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Sexual Precocity in a 16-Month-Old
/ Z% p" ?. C( P4 V0 h3 N6 lBoy Induced by Indirect Topical
, d. e/ k5 g) f" r' I- u; S! aExposure to Testosterone
7 c' n* z, ]2 _" }0 MSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% H `5 D/ ]3 I+ B' S! B
and Kenneth R. Rettig, MD1
4 V6 Y. r4 `6 S0 VClinical Pediatrics5 U* d) |9 w( ^+ _" A
Volume 46 Number 6
, O; m/ X* D' P- ]0 y& h+ vJuly 2007 540-543
w! S, h. {+ _© 2007 Sage Publications
* H7 r9 g( {( q: n0 I+ R: N# ^$ N10.1177/0009922806296651
0 Z. A. N2 c; M- J+ Qhttp://clp.sagepub.com
4 B' o+ _+ t9 @) j' }- q( l- E5 \: I* rhosted at
8 f1 V3 W7 s B* O5 Q' Q2 x& hhttp://online.sagepub.com
8 U; Z9 a9 h7 z2 b1 ~Precocious puberty in boys, central or peripheral,& V6 ^6 P3 ^/ r1 w8 n, Y, n
is a significant concern for physicians. Central$ W1 |5 K, H+ o" v j
precocious puberty (CPP), which is mediated, P3 ?6 G s/ W! ?
through the hypothalamic pituitary gonadal axis, has6 ?3 ^' S* C: Z! K) `: W& m1 K, Z
a higher incidence of organic central nervous system
! N, O! m# J: T$ e( hlesions in boys.1,2 Virilization in boys, as manifested- R. [4 f0 T" s( U0 N7 `
by enlargement of the penis, development of pubic! H. Y6 W9 K8 X. t) [: K0 s
hair, and facial acne without enlargement of testi-
4 H$ B# S1 S# G- m' mcles, suggests peripheral or pseudopuberty.1-3 We: z3 \7 v" | P9 y
report a 16-month-old boy who presented with the$ ~* s6 ]+ z I: w* z6 f% o4 x G1 ~
enlargement of the phallus and pubic hair develop-
/ a3 _& Z5 X. Y/ _3 r/ y4 yment without testicular enlargement, which was due
9 X) J ]3 r+ Bto the unintentional exposure to androgen gel used by
1 K3 r9 Q2 `* Q+ d# [3 othe father. The family initially concealed this infor-
6 `( V8 A+ M3 e6 {) e; X* u0 Q, qmation, resulting in an extensive work-up for this5 ?7 }9 o/ p/ }! n0 ~8 j# W$ c
child. Given the widespread and easy availability of
# z9 A4 }$ N/ y3 b7 g; N/ Vtestosterone gel and cream, we believe this is proba-
% T7 [8 U' d, n A3 m. A Q3 Kbly more common than the rare case report in the# i- y4 U5 G2 o, Q9 d3 Y4 f, J
literature.4! [+ s2 B4 P% k' ]
Patient Report; z0 R+ |; ]5 F+ I" M0 j8 X" C( E9 ]
A 16-month-old white child was referred to the
5 a, W# V9 u% n$ c2 Nendocrine clinic by his pediatrician with the concern
H2 k. N0 u* z. a8 _: R Z- Kof early sexual development. His mother noticed
P0 |. U$ ^+ glight colored pubic hair development when he was* T3 F2 ]9 I$ H( |1 D0 u! s
From the 1Division of Pediatric Endocrinology, 2University of
* k0 H) l- q+ a I% s) }South Alabama Medical Center, Mobile, Alabama.
5 O. \ Z) W3 N+ a6 ?Address correspondence to: Samar K. Bhowmick, MD, FACE,
# q% ^8 m7 q5 I# O$ D8 q8 l4 R2 |6 ^Professor of Pediatrics, University of South Alabama, College of/ j2 ]6 }% C" u. P0 t2 ?( O
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 h) F0 J4 y6 G7 S8 p
e-mail: [email protected].( o6 ^* ?% x; o/ C' A
about 6 to 7 months old, which progressively became7 P$ O7 a9 V- E# ~
darker. She was also concerned about the enlarge-
' R5 B r0 D2 M3 S! iment of his penis and frequent erections. The child
. V2 X& ]& x8 w; L, cwas the product of a full-term normal delivery, with
5 P* L1 i$ s' u( Y! m# aa birth weight of 7 lb 14 oz, and birth length of
( p& h1 z( |- j20 inches. He was breast-fed throughout the first year- g" p7 B, u# x/ w1 p" F" T( Y
of life and was still receiving breast milk along with
8 V( ]# h' N9 psolid food. He had no hospitalizations or surgery,6 y; K2 w! I6 h4 F4 ]* Z! X; {" ~* }4 C' H
and his psychosocial and psychomotor development$ r+ p+ p$ x. b# i* M
was age appropriate.
