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Sexual Precocity in a 16-Month-Old- v& U. @% Q0 I# Q; ]& ?" Q
Boy Induced by Indirect Topical
9 S: j% q/ G0 s% K8 _Exposure to Testosterone
1 Z0 w( y" g7 k- F( y3 Q; lSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; o! C) h3 M# V1 j5 ~5 N, vand Kenneth R. Rettig, MD1. a1 e: N9 m# r) J" d0 Y6 v
Clinical Pediatrics
6 F) t0 E* j# i2 w/ L5 l& L) NVolume 46 Number 68 K& b, q& s9 j. e* ? G2 i3 P
July 2007 540-5430 ~4 Z1 `8 x) u0 l9 j
© 2007 Sage Publications
* l& [; J$ Y& A( C5 R6 _- O8 O10.1177/0009922806296651/ @1 R- _) x9 G, O* t! _& u
http://clp.sagepub.com
. F3 N! R: z* _; n, `6 e ?& G$ Jhosted at- ~6 j# p9 k, j
http://online.sagepub.com
X8 x( E" q, r! y4 l1 uPrecocious puberty in boys, central or peripheral,/ O0 L# i% i( E0 [; j- j
is a significant concern for physicians. Central9 k, H. C5 E1 Z/ ^; V
precocious puberty (CPP), which is mediated
8 W2 ]: b# f) \" C0 Q! ithrough the hypothalamic pituitary gonadal axis, has# e% v5 m, Q# N- j: I0 K5 d2 x
a higher incidence of organic central nervous system
: a! M$ \# L* S8 l+ ]lesions in boys.1,2 Virilization in boys, as manifested: m3 C1 d( Q; Y2 m6 i' G {$ y
by enlargement of the penis, development of pubic
2 `1 o8 {! x J/ ^hair, and facial acne without enlargement of testi-
8 W" s( V' a) ?/ Ocles, suggests peripheral or pseudopuberty.1-3 We) W' j- a: ^3 R+ o5 \) }
report a 16-month-old boy who presented with the; e) z Y# a! P; m) m9 P1 k! `( }2 {* V
enlargement of the phallus and pubic hair develop-
V: I7 G0 o7 Xment without testicular enlargement, which was due h q: V) U6 V1 k
to the unintentional exposure to androgen gel used by( v( {2 W2 N0 ^# |1 y: d. ]
the father. The family initially concealed this infor-
& E/ B+ a( X3 V: b5 Ymation, resulting in an extensive work-up for this
a7 t, A9 ~$ a7 z; \child. Given the widespread and easy availability of
/ `( P0 D4 K$ {; gtestosterone gel and cream, we believe this is proba-
/ w8 ^5 p2 D7 h+ q: ybly more common than the rare case report in the
0 U. L3 D. H- Aliterature.4# h; Z, N, ]( ]- l8 \* j
Patient Report
; ]! A3 D9 `7 n& F( @: g! k2 {" nA 16-month-old white child was referred to the$ u- O% G& e+ B) Z/ Q
endocrine clinic by his pediatrician with the concern
6 E' k q( }7 `. u; @' gof early sexual development. His mother noticed) A4 v8 }, N: ?( f
light colored pubic hair development when he was+ q7 g$ N! v3 F( G# F
From the 1Division of Pediatric Endocrinology, 2University of
K4 ?, w- |; U2 iSouth Alabama Medical Center, Mobile, Alabama.2 d( B3 u' D+ {! m y; j
Address correspondence to: Samar K. Bhowmick, MD, FACE,
+ I. T7 r4 c% @- W; ]Professor of Pediatrics, University of South Alabama, College of+ ~. s/ ?3 F- S$ p7 V) y, c; |' D
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
9 s; m: C* _) i1 U) O( x: pe-mail: [email protected]. \) l* z8 Q. y, r" e+ D
about 6 to 7 months old, which progressively became
1 P6 ]7 k9 q* a# z' A- Q5 M5 sdarker. She was also concerned about the enlarge-
7 I' ]1 }5 n2 v8 rment of his penis and frequent erections. The child+ n* O* U' z4 _8 K* |6 n Y3 {4 }
was the product of a full-term normal delivery, with/ F9 G" N- G! d# D5 a8 Y
a birth weight of 7 lb 14 oz, and birth length of
6 g9 @3 B1 n3 V3 x" [ j20 inches. He was breast-fed throughout the first year' D8 N! _& j/ [8 {
of life and was still receiving breast milk along with
) N( d8 Z7 H) a* {( jsolid food. He had no hospitalizations or surgery,
/ r$ i5 O& r B% u8 P3 `. qand his psychosocial and psychomotor development' }% a1 G/ Q. ~" u, a1 i( b
was age appropriate.
