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Sexual Precocity in a 16-Month-Old. q, v" n) w9 h5 `
Boy Induced by Indirect Topical; v, s0 k/ g* @ }9 w
Exposure to Testosterone n8 n' L* Y/ X9 G: Q3 n
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2, j, w. @& J* |3 I2 g% E z& I
and Kenneth R. Rettig, MD1) B/ i! p' q6 y2 q. }
Clinical Pediatrics
8 f9 z* w; N% A, k6 vVolume 46 Number 6+ }; p1 o, w1 h* W: @- O1 `
July 2007 540-543
/ o5 T# B3 [7 M: t© 2007 Sage Publications+ Z0 c" g% f( X2 t2 S' [
10.1177/00099228062966513 f- G# M$ g+ w: H! p, c
http://clp.sagepub.com
4 l( U, J( N7 L+ N2 x Rhosted at
4 u- W8 C% ?0 e6 ^( ahttp://online.sagepub.com+ _7 N& K% O' O( Q( I* O! z& ]
Precocious puberty in boys, central or peripheral,
6 q z% B, h v3 B4 K1 q5 Z( @) Ois a significant concern for physicians. Central
! E" g- j) m8 Hprecocious puberty (CPP), which is mediated
7 w- u) E$ n1 K: |2 f; T( Rthrough the hypothalamic pituitary gonadal axis, has
. e8 [: Q1 G& m) ]/ ?1 ^4 L: [a higher incidence of organic central nervous system
7 N4 E) o% z- H- `4 ~8 V+ ]lesions in boys.1,2 Virilization in boys, as manifested
7 o2 U; }( N* ?by enlargement of the penis, development of pubic
7 D0 T5 @# d. ~( s! Rhair, and facial acne without enlargement of testi-
" C- V# S% a4 M; S6 m5 j' @cles, suggests peripheral or pseudopuberty.1-3 We
, B, [4 _/ V- wreport a 16-month-old boy who presented with the) w1 L# t# s3 L0 U* u
enlargement of the phallus and pubic hair develop-, I8 s7 j1 I# G
ment without testicular enlargement, which was due+ }2 R& O! x& l2 `- q* x
to the unintentional exposure to androgen gel used by
. s5 L! q% ^( E2 e0 l# pthe father. The family initially concealed this infor-; }0 r& H4 {" k& E) [7 c* ?
mation, resulting in an extensive work-up for this2 a& {9 {8 [' Z, ?8 o s9 g- C* S
child. Given the widespread and easy availability of
$ r! U8 Z9 P' E* D- {6 ntestosterone gel and cream, we believe this is proba- m# u9 d; W9 |9 Q* W
bly more common than the rare case report in the& B0 B/ g3 \) e; |1 {; x
literature.45 T2 F& G, D6 f# i( Y% M
Patient Report
# F- b5 m8 O! N" S2 n) ` X2 ZA 16-month-old white child was referred to the
* [. Z f1 f8 G3 P, wendocrine clinic by his pediatrician with the concern3 } W# l& q$ d
of early sexual development. His mother noticed
% J2 ?6 |( `. slight colored pubic hair development when he was) A# ?9 Q0 S3 ~7 v+ c
From the 1Division of Pediatric Endocrinology, 2University of
6 z8 e* j4 N. gSouth Alabama Medical Center, Mobile, Alabama.
6 L/ @. H' v) TAddress correspondence to: Samar K. Bhowmick, MD, FACE,! a. H& a. N0 x* \/ C% V5 B) R' w) F
Professor of Pediatrics, University of South Alabama, College of" W' Q- u- u* h7 U/ b& \; Y( E0 z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 ]- A& T: y/ w9 |; A
e-mail: [email protected].
' J! U3 A4 q! L( j0 Rabout 6 to 7 months old, which progressively became
7 p' Z/ D( o# e8 Z! l/ Adarker. She was also concerned about the enlarge-6 a2 m" f+ h$ v" C
ment of his penis and frequent erections. The child1 S) {1 t5 d( C* Q
was the product of a full-term normal delivery, with5 G& o3 z, m- F4 f5 s# ?" b
a birth weight of 7 lb 14 oz, and birth length of
5 s/ H& z5 w, d/ ~20 inches. He was breast-fed throughout the first year
; r' g" L Z4 G2 s3 L) eof life and was still receiving breast milk along with$ O9 k1 c& I% @; s* V9 b+ ~
solid food. He had no hospitalizations or surgery,+ B9 l: ` R& C* s2 x/ B
and his psychosocial and psychomotor development
( J# @+ ]# h+ M" c7 Gwas age appropriate.