$ `+ X, s- e9 ~" _$ P5 jThe family history was remarkable for the father,
8 F p7 M0 ]) b: A$ X2 b2 qwho was diagnosed with hypothyroidism at age 16,0 l5 n8 n) C# \+ j- ^
which was treated with thyroxine. The father’s
) N' f$ T, j3 A% o- ~' B' jheight was 6 feet, and he went through a somewhat
) K! J/ B- |$ F/ Learly puberty and had stopped growing by age 14.
/ Z7 M1 ]2 z. I/ l/ E4 {% N, VThe father denied taking any other medication. The/ g2 b# m. ]$ [& r' }6 h
child’s mother was in good health. Her menarche# z5 w/ x6 ^" b- b" Q
was at 11 years of age, and her height was at 5 feet
* `1 A! Z/ z: j- [8 c6 Y c$ Z) ?5 inches. There was no other family history of pre-( f" e0 n; G2 \: N# m
cocious sexual development in the first-degree rela-. } c/ a- y5 n' z1 d/ r
tives. There were no siblings.8 O# m9 T( q& k$ z; d; L7 C0 [
Physical Examination
; Q% ~/ j( [3 U5 aThe physical examination revealed a very active,; R) `4 V, `* P7 M" F% ]9 S1 Y ]' @
playful, and healthy boy. The vital signs documented
+ Q7 y( h* S% p1 K& I; {1 j) ^a blood pressure of 85/50 mm Hg, his length was, V0 w v: S# U* q. w
90 cm (>97th percentile), and his weight was 14.4 kg X# A4 v/ \. N" b+ ]+ ]- w
(also >97th percentile). The observed yearly growth
7 _% f$ z: @* Mvelocity was 30 cm (12 inches). The examination of' Z5 ^8 j% `9 J/ T8 t/ \% s
the neck revealed no thyroid enlargement.
# T" b1 q! ^/ y1 DThe genitourinary examination was remarkable for
% d" U4 a/ ] R" I4 [- c; E5 O" Genlargement of the penis, with a stretched length of
8 S1 S# C# b' S. S6 P7 G8 cm and a width of 2 cm. The glans penis was very well
( b/ I' q0 K. `4 _; y9 Cdeveloped. The pubic hair was Tanner II, mostly around! ~( x _: D" \; q# x
540: F, N1 u$ s- D; O# d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 K2 Z' W* o' Z; i- l, Y, pthe base of the phallus and was dark and curled. The; Y$ A' A( n) \# T1 K8 _
testicular volume was prepubertal at 2 mL each.
9 ~' t. T' m5 @1 ?( g- @. \The skin was moist and smooth and somewhat
U6 V. S5 E1 h1 _, G7 V( Zoily. No axillary hair was noted. There were no; N/ `3 w8 p% P& O
abnormal skin pigmentations or café-au-lait spots.
# }' B R, B7 x: zNeurologic evaluation showed deep tendon reflex 2+/ g- r$ Z: F; h
bilateral and symmetrical. There was no suggestion3 V- g" \, M9 E% d
of papilledema.9 }' c% I6 N* G' Q# c
Laboratory Evaluation
, J4 A4 }- M$ i' D/ j% oThe bone age was consistent with 28 months by& }( N+ \. c$ Z8 |7 [, O: B- G" |7 J
using the standard of Greulich and Pyle at a chrono-- g5 Y4 B2 h. k7 n1 {$ B: d3 Y
logic age of 16 months (advanced).5 Chromosomal) \" J: j) N# O. }5 B, f1 [& S1 v
karyotype was 46XY. The thyroid function test
" I, z% R8 R: L% r* oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-$ H# i8 d% o: u0 s
lating hormone level was 1.3 µIU/mL (both normal).
