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Sexual Precocity in a 16-Month-Old
- T% k2 P8 }( j$ L+ `: lBoy Induced by Indirect Topical
* d! J) `3 y8 Y9 Z3 bExposure to Testosterone! ~9 f- v- M0 R
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 ~; @8 Q9 h1 Q' P7 v' W. B- eand Kenneth R. Rettig, MD12 u5 q |8 F& _: z2 ]
Clinical Pediatrics
6 b7 N4 s$ H' mVolume 46 Number 67 X0 S- Z/ m( y. K E0 H
July 2007 540-543# J) K z/ F9 f; [
© 2007 Sage Publications0 X* h- d1 K g p2 g
10.1177/0009922806296651
0 g. Q6 D& c# C+ O+ s8 q y' I, ]( K* thttp://clp.sagepub.com- Q3 C: o- I1 m" T3 F* f4 ^8 v/ O
hosted at
- @4 J7 }, q6 p5 [http://online.sagepub.com6 ~: P" a3 ?- w7 S$ ^7 _
Precocious puberty in boys, central or peripheral, O9 F% g/ `; E# ~
is a significant concern for physicians. Central
4 x4 v1 }3 Z5 C& L& o" yprecocious puberty (CPP), which is mediated
3 B* c* a$ G0 e* l }) c7 i+ Ethrough the hypothalamic pituitary gonadal axis, has
. ]7 D5 r# `/ h Y' X$ g0 A! Q" G4 da higher incidence of organic central nervous system
2 m1 L. S4 O4 d6 I; y/ ^lesions in boys.1,2 Virilization in boys, as manifested
+ k6 v" y1 X; \by enlargement of the penis, development of pubic
: h9 U( L" \8 u4 Bhair, and facial acne without enlargement of testi-( m# A. b' G6 k" {6 a) P
cles, suggests peripheral or pseudopuberty.1-3 We
8 L$ V& l. i0 Oreport a 16-month-old boy who presented with the7 m; J- X2 F% z- Y/ t2 W# g
enlargement of the phallus and pubic hair develop-) K6 c- w: t9 U+ T% h5 }1 }, E; h7 @
ment without testicular enlargement, which was due
) k: f3 j/ k' @1 v. Fto the unintentional exposure to androgen gel used by9 r( N, q* n: |% A4 T, f( i
the father. The family initially concealed this infor-0 |$ N/ P! N$ S: l" j
mation, resulting in an extensive work-up for this
7 u- Z/ u, [" {( ~! Q& Cchild. Given the widespread and easy availability of
& a6 t) w/ F, S% wtestosterone gel and cream, we believe this is proba-
% L+ V X: L( P3 e& X6 H5 @( Gbly more common than the rare case report in the: o& b5 Y9 S" g* i* r, S
literature.4
) J8 k. U! U; P3 D' bPatient Report
1 y5 I1 A7 \4 Q& v8 k) OA 16-month-old white child was referred to the
2 }. D3 {- d [5 B! F! A4 t1 lendocrine clinic by his pediatrician with the concern
( p: Z, Z. `: jof early sexual development. His mother noticed* d7 y" t3 y* E- h* Z% X+ y" g& g
light colored pubic hair development when he was! I: _0 ~, ]* Y1 N, A, H3 N7 Z
From the 1Division of Pediatric Endocrinology, 2University of6 a W( [# s5 `* P
South Alabama Medical Center, Mobile, Alabama.- h' m8 I# Z" N+ v9 U
Address correspondence to: Samar K. Bhowmick, MD, FACE,
& a' F9 M$ I) C( H& E+ jProfessor of Pediatrics, University of South Alabama, College of9 w. A% @ U7 X- A3 e$ \
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 w* g9 d5 U9 p" O3 O6 u( N# R0 ee-mail: [email protected].
