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Sexual Precocity in a 16-Month-Old
% {, a. y3 N; g8 @5 } H, e1 G7 XBoy Induced by Indirect Topical
^4 {" [6 N$ y4 g+ |Exposure to Testosterone* ~3 t+ m3 O4 Q$ m; W
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- @1 _+ |$ y8 A( Y4 X' s
and Kenneth R. Rettig, MD1: k- \9 g9 P9 d% t: O+ A @
Clinical Pediatrics
! Z9 ~, V9 s6 S! G# A. I0 i* m# u3 jVolume 46 Number 6
0 g9 @' j0 ^& ^. ^: {/ iJuly 2007 540-543+ [& Z; v4 s6 }! e8 }: |7 [
© 2007 Sage Publications* j# B# z# N; y# K3 d9 l
10.1177/00099228062966516 p$ |: b% O/ i5 }
http://clp.sagepub.com
7 _; Z( j$ ^! p; S; }hosted at2 Z6 U+ H% S0 K! u; j, O+ g
http://online.sagepub.com
6 N! U, J' |3 Y( y6 t5 WPrecocious puberty in boys, central or peripheral,2 L- x) Z4 c( c8 Y/ U/ h6 e# ]4 ]
is a significant concern for physicians. Central! c) ?8 C* r& ]( E( ^- n0 ^
precocious puberty (CPP), which is mediated6 B4 x# ^ T1 F# Y
through the hypothalamic pituitary gonadal axis, has$ P$ ]8 }& r M; p. A& L+ ^
a higher incidence of organic central nervous system
8 k" c( l1 E/ a1 s% |# v% _lesions in boys.1,2 Virilization in boys, as manifested& }$ C, B F s; S0 n
by enlargement of the penis, development of pubic% d$ A' L& g7 C% b
hair, and facial acne without enlargement of testi-
2 d" b1 \- s: D' m" {: ucles, suggests peripheral or pseudopuberty.1-3 We
* C1 K- |. e4 G/ ireport a 16-month-old boy who presented with the/ Z0 ^; H- e# w: Y3 R/ P" c# {
enlargement of the phallus and pubic hair develop- Q8 G" p; \1 u& z
ment without testicular enlargement, which was due/ v! N- ^6 k0 d; H( ^
to the unintentional exposure to androgen gel used by# p; ]+ {- V1 Y
the father. The family initially concealed this infor-! P9 e- E& Z; C4 p7 V' a
mation, resulting in an extensive work-up for this1 i( J' |5 ?+ S: G) o' ^
child. Given the widespread and easy availability of
+ ?/ {- I( {0 f+ I: {testosterone gel and cream, we believe this is proba-9 H) H9 l3 ^8 v9 w
bly more common than the rare case report in the8 V0 [# f! w6 }. y( P
literature.4; F8 m' A( @' _3 U' Z
Patient Report" ^4 Z/ u6 o' Z# q8 `4 s: y' m* b
A 16-month-old white child was referred to the
7 w: Y7 s! k, ^& S: w- _ k% ]1 qendocrine clinic by his pediatrician with the concern" R4 b# i; @5 a4 Z c$ U/ w
of early sexual development. His mother noticed
* L0 `) Q6 F! J% {" g' k3 b( mlight colored pubic hair development when he was
' V7 I( E- c, J5 h' MFrom the 1Division of Pediatric Endocrinology, 2University of: r4 K& m4 F4 R; j2 L2 b3 i
South Alabama Medical Center, Mobile, Alabama.
