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Sexual Precocity in a 16-Month-Old
* I+ u* L: s( H1 Z zBoy Induced by Indirect Topical
9 |* M7 M& H) @& AExposure to Testosterone
A6 j/ k }8 b0 Q3 m9 P6 _6 r9 I* YSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! \, K1 H1 Z5 @0 c: u ^
and Kenneth R. Rettig, MD1
% M! d& H0 t- R3 T( BClinical Pediatrics
; }! A1 M( T& AVolume 46 Number 6
6 `9 D- h; l; U% ^7 I$ y$ RJuly 2007 540-543" r: n4 ~$ E+ y2 ]$ K5 X
© 2007 Sage Publications' K* u7 J: a& N4 k2 Y2 ~/ C
10.1177/0009922806296651# \8 {7 V @6 s0 `7 J @
http://clp.sagepub.com. p& N% f5 p; X6 N7 |
hosted at
' j9 f8 |7 l; L3 Z& @! B p7 `; i0 F+ zhttp://online.sagepub.com
6 A, b: J3 c5 U+ I" APrecocious puberty in boys, central or peripheral,: ~% o( G: D3 \' c2 u( O
is a significant concern for physicians. Central
; D: y, d4 P' o, D) {, Pprecocious puberty (CPP), which is mediated9 d* [8 d; \" A2 w! A
through the hypothalamic pituitary gonadal axis, has
2 H' X( B# k$ `9 @% x6 U; L' Sa higher incidence of organic central nervous system D1 F8 g2 @/ e! ^* k
lesions in boys.1,2 Virilization in boys, as manifested
: J4 I/ v# y1 s; A$ @8 p* f4 rby enlargement of the penis, development of pubic
, P' Q: Y6 g, D6 q( a' uhair, and facial acne without enlargement of testi-$ Y* t" p- x1 D8 t" d. e0 e
cles, suggests peripheral or pseudopuberty.1-3 We( S8 g: n2 q# [, O( [: A
report a 16-month-old boy who presented with the2 v7 Q, u- s/ q) F4 q
enlargement of the phallus and pubic hair develop-
! v3 ^: {, p- n! N5 F5 _ment without testicular enlargement, which was due
. z2 Z. c$ p# C U) @to the unintentional exposure to androgen gel used by
; d+ V0 x! H/ |4 T0 I* r2 Hthe father. The family initially concealed this infor-
: l# ]0 C1 x' o2 U5 `# }mation, resulting in an extensive work-up for this% v7 t5 B4 D5 W3 h& f
child. Given the widespread and easy availability of6 q4 t) a4 l6 i0 s% N" [; c
testosterone gel and cream, we believe this is proba-
; u2 ]/ z+ x9 G2 e! W# Lbly more common than the rare case report in the
j4 s2 }* o& x- e$ k: f0 pliterature.47 K" e( a0 j, s: C5 L1 M
Patient Report
, D* c0 b y' a4 IA 16-month-old white child was referred to the9 }( m0 m. G6 k& U( L# @: G
endocrine clinic by his pediatrician with the concern1 U9 }8 D; j! D4 D+ S. G' W4 T
of early sexual development. His mother noticed
* G" l' A8 t. ?/ S6 ]8 f2 ~light colored pubic hair development when he was5 E8 Z' E: s7 S" G0 K& f: {
From the 1Division of Pediatric Endocrinology, 2University of
7 ^+ X6 b8 `. S- z. ~South Alabama Medical Center, Mobile, Alabama.
. |! k" n9 b! T4 f% o9 bAddress correspondence to: Samar K. Bhowmick, MD, FACE,; v/ C+ [" \- v& k; q4 g) r; g
Professor of Pediatrics, University of South Alabama, College of+ b5 ^* h6 h6 Q( T% \4 U
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( a: s1 \! ? a/ j& G2 r$ V3 K: V& Y
e-mail: [email protected].