2 {# p a$ M( W3 w% \about 6 to 7 months old, which progressively became
5 q* V2 q: Z% m5 \/ C7 d- hdarker. She was also concerned about the enlarge-4 n# U4 x# u: \
ment of his penis and frequent erections. The child
9 j, q2 s! E4 U( k6 z( c; a$ F( Hwas the product of a full-term normal delivery, with) b/ Q, P0 g* d" R# g* e5 j
a birth weight of 7 lb 14 oz, and birth length of
# M" L0 \& r3 V/ n20 inches. He was breast-fed throughout the first year* o/ a0 j5 W& | k
of life and was still receiving breast milk along with: M" L+ c* |. O) l- w
solid food. He had no hospitalizations or surgery,
5 D2 S/ V# j2 @3 G6 J7 Kand his psychosocial and psychomotor development
; S/ R. h' x0 Z7 |- Zwas age appropriate.; }2 Y! r3 q1 d8 Q, B
The family history was remarkable for the father,
# A# ~3 M8 }1 C- R& J6 o& o& wwho was diagnosed with hypothyroidism at age 16,5 C1 r4 ^$ E7 v
which was treated with thyroxine. The father’s
$ M3 R+ B" @1 B8 g: e) p }. theight was 6 feet, and he went through a somewhat
, p0 Y/ ]& o% X8 nearly puberty and had stopped growing by age 14.
; Q/ s; h7 [% X3 s6 \The father denied taking any other medication. The* I2 {2 C* {7 P9 E, x' T' R2 a
child’s mother was in good health. Her menarche
5 t6 x) |8 y u% B: o+ xwas at 11 years of age, and her height was at 5 feet
6 W1 @% ]! m# K T( @4 |5 inches. There was no other family history of pre-
3 Q, A6 J$ N7 n: x0 R$ f$ Scocious sexual development in the first-degree rela-
" c* O- {; A7 \# I! Ptives. There were no siblings.* P: v: G9 |5 ?. n/ ^2 c8 X
Physical Examination% q+ o8 `$ }3 ]; [1 s7 d" J
The physical examination revealed a very active,
' j6 F8 I& P2 N( T& I4 a# |playful, and healthy boy. The vital signs documented8 g: K' v1 n4 ]4 s6 W5 C
a blood pressure of 85/50 mm Hg, his length was
9 U2 c# P* p" y90 cm (>97th percentile), and his weight was 14.4 kg4 K# z9 t' \9 }4 O
(also >97th percentile). The observed yearly growth4 i5 ^9 V" w; \1 M
velocity was 30 cm (12 inches). The examination of* R/ Y# g% l g1 ^
the neck revealed no thyroid enlargement.' p, [% B% r) g, ~3 [( a
The genitourinary examination was remarkable for
* Y" S8 j& D- T2 Cenlargement of the penis, with a stretched length of
1 g2 g$ @0 G. o! {5 U8 cm and a width of 2 cm. The glans penis was very well
( v/ F% w2 M+ E3 W) bdeveloped. The pubic hair was Tanner II, mostly around# z0 y( c: ]: V3 D/ n, ]0 i; E
540( F7 z1 _6 L! g0 X6 l( [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 u c8 Y6 I8 Uthe base of the phallus and was dark and curled. The K" ^4 P( j, G: n5 d
testicular volume was prepubertal at 2 mL each.
" ]* |+ O1 ?% w) R. dThe skin was moist and smooth and somewhat7 }$ w2 N& [, W4 I8 m3 S
oily. No axillary hair was noted. There were no6 K' l+ \& y* j* t' x7 k
abnormal skin pigmentations or café-au-lait spots.