7 N- {; I% I' Z0 T3 ^Address correspondence to: Samar K. Bhowmick, MD, FACE,
|, c1 I" O. n4 d, b2 g# wProfessor of Pediatrics, University of South Alabama, College of
) r6 V9 f- z B: nMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# n- y5 @: K. i6 @% O- r
e-mail: [email protected].- V8 D8 F! c$ y* F0 p+ {1 b, @
about 6 to 7 months old, which progressively became% k. D, f& u* L- j: ^
darker. She was also concerned about the enlarge-
+ X+ u; j6 ]- @! f/ m; j. ~ment of his penis and frequent erections. The child
: e+ g: b( p+ X9 B8 l" L9 wwas the product of a full-term normal delivery, with
) X6 E. t' O/ }8 c% E3 c' @a birth weight of 7 lb 14 oz, and birth length of% z* U; v6 k9 J- b2 X. i
20 inches. He was breast-fed throughout the first year7 Y! L$ ]4 B6 Z$ {. s6 |$ k5 K
of life and was still receiving breast milk along with
( x; ~! q5 l2 `' q9 wsolid food. He had no hospitalizations or surgery,! p# o6 t4 K% i+ y/ c
and his psychosocial and psychomotor development
( }6 [. K9 \2 m1 s2 Bwas age appropriate.: [! D, J2 O) _
The family history was remarkable for the father,
% n. d$ ]; ^4 I% zwho was diagnosed with hypothyroidism at age 16,
5 J/ Y' `, c! v j! r( ?which was treated with thyroxine. The father’s
4 q4 C6 m& W9 P8 R' b! lheight was 6 feet, and he went through a somewhat( _* \+ _; C4 w* ~% s$ k
early puberty and had stopped growing by age 14.' `( {* j$ m; g/ ]- o
The father denied taking any other medication. The
$ q8 v8 E' z0 i, G G$ Schild’s mother was in good health. Her menarche: Q7 t: Y3 J H0 K* N" P
was at 11 years of age, and her height was at 5 feet
" W& V# h! d u$ C5 inches. There was no other family history of pre-; ?! _! h7 Y7 o V8 T* t5 X; V9 K
cocious sexual development in the first-degree rela-4 H$ [/ i1 G$ `& Z: n4 R% \
tives. There were no siblings.
( D& r3 b4 Q. }, p/ k0 r7 ~: xPhysical Examination
) r" d8 [8 ~+ r$ C9 Q6 U6 d( N3 xThe physical examination revealed a very active,
U5 B# o1 C& a/ G4 Q" G% vplayful, and healthy boy. The vital signs documented7 b% t* Q8 t) h' w
a blood pressure of 85/50 mm Hg, his length was
. a0 U/ p* D0 p4 t& ~) F4 K90 cm (>97th percentile), and his weight was 14.4 kg
# E3 G2 N0 H9 j3 ^ k(also >97th percentile). The observed yearly growth# D5 g# X( {3 w# O1 x, C3 J: @
velocity was 30 cm (12 inches). The examination of. O6 |( e% @- b7 f( D7 _% } u
the neck revealed no thyroid enlargement.8 T/ f* G1 o6 x, b, E# w5 p
The genitourinary examination was remarkable for$ V3 d4 a. a/ C* C, Y4 f# Y0 F/ t
enlargement of the penis, with a stretched length of
" j% K+ W( r9 v, ~/ ?! W8 cm and a width of 2 cm. The glans penis was very well
2 c V( x% M! [3 W% @developed. The pubic hair was Tanner II, mostly around |$ @6 u7 m$ o4 N2 _- d
540
4 q8 J x6 s* J! q* M: O( \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 u. d, g% M- P1 m- D8 {the base of the phallus and was dark and curled. The" g# j5 Y+ h) g+ @) ]0 v. Z
testicular volume was prepubertal at 2 mL each.
) |) K7 v$ Q/ q5 i% AThe skin was moist and smooth and somewhat
$ }* r/ R4 }! b# R' poily. No axillary hair was noted. There were no. I, y8 _' `9 `0 L1 s1 w' m' V; b
abnormal skin pigmentations or café-au-lait spots.$ u9 k2 H& u" f3 v% L
Neurologic evaluation showed deep tendon reflex 2+
4 R; d9 ~% y' lbilateral and symmetrical. There was no suggestion
z7 M( ]7 @( j5 `- S; Vof papilledema.
, v: y: r F# X h, ZLaboratory Evaluation
7 |/ e" p, z# C W+ e3 aThe bone age was consistent with 28 months by
( ^ p" n' x ?$ |( m \* q9 q; yusing the standard of Greulich and Pyle at a chrono-9 U8 d& s/ E( \+ v" c% x
logic age of 16 months (advanced).5 Chromosomal
9 I G* x1 I% l U# ~. O& f8 [karyotype was 46XY. The thyroid function test
- L' ]- N$ b5 v$ Ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-3 b5 R3 Y! U: M9 D8 L
lating hormone level was 1.3 µIU/mL (both normal).
