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Sexual Precocity in a 16-Month-Old, b, Z9 h. D; X& f0 v2 @
Boy Induced by Indirect Topical
7 h2 k. w4 T. bExposure to Testosterone0 X; m. b# A0 t
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, B# C: k, Z0 q9 Jand Kenneth R. Rettig, MD1
) B6 c! u, G* P! m: vClinical Pediatrics
% \+ Q) ?9 [1 T4 A: l0 @Volume 46 Number 6( w8 b# D5 h9 }( v
July 2007 540-543
7 o2 g; |1 J5 Z" e0 |3 o© 2007 Sage Publications
" q: Q( n1 i0 @* c10.1177/0009922806296651, m; N( ~0 q) T4 G: P
http://clp.sagepub.com% j W# n3 ^3 I
hosted at
+ B9 E9 w z" Zhttp://online.sagepub.com+ D" P8 h$ A7 V* b7 W" H
Precocious puberty in boys, central or peripheral,' Q% _- I, v8 X( B( V2 b
is a significant concern for physicians. Central. ^! B4 `" a; |/ k+ c2 x: g7 h
precocious puberty (CPP), which is mediated
: [9 e# c% z# Rthrough the hypothalamic pituitary gonadal axis, has
2 U& |, H5 J0 g2 k9 ca higher incidence of organic central nervous system: [* @/ A9 g ]' @$ J) L/ f' L9 D
lesions in boys.1,2 Virilization in boys, as manifested
7 P0 s# F, j$ Lby enlargement of the penis, development of pubic
- V ~" Q3 B( n# s" _hair, and facial acne without enlargement of testi-# f8 S% q: S" w( z( U& L) C
cles, suggests peripheral or pseudopuberty.1-3 We
* B7 v r( H p* hreport a 16-month-old boy who presented with the
9 f1 ~ _2 l! ]$ Y" X. P5 henlargement of the phallus and pubic hair develop-) Q/ d+ Q; ]: `* ]" E% w% i
ment without testicular enlargement, which was due
2 t7 ?7 C! R% _* l; o! m, Oto the unintentional exposure to androgen gel used by
0 b1 v5 j9 ^+ P4 M# F+ |* ~the father. The family initially concealed this infor-
3 b0 _7 q4 v- y7 nmation, resulting in an extensive work-up for this: G4 R" G# X- Q6 s9 ^
child. Given the widespread and easy availability of6 A2 E# Q8 U1 c9 e2 n& Q. I/ a
testosterone gel and cream, we believe this is proba-+ V( N% j) U6 k0 [0 C3 P
bly more common than the rare case report in the
2 o9 \6 _! G2 e% z/ E4 Kliterature.4
9 S2 Y$ y( y1 M+ PPatient Report3 m& x& ?. @, k. {/ j
A 16-month-old white child was referred to the K+ P! C* a0 A6 ~
endocrine clinic by his pediatrician with the concern
/ L: B; l) `4 l, g, xof early sexual development. His mother noticed5 {5 O# k }$ u4 ^
light colored pubic hair development when he was
" c4 i( C4 W! U3 Q2 H( ?7 D( X) BFrom the 1Division of Pediatric Endocrinology, 2University of) G+ c. G' L1 H: W. F5 y; ?! }
South Alabama Medical Center, Mobile, Alabama.8 s: C8 J j* n$ K% r
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 J( E7 T7 g8 P
Professor of Pediatrics, University of South Alabama, College of
# d) r/ m0 f& c5 J/ C1 LMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# x8 j3 y3 F. d0 U6 A& V$ H! F
e-mail: [email protected].
) [9 v" A6 `* g+ ~/ x7 t# D! cabout 6 to 7 months old, which progressively became" l) V. ^! [- W( s0 ^
darker. She was also concerned about the enlarge-
6 i n5 W* U- j, ]5 y, ]0 c, fment of his penis and frequent erections. The child! i0 E5 c7 H$ ] f @1 Y- [
was the product of a full-term normal delivery, with
$ W7 v) J# z- E! y& va birth weight of 7 lb 14 oz, and birth length of
; b: ?" b# B" p# q3 U. E0 E20 inches. He was breast-fed throughout the first year" g, m8 U3 p3 J8 s1 f0 x. I
of life and was still receiving breast milk along with
f- X4 w% x0 ^. v4 D& nsolid food. He had no hospitalizations or surgery,
% d- G& M- A$ O2 q8 ]5 jand his psychosocial and psychomotor development5 \6 O- z9 z( y9 d5 m! v
was age appropriate.
