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Sexual Precocity in a 16-Month-Old
, j: ~8 Q- Y. U3 P& a: GBoy Induced by Indirect Topical+ `! p* b8 Z+ F0 h& P( L0 b' b
Exposure to Testosterone
# s+ |, V0 M( _9 K' ^$ C1 ASamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2+ P1 J- H& X8 |
and Kenneth R. Rettig, MD1
+ j- ^2 g) ?& V$ c5 K9 Q/ y' R1 N: D( IClinical Pediatrics
. h' Y/ m) E; c# p, ~Volume 46 Number 6
% y/ q/ g) T; P( t/ \! yJuly 2007 540-5434 v; U7 z' M& Q& p* H# I, v5 ~! Z
© 2007 Sage Publications% A6 A5 Q2 x3 |
10.1177/0009922806296651
+ G" z+ n) a* w! Z) F" |$ m% m+ p! m+ Ehttp://clp.sagepub.com
0 J5 W1 X8 ?6 ~# y. R1 B( mhosted at3 u3 q$ p3 n _( S* S; L' @) W) H
http://online.sagepub.com
* s4 S3 A6 N2 V7 s! I# ZPrecocious puberty in boys, central or peripheral,
+ N7 }; T4 W/ @ \6 t" mis a significant concern for physicians. Central
2 u" c4 v6 d% {7 p7 Tprecocious puberty (CPP), which is mediated
, F- r- Q* ~& d; q3 U& H( S& mthrough the hypothalamic pituitary gonadal axis, has
; z, l& L3 x5 j3 e) S" a1 Na higher incidence of organic central nervous system0 m( j: s, {$ v$ f" O4 D( `
lesions in boys.1,2 Virilization in boys, as manifested
9 ]; m* n+ }; B% s7 L2 zby enlargement of the penis, development of pubic/ \% u4 u5 g+ J8 X1 Y. H
hair, and facial acne without enlargement of testi-
2 L) h# n6 M7 G/ e/ T" S* B( ?cles, suggests peripheral or pseudopuberty.1-3 We
9 ^! [5 ~4 p$ D: H8 Kreport a 16-month-old boy who presented with the, {( I0 T0 ~* |, X, H6 x$ g3 A
enlargement of the phallus and pubic hair develop-
6 P5 S) o) M: L. Ement without testicular enlargement, which was due3 G x M1 D6 X8 }9 X
to the unintentional exposure to androgen gel used by( k0 \" u9 _1 ^8 f; I
the father. The family initially concealed this infor-, ?1 d3 {, G' @9 S/ C( Y d4 W! D
mation, resulting in an extensive work-up for this5 ]; q, R" B" R J- H' l
child. Given the widespread and easy availability of
0 Q: \* { l' b, X1 I" u6 [1 |testosterone gel and cream, we believe this is proba-( U$ L* D% A) [4 i
bly more common than the rare case report in the" I* c2 w# f9 H' ~- `8 ]
literature.4( o6 E- e3 o# o- ~& V) d
Patient Report9 a3 e# Z; A2 K+ h) b
A 16-month-old white child was referred to the
( K" _' U; K7 rendocrine clinic by his pediatrician with the concern6 v* m. s% |, Y- h% `* ]2 _0 ~
of early sexual development. His mother noticed/ b/ p/ A7 g+ [+ `4 F' |2 `4 a
light colored pubic hair development when he was I( M+ S* X# j+ h" {' W7 o0 A7 @. _
From the 1Division of Pediatric Endocrinology, 2University of6 @- x9 C5 [" R1 G/ K3 s
South Alabama Medical Center, Mobile, Alabama.
, B. b, n- t! e# uAddress correspondence to: Samar K. Bhowmick, MD, FACE,( m$ ]' O/ r: s7 D# k# T. m
Professor of Pediatrics, University of South Alabama, College of" C7 h9 C! W" V/ K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297; Q; t9 @" L9 i& } A0 x
e-mail: [email protected].) F n6 O6 A* V
about 6 to 7 months old, which progressively became
% W' C6 B- c. Ndarker. She was also concerned about the enlarge-
1 t* h0 r6 F# B( x: K) R; c% Mment of his penis and frequent erections. The child
# C. ? t1 Y% K8 z8 S3 Kwas the product of a full-term normal delivery, with! b9 J5 S/ v+ `3 R. P
a birth weight of 7 lb 14 oz, and birth length of% t; `8 s: P/ ]5 v
20 inches. He was breast-fed throughout the first year
5 s0 G6 [& D! t9 `of life and was still receiving breast milk along with9 f: {: F" d# u
solid food. He had no hospitalizations or surgery,: I. r, T1 t N; k8 [
and his psychosocial and psychomotor development7 N3 H, n$ @6 d) H- S) D
was age appropriate.