/ p: O2 F2 k6 e5 X- v* H: aThe family history was remarkable for the father,
( e. f: C3 E* T) p( j9 M% Q' Rwho was diagnosed with hypothyroidism at age 16,1 W T& G1 b! u: _
which was treated with thyroxine. The father’s
9 m& }. k4 u8 |height was 6 feet, and he went through a somewhat
R6 c7 s6 v& U& Q; \0 Yearly puberty and had stopped growing by age 14.
4 {( z1 r4 v' X2 K* z, p6 RThe father denied taking any other medication. The
3 t( f2 N% L& x7 B, @) v' ~child’s mother was in good health. Her menarche( |- W% E1 D$ D& @5 M; m4 _
was at 11 years of age, and her height was at 5 feet
$ X- r1 B& g; y! o u7 o5 |5 inches. There was no other family history of pre-
$ q& ~8 O# z1 g* n' r, Vcocious sexual development in the first-degree rela-
, p+ P }4 |1 H/ Stives. There were no siblings.
/ p8 Q6 ~- \7 F3 U5 xPhysical Examination# J' R2 q6 d/ A. @. t
The physical examination revealed a very active,
9 B/ i% b5 w3 V" o& zplayful, and healthy boy. The vital signs documented6 S4 L5 Z5 ?+ b+ [0 N2 k J
a blood pressure of 85/50 mm Hg, his length was
; D# o, m' r" \* W. P90 cm (>97th percentile), and his weight was 14.4 kg
% D" ~& G/ y0 G: B, f5 e6 S(also >97th percentile). The observed yearly growth
4 |5 s5 c, p) |& u) cvelocity was 30 cm (12 inches). The examination of) P8 s6 j- d/ f' j4 D- f" C# G
the neck revealed no thyroid enlargement.
- ^- k1 i* {" c; q+ |0 `The genitourinary examination was remarkable for* [4 i+ k, `) r' {6 n: B: B
enlargement of the penis, with a stretched length of
' S# O& R: ^5 P) e8 cm and a width of 2 cm. The glans penis was very well- t8 {# W' Q3 a, u# I6 X
developed. The pubic hair was Tanner II, mostly around
+ g% B3 G4 [% g3 e: k540
" w7 l0 c8 `* Z1 S9 Xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. k; ]# P3 g( T1 g
the base of the phallus and was dark and curled. The% N1 R" _$ I% |5 x+ e0 g
testicular volume was prepubertal at 2 mL each.
4 Z' X$ T4 d7 n3 J, u) {8 Z. ~The skin was moist and smooth and somewhat7 Q$ G1 R6 v6 C
oily. No axillary hair was noted. There were no% k1 }" L9 t1 ]3 y- i
abnormal skin pigmentations or café-au-lait spots.' Z5 _+ ?& @2 {: l3 M( b& M* E% q
Neurologic evaluation showed deep tendon reflex 2+4 X4 d3 O/ X1 o0 A1 c% o) x
bilateral and symmetrical. There was no suggestion
& Y, e# s4 Q6 _7 yof papilledema.$ ^2 U _$ t( D6 _. k& ^+ q/ y& j6 U1 N
Laboratory Evaluation, L1 i( k( \+ ]( M0 Z% q" ~
The bone age was consistent with 28 months by" v' Y6 |2 h) ]
using the standard of Greulich and Pyle at a chrono-
0 h3 p6 L/ Y2 ~; T6 B1 [9 h$ Xlogic age of 16 months (advanced).5 Chromosomal
& v1 D, r' j! Ekaryotype was 46XY. The thyroid function test
* G# R3 I9 s$ l- g3 T7 G7 Gshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
/ m8 T. i1 ?0 m! wlating hormone level was 1.3 µIU/mL (both normal).
