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Sexual Precocity in a 16-Month-Old
, c! L, z3 T2 i& J1 p* ^! WBoy Induced by Indirect Topical; A! ~. ]0 k3 O+ u% ^
Exposure to Testosterone: R, {. }" e4 a1 {
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 I0 y1 \3 k# r" S
and Kenneth R. Rettig, MD1$ c0 b3 w4 N2 ^1 ]% A3 I( V/ `
Clinical Pediatrics
) X' i1 w+ C( qVolume 46 Number 6
5 b6 K6 n0 ?: Y& h5 mJuly 2007 540-5434 |, \6 \: U* |. v2 }2 S* f9 t
© 2007 Sage Publications
$ I0 c0 v4 j6 v10.1177/0009922806296651% X, t( z4 d+ E- _+ Z8 U) f
http://clp.sagepub.com
5 x2 N, B4 S9 S, chosted at
: V3 U( c. u0 ghttp://online.sagepub.com, ]: g! [1 ^! H0 q @/ B2 f2 c1 o
Precocious puberty in boys, central or peripheral,
# V& v7 l0 D. a. u! P his a significant concern for physicians. Central
. C' w( \ b& N0 C+ i8 k" t2 }precocious puberty (CPP), which is mediated
! ^& Z6 m+ B5 ~5 b9 D" fthrough the hypothalamic pituitary gonadal axis, has
- a" n4 ]+ e3 c# H/ a- @6 x- ^/ Pa higher incidence of organic central nervous system' A$ R# z ~3 Q" A2 N* A
lesions in boys.1,2 Virilization in boys, as manifested+ l' s+ ?$ a1 ]% O1 c1 K( ^
by enlargement of the penis, development of pubic; F: \5 \) m5 ~( I- T% I0 O
hair, and facial acne without enlargement of testi-
$ ^) N/ F* |( U' A3 K8 M% U" M8 Ycles, suggests peripheral or pseudopuberty.1-3 We: T, x) ^8 D: ]1 W3 y
report a 16-month-old boy who presented with the
1 f2 e8 H( r7 t# n1 ?- z* b! W8 f. [enlargement of the phallus and pubic hair develop-
- |8 a1 G3 _3 X0 Nment without testicular enlargement, which was due
( E, c- ]% T! Z2 W" s0 \to the unintentional exposure to androgen gel used by
0 x }1 u; i- f. a8 Z3 Ethe father. The family initially concealed this infor-9 N+ @7 j) Y0 L/ I( r! v" O
mation, resulting in an extensive work-up for this
0 P1 D5 ]- l- r w* S- Q6 {child. Given the widespread and easy availability of6 h+ E. b/ A/ W% z
testosterone gel and cream, we believe this is proba-+ o- I* n3 Y% u9 ^) r/ Z7 @
bly more common than the rare case report in the
) z+ N2 C8 ]+ n- ?literature.4
$ N2 G; v2 n: [9 ]; ?9 N( p" }Patient Report
8 z5 J; l7 r" b7 z1 |" MA 16-month-old white child was referred to the
: ?+ v5 f- t6 ]2 Fendocrine clinic by his pediatrician with the concern
, @8 W# f1 ~1 w7 j& V& Dof early sexual development. His mother noticed1 @. Z; w: W) y- q- C
light colored pubic hair development when he was8 h" {7 H0 {* m% X9 m+ i
From the 1Division of Pediatric Endocrinology, 2University of6 B) ?/ I5 Q' z1 u, Z& y0 L
South Alabama Medical Center, Mobile, Alabama.8 f, X n$ w# k4 V8 J
Address correspondence to: Samar K. Bhowmick, MD, FACE,5 v: S2 Q8 E6 A
Professor of Pediatrics, University of South Alabama, College of
8 J. c; V8 E8 f% S* D( `. nMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 j& V1 D/ \: h' A5 Z8 ge-mail: [email protected].
