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Sexual Precocity in a 16-Month-Old
1 c& Q; p4 Q. U) j' ZBoy Induced by Indirect Topical5 W$ y c. [+ @% p
Exposure to Testosterone0 ~2 d7 ]( B, E; w$ W" p
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: H. E& x( R( `3 Y. R% {! O# a' ~
and Kenneth R. Rettig, MD1
5 _0 L0 ?& @* P: ?5 C; G+ z7 ^. aClinical Pediatrics d9 a7 S% Q. c1 G$ q& }! P$ U
Volume 46 Number 6+ K. c# ? X$ c6 b9 D h5 q t
July 2007 540-543
; U2 }8 W( I& X# c A v' D© 2007 Sage Publications& v, N# e6 h5 o- ~8 a) g# e
10.1177/0009922806296651& w- j2 M0 Q% _) @7 F9 w" c
http://clp.sagepub.com
" J) E, M) Z/ o& bhosted at' }, ?% B" l$ E. I
http://online.sagepub.com
9 m' s. W, e4 K& Z, z) C* DPrecocious puberty in boys, central or peripheral,
6 D7 D! \/ b& a( q- N) bis a significant concern for physicians. Central
8 W% ^6 T U m Q5 ?, mprecocious puberty (CPP), which is mediated/ }7 r5 k# P8 }6 r- o
through the hypothalamic pituitary gonadal axis, has
; C5 y9 r' ~) v! A3 wa higher incidence of organic central nervous system
$ ?: L f3 \4 klesions in boys.1,2 Virilization in boys, as manifested
6 M. ~' H+ J e1 z3 g2 G: `: pby enlargement of the penis, development of pubic
6 U7 l f9 k( v, ahair, and facial acne without enlargement of testi-
: A( Q; f, r0 Y; h) F% ~0 _cles, suggests peripheral or pseudopuberty.1-3 We( m0 U; W) w& K* Z$ ]$ d) \2 E! H0 @
report a 16-month-old boy who presented with the% Z# \& h' c- P; w+ F
enlargement of the phallus and pubic hair develop-
# Y. S! q) `0 z7 X! P8 ]+ ?ment without testicular enlargement, which was due9 e3 o7 T4 s `9 \! B( c: q! q
to the unintentional exposure to androgen gel used by) U3 ^. c0 R7 N' s
the father. The family initially concealed this infor-$ j1 _, U* s/ ^" H
mation, resulting in an extensive work-up for this
+ I* G& D. T5 R. v3 Vchild. Given the widespread and easy availability of3 ?, q! V h% Z1 v4 D( }/ b
testosterone gel and cream, we believe this is proba-
+ W& i* k4 ~5 K: C5 j8 q( Dbly more common than the rare case report in the' ^/ T* K% C! n, A/ {8 d
literature.4: Z, Z+ ]4 ^& K
Patient Report
6 v' {6 ^3 c- [9 QA 16-month-old white child was referred to the( z+ C/ y' ~( W* F% e
endocrine clinic by his pediatrician with the concern2 p# S4 _1 F1 E0 k; f3 _$ L$ d
of early sexual development. His mother noticed
7 Q$ q- z* q" {light colored pubic hair development when he was
" c( p- @3 W# O3 D: m" e0 wFrom the 1Division of Pediatric Endocrinology, 2University of5 F1 a }( J2 X* h5 C& ]- E
South Alabama Medical Center, Mobile, Alabama.
) F2 U: m5 ~9 T2 uAddress correspondence to: Samar K. Bhowmick, MD, FACE,, Q3 S/ v( `* x5 o/ _
Professor of Pediatrics, University of South Alabama, College of
" |4 [ o6 \ R9 z- b. JMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 g$ o* R2 {, j& k* r6 a5 w% E* {5 ?e-mail: [email protected].