" k! y( J/ d# n& o, l+ Q! q$ hThe concentrations of serum electrolytes, blood$ e' h- i# v1 m3 e* J) z
urea nitrogen, creatinine, and calcium all were
7 r7 ? @+ t+ @: C3 z# Lwithin normal range for his age. The concentration e* O9 m1 q0 `. j( \$ Q" m
of serum 17-hydroxyprogesterone was 16 ng/dL
% O% ?' T* { d. z3 K7 q(normal, 3 to 90 ng/dL), androstenedione was 20
& F7 }: @8 M; {4 Y3 Z- `, gng/dL (normal, 18 to 80 ng/dL), dehydroepiandros- P' y4 V; x/ H, E
terone was 38 ng/dL (normal, 50 to 760 ng/dL),, F3 g0 s8 D; h _0 l
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
; o: X J& e2 C; ?4 L. {4 a8 M49ng/dL), 11-desoxycortisol (specific compound S)6 i; w2 c4 a' x
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# ~, C' [( j3 \$ k! W
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total6 E" N! p* T7 |- R& x* O- m
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),) t, d' c y/ k; e; ^
and β-human chorionic gonadotropin was less than
5 {3 f: c' q5 F7 N5 mIU/mL (normal <5 mIU/mL). Serum follicular
* y# j f7 @8 u+ `+ i$ a- Ostimulating hormone and leuteinizing hormone
1 N! g' x& f4 l9 l5 T/ y/ K; ^concentrations were less than 0.05 mIU/mL
8 U# ?# U% `. C( }(prepubertal).
. H, i% V) B& E' ^The parents were notified about the laboratory$ r0 F9 k& g. X+ X
results and were informed that all of the tests were! O- R8 I* R C7 l3 ?* ]
normal except the testosterone level was high. The
* H% [! ?0 p2 [" d0 pfollow-up visit was arranged within a few weeks to
$ `% R1 u7 v4 \0 z& |" S( tobtain testicular and abdominal sonograms; how-* c. ]" F! u5 U+ a: w
ever, the family did not return for 4 months.
4 P3 }2 Q6 O' N7 c& k0 rPhysical examination at this time revealed that the+ r( F9 q( J3 J, W7 b
child had grown 2.5 cm in 4 months and had gained3 ^* p6 m, C/ k5 j. {. E3 h/ v
2 kg of weight. Physical examination remained: S; m. P2 v- {. L4 C
unchanged. Surprisingly, the pubic hair almost com-; [8 O( t% A( X
pletely disappeared except for a few vellous hairs at
) B2 @. Q+ g6 C, c# ]) y& A. kthe base of the phallus. Testicular volume was still 2
+ W' k) T( e' F0 ^3 S& d5 F" i" @, }mL, and the size of the penis remained unchanged.# g! N1 j8 ^5 n
The mother also said that the boy was no longer hav-8 m. T2 h% x9 G, A, h q( V
ing frequent erections.
: g: ]( c& z6 J4 eBoth parents were again questioned about use of
& I$ V! b( ?0 U- y l, Nany ointment/creams that they may have applied to
@& K4 `8 S2 v- [0 @the child’s skin. This time the father admitted the
; z1 Q" l7 h, u' x& CTopical Testosterone Exposure / Bhowmick et al 541
1 I9 _& X9 { Z, a8 D6 o+ iuse of testosterone gel twice daily that he was apply-
. s/ y" J% s: d. Y/ zing over his own shoulders, chest, and back area for
1 E4 R0 ^; y% ]& K1 s1 y# F/ Ma year. The father also revealed he was embarrassed/ \ h$ J: l# _& E% `
to disclose that he was using a testosterone gel pre-7 J8 n- Z- ]) ` f; O* f
scribed by his family physician for decreased libido
O+ ]% L j& j6 J/ M: V3 g* ssecondary to depression.! X- O$ L& S u; {2 ^* E3 x
The child slept in the same bed with parents.
# l. [2 L- s5 ~The father would hug the baby and hold him on his
4 X% s& X9 |& b, K3 gchest for a considerable period of time, causing sig-
1 k O6 E% ~2 N0 [+ B' Lnificant bare skin contact between baby and father.