2 h: w6 c. Q; }The concentrations of serum electrolytes, blood
% X1 ?% _' H4 f- [urea nitrogen, creatinine, and calcium all were+ p+ L* W5 o+ x
within normal range for his age. The concentration
" b6 q6 T. K1 H% ]9 @* ?of serum 17-hydroxyprogesterone was 16 ng/dL
1 {( r9 H5 g7 ~0 P(normal, 3 to 90 ng/dL), androstenedione was 20: Z8 C2 |1 e8 ~, Q$ ~, K% p# @
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; E3 ~% ~- L% K
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. y9 D! Y# v* _' G* g9 Cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 j/ ]& i, L! Z% t1 r49ng/dL), 11-desoxycortisol (specific compound S)4 {& E6 K/ l7 P7 T5 q c0 _
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. ~0 g/ h3 S4 Y9 M+ S% i v4 \- s
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
t. F7 }3 e0 A8 Otestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 n( o% f& ]% f6 I, I( B( ?and β-human chorionic gonadotropin was less than2 l* E, U1 L9 o
5 mIU/mL (normal <5 mIU/mL). Serum follicular7 l. P2 U, O; e
stimulating hormone and leuteinizing hormone1 Q; @, T; [3 A+ f8 h/ c8 M/ r
concentrations were less than 0.05 mIU/mL' h9 _- b# O s9 I* C+ M% t
(prepubertal).* Y; y1 \9 I) ?5 Y0 p- u9 q5 t
The parents were notified about the laboratory) M2 t/ ]! A! c1 H
results and were informed that all of the tests were5 H3 e8 `9 C# s k
normal except the testosterone level was high. The
# m* F) U# E8 Rfollow-up visit was arranged within a few weeks to
- e3 Z- x( {5 m7 W5 Aobtain testicular and abdominal sonograms; how-0 U+ C+ X4 D2 P/ ~" C2 b
ever, the family did not return for 4 months.
; X! H1 K4 G y I# O2 G' \Physical examination at this time revealed that the
9 l: J/ U7 l: ~5 o( c% n0 Cchild had grown 2.5 cm in 4 months and had gained0 c' [3 l! p& D' b( i
2 kg of weight. Physical examination remained
' y3 O5 N0 K0 n0 Q2 R9 i* Zunchanged. Surprisingly, the pubic hair almost com-7 {; i) m) c# n% e1 q% K& L8 C
pletely disappeared except for a few vellous hairs at
E. Z9 f7 ^7 W: A: _the base of the phallus. Testicular volume was still 2* M$ P& j7 c, A7 ^4 z0 j( ]
mL, and the size of the penis remained unchanged.: L3 L$ \# q! `% G
The mother also said that the boy was no longer hav-3 U5 T( J- k' ]2 [4 ` g4 v! l
ing frequent erections.
' V3 j" _6 B1 q$ sBoth parents were again questioned about use of
, |" v% T {% S) H0 V; Nany ointment/creams that they may have applied to
6 |4 r, @! w8 L. \the child’s skin. This time the father admitted the
3 q7 e8 [* _8 r% o( e/ STopical Testosterone Exposure / Bhowmick et al 5410 [% A0 _; m7 @6 x( j
use of testosterone gel twice daily that he was apply-
; [9 m. q& _, e* R# ]$ f6 a# ming over his own shoulders, chest, and back area for, z) j |6 B% @6 H* H/ z: I2 I |
a year. The father also revealed he was embarrassed8 N7 F/ w/ \2 z) Y- p# A
to disclose that he was using a testosterone gel pre-
! F: p ?/ S M; `7 wscribed by his family physician for decreased libido
( l" h) K% j& ~( z6 v) J2 asecondary to depression.
1 [1 S& `. y5 r4 t" [. _The child slept in the same bed with parents.