, r% W" I5 u9 A! M" U: X$ Habout 6 to 7 months old, which progressively became( E1 j$ m: G- e! a8 d$ {" ^8 g& Z
darker. She was also concerned about the enlarge-
8 N/ {% O* Y* w, Wment of his penis and frequent erections. The child
2 [$ N' f, p) M$ y1 @+ |was the product of a full-term normal delivery, with
, g4 `( E0 a1 a" Z- m- v8 x* [5 F0 ia birth weight of 7 lb 14 oz, and birth length of9 ]( S) P; Q2 M$ R5 ?0 ~. e5 ~
20 inches. He was breast-fed throughout the first year) N: A, y% Y/ a% Q6 h! e
of life and was still receiving breast milk along with" s" s9 u `9 d) {
solid food. He had no hospitalizations or surgery,
3 y) ]$ v) m/ O, y1 F5 P9 O7 o. d/ |and his psychosocial and psychomotor development
! R% s8 j0 f- k' ~% Dwas age appropriate.
1 G- o9 z3 Y5 fThe family history was remarkable for the father,
2 I! ^ k8 [- C* r6 Pwho was diagnosed with hypothyroidism at age 16,! ?+ {- m9 T- ]: Z! N- M: R) ~& F
which was treated with thyroxine. The father’s" m2 V, O2 j! ?9 |% ~. u
height was 6 feet, and he went through a somewhat" }3 r' H+ }7 s$ v! e
early puberty and had stopped growing by age 14.' b- M* Z+ i, k) V
The father denied taking any other medication. The3 D( o" g: z# N
child’s mother was in good health. Her menarche' [" V; N& U! o6 _1 Y- \
was at 11 years of age, and her height was at 5 feet; Y9 r) k8 C# [5 L$ t/ M- x
5 inches. There was no other family history of pre-
% v! l, i" f. i2 k7 ecocious sexual development in the first-degree rela-
+ J/ V7 S X. d7 @tives. There were no siblings.
+ v6 D. `0 X* ~. K8 ~: q0 YPhysical Examination
& O2 ^9 ~6 \ |The physical examination revealed a very active,' c7 n* n c: U# C/ L- M, I
playful, and healthy boy. The vital signs documented- O3 X @! b) U! r
a blood pressure of 85/50 mm Hg, his length was6 I% N6 V# {5 M: O" O4 _/ X
90 cm (>97th percentile), and his weight was 14.4 kg# U/ l7 u2 q6 l5 o) L- ^6 z
(also >97th percentile). The observed yearly growth) c7 R" I- i9 l4 c8 z
velocity was 30 cm (12 inches). The examination of4 Y! A& U! c0 e& |/ `" G. v. a, S# E
the neck revealed no thyroid enlargement.
; H/ \) V( {, V: k1 e8 k/ a1 i" }! kThe genitourinary examination was remarkable for1 J9 s; g# S0 t0 ~% `
enlargement of the penis, with a stretched length of
9 ?! n$ ~3 g/ z( ?8 cm and a width of 2 cm. The glans penis was very well
8 z, g+ A# d/ w3 u. }developed. The pubic hair was Tanner II, mostly around1 E3 m3 n( h' o
540$ D) `. Y( c! k) N5 B0 ?, u& A$ }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 Y* H. z! h! j" |1 D/ w7 M+ `the base of the phallus and was dark and curled. The7 B& h9 r/ i8 u A6 h+ X% U
testicular volume was prepubertal at 2 mL each.
0 e' b& `! X+ k' ~" RThe skin was moist and smooth and somewhat/ r, S3 b1 Y' U/ b% K
oily. No axillary hair was noted. There were no' f3 d z, J, d, g8 N, r5 f
abnormal skin pigmentations or café-au-lait spots.