) ]- B+ v7 `$ I: KThe family history was remarkable for the father,
3 o& ]3 w( ~' g1 mwho was diagnosed with hypothyroidism at age 16,
3 f% t; r9 c9 `+ B) q& twhich was treated with thyroxine. The father’s/ G% ^- @, N4 B) M+ e" a
height was 6 feet, and he went through a somewhat2 q0 W/ P) s, {7 O+ e
early puberty and had stopped growing by age 14." Q) v1 n, z$ W0 h5 u3 x0 B
The father denied taking any other medication. The
. L3 H% |: v2 H, Mchild’s mother was in good health. Her menarche" H7 m: m, |) E: }
was at 11 years of age, and her height was at 5 feet7 l# O/ {0 R+ I' f/ A C
5 inches. There was no other family history of pre-
* t+ |3 h! l) `+ S% _* ncocious sexual development in the first-degree rela-4 Z; f9 b" G3 n& C$ T+ K
tives. There were no siblings.$ _# i% ]; u. _* M6 z$ \
Physical Examination
7 r9 p$ {+ D5 J5 HThe physical examination revealed a very active,
: t; g+ o% j; F+ Hplayful, and healthy boy. The vital signs documented
/ F( y! h6 q0 |. D3 J+ ~a blood pressure of 85/50 mm Hg, his length was
: Q j; j. N' ?. e90 cm (>97th percentile), and his weight was 14.4 kg- P7 |6 [$ W+ L/ v9 \
(also >97th percentile). The observed yearly growth
1 s7 a, e: N* i& Lvelocity was 30 cm (12 inches). The examination of
# C0 \3 N& D/ p& d9 y$ j9 dthe neck revealed no thyroid enlargement., A% l) _2 a9 Z
The genitourinary examination was remarkable for
% N1 _0 p$ ?! v3 g2 Y! yenlargement of the penis, with a stretched length of' x* n& R6 x: j5 I/ p# K
8 cm and a width of 2 cm. The glans penis was very well; g( j5 `2 m# h" G# \3 A
developed. The pubic hair was Tanner II, mostly around
% N1 q6 w5 O) i- ~540 O0 [4 Y1 |& d8 d- a: f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. d; v' O8 M; }" T( t
the base of the phallus and was dark and curled. The
6 E2 m# u+ }& Z7 @% K) utesticular volume was prepubertal at 2 mL each.
! d7 d9 n- f7 w# h% u' S- G3 PThe skin was moist and smooth and somewhat1 J9 ~; ^% K% @7 F