* x1 e, k1 H4 k" j. R, X( ^The family history was remarkable for the father,
T; R8 k9 e3 y$ a& Pwho was diagnosed with hypothyroidism at age 16,
$ ]( n) k# e( w8 Y# pwhich was treated with thyroxine. The father’s
7 s5 a& B+ B% I$ S. t X/ _height was 6 feet, and he went through a somewhat$ q* j9 z4 Z8 R( G' [
early puberty and had stopped growing by age 14.6 K6 `- D; M. P0 ^& i8 g
The father denied taking any other medication. The
, ~7 \' ]0 D' _% ^child’s mother was in good health. Her menarche) i( t" L! B( }
was at 11 years of age, and her height was at 5 feet0 B* W5 O, \# J. j+ d6 N
5 inches. There was no other family history of pre-2 ~, I8 V b) _: l1 ?6 {
cocious sexual development in the first-degree rela-# d/ u. G2 }; x6 `
tives. There were no siblings.5 _2 s2 H* ]1 F
Physical Examination
8 D! ?! B3 t% _ X% h6 n* K: pThe physical examination revealed a very active,2 ^4 C* J- v z/ o
playful, and healthy boy. The vital signs documented
0 H1 v+ e7 ], z0 t/ u1 o: va blood pressure of 85/50 mm Hg, his length was
y9 T0 G; q/ z. {. ~5 K w- ~& V/ |90 cm (>97th percentile), and his weight was 14.4 kg
; y1 Q1 g' e; `* m(also >97th percentile). The observed yearly growth
, U% N, @. @; _' T8 Dvelocity was 30 cm (12 inches). The examination of
* b, \* \8 s* Sthe neck revealed no thyroid enlargement.
0 G# | y a; { i. Q/ yThe genitourinary examination was remarkable for
& E" Z& B0 g3 S6 s: ~enlargement of the penis, with a stretched length of/ Q6 }$ ]+ y7 x9 I, q& q, @
8 cm and a width of 2 cm. The glans penis was very well
+ [/ ?% i( d% M& ^) o6 Cdeveloped. The pubic hair was Tanner II, mostly around
4 |4 e9 [( L P$ [" w) P540
' _, v3 z+ }/ I! F5 ]at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) j a' e" m, r
the base of the phallus and was dark and curled. The
* ]* k5 K7 q: h! itesticular volume was prepubertal at 2 mL each.
: ]: U' Z0 M7 R1 ?The skin was moist and smooth and somewhat
9 f; l' `: L* W* _ q# g9 c5 ]; loily. No axillary hair was noted. There were no3 b5 C2 R& i/ K0 n8 h1 j
abnormal skin pigmentations or café-au-lait spots.9 i/ S/ D' M: p: E! Z( b
Neurologic evaluation showed deep tendon reflex 2+
v# a* R1 X+ B' [bilateral and symmetrical. There was no suggestion
6 V$ i# k9 J P3 P; O2 c6 J# ~8 lof papilledema./ ?) X* G1 S$ d2 x
Laboratory Evaluation
) }' G$ q! S) q$ a( F- F+ gThe bone age was consistent with 28 months by* i1 W0 O, S1 T
using the standard of Greulich and Pyle at a chrono-
; Y6 U$ }% p H0 G3 b/ Ologic age of 16 months (advanced).5 Chromosomal+ q& Z8 u& A# d
karyotype was 46XY. The thyroid function test
N, S! x, a0 L- [: cshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
* l2 J; {, h+ L% W0 C2 X4 Rlating hormone level was 1.3 µIU/mL (both normal).