% L8 a2 f2 f7 D# k! NThe father would hug the baby and hold him on his8 Z) }- j2 b! j: h7 H2 ?
chest for a considerable period of time, causing sig-
K* ?! ?' u( i9 E bnificant bare skin contact between baby and father.3 S+ J* a( Q% i. ?2 i
The father also admitted that after the phone call,; k p1 O% {( m
when he learned the testosterone level in the baby' K$ P! ?$ a) M$ t' M7 e
was high, he then read the product information2 }. e/ \; G& z- e) k
packet and concluded that it was most likely the rea-
# F; ^% G2 V0 W: Y Q; a8 vson for the child’s virilization. At that time, they
6 J3 L9 d! ?6 ]/ ^2 Qdecided to put the baby in a separate bed, and the1 R3 J0 |# ~; H1 T- \, m
father was not hugging him with bare skin and had
3 }. ?# `+ A3 e1 O1 R7 Bbeen using protective clothing. A repeat testosterone
* V7 z1 M( Q" I# k( l& O' q6 w& Rtest was ordered, but the family did not go to the
2 ]" f+ V6 R* r7 ^0 Y6 Q. E% n/ klaboratory to obtain the test.; {5 U: U/ D+ v
Discussion) }" }3 P) P1 K2 D8 Q+ @
Precocious puberty in boys is defined as secondary7 @* E; }8 q8 _1 u" K4 Y$ o7 T
sexual development before 9 years of age.1,4, h$ Z+ G: U- ^' W/ |- d
Precocious puberty is termed as central (true) when& K/ m, G) j. P& D% i: Y
it is caused by the premature activation of hypo-7 S4 T9 B. l. x
thalamic pituitary gonadal axis. CPP is more com-2 L2 @8 p0 ~6 `6 K% C3 i* k
mon in girls than in boys.1,3 Most boys with CPP8 S$ |4 W5 E0 N$ A' P7 U
may have a central nervous system lesion that is
( s- f2 L( C! ? S) Iresponsible for the early activation of the hypothal-; ^4 D7 K" H/ o$ J& r
amic pituitary gonadal axis.1-3 Thus, greater empha-
- \$ r8 s# W5 ~6 [sis has been given to neuroradiologic imaging in
" v6 D$ q: I/ V( f7 _boys with precocious puberty. In addition to viril-
( b2 }" F" | T. lization, the clinical hallmark of CPP is the symmet-+ d# @, N# J/ {8 m& a/ C5 S
rical testicular growth secondary to stimulation by# E. X, f, U7 V% h0 J, v& L
gonadotropins.1,3, o: f# g' b% w' |
Gonadotropin-independent peripheral preco-
' K }- d# Y: L4 M( Xcious puberty in boys also results from inappropriate
& k: i% B3 R T9 N' Wandrogenic stimulation from either endogenous or- i7 F* r1 b) c; z# m
exogenous sources, nonpituitary gonadotropin stim- I) X# z& C, O @
ulation, and rare activating mutations.3 Virilizing
! L: W# I; _/ v. g9 X X3 hcongenital adrenal hyperplasia producing excessive8 V/ ^" w/ v u5 J1 F
adrenal androgens is a common cause of precocious
0 N( {7 U! g, [9 V4 e$ e5 r( I' spuberty in boys.3,40 h1 F$ |! _. Y7 J% _
The most common form of congenital adrenal9 t& V6 C, G& {0 B/ I/ a' n/ y
hyperplasia is the 21-hydroxylase enzyme deficiency.