/ s# a! q3 g6 m' c* wabout 6 to 7 months old, which progressively became/ J+ _, u3 p: U4 Q
darker. She was also concerned about the enlarge-6 W. G5 E& f) Y0 ^, ?4 }
ment of his penis and frequent erections. The child
: D6 E+ U, u1 l& twas the product of a full-term normal delivery, with: y1 D" ^3 b4 h1 S
a birth weight of 7 lb 14 oz, and birth length of6 x" Q2 G$ {1 d% d
20 inches. He was breast-fed throughout the first year2 U/ ~. Z, N7 ?% Q3 S
of life and was still receiving breast milk along with
8 w! [( ^7 t- q, Z/ ~1 N6 @solid food. He had no hospitalizations or surgery,
6 G% C, c$ r0 ^$ C. y- a3 rand his psychosocial and psychomotor development
/ r: m! u8 {* D6 v! W3 Z6 v7 Wwas age appropriate.! }! @$ U8 y7 g
The family history was remarkable for the father,
0 [8 Q" ~# K: _3 rwho was diagnosed with hypothyroidism at age 16,1 C" D0 l6 d2 }( g) M- a( H7 K
which was treated with thyroxine. The father’s
+ _% W5 `: i4 A3 X9 B9 dheight was 6 feet, and he went through a somewhat
" V9 u* M0 {' W" cearly puberty and had stopped growing by age 14.
$ |; L9 N" H/ U8 k; g( Z; O& K' u' KThe father denied taking any other medication. The. T5 Q9 _7 t: h
child’s mother was in good health. Her menarche
8 n! M6 A( |1 U: d wwas at 11 years of age, and her height was at 5 feet
: S1 N5 t! k$ j, c5 inches. There was no other family history of pre-
4 N' M0 ~- p. \cocious sexual development in the first-degree rela-
8 \9 J& k5 g) B3 F/ N) }tives. There were no siblings./ ` F* m. t* M) Z' b0 w
Physical Examination. [( p* l/ Q. \+ k8 Q
The physical examination revealed a very active,- b, ~0 y4 P9 G( m! G
playful, and healthy boy. The vital signs documented
7 `6 ^) y/ q! K' q" a5 Y1 }$ ~6 ha blood pressure of 85/50 mm Hg, his length was
% q* v" \4 ~8 X, @/ D- f- U90 cm (>97th percentile), and his weight was 14.4 kg
2 B: o4 W% @7 z$ }(also >97th percentile). The observed yearly growth2 V- ~- B# ] l* v$ S/ X) J
velocity was 30 cm (12 inches). The examination of; W: n/ m$ s+ l2 c0 H
the neck revealed no thyroid enlargement.
$ G7 x$ S( S' C _, L! c5 `The genitourinary examination was remarkable for) k; R( i) M* B8 Z+ `2 K
enlargement of the penis, with a stretched length of
- {" v1 j) ~* y2 v7 W! ?8 cm and a width of 2 cm. The glans penis was very well
: x" c( W8 `6 u/ ydeveloped. The pubic hair was Tanner II, mostly around
( M3 b3 r# k: j$ ]- X. [, Y540
2 B( {# I5 h! f3 Aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) U5 V) i8 i) w' O
the base of the phallus and was dark and curled. The; P- A z- T" C3 C D; P8 [
testicular volume was prepubertal at 2 mL each., ^. w% t( l. B- V7 v/ p2 {
The skin was moist and smooth and somewhat! d! F: |) j7 |4 o, Y2 J- N
oily. No axillary hair was noted. There were no# k) Y* s% f R: q) \! f
abnormal skin pigmentations or café-au-lait spots.
, t% \8 s Q9 i' e9 P6 qNeurologic evaluation showed deep tendon reflex 2+
8 T M7 g$ q# o' I: e; Tbilateral and symmetrical. There was no suggestion
4 @( Y" S* I. P; M4 l) iof papilledema.- M8 u# C5 ?/ o5 w( {! L
Laboratory Evaluation; b- a6 V. L9 s) n! J0 Z
The bone age was consistent with 28 months by, {; p; h7 p1 j
using the standard of Greulich and Pyle at a chrono-
" f( g8 t8 N% u8 o( vlogic age of 16 months (advanced).5 Chromosomal$ U, _6 i$ g( V* Q
karyotype was 46XY. The thyroid function test
6 I+ U" z6 I& @: V$ [4 Gshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
p: H8 Z% u8 S3 z$ o3 @% J: G% ylating hormone level was 1.3 µIU/mL (both normal).$ K7 A5 ^* V! u: I; j& }1 {
The concentrations of serum electrolytes, blood h' [+ e# H+ O' {+ J6 }8 }
urea nitrogen, creatinine, and calcium all were3 ~* _& g$ ]! G$ [& r
within normal range for his age. The concentration0 m( k9 N. D8 ?$ Q5 R3 ?
