I* P5 H H
hair, and facial acne without enlargement of testi-
; y2 @) g+ |, x9 d* Q- d. wcles, suggests peripheral or pseudopuberty.1-3 We
; S0 x1 v% o3 t- x& lreport a 16-month-old boy who presented with the7 I0 G5 x) j% c9 e% Y' P7 N2 n" h
enlargement of the phallus and pubic hair develop-0 x H1 ?3 k2 F4 r" g: A
ment without testicular enlargement, which was due: @' W) [! ^: R" l2 R
to the unintentional exposure to androgen gel used by
4 E- T2 F! i' g( |the father. The family initially concealed this infor-9 ~$ u' X8 d- F! i# ?: }; f: B/ m
mation, resulting in an extensive work-up for this
1 i& d0 e) c+ v* ~% h+ Ochild. Given the widespread and easy availability of7 u7 A r/ A$ a* M
testosterone gel and cream, we believe this is proba-
6 d+ b1 k* T; |+ }bly more common than the rare case report in the* @" ~4 o) r8 C( H$ v3 A7 B' Q
literature.4! i2 g$ P' C# C9 q$ m& P$ O2 q
Patient Report3 @6 N* \* y/ ], ]
A 16-month-old white child was referred to the
# a3 E5 a6 s9 D1 V/ c* _$ }endocrine clinic by his pediatrician with the concern
: J' Y# J+ ^2 j# Pof early sexual development. His mother noticed8 D3 h) {0 Z! X8 l2 U
light colored pubic hair development when he was
/ t7 Y. O1 h! t& v5 l' cFrom the 1Division of Pediatric Endocrinology, 2University of. x2 t8 l6 ?# k2 n! j
South Alabama Medical Center, Mobile, Alabama.
/ G! Y6 K6 c' o5 X- f- VAddress correspondence to: Samar K. Bhowmick, MD, FACE,! o! K7 x8 n1 F* H9 X/ Z- g
Professor of Pediatrics, University of South Alabama, College of
4 O) E0 r3 |4 q) oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 l* I5 h. @! {1 f6 o# }
e-mail: [email protected].& w$ b1 t% O5 H0 I5 _
about 6 to 7 months old, which progressively became. }* w6 m3 k# f1 G" M" p
darker. She was also concerned about the enlarge-
( Z" i7 P8 X$ v* d3 I }$ Y/ ~ment of his penis and frequent erections. The child2 F6 `/ d! G9 r* a G3 F+ `9 p/ g& I
was the product of a full-term normal delivery, with3 J. b4 N4 F# u* S/ l* e+ L
a birth weight of 7 lb 14 oz, and birth length of& ?( K x# X! g. h
20 inches. He was breast-fed throughout the first year* _7 H( B5 _+ u
of life and was still receiving breast milk along with
( l& G) w$ i! V6 }3 Qsolid food. He had no hospitalizations or surgery,
: O! [* Y# i6 H6 a: ]9 Wand his psychosocial and psychomotor development( L; ^5 R" U# c/ M) G/ L' L$ a
was age appropriate.# M, X) a5 U6 ^ `& y* o0 `: @8 p) e
The family history was remarkable for the father,
' f: X) v' N$ h# R5 fwho was diagnosed with hypothyroidism at age 16,
8 w/ N' O) i& j0 W5 }which was treated with thyroxine. The father’s
/ A; _% P" v- i* hheight was 6 feet, and he went through a somewhat
; a9 J: w/ n" ]( L2 Fearly puberty and had stopped growing by age 14.