2 Z0 h; V y& I' tThe 11-β hydroxylase deficiency may also result in( `; q0 k& d9 |! e* y1 N
excessive adrenal androgen production, and rarely,1 `3 _; u( S* Y' U, H
an adrenal tumor may also cause adrenal androgen0 e6 g& c- q* d- B8 f4 f
excess.1,3
7 b1 {; a7 ~1 s) X" Q! G9 m2 k" r1 Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# n. n' T; z- x542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, D% N4 h6 b5 J$ X, \% d$ D, g2 a
A unique entity of male-limited gonadotropin-9 x; I b- V1 e$ T6 e( V* x
independent precocious puberty, which is also known, F! U+ ]* ]" b) n }4 o5 }: r
as testotoxicosis, may cause precocious puberty at a( x5 A4 A. L8 {
very young age. The physical findings in these boys
3 C q6 ?" [3 H0 E+ ]- Hwith this disorder are full pubertal development,
6 X" R; j+ G3 Y1 X) l7 { Iincluding bilateral testicular growth, similar to boys
( J2 G. t2 _% e* N5 d/ _; ?* M4 {* {with CPP. The gonadotropin levels in this disorder
8 I& L1 w7 a! Y) E/ D4 m: w% zare suppressed to prepubertal levels and do not show
7 V) A! c6 F1 t% ? N5 p3 i0 ^pubertal response of gonadotropin after gonadotropin-$ Y% z4 W7 y; R, o) t
releasing hormone stimulation. This is a sex-linked# N3 t# v. [! P; F* D( |3 |
autosomal dominant disorder that affects only
! J3 f1 s3 k+ h1 W/ @( O0 u) C7 zmales; therefore, other male members of the family
7 e/ X2 N% P8 `: m9 `6 u& mmay have similar precocious puberty.3
4 E+ a' t" M' r9 ?+ a! eIn our patient, physical examination was incon-
' j% _" l' a7 n$ Z/ Ksistent with true precocious puberty since his testi-2 [4 X2 Q3 b& o# H* A
cles were prepubertal in size. However, testotoxicosis) @/ I A4 Z" \6 }
was in the differential diagnosis because his father
S$ p* }: k* F4 E- astarted puberty somewhat early, and occasionally,
- E& O8 K. ^# t Q; ?9 D) x9 jtesticular enlargement is not that evident in the" f% d! G/ q4 h% `; F; l1 ^
beginning of this process.1 In the absence of a neg-. n" l* `7 U: y/ y( M
ative initial history of androgen exposure, our
3 O# ]5 e+ f- o7 u* e6 D0 K4 dbiggest concern was virilizing adrenal hyperplasia,
! ]4 C. n+ N; c: J2 W, b! w1 Leither 21-hydroxylase deficiency or 11-β hydroxylase
/ G# ~( q5 M( l4 @; I: [deficiency. Those diagnoses were excluded by find-
. L1 T. @" C" a% P' E9 Iing the normal level of adrenal steroids.
: J" K) L9 ?2 n% B$ G) YThe diagnosis of exogenous androgens was strongly* c! ?& @$ S6 O7 K3 E: ]
suspected in a follow-up visit after 4 months because, J9 K6 ^9 F6 @5 X ]
the physical examination revealed the complete disap-) `5 c3 B) F) c, p$ r7 m( p
pearance of pubic hair, normal growth velocity, and; W9 u" {& X; Y
decreased erections. The father admitted using a testos-- `# I7 c+ S: p( Y6 J0 \
terone gel, which he concealed at first visit. He was
) \( h/ H0 X0 `using it rather frequently, twice a day. The Physicians’
, u1 E# ^6 {. R" c* A# IDesk Reference, or package insert of this product, gel or' }$ K' H8 ?8 V4 {9 |) K
cream, cautions about dermal testosterone transfer to7 M7 X9 q% ~. m6 S
unprotected females through direct skin exposure.9 ]. |9 a; Y w& k
Serum testosterone level was found to be 2 times the+ A7 b v: z# j3 r/ C
baseline value in those females who were exposed to. L) s6 X. }. [1 e) u
even 15 minutes of direct skin contact with their male
* C7 K$ \# l. H6 k, S, S h6 ?/ Vpartners.6 However, when a shirt covered the applica-4 l; C/ X$ \' _( z. n0 [7 Z; a: r
tion site, this testosterone transfer was prevented.# y1 i) [, }; d- K
Our patient’s testosterone level was 60 ng/mL,6 ~1 W) p+ U0 S$ _
which was clearly high. Some studies suggest that
) V1 ?) q9 |7 cdermal conversion of testosterone to dihydrotestos-
6 Y, m/ Y$ h$ C, ]5 Tterone, which is a more potent metabolite, is more5 J( Z. S* X/ U6 w
active in young children exposed to testosterone1 ~6 M8 w6 {, }
exogenously7; however, we did not measure a dihy-. P# X% E2 X9 b4 `/ M1 `+ ^
drotestosterone level in our patient. In addition to
