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Sexual Precocity in a 16-Month-Old: j d& R- ?$ m7 m9 q% v) z
Boy Induced by Indirect Topical
9 ]; B2 G4 ^5 ^- OExposure to Testosterone
3 i, q) F. L kSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: `. d2 l# b; \: R' ~1 }
and Kenneth R. Rettig, MD12 d2 y: U" i/ ]8 h7 k
Clinical Pediatrics
6 ]# U1 c$ k% m( [+ @" j, bVolume 46 Number 69 w' a& N! S; v" T' c! J2 T
July 2007 540-543# r3 S3 T9 S# V5 G% ^, z
© 2007 Sage Publications4 S7 K: o c2 i# d) \# \7 g% [
10.1177/0009922806296651
, c% E6 H. [' \( mhttp://clp.sagepub.com. g# d% `/ l6 f5 c# u7 J8 p- t
hosted at, g$ L) L2 U; F' H( Q4 y
http://online.sagepub.com
+ j" n% t" L# V. K9 R5 n5 P4 dPrecocious puberty in boys, central or peripheral,
- z+ M& L8 U7 S9 x7 \5 ]is a significant concern for physicians. Central
" k* o$ j1 Z) Uprecocious puberty (CPP), which is mediated
( y0 U# |4 @( l2 X1 ?through the hypothalamic pituitary gonadal axis, has
( h% E. I' p: [% Y6 ha higher incidence of organic central nervous system2 k- _( ~$ \2 Z& P. p! V" ?" E
lesions in boys.1,2 Virilization in boys, as manifested
; }+ i0 v! K* i, }1 yby enlargement of the penis, development of pubic
2 u* H9 o4 w( t% X- I1 Qhair, and facial acne without enlargement of testi-
( Z& R7 ~0 U8 C1 H% C( m! m2 Ucles, suggests peripheral or pseudopuberty.1-3 We
* l/ S( n4 z% F8 O9 Z9 }& w# Ereport a 16-month-old boy who presented with the$ O9 N% J) k, C4 y; ] \
enlargement of the phallus and pubic hair develop-. i: V( {3 \) g" i: H+ m
ment without testicular enlargement, which was due
# \! k; {& h/ _to the unintentional exposure to androgen gel used by
8 F' C. o3 W. m# i. W1 Lthe father. The family initially concealed this infor-% F0 O# v; M, S) @; o
mation, resulting in an extensive work-up for this4 I' s: a4 F: T* A& b1 K0 q2 |
child. Given the widespread and easy availability of
% q0 q$ E! V+ q6 M/ ~. w& E" s7 h6 Ltestosterone gel and cream, we believe this is proba-
* |+ _ a, C8 C2 N, T, V1 _3 {- w. vbly more common than the rare case report in the
& }5 [ H1 T8 Wliterature.4( b! j5 E) o: B% Y2 Y l
Patient Report
+ ~/ j6 ~' D# |A 16-month-old white child was referred to the
1 ~- i0 G( ]0 Yendocrine clinic by his pediatrician with the concern! _* ^8 ]3 `$ x# v
of early sexual development. His mother noticed) K, b% ^" E6 l R8 f' t& o3 {. `
light colored pubic hair development when he was' H0 P* t) _7 K* |6 L
From the 1Division of Pediatric Endocrinology, 2University of E* G8 |" u2 N7 y0 Y9 p# r
South Alabama Medical Center, Mobile, Alabama.' k" X j4 }2 K; d
Address correspondence to: Samar K. Bhowmick, MD, FACE,: N' u2 C" q/ O
Professor of Pediatrics, University of South Alabama, College of
3 I& B( @4 X6 N3 q, LMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297; Y+ ?$ }: Z% l1 E
e-mail: [email protected].