) P3 N) S1 z9 n' P) C& sNeurologic evaluation showed deep tendon reflex 2+; l0 Q% ^! g; }3 f) z
bilateral and symmetrical. There was no suggestion
+ J# t/ H& g" i4 @/ Vof papilledema.) l; G. u1 U* @- S: [ }$ H
Laboratory Evaluation
; g: H4 F' x) ^2 i' k8 T+ LThe bone age was consistent with 28 months by
& U, m7 [1 j0 Y7 Q/ @! n3 n/ L. }using the standard of Greulich and Pyle at a chrono-! W0 e2 v7 K! E2 y6 Q* U
logic age of 16 months (advanced).5 Chromosomal9 S. `$ O8 F2 W
karyotype was 46XY. The thyroid function test
" _! ?# O" H1 a: }3 D* \9 lshowed a free T4 of 1.69 ng/dL, and thyroid stimu-9 a7 B" H: }; P# k9 r* m. D
lating hormone level was 1.3 µIU/mL (both normal).; x! G) r/ e' n5 B' [. m/ m& o9 s
The concentrations of serum electrolytes, blood
8 z/ B- B, k w% W2 T" k+ }; kurea nitrogen, creatinine, and calcium all were _2 E; C8 Z' {/ R) [& M
within normal range for his age. The concentration5 T1 w, b& R% }5 |. G8 I
of serum 17-hydroxyprogesterone was 16 ng/dL3 b0 u/ Y4 {3 J+ t7 M- m
(normal, 3 to 90 ng/dL), androstenedione was 20
% c4 T# g! ~9 N2 _& B8 Qng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( K: w! r% e& ~, w* I/ xterone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 r' ]( E0 s9 T; p5 O: xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
3 P# O) _' W% @0 N& ?5 a$ h49ng/dL), 11-desoxycortisol (specific compound S)8 ? g& z( o% I% V) `- B5 X0 z
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
" z) p5 X, o2 X7 c* n! dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
/ _* X, e& X" Z6 r& N9 p5 ]testosterone was 60 ng/dL (normal <3 to 10 ng/dL),& ]' c3 Q- _2 _' |* \
and β-human chorionic gonadotropin was less than3 W/ j' ]& a7 @3 ]/ C- N
5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 D" r0 k) {, u1 H* cstimulating hormone and leuteinizing hormone% u: l" \+ D) O, Z. n2 u
concentrations were less than 0.05 mIU/mL
" ^" ~: F& k" D, z: d, [3 s0 E! b(prepubertal).
! g$ R4 ]6 U( M/ H. |$ fThe parents were notified about the laboratory2 X5 M; N3 s! Q: z# D' V
results and were informed that all of the tests were+ P3 H$ M$ _1 u3 b
normal except the testosterone level was high. The
6 p# h4 D J: L5 f" E, P$ Hfollow-up visit was arranged within a few weeks to7 N# P" O, {$ `9 a% K1 a* j7 v
obtain testicular and abdominal sonograms; how-
4 L+ ~5 l, o7 Q* pever, the family did not return for 4 months./ m8 S! p0 W' |' g" H }, Y
Physical examination at this time revealed that the* o; t- I5 {9 {8 B! |" v: a
child had grown 2.5 cm in 4 months and had gained
4 y9 _- u7 E, w( t2 kg of weight. Physical examination remained
0 X {: ~; v: x) runchanged. Surprisingly, the pubic hair almost com-' O& B2 D) s7 X
pletely disappeared except for a few vellous hairs at- q9 M- z: N1 X, s
the base of the phallus. Testicular volume was still 22 q& ?. V/ B& q
mL, and the size of the penis remained unchanged.
# z3 C. R* v' _% R) N kThe mother also said that the boy was no longer hav-( X, @ F' S5 s7 V
ing frequent erections.
( B& Z& d5 r* O" FBoth parents were again questioned about use of
( w' ]: t8 j0 R% o N; |3 f/ O0 f$ Yany ointment/creams that they may have applied to& w. g' `8 C6 P) \( G; E1 P3 \
the child’s skin. This time the father admitted the
0 s& d" n7 K/ x' hTopical Testosterone Exposure / Bhowmick et al 541
9 G* K: J" F2 h$ \0 X$ O/ Kuse of testosterone gel twice daily that he was apply-
& ~, b4 V- `# P9 N3 ^9 Sing over his own shoulders, chest, and back area for
/ j+ A2 F+ w& x+ U8 Ua year. The father also revealed he was embarrassed# B4 o6 x7 o0 \" r9 J$ Z3 `: P* f
to disclose that he was using a testosterone gel pre-; u _7 h$ M& \+ c, Q/ `, N
scribed by his family physician for decreased libido
" a4 ?' r/ w' i9 Hsecondary to depression.$ b( ]& v7 F) `% n I" r% S5 P
The child slept in the same bed with parents.
