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Sexual Precocity in a 16-Month-Old6 D" T2 G" G, e
Boy Induced by Indirect Topical) J! S g7 s, q, I# Q% _$ [6 Q
Exposure to Testosterone
6 \2 Z1 N1 O+ U3 m8 fSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 _* O# Z/ `4 h4 l7 E
and Kenneth R. Rettig, MD10 _+ l( z( J+ Y0 a
Clinical Pediatrics7 A8 L3 R5 P' h! z
Volume 46 Number 6/ t# L! L1 z3 T* W
July 2007 540-543
' P4 d7 d1 \" l: r) U" B& y# ^© 2007 Sage Publications
$ l2 v% o+ a* h3 F% R10.1177/0009922806296651( Q; A7 C. u! H* J% V
http://clp.sagepub.com
+ V' K3 ?1 _/ f0 }hosted at6 E6 Z3 z. a4 p6 }9 V' U
http://online.sagepub.com
) f$ r9 q \, N3 H3 Z" L7 y$ ^" {Precocious puberty in boys, central or peripheral,
( V, h0 u8 R( k+ O) z; q* ]is a significant concern for physicians. Central
% _0 W9 _9 A4 `) o, H% a! d/ T4 ^precocious puberty (CPP), which is mediated
" F/ U2 u6 M& e8 ithrough the hypothalamic pituitary gonadal axis, has
/ I5 f% V4 [0 d4 L" M, b% I, {a higher incidence of organic central nervous system
5 U% F5 V, C- h# w! E: ilesions in boys.1,2 Virilization in boys, as manifested5 P. b* P" t* ^0 l% h7 B7 g7 g
by enlargement of the penis, development of pubic
7 ?6 f6 C+ Q# l& `0 r" g' p, \hair, and facial acne without enlargement of testi-
) M% u5 O8 Z1 M" O" Icles, suggests peripheral or pseudopuberty.1-3 We
) `4 i- Z; ?3 n breport a 16-month-old boy who presented with the- a) f0 k: m/ h- O/ V8 ]) \
enlargement of the phallus and pubic hair develop-0 O; m; ?! c4 {7 F4 A
ment without testicular enlargement, which was due7 q& n0 i7 ?% ]2 Z8 j) y* ?$ W
to the unintentional exposure to androgen gel used by
- c1 i0 W) l4 G. ?7 N3 _6 C. Gthe father. The family initially concealed this infor-
5 o+ n1 y' M8 r, c5 B' smation, resulting in an extensive work-up for this# ~5 ]7 y# j; X- M/ ]0 E
child. Given the widespread and easy availability of
0 N& k9 K0 O7 p& |testosterone gel and cream, we believe this is proba-' ?9 v, n/ Y6 }6 w; V1 E/ a8 t
bly more common than the rare case report in the
& b0 m9 N! z! y4 A" d' d/ c6 uliterature.4
4 G% O9 Q- r$ @Patient Report
5 k3 L# B8 V6 f- JA 16-month-old white child was referred to the
" X! o: G& a, x. ^; R% bendocrine clinic by his pediatrician with the concern
: h( w8 V. e6 O: T# X4 H1 }of early sexual development. His mother noticed
* ]9 V+ n+ j1 e6 z1 r5 s$ X4 B4 Tlight colored pubic hair development when he was
4 C0 W1 z- `. U0 UFrom the 1Division of Pediatric Endocrinology, 2University of$ M. _ y+ y2 E; ~2 c& r6 t
South Alabama Medical Center, Mobile, Alabama.; Q, D9 h. m) E( k p6 s; j
Address correspondence to: Samar K. Bhowmick, MD, FACE,
3 K' N3 ?* v9 KProfessor of Pediatrics, University of South Alabama, College of& ]+ s; o+ X2 T- J, W* m) @4 H
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297; v6 i. j8 ?% Q! L9 f+ j
e-mail: [email protected].