: E" i- z4 w4 @Neurologic evaluation showed deep tendon reflex 2+
! c# j" Y) N" z8 w5 Cbilateral and symmetrical. There was no suggestion
+ U) j( O) |8 V* Y9 {' |# M( ^of papilledema.3 X: B3 e' _# ~0 K
Laboratory Evaluation
1 e" |# F% i; }! B& ~/ b, w1 e. oThe bone age was consistent with 28 months by. g* Y! I' X" K6 w
using the standard of Greulich and Pyle at a chrono-3 @: U6 z v7 j
logic age of 16 months (advanced).5 Chromosomal. n6 V: Z) s' R: o- S% l$ v
karyotype was 46XY. The thyroid function test; p' ^% O# h3 f( T- a% m( K
showed a free T4 of 1.69 ng/dL, and thyroid stimu-3 k* n* b0 L* D; L1 y; n
lating hormone level was 1.3 µIU/mL (both normal).( m. L/ D% M0 {4 ^) Q- L
The concentrations of serum electrolytes, blood
]9 {% J7 @2 O0 t9 Purea nitrogen, creatinine, and calcium all were% z# ?* W) \; R* \& Q1 S9 i# G
within normal range for his age. The concentration. K- I) M% t3 J, y6 U- ]+ P8 O' }+ d
of serum 17-hydroxyprogesterone was 16 ng/dL
2 j2 f6 Z2 k* n" R+ p(normal, 3 to 90 ng/dL), androstenedione was 20! M7 x' q: K! Z- @" S
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
+ I8 x) m, ~ ]# B' @, vterone was 38 ng/dL (normal, 50 to 760 ng/dL)," R ~5 N" ^( C5 ] K# c
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
" ]- z9 R4 w6 U, p( d49ng/dL), 11-desoxycortisol (specific compound S)/ i5 }: F/ S3 g( ^! O2 o$ T( h, ]
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) \5 A6 _- F( v! W D0 n
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 Z4 E p1 i$ S
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),% m+ u& h h5 \0 z# J. g) j
and β-human chorionic gonadotropin was less than& [$ a4 k9 i. k" D
5 mIU/mL (normal <5 mIU/mL). Serum follicular- s7 y/ `( p# @( Q/ [/ q0 |5 p
stimulating hormone and leuteinizing hormone
/ x, [( D8 }& ^9 O$ x& nconcentrations were less than 0.05 mIU/mL7 v7 U6 w: n- q$ r* O/ D4 A
(prepubertal).3 r' k3 b1 E9 I/ U. x$ Y6 ?4 l6 c
The parents were notified about the laboratory* J$ Z4 E7 D4 y. `: g
results and were informed that all of the tests were4 e) q0 X- O+ u& t2 y
normal except the testosterone level was high. The, F- E; z' x) w
follow-up visit was arranged within a few weeks to
L: _$ {. w) { {0 _obtain testicular and abdominal sonograms; how-6 B. H. R" z: y) |& X& }7 `
ever, the family did not return for 4 months.: _) H* g5 V/ i3 j, l" \- Q& c% b
Physical examination at this time revealed that the
# c& I" u' ^' t4 p& `: {child had grown 2.5 cm in 4 months and had gained
4 z' {* ^7 P2 Y5 b8 U/ g# U. k( N2 kg of weight. Physical examination remained9 N# ]8 ]% _ \
unchanged. Surprisingly, the pubic hair almost com-
! t3 a" `: b+ Y0 e* r# ?: o5 R. Upletely disappeared except for a few vellous hairs at
' j- s3 g0 V# h' u0 n8 @ U( T' Xthe base of the phallus. Testicular volume was still 2
* c& U: P$ c3 k- S; bmL, and the size of the penis remained unchanged.& m" t' J7 w7 m- C( \
The mother also said that the boy was no longer hav-1 y$ e; l/ `" V) d6 z+ N& }$ D) P. m
ing frequent erections.
$ r1 o6 I: }! B7 ?7 dBoth parents were again questioned about use of
/ `2 l# ?2 B. V8 X" zany ointment/creams that they may have applied to) }" s9 c {' T% E
the child’s skin. This time the father admitted the+ t: _+ n5 A8 \) {4 n
Topical Testosterone Exposure / Bhowmick et al 541
6 B$ e3 g- X) g: @use of testosterone gel twice daily that he was apply-8 d$ R; S& Y8 L8 d7 b2 L1 I6 _
ing over his own shoulders, chest, and back area for5 @* p( x' f1 `9 w/ G
a year. The father also revealed he was embarrassed1 [- }% _6 Q9 t/ R8 X
to disclose that he was using a testosterone gel pre-, _& J, M4 |4 F+ y, ~+ \
scribed by his family physician for decreased libido# P3 F& S! A6 V, x) i: w
secondary to depression.8 ], k( J* n8 T1 K' J
The child slept in the same bed with parents.; g0 n8 ~. G2 m$ ^5 {( R' ^7 t1 K
The father would hug the baby and hold him on his
: s( B% H/ E3 x; `3 H( Echest for a considerable period of time, causing sig- z& c, p# z7 _' V
nificant bare skin contact between baby and father.