, B. ^1 u2 U, T7 X$ AThe father would hug the baby and hold him on his/ f5 a4 U) @/ Y) R. A& t6 ?
chest for a considerable period of time, causing sig-
) c0 u( k3 ^4 w" k1 e, jnificant bare skin contact between baby and father.- ^0 S; T' R+ V* U: t
The father also admitted that after the phone call,0 b9 w+ q. L% J( H
when he learned the testosterone level in the baby
8 b2 N h( C2 y/ S x" a. owas high, he then read the product information
. L4 ~: W8 C' i4 ?* n( j" f. fpacket and concluded that it was most likely the rea-
% f9 g; N; u9 L' {, Qson for the child’s virilization. At that time, they# x# t5 o/ H) n' p% |
decided to put the baby in a separate bed, and the2 |, E+ |; Q! Z0 \& b# u- M) x
father was not hugging him with bare skin and had
. \) E- m# p* S; ~6 Ubeen using protective clothing. A repeat testosterone
: _* f% M* C- C6 v1 ]7 s# Xtest was ordered, but the family did not go to the
: S" _0 @ U: \) Blaboratory to obtain the test.! O4 R8 R8 I- C, r. _. D( R
Discussion
$ q) B1 P( S) |( b0 aPrecocious puberty in boys is defined as secondary; k0 t, N5 |. q& H3 F
sexual development before 9 years of age.1,4
% {. i. u' D2 H8 ?! S4 [8 z! n) ^Precocious puberty is termed as central (true) when" T0 T# N$ `6 u+ H5 [4 u% e
it is caused by the premature activation of hypo-0 S5 A n( E$ P$ r6 q( A& D/ ^' i
thalamic pituitary gonadal axis. CPP is more com-
/ V$ d# t+ Q( Kmon in girls than in boys.1,3 Most boys with CPP; b; j# U1 M, \- _7 \7 g1 p
may have a central nervous system lesion that is9 j, p# Y( i2 b7 J/ v
responsible for the early activation of the hypothal-& o! o) Q& `. b* f
amic pituitary gonadal axis.1-3 Thus, greater empha-
7 V! ?. e. h* T7 Y. ^/ R ?- Gsis has been given to neuroradiologic imaging in
. p1 |- E- l) `7 S. X% pboys with precocious puberty. In addition to viril-
. S; Y6 n% z8 | E, p: }# ]ization, the clinical hallmark of CPP is the symmet-- q* p" x9 C h2 m& N
rical testicular growth secondary to stimulation by L }4 y2 x8 F8 t
gonadotropins.1,3
) N; S# r/ }) Z8 d7 L/ ^Gonadotropin-independent peripheral preco-/ k1 z! t& O" e1 ]9 [6 X
cious puberty in boys also results from inappropriate
$ j9 C" P/ ^7 |0 q: xandrogenic stimulation from either endogenous or% w8 J8 }# l. [; B- T8 i2 `
exogenous sources, nonpituitary gonadotropin stim-
% U; n K3 |4 s7 Sulation, and rare activating mutations.3 Virilizing
+ W5 H: [3 K' r2 h _( ^9 vcongenital adrenal hyperplasia producing excessive$ A$ Y( [, T7 Y* @, D
adrenal androgens is a common cause of precocious
" L7 P |5 G# @% I! f6 |puberty in boys.3,4
0 ?: F! v8 X7 a1 O# ~& T; cThe most common form of congenital adrenal- E7 a! q; l. g
hyperplasia is the 21-hydroxylase enzyme deficiency./ y; y$ w7 O/ H/ A- u" | Z* w/ r$ V
The 11-β hydroxylase deficiency may also result in
: q, v/ m) d9 l+ ?: ]excessive adrenal androgen production, and rarely,
. @" K; Q" G) ^1 g9 K# c* e) Oan adrenal tumor may also cause adrenal androgen
& B4 f) w* b i3 {" Fexcess.1,3
- Y! q! |/ ~$ ~; p" J( Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 h6 n n! N. z7 \4 d. R& k( U9 N
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! U! J7 T( t' m2 _6 u# a+ V
A unique entity of male-limited gonadotropin-
; g& \, p8 W2 M2 Lindependent precocious puberty, which is also known, k1 O7 m% I# p( L! k
as testotoxicosis, may cause precocious puberty at a
9 r, o+ a; A* @5 ]very young age. The physical findings in these boys
! [/ ]# j% E2 F2 ~0 t7 s+ S: M" swith this disorder are full pubertal development,/ V& N* O% k) T