/ B) G( H; m4 I u6 D9 Q& e0 Nabout 6 to 7 months old, which progressively became& F i( a. L0 S5 S# M( y. i
darker. She was also concerned about the enlarge-4 M# ?8 @! _% r$ x; ?1 P+ t
ment of his penis and frequent erections. The child
1 Y, h$ [! y. g6 q9 B. Twas the product of a full-term normal delivery, with
/ _8 A* k3 Y7 ^$ ha birth weight of 7 lb 14 oz, and birth length of5 L* V, N; }% j( m2 o
20 inches. He was breast-fed throughout the first year3 e4 J6 V3 m+ _( y6 S: ^$ u
of life and was still receiving breast milk along with
4 [6 y$ n0 a' K3 d# Csolid food. He had no hospitalizations or surgery,/ z& Y B, s j: J! |
and his psychosocial and psychomotor development" Y- h/ _2 ~) i! A) v1 c
was age appropriate.! z9 ]; Q; x! {& m0 t2 |+ i' J, q# p
The family history was remarkable for the father,% ?5 A# H! d7 X1 I! j4 n- z
who was diagnosed with hypothyroidism at age 16,4 k5 J) s% s$ a" t0 u/ |( K5 v E
which was treated with thyroxine. The father’s" T8 P1 I6 I9 p. u
height was 6 feet, and he went through a somewhat$ X7 G# t: M/ s, i% {
early puberty and had stopped growing by age 14.( ~- g2 G \, d) w, j9 M1 r4 I
The father denied taking any other medication. The6 T, W, B# I6 F% `, e7 ~7 p0 S
child’s mother was in good health. Her menarche6 b! x# @& l5 P3 _3 ~
was at 11 years of age, and her height was at 5 feet
8 f# s! O" `- Y4 J7 P: k5 inches. There was no other family history of pre-, Z* Y$ Y, l0 |$ p, s
cocious sexual development in the first-degree rela-, C% q P4 E( M: w
tives. There were no siblings.$ X `: p6 j* q- i$ V7 g5 i
Physical Examination
- H0 K( {: g' j6 c5 zThe physical examination revealed a very active,
, Z1 U8 c# [! \playful, and healthy boy. The vital signs documented/ F, g. [# d" }. z7 I# P
a blood pressure of 85/50 mm Hg, his length was5 Q" s6 J7 L4 i9 }0 p$ u. m$ E& E9 h4 a
90 cm (>97th percentile), and his weight was 14.4 kg" f7 B) u! O8 c0 F. }$ g% h
(also >97th percentile). The observed yearly growth" v* H' U2 G4 o) J
velocity was 30 cm (12 inches). The examination of3 A- N" B0 Q. H2 S9 R
the neck revealed no thyroid enlargement.
" z% [6 @- Z8 M9 P3 x, v1 NThe genitourinary examination was remarkable for
* l4 W$ m3 Y* C" Q( fenlargement of the penis, with a stretched length of
$ U5 M$ |) ?/ }' m5 b0 K; N8 cm and a width of 2 cm. The glans penis was very well/ ^3 ~" C0 m1 v7 u1 {& V* S
developed. The pubic hair was Tanner II, mostly around1 a/ T7 N- U) P+ }
5400 s+ Z& g# O- w r4 J2 g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& e( T1 z3 G( Fthe base of the phallus and was dark and curled. The0 E) l s, }3 {8 C4 j: G, ?+ D
testicular volume was prepubertal at 2 mL each.
1 Y$ T; M1 ?' @6 K E& SThe skin was moist and smooth and somewhat
& l3 s+ t1 a$ R8 P+ {0 t. f$ Goily. No axillary hair was noted. There were no
( r# u5 s& a) B1 Uabnormal skin pigmentations or café-au-lait spots.5 K- }7 R8 J2 q3 I8 f, V" J
Neurologic evaluation showed deep tendon reflex 2+
8 V; ]7 p) D$ J: u1 G; y Ubilateral and symmetrical. There was no suggestion
c) y2 V& D6 K9 ]" dof papilledema.+ K- w' p. j+ G6 Z9 q
Laboratory Evaluation
. S% q- J/ c" BThe bone age was consistent with 28 months by3 \! ]! ]% T4 d3 W) \
using the standard of Greulich and Pyle at a chrono-) ~8 S/ ~0 Y6 t: M* y/ R( P
logic age of 16 months (advanced).5 Chromosomal1 b3 W# A9 _0 b
karyotype was 46XY. The thyroid function test3 I% q3 s4 r- }. |
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
, B3 d# r8 x% ?% ~8 Olating hormone level was 1.3 µIU/mL (both normal).