- ~8 D) T" m; j7 W# _6 i& g' J( F! gThe father denied taking any other medication. The1 w8 X% _/ w! e* f2 P
child’s mother was in good health. Her menarche
9 d. g, F" Y! P1 U. zwas at 11 years of age, and her height was at 5 feet% H" y M' M3 a5 T* {4 S- N) T
5 inches. There was no other family history of pre-) l2 f2 i' Q0 a5 Z3 h) F+ @* I- W
cocious sexual development in the first-degree rela-: L, _3 U9 S g$ c" P `0 Z9 c
tives. There were no siblings.
s P4 Y5 f: M" o- gPhysical Examination. D# X0 v, {( q x# {, L
The physical examination revealed a very active,
. h/ n1 `! q6 w$ vplayful, and healthy boy. The vital signs documented; V+ |8 e# X4 {! Q- `. B6 X' k% H' _
a blood pressure of 85/50 mm Hg, his length was8 r5 E& K% f* I* k
90 cm (>97th percentile), and his weight was 14.4 kg3 _ C/ g5 m% x! x" k1 s
(also >97th percentile). The observed yearly growth0 N) J' h, D+ g2 Z; W; q; j$ A* P8 b$ `
velocity was 30 cm (12 inches). The examination of) E& k, x1 ]: v
the neck revealed no thyroid enlargement.
5 V" O# Q7 Z! q2 [% {& ]9 ZThe genitourinary examination was remarkable for
. _% D- a i& L( jenlargement of the penis, with a stretched length of2 M6 m4 @/ R# B k
8 cm and a width of 2 cm. The glans penis was very well
1 l9 \+ X, p1 O8 L: Q" [( Fdeveloped. The pubic hair was Tanner II, mostly around" h; `" |# @. k! ^& C" T
540. `- I# C: v. U ^4 i" k
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" \% F! W- [/ S: e7 rthe base of the phallus and was dark and curled. The
5 Y% V0 _- B; _- {5 Htesticular volume was prepubertal at 2 mL each.& |6 z, f, l1 }6 H: D6 Y
The skin was moist and smooth and somewhat
- x( p9 Q" _# _$ boily. No axillary hair was noted. There were no6 N9 W, k" l7 @+ p2 [0 k* L
abnormal skin pigmentations or café-au-lait spots.) ?5 |; z: q: W( [! c
Neurologic evaluation showed deep tendon reflex 2+
6 c6 d5 y8 _% L( e& `8 l# R6 }( z' n7 _bilateral and symmetrical. There was no suggestion
! ~+ I$ t# u( z. K9 {6 e! aof papilledema.
, g- b* ]1 g" |Laboratory Evaluation+ g% V8 d: b' W, e
The bone age was consistent with 28 months by: ^+ N7 J' U! v& ?5 ^1 n# K
using the standard of Greulich and Pyle at a chrono-# N! Y8 i4 t& h
logic age of 16 months (advanced).5 Chromosomal
9 k4 F: [4 B- U0 a! @- Ckaryotype was 46XY. The thyroid function test7 P W% d, W; q$ Q3 j5 c6 _7 q; E0 X- C
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
' f$ y0 L# I( r( s' Ilating hormone level was 1.3 µIU/mL (both normal).
0 B6 R, Z5 T+ G: AThe concentrations of serum electrolytes, blood
T" O: `' s* Z/ Curea nitrogen, creatinine, and calcium all were4 J( p* S( H6 L9 v
within normal range for his age. The concentration& \7 \7 n! _. h5 R3 M% t
of serum 17-hydroxyprogesterone was 16 ng/dL
& t7 J5 T$ R: V; H- D(normal, 3 to 90 ng/dL), androstenedione was 20
1 b$ A y; @6 U+ {ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
$ s6 {7 Q5 e h( _* W/ Qterone was 38 ng/dL (normal, 50 to 760 ng/dL),
) B& m6 H8 V7 G% K+ y. Wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to, F, L( K9 _% X% A: h7 Z7 e
49ng/dL), 11-desoxycortisol (specific compound S)- A9 c, H1 H) P; y
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 A1 h% y2 H- ^( ~8 B3 q+ W