( b1 t+ D8 {$ T4 _8 n9 Oabout 6 to 7 months old, which progressively became7 O# d) v2 B" j& [2 W
darker. She was also concerned about the enlarge-6 C6 S4 b" D+ y! ]
ment of his penis and frequent erections. The child$ i! @5 x1 V& \
was the product of a full-term normal delivery, with
# Q6 \7 p) V7 d' v& k1 X% |$ O4 Ra birth weight of 7 lb 14 oz, and birth length of) U5 v- |$ g3 v+ a1 L: U( G
20 inches. He was breast-fed throughout the first year% g& F$ }8 O* i3 n! b7 t' }
of life and was still receiving breast milk along with `$ z) o$ u. f2 s" M" L1 ?
solid food. He had no hospitalizations or surgery,7 `2 E$ S% K- h M* |+ h
and his psychosocial and psychomotor development
! B8 V1 d& {" P" T4 o$ {# Zwas age appropriate.9 [. T/ [) y6 i. t) f1 x
The family history was remarkable for the father,
d; U1 Q# d: ]* lwho was diagnosed with hypothyroidism at age 16,6 g. p) U* B6 g' Q5 U7 V. x5 c! M/ I
which was treated with thyroxine. The father’s6 p+ _, F5 R) f/ N) Q
height was 6 feet, and he went through a somewhat, a4 w6 j9 e- |% K- ?: E5 K9 l
early puberty and had stopped growing by age 14.
7 E" }. T, u! b7 Y& s% `# [The father denied taking any other medication. The
: ?5 K; _; W* ^& g+ @) T+ Pchild’s mother was in good health. Her menarche' ~; G# L X" n
was at 11 years of age, and her height was at 5 feet, s- o. a, m' B7 L% n6 R1 o9 Y# ^
5 inches. There was no other family history of pre-
- t& Y/ \% p' |( d: i* ycocious sexual development in the first-degree rela-
' ^$ x8 b3 | U6 A2 } J6 Dtives. There were no siblings.
% V- Z) J0 h5 S0 \% W4 k9 }Physical Examination) Q" ?5 m* y1 |% V' P! I- K( V- \# P
The physical examination revealed a very active, q: F4 l! F' P
playful, and healthy boy. The vital signs documented8 H1 {. T( U7 p$ k
a blood pressure of 85/50 mm Hg, his length was, `: y! t1 |8 e8 ?. M
90 cm (>97th percentile), and his weight was 14.4 kg5 T" y3 t, {) p6 k, Q+ e1 O
(also >97th percentile). The observed yearly growth/ R7 t6 j) _9 ?, k
velocity was 30 cm (12 inches). The examination of* D$ S8 K) \. B" V& j# o
the neck revealed no thyroid enlargement.
; ]2 v: o4 {3 i& X4 r% HThe genitourinary examination was remarkable for2 Q, h$ V& d1 J( l( x
enlargement of the penis, with a stretched length of4 s V) }/ t9 }, `
8 cm and a width of 2 cm. The glans penis was very well
/ z6 ~. J9 y. [! Vdeveloped. The pubic hair was Tanner II, mostly around R9 I9 J7 G: P* t
540
6 k. O0 ^; n4 \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
E, a7 Q' x% Q; Sthe base of the phallus and was dark and curled. The% U- |* k' m: Q9 h! L
testicular volume was prepubertal at 2 mL each.
& h$ }1 _# i# w! L- CThe skin was moist and smooth and somewhat
. {9 I* e/ @( Z K, Yoily. No axillary hair was noted. There were no
8 O/ E" b5 J# |4 z% c4 F- H; l3 iabnormal skin pigmentations or café-au-lait spots.6 S3 T- z! X0 _
Neurologic evaluation showed deep tendon reflex 2+
9 ^& I1 T% v9 I* Vbilateral and symmetrical. There was no suggestion
, h P, }9 |/ ]+ bof papilledema.: d9 w0 A- }2 P2 Z7 l
Laboratory Evaluation5 a. y6 q* T+ R s: ~- k
The bone age was consistent with 28 months by
B' Z) g7 \- v+ ^ s' ]+ Uusing the standard of Greulich and Pyle at a chrono-
2 s& h2 S8 u, @% p( blogic age of 16 months (advanced).5 Chromosomal
3 T4 T$ ]9 ?7 lkaryotype was 46XY. The thyroid function test
' H" i9 z% x$ [) }7 p& n% y1 ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 L. T4 |4 h" P+ w3 }: x
lating hormone level was 1.3 µIU/mL (both normal).