' L1 S) @, x- `& vThe concentrations of serum electrolytes, blood
. x/ z5 j1 h8 `( L" qurea nitrogen, creatinine, and calcium all were2 |* I$ K/ g4 y* G0 }" e% F
within normal range for his age. The concentration
6 ^; d6 y( \( y, R Kof serum 17-hydroxyprogesterone was 16 ng/dL
0 \, C6 P$ m8 Z# {" z" g- ^(normal, 3 to 90 ng/dL), androstenedione was 20
& h8 e. b0 f0 v3 h4 g7 s6 \2 @ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ L/ l8 q/ \: Y) I; ^5 x/ l0 _5 N1 tterone was 38 ng/dL (normal, 50 to 760 ng/dL),- N) p) h' |1 f* h6 W& B: e: D8 F
desoxycorticosterone was 4.3 ng/dL (normal, 7 to8 e' x9 i& D+ G5 _7 e
49ng/dL), 11-desoxycortisol (specific compound S)
0 k* \2 w" g. k$ o4 ?$ Wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 K8 c5 T$ O ]6 N+ P. [* u3 xtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 C+ t+ W8 `* R; K5 b6 O
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),! w2 a' D' x9 Y5 E& j7 J% V- Q" H* m+ A) T
and β-human chorionic gonadotropin was less than7 ]6 m4 K3 \2 O: H
5 mIU/mL (normal <5 mIU/mL). Serum follicular) H- w& x. F( I6 k4 I6 s! B ?2 O
stimulating hormone and leuteinizing hormone1 W1 G( E& }) y7 \% a/ d' d
concentrations were less than 0.05 mIU/mL& y& F1 y7 c1 T2 X, {, x, a
(prepubertal).
" H, R' Z) Z3 }The parents were notified about the laboratory3 g2 n1 \& m! [3 u# C* ^% I* f; I6 O
results and were informed that all of the tests were
9 q6 S K) N9 ]6 q4 cnormal except the testosterone level was high. The; X! d( o8 A- \/ }7 {; M( Q
follow-up visit was arranged within a few weeks to
( U l. N, U Nobtain testicular and abdominal sonograms; how-2 x% K( {4 @$ ?/ C! i! r) I( _
ever, the family did not return for 4 months.
* q4 v1 \8 I9 u/ L3 w* f$ b* T- H2 RPhysical examination at this time revealed that the1 P3 l* i, N! h: [
child had grown 2.5 cm in 4 months and had gained; }! ]- u; A6 _
2 kg of weight. Physical examination remained' D# B) S9 w+ u8 y
unchanged. Surprisingly, the pubic hair almost com-
7 u- T( }* k$ }; t9 a+ ^pletely disappeared except for a few vellous hairs at
' ], P& c/ o% M8 q9 lthe base of the phallus. Testicular volume was still 2( G. i" V0 c' u5 @- |; I
mL, and the size of the penis remained unchanged.
# `6 L' w, t8 z* b1 k6 b. ^; ?The mother also said that the boy was no longer hav-
: B& @4 a1 |4 E/ D8 N7 ~* ying frequent erections.( |4 n8 }9 \/ g% w0 ~5 S6 Y! s
Both parents were again questioned about use of
( p1 j6 ?# G: K" t" _! ^" p( xany ointment/creams that they may have applied to! J. {1 X9 w6 ~; A3 D
the child’s skin. This time the father admitted the
# \4 j; G+ x3 M, e% j$ HTopical Testosterone Exposure / Bhowmick et al 541
{. ?6 V* A# P0 Z7 z$ W2 Ouse of testosterone gel twice daily that he was apply-
7 z1 T% ^$ f( w- z2 ning over his own shoulders, chest, and back area for9 P, l, P/ D0 P" T
a year. The father also revealed he was embarrassed _2 P1 |& l3 ~ h4 c9 {2 e [! h1 A
to disclose that he was using a testosterone gel pre-% J6 E3 N' d6 _
scribed by his family physician for decreased libido! G" u, Z6 ~- Z r! g
secondary to depression.
. r* p$ |9 X: iThe child slept in the same bed with parents.
4 }9 k: z. u) AThe father would hug the baby and hold him on his
9 A( u: }0 n* F: K; ychest for a considerable period of time, causing sig-
2 g" p& e" h/ s+ O' s0 ~nificant bare skin contact between baby and father.