0 s6 k4 O A: f5 Y0 X [) u! r0 j1 jThe father also admitted that after the phone call,+ c2 I. H) q+ t) l0 q d
when he learned the testosterone level in the baby
5 j5 `6 ^3 v2 D$ [% v$ c( w* Gwas high, he then read the product information/ U. \9 q2 l' g& K+ n) S* T* F4 p
packet and concluded that it was most likely the rea-1 q2 R' |1 l: ? E3 s2 j
son for the child’s virilization. At that time, they. C1 F) A- w# S, _! ]# j
decided to put the baby in a separate bed, and the& q, b& J. i4 W
father was not hugging him with bare skin and had
& e5 U# n R9 } b. n/ Gbeen using protective clothing. A repeat testosterone
& T! Y/ A+ m, t0 Ctest was ordered, but the family did not go to the
( O3 c0 B1 i! B& l0 b) v8 d0 ^laboratory to obtain the test.
% Z# V" P9 i& a4 i, P1 ^+ FDiscussion& ~- ]/ L. _) c I9 J3 u
Precocious puberty in boys is defined as secondary: u. C9 a" L$ s3 }9 O
sexual development before 9 years of age.1,4: M5 S7 ~1 S: z
Precocious puberty is termed as central (true) when" q( d) K( }/ ]
it is caused by the premature activation of hypo-
' u& s& n" t: T, a* v8 tthalamic pituitary gonadal axis. CPP is more com-
+ w5 g, U- {. g& |' t, Nmon in girls than in boys.1,3 Most boys with CPP
3 d2 g7 B5 p }8 O2 nmay have a central nervous system lesion that is- c. s6 K8 P$ O5 O3 y1 z- j
responsible for the early activation of the hypothal-+ @3 g7 L$ n3 T R$ Q$ z
amic pituitary gonadal axis.1-3 Thus, greater empha-
O2 U! }" A y6 Gsis has been given to neuroradiologic imaging in8 ?0 P7 O2 O( c7 p+ e' R
boys with precocious puberty. In addition to viril-, Z. v% \+ a1 G. Y9 h+ n/ ?
ization, the clinical hallmark of CPP is the symmet-$ o9 f; W5 Y4 ?; a8 u& J9 H
rical testicular growth secondary to stimulation by
7 b+ h* }* q& u( S, t+ [) |7 [4 H: ggonadotropins.1,3
( s4 f; w6 v x R* M/ c$ ~Gonadotropin-independent peripheral preco-
# r! `- n7 N4 N: ^cious puberty in boys also results from inappropriate- l6 Q y1 B6 Q6 e7 h ?4 O
androgenic stimulation from either endogenous or
' E4 G- G. T: u0 h: l6 K4 I* x8 Oexogenous sources, nonpituitary gonadotropin stim-
) c& E+ O0 w& z' u6 \! hulation, and rare activating mutations.3 Virilizing* a, ~; x$ ]0 }7 J- C, e7 b4 r) p) P
congenital adrenal hyperplasia producing excessive( v: V2 i9 J" T, `2 l& n
adrenal androgens is a common cause of precocious J/ [% \6 _8 V# Z' ?/ G' @
puberty in boys.3,4
/ M+ l" P( i! C0 x7 b2 XThe most common form of congenital adrenal
1 K' ?1 P; ^# p" w) t- f/ ?hyperplasia is the 21-hydroxylase enzyme deficiency.1 j5 ^/ C$ O3 ]5 o) p
The 11-β hydroxylase deficiency may also result in
Y3 o5 u, O/ p% hexcessive adrenal androgen production, and rarely,0 z: Q( k, L4 W0 X0 j
an adrenal tumor may also cause adrenal androgen
$ s' K7 i% ^, {excess.1,30 U3 f$ g% K v5 {7 K$ c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% f1 q3 c* |) c( J/ z5 I2 A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; @) E9 H; G) Y/ a8 E, {, z2 IA unique entity of male-limited gonadotropin-
