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Sexual Precocity in a 16-Month-Old* z( O% T: |0 A
Boy Induced by Indirect Topical; [( C! U5 z2 X: p0 @ ?+ ]
Exposure to Testosterone# ^ t/ |$ B4 E8 o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 o/ P4 o4 D7 ]1 r5 u& pand Kenneth R. Rettig, MD1! O% ], U6 q N2 W! n# u
Clinical Pediatrics \& k1 F2 m' X6 `' j" c: G
Volume 46 Number 6
+ x2 p" a7 d5 `! U7 v; G( hJuly 2007 540-543% i9 Q6 d& a' |4 ^5 [+ N0 P) ^
© 2007 Sage Publications
' s+ s8 v* y( y' X* b7 g0 t10.1177/0009922806296651/ f+ t1 I4 m' D
http://clp.sagepub.com, X* i' T: `8 h
hosted at
; m3 o3 w+ _/ e$ M7 Ihttp://online.sagepub.com: w/ L2 S( Z) Y. h1 _* r% n2 n9 }" s* p
Precocious puberty in boys, central or peripheral,
) `9 N* ^9 j: G* @( h z0 Ris a significant concern for physicians. Central
4 b6 o4 @! S6 J5 ^/ P% h& x+ Kprecocious puberty (CPP), which is mediated' b) B5 T" {6 Y' J0 Y, f% E( E
through the hypothalamic pituitary gonadal axis, has
% U1 D" [ l& U2 m$ }2 sa higher incidence of organic central nervous system
9 C) B0 N. u' G5 q3 o/ Y# |* Mlesions in boys.1,2 Virilization in boys, as manifested
5 Z2 y5 F8 y8 Q/ B- k7 D: r9 kby enlargement of the penis, development of pubic) D- F# B/ b( D$ f5 W
hair, and facial acne without enlargement of testi-
4 y8 w5 q5 s2 J% x4 p$ jcles, suggests peripheral or pseudopuberty.1-3 We/ b4 @" M" G: \8 R' B9 Q1 m% Y* J
report a 16-month-old boy who presented with the
) x/ y9 x0 n% Q4 a* N* Aenlargement of the phallus and pubic hair develop-3 C, @2 K# \5 V: x7 f
ment without testicular enlargement, which was due6 j& _' C$ M$ A g# [+ \9 l
to the unintentional exposure to androgen gel used by8 q3 |! _0 @4 P6 k- n! g$ H
the father. The family initially concealed this infor-, u4 s5 O) ?* d( c; j
mation, resulting in an extensive work-up for this% J. E; m% ?$ B0 H4 O+ |4 ?3 {; ~) m
child. Given the widespread and easy availability of9 P' O) n- J8 e8 o6 W
testosterone gel and cream, we believe this is proba-
7 m' ~5 |* K/ g( {9 v/ a# Gbly more common than the rare case report in the0 Q: s! v& Y# F2 S+ F
literature.4* ~6 @, P6 W5 n( j4 ]3 [$ @4 c
Patient Report
+ D* G/ P1 p; K7 l6 rA 16-month-old white child was referred to the& c. O6 j. \' d- ~5 v+ b# @7 q
endocrine clinic by his pediatrician with the concern* T. g8 p$ c: m0 v4 L6 A/ h
of early sexual development. His mother noticed5 e! {* p. X) V$ o# D# ~6 p
light colored pubic hair development when he was
8 g2 a! t) [2 w+ w( j/ oFrom the 1Division of Pediatric Endocrinology, 2University of
( f- B4 f! X( h$ a( }South Alabama Medical Center, Mobile, Alabama.