8 u" g$ z# Y/ U2 ^9 r* ]The concentrations of serum electrolytes, blood5 V4 h& X4 H' O4 F1 Y+ c
urea nitrogen, creatinine, and calcium all were
7 J8 ?2 z) T) o* m- A# h uwithin normal range for his age. The concentration
. \+ q g7 R1 dof serum 17-hydroxyprogesterone was 16 ng/dL2 K- b2 b! h% S) L6 D1 _
(normal, 3 to 90 ng/dL), androstenedione was 20
, N) w z% V. O7 `( S! }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 a/ u L0 d( J4 r6 p7 O! Q. nterone was 38 ng/dL (normal, 50 to 760 ng/dL),
* s' r, l" F& J9 F- ddesoxycorticosterone was 4.3 ng/dL (normal, 7 to: H- w$ {5 h% P: E ^/ g) n. _: E0 ^
49ng/dL), 11-desoxycortisol (specific compound S)
0 p( K8 D: p* G- X8 v& S S: rwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: ~ J6 a* d3 w* `- k2 `8 j' otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 z$ Q" }6 Q2 R1 e. @' etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ N% s2 f' `# @; h# U- K+ F! u' [and β-human chorionic gonadotropin was less than3 ~% y' n7 i/ Y; X5 H% Y6 Z
5 mIU/mL (normal <5 mIU/mL). Serum follicular% |) c5 h& n/ \0 O$ L) b3 ?
stimulating hormone and leuteinizing hormone
, o7 o" @2 c8 Q* v6 ]6 L3 c M( dconcentrations were less than 0.05 mIU/mL* F- \6 F; {' Y+ l% B1 t3 ^
(prepubertal).
% L" m; T8 e* K+ j* SThe parents were notified about the laboratory
8 ~! m7 Z1 i. E/ V2 @" F, F7 j# s. @results and were informed that all of the tests were2 Z& P# M9 u: z0 H: e( d
normal except the testosterone level was high. The3 T: e x& \9 n7 I) _
follow-up visit was arranged within a few weeks to
4 n: j4 o7 h/ J: C3 jobtain testicular and abdominal sonograms; how-& h% x9 S% r% X0 A9 t7 Q P: e
ever, the family did not return for 4 months.6 D; f$ M! E. v, G8 C/ L" f
Physical examination at this time revealed that the& S. F8 t5 N' Q% N) T, e2 [7 B5 \
child had grown 2.5 cm in 4 months and had gained; a0 ^' I# W! I# T$ D. b4 {( ?3 l
2 kg of weight. Physical examination remained9 n) l: R9 c6 _ \& W4 P) l( R8 w5 q
unchanged. Surprisingly, the pubic hair almost com-
, [8 D7 k' Y0 z+ Y) fpletely disappeared except for a few vellous hairs at
, V+ R3 V9 `7 o Z1 B& ?; kthe base of the phallus. Testicular volume was still 21 i; P, N- G* o8 [
mL, and the size of the penis remained unchanged.' q9 ]4 U+ H: \3 S c- U; E9 n) S
The mother also said that the boy was no longer hav-
2 Z* S* D I+ ~; P/ @ing frequent erections.* l! y9 k' _/ i3 d
Both parents were again questioned about use of# X- J9 f. B9 @9 D& y! t. c4 h2 m- q
any ointment/creams that they may have applied to0 s# ~, h- g5 Z& u
the child’s skin. This time the father admitted the/ W- z7 s8 S. Q- g; D Q* [
Topical Testosterone Exposure / Bhowmick et al 5413 g7 U0 r7 R$ Q0 N+ V
use of testosterone gel twice daily that he was apply-, k" ^, z7 G& l% I4 B3 H
ing over his own shoulders, chest, and back area for* q+ y, J+ G! |: ]. S, M; l0 a
a year. The father also revealed he was embarrassed
3 J$ b, }) j' N( vto disclose that he was using a testosterone gel pre-
% G9 K7 v0 J0 y) L H0 B+ gscribed by his family physician for decreased libido
$ i6 s$ j! {% R6 y8 A! nsecondary to depression.