. p; `7 d W3 k' ZThe father also admitted that after the phone call,
4 N! H; E0 [% O# G' ~0 r7 ywhen he learned the testosterone level in the baby5 Q; W/ s8 d% g- J7 s
was high, he then read the product information: b1 x( N' E! S. O6 Y- q' B' \
packet and concluded that it was most likely the rea-; N$ ]+ e7 w1 L% Z& `: H
son for the child’s virilization. At that time, they8 l2 {7 K6 d0 Y5 M5 y
decided to put the baby in a separate bed, and the
& x+ w0 j. B) O5 s* J& ^father was not hugging him with bare skin and had8 |. M' A: ?1 g' X8 w
been using protective clothing. A repeat testosterone
- G. B$ H2 p0 j' w) Atest was ordered, but the family did not go to the5 g6 h! P% b; z- v
laboratory to obtain the test.
( K' V! Q" O* f5 RDiscussion
$ Y g, g* s/ K9 f& N" e% b% nPrecocious puberty in boys is defined as secondary
# h' E4 w9 |& t& y8 G! u" z1 k' Gsexual development before 9 years of age.1,4
6 v: }* S' I8 F" ^; g2 E" t) }Precocious puberty is termed as central (true) when
7 e+ v3 @7 a" _$ Bit is caused by the premature activation of hypo-1 s0 G" }6 T9 j- k$ `6 s7 Q( P9 j
thalamic pituitary gonadal axis. CPP is more com-) J5 G7 c; S+ r3 V) ]
mon in girls than in boys.1,3 Most boys with CPP
$ X! k' f, K1 P5 {0 C+ m0 Omay have a central nervous system lesion that is
& I3 t) M. x: D; @$ Oresponsible for the early activation of the hypothal-5 l# y- f1 R |+ v
amic pituitary gonadal axis.1-3 Thus, greater empha-
6 u% E. h6 ?4 asis has been given to neuroradiologic imaging in
- ^2 B7 W: B. R$ K& hboys with precocious puberty. In addition to viril-5 k5 O8 U3 ]5 Z- z
ization, the clinical hallmark of CPP is the symmet-$ O7 V2 c8 ~+ A7 r" a
rical testicular growth secondary to stimulation by l5 n% z- K& k0 ~, C& x
gonadotropins.1,3
+ S( x% W1 Q1 C- lGonadotropin-independent peripheral preco-3 o) v. ^* @9 g- X
cious puberty in boys also results from inappropriate$ D, u: l) f1 F. m1 `! y/ z$ \; i
androgenic stimulation from either endogenous or
4 P. A7 B& {2 X2 W7 U* fexogenous sources, nonpituitary gonadotropin stim-
* i& y2 X/ v' v/ yulation, and rare activating mutations.3 Virilizing
' i& {2 M2 s m& Jcongenital adrenal hyperplasia producing excessive0 w; @' t+ m' O4 r3 j) }
adrenal androgens is a common cause of precocious
: C4 [3 ]0 r4 kpuberty in boys.3,4# B8 F: X1 p y- z$ W
The most common form of congenital adrenal# T$ T. y" \+ C5 b3 P" x
hyperplasia is the 21-hydroxylase enzyme deficiency.. f$ {$ f5 z# q6 @: `3 T* V4 |
The 11-β hydroxylase deficiency may also result in* y1 z T9 {4 M. X
excessive adrenal androgen production, and rarely,6 C8 [+ Q# M/ ~3 w
an adrenal tumor may also cause adrenal androgen# @3 b" B) L0 Y7 P0 O
excess.1,3
2 N2 f! |; I2 |) Z% fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 A+ j+ B( _. T2 b7 W3 t542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 b( ?' J) Q9 v2 E/ \A unique entity of male-limited gonadotropin-7 Z& d3 P4 s' s8 @
independent precocious puberty, which is also known
5 ]: k+ ~5 g' {7 L& |. H ?$ Zas testotoxicosis, may cause precocious puberty at a4 B; F9 y* d+ u( j
very young age. The physical findings in these boys
0 o$ {" c: x" V$ n+ Bwith this disorder are full pubertal development,
$ l3 _8 B5 p7 D. c% k$ rincluding bilateral testicular growth, similar to boys