) p8 E0 L6 }, Q" F6 sabout 6 to 7 months old, which progressively became, c q% U K# O" I7 o7 z) m. y
darker. She was also concerned about the enlarge-" a9 y" u0 O+ O: K/ l# z
ment of his penis and frequent erections. The child
7 D: h! m( w4 u" awas the product of a full-term normal delivery, with( C5 h$ s9 U" M& _3 K6 K8 [
a birth weight of 7 lb 14 oz, and birth length of: t C& g' G; C
20 inches. He was breast-fed throughout the first year' b( v2 u' w5 b6 K+ N
of life and was still receiving breast milk along with
6 U! o. d, m9 b+ _, t0 ?- |solid food. He had no hospitalizations or surgery,
* Z* g& {, ]1 O+ Y# q% Z( |" t3 Mand his psychosocial and psychomotor development
8 @( ^. C- T. ]$ ]6 X. pwas age appropriate.
) a/ j, o" ?4 K8 h1 l6 T1 ?The family history was remarkable for the father,
! R) S# l- C9 d. j: J0 U! x% hwho was diagnosed with hypothyroidism at age 16,
, {5 Q/ o6 C, _7 Gwhich was treated with thyroxine. The father’s
0 W. Q7 }$ @, Gheight was 6 feet, and he went through a somewhat+ x& X* b+ F4 y9 i, h
early puberty and had stopped growing by age 14.5 S7 z* L( A5 `% {* w% |! \/ ^' v
The father denied taking any other medication. The
; u, \3 c1 F& F1 Lchild’s mother was in good health. Her menarche
# t7 S0 S9 V: A3 I: ^# Qwas at 11 years of age, and her height was at 5 feet
& ?! `4 l4 @# X9 S' V5 inches. There was no other family history of pre-( Z7 K! `4 T1 O
cocious sexual development in the first-degree rela-
2 l5 w, c, D$ A( qtives. There were no siblings.6 T6 `( q. P/ m: h1 D! h
Physical Examination8 m/ ~( Y$ p' Z. {5 T, g% ^- l
The physical examination revealed a very active,
9 A+ r: M6 H0 p, Rplayful, and healthy boy. The vital signs documented+ z5 Y: \' n% V& l
a blood pressure of 85/50 mm Hg, his length was( Z& G- [0 i5 y% t, U
90 cm (>97th percentile), and his weight was 14.4 kg) [. i+ [' U8 {$ N" }7 _2 }6 Y
(also >97th percentile). The observed yearly growth
3 B9 M3 `8 F) `& s: I4 x( }( i) hvelocity was 30 cm (12 inches). The examination of3 r# u2 T! _- Y+ ^( ~; b6 V# C \
the neck revealed no thyroid enlargement.' L2 i- d, j( p4 Z
The genitourinary examination was remarkable for
, X9 g- N" K0 \enlargement of the penis, with a stretched length of
. w& h+ a' Y% [% z7 k8 cm and a width of 2 cm. The glans penis was very well
6 `; G- j. j2 {, A3 kdeveloped. The pubic hair was Tanner II, mostly around
# Y3 S5 U0 ~0 B) L8 W) n5401 `0 p; U8 `$ o2 E' C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" w" W/ i8 r# V' H0 Fthe base of the phallus and was dark and curled. The
( g8 M' H! L( V. H& N+ Q& y: atesticular volume was prepubertal at 2 mL each.4 M! k7 K: Q1 D& W% d9 s
The skin was moist and smooth and somewhat' I5 U# n: O" G+ ]8 z, g$ V
oily. No axillary hair was noted. There were no' _, h. l' B+ W, x, {8 J
abnormal skin pigmentations or café-au-lait spots.
" U& m( I4 Q! M$ n" W) ?' Z/ C; _7 RNeurologic evaluation showed deep tendon reflex 2+; ?; v/ @3 J9 N' c& Q! @
bilateral and symmetrical. There was no suggestion
# v% \( e, ~. m5 B. y5 Jof papilledema.
. o. U4 J- x' ?; A% l. PLaboratory Evaluation
" }: U9 H* f1 vThe bone age was consistent with 28 months by/ c# U7 W& d& f7 ~
using the standard of Greulich and Pyle at a chrono-
$ p! c' M& x# g. u6 Z$ {logic age of 16 months (advanced).5 Chromosomal
& @ t# Y4 z' Kkaryotype was 46XY. The thyroid function test6 J$ s2 l" P K
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
: Z& B2 \/ x; D7 s z4 x( Q7 {+ Olating hormone level was 1.3 µIU/mL (both normal).