6 t* D- P" F! a+ W# j4 G' J$ FThe concentrations of serum electrolytes, blood) k# \9 P% U$ [: U9 w5 L+ u0 ?
urea nitrogen, creatinine, and calcium all were
" s5 T+ \$ H8 Z9 O# Xwithin normal range for his age. The concentration
: ]$ F3 z$ n) g$ Y( m i* @# Lof serum 17-hydroxyprogesterone was 16 ng/dL4 i2 M1 a% n A$ h
(normal, 3 to 90 ng/dL), androstenedione was 20
; ]3 d. H* ?/ @, F/ Q/ jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: e- C/ R8 {0 t/ K, E
terone was 38 ng/dL (normal, 50 to 760 ng/dL),2 f: x7 C# Y. |, _, A, U" p
desoxycorticosterone was 4.3 ng/dL (normal, 7 to! }; z7 s) z4 K) R! E+ I
49ng/dL), 11-desoxycortisol (specific compound S)8 w) b% w8 D0 z, k: c' t
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ ]% H( f3 F t# O% etisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# p! Z" m4 d1 t9 N7 {
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ A. m! y5 [' {/ K2 Q# C" band β-human chorionic gonadotropin was less than
4 p/ ^6 U5 S& O9 q4 ~2 n5 mIU/mL (normal <5 mIU/mL). Serum follicular
# i; E; w; n% ]+ ~6 wstimulating hormone and leuteinizing hormone! L, D1 z6 d6 x
concentrations were less than 0.05 mIU/mL
" D! ]1 ]% W; w3 W(prepubertal).3 a9 W: U1 O# {1 b, O) w% v
The parents were notified about the laboratory1 x9 W/ W6 X% i
results and were informed that all of the tests were& n. c" Q) g) z D" V/ Y7 O, N
normal except the testosterone level was high. The
* K/ }" U: d- F/ A+ Sfollow-up visit was arranged within a few weeks to' X$ ~) Z! A4 d- Z
obtain testicular and abdominal sonograms; how-
8 H0 [/ j' g3 D; e4 B$ }/ Vever, the family did not return for 4 months.- A( @, O0 U8 u Y. I9 W* H( S! X9 |
Physical examination at this time revealed that the$ e9 I k3 p+ S0 B
child had grown 2.5 cm in 4 months and had gained c! M: [! o" Q
2 kg of weight. Physical examination remained5 I# L* R- _! C/ c; P
unchanged. Surprisingly, the pubic hair almost com-
# d# V& a2 c& h* Q7 @6 W" ]; Ipletely disappeared except for a few vellous hairs at
9 D; X* u- v6 G& Z* wthe base of the phallus. Testicular volume was still 2+ g* z# N/ j9 K) I; I; |
mL, and the size of the penis remained unchanged.) \ x' Q4 |2 {1 |
The mother also said that the boy was no longer hav-/ r7 j: }" e: U" K
ing frequent erections.
% W! v4 h) U uBoth parents were again questioned about use of
; I8 j* @# T T7 L' T% Fany ointment/creams that they may have applied to+ f% E2 b3 f# ^! y7 l, \- j
the child’s skin. This time the father admitted the
2 \3 o5 v$ k( e0 g+ x# oTopical Testosterone Exposure / Bhowmick et al 5411 j9 }) N: _" o
use of testosterone gel twice daily that he was apply-0 N( H' z! q! g! F0 I- F0 n& o
ing over his own shoulders, chest, and back area for
$ n& P- k! x4 f* B# h0 {3 Qa year. The father also revealed he was embarrassed1 a) M$ \2 D: P% k8 C$ z
to disclose that he was using a testosterone gel pre-6 t3 c0 s9 h; w' b$ q. E
scribed by his family physician for decreased libido3 R& ]: _& l- ?' ?6 S+ Z4 |. v% N7 O
secondary to depression.
- ?! x6 t; ?8 ^5 UThe child slept in the same bed with parents., i/ ?4 w* k y* O+ n) \5 v8 K
The father would hug the baby and hold him on his
! ?9 U& e: c; \6 Wchest for a considerable period of time, causing sig-8 N$ @1 T/ j3 e$ b7 b7 ?; m$ T, c- [ n) S
nificant bare skin contact between baby and father.; `' Y7 o D/ p& C
The father also admitted that after the phone call,
5 {+ n9 D( Q$ }2 k& ywhen he learned the testosterone level in the baby
* K6 a8 E' s" N% bwas high, he then read the product information4 w7 ]- `* @- ^2 K% u# N% G0 _
packet and concluded that it was most likely the rea-
( `8 \! K3 l1 c1 Mson for the child’s virilization. At that time, they
8 w% V4 K! e) _9 ydecided to put the baby in a separate bed, and the
0 h9 s x9 j* I/ C5 [* ~father was not hugging him with bare skin and had
, K3 {6 I, |$ P% ybeen using protective clothing. A repeat testosterone; O' a! {( g% G7 |4 z; n
test was ordered, but the family did not go to the7 e* [; T8 Q" n v6 F3 u1 i
laboratory to obtain the test.
