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Sexual Precocity in a 16-Month-Old
* i: l2 u8 M# HBoy Induced by Indirect Topical
' \ I! {+ J9 O4 {/ \Exposure to Testosterone
1 R; |: g" Q" k/ T4 I# hSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. f& a/ s4 c z+ W5 p) I/ G4 b8 eand Kenneth R. Rettig, MD1
/ g+ U7 ~+ L+ o, E9 VClinical Pediatrics' M9 n4 q$ a1 f8 {, e$ [
Volume 46 Number 6/ l" Q9 W, w- k ~) }' |' `
July 2007 540-543
4 X9 f0 U( ~( C& @! h© 2007 Sage Publications, g' ]# H" a- E
10.1177/0009922806296651
8 ]1 W* g) U8 n: v2 f0 W6 Ohttp://clp.sagepub.com* {6 H5 ?( N9 N; `' g- `
hosted at3 _* b4 F: T; F1 k
http://online.sagepub.com7 n ~2 q6 i1 E. W4 z+ z
Precocious puberty in boys, central or peripheral,* p6 a/ L) |" b2 N% o; L$ ?
is a significant concern for physicians. Central8 |- Y, O' t& o4 e& z& F" [) c
precocious puberty (CPP), which is mediated
" L- |- Z1 P6 y3 b6 p+ n; a) Wthrough the hypothalamic pituitary gonadal axis, has
E) J, k* m! s/ e+ la higher incidence of organic central nervous system: Y, |& f/ z) K) m e5 v! O8 f
lesions in boys.1,2 Virilization in boys, as manifested
: H- }% \, M% V5 [! t! Xby enlargement of the penis, development of pubic- J) T" H) Y: U3 r
hair, and facial acne without enlargement of testi-
+ p8 v8 J% f: ]! D, n5 `cles, suggests peripheral or pseudopuberty.1-3 We
P% Z8 J& F& R9 ]2 M0 f$ Qreport a 16-month-old boy who presented with the8 q9 h4 f6 T- i+ q J$ L, c
enlargement of the phallus and pubic hair develop-
* f8 B8 t, x& w( `* U2 h+ k) P, Mment without testicular enlargement, which was due ^# N8 A" D5 I6 F% O5 {
to the unintentional exposure to androgen gel used by
( p% `; B5 t5 c* \the father. The family initially concealed this infor-
+ O6 x! ^2 f# n9 q" |mation, resulting in an extensive work-up for this
8 `! G' S3 p4 Q0 u) {child. Given the widespread and easy availability of/ h' v. }$ @) A) C, [" X: t* f$ X
testosterone gel and cream, we believe this is proba-. k+ p1 L8 X& W8 O: O
bly more common than the rare case report in the
/ O; a$ v8 \ l/ I9 f* {literature.41 ?; a& ]$ O* B& O
Patient Report
+ z! \8 Z5 d0 ^, |9 rA 16-month-old white child was referred to the
. h( y9 r# D) H/ j5 d9 D8 d3 mendocrine clinic by his pediatrician with the concern
, d! Q/ ?0 E% m! @of early sexual development. His mother noticed
6 O9 E4 Z& _& h: f& }" i6 nlight colored pubic hair development when he was
8 D4 I c, h- j" P) SFrom the 1Division of Pediatric Endocrinology, 2University of
3 @. }/ \! ^* @; c9 R" t/ }South Alabama Medical Center, Mobile, Alabama.# k+ g, L/ g0 P, F
Address correspondence to: Samar K. Bhowmick, MD, FACE,( F, D/ C2 t1 l4 @3 M
Professor of Pediatrics, University of South Alabama, College of% { u& T5 r$ x( |1 h0 c
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# x. F( y3 [1 l
e-mail: [email protected].
3 ]. w3 w" [/ cabout 6 to 7 months old, which progressively became' ?+ k% ^$ @: \8 f& ?$ q+ A3 A g, D
darker. She was also concerned about the enlarge-
* |) o D+ [3 ]' j& o9 x5 i. l5 l) Pment of his penis and frequent erections. The child3 W& p+ y( R% m% o- ?2 `
was the product of a full-term normal delivery, with
7 j3 j" J' _) |5 l% ca birth weight of 7 lb 14 oz, and birth length of1 b; y* d8 _. x/ j; w
20 inches. He was breast-fed throughout the first year
! F( b2 k. `# v/ k5 hof life and was still receiving breast milk along with( [" ]& m+ x5 f$ s4 X
solid food. He had no hospitalizations or surgery,' H& {. \( B2 v' t8 N0 D U8 \
and his psychosocial and psychomotor development
( E5 A- {+ d2 Y6 m4 ewas age appropriate.