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: s8 n+ ]# _7 H. H& G
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
' D! v5 g. x7 Z/ o* m" ~# Hand β-human chorionic gonadotropin was less than! o% o4 _1 x8 o/ [8 \
5 mIU/mL (normal <5 mIU/mL). Serum follicular4 g6 X7 o/ A3 Z1 Q1 o
stimulating hormone and leuteinizing hormone
9 I- Y$ d& O9 l1 i4 D3 G1 _concentrations were less than 0.05 mIU/mL9 B$ c: O! `1 ~/ y$ S+ A# P: ^
(prepubertal).5 `/ ~6 v- B+ K. g; E( w2 B+ n8 I
The parents were notified about the laboratory
3 ^3 y, N4 L8 L, \& H% jresults and were informed that all of the tests were! o6 \( j+ P: z: h, R5 s
normal except the testosterone level was high. The
U; N3 ?+ K" \follow-up visit was arranged within a few weeks to5 Z+ t) F- | H$ t- J1 ~
obtain testicular and abdominal sonograms; how-
4 M- ]2 @+ _. G! Y% T" lever, the family did not return for 4 months.- J0 u7 n) k& @" ?: j, t! z D
Physical examination at this time revealed that the
6 ]! V* h2 o z6 J. o+ Xchild had grown 2.5 cm in 4 months and had gained
) [2 m7 Q6 r" |2 kg of weight. Physical examination remained
E$ {3 Y2 C% D9 {+ |unchanged. Surprisingly, the pubic hair almost com-
, u2 Y: J/ R0 c: }% R9 ?pletely disappeared except for a few vellous hairs at
, w7 m5 [ w$ a1 q& T, ] |the base of the phallus. Testicular volume was still 29 x1 v9 R) Q% T" z
mL, and the size of the penis remained unchanged.
% ~7 s4 A. i9 \The mother also said that the boy was no longer hav-
3 E/ f8 I- }6 P0 ~. Ding frequent erections.9 S5 `; P! c# Y, j, X
Both parents were again questioned about use of% i' X6 I% P; X9 E" @
any ointment/creams that they may have applied to
y+ g* a& m6 Jthe child’s skin. This time the father admitted the2 D% I: a* X+ ^9 C1 r7 M
Topical Testosterone Exposure / Bhowmick et al 541- d4 D) h! v+ Q+ D4 {
use of testosterone gel twice daily that he was apply-
! H0 |; e8 C. G/ S6 X6 T! @; R" h; F: _ing over his own shoulders, chest, and back area for* s4 x5 C( R7 m2 k! `9 g+ G
a year. The father also revealed he was embarrassed
" V% n9 H/ i. P" w, d/ Sto disclose that he was using a testosterone gel pre-$ a! K& i& u9 {, n
scribed by his family physician for decreased libido# e. g+ `* F7 s V! J% V& u! ?
secondary to depression.
9 H6 E1 _! e" v% JThe child slept in the same bed with parents.# i5 Q! K* ~3 L$ }' v% S
The father would hug the baby and hold him on his) m2 R9 Q4 v6 m0 ~! u
chest for a considerable period of time, causing sig-8 p, H% C6 W6 {8 |
nificant bare skin contact between baby and father.% r% {4 Y$ M. y+ h2 J( H
The father also admitted that after the phone call,
/ g" f, u3 q; k+ u8 Hwhen he learned the testosterone level in the baby" Z/ I" r! |2 \
was high, he then read the product information
7 B, r" ^5 P0 _: ypacket and concluded that it was most likely the rea-
. E0 G; b1 s( x; xson for the child’s virilization. At that time, they
; G- ?! g% [* H. c! ]& c* }7 hdecided to put the baby in a separate bed, and the8 `1 }# C+ t* E d
father was not hugging him with bare skin and had. u# H- v& s5 T* G1 k' G, j4 @$ Q
been using protective clothing. A repeat testosterone
1 l* m6 f' O+ h% Y3 ~3 `5 S" A- gtest was ordered, but the family did not go to the) |3 q z+ Y2 m: v) x4 M; o3 i
laboratory to obtain the test.