# C. r1 h5 Z/ J& N n+ MThe concentrations of serum electrolytes, blood* Q8 p N2 K7 s! H
urea nitrogen, creatinine, and calcium all were/ @8 x' I4 y2 Y3 A( D9 F) d& K9 @
within normal range for his age. The concentration
! C6 f' \$ {+ I2 W8 S) l, n2 Yof serum 17-hydroxyprogesterone was 16 ng/dL
' e$ C& x( Y! G(normal, 3 to 90 ng/dL), androstenedione was 20
6 @% w/ D) R& y: G* V- Hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 u8 p" Z7 E! U! W b7 }) N. l% aterone was 38 ng/dL (normal, 50 to 760 ng/dL),4 i% Z! o7 ?6 J! l2 v" C ]/ u
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 _+ B7 W3 J; C
49ng/dL), 11-desoxycortisol (specific compound S)- {3 A& V7 |1 F( s; A
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% H" A: L: n/ W9 k% s7 m+ ? @
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; N. x1 P- |9 Ktestosterone was 60 ng/dL (normal <3 to 10 ng/dL),. v* o/ C8 |# I8 y7 f" o+ W" r/ |8 z
and β-human chorionic gonadotropin was less than
9 _ k8 N- G' t$ b' n5 mIU/mL (normal <5 mIU/mL). Serum follicular
: H0 p# X8 Y2 H _- ^1 fstimulating hormone and leuteinizing hormone0 U, \4 E7 a1 @3 s& o: b" j3 U1 r
concentrations were less than 0.05 mIU/mL
+ a! \' @' l) W7 H1 S: \(prepubertal).9 n. t' D) g% @3 g6 O, X: `
The parents were notified about the laboratory9 q& S6 [( \$ X$ R) a* }; E+ e* j
results and were informed that all of the tests were, S6 L% t- D6 C8 c4 L8 B' L
normal except the testosterone level was high. The
2 p7 X2 |5 k, ?- ?& [8 p' s3 P) }" pfollow-up visit was arranged within a few weeks to
! a0 V" A& X$ V4 Q2 cobtain testicular and abdominal sonograms; how-/ S6 X5 J+ F3 H5 y) s" w" N) Y5 {
ever, the family did not return for 4 months.$ U9 B- X( ~7 a6 p: F. a) C
Physical examination at this time revealed that the. |/ s6 S8 G- e3 N X5 _1 s* t
child had grown 2.5 cm in 4 months and had gained, O0 E! }/ X( `- t
2 kg of weight. Physical examination remained2 s& |; q! a" d% r# w
unchanged. Surprisingly, the pubic hair almost com-0 c& Z; K* p% w6 s# L
pletely disappeared except for a few vellous hairs at0 t, @. N2 Q- g
the base of the phallus. Testicular volume was still 2
9 @9 A/ U$ E: \. O4 f" B; G/ D8 l4 i" mmL, and the size of the penis remained unchanged.! N/ `% |9 s0 t) w; y' f
The mother also said that the boy was no longer hav-1 t" n5 L& i9 B X: F) X
ing frequent erections.
+ g6 G4 O6 b& Q* n( O/ N7 kBoth parents were again questioned about use of3 \* v* v6 ?6 K/ M/ s7 z
any ointment/creams that they may have applied to
% s5 _; Z: U. t+ R& W/ O; gthe child’s skin. This time the father admitted the( B6 M% o, O6 r! [, v$ s
Topical Testosterone Exposure / Bhowmick et al 541$ ^! T' V0 P; G7 ^9 q$ U
use of testosterone gel twice daily that he was apply-
1 e |" M& ^( [& |ing over his own shoulders, chest, and back area for
* }% [- w" K9 Pa year. The father also revealed he was embarrassed
% x( w3 c g# g" }- l( b: m% ^1 R9 c/ Kto disclose that he was using a testosterone gel pre-
/ z" S: N# f3 l1 S- R |( y! [scribed by his family physician for decreased libido1 }/ Q: V5 c3 G; u; n# \
secondary to depression.: Z! f) U$ k( s0 q$ S- J
The child slept in the same bed with parents.