including bilateral testicular growth, similar to boys/ S9 ]1 }: b8 J
with CPP. The gonadotropin levels in this disorder6 Y; f: F0 q; l( |! i
are suppressed to prepubertal levels and do not show
( O# K5 z3 t% V/ C! \% \* mpubertal response of gonadotropin after gonadotropin-* A& A2 H# S- J! K3 I8 p Q1 o
releasing hormone stimulation. This is a sex-linked
8 s$ p3 Y# S5 J6 F! P" ^autosomal dominant disorder that affects only
, f3 o0 ?( z, P" zmales; therefore, other male members of the family
. r; i& E' J) |* }% S* B- l' a; I+ Kmay have similar precocious puberty.3
4 D7 }( u7 U h! V- E1 V6 `+ `In our patient, physical examination was incon-# x9 k5 p( B2 x$ U H
sistent with true precocious puberty since his testi-' Z5 J9 r6 ?. Z2 p* d
cles were prepubertal in size. However, testotoxicosis
) w0 D4 }/ k9 ~7 Y& }2 i: owas in the differential diagnosis because his father* a3 g! x4 g" g$ y5 b2 K
started puberty somewhat early, and occasionally," J* N1 ~* Z% r e' w
testicular enlargement is not that evident in the
, N0 @3 @- ^- I! A/ v2 V- ~- Wbeginning of this process.1 In the absence of a neg-
1 C: S% S0 Z3 m% G- c( u4 E7 cative initial history of androgen exposure, our
7 {& z+ B% r, M/ b" z, z+ s! Abiggest concern was virilizing adrenal hyperplasia,. Y/ w- X/ a2 N
either 21-hydroxylase deficiency or 11-β hydroxylase5 _+ n! [! E# t4 B
deficiency. Those diagnoses were excluded by find-
3 f$ C$ I3 a% i0 l4 xing the normal level of adrenal steroids.- C: i4 R! Y- ` M
The diagnosis of exogenous androgens was strongly) x! Q6 y6 o0 V% @
suspected in a follow-up visit after 4 months because
1 n( P% l M6 r3 Q+ k- Kthe physical examination revealed the complete disap-
8 p. T- L; ^2 y$ h! dpearance of pubic hair, normal growth velocity, and
& k4 [" _# g2 V+ p/ udecreased erections. The father admitted using a testos-; o. p. p* ]! s
terone gel, which he concealed at first visit. He was
: E# V8 K" t8 O3 a: n( uusing it rather frequently, twice a day. The Physicians’( X/ I4 P4 o8 c) N
Desk Reference, or package insert of this product, gel or: I) b Q' z8 ^2 H: ]! h& `$ D6 `
cream, cautions about dermal testosterone transfer to
1 m! D% s# w0 gunprotected females through direct skin exposure.
7 m$ T6 ~- j+ t' e8 o, t( ~Serum testosterone level was found to be 2 times the
) p2 e F% m0 h( Z o" Wbaseline value in those females who were exposed to2 z0 a% O" h& s" b1 W/ D0 {
even 15 minutes of direct skin contact with their male+ \* E! W6 `( @# T8 M
partners.6 However, when a shirt covered the applica-
: i8 j7 I+ @- b2 vtion site, this testosterone transfer was prevented.- Z7 H7 _- y! v2 h6 u
Our patient’s testosterone level was 60 ng/mL,, Y3 z1 d! c4 d, L
which was clearly high. Some studies suggest that, V" N4 b) l* z+ b
dermal conversion of testosterone to dihydrotestos-7 u7 x/ F$ Q4 C K
terone, which is a more potent metabolite, is more1 R1 j1 C. \, ^$ E
active in young children exposed to testosterone) G7 ? l! T/ s4 m( @0 ^4 R
exogenously7; however, we did not measure a dihy-
9 T9 a6 x% F% ] h4 N$ L( y" f7 p0 Bdrotestosterone level in our patient. In addition to$ }+ c! k' o/ R4 @" A" [1 e
virilization, exposure to exogenous testosterone in5 I. l0 V1 h5 M4 ^ Y
children results in an increase in growth velocity and
8 _) G0 @' S" i9 j9 l0 Vadvanced bone age, as seen in our patient." s( _8 b7 j7 n0 M" c) `- {: I
The long-term effect of androgen exposure during
. n5 `/ ^! h0 S. A6 ~' ?early childhood on pubertal development and final3 Y& m$ |: G8 {
adult height are not fully known and always remain