3 j6 m/ d: `. ?8 Q: K4 wDiscussion! x$ R# M$ `$ D2 t+ D+ K
Precocious puberty in boys is defined as secondary) ]5 f3 }$ p# {7 u( z
sexual development before 9 years of age.1,4
, i+ z+ j1 A) f5 kPrecocious puberty is termed as central (true) when
6 t& q0 `2 I$ V M+ |it is caused by the premature activation of hypo-$ ?2 t+ x: d! l1 U
thalamic pituitary gonadal axis. CPP is more com-
o* E& u3 v: z$ G. F% Jmon in girls than in boys.1,3 Most boys with CPP# s X, R( Y% E5 X) i, y
may have a central nervous system lesion that is
2 X4 m/ X# h5 nresponsible for the early activation of the hypothal-
+ |7 f$ S4 ~7 t# |& h' ~, Oamic pituitary gonadal axis.1-3 Thus, greater empha-
$ J8 y* _, E. E, k" F) |sis has been given to neuroradiologic imaging in
+ Q4 [+ k9 J& O+ ?boys with precocious puberty. In addition to viril-
# p& w K3 ~' h I- R+ I3 Oization, the clinical hallmark of CPP is the symmet-
7 N8 l6 H' {; d% ?: p/ c: }rical testicular growth secondary to stimulation by8 G r/ l, O: _: R( v' C8 \
gonadotropins.1,3+ Z* d3 f9 n. ?6 f
Gonadotropin-independent peripheral preco-
_6 S x$ y, O* u9 f; L! S, tcious puberty in boys also results from inappropriate
* F. S5 ?1 k) Y3 U1 b& E( w4 wandrogenic stimulation from either endogenous or$ ?9 N2 I) ]5 G7 H* |7 M* h0 u& T6 `
exogenous sources, nonpituitary gonadotropin stim-
! I/ D, i7 G- v. {/ l3 X: D: Qulation, and rare activating mutations.3 Virilizing
* r6 N0 i/ O3 |4 m# fcongenital adrenal hyperplasia producing excessive
+ @% c8 ]: X+ @! {: d1 Z2 [6 Gadrenal androgens is a common cause of precocious y% ]" @) V3 s+ j" R/ t5 h" `
puberty in boys.3,4
# p& ]: [) K. F3 X+ A1 ?8 q$ rThe most common form of congenital adrenal
3 z. s" A/ l# S) N6 Z* _7 ghyperplasia is the 21-hydroxylase enzyme deficiency.
( ]1 C4 i0 r, }8 |8 hThe 11-β hydroxylase deficiency may also result in
8 q1 j3 _! d& m+ R6 O' U4 D$ u1 Aexcessive adrenal androgen production, and rarely,
" |& v2 J, @% @, ^& ean adrenal tumor may also cause adrenal androgen$ ~3 p* P3 G, r: a: T
excess.1,3
* b7 I$ [& g3 M- Vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- x6 a2 d: r+ V7 |5 C; t& ~7 S+ M
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 W8 }1 w) k5 rA unique entity of male-limited gonadotropin-5 [! Y$ o" q3 E1 d
independent precocious puberty, which is also known& B" {! w' M' w
as testotoxicosis, may cause precocious puberty at a
6 D J/ ^: o& V; B$ s8 ?7 }9 I$ u% a+ |1 ^very young age. The physical findings in these boys" n4 h! ^" } A# c- x& q" \$ _
with this disorder are full pubertal development,# N( D7 s: F0 ]3 G1 S+ x) c
including bilateral testicular growth, similar to boys
( L. w; P' X' C0 J! c$ ^* pwith CPP. The gonadotropin levels in this disorder8 F; P8 I8 u7 F
are suppressed to prepubertal levels and do not show
3 `4 U+ `5 ~& |: i b% T! Q3 zpubertal response of gonadotropin after gonadotropin-+ v4 k3 E- X+ V6 Q5 i4 A C4 B6 L
releasing hormone stimulation. This is a sex-linked( x/ E6 _! @, [9 ?1 f
autosomal dominant disorder that affects only
0 _! T9 z7 T9 F6 u! ?3 L! wmales; therefore, other male members of the family9 G \ I- _8 w1 z
may have similar precocious puberty.3( A5 F5 s( J3 z$ E. V
In our patient, physical examination was incon-
( s& J7 b9 Z- w: F3 B0 _- K osistent with true precocious puberty since his testi-- O! H8 U; @2 A7 `. [
cles were prepubertal in size. However, testotoxicosis& S& p w& r" a6 ?$ X) {
was in the differential diagnosis because his father; a; b; u8 Q7 L7 f6 I0 U% N% {# {
started puberty somewhat early, and occasionally,
0 \! R" }% @8 |! l" jtesticular enlargement is not that evident in the
- u+ ]1 U/ u5 J/ K1 |& A+ Fbeginning of this process.1 In the absence of a neg-
2 S% N/ o' |; q$ ?: u2 N5 L& ~ative initial history of androgen exposure, our
5 b$ g( b4 H, s: K% b( {& _$ }6 t) ~biggest concern was virilizing adrenal hyperplasia,
g" j8 c4 g. ~2 f! G7 Q0 ]& seither 21-hydroxylase deficiency or 11-β hydroxylase0 l* I, V. x8 m. A0 C6 l/ u
deficiency. Those diagnoses were excluded by find-
' r$ J# R! j1 ^& b& jing the normal level of adrenal steroids.