$ l! D$ @ R0 Y n6 L' GThe family history was remarkable for the father, ?( O, m6 h+ _$ q6 |4 x* G+ ^' w
who was diagnosed with hypothyroidism at age 16,9 a& b& T0 m5 Z' b- ]7 P3 P, G
which was treated with thyroxine. The father’s2 f8 G! u" c+ q/ ?
height was 6 feet, and he went through a somewhat- L* e; m- Q" w( T& P4 I! O
early puberty and had stopped growing by age 14.
' S/ c) _3 K0 ^The father denied taking any other medication. The
! n7 j3 \, g& wchild’s mother was in good health. Her menarche
* N3 M6 c$ B' F9 I- B5 Qwas at 11 years of age, and her height was at 5 feet6 s4 G5 ^8 v/ _2 ~6 m
5 inches. There was no other family history of pre-( |5 [+ n3 y7 `: ~. n$ h# ^
cocious sexual development in the first-degree rela-( b Z8 r1 @% J) s% r: Y3 \6 X
tives. There were no siblings.3 f3 ]$ ?, @" w7 d5 T, Q6 e
Physical Examination
1 o4 c E# f2 D2 J" L/ x9 |7 ` kThe physical examination revealed a very active,
+ c8 t5 a# V" c; z. v$ Oplayful, and healthy boy. The vital signs documented
& W9 O; g9 J/ d) S6 {, z' q; T7 Ga blood pressure of 85/50 mm Hg, his length was
$ N( L- I J4 y1 G90 cm (>97th percentile), and his weight was 14.4 kg( p7 @% m- j( N) [ l
(also >97th percentile). The observed yearly growth
$ J* X1 p/ k1 g6 Hvelocity was 30 cm (12 inches). The examination of
0 `! I. H0 ?, [" mthe neck revealed no thyroid enlargement.
8 C3 p# q& g6 s" m; vThe genitourinary examination was remarkable for
* U5 z8 i* M( _, B/ Nenlargement of the penis, with a stretched length of- X1 N/ x2 X$ J' H# S
8 cm and a width of 2 cm. The glans penis was very well
: p0 L5 W% T; _6 g) p$ pdeveloped. The pubic hair was Tanner II, mostly around X/ p# a+ M3 L
5406 @7 D, K! ^7 `( z2 _% {' D
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; v. S2 o" n9 ]2 a w3 b2 c+ q* N8 Bthe base of the phallus and was dark and curled. The
3 O( H7 @( F# H1 {: p% Q: ^testicular volume was prepubertal at 2 mL each.. e; [, e- L- m" K+ S' l# G% p; v
The skin was moist and smooth and somewhat8 b: I: i8 k" F- Y$ M5 Q
oily. No axillary hair was noted. There were no
2 v$ B6 |/ y9 \+ S9 o* U& v5 fabnormal skin pigmentations or café-au-lait spots.
! j6 G* G2 W; o PNeurologic evaluation showed deep tendon reflex 2+: x; ~+ [0 M: d2 o" X3 Y: F
bilateral and symmetrical. There was no suggestion+ v+ B( N/ [& w& ]0 b
of papilledema.
7 N I: c% Y; o: k$ yLaboratory Evaluation3 D$ I& O2 @! r3 f) K* c, G
The bone age was consistent with 28 months by* p. b7 m& u* {- r; T
using the standard of Greulich and Pyle at a chrono-3 g6 A+ M7 _6 [) y- w$ U
logic age of 16 months (advanced).5 Chromosomal
. Q% W7 Y5 W9 s! Skaryotype was 46XY. The thyroid function test
* `6 Y# T: j8 ]6 Mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-9 n' i$ C* M8 N3 n: ?
