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Sexual Precocity in a 16-Month-Old
" M7 x$ e. S* r! \0 g0 b# UBoy Induced by Indirect Topical3 v3 w( ~" y! B& p( K5 Y
Exposure to Testosterone/ \% g, N: y' a4 K' X) u2 x
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 e: W5 G' _- n( N: b. X( }
and Kenneth R. Rettig, MD1
$ R, l+ l* Y# {$ L) nClinical Pediatrics
) z# Q4 o, Z2 z6 G- g+ `Volume 46 Number 6
; G3 @) v+ V9 W4 l# ]July 2007 540-543# Z+ A/ w5 q' S+ ^
© 2007 Sage Publications
. r _6 v' v0 P- B10.1177/0009922806296651- O6 C3 s8 |! {3 G0 z
http://clp.sagepub.com$ [& [# K! \! W8 t- v9 S
hosted at; w. _1 J8 {5 M3 I t; u5 c
http://online.sagepub.com$ X' m* {7 w, j) X* R+ z$ \
Precocious puberty in boys, central or peripheral,7 Q: \8 R$ l9 k$ n0 p
is a significant concern for physicians. Central
5 E9 z" L& p3 o, c, pprecocious puberty (CPP), which is mediated
4 U3 v9 E" c* G) Sthrough the hypothalamic pituitary gonadal axis, has
1 c9 V: C$ Y1 a. J+ F0 ^a higher incidence of organic central nervous system6 Q$ H, d C1 R C- c5 N
lesions in boys.1,2 Virilization in boys, as manifested
9 Z' {5 s9 b3 a I$ [1 sby enlargement of the penis, development of pubic
) j+ e! w) ^1 Z# I2 ~hair, and facial acne without enlargement of testi-
m C- t- I7 U9 Ecles, suggests peripheral or pseudopuberty.1-3 We0 F' J/ k* ?5 d) w L
report a 16-month-old boy who presented with the" f6 w1 t7 G2 { M2 |" c5 `
enlargement of the phallus and pubic hair develop-. w+ a! t* s8 J7 U# h- W7 K
ment without testicular enlargement, which was due
2 l* ]2 J- a7 S L2 mto the unintentional exposure to androgen gel used by
/ c1 M8 T2 y% p0 T3 e; C. pthe father. The family initially concealed this infor-: w0 \% V- N! f; I4 H
mation, resulting in an extensive work-up for this
4 n+ I' I) G) g; }7 ]9 F4 Ychild. Given the widespread and easy availability of
& P% v0 f' B6 W$ Mtestosterone gel and cream, we believe this is proba-8 W: P( ?/ h/ H. w6 v* W. v
bly more common than the rare case report in the# ]9 t; F1 j4 H$ S
literature.4
8 |1 H7 l/ m Q8 J! L- ]Patient Report
/ b' c! B# i& E* r/ J& W2 C7 k" ?A 16-month-old white child was referred to the2 Y8 @, a- y/ P) j1 M- Q
endocrine clinic by his pediatrician with the concern5 Z1 a0 L! H o8 j K1 V4 F
of early sexual development. His mother noticed# I; i' Y2 r5 q5 C
light colored pubic hair development when he was* W; y& n. e+ W( \) N
From the 1Division of Pediatric Endocrinology, 2University of/ V! P. Z# G- `3 B: k. c
South Alabama Medical Center, Mobile, Alabama.& G1 ]6 r: L6 y8 G, z; a. G
Address correspondence to: Samar K. Bhowmick, MD, FACE,6 ]3 m" g; g, n& u6 D
Professor of Pediatrics, University of South Alabama, College of$ `) a5 c& p9 x0 q
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;* @) G% E* Z) R& ^2 \4 m% b9 ~
e-mail: [email protected].. y: ]& w5 C* N. W9 S" ]
about 6 to 7 months old, which progressively became
9 L: V m8 G+ Q# ^4 q. Ddarker. She was also concerned about the enlarge-
& t$ M6 a1 ?2 y5 ?9 cment of his penis and frequent erections. The child
0 ]& }3 l; r6 ]1 `8 u/ d( P" Ywas the product of a full-term normal delivery, with$ c& s+ S% e! Y3 C$ u
a birth weight of 7 lb 14 oz, and birth length of
8 `. N7 G8 n" {; A# d8 K20 inches. He was breast-fed throughout the first year$ b+ L4 f0 u4 W/ n8 T
of life and was still receiving breast milk along with- I: p( s$ S' U# o5 D9 @
solid food. He had no hospitalizations or surgery,7 g- @2 W! Z) Q6 h" N; Q
and his psychosocial and psychomotor development
( p: S' L( F5 ~$ ?. [0 Fwas age appropriate.