& Z: R4 @# y1 V- n$ O/ Kwith CPP. The gonadotropin levels in this disorder
; h# H D9 S6 D8 q. G& {6 y. Ware suppressed to prepubertal levels and do not show
9 E' p4 s( P8 X6 [& Spubertal response of gonadotropin after gonadotropin- N% r" i+ l. U( N- X
releasing hormone stimulation. This is a sex-linked7 K% Y& g6 y' u9 b7 u
autosomal dominant disorder that affects only
6 T7 K3 h& s Q& zmales; therefore, other male members of the family U9 y. K7 r$ N2 l. w8 f
may have similar precocious puberty.35 }/ x, ~& Q$ z% f# |
In our patient, physical examination was incon-6 P; g+ G5 b1 ?) O5 K5 n
sistent with true precocious puberty since his testi-
* c& I9 k7 z- ecles were prepubertal in size. However, testotoxicosis
( V8 z# D }7 I' h3 ] q" awas in the differential diagnosis because his father
. b) d) _. J1 X9 [started puberty somewhat early, and occasionally,
" a0 W/ v+ @- ?0 B4 o: ?( Qtesticular enlargement is not that evident in the
( V" I- F. z* y0 i3 Mbeginning of this process.1 In the absence of a neg-6 Y3 e+ ~' F7 \0 `2 T
ative initial history of androgen exposure, our7 t, e7 O7 _/ H' N2 a. @6 S8 a' W) E
biggest concern was virilizing adrenal hyperplasia,
: O* ~& c3 s" J Ieither 21-hydroxylase deficiency or 11-β hydroxylase
7 `0 W2 ^! Z! K. d$ F. a4 q& sdeficiency. Those diagnoses were excluded by find-0 t8 f3 B" [3 ^+ ~! f& p
ing the normal level of adrenal steroids.5 h- i# r5 r8 R8 L
The diagnosis of exogenous androgens was strongly5 A- V& Y; `) k4 t: y( b2 N! l
suspected in a follow-up visit after 4 months because9 s: i$ d' D* C0 w6 V
the physical examination revealed the complete disap-# I& s% G5 U! I. ]) {+ G
pearance of pubic hair, normal growth velocity, and
- i1 T7 B+ }# Y$ L6 }! ^& B" i& fdecreased erections. The father admitted using a testos-( y, A0 s. ?7 O$ u( [
terone gel, which he concealed at first visit. He was
8 |" x' v [- }2 `' J( eusing it rather frequently, twice a day. The Physicians’9 \" Q" C4 q" L2 _# d$ f
Desk Reference, or package insert of this product, gel or/ F, q* \# e: o9 ~
cream, cautions about dermal testosterone transfer to# U+ V8 D7 V) g! z" x! G
unprotected females through direct skin exposure.
# P- I/ P4 V- ^Serum testosterone level was found to be 2 times the6 Q+ i. s0 `4 t _, V P
baseline value in those females who were exposed to1 R9 O: q% A, b- C& F, z" @
even 15 minutes of direct skin contact with their male! e/ u+ @, E3 N
partners.6 However, when a shirt covered the applica-: J3 W' ?/ k8 r6 h- i
tion site, this testosterone transfer was prevented.8 w) k5 j Z2 }
Our patient’s testosterone level was 60 ng/mL,
' z% t* x, J/ ~: r! q* Mwhich was clearly high. Some studies suggest that
( u/ y" B& U3 ^7 Gdermal conversion of testosterone to dihydrotestos-% _! Z5 m7 ~+ v& |$ J
terone, which is a more potent metabolite, is more* z+ R9 u9 W: [: ~; V
active in young children exposed to testosterone6 P2 U) b; `/ }. @4 J
exogenously7; however, we did not measure a dihy-( j' }1 e( `# f$ N
drotestosterone level in our patient. In addition to
" W/ a$ G2 u+ \7 q, q0 n5 S; K3 |virilization, exposure to exogenous testosterone in
; S4 M, |) B' h7 E2 ~" \2 Q: [3 Schildren results in an increase in growth velocity and2 w( h4 H4 }2 Y6 ~+ c
advanced bone age, as seen in our patient.! o8 G+ N7 C+ D
The long-term effect of androgen exposure during, F4 \' z6 ?& ?