lating hormone level was 1.3 µIU/mL (both normal).- r1 R) x9 E: j5 Z [ f
The concentrations of serum electrolytes, blood
7 b- M! J7 D E# eurea nitrogen, creatinine, and calcium all were8 A7 X u: }4 @5 s6 a& f: {: e8 z5 u
within normal range for his age. The concentration( w; ^; I7 q) R$ `0 R8 r
of serum 17-hydroxyprogesterone was 16 ng/dL
& {3 ?! x l) ?; ](normal, 3 to 90 ng/dL), androstenedione was 20
m$ v+ Y# U% v* y2 E3 w: x; Hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, C2 X* m% Q6 `6 [& E$ Xterone was 38 ng/dL (normal, 50 to 760 ng/dL),
& |4 s3 Z8 Y# c9 }" l; X8 |" w. wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to6 B; h: |( w1 `5 o; C1 N$ F! e
49ng/dL), 11-desoxycortisol (specific compound S)8 o6 x9 D/ \1 ^5 n* j" @6 W
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 n h! S8 Q4 u6 Jtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 x+ v ^3 B! a8 q' I. Ltestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 w# F" e7 W* D; l, ?9 Zand β-human chorionic gonadotropin was less than' u6 f/ l: t2 t' n: T
5 mIU/mL (normal <5 mIU/mL). Serum follicular
# n( O: k. v1 G! x/ astimulating hormone and leuteinizing hormone( k9 v \1 I q. I# ~$ Z0 t* h
concentrations were less than 0.05 mIU/mL
8 Y9 x) D; s: ?3 W9 S$ n(prepubertal).
: L% X) N& H- C( ~The parents were notified about the laboratory
1 F0 E7 Q4 B* U0 Bresults and were informed that all of the tests were8 Q6 ?' R4 N! ~& `) d$ S
normal except the testosterone level was high. The
) d1 T% w0 V2 l3 j- O+ Wfollow-up visit was arranged within a few weeks to
. j; A+ o: S) X9 A5 [! fobtain testicular and abdominal sonograms; how-
! h6 c% Z: v" ^$ f1 Bever, the family did not return for 4 months.
$ d) q( D' H `) J4 ]1 APhysical examination at this time revealed that the' t, `1 G0 Q( M) {
child had grown 2.5 cm in 4 months and had gained
2 ~6 y; F* P- z0 t6 r3 \2 kg of weight. Physical examination remained+ W/ Z+ i8 _ K) y
unchanged. Surprisingly, the pubic hair almost com-; V: R8 P* w }7 n; f* U8 y
pletely disappeared except for a few vellous hairs at+ o9 s; s. h& ^
the base of the phallus. Testicular volume was still 2
# @% H% L$ M8 s R: J1 s4 [mL, and the size of the penis remained unchanged.9 _+ [* W8 n f0 c }
The mother also said that the boy was no longer hav-0 D8 d6 G# G# S) A4 U# N4 V) P
ing frequent erections.
8 R* N a' {. Z8 m, }' F3 i& qBoth parents were again questioned about use of
2 i, d- ]0 M$ q8 w' T* \( v4 Many ointment/creams that they may have applied to6 F5 I6 F. }# Z& K' X5 L2 P% ]
the child’s skin. This time the father admitted the
/ H W( P( b- n2 oTopical Testosterone Exposure / Bhowmick et al 541 E% C* @3 b9 L+ H* f, _& [6 E; A5 U5 {
use of testosterone gel twice daily that he was apply-; D. S) y9 y4 l; Z
ing over his own shoulders, chest, and back area for7 `2 V" @$ m' R: L/ @) I0 q
a year. The father also revealed he was embarrassed
) J( @% R0 m4 l8 b1 o8 l6 R3 jto disclose that he was using a testosterone gel pre-
) x' U/ v9 m# A0 k1 escribed by his family physician for decreased libido1 K# V. n; j+ q7 M- W9 P( Q7 _
secondary to depression.
V4 o( G `) D8 q- o! K; K4 k+ U- oThe child slept in the same bed with parents.4 ?0 W& J" l8 m( j; A5 y' I! g0 ~
The father would hug the baby and hold him on his
2 b. [9 O! F2 mchest for a considerable period of time, causing sig-
$ A! {+ k( s1 E1 L1 y8 e1 Snificant bare skin contact between baby and father./ b# e: q0 E: K! \* z
The father also admitted that after the phone call,
) u ?0 Z7 {4 V. A/ ewhen he learned the testosterone level in the baby, N, z% f' g0 F4 v+ @& m- Q+ y
was high, he then read the product information
. |0 X$ K" F" M" I4 o9 F; apacket and concluded that it was most likely the rea- s; B, A/ Z2 m, V! h
son for the child’s virilization. At that time, they' e3 c& p7 b' k! D" Z; Z
decided to put the baby in a separate bed, and the
7 s8 k2 B/ d& I9 b6 m! Mfather was not hugging him with bare skin and had
5 p$ Q3 r( J$ M8 ibeen using protective clothing. A repeat testosterone5 i- D0 T. H, ?7 a" J3 U- e
test was ordered, but the family did not go to the
% i) k" {* q) r x/ D- ]6 U) rlaboratory to obtain the test.