: [" P( h2 }8 o& j: V& Y# Fvirilization, exposure to exogenous testosterone in
6 y" ?3 j/ [' i5 K5 a' J6 b1 tchildren results in an increase in growth velocity and/ }. h6 @, Q. q. p2 D
advanced bone age, as seen in our patient.3 N2 X( O5 ^ z+ B6 b. q
The long-term effect of androgen exposure during
- F! T4 M6 _/ k5 {' m$ @8 _- ?6 [early childhood on pubertal development and final8 Q: e% I; i: l7 f! d+ U
adult height are not fully known and always remain0 e! ] ~0 X* @& w; e! d
a concern. Children treated with short-term testos-
3 B# K4 B. h$ ~, {$ e: C+ v' Mterone injection or topical androgen may exhibit some8 J. n7 Q% q' e, y X, E1 A5 {6 {' Z/ ]
acceleration of the skeletal maturation; however, after, e$ V- h- z2 Q, N( C- `
cessation of treatment, the rate of bone maturation( ^# G4 k* n& U+ D8 D
decelerates and gradually returns to normal.8,94 h0 G4 a3 T( G/ ?; Y
There are conflicting reports and controversy
+ m2 c: s3 n* L% Y bover the effect of early androgen exposure on adult
8 S* q) q' s) A7 f, t) M0 s; Lpenile length.10,11 Some reports suggest subnormal
! H5 O8 \, L+ [7 t2 i2 W8 aadult penile length, apparently because of downreg-; H! i& e' f( B4 \
ulation of androgen receptor number.10,12 However,
7 r: I) Q' P- YSutherland et al13 did not find a correlation between5 b( e, W' _# k$ {8 ^
childhood testosterone exposure and reduced adult
3 L- K' N" e) `' D- mpenile length in clinical studies." ` ?% v/ X) v1 q$ k+ p- R. @
Nonetheless, we do not believe our patient is
" [; s; {7 A$ s; agoing to experience any of the untoward effects from
8 D# d2 R; \$ R, Dtestosterone exposure as mentioned earlier because- m) e3 ?/ k6 A6 m0 a* R
the exposure was not for a prolonged period of time.3 j' \, r" x" P* S( h6 |9 `. e, o; [
Although the bone age was advanced at the time of
* h- n, F, M1 N% ~diagnosis, the child had a normal growth velocity at+ a. `, [0 x+ r
the follow-up visit. It is hoped that his final adult. V/ h4 X3 S5 Y8 N1 d
height will not be affected.
: Q/ B3 E+ b( y: A, I! ^Although rarely reported, the widespread avail-
+ }, Q" _5 k* ~& C6 c# aability of androgen products in our society may' M* V" q( {- C P& u& Z: j5 U1 c
indeed cause more virilization in male or female0 H# I& i3 r" O- v% Z* Y
children than one would realize. Exposure to andro-( J& b4 H; F z6 C$ }: ]" s
gen products must be considered and specific ques-7 K8 y5 O0 e' P
tioning about the use of a testosterone product or
7 J, w2 j$ S4 a9 Ngel should be asked of the family members during: R) v6 i& x I# [; {
the evaluation of any children who present with vir-
2 }9 o/ i2 h, R0 i; k" N# Filization or peripheral precocious puberty. The diag-6 u3 M) v, D8 F3 [
nosis can be established by just a few tests and by+ S$ \6 _- G0 v8 A; ^
appropriate history. The inability to obtain such a. Y! g9 _0 q6 E% w7 J! n% F1 ?$ E
history, or failure to ask the specific questions, may
6 W9 n1 U6 B' G' [- qresult in extensive, unnecessary, and expensive. |' p4 t% r' R6 v5 ~7 ^6 }
investigation. The primary care physician should be: l- g$ [/ t1 q4 g$ X0 _: A% r
aware of this fact, because most of these children
0 ~8 F1 l) Z$ t3 |. v& }1 |' X6 qmay initially present in their practice. The Physicians’! P! c+ v/ a B% x
Desk Reference and package insert should also put a6 |! P1 n9 {! f( u$ k+ E
warning about the virilizing effect on a male or
( V3 ]+ W& ~ a1 V4 sfemale child who might come in contact with some-
# `0 ]' X# X sone using any of these products.
m. m; c3 j# Q/ n' p0 M5 k5 BReferences
`' p9 v7 {4 q$ N! |8 E1. Styne DM. The testes: disorder of sexual differentiation
X' _& M0 ]9 P$ A- E& Q/ d* Hand puberty in the male. In: Sperling MA, ed. Pediatric" ?9 C* T/ `9 T; ~' L
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders; Q, N8 P- k# I6 s2 Y* Y
2002: 565-628.4 |! N% b: N/ ]/ |
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: r+ V# n) M" U( [& hpuberty in children with tumours of the suprasellar pineal |
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