0 K+ Z# H2 N0 p xindependent precocious puberty, which is also known
% ^2 L. |& T& N$ R9 g4 oas testotoxicosis, may cause precocious puberty at a+ Y& w" e8 e- s* {
very young age. The physical findings in these boys/ u3 L! Q% w: i" Y5 y. Q" ^4 Z
with this disorder are full pubertal development,
2 }$ g2 U) E D( p5 p1 ^( Xincluding bilateral testicular growth, similar to boys4 S# F- z" ]. Y& O" }: L8 [
with CPP. The gonadotropin levels in this disorder/ F0 j% }9 ]2 g5 z9 h' ^0 s
are suppressed to prepubertal levels and do not show F5 W, S. z# M o2 g2 f
pubertal response of gonadotropin after gonadotropin-9 Z9 C0 Q5 I- D! B8 Z2 X
releasing hormone stimulation. This is a sex-linked
- F( u( w: O+ m; _1 n8 U; Cautosomal dominant disorder that affects only9 E$ P3 R. W% W! u
males; therefore, other male members of the family
- H2 h* n6 c5 N# W; }may have similar precocious puberty.3
+ @9 J5 w0 {5 {' cIn our patient, physical examination was incon-9 d; Z9 o3 R6 U5 e1 }7 a. d- E
sistent with true precocious puberty since his testi-$ E$ t2 b' G! Q& U+ o( Z9 I
cles were prepubertal in size. However, testotoxicosis
- ^1 e; t" a$ _" Z: m8 Twas in the differential diagnosis because his father
: o m, q- M+ r- estarted puberty somewhat early, and occasionally,5 T5 M2 d& \8 C2 A. G0 w
testicular enlargement is not that evident in the
0 q; O, i1 Y6 Qbeginning of this process.1 In the absence of a neg-* m, @3 s! r: }3 S! M% t! A! m
ative initial history of androgen exposure, our
% g9 X* c% r- m5 @6 Hbiggest concern was virilizing adrenal hyperplasia,3 ~- U T* D& w! J' k& V
either 21-hydroxylase deficiency or 11-β hydroxylase
# ^0 }/ [( k" R2 Z7 J0 `deficiency. Those diagnoses were excluded by find-( m* U3 m9 t" H6 W. h7 ~1 l2 ~
ing the normal level of adrenal steroids. [ N: _( ^0 y4 n
The diagnosis of exogenous androgens was strongly0 o6 D& |# E8 r: f6 x0 T# O/ V, g
suspected in a follow-up visit after 4 months because
6 i9 @' f% @3 q- @9 Sthe physical examination revealed the complete disap-" H' n- P. O9 C. E2 q' i
pearance of pubic hair, normal growth velocity, and
. ?) c5 E/ Z/ P, {. r6 f7 ?) Xdecreased erections. The father admitted using a testos-
' D% ~* T# F% E! \' qterone gel, which he concealed at first visit. He was' x! B! b3 [4 e( J- z- F& O4 w' d
using it rather frequently, twice a day. The Physicians’
1 s2 N. W! Z% S$ ^7 R0 PDesk Reference, or package insert of this product, gel or$ o/ z- b3 a. i5 U# R) J2 u
cream, cautions about dermal testosterone transfer to' x( s; R3 ?- F% Y2 u
unprotected females through direct skin exposure.' x4 `: C( x; J' a7 p, w
Serum testosterone level was found to be 2 times the
0 Z$ z' n0 @$ r' l0 ^baseline value in those females who were exposed to4 V, n4 \, f. F9 f9 ^
even 15 minutes of direct skin contact with their male
4 R: i9 V: y% [/ w% ?. Epartners.6 However, when a shirt covered the applica-0 A V# c7 l: P. n% n* |8 |
tion site, this testosterone transfer was prevented.