. \. C2 r5 R4 |4 ?Discussion
Z, I4 i6 M5 B0 c4 FPrecocious puberty in boys is defined as secondary
# N0 h0 }+ j6 `8 N% C- a, Y6 gsexual development before 9 years of age.1,40 r2 b+ I$ a! A J# c7 G* v; g* ~) y$ I7 t
Precocious puberty is termed as central (true) when
- R6 y4 N2 @. t* e6 m+ Kit is caused by the premature activation of hypo-/ Q6 J B P2 t
thalamic pituitary gonadal axis. CPP is more com-
% n8 t4 X) r7 K5 Hmon in girls than in boys.1,3 Most boys with CPP' h. ]! ^ N( K$ B
may have a central nervous system lesion that is/ }- [1 ~$ P1 V4 h8 i0 {0 j. q
responsible for the early activation of the hypothal-
4 O5 i& f9 E6 V4 O# H1 Uamic pituitary gonadal axis.1-3 Thus, greater empha-
3 y/ j! ?, n5 C$ X+ dsis has been given to neuroradiologic imaging in& G1 p3 ^1 M& z
boys with precocious puberty. In addition to viril-
( q" z5 D! H* U6 `$ i- Lization, the clinical hallmark of CPP is the symmet-
9 d9 |- R" v# g7 ^rical testicular growth secondary to stimulation by
$ Q0 c, `- q: I h' @( rgonadotropins.1,3
: v: J1 C1 r8 TGonadotropin-independent peripheral preco-
* g, X4 n, t1 H: `: Fcious puberty in boys also results from inappropriate) l" z/ x" o! d& Z8 A' p$ P6 B0 D
androgenic stimulation from either endogenous or
$ N- i, G5 E& f/ gexogenous sources, nonpituitary gonadotropin stim-
: f5 \+ @8 g" nulation, and rare activating mutations.3 Virilizing
3 e' n# R# n# ]: z. icongenital adrenal hyperplasia producing excessive z( v. p. W; E0 M) \. `" X
adrenal androgens is a common cause of precocious7 v$ N" r" y! v$ {+ L5 s2 I% S
puberty in boys.3,4+ @: P) _9 o+ y& @3 t
The most common form of congenital adrenal
8 ?/ t/ h( L( q! N+ chyperplasia is the 21-hydroxylase enzyme deficiency.. R1 E9 X# g2 r% m# m# h% ]
The 11-β hydroxylase deficiency may also result in, G8 x p) a/ Q* p Z
excessive adrenal androgen production, and rarely,/ L: M" c5 U) |7 f
an adrenal tumor may also cause adrenal androgen& l" g- O [& L' r
excess.1,3. ?( i U' T: g& _1 l
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" X2 [ j: u- O0 d7 Z6 O
542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 O O( r3 k; b5 b% f! i# p
A unique entity of male-limited gonadotropin-, c) E) V5 R6 j8 T7 F" u3 l
independent precocious puberty, which is also known
% L. I7 H. l1 ias testotoxicosis, may cause precocious puberty at a, d9 |9 r, q0 q) U$ @0 x8 x; y$ W
very young age. The physical findings in these boys
; \" ?5 ~4 B2 B6 @3 I q+ R# ]; iwith this disorder are full pubertal development,
' L5 ]9 P/ v4 I! k9 ]including bilateral testicular growth, similar to boys) i) o( M) d4 O3 j
with CPP. The gonadotropin levels in this disorder3 G/ ?7 ]0 ~6 a* ?9 `4 h2 F
are suppressed to prepubertal levels and do not show
' b% R p3 H4 ?& w% }* Cpubertal response of gonadotropin after gonadotropin-
} `) j! y* Y$ x& P/ G0 L) Zreleasing hormone stimulation. This is a sex-linked' }* f" z" K8 |) q* z% i9 W
autosomal dominant disorder that affects only
4 _6 M1 e! {8 emales; therefore, other male members of the family
3 E! T! I& T% i5 ]. dmay have similar precocious puberty.3
- R' ~) _6 D, W) ]$ L, y: vIn our patient, physical examination was incon-
4 |4 v0 J8 e# y( }& _3 ssistent with true precocious puberty since his testi-0 T/ [% Y0 C+ G/ A1 h
cles were prepubertal in size. However, testotoxicosis
( R+ h- r A. P2 P, Hwas in the differential diagnosis because his father
; r% l, g8 x; @7 u- ostarted puberty somewhat early, and occasionally,
. v; J1 ]. n' b4 c1 U$ s* z( Stesticular enlargement is not that evident in the