" ]5 x- k; q9 @The family history was remarkable for the father,( d K4 p x+ _. j
who was diagnosed with hypothyroidism at age 16,
% p0 a* K. i! T$ c$ Y% Cwhich was treated with thyroxine. The father’s, W6 D. X# b- A. c6 g& T
height was 6 feet, and he went through a somewhat. L- B$ J! |# {' }& G
early puberty and had stopped growing by age 14.
0 j/ R5 ^- Z2 q0 u. VThe father denied taking any other medication. The8 {2 J0 B0 c7 ]: f' d8 F
child’s mother was in good health. Her menarche
% O# ?* q$ g3 g0 |5 V4 }2 N) Vwas at 11 years of age, and her height was at 5 feet& E1 r- E p" ^! a/ n% n* L
5 inches. There was no other family history of pre-
r2 Q* ^6 H b* W. Xcocious sexual development in the first-degree rela-
8 [; M* i; d Q& i2 u+ ], O( ptives. There were no siblings.$ e' F _" z6 W/ L$ n, T- E
Physical Examination
9 e( |. `- x. X8 YThe physical examination revealed a very active,0 Z* F Z( A' M6 P
playful, and healthy boy. The vital signs documented' d! ?5 |) x6 @$ z0 A2 ~) j3 F
a blood pressure of 85/50 mm Hg, his length was& c+ ]2 f, y5 N: s0 N* I6 E- Z! X
90 cm (>97th percentile), and his weight was 14.4 kg% }" n3 \8 k4 y
(also >97th percentile). The observed yearly growth* o* u: H: T8 M# a9 w+ I. }( ~
velocity was 30 cm (12 inches). The examination of& F, n. W1 d5 z* P. H; N/ k0 {" C
the neck revealed no thyroid enlargement.
6 @( N6 c: i$ q) f/ UThe genitourinary examination was remarkable for! b8 |5 c, L0 y4 X2 I0 F' o1 {+ H
enlargement of the penis, with a stretched length of
( O1 g: K3 b# h8 cm and a width of 2 cm. The glans penis was very well# S$ X$ U% d5 s8 ]2 c* y! W
developed. The pubic hair was Tanner II, mostly around
/ ~7 D U- @# R% E5 D* m540
8 C& Q$ J6 ]+ u% b7 xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* I; I0 O4 h9 X8 Q! u0 o/ r
the base of the phallus and was dark and curled. The; Z; y/ Z/ V; f2 s
testicular volume was prepubertal at 2 mL each.
5 c0 }4 a5 }% o8 |# EThe skin was moist and smooth and somewhat
& M! j/ ]! M7 Woily. No axillary hair was noted. There were no
% b- u& [$ l( x3 \3 a" n2 { xabnormal skin pigmentations or café-au-lait spots.
" `( m( Z3 Z* I8 U! D/ v$ XNeurologic evaluation showed deep tendon reflex 2+$ a5 \! h! c# q* x- _4 U$ G