6 Z3 R3 Y- w& C ~# ~The diagnosis of exogenous androgens was strongly5 B u$ ], Y+ x4 n9 W: h: W K' \
suspected in a follow-up visit after 4 months because
9 ^9 @ h* u3 p) T8 X5 }; Q& v& ?8 fthe physical examination revealed the complete disap-7 V9 f; q, }- X* k) Q4 z0 `
pearance of pubic hair, normal growth velocity, and
@6 z0 m: g" Xdecreased erections. The father admitted using a testos-: \1 w2 X7 ^5 E* Y
terone gel, which he concealed at first visit. He was
9 S2 h3 Q! m) f' Yusing it rather frequently, twice a day. The Physicians’3 _" Q! T' T/ h) L# D1 c2 x5 k
Desk Reference, or package insert of this product, gel or: P3 F; p9 w1 W( X* n
cream, cautions about dermal testosterone transfer to
( o- l% M, l1 m- K- Y# Uunprotected females through direct skin exposure.3 U8 Y0 A2 d, x0 @: Q1 K6 }
Serum testosterone level was found to be 2 times the
- ^0 i% a% P9 z9 `0 o f$ U5 Qbaseline value in those females who were exposed to
7 _: c& p, C6 K* r1 J: b" Zeven 15 minutes of direct skin contact with their male6 P* b9 H3 {, |* m# B
partners.6 However, when a shirt covered the applica-6 R# I# I' {. [
tion site, this testosterone transfer was prevented.; V" W, Z' W i- b: ~& F4 s
Our patient’s testosterone level was 60 ng/mL,
m3 c+ f& f! B' Fwhich was clearly high. Some studies suggest that# g9 S0 P9 g, e
dermal conversion of testosterone to dihydrotestos-
& ?! A' Q& X6 A& T! b" p! \, ^terone, which is a more potent metabolite, is more
$ A2 j8 w) r& T; ]active in young children exposed to testosterone8 S/ Z- _# O$ \0 r
exogenously7; however, we did not measure a dihy-# A3 c3 y$ P9 |, d$ [' m) N6 ]
drotestosterone level in our patient. In addition to
' Q/ d# ?! M: }: e9 M% Pvirilization, exposure to exogenous testosterone in
. s `: @! A+ f4 E) Schildren results in an increase in growth velocity and
. R: a1 q' I/ T: G" n# Fadvanced bone age, as seen in our patient.