7 n. E7 T5 F. i `! Z8 U' rThe father would hug the baby and hold him on his
; j- }) K5 J- u. W! Rchest for a considerable period of time, causing sig-$ n: J# a; S4 `& Q; o, B- N
nificant bare skin contact between baby and father.3 Q l3 B% t+ m- p4 n) X5 i7 {
The father also admitted that after the phone call,& u F# [$ \, }! J' _2 f5 e- x/ Z* I. M" y
when he learned the testosterone level in the baby# Q$ I) H0 M5 F6 [- x. t* c
was high, he then read the product information; Q3 N3 p( O$ \3 @/ [/ H% @1 \
packet and concluded that it was most likely the rea-
* k9 K4 M$ q9 [+ Yson for the child’s virilization. At that time, they
' r" v+ \! ~4 J. t. \decided to put the baby in a separate bed, and the$ I: z( w# H& W( N$ Z3 I7 I
father was not hugging him with bare skin and had
& G5 J# e/ U% h) ^2 G# ]. Fbeen using protective clothing. A repeat testosterone$ W, f: S8 E8 r0 r1 \4 L6 P x5 T
test was ordered, but the family did not go to the$ ]6 D" }/ t5 Y4 e4 g# I" I2 _
laboratory to obtain the test.
6 b# B7 D F% @; K n" ^* ADiscussion
4 k) g' B/ F6 D/ \; t$ u5 j3 w) IPrecocious puberty in boys is defined as secondary
6 i! F1 m! B$ h, e v7 ksexual development before 9 years of age.1,48 C# y9 r1 C) u, z, Y
Precocious puberty is termed as central (true) when) R# ^. g( I2 \9 c# |
it is caused by the premature activation of hypo-$ Z; t c2 {! m
thalamic pituitary gonadal axis. CPP is more com-
. k* {( C( z3 ~( r: v2 X/ u0 qmon in girls than in boys.1,3 Most boys with CPP
2 {/ I* h; K* a& O) m# g$ Y! Wmay have a central nervous system lesion that is) u& m N2 Y. C% B0 l/ ?# w
responsible for the early activation of the hypothal-7 ~# H# x7 T+ `$ s2 n
amic pituitary gonadal axis.1-3 Thus, greater empha-9 d7 [, n7 U% E- b4 d( k' o
sis has been given to neuroradiologic imaging in
w$ e! H) q6 _/ O5 M. |+ K% Lboys with precocious puberty. In addition to viril-) ]1 `3 @0 Q, [5 {" W8 t3 |% t4 J
ization, the clinical hallmark of CPP is the symmet-+ X r* g4 z. N4 S, P& B- f
rical testicular growth secondary to stimulation by4 `5 p# u1 a# J# E; B+ Y
gonadotropins.1,3 \4 M# h% q6 g1 f/ |
Gonadotropin-independent peripheral preco-6 D& `( y) C' ~8 b
cious puberty in boys also results from inappropriate
$ h2 a) [) S8 r' w% }androgenic stimulation from either endogenous or
2 y" r3 J$ X6 p3 u/ T4 \exogenous sources, nonpituitary gonadotropin stim-
7 o$ m' s3 K, j" [ulation, and rare activating mutations.3 Virilizing+ Q% I" b1 ?- b1 V3 }- H
congenital adrenal hyperplasia producing excessive- h1 N' v# l& B/ M
adrenal androgens is a common cause of precocious# E! U+ }, W9 Z9 C/ B
puberty in boys.3,4
8 R+ H, d1 k2 _$ o M; A7 OThe most common form of congenital adrenal
4 m" |) J G6 X5 O8 r0 u( H8 Mhyperplasia is the 21-hydroxylase enzyme deficiency.