; f2 X" k$ \/ |2 s7 f6 E1 G. VThe child slept in the same bed with parents.% `5 u8 p) R; U7 g
The father would hug the baby and hold him on his
+ ^* G" p/ k/ C0 V# C; E, Kchest for a considerable period of time, causing sig-
/ W6 ?$ T! {4 b1 c$ P# n! u) p+ Onificant bare skin contact between baby and father.6 N, H. L* y, t1 F
The father also admitted that after the phone call,
7 \( G. M7 v* C: {when he learned the testosterone level in the baby
$ j0 c2 s9 D: J% s/ h1 }$ Q {( awas high, he then read the product information
1 B% u5 n u9 }; @6 A* upacket and concluded that it was most likely the rea-* C3 d% e/ K4 z* b+ s t
son for the child’s virilization. At that time, they
# B8 C) T3 j6 |' x4 Idecided to put the baby in a separate bed, and the A; {% T$ p; n$ b3 D, M m
father was not hugging him with bare skin and had
- i7 T! N5 p) l2 I, c5 p) Xbeen using protective clothing. A repeat testosterone/ s% e! x, H6 K2 @& V& G
test was ordered, but the family did not go to the
* X% h# h W1 ~) z7 y7 |- ulaboratory to obtain the test.0 u" [: X4 r3 M0 U3 ?, h* C; h$ w
Discussion" g0 m R6 I, Q/ s# N: k2 R
Precocious puberty in boys is defined as secondary
7 R X5 o& b- Q; `sexual development before 9 years of age.1,4 k! Y6 D% j2 O
Precocious puberty is termed as central (true) when
- x5 ^7 ?+ A7 T2 L3 ]* @8 {; Y6 ~it is caused by the premature activation of hypo-
/ \8 j2 ?& X( S; u* X' u, s0 Vthalamic pituitary gonadal axis. CPP is more com-, @( Y0 ?% {6 S. x- ^5 I% H* F+ ?
mon in girls than in boys.1,3 Most boys with CPP4 [6 w# Y& v3 Q! f
may have a central nervous system lesion that is
0 A4 x5 ~1 t: m0 b# ~ _$ C P# {* Presponsible for the early activation of the hypothal-7 Q7 n9 N! d/ x5 B
amic pituitary gonadal axis.1-3 Thus, greater empha-
9 N/ L- r% w3 |7 _3 zsis has been given to neuroradiologic imaging in3 x4 u+ D; I3 g1 }# y9 h. ~
boys with precocious puberty. In addition to viril-& [3 c* j$ Z8 O% Q3 b9 f
ization, the clinical hallmark of CPP is the symmet-) m2 H! C8 L8 K4 u9 u
rical testicular growth secondary to stimulation by% \4 w) Y: W6 A* W5 Q
gonadotropins.1,3( O/ R# m% @8 A/ O; o; i( w9 F
Gonadotropin-independent peripheral preco-
5 w9 m0 k, L7 Y/ Ncious puberty in boys also results from inappropriate" }# } ?) X( y. Q7 u* l7 N: S5 W
androgenic stimulation from either endogenous or
) y. i. P* W3 h# `exogenous sources, nonpituitary gonadotropin stim-
/ c: R: F& @ {9 c9 Y- M, Y l0 o# Xulation, and rare activating mutations.3 Virilizing2 Z/ t5 _2 F1 [3 a# H7 {! V
congenital adrenal hyperplasia producing excessive
# @" }% `& z" V- K/ _. Nadrenal androgens is a common cause of precocious# M' p+ ]6 U4 U: { T' y
puberty in boys.3,4
7 Q0 [% l- `$ G; a( j3 d* F' EThe most common form of congenital adrenal
7 m' N2 P d& S: Dhyperplasia is the 21-hydroxylase enzyme deficiency.. N. k' o& S3 O- b0 u: a
The 11-β hydroxylase deficiency may also result in0 q* R6 D/ M) z8 t6 U7 a5 D# [. o
excessive adrenal androgen production, and rarely,3 Z; h6 T8 b2 D+ m0 h5 ], r+ {! T
an adrenal tumor may also cause adrenal androgen
% ]% i" [- _3 ~8 u; _0 ~; a. pexcess.1,3
\0 g7 ^# d. e" ~% eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 C: A. u8 D& c, x1 h8 q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 _8 Z3 e6 p! ]9 w# v0 hA unique entity of male-limited gonadotropin-
& J3 Y. q9 l3 ~2 x3 Xindependent precocious puberty, which is also known
3 e% W: ^; q) _% ^$ `* H; g* _as testotoxicosis, may cause precocious puberty at a