9 S0 c4 z, x0 ^0 FAddress correspondence to: Samar K. Bhowmick, MD, FACE,
& m7 [6 p9 c5 H, N; _Professor of Pediatrics, University of South Alabama, College of7 j: e8 _$ O. g+ P n# V# \
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% u+ y+ A+ M+ ]: Z p# X
e-mail: [email protected].% z# c$ Y1 s, M3 o p
about 6 to 7 months old, which progressively became6 X" }7 w; c3 w$ V$ c2 e! I1 z
darker. She was also concerned about the enlarge-
* K( J# A% h G& I2 Y' Kment of his penis and frequent erections. The child1 }) \! a3 q2 J4 M
was the product of a full-term normal delivery, with9 _) P+ g' b$ ^
a birth weight of 7 lb 14 oz, and birth length of
( P: ^0 O8 [4 S8 `. ?& u9 h20 inches. He was breast-fed throughout the first year
# _' w) L1 l8 uof life and was still receiving breast milk along with& T" D4 [5 ?. W! G
solid food. He had no hospitalizations or surgery,0 }4 t K; t# x. t7 c2 y
and his psychosocial and psychomotor development
7 R5 U4 I, Q- {" {0 @1 X3 ~- p3 }0 p7 ewas age appropriate.3 K$ L7 Y% X* ^" k# p7 M0 H5 Y0 n7 V# M
The family history was remarkable for the father,
, w8 { O+ q; i. Owho was diagnosed with hypothyroidism at age 16,4 ]! |# L+ H+ c. }4 J3 D6 ]! ?$ u
which was treated with thyroxine. The father’s7 l# `8 i2 [+ y; T: f( G6 {$ Z3 @
height was 6 feet, and he went through a somewhat
3 N3 K. X: L. M1 Mearly puberty and had stopped growing by age 14.
' {- c# |. N+ Z/ A& X0 wThe father denied taking any other medication. The
7 n* ] |4 E. c7 echild’s mother was in good health. Her menarche+ j& K3 b. {6 k6 C" o
was at 11 years of age, and her height was at 5 feet
- `/ y) U! W3 G8 ~! F5 inches. There was no other family history of pre-
! `8 i/ B* ^% h$ vcocious sexual development in the first-degree rela-
" w5 \' x( f4 F4 [tives. There were no siblings." P. n( N2 x5 U
Physical Examination6 W8 o5 z9 O% |# s0 l
The physical examination revealed a very active,+ z7 H* K4 |* b% Y2 {9 ?
playful, and healthy boy. The vital signs documented
% x* e% h) G# k# N, o6 d1 qa blood pressure of 85/50 mm Hg, his length was" v3 {/ p& q3 a/ X% c, l
90 cm (>97th percentile), and his weight was 14.4 kg" p r2 R; J6 a+ b& o" ]6 Z
(also >97th percentile). The observed yearly growth+ C' Y6 L$ r, z* l/ @/ o, N
velocity was 30 cm (12 inches). The examination of
7 X E6 @ X- n9 `' Lthe neck revealed no thyroid enlargement.7 z% j+ m% x9 ]$ D5 I' J
The genitourinary examination was remarkable for
9 v2 k3 p. p2 P2 @ L* Denlargement of the penis, with a stretched length of
! u; |, b: T; d( g. w0 {2 B8 cm and a width of 2 cm. The glans penis was very well
3 U4 I3 S' d+ }! R' u' g. Gdeveloped. The pubic hair was Tanner II, mostly around
0 E+ Q: S* K% h' x5 r540
. o9 g/ C0 X, Y( C' Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 _. ?3 i7 ]. T z
the base of the phallus and was dark and curled. The# F- u% Y5 d: ~( U6 t5 A# X2 y* q
testicular volume was prepubertal at 2 mL each.
$ H. {% M4 u3 ~+ z5 l) KThe skin was moist and smooth and somewhat8 l4 a$ D% y4 t5 K" Z- `$ _
oily. No axillary hair was noted. There were no
; q+ V' @5 {: ~, q$ |abnormal skin pigmentations or café-au-lait spots.
% q# a" Y* U: b9 F; R# ^' UNeurologic evaluation showed deep tendon reflex 2+
$ l D/ U: A$ b0 `bilateral and symmetrical. There was no suggestion
' H* v0 p! i8 E% I' k% xof papilledema.
" t2 e6 M4 n- _1 hLaboratory Evaluation
# j/ C0 a. S" G2 j( B k* GThe bone age was consistent with 28 months by( u0 G4 i7 F) z& r- v
using the standard of Greulich and Pyle at a chrono-) q" i0 d% r' S3 }/ T; O4 s) |8 A
logic age of 16 months (advanced).5 Chromosomal/ ^8 A* l) ]+ i
karyotype was 46XY. The thyroid function test
/ C% C# Q4 O# U8 Y! Vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
. F3 {. M* h% p2 K& G Qlating hormone level was 1.3 µIU/mL (both normal).