! C2 E5 t* B& Xa concern. Children treated with short-term testos-: _9 r- D* T. J( \9 T; f8 z
terone injection or topical androgen may exhibit some
% {! w: v r9 R( W. o3 H! l3 o1 Cacceleration of the skeletal maturation; however, after& n6 C) g! S/ x1 j3 ^: o
cessation of treatment, the rate of bone maturation( h! T% B# v) d3 e8 F
decelerates and gradually returns to normal.8,94 R! ?7 o) G" }8 h5 o
There are conflicting reports and controversy
$ @3 t, x( p: ]: w. r! }over the effect of early androgen exposure on adult
2 e' G1 G% b' u9 v6 _; k: r3 [! npenile length.10,11 Some reports suggest subnormal
+ v. }" k; G. oadult penile length, apparently because of downreg-) v0 ^0 i2 u1 M* { ~
ulation of androgen receptor number.10,12 However,+ }, Q2 ^+ b# u' \# v
Sutherland et al13 did not find a correlation between) d1 F' T8 e. u% u
childhood testosterone exposure and reduced adult
; T1 k$ }0 }' ^0 Rpenile length in clinical studies.) [ G! Q. |5 G# ]2 o4 T& M
Nonetheless, we do not believe our patient is0 V- a: s. t9 a6 q
going to experience any of the untoward effects from
# h9 `2 H- ?" z3 L* |testosterone exposure as mentioned earlier because2 o* i, ]& `+ F+ x7 W7 w o, B
the exposure was not for a prolonged period of time.
3 q% X) {: |$ S5 Y- W& UAlthough the bone age was advanced at the time of
) _7 O8 h& R, w8 C3 e; |diagnosis, the child had a normal growth velocity at
! l1 S3 p1 \# {- G: zthe follow-up visit. It is hoped that his final adult2 m& {2 L! X: D6 M' [$ A: T7 e
height will not be affected.
/ E) t8 o6 B( `; y, ZAlthough rarely reported, the widespread avail-
. H; Q0 ^ ^& Wability of androgen products in our society may
3 Q4 H" {2 U& V7 n' P1 Z+ C5 o7 `6 h" Q: vindeed cause more virilization in male or female
. c3 z% Q+ T3 ]. J$ b6 S9 _children than one would realize. Exposure to andro-4 ~- Y; ]1 B: ?+ ^5 _ G% h. G
gen products must be considered and specific ques-
5 E8 A8 z6 B* `) Z9 P9 J% {/ Ptioning about the use of a testosterone product or$ p, N; h& H. Z; W# R1 h
gel should be asked of the family members during
4 v. X9 l, \4 k6 I0 k6 J# \the evaluation of any children who present with vir-- V I8 S4 B( i6 r# k' n" N
ilization or peripheral precocious puberty. The diag-
6 \$ u8 _, k- n7 ?( E6 Vnosis can be established by just a few tests and by/ \* F3 A' C$ T: [8 P! Y
appropriate history. The inability to obtain such a7 }' B: m! m8 b
history, or failure to ask the specific questions, may3 I. ^+ C( f5 R3 \
result in extensive, unnecessary, and expensive
+ b# B5 I, K( l( M- F6 binvestigation. The primary care physician should be
4 m" o+ N& F$ D6 jaware of this fact, because most of these children
* P$ N' I( H4 ~6 \7 R2 z, @may initially present in their practice. The Physicians’
3 v% {/ H! o3 N0 W% E' h2 Q" eDesk Reference and package insert should also put a# R8 u1 J: w+ d) k1 C0 Y4 K
warning about the virilizing effect on a male or
6 p$ L. l, P# l6 i5 `( rfemale child who might come in contact with some-( \* q+ W3 b6 p4 R5 a
one using any of these products.3 N0 q, l5 l: F- u
References' T; g6 }" l6 }$ ^4 J- f$ u9 D
1. Styne DM. The testes: disorder of sexual differentiation( |4 t. N) F$ ?: O5 }! a
and puberty in the male. In: Sperling MA, ed. Pediatric
0 i$ T, Z @. z* v" xEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 m& y- A6 a7 Y" A( `2002: 565-628.
% d+ @( `* Z0 ^4 G2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious7 k/ b# c4 ]: L" c% I/ t9 a
puberty in children with tumours of the suprasellar pineal |
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