1 a) Z, Q4 h4 _- E/ A, v9 WDiscussion2 J# n/ i3 ~5 x" |* g
Precocious puberty in boys is defined as secondary
* M x2 R' o5 Y2 h9 a8 _) tsexual development before 9 years of age.1,4/ \) Q7 c' y' O; V/ f2 B
Precocious puberty is termed as central (true) when8 O }# |* b( t& Z
it is caused by the premature activation of hypo-9 u1 ~2 j7 X/ C
thalamic pituitary gonadal axis. CPP is more com-
4 y& [1 q I9 m+ qmon in girls than in boys.1,3 Most boys with CPP2 a5 Y9 f. D1 ^/ e* h8 x& H- L
may have a central nervous system lesion that is
/ H- ]9 |/ S6 ~ p* K( p0 Y+ h) Dresponsible for the early activation of the hypothal-3 @: s. k H, L4 h' X+ n
amic pituitary gonadal axis.1-3 Thus, greater empha-
$ N8 L+ G- w0 `4 o' N3 `! D/ P( isis has been given to neuroradiologic imaging in
2 U& l/ L4 L5 R0 U8 G# pboys with precocious puberty. In addition to viril-; v" X/ h) X- w# o* m: a
ization, the clinical hallmark of CPP is the symmet-. G7 ?) K- {, W2 ?
rical testicular growth secondary to stimulation by A/ p3 J4 F, R v8 H
gonadotropins.1,3& o# m2 i7 ]' |; E8 \ ]
Gonadotropin-independent peripheral preco-6 X) x, V; r, P2 q$ z% i; Y4 M0 W- Z
cious puberty in boys also results from inappropriate0 o, L4 i( A! Q4 E
androgenic stimulation from either endogenous or5 ^+ W9 c! J) g$ l: n$ j8 s
exogenous sources, nonpituitary gonadotropin stim-6 U: u+ {5 ]5 F: p
ulation, and rare activating mutations.3 Virilizing
& L8 H1 ^) J. k/ ]: R% D7 R9 ~0 Scongenital adrenal hyperplasia producing excessive
) @4 O% a' H6 `# S7 `adrenal androgens is a common cause of precocious1 X F$ K# h! `$ d. c# j6 p
puberty in boys.3,4# a. E2 M0 l3 e! T1 Y' U( r
The most common form of congenital adrenal
# e* O/ ^# N+ k+ R5 Uhyperplasia is the 21-hydroxylase enzyme deficiency.
8 R4 w0 M- t4 L6 |+ R( H! FThe 11-β hydroxylase deficiency may also result in) @4 _ O6 W5 t# m b
excessive adrenal androgen production, and rarely,
; q! A1 `* { i+ T8 v3 Wan adrenal tumor may also cause adrenal androgen
8 b5 w2 L# b( C+ X' A4 R6 a" B8 [excess.1,3
4 ?2 s* X R( L, d) }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 i( C6 s. E8 S' ?5 J+ L1 P
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! |# I! W, e0 c9 e" }A unique entity of male-limited gonadotropin-
8 G$ c# ]$ M9 |7 L( K( ]1 U3 Z6 X2 mindependent precocious puberty, which is also known
1 M3 A# |/ }- Y" mas testotoxicosis, may cause precocious puberty at a4 c9 J7 B/ }2 _, j7 a5 e* w1 z
very young age. The physical findings in these boys4 A- Z( V' j" K3 `
with this disorder are full pubertal development,
( P: l0 M" J9 A0 ~) R; R% \$ wincluding bilateral testicular growth, similar to boys
3 M, N- o# h9 C$ jwith CPP. The gonadotropin levels in this disorder8 N0 u+ s* q. O" ?
are suppressed to prepubertal levels and do not show
3 u- @$ t+ Z6 \pubertal response of gonadotropin after gonadotropin-0 b2 {5 l+ Z: j0 l& ?