8 q3 T9 w2 `6 I2 b7 [( HThe concentrations of serum electrolytes, blood
4 E# C4 _7 M# w5 Q$ b0 surea nitrogen, creatinine, and calcium all were! O# S2 R A5 d- M% N" s2 x/ Q9 W
within normal range for his age. The concentration
( q6 s. R1 p* N" Q0 a) M! zof serum 17-hydroxyprogesterone was 16 ng/dL
1 P6 h! |3 I& B Q% H(normal, 3 to 90 ng/dL), androstenedione was 20- ~9 I, R& \" m" _
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 R- b" d! a$ \$ x! \4 f
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 ?# w" x: q$ }4 Rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( k; G% w, Z) s. [49ng/dL), 11-desoxycortisol (specific compound S)
* A0 ~* g9 _8 Z e$ u+ mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 b& c$ t. }" l$ c6 {
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
# j5 c* i- `; R: l9 p- G) P9 gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 d q% y8 n) P# [6 {0 ]% H
and β-human chorionic gonadotropin was less than: b! i9 V- V8 S _
5 mIU/mL (normal <5 mIU/mL). Serum follicular7 ?/ V+ b0 M: q3 \" Q6 T
stimulating hormone and leuteinizing hormone
# v9 B; O; x+ l: p3 m& }concentrations were less than 0.05 mIU/mL
" D9 c, K. N- a/ x/ g(prepubertal).3 c( @9 O$ ^/ S" v ^
The parents were notified about the laboratory2 }% p: C" I8 g; g% O5 G/ \
results and were informed that all of the tests were
. a) G$ V% h9 ^/ Hnormal except the testosterone level was high. The
' B. p' n' A4 ^4 e5 g! C6 z, E# ~; _0 kfollow-up visit was arranged within a few weeks to
# g! G+ K1 p$ U; a# V4 robtain testicular and abdominal sonograms; how-
- C5 W9 l+ o: K; C; J5 h9 H0 d1 hever, the family did not return for 4 months.& h2 I( D+ V! k* e6 V6 Q; W
Physical examination at this time revealed that the
3 X; A, E/ f! f% }* hchild had grown 2.5 cm in 4 months and had gained' T$ ~0 _- M% L2 Q. z/ j6 Q3 R
2 kg of weight. Physical examination remained
2 l9 n! z( o: e. v1 P: Y! k; E" P4 _4 Tunchanged. Surprisingly, the pubic hair almost com-
1 T: I; |# ? j$ h) a. U$ hpletely disappeared except for a few vellous hairs at l: r3 l+ {% `
the base of the phallus. Testicular volume was still 23 q u! ~ }4 R0 D" E. M1 ?
mL, and the size of the penis remained unchanged.. ?( O T# K$ n5 G% k$ v
The mother also said that the boy was no longer hav-
) i# H8 o( l; k Z$ e3 Q6 Z$ n' Iing frequent erections.: @! d2 U' E# R, M7 j
Both parents were again questioned about use of
& P1 F0 {. [4 ]' b9 [any ointment/creams that they may have applied to0 u1 P9 G! `/ j: P# G
the child’s skin. This time the father admitted the
% B! P; D9 g0 \3 {4 ETopical Testosterone Exposure / Bhowmick et al 541
$ m* @$ g: R/ f% n7 Zuse of testosterone gel twice daily that he was apply-
$ [" K0 j M2 {) Uing over his own shoulders, chest, and back area for3 i7 B8 y8 A( W; Z
a year. The father also revealed he was embarrassed0 a ^% g. G# D+ b2 ^: ?
to disclose that he was using a testosterone gel pre-
( ?: K. F/ {/ E# B( L9 G, T8 J0 G1 Cscribed by his family physician for decreased libido7 p& c% P+ P+ y; v
secondary to depression.