' [0 H) a* D7 u" I# d1 Ibeginning of this process.1 In the absence of a neg-
5 ?$ h: F2 C+ M, n' iative initial history of androgen exposure, our
% A6 x- H3 i/ I! Cbiggest concern was virilizing adrenal hyperplasia,
; Q: j U3 ~5 ^% R$ _either 21-hydroxylase deficiency or 11-β hydroxylase
) p7 U! y$ k* d2 u1 I- E' b$ G( Q. |) Qdeficiency. Those diagnoses were excluded by find-/ h) h# J$ g5 t3 t2 c
ing the normal level of adrenal steroids.
1 |2 T. D4 a; q: wThe diagnosis of exogenous androgens was strongly4 ^( t, `# ^0 k+ }- o. H4 S
suspected in a follow-up visit after 4 months because
3 H7 _* T' K$ |+ w2 p7 X6 D7 Ithe physical examination revealed the complete disap-
/ q: }; B: M% n* Y, M/ `4 Zpearance of pubic hair, normal growth velocity, and
+ W. I, s8 t4 Z, ?decreased erections. The father admitted using a testos-
. P! U. D6 s& E& Yterone gel, which he concealed at first visit. He was* o. @3 F- {4 }0 k* L- u
using it rather frequently, twice a day. The Physicians’
% p, [7 [! n$ ?3 WDesk Reference, or package insert of this product, gel or- C+ x! ~- C; O e3 ]- z/ y
cream, cautions about dermal testosterone transfer to; r, M9 d% |2 W6 e( T: P
unprotected females through direct skin exposure.8 h+ }5 R8 ?6 t" p: J
Serum testosterone level was found to be 2 times the
* h) h2 |, H# ]. mbaseline value in those females who were exposed to
% j- L' f" q' xeven 15 minutes of direct skin contact with their male
- K" d, s' Y7 }; s& y9 N& [partners.6 However, when a shirt covered the applica-5 w' D* P" P: e/ i7 H( I" b% I
tion site, this testosterone transfer was prevented." l' E* z5 e0 k9 U) H
Our patient’s testosterone level was 60 ng/mL,9 M, w7 f8 w0 S# w' L1 h! L
which was clearly high. Some studies suggest that
6 l- Y. O( ~/ T% G1 b. k" xdermal conversion of testosterone to dihydrotestos-) s- }- Z. E0 L5 ]# ?, A$ [: v
terone, which is a more potent metabolite, is more6 O) w% p0 {" w" ]7 {
active in young children exposed to testosterone
4 f: [8 |; H4 t+ N7 eexogenously7; however, we did not measure a dihy-
7 U; c+ m* ?8 M+ K7 u9 x% B6 {drotestosterone level in our patient. In addition to1 R! H% D& _$ r+ V# ~% U9 Y5 U
virilization, exposure to exogenous testosterone in4 B. P4 Q9 I( p9 ]# o
children results in an increase in growth velocity and% m' T3 @- O3 f6 Q8 N9 H
advanced bone age, as seen in our patient.' J( ]" E5 n" O" D
The long-term effect of androgen exposure during/ a) \0 u. q/ Q4 f
early childhood on pubertal development and final
9 F( v; e. {) {' ?; m6 s- D' u( ^adult height are not fully known and always remain
+ B2 U- t, D$ z E. Y9 Ya concern. Children treated with short-term testos- I) D, n7 l6 l3 |# |, o0 p8 B$ n
terone injection or topical androgen may exhibit some7 r/ _3 |& h- y9 p+ x2 j
acceleration of the skeletal maturation; however, after/ f; r, ]. A, }6 K$ `
cessation of treatment, the rate of bone maturation
; S6 k$ m" j' Edecelerates and gradually returns to normal.8,9
* `$ r3 F3 m/ r0 P5 ZThere are conflicting reports and controversy
! X2 W! }2 v6 R+ V" X# @2 H7 ?) d/ {: kover the effect of early androgen exposure on adult
' d' r1 L# E; B6 gpenile length.10,11 Some reports suggest subnormal4 B- M" r( k3 @& D' M
adult penile length, apparently because of downreg-
, ]& }2 |4 d# O4 A0 x) fulation of androgen receptor number.10,12 However,
1 ?( R. r6 h0 J: u! A' BSutherland et al13 did not find a correlation between, C; M' w. u- b6 @) }6 c1 z! ], U8 Z/ d
childhood testosterone exposure and reduced adult
; |6 E) Y4 ]5 r7 g' L# Mpenile length in clinical studies.