- c, |( a+ Z5 x+ r1 p$ o% h* KThe father also admitted that after the phone call,
3 G* l7 W; y7 Ywhen he learned the testosterone level in the baby3 ?8 H0 }! N" V- \3 e
was high, he then read the product information4 T. X6 W& c+ a$ a" _6 U
packet and concluded that it was most likely the rea-' W+ ^1 }) ^0 u/ p* [% K6 c
son for the child’s virilization. At that time, they4 [1 N5 ~. f R: Z* y( C
decided to put the baby in a separate bed, and the5 `- W& k( K& H: n
father was not hugging him with bare skin and had# A! |- S# f$ s, A7 M# T
been using protective clothing. A repeat testosterone, l, }1 v) t) |8 A
test was ordered, but the family did not go to the0 ?2 C$ R" l. E0 [
laboratory to obtain the test.8 P9 w1 B/ w5 l# y6 y
Discussion' Z" e9 V; @2 Y( m( k
Precocious puberty in boys is defined as secondary
* A! H/ A4 _# Q* R' Esexual development before 9 years of age.1,4; g, |1 @9 c5 T- _; l" e& I
Precocious puberty is termed as central (true) when" H- N7 f3 k# y8 j c. f
it is caused by the premature activation of hypo-' {5 s9 [5 _ g8 A# {
thalamic pituitary gonadal axis. CPP is more com-& w. `: i- n3 u. Y5 ?+ x3 n. C; h
mon in girls than in boys.1,3 Most boys with CPP; j. c0 \6 K. a( H
may have a central nervous system lesion that is. c- N9 J0 ^2 W9 O: P8 U& Y
responsible for the early activation of the hypothal-. F( b5 U1 i9 J
amic pituitary gonadal axis.1-3 Thus, greater empha-
0 f( }: z1 _- ~" c$ _0 }sis has been given to neuroradiologic imaging in
. Q! ]6 I) N2 A1 a$ S# @2 P: z; [& cboys with precocious puberty. In addition to viril-9 Q1 _5 Z6 D- B# k: W3 n1 O5 L
ization, the clinical hallmark of CPP is the symmet-' ?8 F% J$ {( ]8 q! N- c0 Z
rical testicular growth secondary to stimulation by& M* p a, B* `4 W7 y# x* n
gonadotropins.1,3
! z+ J! o" n. [, O+ C" }Gonadotropin-independent peripheral preco-, l6 h1 u2 ^: P* g* S
cious puberty in boys also results from inappropriate8 }8 D- q9 Q3 m! E" g7 O
androgenic stimulation from either endogenous or
) E9 A) u6 i- U; f. Oexogenous sources, nonpituitary gonadotropin stim-" `, k" [4 q8 {3 L* Z1 e1 E
ulation, and rare activating mutations.3 Virilizing2 B6 H3 a& v2 a. Y- e% Z" S9 y: V" h
congenital adrenal hyperplasia producing excessive! Q1 R* c' }6 T
adrenal androgens is a common cause of precocious
! t! }$ r' D1 S+ d( J0 xpuberty in boys.3,44 u8 M. y9 ^2 a0 z$ i" d
The most common form of congenital adrenal4 v8 f3 i- x1 D0 d3 |
hyperplasia is the 21-hydroxylase enzyme deficiency.