oily. No axillary hair was noted. There were no% v, _' q9 @! Z6 A
abnormal skin pigmentations or café-au-lait spots.( P! { M) r2 Z0 r5 V7 l3 _
Neurologic evaluation showed deep tendon reflex 2+# Y) H7 q, G' k) S, A( V
bilateral and symmetrical. There was no suggestion
7 J6 L3 o4 L: @6 k fof papilledema.
7 }3 u% w4 O& z i: }: S* H$ ?Laboratory Evaluation- T2 i. w' I& _. ]4 z! h( w
The bone age was consistent with 28 months by$ v. l# N% m# ~- V) u* [
using the standard of Greulich and Pyle at a chrono-
4 w& h: |0 A) w, Slogic age of 16 months (advanced).5 Chromosomal
' B: r8 S$ \, |/ M& X/ q6 nkaryotype was 46XY. The thyroid function test
. k" ^. e/ a) [% n) Ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 K! P4 I( k( K- o3 R; ]. p qlating hormone level was 1.3 µIU/mL (both normal).+ R% D( \* j( e" E
The concentrations of serum electrolytes, blood( h t% M5 s4 j2 @% u
urea nitrogen, creatinine, and calcium all were
. H& k5 b, H1 B- T* ~within normal range for his age. The concentration4 R) H) L# Q! q9 B& O( p
of serum 17-hydroxyprogesterone was 16 ng/dL8 [) [& |) t# A( F2 O
(normal, 3 to 90 ng/dL), androstenedione was 20" F' G: w4 f6 G* _4 w) U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 D# `( F0 y# o* Uterone was 38 ng/dL (normal, 50 to 760 ng/dL),
& ^) Z$ V; o8 Y4 H5 Z- D$ cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
! m3 S5 G* e7 X49ng/dL), 11-desoxycortisol (specific compound S)
$ ~7 Y8 ]# r8 [/ P6 dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, E+ X$ u( L, R0 P) X. e) G
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 |$ m) P$ R! n8 e: v: F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ H! |$ v' ^% ~ O4 Nand β-human chorionic gonadotropin was less than4 K0 _ B7 t, R( z, f7 r S
5 mIU/mL (normal <5 mIU/mL). Serum follicular, L' W- x& D+ T& H5 H0 \( ^
stimulating hormone and leuteinizing hormone4 F3 ~/ O( s& I3 f0 q; n
concentrations were less than 0.05 mIU/mL
; l$ e# H; b6 O- D8 u(prepubertal).2 ~$ L4 T$ m/ ]1 m
The parents were notified about the laboratory
" `9 c6 n3 x+ i" G7 `8 B- ]* ?results and were informed that all of the tests were ~' l8 J& `- q6 W6 o5 P
normal except the testosterone level was high. The
8 Z+ X" H# p: Pfollow-up visit was arranged within a few weeks to
3 N0 t' V$ B' Q% r8 Zobtain testicular and abdominal sonograms; how-
; f7 H9 }+ j7 v4 Z: j' Uever, the family did not return for 4 months.
, C' K \7 q4 h% D0 o" JPhysical examination at this time revealed that the) Q5 q' @$ }, f! w2 l! F
child had grown 2.5 cm in 4 months and had gained
& Z5 C6 I# G \# o, |2 kg of weight. Physical examination remained, g' D) l0 y. E+ O' k8 |( ]
unchanged. Surprisingly, the pubic hair almost com-
5 |5 V* L+ J1 J( b. f1 ], J! Tpletely disappeared except for a few vellous hairs at) c$ U4 b& L! ~- A
the base of the phallus. Testicular volume was still 20 t" D) S' {- T3 {& f% m
mL, and the size of the penis remained unchanged.) ?9 |) ^1 ~0 _
The mother also said that the boy was no longer hav-" m- O& @$ j8 H( V1 @7 V# u( n ]0 l0 x
ing frequent erections.
, c5 _# w2 w, B3 f/ Y/ @ H+ YBoth parents were again questioned about use of9 W: \0 k; X% z5 X
any ointment/creams that they may have applied to
- f9 X2 D/ t% o) O8 @/ k/ f9 H+ {, }4 Mthe child’s skin. This time the father admitted the$ @( J$ s8 l! }8 b
Topical Testosterone Exposure / Bhowmick et al 541- a) Y" _# k- k& Q* P
use of testosterone gel twice daily that he was apply-% o( y, @7 [6 P, g" {9 m) d
ing over his own shoulders, chest, and back area for
; s2 Y! C) T" H& l! _a year. The father also revealed he was embarrassed! L; X' A: R/ b) j& {
to disclose that he was using a testosterone gel pre-
; U$ G A, E( }% u/ |. T6 {scribed by his family physician for decreased libido( m" c; n8 Z( }5 B/ |& I+ q
secondary to depression.
" p, F5 e3 D" U9 |' m# ], eThe child slept in the same bed with parents.