& c* T; Q8 ^8 E" F" N8 `# SThe concentrations of serum electrolytes, blood
/ C- E( W* |8 vurea nitrogen, creatinine, and calcium all were( d ]; t3 I3 @9 x; F# r
within normal range for his age. The concentration" ?. x4 ^5 H) r7 x( |6 ]+ R' g
of serum 17-hydroxyprogesterone was 16 ng/dL
, [. F* B8 I! A+ F: r8 N9 |9 A1 a(normal, 3 to 90 ng/dL), androstenedione was 204 k& Q7 d/ a% x. x
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
* K6 \1 x( B. `, K0 H9 `5 pterone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 ^$ ]3 m: B `desoxycorticosterone was 4.3 ng/dL (normal, 7 to) i. u8 n: M" L: i7 Y" {* v T
49ng/dL), 11-desoxycortisol (specific compound S) F9 B2 i# J1 J2 P# O2 P
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( F/ w( }# M" o ^" e. t
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, S: H* O5 m( Y0 H' i5 Mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ _: h% M' D/ _. B5 @+ E" r+ ^and β-human chorionic gonadotropin was less than
3 ^) R6 q$ s+ t5 {& Z0 S5 mIU/mL (normal <5 mIU/mL). Serum follicular6 `: t3 \8 e- I" c$ m: |. s
stimulating hormone and leuteinizing hormone
1 O( i& k* r/ o. [, B. D4 n; V7 @concentrations were less than 0.05 mIU/mL9 d# O/ H& x7 ?/ V
(prepubertal)., k$ X- z1 Q# }+ X) P
The parents were notified about the laboratory; ^; x1 |4 E% l# C9 A
results and were informed that all of the tests were- k! f: E- W3 T
normal except the testosterone level was high. The# Y. x; m; d9 h7 K+ C
follow-up visit was arranged within a few weeks to# c; Y, ^& _, g. S
obtain testicular and abdominal sonograms; how-
8 {! V2 `( [6 ], F! _& Hever, the family did not return for 4 months.
0 G* g9 S9 p. s5 NPhysical examination at this time revealed that the5 l. K2 G( @2 p6 \. y
child had grown 2.5 cm in 4 months and had gained
6 J5 t6 B) ^3 R2 ^2 kg of weight. Physical examination remained
( h8 S8 a, }* r% ^* W5 S+ kunchanged. Surprisingly, the pubic hair almost com-' u" |* H0 F9 a5 k& j5 \
pletely disappeared except for a few vellous hairs at+ k( _' O% z* _ D
the base of the phallus. Testicular volume was still 2) Y: i; m! B1 W% l
mL, and the size of the penis remained unchanged.2 [* B% @$ A5 o: m8 [0 t' c4 c
The mother also said that the boy was no longer hav-9 [" E& n5 g/ X; G
ing frequent erections.) M6 B, ~! y# g. k5 U/ V
Both parents were again questioned about use of
5 e* t/ V1 R8 D) }. F: b0 x# lany ointment/creams that they may have applied to9 X; `) Z, T3 i* M1 I1 x$ L
the child’s skin. This time the father admitted the6 `* [+ O5 U6 y+ _$ o2 T
Topical Testosterone Exposure / Bhowmick et al 541* y( F% H3 o! s2 v: b
use of testosterone gel twice daily that he was apply-
/ G8 {: b* Y- h' L9 h4 qing over his own shoulders, chest, and back area for
8 H" T$ A& B }" f* wa year. The father also revealed he was embarrassed" R$ F) ?# l1 A( ?
to disclose that he was using a testosterone gel pre-
2 I7 w; ^9 q- \9 }" ]scribed by his family physician for decreased libido' @$ Y% r6 Z1 C4 v9 S- \+ L
secondary to depression.6 G5 e) o% m. {* n9 x* o5 n$ J
The child slept in the same bed with parents.