& w% }* }; I5 o, v% d) ?5 [+ n: n! d0 TThe child slept in the same bed with parents.: Y; k5 e# J" k1 g' J; T4 l
The father would hug the baby and hold him on his
6 n2 ~" p; X( x- T5 z: a$ ^+ Jchest for a considerable period of time, causing sig-! P# ]7 {& W! v* u5 c- e. |
nificant bare skin contact between baby and father.: Y: n5 E+ i7 ~- b) [: a6 J8 S
The father also admitted that after the phone call,
* P6 E3 d( g* y V4 M( b- W, Twhen he learned the testosterone level in the baby7 ?) E0 b7 J2 V/ k& z. C# X
was high, he then read the product information/ @- v" F. p7 B! F
packet and concluded that it was most likely the rea-
# D Y: @' O/ @0 G2 c: ^/ ?son for the child’s virilization. At that time, they+ @6 {& q2 h0 w' ^8 F& l/ ^+ q
decided to put the baby in a separate bed, and the
0 u4 o+ G2 j) ]6 }9 l; _2 n8 vfather was not hugging him with bare skin and had* {* k0 r" V7 R
been using protective clothing. A repeat testosterone: @6 g. O8 o2 r& O6 R8 n2 S7 P! V
test was ordered, but the family did not go to the
# ], H. [4 E# l6 H$ F- Vlaboratory to obtain the test.
1 l# \% R' R) c/ G& j. f ~Discussion
7 `" ^. y/ T$ OPrecocious puberty in boys is defined as secondary! M, i6 U9 N+ k- r
sexual development before 9 years of age.1,4
: ?5 p# Q1 [- [* y* P2 E7 tPrecocious puberty is termed as central (true) when
+ Y) p- ^+ ?# _6 c& Y! hit is caused by the premature activation of hypo-* Z& N3 Q+ s6 }% S6 n) @$ n9 e1 p- p
thalamic pituitary gonadal axis. CPP is more com-
# E$ c# h. P9 pmon in girls than in boys.1,3 Most boys with CPP
- k, g2 {5 H/ B. Zmay have a central nervous system lesion that is; {8 y( F7 p, O( `9 {# E2 X
responsible for the early activation of the hypothal-0 E5 j. R3 A) w# b; ?
amic pituitary gonadal axis.1-3 Thus, greater empha-
$ n" ]: C5 |: i2 J7 `- Jsis has been given to neuroradiologic imaging in! \9 G" {. P+ A" u$ U4 O+ Q6 d
boys with precocious puberty. In addition to viril-9 U( N5 G+ W, e V$ G
ization, the clinical hallmark of CPP is the symmet-
6 J0 M. E& P# frical testicular growth secondary to stimulation by; m1 g8 H( U7 j8 L% ?* r& V
gonadotropins.1,3) \9 w8 u% e. [- ^
Gonadotropin-independent peripheral preco-( `% l; j+ @& x; ~6 R2 [
cious puberty in boys also results from inappropriate
+ X' }- F6 X, \" L" m0 ^androgenic stimulation from either endogenous or
( q: e) M; A0 s4 mexogenous sources, nonpituitary gonadotropin stim-
* O5 R* M+ c- v+ U0 t& Z3 Hulation, and rare activating mutations.3 Virilizing
6 k( h3 I2 S6 Ycongenital adrenal hyperplasia producing excessive
3 _% B- e) N& Yadrenal androgens is a common cause of precocious
$ @* J# h: l8 F( s4 ppuberty in boys.3,48 K% X9 c) B2 p$ C& J
The most common form of congenital adrenal- ~( |, t" X5 O9 l% F e) S' D4 g
hyperplasia is the 21-hydroxylase enzyme deficiency.$ H1 z, J( d; T8 R! M( w
The 11-β hydroxylase deficiency may also result in* P1 X, M$ X. W1 {
excessive adrenal androgen production, and rarely,: g5 Y3 z, R, N! v$ ]
an adrenal tumor may also cause adrenal androgen
2 J4 ?3 T5 x( G7 h4 ]' q' l$ i5 t ]! ^excess.1,3: k4 q" a/ D& C+ P5 W" C8 i) }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' {: T* H% z& | j: ]5 B% N542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& u" c6 f- a. o3 r4 W- V& O# p
A unique entity of male-limited gonadotropin-' }& R6 t# E7 r. p# x& p
independent precocious puberty, which is also known. f6 h% c( g1 E( j( U5 G