of serum 17-hydroxyprogesterone was 16 ng/dL
. Z' H3 t& [5 p N7 j5 z( w; ?# b(normal, 3 to 90 ng/dL), androstenedione was 20
' f7 R7 p1 N; e6 R) Z6 J: dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 F l2 `3 y' h) h( G+ X
terone was 38 ng/dL (normal, 50 to 760 ng/dL),. j" w: U2 P5 O
desoxycorticosterone was 4.3 ng/dL (normal, 7 to% z" H' Y! ]8 U: R
49ng/dL), 11-desoxycortisol (specific compound S)
$ ?" K- R0 P0 D3 {was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
0 e$ J+ |* V' M0 Ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 T. o& e/ ?7 x4 _" b9 ~
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
' k0 u/ C7 |" U* ^/ tand β-human chorionic gonadotropin was less than
. f3 f: A5 P4 `: L5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 d8 V! ?7 G y% O- q* N$ zstimulating hormone and leuteinizing hormone
2 a5 S1 j' d+ |concentrations were less than 0.05 mIU/mL
7 R+ f; A$ W+ g) m2 ^(prepubertal).
/ p3 Q; z9 b% `( }- f, U1 zThe parents were notified about the laboratory
3 q# j: Z7 @# p! U. a( M7 v) K p2 qresults and were informed that all of the tests were7 A& X, a' N4 R( [2 L1 Y- `' E) R1 j
normal except the testosterone level was high. The4 ?0 A% a1 e" W7 K
follow-up visit was arranged within a few weeks to
; H/ H+ t3 R- l% Q O0 M1 hobtain testicular and abdominal sonograms; how-& x$ ]) |8 L1 t2 }
ever, the family did not return for 4 months.
, \: G1 R% R* }% U+ o8 k5 QPhysical examination at this time revealed that the
+ _. ?2 }5 ?$ \8 S" C8 _( M% j" mchild had grown 2.5 cm in 4 months and had gained" X# \5 h3 T; g. T: r
2 kg of weight. Physical examination remained! x7 D8 }% r3 h3 P; c$ M2 P# H8 j
unchanged. Surprisingly, the pubic hair almost com-
# b# u$ ]0 A% npletely disappeared except for a few vellous hairs at0 K1 E" J/ `8 o: L! m6 z
the base of the phallus. Testicular volume was still 2. u9 H% U L" [/ Y
mL, and the size of the penis remained unchanged.
. m/ s) y, h" G0 z: n6 ZThe mother also said that the boy was no longer hav-
' e3 ^. d& ?* [3 V* X, y1 Jing frequent erections.1 s& m3 X8 Z' l1 b
Both parents were again questioned about use of$ Q6 ?, ^- Q7 h! V* @3 e
any ointment/creams that they may have applied to3 M, c2 h, | D2 ~5 I
the child’s skin. This time the father admitted the/ }/ |+ ^( ^# U8 F5 l6 x
Topical Testosterone Exposure / Bhowmick et al 541
0 g6 P/ i' G( Ouse of testosterone gel twice daily that he was apply-! t4 l9 b0 G( ?' y. h% L7 I) j% H
ing over his own shoulders, chest, and back area for6 F( z2 |+ s+ L0 i/ Z/ H
a year. The father also revealed he was embarrassed% e! ~4 e" {( ]% v. L: Q( z9 a
to disclose that he was using a testosterone gel pre-
% y2 H7 b7 e8 }; |8 x; Q/ Lscribed by his family physician for decreased libido! H% e1 e( \0 F3 n5 `
secondary to depression.
2 w5 J( I9 {& ^; o& e( l. fThe child slept in the same bed with parents.
7 c9 [7 B! Y+ RThe father would hug the baby and hold him on his
0 Q) U0 j' K1 R4 b0 U echest for a considerable period of time, causing sig-
4 a. i7 c# m* u$ O; {* gnificant bare skin contact between baby and father.