; B, A& p! J+ g# V8 b, d9 {The 11-β hydroxylase deficiency may also result in
" K9 e. j, y4 j& l5 _/ Aexcessive adrenal androgen production, and rarely,$ n, n9 p- U; Z0 Z
an adrenal tumor may also cause adrenal androgen
" J6 c" i$ E1 c% l$ [+ Z; M8 O8 Eexcess.1,3
9 `4 Z8 s3 F9 M Z4 q' ^, Z% {7 Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
e& @, q3 `! s+ ?. V! T2 w4 K+ ]$ P542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% y9 w& `4 M& Q6 A4 y: jA unique entity of male-limited gonadotropin-
- m* h E- Z0 h* ?% xindependent precocious puberty, which is also known1 M, n" }4 t' t$ P
as testotoxicosis, may cause precocious puberty at a
" v$ [3 q* q" Dvery young age. The physical findings in these boys
; S% {/ [! d" d# V7 F* T% q. `% twith this disorder are full pubertal development,) W& o1 M$ s. J: `" v
including bilateral testicular growth, similar to boys
+ T/ q/ |# i) Pwith CPP. The gonadotropin levels in this disorder2 M- P: D. [1 T1 x7 {
are suppressed to prepubertal levels and do not show
+ B, L: v1 N) z, Ppubertal response of gonadotropin after gonadotropin-5 X1 ~* d! s. l1 B, p% m* u
releasing hormone stimulation. This is a sex-linked) s1 p8 `1 n9 r$ l
autosomal dominant disorder that affects only* b9 S! @' {* R8 x+ c4 b- T4 X
males; therefore, other male members of the family
) B4 |7 k+ `" a' N2 I% P/ g6 Pmay have similar precocious puberty.3+ B8 c; b2 Z8 K/ W
In our patient, physical examination was incon-1 b O: t' ?+ y9 Q. W) K
sistent with true precocious puberty since his testi-
- t- D8 L7 e. M5 wcles were prepubertal in size. However, testotoxicosis
. L5 ]. i2 P# [was in the differential diagnosis because his father! Y; B2 G# r/ _, L
started puberty somewhat early, and occasionally,2 @3 T! d$ b- M/ J: l* A8 P* x
testicular enlargement is not that evident in the# m6 l3 [$ G8 b- P/ f/ y2 A% G q
beginning of this process.1 In the absence of a neg-
6 m8 m5 ^% f: `/ t) sative initial history of androgen exposure, our
s8 W$ w8 Q: Y$ M' ebiggest concern was virilizing adrenal hyperplasia,
7 z; x" `) G1 l; i) J+ ?5 |: qeither 21-hydroxylase deficiency or 11-β hydroxylase
! w9 C, {: I9 E& q1 ndeficiency. Those diagnoses were excluded by find-% c6 |+ z) B7 S- v: K. ^
ing the normal level of adrenal steroids.7 Y- T0 G: V+ N& A7 M9 f! c, t* i w
The diagnosis of exogenous androgens was strongly0 k3 Y6 [+ s! @9 u! o2 ~
suspected in a follow-up visit after 4 months because/ i: Q. w- \- _$ |7 H
the physical examination revealed the complete disap-
: z6 F6 A4 z8 f. R' Gpearance of pubic hair, normal growth velocity, and* E$ e. }5 a" b: }
decreased erections. The father admitted using a testos-
$ A- s) E0 P( I9 |8 j1 Rterone gel, which he concealed at first visit. He was
4 t D" m" Z8 V" ~using it rather frequently, twice a day. The Physicians’ g1 a7 Y) J/ E# D3 g
Desk Reference, or package insert of this product, gel or
: D" e5 ~( G- U! M" h8 A- }cream, cautions about dermal testosterone transfer to
, A* [# G) D: l2 Wunprotected females through direct skin exposure.
2 H. ?/ A' J9 \) w+ K8 VSerum testosterone level was found to be 2 times the# a$ ~: w' K3 Z; l+ _" y
baseline value in those females who were exposed to
& T( r3 s' v( X* k! m6 |even 15 minutes of direct skin contact with their male
% X$ O h. b. O' A& e$ Fpartners.6 However, when a shirt covered the applica-4 o! n& l4 r7 ?# h! ^/ B( |
tion site, this testosterone transfer was prevented.
' N7 p- w1 X/ P) Q( COur patient’s testosterone level was 60 ng/mL, e d3 L- v7 P2 N
which was clearly high. Some studies suggest that
0 F6 T4 [; ~4 V8 `# W& m7 Edermal conversion of testosterone to dihydrotestos-
9 v; v6 ?+ h. _, O3 yterone, which is a more potent metabolite, is more2 t; K4 v% S4 X7 U( x- X
active in young children exposed to testosterone
, T2 K+ ^4 n1 a' I3 Z0 w1 hexogenously7; however, we did not measure a dihy-, S# V' [3 u: h" o
drotestosterone level in our patient. In addition to2 E8 a& x$ c3 `5 x- g* A
virilization, exposure to exogenous testosterone in
3 R+ f& Z0 j% ?1 A$ {5 c* lchildren results in an increase in growth velocity and
# M/ z7 U$ ^, n. L0 ^, Eadvanced bone age, as seen in our patient. ^( Y5 E" X. A, H* ]8 x7 t% T9 u" `
The long-term effect of androgen exposure during. @6 f3 R+ q! V! j4 [2 ^. W- @: N7 ?