+ m* p1 a5 a1 O+ Xvery young age. The physical findings in these boys
- y+ |- V: ]* Vwith this disorder are full pubertal development,8 A; c/ P1 W: o' |/ I" u0 C
including bilateral testicular growth, similar to boys0 t! ?2 J0 r- \& P" S, H
with CPP. The gonadotropin levels in this disorder
/ i. H* e' |! C, @4 B; _are suppressed to prepubertal levels and do not show
2 O' N( b. @. _# bpubertal response of gonadotropin after gonadotropin-7 g. b) Y4 C0 }7 Y% ?) }
releasing hormone stimulation. This is a sex-linked
+ f, G% ~2 f! q( A! z$ I* sautosomal dominant disorder that affects only0 G% d2 l' M5 w- r% k
males; therefore, other male members of the family
; |9 \& ?0 a, W4 Emay have similar precocious puberty.3
3 e! k2 i; X+ x( Z U, VIn our patient, physical examination was incon-- {% i! v7 G, k# z- r
sistent with true precocious puberty since his testi-6 ?* Y9 L6 Z6 m1 f7 e8 \/ W
cles were prepubertal in size. However, testotoxicosis
/ M }( m) C- Q# ]* i2 ~$ Iwas in the differential diagnosis because his father
' P% {+ }7 P( E+ Xstarted puberty somewhat early, and occasionally,$ O$ T. M- K3 [1 p
testicular enlargement is not that evident in the3 Q- [$ J% D1 S, b
beginning of this process.1 In the absence of a neg-
! `5 ^2 U0 I& Y" kative initial history of androgen exposure, our0 y1 q' R) L5 H& `/ c0 f! e% u ]8 ~
biggest concern was virilizing adrenal hyperplasia, @& C! N: {9 c" \9 p
either 21-hydroxylase deficiency or 11-β hydroxylase- H3 Z1 B& V( s* K7 D% _( O
deficiency. Those diagnoses were excluded by find-
* N- F+ M* Z3 k. W- xing the normal level of adrenal steroids.& X: N. Q% ~( d+ _
The diagnosis of exogenous androgens was strongly
5 R* J! B" y2 @. `4 C4 |! d, esuspected in a follow-up visit after 4 months because9 K3 G* c# q. S8 t0 w
the physical examination revealed the complete disap-$ |# K0 k+ P) K4 d6 X- _
pearance of pubic hair, normal growth velocity, and
6 O q/ m4 k1 u3 |& ?9 M1 h3 t* Z5 wdecreased erections. The father admitted using a testos-
. y7 }! Y4 J6 D. @1 tterone gel, which he concealed at first visit. He was) _* w% P. i1 K
using it rather frequently, twice a day. The Physicians’
* i; v9 x/ l# q0 F% X! \ SDesk Reference, or package insert of this product, gel or2 d. g: ?/ Z- B6 t
cream, cautions about dermal testosterone transfer to
9 S- o( k, z1 qunprotected females through direct skin exposure.# L5 F; w/ g7 Q/ ~5 x$ ` l
Serum testosterone level was found to be 2 times the/ f7 ]- j3 n3 W1 T
baseline value in those females who were exposed to
4 a9 U% U0 |; C, Q, t+ Ueven 15 minutes of direct skin contact with their male
) [2 G% [. V% [; Fpartners.6 However, when a shirt covered the applica-
6 }: U$ X9 X' v7 Z2 b- L2 S+ X7 etion site, this testosterone transfer was prevented.
' f! i8 S3 z. ]/ _% ?Our patient’s testosterone level was 60 ng/mL,
& Q. p# D' [0 a# O, R9 a; m$ Twhich was clearly high. Some studies suggest that
: l4 l+ _& S/ e- Idermal conversion of testosterone to dihydrotestos-
3 R9 n5 V& P2 p9 I& }terone, which is a more potent metabolite, is more& [, M- C1 C* |: k- C: d5 q& q
active in young children exposed to testosterone: b0 M6 j. Y9 |: ^. ?
exogenously7; however, we did not measure a dihy-: \+ ^; ~. o) G( B
drotestosterone level in our patient. In addition to
2 Z# O( `% ]% S$ Zvirilization, exposure to exogenous testosterone in$ f/ g. a' N% i# i# [
children results in an increase in growth velocity and
! l+ R5 b8 x" o" I: }advanced bone age, as seen in our patient.