as testotoxicosis, may cause precocious puberty at a$ ^' }( ^# l3 i
very young age. The physical findings in these boys
% Z2 Y2 u- s; ]8 t9 P* Ywith this disorder are full pubertal development,
$ E8 @! [( y% d; k/ I3 bincluding bilateral testicular growth, similar to boys
\* H+ e. }7 J: `with CPP. The gonadotropin levels in this disorder
0 L$ {* t& E0 x3 x3 ^are suppressed to prepubertal levels and do not show
2 C" X7 J: g+ I$ i7 t; {pubertal response of gonadotropin after gonadotropin-
3 g I p7 Q3 B) A# Mreleasing hormone stimulation. This is a sex-linked
, Z7 ^( w+ s2 e0 r" C9 Iautosomal dominant disorder that affects only
7 `" s, n, K. a/ f4 ^! Wmales; therefore, other male members of the family+ b- V: x# U5 G0 g& f) }
may have similar precocious puberty.3" g$ j' L, d U5 b( Y
In our patient, physical examination was incon-
1 R( s. {' T- b' o8 L p: X! hsistent with true precocious puberty since his testi-
, K) L$ A# O$ Z& C" Acles were prepubertal in size. However, testotoxicosis
2 a( I- Q- C! `( rwas in the differential diagnosis because his father& t' e+ r* \' d, S: F
started puberty somewhat early, and occasionally,
) Q& j+ t# z% [- c9 Q6 Vtesticular enlargement is not that evident in the0 C A# }0 I) ]/ l, X
beginning of this process.1 In the absence of a neg-
( k3 H$ m7 k/ }ative initial history of androgen exposure, our( b; \) U, ~2 H
biggest concern was virilizing adrenal hyperplasia,/ L5 R# E* e9 l. t. a
either 21-hydroxylase deficiency or 11-β hydroxylase
5 U+ S) z7 [; i9 H' x' b+ ?7 ]) Odeficiency. Those diagnoses were excluded by find-/ D+ y. F: A! V+ S7 @, ]
ing the normal level of adrenal steroids.- p( @8 `2 R1 N* S: b% b; {! q
The diagnosis of exogenous androgens was strongly
- V6 m6 z+ U- q# \suspected in a follow-up visit after 4 months because
/ k6 m4 T' n/ v2 R% k# Uthe physical examination revealed the complete disap-1 ^* C; \; r/ q/ ~" f4 ?
pearance of pubic hair, normal growth velocity, and
$ D8 L& e7 a% W: M; Edecreased erections. The father admitted using a testos-, ]7 c. D$ }4 J; n
terone gel, which he concealed at first visit. He was
* q$ \* x3 [: g$ B& ]using it rather frequently, twice a day. The Physicians’
* I; S6 a/ }) L, y a1 L; `0 uDesk Reference, or package insert of this product, gel or
. N. S4 H1 I0 l5 w9 z7 ccream, cautions about dermal testosterone transfer to2 U. i1 l/ ?/ f8 V
unprotected females through direct skin exposure.
" A% s/ J# n5 e* D. O+ z8 z4 _5 SSerum testosterone level was found to be 2 times the
. b- W& ]9 }, R" Zbaseline value in those females who were exposed to9 ^5 B( S1 }% ]8 \+ X
even 15 minutes of direct skin contact with their male
+ r8 ?$ U# \0 u6 fpartners.6 However, when a shirt covered the applica-
' G; m$ S' v, Ption site, this testosterone transfer was prevented.
$ `9 U! ~: l: R4 i( V5 qOur patient’s testosterone level was 60 ng/mL,
' E& b: d# B; L0 P; d& xwhich was clearly high. Some studies suggest that K4 R/ i8 U0 E9 ?, e
dermal conversion of testosterone to dihydrotestos-5 B; k* x! m z, w: F+ _
terone, which is a more potent metabolite, is more: v; d i1 H% ?# g: G; E
active in young children exposed to testosterone; y: L: T% V+ l5 i3 E$ m9 R
exogenously7; however, we did not measure a dihy-
9 `3 ~- C8 x7 bdrotestosterone level in our patient. In addition to
, z7 ]" Q1 M6 r, dvirilization, exposure to exogenous testosterone in# E! p8 e8 X$ R, y