releasing hormone stimulation. This is a sex-linked* D0 C8 ]8 d; i6 V: D \5 F1 r
autosomal dominant disorder that affects only, y D- `. `& v
males; therefore, other male members of the family3 G: ?# j& J( [2 G2 X% c! U
may have similar precocious puberty.3
& @: t) L: ^& ? W |; {& FIn our patient, physical examination was incon-
5 L8 B' ?3 `- Z1 tsistent with true precocious puberty since his testi-
# |3 L0 ]8 P0 E% Dcles were prepubertal in size. However, testotoxicosis; ^( h- F @9 i7 }, _
was in the differential diagnosis because his father
& ?8 L. U7 K! d4 y/ }& Vstarted puberty somewhat early, and occasionally,: V8 A, V+ q6 |6 e2 y1 }2 q
testicular enlargement is not that evident in the
' ~4 N4 p5 T3 b( o$ W5 xbeginning of this process.1 In the absence of a neg-
7 x% R$ p1 y4 J3 w* n- i3 rative initial history of androgen exposure, our% E: v( z4 b+ {" {! ~
biggest concern was virilizing adrenal hyperplasia,3 W) S/ M& a1 \/ Y+ f
either 21-hydroxylase deficiency or 11-β hydroxylase
C7 [) m6 d' M( b+ kdeficiency. Those diagnoses were excluded by find-, ^: W9 P/ O e+ i9 O. S4 }, g: a- L! \
ing the normal level of adrenal steroids.
) ^% \1 C5 N* B% O0 `) |The diagnosis of exogenous androgens was strongly9 g5 c: _2 P8 c; v
suspected in a follow-up visit after 4 months because
2 J8 O4 L. q/ F+ ~5 W. Wthe physical examination revealed the complete disap-
9 Q# o" G- `2 _, C) V6 Tpearance of pubic hair, normal growth velocity, and) P: b) T# O/ {% ~
decreased erections. The father admitted using a testos-
* _' Y; g/ E8 }9 Uterone gel, which he concealed at first visit. He was4 ^! V( I$ x) w" o* }* C* X
using it rather frequently, twice a day. The Physicians’- W5 j1 f! R" J5 f, P; Y
Desk Reference, or package insert of this product, gel or
& r& s% l7 s5 ^& ecream, cautions about dermal testosterone transfer to8 B1 u/ m6 @. l2 O; y8 l# P
unprotected females through direct skin exposure.# b# s. v& ]: a" W4 P1 X& r
Serum testosterone level was found to be 2 times the/ q, v, ~9 o5 E3 D* u% M
baseline value in those females who were exposed to
* ~* W: q# x! A, D+ |8 D- f; meven 15 minutes of direct skin contact with their male
5 F/ `, ]7 T" K& Fpartners.6 However, when a shirt covered the applica-
0 v! s( N5 `3 s& {4 j+ gtion site, this testosterone transfer was prevented.