1 P+ j! }! `: O ^8 wThe father would hug the baby and hold him on his' y' M2 S/ i2 s# I/ q/ F/ v
chest for a considerable period of time, causing sig-
{- A& ]2 H0 [" {nificant bare skin contact between baby and father.. }2 I4 C' G0 M: ?5 Y6 _
The father also admitted that after the phone call,
; d9 b; i$ _5 |, m8 z* {when he learned the testosterone level in the baby
5 `: y% x1 g! s- C# T" Y: D7 M% wwas high, he then read the product information; n+ }2 |, s1 X& F1 [- I: {5 v
packet and concluded that it was most likely the rea-
) A T6 J0 J. r. z G7 Lson for the child’s virilization. At that time, they: B0 _ \& s/ L- }, q. z% Z6 k$ l" Z
decided to put the baby in a separate bed, and the
- H3 c9 _7 m* Y* `6 tfather was not hugging him with bare skin and had
2 N+ K8 p) L0 N# i. ]* Y; Ibeen using protective clothing. A repeat testosterone1 O' @: v' b0 f& j6 `
test was ordered, but the family did not go to the
6 Y, A5 ?8 z7 C. t2 c y4 T) C) Glaboratory to obtain the test.
" L3 ~4 `) B8 z9 ^Discussion9 @* d; P$ o j2 s5 Z$ j6 [
Precocious puberty in boys is defined as secondary
( } \7 b5 J) \8 C' y. J9 ~9 fsexual development before 9 years of age.1,4
; ]: R+ s8 |4 ~1 f9 GPrecocious puberty is termed as central (true) when
0 I# b1 L Z0 }# rit is caused by the premature activation of hypo-; L& }: w% l/ |2 `" b
thalamic pituitary gonadal axis. CPP is more com-4 n D; U' y( R9 \4 G
mon in girls than in boys.1,3 Most boys with CPP. U6 \4 x3 f. ]4 v) p8 D: G5 E, \
may have a central nervous system lesion that is
3 R$ x& U! Z* S; f5 l' I2 Yresponsible for the early activation of the hypothal-" N$ c- b( r4 a3 |1 [6 U- H6 Y. g
amic pituitary gonadal axis.1-3 Thus, greater empha-
2 @1 S- V% Z& \7 w3 M8 V$ bsis has been given to neuroradiologic imaging in6 m! S" m( D( N |9 i
boys with precocious puberty. In addition to viril-
2 O! A3 m/ R6 R# j+ _9 j. Bization, the clinical hallmark of CPP is the symmet-/ R2 T+ I) ?& |
rical testicular growth secondary to stimulation by2 R* w7 a* X% @
gonadotropins.1,3$ ?# v6 G3 z$ `" b4 O# k
Gonadotropin-independent peripheral preco-
1 U0 Q5 z3 P. e! J1 A# q9 h' h) _, Xcious puberty in boys also results from inappropriate# i) N! L) C8 L; z4 c6 x
androgenic stimulation from either endogenous or
% i# G; i; t/ S _/ texogenous sources, nonpituitary gonadotropin stim-: \+ `! M2 G3 y0 Q& ~
ulation, and rare activating mutations.3 Virilizing
Q8 u/ ~ W' x, R" L: Tcongenital adrenal hyperplasia producing excessive
# R- E( M1 C$ g$ kadrenal androgens is a common cause of precocious
. _% w8 P2 {% n, c, jpuberty in boys.3,4
5 A+ _. y) Q) W$ T+ Y& S- l+ jThe most common form of congenital adrenal
/ L6 S; R7 f1 n4 A; D ^hyperplasia is the 21-hydroxylase enzyme deficiency.( i: Q% O+ y" l" e
The 11-β hydroxylase deficiency may also result in
. c- a% D( l0 D# e1 M" s1 y4 Mexcessive adrenal androgen production, and rarely,
9 c3 }, P( b* Van adrenal tumor may also cause adrenal androgen2 g; M" Q4 y. R
excess.1,3% R) F- B( d5 m% G, p
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, P" t6 N9 e5 Y5 [$ O+ ?. _542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' Y" ]: P$ W7 L3 M. V [) Z* ]' U
A unique entity of male-limited gonadotropin-, ] K1 X2 G) i& K* \& c
independent precocious puberty, which is also known
+ W6 I. R- Z! \5 m8 Aas testotoxicosis, may cause precocious puberty at a
8 H; k+ F2 _1 [1 [very young age. The physical findings in these boys