+ o& J4 ?) U' I# Q9 ^* ZThe 11-β hydroxylase deficiency may also result in; j$ j& L! r: I" P7 l* d
excessive adrenal androgen production, and rarely,( e1 t. ^! z2 f: R E; i
an adrenal tumor may also cause adrenal androgen: E6 d; V9 | E- h
excess.1,3" v5 H+ b( S0 u6 o5 R* ?( [0 d$ p
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' |' B q t; L0 g6 a+ \2 g6 n. J542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! a) [! H2 D- m9 gA unique entity of male-limited gonadotropin-
! ^( h: d' _& L# r! Cindependent precocious puberty, which is also known5 D& g1 \0 [% r) p
as testotoxicosis, may cause precocious puberty at a, x; T/ W; H1 O: o
very young age. The physical findings in these boys2 H0 ]! p3 L+ P8 K4 f
with this disorder are full pubertal development,9 W. \' ~+ R" V( Y, H+ g
including bilateral testicular growth, similar to boys: L2 |. Z p* u8 ?3 r
with CPP. The gonadotropin levels in this disorder& |3 {" J$ w! r1 @% Y2 H2 k; Y
are suppressed to prepubertal levels and do not show' ]: g3 z5 b8 D, A
pubertal response of gonadotropin after gonadotropin-
/ [8 n2 B6 q2 k7 vreleasing hormone stimulation. This is a sex-linked
, e) d2 f4 \. s t% g9 `( ^autosomal dominant disorder that affects only! E, g6 B, I |5 Q) R6 Q7 r# ?: t
males; therefore, other male members of the family. M {. Q& T( K8 z+ p
may have similar precocious puberty.3
+ H/ c, g0 s3 ]5 W; U+ t/ @7 eIn our patient, physical examination was incon-
4 w! K8 r- @5 g. V( h1 a$ ~sistent with true precocious puberty since his testi-
# f: O, G, M& v' c$ P7 l9 r3 Wcles were prepubertal in size. However, testotoxicosis
8 X# n z& _5 `0 l6 V4 M+ Pwas in the differential diagnosis because his father( m& C6 J M7 g! w
started puberty somewhat early, and occasionally,8 Q, q( f" A/ S0 n5 G
testicular enlargement is not that evident in the) l- J" M$ |# i
beginning of this process.1 In the absence of a neg-2 C" ]9 m2 J/ \1 p6 w
ative initial history of androgen exposure, our
/ v9 B$ v- g1 M' U6 G8 P, jbiggest concern was virilizing adrenal hyperplasia,, _8 k% r l3 G5 S, ? L
either 21-hydroxylase deficiency or 11-β hydroxylase, D% d* M' Q' \9 J( v* i
deficiency. Those diagnoses were excluded by find-
/ c: _+ D7 J$ n" L* xing the normal level of adrenal steroids.; p, G6 i+ N$ S# I) n- ^- d+ J
The diagnosis of exogenous androgens was strongly3 G+ e. N5 [: T; J! y- a
suspected in a follow-up visit after 4 months because2 k( K/ Q# I6 j; b
the physical examination revealed the complete disap-# k3 D, ?6 a' `1 P0 o
pearance of pubic hair, normal growth velocity, and9 G3 e7 J$ F7 y b9 I1 y$ I
decreased erections. The father admitted using a testos-
5 h" j' Z& y4 K9 cterone gel, which he concealed at first visit. He was1 a/ w I* _& H* K$ O1 H
using it rather frequently, twice a day. The Physicians’
^. F7 d' v/ J2 C+ JDesk Reference, or package insert of this product, gel or e: w. W5 [7 `/ P; ^$ a
cream, cautions about dermal testosterone transfer to0 o y& v/ W. q6 ?1 e
unprotected females through direct skin exposure.9 u. g( T4 s# Q# I
Serum testosterone level was found to be 2 times the% ~! Z* w2 Y1 ?3 h( f) e- u0 M: o
baseline value in those females who were exposed to
* j' l M2 a2 @, oeven 15 minutes of direct skin contact with their male
' d- g; J6 E; w! J( d/ \) {partners.6 However, when a shirt covered the applica-) m( P1 J( U6 w0 D! F3 g# y
tion site, this testosterone transfer was prevented.1 o# P( y; ^5 D! E5 |% T
Our patient’s testosterone level was 60 ng/mL,
; |4 m6 g/ }# ^- f$ Kwhich was clearly high. Some studies suggest that
9 ~9 }1 T8 f0 O3 F' Ndermal conversion of testosterone to dihydrotestos-
0 N5 C( x- `7 oterone, which is a more potent metabolite, is more
" r6 r) V( o1 G( X6 D3 _active in young children exposed to testosterone2 i" R7 E0 ]/ p2 A) Z! Z
exogenously7; however, we did not measure a dihy-$ A$ t+ B8 u% u) R. d) M
drotestosterone level in our patient. In addition to$ `* f9 k, S: ~ N: R5 r I