* Z4 X* V! p7 z, eNonetheless, we do not believe our patient is
6 Y7 }& ]3 j* @. o4 Igoing to experience any of the untoward effects from* r1 O4 F. C8 ~$ T q
testosterone exposure as mentioned earlier because
8 B) j% @ t4 \, Ithe exposure was not for a prolonged period of time.
: J- o2 ^/ D4 L5 p* A8 G7 ZAlthough the bone age was advanced at the time of
/ }, u- H+ E7 q, c) o. t9 C0 {6 `diagnosis, the child had a normal growth velocity at# l* q [; l; a" }! B5 N( {
the follow-up visit. It is hoped that his final adult
8 g7 I" `% y/ d9 y, Dheight will not be affected.0 o3 x4 a6 V4 u7 y' ~6 |6 v
Although rarely reported, the widespread avail-
( G9 u" W+ b6 Jability of androgen products in our society may5 ~" {3 ^4 T, w9 P" L
indeed cause more virilization in male or female& w' f+ z/ p0 D( c0 k. L$ U0 K
children than one would realize. Exposure to andro-3 I! s6 i% s- {; y6 |$ O
gen products must be considered and specific ques-
% e, r. ]8 ~- ]/ w ftioning about the use of a testosterone product or$ r8 u9 I: _8 v2 @2 y
gel should be asked of the family members during: Z- r1 g3 a% l8 j* |: q/ N1 N* B
the evaluation of any children who present with vir-% W! R; g& ?9 Z3 M0 [' P' H) s1 L
ilization or peripheral precocious puberty. The diag-! K. |) E1 R8 V, ~9 f0 b$ r
nosis can be established by just a few tests and by4 a' O$ ~( W: A
appropriate history. The inability to obtain such a' G4 S7 f+ ]5 j1 l4 P
history, or failure to ask the specific questions, may
: W: T* c. o+ tresult in extensive, unnecessary, and expensive
# D" D( N0 P$ l, V- E' X& qinvestigation. The primary care physician should be
* _$ y" t+ E7 w1 I7 Qaware of this fact, because most of these children& J: L- V# c4 W# _5 c
may initially present in their practice. The Physicians’& i5 N4 Y1 N' ?7 |" n" ^1 n
Desk Reference and package insert should also put a
* o* b. w- u8 ^% hwarning about the virilizing effect on a male or
6 b8 L7 q/ U: ]/ N, d, H4 C6 q* u9 Vfemale child who might come in contact with some-
+ W- k2 R0 F' J4 J* H2 ~/ oone using any of these products.; G' u4 x* t7 k% Y: R
References; S* Q3 U8 Z4 Y
1. Styne DM. The testes: disorder of sexual differentiation6 C5 v. l: J) l6 f
and puberty in the male. In: Sperling MA, ed. Pediatric
; g1 v4 }7 X, @3 lEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 o# V) V2 ~3 F1 R. X- S. n2002: 565-628.
! I8 @) o3 q0 v2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; t8 v2 W' d7 {7 [
puberty in children with tumours of the suprasellar pineal |
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