" e _% v- T5 w0 W" {; K! W8 wThe father would hug the baby and hold him on his
8 u( B7 ?/ j3 {- B9 jchest for a considerable period of time, causing sig-/ e' R' q: X3 q3 M, Z
nificant bare skin contact between baby and father.; ?+ ^; [) V' ?+ v
The father also admitted that after the phone call," `: U+ r, S6 E$ K
when he learned the testosterone level in the baby6 N& C3 V$ m% n7 s6 U; l
was high, he then read the product information1 `+ K" k1 ~4 x% n; L! G
packet and concluded that it was most likely the rea-
1 M% } o: _7 K3 B n1 n5 Z9 {son for the child’s virilization. At that time, they
- T3 b3 A; Y* g. @7 j0 ~decided to put the baby in a separate bed, and the
5 k0 ^9 \0 b; T- h( b5 C7 D9 hfather was not hugging him with bare skin and had
1 T9 M) F$ L: T: kbeen using protective clothing. A repeat testosterone
4 J' Y5 m! y0 I- i4 l* ltest was ordered, but the family did not go to the
, i& V; O; x2 U ylaboratory to obtain the test.; a3 e$ H {# Z( @) n0 |
Discussion, k; Z9 Z& e3 P. w
Precocious puberty in boys is defined as secondary
: n- O9 z6 D. h# L: msexual development before 9 years of age.1,4: u o( ~3 i7 K7 Z0 ~
Precocious puberty is termed as central (true) when
- H2 ?" _: p" X ^. H/ |; L7 Y) N# oit is caused by the premature activation of hypo-! z2 p6 S; A8 x6 v; n8 f5 Q9 E
thalamic pituitary gonadal axis. CPP is more com-4 Q( t' r/ {( T9 R, }$ c) }7 d
mon in girls than in boys.1,3 Most boys with CPP
) \% @. B" P9 t& U# y4 D- Vmay have a central nervous system lesion that is
# T9 r$ H) o' ] n7 F6 vresponsible for the early activation of the hypothal-
, M$ e$ \7 v( S* G! Oamic pituitary gonadal axis.1-3 Thus, greater empha-
3 R0 S3 U2 c& m q' t$ Isis has been given to neuroradiologic imaging in7 Y! F; q8 W- v1 ]$ z
boys with precocious puberty. In addition to viril-% \5 b$ s# O8 U% h" y
ization, the clinical hallmark of CPP is the symmet-
2 z' a" N! O6 G, H8 V% n* J3 F$ zrical testicular growth secondary to stimulation by
. A+ w$ R0 z1 Y# j) ygonadotropins.1,3
- f( S. _; I- @1 L3 P: I5 fGonadotropin-independent peripheral preco-
6 P+ k; {$ o9 lcious puberty in boys also results from inappropriate
: W; f6 v4 ?* X& L: {/ C2 }+ k* dandrogenic stimulation from either endogenous or; N, t$ M q, h( K1 R
exogenous sources, nonpituitary gonadotropin stim-
p: o2 ?6 f9 R5 U6 J) Z1 C ]7 rulation, and rare activating mutations.3 Virilizing$ X! k" Z3 y+ Y' i9 b( o# B* Y I
congenital adrenal hyperplasia producing excessive
/ f9 C+ T" ?7 P- }# I* f2 tadrenal androgens is a common cause of precocious5 j/ `9 [$ U: o+ N3 y
puberty in boys.3,4
$ l$ {/ Q) Z6 Z6 ~( I0 H8 oThe most common form of congenital adrenal
) _5 d7 B `) mhyperplasia is the 21-hydroxylase enzyme deficiency.3 k$ q5 i% q/ g4 d6 j4 F
The 11-β hydroxylase deficiency may also result in* r- J' b. m$ m5 v
excessive adrenal androgen production, and rarely,4 Q$ c9 P6 }, n% D: o8 @; v$ N
an adrenal tumor may also cause adrenal androgen
' q6 s6 ?6 E" e" S, N! F$ D9 {$ ?excess.1,30 w }/ t7 w {$ n( f3 `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ j6 s2 V! e: i
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ D4 W; d9 g, } p, g- nA unique entity of male-limited gonadotropin-
7 m. x7 ~8 X# c6 M% ~+ P& Nindependent precocious puberty, which is also known
5 a/ ?5 l. o. ?; H) ~1 Ias testotoxicosis, may cause precocious puberty at a4 U( D ~9 f- v# h; o! C
very young age. The physical findings in these boys: j$ |) t) e7 ^$ K, K. @2 w