virilization, exposure to exogenous testosterone in
; B, W ]2 o r* Z- _children results in an increase in growth velocity and: R/ ?7 M3 |& [* Y$ K2 M) c
advanced bone age, as seen in our patient.# {: R/ o; a7 @4 R5 E/ p
The long-term effect of androgen exposure during# {: I0 u+ T) y; y3 R Q
early childhood on pubertal development and final
3 L# P" R: ?/ o9 w2 c0 M) Q8 Dadult height are not fully known and always remain
) @, B$ E7 P) N5 ^) q: D$ {a concern. Children treated with short-term testos-
$ r, ]1 `) C1 j2 ?3 ~* H/ Qterone injection or topical androgen may exhibit some
! ~8 A! R6 B" b5 P: v! H; g8 M$ N6 yacceleration of the skeletal maturation; however, after# x$ e4 F( n% Q& i0 R
cessation of treatment, the rate of bone maturation
' n+ V: Y/ H p# B0 Gdecelerates and gradually returns to normal.8,9+ [: D8 I9 t4 S2 Q6 M
There are conflicting reports and controversy# \1 s' p4 @& N4 ^6 G* k. d
over the effect of early androgen exposure on adult- o: R) n) a5 b" ^, B$ L
penile length.10,11 Some reports suggest subnormal" G5 L5 T2 K* h% X
adult penile length, apparently because of downreg-
4 c+ M8 Z b( U7 ]ulation of androgen receptor number.10,12 However,
; H; e9 e3 U0 JSutherland et al13 did not find a correlation between
4 O, A% Z; X7 R) r& Q' \childhood testosterone exposure and reduced adult
, K9 y1 K" P0 F& q# openile length in clinical studies.% y. ^& e9 m3 O) U+ z8 E. ^
Nonetheless, we do not believe our patient is
% a2 B2 A) y: l4 i2 h+ Y$ Hgoing to experience any of the untoward effects from) @( x0 d! e) x l O. \
testosterone exposure as mentioned earlier because
) t' f* ^# c) K0 V$ X- }8 U' Xthe exposure was not for a prolonged period of time.
9 f# ~! r3 @5 w. A- L+ W& c0 j0 RAlthough the bone age was advanced at the time of
0 l l' y5 d" L0 g0 y0 }' wdiagnosis, the child had a normal growth velocity at
2 h* E# ~* G+ j) _/ }# U( mthe follow-up visit. It is hoped that his final adult
, T& l8 ?. @- b" Dheight will not be affected.; u% O3 ]! N! |; ~6 ?4 Q e* n
Although rarely reported, the widespread avail-
) ^+ c3 E( W$ J& q Kability of androgen products in our society may, D: N, L5 E3 j, n9 O j
indeed cause more virilization in male or female; k, s8 f9 ]$ M# {
children than one would realize. Exposure to andro-( p7 u4 v% r! C
gen products must be considered and specific ques-
* M5 ]$ R4 E! e @tioning about the use of a testosterone product or
: I7 I" {6 u! v$ i5 ^( ugel should be asked of the family members during
0 i8 H0 V& Y& J! t+ dthe evaluation of any children who present with vir-8 n0 d" N" c7 W- `( D7 G& ~
ilization or peripheral precocious puberty. The diag-: A/ Y$ x8 s0 @ c3 s/ ^7 T2 m
nosis can be established by just a few tests and by
* @; y+ }/ d) [6 }5 rappropriate history. The inability to obtain such a/ R6 q4 \& N# i/ y* _4 k& H. f
history, or failure to ask the specific questions, may
# x) ^8 y# D E* p: |5 z0 O- hresult in extensive, unnecessary, and expensive
; T4 @5 h4 k" N% n% I. w2 w0 ?investigation. The primary care physician should be
5 O6 G) l6 }1 X7 Naware of this fact, because most of these children$ n9 ^, r# `0 P4 r) ~! ]1 v5 i8 D
may initially present in their practice. The Physicians’! j, F0 B% U* Q4 ]
Desk Reference and package insert should also put a2 o; D* B2 ?+ p
warning about the virilizing effect on a male or
! M8 n' L; }+ i. G: i9 vfemale child who might come in contact with some-, b" g3 `! D* @. R( ^8 `* \
one using any of these products.
- s' B/ R5 j' q! V: A0 l$ dReferences' } Q6 }+ H1 y
1. Styne DM. The testes: disorder of sexual differentiation7 K" o# Z3 F/ M) d
and puberty in the male. In: Sperling MA, ed. Pediatric+ A( {- `, m) M% h3 A& X3 ?
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 M7 r' H( B& E% Q, ~- }4 H8 c2002: 565-628.9 U, Y6 h7 i2 m; q8 b5 `
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 O4 M) g7 t$ C2 Apuberty in children with tumours of the suprasellar pineal |
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