/ a$ p0 _" X3 Z" E8 f. }5 |$ ]The long-term effect of androgen exposure during
# l3 L. ^2 `/ ] |' S7 hearly childhood on pubertal development and final7 W- g! b& y: G* L& x( I8 o F
adult height are not fully known and always remain
/ b" F. n1 `5 c) Y( ma concern. Children treated with short-term testos-2 w3 e, v( l' T, p" u
terone injection or topical androgen may exhibit some8 w8 O$ b/ h8 x0 @. s1 Y+ X
acceleration of the skeletal maturation; however, after: b; _ P ?5 c8 A" n* w) J
cessation of treatment, the rate of bone maturation
2 e2 f# {7 m7 Tdecelerates and gradually returns to normal.8,9; ~4 Q& [2 f5 W2 h
There are conflicting reports and controversy7 J. X4 A6 p7 s! H6 Z0 J8 [
over the effect of early androgen exposure on adult
; d& M- K Q% W! s9 X9 o; {penile length.10,11 Some reports suggest subnormal
0 Y5 y) d! v% c1 wadult penile length, apparently because of downreg-
$ M2 {( R2 J" c( ]8 y; K0 }ulation of androgen receptor number.10,12 However,
7 p6 O5 V2 b4 a8 k( a4 {3 L$ JSutherland et al13 did not find a correlation between6 F3 g# W3 R6 y+ m
childhood testosterone exposure and reduced adult0 n1 [. v; x. x) M! |% d
penile length in clinical studies.
: ?$ s w8 P0 c/ z7 PNonetheless, we do not believe our patient is
% D' Y2 V& _2 ]& N5 `: qgoing to experience any of the untoward effects from
, O. P; E2 A) W0 {, htestosterone exposure as mentioned earlier because
; E7 x3 ^( t5 [9 Ithe exposure was not for a prolonged period of time.* S% T; D" \6 {
Although the bone age was advanced at the time of
9 }; z' r) D1 B. w/ v$ _7 p( H* g A/ Mdiagnosis, the child had a normal growth velocity at8 H- m$ N+ N6 k! A: @
the follow-up visit. It is hoped that his final adult3 `, k3 w1 d [$ O( Y
height will not be affected.8 `* p( Z9 O% n: x$ F
Although rarely reported, the widespread avail-
4 F6 y4 u2 X' D7 k3 j! [ability of androgen products in our society may8 d% E, d1 @ m% [
indeed cause more virilization in male or female
2 Q8 @& W' E/ J2 I& u. w" F, bchildren than one would realize. Exposure to andro-1 O: X) e0 b" O$ q& s+ A7 c
gen products must be considered and specific ques-# E. K* u/ N2 t" ]- f# l: l
tioning about the use of a testosterone product or' N& V' S) N; L% }# v k
gel should be asked of the family members during4 U+ D) e0 n2 Q' C4 C
the evaluation of any children who present with vir-; U/ E! N+ @1 g5 L: Y$ G( d$ V
ilization or peripheral precocious puberty. The diag-
5 [/ |* v* R3 J9 p7 t. ~" inosis can be established by just a few tests and by
- R4 N+ D, G0 w$ H* Iappropriate history. The inability to obtain such a% K3 P% t: v7 v* Q
history, or failure to ask the specific questions, may
; w0 @5 |7 M4 ]result in extensive, unnecessary, and expensive
M* e! d' N; r# qinvestigation. The primary care physician should be
$ T/ \. z, T6 F7 uaware of this fact, because most of these children$ d! ~! d7 i) g4 m% x0 g7 Y
may initially present in their practice. The Physicians’5 y( G/ L/ ]! t {
Desk Reference and package insert should also put a
, k, H3 _9 n, ~( T- j3 T# i6 Zwarning about the virilizing effect on a male or
. Y7 t3 N3 } Zfemale child who might come in contact with some-
3 @$ _" K" _+ F9 t3 s% C' mone using any of these products.
- U0 ^9 D8 o! ^! d& J( MReferences
4 s: c ^9 r2 |; X" v* }& m1. Styne DM. The testes: disorder of sexual differentiation }' r0 N! `1 B/ d4 q, Z- U5 h: H
and puberty in the male. In: Sperling MA, ed. Pediatric# C7 X% I' O5 a' S1 K. h s3 a
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 i8 I6 t# R. \3 l3 K6 n* G" h2002: 565-628.' _, n9 f% |- F. {& T3 f% z
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 R, i. `) L# i7 T' O: Kpuberty in children with tumours of the suprasellar pineal |
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