, A7 G( ~* [1 p) c4 b+ J4 q `Our patient’s testosterone level was 60 ng/mL,1 E2 F9 d3 {5 a9 d" c
which was clearly high. Some studies suggest that
! b: }2 B) h$ U) m0 ^0 bdermal conversion of testosterone to dihydrotestos-5 K* L' o8 Q/ x. E
terone, which is a more potent metabolite, is more3 Y2 P' ? M# {- p
active in young children exposed to testosterone
2 T; Q$ E$ T% R3 Nexogenously7; however, we did not measure a dihy-
% n3 m W% i# r+ k3 N' rdrotestosterone level in our patient. In addition to
2 m' z( s0 T0 @( o2 kvirilization, exposure to exogenous testosterone in- b/ B$ z0 p9 W; J
children results in an increase in growth velocity and
- S' r. E6 e* h9 g1 L+ Eadvanced bone age, as seen in our patient.3 e9 s! |5 N7 H( B. G" k
The long-term effect of androgen exposure during
7 W/ U- {" |' M% Y3 h' Oearly childhood on pubertal development and final; i( \9 A. h1 u5 d) T
adult height are not fully known and always remain! X9 a* B1 T8 _. e
a concern. Children treated with short-term testos-
1 N' `% ~0 r* w6 J, f$ T" l6 q( Nterone injection or topical androgen may exhibit some
n( \ R& ?+ j! ]* Vacceleration of the skeletal maturation; however, after! _, d0 d4 O9 g0 B1 I* i: r3 H" z
cessation of treatment, the rate of bone maturation7 T. } O n$ d" G2 N) }; u
decelerates and gradually returns to normal.8,9
! _ |$ b+ X+ h2 K/ W- z0 D$ xThere are conflicting reports and controversy, i" n) h1 n/ ~8 T2 q
over the effect of early androgen exposure on adult A$ z( M, H, }( \6 W
penile length.10,11 Some reports suggest subnormal* ^' R5 y. f5 r! Q4 N/ U
adult penile length, apparently because of downreg-# X2 W4 B$ e: K. a* Z7 \
ulation of androgen receptor number.10,12 However,2 B, y. f6 @$ k1 V0 V D6 x2 q
Sutherland et al13 did not find a correlation between
0 v1 s2 v; x7 ^. G, hchildhood testosterone exposure and reduced adult4 I8 N/ F' f* }* b, @
penile length in clinical studies.; e2 m7 z0 E0 a! P* n: O
Nonetheless, we do not believe our patient is
; K$ Y1 r2 R& M- u; h Bgoing to experience any of the untoward effects from! g9 {* q) r# A! I6 k6 E& R' `8 E
testosterone exposure as mentioned earlier because
% K/ A+ ]" a& r- fthe exposure was not for a prolonged period of time.: q( |9 d- k5 S9 i
Although the bone age was advanced at the time of9 R/ P. U% J* B+ [% `$ m/ ^6 V
diagnosis, the child had a normal growth velocity at
8 V' l5 N. F G( \the follow-up visit. It is hoped that his final adult+ f5 V( F* j3 p6 Q" F; p7 s& Y/ c7 @
height will not be affected.
8 c6 k( U! O+ F" G9 E, A. i' G! HAlthough rarely reported, the widespread avail-4 H: s: N0 r. ~% w, z
ability of androgen products in our society may' u! Z' [( [4 h, x S' M* F
indeed cause more virilization in male or female
' [: u3 ~% x: W( echildren than one would realize. Exposure to andro-
& @' @, S! v ~gen products must be considered and specific ques-
5 Y' s& {, |, V' d. J6 ^# ~/ Z5 rtioning about the use of a testosterone product or
6 p- I; |# t% lgel should be asked of the family members during( t. M2 g; e0 i
the evaluation of any children who present with vir-2 h: v: y1 R9 D; F7 Q% d6 w6 y
ilization or peripheral precocious puberty. The diag-
4 v: c& b$ J) X9 J; f+ P* O& _' u) ^" anosis can be established by just a few tests and by
7 ]* A" h" [# D/ x) Oappropriate history. The inability to obtain such a# M3 e" M$ P. m2 P7 \1 e/ p
history, or failure to ask the specific questions, may
1 o1 N8 `# h4 z" A- M9 n+ lresult in extensive, unnecessary, and expensive- U4 L8 h! j$ Z; V7 Z
investigation. The primary care physician should be7 k( {% Q: R( L1 _7 m
aware of this fact, because most of these children% l1 y8 [. ?, o2 S1 X! u Y/ r
may initially present in their practice. The Physicians’ O- D5 F! ]! I6 N& e+ [ O) U \
Desk Reference and package insert should also put a4 G5 y) T7 A6 Z+ m# g& U1 ^* }3 P0 t
warning about the virilizing effect on a male or
# K) G( \# i: r/ c1 ]& y$ _female child who might come in contact with some-
! ~7 c$ ?+ j8 D* v5 Cone using any of these products.7 ^; }6 W* r1 L$ s$ Z
References
7 Y" X& b& a _6 J( J) i1. Styne DM. The testes: disorder of sexual differentiation
M! c1 ?, D" ^/ k2 w2 i# b0 uand puberty in the male. In: Sperling MA, ed. Pediatric9 F5 S& J9 z6 J
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ H! e6 c7 `. u: r! K9 |7 `, T4 G2002: 565-628.
, g" t- `1 _5 n/ g/ F" P2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious5 [ ~) u. c1 A; G/ ~7 @
puberty in children with tumours of the suprasellar pineal |
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