! P8 S; v& K( c. i1 X+ a( pThe long-term effect of androgen exposure during9 a' H1 e1 p4 ^$ A0 k q$ N2 k! O. ^9 P
early childhood on pubertal development and final$ Z5 {2 Z; q2 U
adult height are not fully known and always remain0 G2 m% i( U' G1 r$ s
a concern. Children treated with short-term testos-. I9 V. i ^5 W* t
terone injection or topical androgen may exhibit some
+ t1 M4 c; Q: qacceleration of the skeletal maturation; however, after* y6 @( s; G2 S2 {" N$ Q
cessation of treatment, the rate of bone maturation5 Z* O6 ^5 z* Q
decelerates and gradually returns to normal.8,9
0 e7 l% ~9 y, Z5 }9 a- N4 pThere are conflicting reports and controversy3 @* `% _3 g( {2 w6 ?+ e" a
over the effect of early androgen exposure on adult
( J" H% [2 r) v! mpenile length.10,11 Some reports suggest subnormal
& z" C) A, M+ L! cadult penile length, apparently because of downreg-
& k6 t: R. Q" _1 S `% fulation of androgen receptor number.10,12 However,% r+ N# J* N! P: l
Sutherland et al13 did not find a correlation between& ]5 @0 h/ C. [
childhood testosterone exposure and reduced adult
% C$ j& p4 N; |" a7 U) K+ t2 mpenile length in clinical studies.% E/ @: {4 B2 n& ]$ K& b8 a" V
Nonetheless, we do not believe our patient is
6 Y: _6 g! g1 J3 j+ _- Y" Zgoing to experience any of the untoward effects from) C @. u+ v& `1 L; L2 o$ e
testosterone exposure as mentioned earlier because" G7 u4 n) B" `6 {
the exposure was not for a prolonged period of time.( Q7 {: H% I4 H, H2 F
Although the bone age was advanced at the time of! R4 R$ p/ P a) V& ^+ ~/ B
diagnosis, the child had a normal growth velocity at
A( ]# X) h3 P3 ]9 ?. O0 Tthe follow-up visit. It is hoped that his final adult
( C( z" S( L' g7 R: iheight will not be affected.
. Y0 f: Z9 Z. J# iAlthough rarely reported, the widespread avail-8 ~; L9 m) z2 r3 t9 b9 r5 j3 @
ability of androgen products in our society may- U" R, z% ]% |: E4 w+ i' w
indeed cause more virilization in male or female
' N2 z X0 X4 E6 ~/ ?4 dchildren than one would realize. Exposure to andro-) R) ^' `3 l5 Q, z% u6 k
gen products must be considered and specific ques-
7 ~) M8 k o( `# {) [' w ]tioning about the use of a testosterone product or% N* r3 M+ @; |' H1 k( p
gel should be asked of the family members during
: r' y5 M7 Q- Jthe evaluation of any children who present with vir-+ y! Q# g9 d! W! q
ilization or peripheral precocious puberty. The diag-0 w+ \5 d! ?3 U2 S" h+ ^ n+ T
nosis can be established by just a few tests and by
3 t$ i4 l6 s- a( \/ v" Aappropriate history. The inability to obtain such a
" ?" l" n4 c% ]" Uhistory, or failure to ask the specific questions, may
% A2 F: o a% e0 R: Tresult in extensive, unnecessary, and expensive! d7 T+ g" n/ Y
investigation. The primary care physician should be
$ n/ @2 n2 B' B. {& ~2 P9 A- iaware of this fact, because most of these children
0 U+ v2 X% d# @2 q& m( Vmay initially present in their practice. The Physicians’0 s# g/ F" Y- K l) k9 v1 J* \
Desk Reference and package insert should also put a. v; g6 K% O( M* y
warning about the virilizing effect on a male or$ n8 a1 w+ O; o0 `% v) V+ \0 F
female child who might come in contact with some-
( k: X$ o! v0 W5 C0 Y3 ^* Yone using any of these products.
- K% f) J) b/ x1 g( O vReferences7 I) s/ J; n+ U7 X# u# z; ~
1. Styne DM. The testes: disorder of sexual differentiation0 X& \7 Z! Y( }6 c2 f, ^
and puberty in the male. In: Sperling MA, ed. Pediatric
6 i& Q& g2 R+ NEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
2 e( b% T1 J1 G# r6 P; R2002: 565-628.
& j; s/ _; X0 E$ s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 M/ `8 }" c0 ]. P& C3 e
puberty in children with tumours of the suprasellar pineal |
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