9 E$ ~5 s& u+ @5 v+ ]Our patient’s testosterone level was 60 ng/mL,7 l" h8 N' N: n) h/ i7 u
which was clearly high. Some studies suggest that
& q V8 S) g: ?, Ddermal conversion of testosterone to dihydrotestos-
5 ?5 T; T! ]+ k" \& k" X3 ?. f4 Gterone, which is a more potent metabolite, is more! p' h1 x. N+ t, ^7 |' [2 A
active in young children exposed to testosterone
; b% T2 z b( ^. Q2 iexogenously7; however, we did not measure a dihy-
) U5 c# J) J8 _7 ~drotestosterone level in our patient. In addition to- \$ r" p# S) ^
virilization, exposure to exogenous testosterone in
* K& Q* Q- g" w" wchildren results in an increase in growth velocity and
9 t1 v" p3 E: p5 e! Vadvanced bone age, as seen in our patient.9 z% o7 ]' L6 l. h9 D
The long-term effect of androgen exposure during
) q$ W9 h: z# F, z1 {& @) T, d ~% i! yearly childhood on pubertal development and final4 s4 N. i+ _, J B
adult height are not fully known and always remain
2 o" p( x; e, {- Ka concern. Children treated with short-term testos-* T' L/ C2 @/ S! y9 h% F$ a. x
terone injection or topical androgen may exhibit some! }6 l5 x4 _, B9 Z
acceleration of the skeletal maturation; however, after
3 E( y7 R% w# N q+ b! Dcessation of treatment, the rate of bone maturation" {7 m) K' C# `2 m$ _( K: s
decelerates and gradually returns to normal.8,9
* T7 {: E4 E% e# s! p4 ZThere are conflicting reports and controversy% x6 P) W+ t* K) ]/ n" n: ]" _
over the effect of early androgen exposure on adult- e. O+ r5 f8 u
penile length.10,11 Some reports suggest subnormal5 G. d0 P( @* B
adult penile length, apparently because of downreg-
; j6 u/ y9 c7 M3 d- O4 g$ J5 Z) Yulation of androgen receptor number.10,12 However,
+ G! d7 g, v: n, D# ~6 m% [' `# `Sutherland et al13 did not find a correlation between
- `* j4 A9 g1 Z# S. I5 ^childhood testosterone exposure and reduced adult) W8 w( z2 s/ M4 x y# E" {
penile length in clinical studies.; U9 y- p" i) h% x, M
Nonetheless, we do not believe our patient is0 s- c+ k6 F- x" I& ?9 x) X
going to experience any of the untoward effects from& A! K2 S( F3 M5 V
testosterone exposure as mentioned earlier because
- ?: ?7 v- o/ E0 m6 ?the exposure was not for a prolonged period of time., S: O" w% ^6 p! A! g% T0 c( L
Although the bone age was advanced at the time of& y& Q8 @% u3 ] ^4 o
diagnosis, the child had a normal growth velocity at
! j& n, n- w H$ F+ s. @3 g5 Lthe follow-up visit. It is hoped that his final adult+ J5 `7 E# I K6 ~/ m* Y& u
height will not be affected.
) R4 p/ v! O! t( ZAlthough rarely reported, the widespread avail-7 w+ T6 \/ L% \$ z
ability of androgen products in our society may% y. \9 G6 a7 S, |6 _
indeed cause more virilization in male or female/ Y* z, {0 v& J7 c8 J6 B
children than one would realize. Exposure to andro-
: a- B& g3 ~% z; \gen products must be considered and specific ques-
. ]( R$ z% A( A/ _2 f/ K0 `tioning about the use of a testosterone product or. W- |; P! m. o7 \2 M4 x' f4 U
gel should be asked of the family members during
. |! G! T% r6 ]5 D4 Othe evaluation of any children who present with vir-
$ U0 e$ t% `* `4 p9 iilization or peripheral precocious puberty. The diag-5 ?; w, c. T6 H! r4 M) r2 t
nosis can be established by just a few tests and by* v8 k3 X: X' Z8 K3 G
appropriate history. The inability to obtain such a
7 ?% s: q6 l H. }/ V) }. X1 chistory, or failure to ask the specific questions, may
- h/ o. B, ?- R" _! y0 Kresult in extensive, unnecessary, and expensive5 u+ v" q3 m1 M9 B' V
investigation. The primary care physician should be1 Q/ O8 L1 C7 v+ |8 @3 K
aware of this fact, because most of these children; M3 x4 o& W0 u' \2 U
may initially present in their practice. The Physicians’
) H1 [5 ?. B. H1 B* {Desk Reference and package insert should also put a* B$ }- H1 L+ Y, S; N r! B* q
warning about the virilizing effect on a male or3 p4 L2 o' k0 i0 X c& T$ k
female child who might come in contact with some-7 c4 n7 A( `( y V, }/ \) q+ |
one using any of these products.
% ^9 r: k5 q5 i4 e' ]' T OReferences
# ]1 x% Q, x+ d/ P1. Styne DM. The testes: disorder of sexual differentiation h( e, o* \ b/ S1 F
and puberty in the male. In: Sperling MA, ed. Pediatric6 y% R& T/ b$ v- R% ~
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* D D- O% k$ R$ l! U) T# J
2002: 565-628.5 @0 U/ @) n2 t4 K5 S4 l! ]
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 y9 ?" n& n" R( n( r! z
puberty in children with tumours of the suprasellar pineal |
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