bilateral and symmetrical. There was no suggestion
# p# ^2 M5 {/ y# v) }/ f" ~% Lof papilledema.
! U" s/ a9 P x7 ^; O! jLaboratory Evaluation
: U* T! k. m0 i' U$ ~1 [5 W# v# JThe bone age was consistent with 28 months by
% ]4 w" x+ `9 Yusing the standard of Greulich and Pyle at a chrono-
7 X9 E- J8 X1 @$ a; R( Vlogic age of 16 months (advanced).5 Chromosomal4 k: Y, C M* j5 q# z# `
karyotype was 46XY. The thyroid function test" z! l! j- h) z: M$ B3 |2 O
showed a free T4 of 1.69 ng/dL, and thyroid stimu-0 t0 x8 G. }& x S2 t- a
lating hormone level was 1.3 µIU/mL (both normal).( o% c: ~: w1 H6 U0 E' J5 L
The concentrations of serum electrolytes, blood
6 e5 ~6 n0 B. `urea nitrogen, creatinine, and calcium all were
5 ?0 S# q7 @+ M4 ?* kwithin normal range for his age. The concentration4 H( C- ~/ Z5 u. \* T3 y
of serum 17-hydroxyprogesterone was 16 ng/dL: e5 Y. f" V$ P+ {+ s4 L, B
(normal, 3 to 90 ng/dL), androstenedione was 20+ O7 _. f' \1 p' X; G. g+ U S
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 y, a) k8 l T; }0 e
terone was 38 ng/dL (normal, 50 to 760 ng/dL),1 E+ X5 ?& c! {6 G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to* O% ?. I7 |9 |/ s! `
49ng/dL), 11-desoxycortisol (specific compound S)
/ ?3 s5 T6 D# S. i6 W) v1 \8 L: D" nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
- p1 ^/ N$ {$ W# s8 X6 Wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 ?+ t w8 x7 D* L( ~& c7 s# b4 E
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ v& t5 I$ k9 g! t
and β-human chorionic gonadotropin was less than
, Y* f2 G6 ~. N6 H# E) p5 mIU/mL (normal <5 mIU/mL). Serum follicular2 O1 u* }' H* ^1 y# X
stimulating hormone and leuteinizing hormone+ \. f- ^+ c! ^( X+ g
concentrations were less than 0.05 mIU/mL. l" C% Q- O; s& ]7 `3 E
(prepubertal).
' l( d6 d2 n/ j; [The parents were notified about the laboratory+ E6 I- x& Z9 U% [! f; `
results and were informed that all of the tests were
! W3 V# V5 Q* q. G4 Lnormal except the testosterone level was high. The
" O: q+ j3 O; @7 xfollow-up visit was arranged within a few weeks to, S" z5 W' w( j' q f2 [) {" n
obtain testicular and abdominal sonograms; how-$ h1 ?( E- \+ R2 {/ Q
ever, the family did not return for 4 months.
. l! ~! G1 t1 i% Z. bPhysical examination at this time revealed that the
) t! o6 T: x- V& P W3 J! R# B" Wchild had grown 2.5 cm in 4 months and had gained
8 c; l! K/ i% X( V2 kg of weight. Physical examination remained
0 m0 t s9 I: v1 u( o6 M0 |4 Kunchanged. Surprisingly, the pubic hair almost com-
. l5 ?* m- g$ S, j% L: p6 ppletely disappeared except for a few vellous hairs at1 T1 l5 P/ H& m8 b$ W
the base of the phallus. Testicular volume was still 2* H3 A* o# b$ [* H" {" Z% ~7 c* m
mL, and the size of the penis remained unchanged.$ B7 x# o5 s; u3 x7 P
The mother also said that the boy was no longer hav-, i# V2 j: |" I9 W( A
ing frequent erections.
) B0 K6 a8 ~3 J; e9 Q0 Y% a: sBoth parents were again questioned about use of
& ^/ a* J! b4 Q* Zany ointment/creams that they may have applied to
; M2 y, {+ k: D5 l. nthe child’s skin. This time the father admitted the
3 w1 J/ Z, e0 E; }4 bTopical Testosterone Exposure / Bhowmick et al 5418 T# ]8 i6 e8 h; ?
use of testosterone gel twice daily that he was apply-
/ h/ _: D* N' T; @% A9 w6 U0 Ting over his own shoulders, chest, and back area for
J* C, c$ h( z) qa year. The father also revealed he was embarrassed2 K+ f" i7 ~: ~
to disclose that he was using a testosterone gel pre-
- N5 k* u" i4 U8 g. T4 R+ Vscribed by his family physician for decreased libido
8 u2 m6 D) J4 v9 Vsecondary to depression.
2 `5 ^$ a- {+ s- G/ s. ?5 N% aThe child slept in the same bed with parents.
2 S) E) a7 |) i h' QThe father would hug the baby and hold him on his
, v: q) g. R, q+ E2 q! e1 ]chest for a considerable period of time, causing sig-
. G4 r# ^9 m) J( g+ G7 Z1 }nificant bare skin contact between baby and father.