with this disorder are full pubertal development,
. i* q) y0 R/ f" k& E% Zincluding bilateral testicular growth, similar to boys# J7 v$ u, C2 k2 @
with CPP. The gonadotropin levels in this disorder
$ ]3 i9 z' I0 x/ S! }/ L3 jare suppressed to prepubertal levels and do not show5 [& M' g, y3 e [! }- Q: Q8 B
pubertal response of gonadotropin after gonadotropin- T0 N& _' \5 ~6 b: r
releasing hormone stimulation. This is a sex-linked
1 x4 @' o) u- q% O0 Zautosomal dominant disorder that affects only" }$ L7 B6 t. r- I: {# @
males; therefore, other male members of the family" t. T8 X- z1 ]1 Z# X# s# _
may have similar precocious puberty.3
2 O- A& U1 ^" C* VIn our patient, physical examination was incon-& M+ f4 \0 x2 ?4 |' X
sistent with true precocious puberty since his testi-' F+ x0 k+ E# [& C. l/ m
cles were prepubertal in size. However, testotoxicosis& t& Y' A! q( \
was in the differential diagnosis because his father1 }0 S8 S- P: M3 u! D6 z
started puberty somewhat early, and occasionally,: Y. [0 ~, a0 W
testicular enlargement is not that evident in the
5 O6 R# w# T7 s9 \beginning of this process.1 In the absence of a neg-
) ~" }: V6 d; J5 Y5 `1 O: Eative initial history of androgen exposure, our$ I) G! |! s9 e8 o' J" l
biggest concern was virilizing adrenal hyperplasia,, Y& |' k F+ _& H" ~2 f0 g/ Y
either 21-hydroxylase deficiency or 11-β hydroxylase& p% |8 O3 @% `" Y I. b
deficiency. Those diagnoses were excluded by find-7 G& \0 @' }4 f4 G+ c$ m5 [
ing the normal level of adrenal steroids.: C7 I! Z- K/ M" Q
The diagnosis of exogenous androgens was strongly
' `7 E4 }$ C& y+ Gsuspected in a follow-up visit after 4 months because3 | T3 e7 j$ K, x0 U
the physical examination revealed the complete disap-
, y6 e$ N# C' {; Q* t2 ]pearance of pubic hair, normal growth velocity, and: ?1 c+ c6 [, X4 O5 J
decreased erections. The father admitted using a testos-
' B. j0 f; Z4 v* y6 z" uterone gel, which he concealed at first visit. He was
5 L3 a2 {1 z3 D* q/ Y4 Susing it rather frequently, twice a day. The Physicians’
5 D2 p# j) ]8 A# _- `Desk Reference, or package insert of this product, gel or
/ f6 l5 S/ Q% M9 W L- Y! wcream, cautions about dermal testosterone transfer to* i4 Y8 m* Q/ y' M J3 O. z
unprotected females through direct skin exposure.
& l5 X2 R' f5 E! q7 q! ASerum testosterone level was found to be 2 times the
6 r2 J' U- s- q$ n9 u; B0 y6 sbaseline value in those females who were exposed to
. K2 L S+ @2 W1 K: Aeven 15 minutes of direct skin contact with their male. D+ d! n/ I }* @5 K& z, p% ^
partners.6 However, when a shirt covered the applica-
! j5 |8 U- J# {; D/ M2 w* htion site, this testosterone transfer was prevented.5 i' H1 e+ A' @9 Z4 V. W, o
Our patient’s testosterone level was 60 ng/mL,+ S$ {; K" P* {0 @3 T
which was clearly high. Some studies suggest that
" W( W! o9 r& t( q0 f2 g$ ldermal conversion of testosterone to dihydrotestos-
1 a& d: f- X1 o# E" M6 v5 Bterone, which is a more potent metabolite, is more
6 u8 E2 w( L. |. `# ]8 Yactive in young children exposed to testosterone# C$ l1 X7 \+ E- Z. S- K; z* t
exogenously7; however, we did not measure a dihy-& ^4 Z( v9 _% Q! ?0 r5 @
drotestosterone level in our patient. In addition to6 p. }! I7 f% f$ H) g& U
virilization, exposure to exogenous testosterone in7 I$ S3 O1 n, I# ~* d, \
children results in an increase in growth velocity and/ M* ]# m# `& _, R0 J% X2 y# b* N" q
advanced bone age, as seen in our patient.