- ~# E' Y* J0 z* t: NThe father also admitted that after the phone call,+ _: o/ I: n9 b
when he learned the testosterone level in the baby! u! [5 L2 |) O( n' o
was high, he then read the product information
) o( x. o8 `/ @. a5 s, E# B* \packet and concluded that it was most likely the rea-
- O$ ]7 Y; k( ^ O7 Uson for the child’s virilization. At that time, they7 _; q! Y1 ~! {, E, S
decided to put the baby in a separate bed, and the
# n5 p4 A, l. s* E; } Kfather was not hugging him with bare skin and had" B& @! u& M: ^
been using protective clothing. A repeat testosterone1 k/ W" h- U5 u" C
test was ordered, but the family did not go to the. J* T, @& z% k4 L
laboratory to obtain the test.( [ |9 D0 K6 a* |. t) b
Discussion! s- q) X& i2 o: N& A& O; R3 N
Precocious puberty in boys is defined as secondary
% Y1 z& ], b$ J& Xsexual development before 9 years of age.1,4
# F. ?. N% q: F) [0 k) f/ W jPrecocious puberty is termed as central (true) when2 B- C# w* y5 L/ S: J( X
it is caused by the premature activation of hypo-/ }1 e' [, f, a: F
thalamic pituitary gonadal axis. CPP is more com-
% e j1 W8 g4 y: K$ o; h; o' R" F, Wmon in girls than in boys.1,3 Most boys with CPP
2 ~ D$ y: C: ~9 C7 a( p$ pmay have a central nervous system lesion that is
$ N p _3 G; m; O6 jresponsible for the early activation of the hypothal-
& C! D$ [$ g, R: O2 uamic pituitary gonadal axis.1-3 Thus, greater empha-
6 |7 k' G5 R; H) ]4 Asis has been given to neuroradiologic imaging in
! Q; a- Z9 {! U6 l) C' C- p2 G* Iboys with precocious puberty. In addition to viril-3 d! {" X% K6 M0 b( K; ~# f/ @; D
ization, the clinical hallmark of CPP is the symmet-2 Q7 \5 b/ q4 t; W! j( l2 S- r: S9 b
rical testicular growth secondary to stimulation by
% Z5 ]9 a& }7 ], Q, W* p0 J; Ogonadotropins.1,3# E: I- n- P1 r$ p8 w7 @
Gonadotropin-independent peripheral preco-
4 y/ R1 W7 K& G; j! i* hcious puberty in boys also results from inappropriate
* e8 c% v0 K2 z. X: vandrogenic stimulation from either endogenous or
5 [% j( k" n: B# k6 q6 U, G5 _exogenous sources, nonpituitary gonadotropin stim-
) H+ u/ \& o0 \0 j' I8 C- iulation, and rare activating mutations.3 Virilizing
2 V5 ]% {4 H2 e7 j, U5 lcongenital adrenal hyperplasia producing excessive
+ [ g( \# g7 |4 N& C( u, h! ^3 _adrenal androgens is a common cause of precocious
" B# B1 T' B; J0 o( opuberty in boys.3,4; Y3 k$ t* Y5 _" i- F( \
The most common form of congenital adrenal
0 v3 S- t) ~2 B7 j0 P7 E% e: whyperplasia is the 21-hydroxylase enzyme deficiency.1 J1 H2 }3 l! n! F# w) W9 w
The 11-β hydroxylase deficiency may also result in8 v, H- S$ H1 A' [! Q
excessive adrenal androgen production, and rarely,+ z. w; ^1 ~: ?" F/ Q
an adrenal tumor may also cause adrenal androgen
( S2 z; y" d. ~; f: ` Jexcess.1,3 h6 W6 I7 h6 Y7 s- t
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* @9 }& b F7 g& N4 O+ x542 Clinical Pediatrics / Vol. 46, No. 6, July 20077 M. u4 Q: F& |
A unique entity of male-limited gonadotropin-, l. _4 ?! O% s, a$ z
independent precocious puberty, which is also known) j4 o% R, v! c" k% f; ?. L5 m
as testotoxicosis, may cause precocious puberty at a3 h: }( R3 a% L* O/ N3 A
very young age. The physical findings in these boys. t# N+ {3 H0 b6 T
with this disorder are full pubertal development,7 W; o: V. r c$ r! D; l, {" ]2 ]
including bilateral testicular growth, similar to boys
2 c2 ?: u) E& @ r+ jwith CPP. The gonadotropin levels in this disorder
& O5 h, l2 w- Aare suppressed to prepubertal levels and do not show" L# r5 f3 w' B! U+ _" Z; B& X" M0 P
pubertal response of gonadotropin after gonadotropin-8 I) f4 @* Y- n! b" F
releasing hormone stimulation. This is a sex-linked9 Z% s+ k6 ?; X# x0 f5 ?