, |. k* x6 v2 o; p$ `& ~The father also admitted that after the phone call,
, _" A' H* H- x* R6 fwhen he learned the testosterone level in the baby
; r8 g' V/ ~ g _6 H' Y9 @- lwas high, he then read the product information7 {, Q- e2 _ D' X0 L/ p. L
packet and concluded that it was most likely the rea-, L) ^8 Q2 U3 S4 c
son for the child’s virilization. At that time, they
0 A1 P* D; M5 Y+ j9 q' R# fdecided to put the baby in a separate bed, and the
/ P0 ^; `9 |: @- `. l) ]father was not hugging him with bare skin and had8 ]9 h. x U; n% \0 ]. Q1 Q+ R5 e7 y
been using protective clothing. A repeat testosterone
5 _* M* {0 I$ ~% Q1 o: mtest was ordered, but the family did not go to the
8 v- O1 m0 `3 h: S6 o; Y2 ^9 }1 Q qlaboratory to obtain the test.
- P7 `3 t* j2 D& HDiscussion
( H, F! o3 U# rPrecocious puberty in boys is defined as secondary& z9 c+ O# @- v' D3 s, p* m V
sexual development before 9 years of age.1,47 Q8 s; s$ _: G! X4 H* o& u; \% s
Precocious puberty is termed as central (true) when* f, [" x% u9 b. Q: C
it is caused by the premature activation of hypo-
# N. J' d0 N" {. @ R( a# Othalamic pituitary gonadal axis. CPP is more com-! ? f' G6 ~4 d2 g3 ] J
mon in girls than in boys.1,3 Most boys with CPP
: t5 d* a7 H; J2 Dmay have a central nervous system lesion that is
: h2 ?4 S G3 S7 _7 J2 iresponsible for the early activation of the hypothal-
9 s9 A3 l0 g9 i4 s0 T8 P0 ~4 Mamic pituitary gonadal axis.1-3 Thus, greater empha-4 v6 ` m" u& b7 i
sis has been given to neuroradiologic imaging in
, e/ V( l+ T" o5 ~2 Nboys with precocious puberty. In addition to viril-# O3 w1 h# s9 x
ization, the clinical hallmark of CPP is the symmet-, X2 B. S7 k/ B S
rical testicular growth secondary to stimulation by0 d& @$ I* N; E; V! [% l0 E7 i9 l
gonadotropins.1,31 P0 p6 f0 p; A! k4 `4 f/ W
Gonadotropin-independent peripheral preco-6 G3 [5 I8 A3 N, f2 x+ C- }. f
cious puberty in boys also results from inappropriate
1 |4 T' s. e$ F$ h- Zandrogenic stimulation from either endogenous or
/ M6 B1 C* m/ y' Pexogenous sources, nonpituitary gonadotropin stim-
6 c3 O* C- r) r" Fulation, and rare activating mutations.3 Virilizing
$ _; H, |; l4 W8 V" qcongenital adrenal hyperplasia producing excessive
9 i+ ?& F& {- R; r% Uadrenal androgens is a common cause of precocious
+ u, _# h0 C; g0 N4 {2 H' z- |: x" \puberty in boys.3,4) O) `1 G# p( z9 [& J
The most common form of congenital adrenal3 m, q( W0 N4 Q$ M$ r
hyperplasia is the 21-hydroxylase enzyme deficiency.