0 |. W5 I+ G. Qwith this disorder are full pubertal development,& C- v8 Q# O1 `4 o1 `
including bilateral testicular growth, similar to boys/ M! e* d+ K9 m# M s; O
with CPP. The gonadotropin levels in this disorder% s8 Z# n. Y6 h' k4 b
are suppressed to prepubertal levels and do not show. a- H8 `# b; K% o, a% l
pubertal response of gonadotropin after gonadotropin-4 G" j1 k+ b! h4 ]
releasing hormone stimulation. This is a sex-linked
( V: F( P5 h$ m3 i: C9 m; eautosomal dominant disorder that affects only7 G8 Q9 g3 R; Q* W2 Z% d4 f
males; therefore, other male members of the family
9 w! I* ~9 R) Mmay have similar precocious puberty.3% V$ Y" K) e+ G# B d) e7 f+ g9 B
In our patient, physical examination was incon-
% j9 A& i- y% e/ ~7 a2 {+ Wsistent with true precocious puberty since his testi-; T* S0 y1 |7 t
cles were prepubertal in size. However, testotoxicosis
/ o. w8 ~8 X4 y* Q2 w+ E, Wwas in the differential diagnosis because his father, v, O ~ N! s& N5 M7 I5 o: a
started puberty somewhat early, and occasionally,
q! T3 l8 p" D% W( Qtesticular enlargement is not that evident in the0 \1 `% o: t: |; Y9 p
beginning of this process.1 In the absence of a neg-" R1 {( `1 L2 W6 A v( a; f R
ative initial history of androgen exposure, our
1 x P: n$ f7 _5 j& j3 Fbiggest concern was virilizing adrenal hyperplasia,
% ^$ r" s$ V: @8 Z1 z6 _either 21-hydroxylase deficiency or 11-β hydroxylase% `- e( V: M- i5 O' ~; w
deficiency. Those diagnoses were excluded by find-
9 J2 ?& R+ t4 W* p* O1 Q9 K% cing the normal level of adrenal steroids.! R; l- r2 d2 Q4 u
The diagnosis of exogenous androgens was strongly
, ^ X% J9 P# W/ l" Jsuspected in a follow-up visit after 4 months because
- m% [2 n8 c! Ethe physical examination revealed the complete disap-) @$ I u6 x6 M. `8 _3 o
pearance of pubic hair, normal growth velocity, and
* _2 O7 i. _ T+ ^- F1 |7 zdecreased erections. The father admitted using a testos-, ~( M! v% c2 c% x( S; m* c( P- |
terone gel, which he concealed at first visit. He was- m# c+ s+ ^' Y: y7 e5 _0 r. m- Z
using it rather frequently, twice a day. The Physicians’- f8 t3 L. Q g$ m
Desk Reference, or package insert of this product, gel or
" I9 O- `* e9 _3 ?! |cream, cautions about dermal testosterone transfer to
- L/ [% M# w* b5 K( \unprotected females through direct skin exposure.7 ~) [9 H5 h' k s/ g3 f- p) ^
Serum testosterone level was found to be 2 times the+ B! s7 C( }' F3 l& g
baseline value in those females who were exposed to7 A- O% g) B& q: l/ }1 k/ `7 I( d8 Y
even 15 minutes of direct skin contact with their male
2 N1 b& D c6 y/ s7 Cpartners.6 However, when a shirt covered the applica-1 k* b- U7 [+ t
tion site, this testosterone transfer was prevented.2 i: b1 l' L" T# v; Y9 [ _# P
Our patient’s testosterone level was 60 ng/mL,
; C: a: t8 W- Q: iwhich was clearly high. Some studies suggest that
4 V9 p1 x3 n" D$ o3 v5 |" udermal conversion of testosterone to dihydrotestos-
3 B5 M+ B4 y. q. ^/ \7 ~terone, which is a more potent metabolite, is more1 p9 Q+ r9 ^8 |& F4 A5 T
active in young children exposed to testosterone
" d8 M( r3 X/ D+ u7 N5 `exogenously7; however, we did not measure a dihy-
& H: G& p2 l, R* r8 H. s1 d3 o9 Sdrotestosterone level in our patient. In addition to0 [ `1 X( [ \( T; I8 b* o
virilization, exposure to exogenous testosterone in- ~9 W& J% h9 x: B
children results in an increase in growth velocity and% _' y* |6 _4 C3 {/ b
advanced bone age, as seen in our patient.