early childhood on pubertal development and final+ {* J5 j0 [* p0 p2 ]
adult height are not fully known and always remain
1 c3 j8 d0 P ^9 a/ n- G( a2 na concern. Children treated with short-term testos-' }# w/ B, z* H0 U3 \- m; \: v
terone injection or topical androgen may exhibit some a5 k* l& F$ Q* P+ j6 h) o
acceleration of the skeletal maturation; however, after
" ]7 N0 U6 n( E; ocessation of treatment, the rate of bone maturation
9 p& K+ b3 W2 Y5 u8 @/ `7 ?decelerates and gradually returns to normal.8,9: m$ I: X$ U1 G3 D' \& F
There are conflicting reports and controversy7 A( z9 B: c$ n6 J+ x2 c2 X" k3 D
over the effect of early androgen exposure on adult4 B6 d- j: b% {& O+ V: y
penile length.10,11 Some reports suggest subnormal
0 m2 M4 y _3 R; @$ c- d4 x7 [7 wadult penile length, apparently because of downreg-
; B5 N) M1 W+ e9 J" n6 r3 g& Zulation of androgen receptor number.10,12 However,
7 k& W+ O3 b7 U& C vSutherland et al13 did not find a correlation between. u! b! w( i7 ~% v9 c5 Z
childhood testosterone exposure and reduced adult9 l0 n0 |) d8 v6 F) o+ P1 x
penile length in clinical studies.
$ T; z1 J- \9 ?) y/ O7 BNonetheless, we do not believe our patient is( r7 b- }; }9 T# Y3 ]& b8 b
going to experience any of the untoward effects from8 [ w3 T5 x: `
testosterone exposure as mentioned earlier because p: t5 d0 j- w4 L+ a
the exposure was not for a prolonged period of time.
# C3 { }: Z. }# iAlthough the bone age was advanced at the time of- S; ~5 L ~3 u m
diagnosis, the child had a normal growth velocity at
" l6 {( f ?4 m [& h2 R2 othe follow-up visit. It is hoped that his final adult
. N% s( D# j3 k. `& J' A+ d qheight will not be affected.
0 n0 [+ _* q& Q D: W$ E" Q1 _Although rarely reported, the widespread avail-" @& @8 a4 d1 Z+ k s8 U7 b6 d. n
ability of androgen products in our society may* g4 i) H% U& ^$ {9 d
indeed cause more virilization in male or female
9 u) N' ~6 P* d" |+ U/ o# Dchildren than one would realize. Exposure to andro-
' d# b0 |4 @; h3 v- {/ @8 B5 t: Ygen products must be considered and specific ques-
1 X/ Y. {' i) F6 y7 R* _. P- \ ltioning about the use of a testosterone product or
) e3 }- P) V0 U' S9 B$ r W# V M3 ]gel should be asked of the family members during1 U: y2 e6 F+ } r
the evaluation of any children who present with vir-
5 v7 S( V: Q# R3 m$ L' |: X' ], lilization or peripheral precocious puberty. The diag-7 F, F# \. v7 O% ^3 J) }
nosis can be established by just a few tests and by% m) |( C- F- `- Y; Y, s: M+ x- j
appropriate history. The inability to obtain such a
2 i! r$ t2 x) G- d& H0 mhistory, or failure to ask the specific questions, may
) O3 ^5 z! p V3 i6 g9 P2 \result in extensive, unnecessary, and expensive
3 r) B! K* H. y8 k# V0 ]. r. Kinvestigation. The primary care physician should be* z4 L) t' ^4 m) f4 o! k6 c" p
aware of this fact, because most of these children
3 {0 n- g9 z3 k6 i: Tmay initially present in their practice. The Physicians’% Y% B- r+ {. q$ n* u8 r, W
Desk Reference and package insert should also put a8 _3 b; f5 p" u& ~& D8 y1 @
warning about the virilizing effect on a male or
; h7 c" s0 C7 L: x4 t/ T+ K9 V3 Pfemale child who might come in contact with some-
, M& ^* i6 H3 U0 C. D! ]one using any of these products.; L2 @# f" |0 s6 m0 _4 m& @
References/ R1 s# z) P8 ]9 K$ T6 T0 q
1. Styne DM. The testes: disorder of sexual differentiation5 N9 a) x7 G B$ w9 K6 L
and puberty in the male. In: Sperling MA, ed. Pediatric2 b/ _7 x- j4 V, r
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;' u. Y. l5 \5 d2 C
2002: 565-628.
9 m3 ?/ f/ n5 b! x7 O9 e7 u$ T2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, {5 q" V* Y6 `; u, t
puberty in children with tumours of the suprasellar pineal |
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