children results in an increase in growth velocity and
2 R7 V* N) ~" R0 g! d# z5 c6 }9 W2 sadvanced bone age, as seen in our patient.
% Q) e: ]: n5 Y5 F5 X8 k6 L- PThe long-term effect of androgen exposure during, K. H. O5 C( J: V( o/ {) ^9 l
early childhood on pubertal development and final. R) T! L' b3 s
adult height are not fully known and always remain& L4 K2 q+ p8 [$ f/ A
a concern. Children treated with short-term testos-
6 M/ v& e& r, f k5 \* }5 N0 h/ Iterone injection or topical androgen may exhibit some
6 ?- A, \6 G' J0 Gacceleration of the skeletal maturation; however, after1 d, ~1 | _1 @. W
cessation of treatment, the rate of bone maturation" a' R5 Z7 w( N% C- n( x Y
decelerates and gradually returns to normal.8,9
4 f* G( Q# ]" U( p0 v7 M* DThere are conflicting reports and controversy
" l( H& k6 v6 n/ s. `0 c+ Vover the effect of early androgen exposure on adult
* p6 |' m! s( q0 ypenile length.10,11 Some reports suggest subnormal. B2 V) T8 U8 N
adult penile length, apparently because of downreg-9 i* p, B: U. ~' H0 f
ulation of androgen receptor number.10,12 However,: ?; q% Y- k! @) f! a; Z
Sutherland et al13 did not find a correlation between/ V8 G2 x: |% `& Q" O" A( w: M
childhood testosterone exposure and reduced adult* D3 x. u B$ i" O
penile length in clinical studies. ]( o# r5 Y) N( I) U6 r. f& ?9 z
Nonetheless, we do not believe our patient is
& t1 `" Q3 O& @* b) ?1 z sgoing to experience any of the untoward effects from
" Y u# a! y; n; p5 e" ^testosterone exposure as mentioned earlier because
/ \: u w( R: r1 B+ b+ athe exposure was not for a prolonged period of time.
3 ?% i1 R0 I. t& M. v- F; ^% q. P5 G9 jAlthough the bone age was advanced at the time of( a2 s f# c' S* Y
diagnosis, the child had a normal growth velocity at
6 N( g8 [4 U* e% T1 P6 lthe follow-up visit. It is hoped that his final adult
3 I9 B$ E: ?9 o6 m" w# N# m" B W, A" rheight will not be affected.) p1 v9 e0 W4 E& Q* o7 w
Although rarely reported, the widespread avail-
7 L) u, A4 e: f2 m( O, A8 l1 [ability of androgen products in our society may
* A& D- P" _8 h1 N1 Cindeed cause more virilization in male or female% e% O/ j7 i/ J% u, c6 V' x+ N
children than one would realize. Exposure to andro-
& b8 }# y5 J+ l7 ?gen products must be considered and specific ques-: ]3 H. k+ C( |% R( ^
tioning about the use of a testosterone product or' ]) q, W q0 F+ F/ v
gel should be asked of the family members during
. A* c6 S9 P4 G9 y3 A2 u+ Uthe evaluation of any children who present with vir-
* f, j. v4 o; Q- g; o$ Kilization or peripheral precocious puberty. The diag-5 @ J7 E. _0 W. ]1 k
nosis can be established by just a few tests and by _% h! ~5 b6 p- e
appropriate history. The inability to obtain such a
- Q' h- ^8 r) u+ Y. whistory, or failure to ask the specific questions, may
9 C' s; Z2 O" [/ p& B) Wresult in extensive, unnecessary, and expensive
( J$ _ g4 |' J; k5 g. {investigation. The primary care physician should be! M6 h9 H- s3 G5 i$ B0 I
aware of this fact, because most of these children
0 M+ M0 r+ A2 Zmay initially present in their practice. The Physicians’
5 G0 M, V4 g1 X- z% o0 |Desk Reference and package insert should also put a2 s; A* @5 H( i1 M
warning about the virilizing effect on a male or& K# ^. T( g- r) h1 A4 L8 S; m/ p; C
female child who might come in contact with some-
8 g! Y* ~0 L* O$ G- k* \one using any of these products.! G6 \1 i! \/ Q \
References
8 |' f/ V' c: \5 [8 u1. Styne DM. The testes: disorder of sexual differentiation
: ?, T9 U, e* o/ c3 k! n5 Jand puberty in the male. In: Sperling MA, ed. Pediatric
) r4 P' k; m( v! G" z. kEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" K1 {$ V( p s: l2 [ J# M2002: 565-628.3 Y3 z/ {3 W- s
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) q; m/ l, Z. Z
puberty in children with tumours of the suprasellar pineal |
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