autosomal dominant disorder that affects only
+ ]4 P4 b0 S! [9 o3 n L$ w1 Lmales; therefore, other male members of the family4 p- _7 _0 h5 z
may have similar precocious puberty.3. \6 P0 H3 G$ f/ T- W1 T5 X N
In our patient, physical examination was incon-
" g! L$ A- J/ W. S& A* h% tsistent with true precocious puberty since his testi-/ F, C' T4 V5 I
cles were prepubertal in size. However, testotoxicosis
6 ~; J; p2 t# l+ f2 k* D Uwas in the differential diagnosis because his father7 u% e$ M7 |+ N) F
started puberty somewhat early, and occasionally,
+ l+ R# i! S A" Y4 O$ y6 ^testicular enlargement is not that evident in the+ h8 [3 @7 X& J5 ~
beginning of this process.1 In the absence of a neg-; t& j7 d( m% e$ R% y
ative initial history of androgen exposure, our
9 B" Z+ T+ b1 U: Xbiggest concern was virilizing adrenal hyperplasia,9 M* }! m! {$ k9 J+ D6 i
either 21-hydroxylase deficiency or 11-β hydroxylase: }' m! Z7 l7 f" z! \) [3 B
deficiency. Those diagnoses were excluded by find-0 C; e& p) @, J0 w
ing the normal level of adrenal steroids.% W6 H" q, F6 G1 J/ ]7 h. N
The diagnosis of exogenous androgens was strongly
6 _! \; E" n) v/ ^suspected in a follow-up visit after 4 months because8 f1 q7 n2 H4 p5 q. @
the physical examination revealed the complete disap-
c" J. b+ |7 v! Apearance of pubic hair, normal growth velocity, and6 P# w( {" ? A7 o3 e" b
decreased erections. The father admitted using a testos-
V4 Y# v$ f3 sterone gel, which he concealed at first visit. He was
* T' G4 |3 t9 R2 L. Jusing it rather frequently, twice a day. The Physicians’
( p: o! E E# a& x H' G, Z7 h4 Q) WDesk Reference, or package insert of this product, gel or
! h5 W. s2 {: E. Kcream, cautions about dermal testosterone transfer to" f) e, Y5 ~& K0 M) n1 ]' G
unprotected females through direct skin exposure.. `* s" Z' n) f2 w. E2 |# [# B$ }
Serum testosterone level was found to be 2 times the# `8 S( y+ n, c; r9 u4 O; }; M
baseline value in those females who were exposed to
* x$ h+ Y' ]& ? aeven 15 minutes of direct skin contact with their male
* M) d2 ?* `3 J1 z8 ]* npartners.6 However, when a shirt covered the applica-
* K! O: W3 `" d& x& z7 o* ntion site, this testosterone transfer was prevented. d% |) K5 J4 Q8 K* }; {
Our patient’s testosterone level was 60 ng/mL,
. w+ }$ Q5 l2 g. w8 D" E6 q/ f$ Dwhich was clearly high. Some studies suggest that' p4 }" o1 E7 k
dermal conversion of testosterone to dihydrotestos-
6 Z/ `( r/ e" K8 ?2 _* Hterone, which is a more potent metabolite, is more2 F! J7 X, T/ i
active in young children exposed to testosterone
7 N( M4 _- a* R5 Uexogenously7; however, we did not measure a dihy-; x0 z- m. _. x5 r% B D
drotestosterone level in our patient. In addition to
' _9 c7 X* x( ]6 x' n4 v/ ^) l3 ^virilization, exposure to exogenous testosterone in% }4 @5 o* u: z* Q c6 `
children results in an increase in growth velocity and
/ v+ C9 b0 J5 F1 M3 [! M- j# k. ]advanced bone age, as seen in our patient.