2 X: ]# |: ]9 bThe 11-β hydroxylase deficiency may also result in
! E+ \3 X' v: w: @excessive adrenal androgen production, and rarely,/ B0 @# }+ [, a& q
an adrenal tumor may also cause adrenal androgen4 ~. n7 n" k$ x% k, N- O
excess.1,3! e% o; c3 q9 o& A$ C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 @/ W# b" n. b1 S) R3 T
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! z# m, q% V- s8 c. e' yA unique entity of male-limited gonadotropin-
, K& Z$ A" Y2 zindependent precocious puberty, which is also known5 R6 O/ g, I2 ^% q$ b _
as testotoxicosis, may cause precocious puberty at a2 |4 ~8 o ~* i/ {
very young age. The physical findings in these boys/ t7 Z0 E/ H7 e4 L; @- R8 `
with this disorder are full pubertal development,1 A* `; ]) Y0 s- L' B
including bilateral testicular growth, similar to boys6 B P2 j6 z v% Z* n6 ?. l
with CPP. The gonadotropin levels in this disorder8 Q/ S/ ^/ `$ W! d, Z( o, U
are suppressed to prepubertal levels and do not show0 g: G& P5 K; B+ x- M
pubertal response of gonadotropin after gonadotropin-
: v; w I- ?% ^! c2 freleasing hormone stimulation. This is a sex-linked. v T, b! ~& ~4 r
autosomal dominant disorder that affects only; q) W9 T- w4 q
males; therefore, other male members of the family$ U3 {' P4 x* B" Y; F! A
may have similar precocious puberty.37 V2 I1 e+ o% G
In our patient, physical examination was incon-* M# D! j+ c; S3 o$ Y1 z
sistent with true precocious puberty since his testi-
6 P, ], s2 i& @3 s5 G; C, acles were prepubertal in size. However, testotoxicosis
$ E0 H% {( f0 uwas in the differential diagnosis because his father2 ?2 d6 S& y* k, A& P
started puberty somewhat early, and occasionally,
5 b( F, s' q8 X' E' utesticular enlargement is not that evident in the
9 e" Y6 v; o, T$ h/ `$ `4 hbeginning of this process.1 In the absence of a neg-* |0 t$ i+ a8 ?/ A" o l+ F
ative initial history of androgen exposure, our0 E. W* d: Z' ?, f! Q6 ?
biggest concern was virilizing adrenal hyperplasia, D) b" I8 [2 R! V! b
either 21-hydroxylase deficiency or 11-β hydroxylase) X: G) D0 H5 I# i& I0 ]- Y2 B; G
deficiency. Those diagnoses were excluded by find-
& v1 A- ]( i8 @- C. Ying the normal level of adrenal steroids.9 i- X5 w$ U, Y3 L0 _* W' x4 ^2 z" P- I: A
The diagnosis of exogenous androgens was strongly
- `0 b0 g% Z0 |; X8 gsuspected in a follow-up visit after 4 months because$ l$ j- K: j% {( w
the physical examination revealed the complete disap-
3 g, W' c% L1 i( gpearance of pubic hair, normal growth velocity, and
* Q0 }6 k; x% c. t0 {( hdecreased erections. The father admitted using a testos-
7 {7 _; h6 L# g7 {terone gel, which he concealed at first visit. He was
, y$ [- _) _9 @4 Musing it rather frequently, twice a day. The Physicians’
1 M" w2 _9 e3 @/ S0 qDesk Reference, or package insert of this product, gel or# o+ i# o0 x' M# Q% ~ y$ W
cream, cautions about dermal testosterone transfer to
% Z0 {( X/ I& h6 I: m7 v7 gunprotected females through direct skin exposure.
3 C. u; C0 Z& D5 R$ V+ j4 PSerum testosterone level was found to be 2 times the! A! v3 b+ z$ u
baseline value in those females who were exposed to1 C8 n0 Z, N# y
even 15 minutes of direct skin contact with their male. ?( X0 D5 k' `' ]
partners.6 However, when a shirt covered the applica-' O/ A2 B9 s _) p8 F" o1 W
tion site, this testosterone transfer was prevented.
' K* D2 W: c7 ]2 AOur patient’s testosterone level was 60 ng/mL," f" f4 q) N; c. H. q% f
which was clearly high. Some studies suggest that4 ]* N1 h6 o2 x+ M4 C2 u
dermal conversion of testosterone to dihydrotestos-9 _% z8 o# B" I P. ?$ X' P5 ?8 ^
terone, which is a more potent metabolite, is more
1 T$ |2 L; C6 P) Mactive in young children exposed to testosterone
9 L i) J, Y* h1 [; ]exogenously7; however, we did not measure a dihy-8 J' n4 H3 }- f# X# v
drotestosterone level in our patient. In addition to
) h: T( s$ W2 ?9 R, Hvirilization, exposure to exogenous testosterone in4 T' I. y$ E* G5 y( w& @
children results in an increase in growth velocity and
$ h$ l# v. C2 ^4 a4 O$ ` D+ \* H3 Aadvanced bone age, as seen in our patient.