' T0 A \; x/ I: nThe long-term effect of androgen exposure during2 r# R! d7 {, ^* E9 s
early childhood on pubertal development and final
4 A6 H: [6 W5 A( {! @& |adult height are not fully known and always remain: x! r: k& y2 [
a concern. Children treated with short-term testos-
3 f, v7 N x/ D& `( yterone injection or topical androgen may exhibit some) D& ~2 s+ T* m7 g' d
acceleration of the skeletal maturation; however, after
% x; U8 R& @8 j1 p8 gcessation of treatment, the rate of bone maturation
6 L6 B1 t, b, M' N( Bdecelerates and gradually returns to normal.8,9 m( s7 K- P3 c5 v0 L; u. p8 h2 o
There are conflicting reports and controversy
6 ^7 `( D9 |+ g& T2 l9 ~1 v1 Yover the effect of early androgen exposure on adult$ `: G) H# I+ ~1 @6 r2 _5 C
penile length.10,11 Some reports suggest subnormal
2 M6 c! C7 x+ ?3 |: {- S" \adult penile length, apparently because of downreg-4 H8 \3 Y( I) |7 W- R" \1 j) N
ulation of androgen receptor number.10,12 However,
5 }) y4 W4 _/ c% K9 }! f' s0 M) `. GSutherland et al13 did not find a correlation between
: Z1 D# L$ {4 @/ b: r' uchildhood testosterone exposure and reduced adult
, ] s7 A; m( `3 spenile length in clinical studies.0 x( L8 ` ^3 W% X8 s" w
Nonetheless, we do not believe our patient is: p! v: A: l% e% e5 t( V4 m3 k$ ^
going to experience any of the untoward effects from
" V5 Y* P6 H1 f# r; E1 r% Ctestosterone exposure as mentioned earlier because
! m( W/ y q, D, M- Y) U4 Tthe exposure was not for a prolonged period of time.
' ]. w2 b! Q, H6 b& H fAlthough the bone age was advanced at the time of
5 ^6 r( [3 P, {8 D+ c) [diagnosis, the child had a normal growth velocity at) N o' W' |, C3 z" b) Z
the follow-up visit. It is hoped that his final adult
6 F# E5 j7 k+ d. z) `height will not be affected.( I& q" L9 r( p5 v! N# R
Although rarely reported, the widespread avail-2 c. K# @' _+ D) S
ability of androgen products in our society may
' c! u) U1 C2 {/ w% |' g1 Oindeed cause more virilization in male or female
5 W; W6 w" u# `, o6 B, cchildren than one would realize. Exposure to andro-
; r' Q8 L% `3 c& t7 v' Z4 D6 tgen products must be considered and specific ques-
, S( v. v+ s6 c4 |, ationing about the use of a testosterone product or9 K1 c [6 F3 e! d4 G
gel should be asked of the family members during+ o8 o8 F x; ` X, \% C9 K
the evaluation of any children who present with vir-( s+ K: ]9 P7 a- D
ilization or peripheral precocious puberty. The diag-' e8 K4 P0 ?( [4 Y; P
nosis can be established by just a few tests and by, B8 I4 v7 H( S
appropriate history. The inability to obtain such a
7 p/ H" v( z6 x9 fhistory, or failure to ask the specific questions, may
8 E( l; G3 a% o: |7 C0 Jresult in extensive, unnecessary, and expensive& c3 U& g* A" M! L
investigation. The primary care physician should be! Z1 L9 U& f- p) v$ ~# G! g
aware of this fact, because most of these children( ]1 H: E: z3 K" e9 `7 r
may initially present in their practice. The Physicians’* c# L, F- D6 ~: g, Y
Desk Reference and package insert should also put a; U& a/ v6 R" i1 P2 V( C- S- G
warning about the virilizing effect on a male or8 [$ p0 [& ?. i; [
female child who might come in contact with some-
6 c. Y8 q% Q& ^' Lone using any of these products.
9 k3 L" P: L5 A5 A3 W) NReferences
+ L* Q* {8 b* {. U3 T1. Styne DM. The testes: disorder of sexual differentiation
2 e" G) L3 {+ I3 S! Z, I8 Dand puberty in the male. In: Sperling MA, ed. Pediatric# ?9 D5 D& z7 I6 \
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, f7 p, W. L! E: F/ m/ q1 u( ]
2002: 565-628.0 v. I7 S7 R' s7 ?3 e5 f2 f+ K
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 @& O; `$ w2 f4 lpuberty in children with tumours of the suprasellar pineal |
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