early childhood on pubertal development and final' _2 n1 A4 E% f$ X; j! O; z8 J
adult height are not fully known and always remain
6 ], p' p/ M0 ~# c0 h. q# ga concern. Children treated with short-term testos-9 N$ S: y2 i( {: A' ^- N3 k6 f" v
terone injection or topical androgen may exhibit some
" s( O1 j2 r( g# e; q# {2 W6 m7 @9 Yacceleration of the skeletal maturation; however, after+ T4 k! r& P# i( u5 i
cessation of treatment, the rate of bone maturation
: W2 |( ~; K' b) ]5 `3 |decelerates and gradually returns to normal.8,9
: [: U3 ~2 F+ t8 `9 u, v) v0 WThere are conflicting reports and controversy
* Y- E5 p* V3 N$ Pover the effect of early androgen exposure on adult5 j+ r& N2 P% m, e
penile length.10,11 Some reports suggest subnormal
$ W" b+ g& k' S& t+ x* w. O! jadult penile length, apparently because of downreg-, v7 p6 O3 X6 d4 z" m3 H
ulation of androgen receptor number.10,12 However,/ n( E: g- O. D% m
Sutherland et al13 did not find a correlation between
/ o3 W2 y5 n: C2 e1 M9 \childhood testosterone exposure and reduced adult$ U. V7 O% h: t
penile length in clinical studies.
, s( ]; B5 `9 }1 SNonetheless, we do not believe our patient is
9 F$ k. n4 o: o* h; t! vgoing to experience any of the untoward effects from
; L0 w( s2 n* @testosterone exposure as mentioned earlier because R% A9 F2 K7 [+ X, s2 h
the exposure was not for a prolonged period of time.$ V! G# x- b, K$ n+ }
Although the bone age was advanced at the time of
1 b* N; q- I# ?$ Qdiagnosis, the child had a normal growth velocity at
8 X3 v3 T, {2 ~/ h8 hthe follow-up visit. It is hoped that his final adult, q! _) D' l! t1 n2 ?: n% ~
height will not be affected. `( y% L5 v8 |0 c: z
Although rarely reported, the widespread avail-! `6 X3 L" y" W
ability of androgen products in our society may" j* S$ i3 f/ O9 b- ^ b) X
indeed cause more virilization in male or female
+ g p" n8 ^- x' V9 h/ {2 y# Kchildren than one would realize. Exposure to andro-
& H# y7 h8 I* k6 {# fgen products must be considered and specific ques-7 ~) F" {' u8 z. b
tioning about the use of a testosterone product or
9 o2 z9 M* ^$ o6 X- t; @gel should be asked of the family members during
9 u# |! x2 z1 h: ^0 ithe evaluation of any children who present with vir-6 O0 [ U' |9 y) m: O
ilization or peripheral precocious puberty. The diag-
6 Q7 j, d6 ?; h, r1 Cnosis can be established by just a few tests and by
/ }2 [" Y6 N6 Aappropriate history. The inability to obtain such a
t! {" T5 K$ ~# mhistory, or failure to ask the specific questions, may4 n+ u4 |: z$ g F4 L
result in extensive, unnecessary, and expensive
0 \' Y( V: z% K" dinvestigation. The primary care physician should be6 q8 A( e4 I; `( p( @! @
aware of this fact, because most of these children
) R4 _& p$ S$ T* X$ Amay initially present in their practice. The Physicians’
& M* [* q$ A# F. BDesk Reference and package insert should also put a
) V* i4 m5 L, @. u" p; ]& Z7 b# \warning about the virilizing effect on a male or$ S8 p1 U0 C' B e
female child who might come in contact with some-$ P* N" w; x0 _
one using any of these products.
. {% q$ N. F+ F* J$ q1 s. IReferences1 s1 B" m9 z! z% a5 r& G9 B
1. Styne DM. The testes: disorder of sexual differentiation0 Q- A; ]( v. }, f" X
and puberty in the male. In: Sperling MA, ed. Pediatric
: |* k. | [* u$ F, G( W% g% XEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
! w7 b% n4 C2 n) e3 T2002: 565-628.
- @( u# D) b& F, T7 ]# |6 a2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 v; l, W$ l d Wpuberty in children with tumours of the suprasellar pineal |
|