$ z9 s4 m5 r+ W F. mThe long-term effect of androgen exposure during
( j) @+ j: `) {) Y# S- v* s) ~early childhood on pubertal development and final
& {+ h7 j! P$ P* k" i) `) z0 j1 A) Qadult height are not fully known and always remain9 o4 q* n- B3 n' \: d# |
a concern. Children treated with short-term testos-
8 c3 Y3 d. e1 y [9 r" Z) ]$ N& U5 Oterone injection or topical androgen may exhibit some$ F5 {* G; o2 H9 F& L" G+ V
acceleration of the skeletal maturation; however, after: f& I2 \" p' ?0 ]: r' d0 p+ A! _
cessation of treatment, the rate of bone maturation
/ E4 M) C% A! ~! w: t/ W4 m# y- @decelerates and gradually returns to normal.8,9+ E0 C8 T8 M* j, h3 n7 z& R
There are conflicting reports and controversy2 g1 X# v( a3 A- U5 |1 B
over the effect of early androgen exposure on adult
) L0 B* G% G7 M8 } r- n$ o! G! wpenile length.10,11 Some reports suggest subnormal
7 l+ P6 {, ] x$ iadult penile length, apparently because of downreg-
/ C2 \# L5 H: I8 p5 C7 A$ i1 dulation of androgen receptor number.10,12 However,0 N. N L S# q6 \5 y$ ?. N
Sutherland et al13 did not find a correlation between4 P8 y) t5 S. B0 a
childhood testosterone exposure and reduced adult
( Z( C; R1 B! N8 u" C" Zpenile length in clinical studies.( P4 L) e/ h' }+ C9 R: d
Nonetheless, we do not believe our patient is6 W; B) R$ \5 j( q: x8 d( u5 J, h
going to experience any of the untoward effects from
+ V. D* g! h8 i. u) ~testosterone exposure as mentioned earlier because
" B- j" Y, ^) y7 c( M/ jthe exposure was not for a prolonged period of time.
/ { F+ t3 Y' t9 G8 M9 UAlthough the bone age was advanced at the time of' q# X) d3 _& e( a; q8 K" E& R$ t4 c( Z
diagnosis, the child had a normal growth velocity at
+ v3 |: ^$ k4 p2 J/ gthe follow-up visit. It is hoped that his final adult
: k& j( _/ G. M" N: Vheight will not be affected.2 z* Q1 Q% w3 }8 Z x
Although rarely reported, the widespread avail-
2 `7 ^4 } T/ N! e9 yability of androgen products in our society may
* |" G7 Z/ k, h7 f) Nindeed cause more virilization in male or female
. ^$ i: u% w( q4 K) Mchildren than one would realize. Exposure to andro-# G; P; _' {- _0 D: C
gen products must be considered and specific ques-& h' w4 d& z2 T& z* o# V
tioning about the use of a testosterone product or
0 @9 K7 v1 C' _6 fgel should be asked of the family members during# Z K2 I7 U, N, E. @
the evaluation of any children who present with vir-0 D* N; m- Z0 S3 N: b
ilization or peripheral precocious puberty. The diag-
& I7 r: j% [6 unosis can be established by just a few tests and by' t. k4 `5 B5 ?$ D( M1 m
appropriate history. The inability to obtain such a
9 t8 f: t8 `7 ]) |history, or failure to ask the specific questions, may
! c4 o! r& ]; Q7 r" ^" U4 }result in extensive, unnecessary, and expensive
) r5 {- G/ I% k# I) rinvestigation. The primary care physician should be; W, v+ g( P2 a) i/ O/ I5 i7 h
aware of this fact, because most of these children
+ Y) y9 j% T3 c/ ?, N5 f' h8 w# imay initially present in their practice. The Physicians’$ o, G3 X' U9 Y& ~( f6 b: W
Desk Reference and package insert should also put a+ Z$ V @# N4 w5 l; @. A% `1 n
warning about the virilizing effect on a male or) n: H% {# j0 t$ R2 O
female child who might come in contact with some-
+ a$ s" a$ U$ z! c: v2 J8 rone using any of these products.
4 n( N: o1 Y+ G0 q6 AReferences
; B" f4 \: A/ K: w5 H: b. p8 M1. Styne DM. The testes: disorder of sexual differentiation
* ?5 D U, [0 H0 v2 ~6 I- vand puberty in the male. In: Sperling MA, ed. Pediatric
: r) ?+ V3 j9 u" j7 GEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
0 A- z5 k% K7 @" F9 Y0 g2002: 565-628." c/ e0 D3 C4 w- H/ a; ^! ]
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- H: d; T) v2 R+ S7 o2 N$ d
puberty in children with tumours of the suprasellar pineal |
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