$ a+ y3 Z% f+ u' h* X, l6 `$ cThe long-term effect of androgen exposure during! ~9 x( O7 J; F/ l( e/ e
early childhood on pubertal development and final2 e% d. F; a7 `
adult height are not fully known and always remain
) E4 G( _3 I s0 M- ?a concern. Children treated with short-term testos-9 }% L f0 ?9 M( `+ ^* s
terone injection or topical androgen may exhibit some3 ]1 W7 A" e0 Z0 {# I% i4 g; `
acceleration of the skeletal maturation; however, after
8 g6 ?6 d* C2 h7 u* `& @; _cessation of treatment, the rate of bone maturation
S. P+ @- I. h0 I4 Jdecelerates and gradually returns to normal.8,9
8 j l2 j$ V2 R" sThere are conflicting reports and controversy8 d0 T; G: W" `
over the effect of early androgen exposure on adult
- T: C0 f& k* X4 Bpenile length.10,11 Some reports suggest subnormal6 W6 d+ ]4 `- g; Q
adult penile length, apparently because of downreg-
# n; u& C5 [' R& o; [' Qulation of androgen receptor number.10,12 However,
2 r, S, i' u' r4 \3 k" HSutherland et al13 did not find a correlation between
# M6 @ l& Q2 @. ~childhood testosterone exposure and reduced adult
9 s |, ]/ g* ] l+ q) b. L# Apenile length in clinical studies.! L$ c$ b/ Z: Q4 Q3 i
Nonetheless, we do not believe our patient is
$ O- @$ j1 f) u0 R& R9 @$ D/ Ogoing to experience any of the untoward effects from& {( ?" v7 h2 _4 r3 O. U; ~0 h$ [7 X
testosterone exposure as mentioned earlier because
& J- E' }6 F1 C6 gthe exposure was not for a prolonged period of time.+ ~% b4 S$ M2 Y6 _4 g* ~
Although the bone age was advanced at the time of) L& m( _; ? L1 n- M6 z. \! k8 f
diagnosis, the child had a normal growth velocity at# ~1 x3 Z9 Z9 ^, S% c. |: z( g
the follow-up visit. It is hoped that his final adult
9 e+ x3 q, ?9 {8 H7 l' {height will not be affected.! W& q# ^9 J7 E/ c
Although rarely reported, the widespread avail-
5 p! D$ w3 L$ D6 c+ rability of androgen products in our society may! C+ n& P8 {1 w' u
indeed cause more virilization in male or female5 C- B$ x q; u" P5 g9 f. p
children than one would realize. Exposure to andro-. i1 ]; L6 ?7 g O( ]( K
gen products must be considered and specific ques-3 `$ W$ y$ ~ W5 }
tioning about the use of a testosterone product or ?3 W; e4 J" b) T* H8 }' d
gel should be asked of the family members during
- g' T" l0 p$ W1 j x1 Tthe evaluation of any children who present with vir-
& G% P' ]9 {7 E( B0 L! s4 i3 vilization or peripheral precocious puberty. The diag-, i9 L( K Q1 w& [
nosis can be established by just a few tests and by
/ u% g, ~; [" \) c6 b9 C P1 jappropriate history. The inability to obtain such a
3 N/ x; D5 y4 n. J# Whistory, or failure to ask the specific questions, may
+ {( V7 s6 r& ?' wresult in extensive, unnecessary, and expensive
: G: T: L. d9 t- ]4 K3 a- }investigation. The primary care physician should be
# F4 r. d R9 G$ r8 S) |' Kaware of this fact, because most of these children
4 }+ \4 J _; ^+ M3 k- Jmay initially present in their practice. The Physicians’
7 X# E, J0 t* n; V: X( C CDesk Reference and package insert should also put a" @: P' d! T) |$ w5 f: b% e+ x: C
warning about the virilizing effect on a male or. K: @! Z& S* h+ ]# Z
female child who might come in contact with some-
3 {! R0 a/ N1 [9 n r% jone using any of these products.
9 d5 `1 G! a ^3 _( e$ EReferences
" F" M: a0 ^9 n" I1. Styne DM. The testes: disorder of sexual differentiation% J) `% L1 m! d8 `8 z# \) a. V
and puberty in the male. In: Sperling MA, ed. Pediatric
; Z6 h5 s$ m$ a$ xEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: f4 l. _- n0 ?, }& X2002: 565-628.
! b1 R" r2 m% z+ Q1 o) ]2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( G! P: V: p* m, K1 X0 k: i8 K
puberty in children with tumours of the suprasellar pineal |
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