" c: r, f. I' t: c3 HThe long-term effect of androgen exposure during
2 E: L) }! g8 c( Bearly childhood on pubertal development and final& h- x, A) h5 U9 m( M
adult height are not fully known and always remain
$ }; O6 X6 }. ^# n" N' @! Z" ^a concern. Children treated with short-term testos-) m/ a: G. S5 L1 [4 N5 Y% U$ t
terone injection or topical androgen may exhibit some
g0 C0 O6 Z3 @* [, o( A# a' Lacceleration of the skeletal maturation; however, after( [7 o2 J6 I6 h2 z8 @
cessation of treatment, the rate of bone maturation+ J& f0 M, y$ D B6 w \
decelerates and gradually returns to normal.8,96 E0 l( s2 Z/ y( u( T; z$ Y. ] q) E
There are conflicting reports and controversy6 Y% C5 {1 O. I
over the effect of early androgen exposure on adult
) v5 Q4 i8 d3 K% lpenile length.10,11 Some reports suggest subnormal
7 L1 Y. v# _* X2 ?9 J& J& y) a2 D' Zadult penile length, apparently because of downreg-
/ G( x7 ^( a/ q8 I5 L$ fulation of androgen receptor number.10,12 However,
: d* R: ]& C _5 H9 f6 P" rSutherland et al13 did not find a correlation between+ \* A8 b2 X; c, }& Y. k# p/ [
childhood testosterone exposure and reduced adult
; O$ c' ^ s/ h% r" @ npenile length in clinical studies.
5 B% f, m/ H7 L7 p9 o1 }; C4 ANonetheless, we do not believe our patient is) h8 {; u( F- J: D' G4 d
going to experience any of the untoward effects from1 d' T3 \! q( z) ^" e: y
testosterone exposure as mentioned earlier because
/ q) A8 n2 A- fthe exposure was not for a prolonged period of time.. U" c& x& l: _* K P9 n& o. c6 f% P
Although the bone age was advanced at the time of
* O& }& O) O% ~" h, N# o1 w2 ddiagnosis, the child had a normal growth velocity at3 H! Y1 |6 @% B4 o3 R0 Q7 P
the follow-up visit. It is hoped that his final adult
. U: f/ g1 i4 w/ O; H8 j- v. o/ f. Pheight will not be affected.
" Y$ P. p: A. f1 Z! Q @2 ]7 B; dAlthough rarely reported, the widespread avail-# @' ^; q! `- K) F" y) `' R4 E
ability of androgen products in our society may
* R0 e5 h! c1 @" q" Mindeed cause more virilization in male or female9 y8 o/ w, S' y
children than one would realize. Exposure to andro-! k" y9 m$ P5 y6 W. h
gen products must be considered and specific ques-. O1 R' i$ ~& {. e8 U
tioning about the use of a testosterone product or
" I$ g1 s( y$ vgel should be asked of the family members during. [! ]/ e* O2 ]7 t' C6 x
the evaluation of any children who present with vir-6 k' X- A" Y* Y2 t9 y% M+ v
ilization or peripheral precocious puberty. The diag-
. R0 a$ x- C, ]$ }2 L0 y- K0 ]nosis can be established by just a few tests and by5 \+ ~" P+ P, A. i0 h
appropriate history. The inability to obtain such a
! @$ z' \( y& p T- r! J2 ^history, or failure to ask the specific questions, may
5 i1 u" I7 ]" u* E% e: }result in extensive, unnecessary, and expensive$ F1 @4 J ~* b
investigation. The primary care physician should be
; S7 S% `! f$ h5 e. P: faware of this fact, because most of these children2 v2 G3 @* f, k% G+ F
may initially present in their practice. The Physicians’$ a9 z+ j. Q' ]" ^$ { \
Desk Reference and package insert should also put a9 D; Z" F& s! W$ s' F& N; T, n
warning about the virilizing effect on a male or
. a9 t* y# V# o8 m- c. x0 gfemale child who might come in contact with some-6 o$ x4 _; b2 [" s4 y
one using any of these products." s+ @/ i5 @% d1 X: z1 G
References
: X1 E' J2 a' f! Y7 a1 q1. Styne DM. The testes: disorder of sexual differentiation
) u! B: L! r; Z; {and puberty in the male. In: Sperling MA, ed. Pediatric) D. K% D4 U7 k; U
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 S, Y$ }6 _- I ~6 _' b T1 E0 Q2002: 565-628.5 a a; O5 z) M% q9 J( U: [. T8 |, T8 a
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' ]6 h$ P- M/ `7 ^1 z; T! ?
puberty in children with tumours of the suprasellar pineal |
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