7 M5 N) S0 ~. @4 l( K3 E RThe family history was remarkable for the father,! D+ Z" ^* P( h, W
who was diagnosed with hypothyroidism at age 16,9 b$ y% J" T3 A& w* L9 \4 H
which was treated with thyroxine. The father’s- g: @' P' V2 }8 u( Z! r
height was 6 feet, and he went through a somewhat
. g: E- k0 v! Y Z9 q5 D/ Cearly puberty and had stopped growing by age 14.+ m8 I, f( `; |/ |2 A
The father denied taking any other medication. The/ J: N8 E( Y; b/ D
child’s mother was in good health. Her menarche
5 a" @/ ?# `( `. }# Uwas at 11 years of age, and her height was at 5 feet( D4 f9 V' A$ I6 k' o* @
5 inches. There was no other family history of pre-
; |/ {7 ]. v. E6 ^: d: O/ }cocious sexual development in the first-degree rela-
3 \% l* `0 f9 I4 Wtives. There were no siblings.
! t1 Z* q% I3 G3 EPhysical Examination
0 ]$ @" x" A- e# X% t5 [- NThe physical examination revealed a very active," {4 q! G% Q$ }2 `3 `
playful, and healthy boy. The vital signs documented& y% Q7 [9 j; s) t) {3 A
a blood pressure of 85/50 mm Hg, his length was
]" ?7 `( N9 l& |90 cm (>97th percentile), and his weight was 14.4 kg
1 U" b. j, j$ s. E0 Z& k(also >97th percentile). The observed yearly growth! |- m% C- r2 b' J. v! a0 k- [
velocity was 30 cm (12 inches). The examination of
r; H4 ^- }: A4 B, Gthe neck revealed no thyroid enlargement.
+ w6 y2 |8 y1 W- SThe genitourinary examination was remarkable for9 l+ s/ |0 ] Q2 h0 W. U- P, ~1 Y
enlargement of the penis, with a stretched length of. e8 B4 a& @- i: P
8 cm and a width of 2 cm. The glans penis was very well ^- O. D2 w/ ], f3 ?+ K" r
developed. The pubic hair was Tanner II, mostly around
% O$ o$ p. _; V8 @' |' P540: b0 C; y5 d! D: _
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 _; n$ o: E9 y' V& n7 k" N
the base of the phallus and was dark and curled. The
" l4 _4 s" I' U+ c$ Y3 g: \testicular volume was prepubertal at 2 mL each.' o2 \ s" N9 a0 Q% [
The skin was moist and smooth and somewhat' G- f+ N, f7 q5 [) u
oily. No axillary hair was noted. There were no+ A* j2 G+ \, h* l9 p+ r4 Q) \% A
abnormal skin pigmentations or café-au-lait spots.
& c% e$ E) r% C, Z3 @( |7 TNeurologic evaluation showed deep tendon reflex 2+$ {7 m8 e' U* r1 H% n
bilateral and symmetrical. There was no suggestion1 @ P% `. X, H' R
of papilledema.5 m# E* Z0 r6 u4 E% K5 f# T
Laboratory Evaluation! a) i0 x; ^! i$ N/ z/ J1 n) o8 l
The bone age was consistent with 28 months by
3 N% d) q: z/ c, U4 q3 T2 zusing the standard of Greulich and Pyle at a chrono- L1 p& }* A! Q! `0 O" \# d/ P% p \
logic age of 16 months (advanced).5 Chromosomal
8 I6 ~% a, l, Q, s, y/ mkaryotype was 46XY. The thyroid function test* z3 T9 F% M# F* D6 t
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
" K1 A# A3 _( ]- X! }3 |lating hormone level was 1.3 µIU/mL (both normal).0 Y( E1 n+ s! b
The concentrations of serum electrolytes, blood# M/ x: b+ B1 q U- \
urea nitrogen, creatinine, and calcium all were5 O! a3 ]7 m6 G+ q/ [: g# e8 P' H
within normal range for his age. The concentration& S1 \9 x5 y0 f5 q; W
of serum 17-hydroxyprogesterone was 16 ng/dL, Q+ |" W" W) {! G5 b8 [$ ^5 f
(normal, 3 to 90 ng/dL), androstenedione was 20
r: w2 M6 f( d8 {& png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
9 m$ x2 `- ^) A0 M9 N# e! z! tterone was 38 ng/dL (normal, 50 to 760 ng/dL),
% O! S7 f9 K* c* d. F, [desoxycorticosterone was 4.3 ng/dL (normal, 7 to
3 F) {/ M7 P) ~! z% z' a49ng/dL), 11-desoxycortisol (specific compound S)' j9 M8 V9 x+ B4 g
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, C- F: h. C% v, E( `7 {; C
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. K! Y8 h! o l0 [, }" [) r7 ftestosterone was 60 ng/dL (normal <3 to 10 ng/dL),% e$ }/ [8 _. [- T3 l
and β-human chorionic gonadotropin was less than |& w+ a' M1 p: X( E
5 mIU/mL (normal <5 mIU/mL). Serum follicular
; x9 Y6 `# D: E/ F1 j% \, }! Xstimulating hormone and leuteinizing hormone, @4 U: C) ~- D# P% U% M7 v
concentrations were less than 0.05 mIU/mL
! u) ^; [0 G3 ^(prepubertal).' S6 L; u# ]/ t: p& g* K+ O
The parents were notified about the laboratory
' s- S* y9 V" Xresults and were informed that all of the tests were, `6 u& k( m$ ~* O% D; Y4 H9 j* ]- k
normal except the testosterone level was high. The
1 C) z. b7 m' E( p! H5 s- pfollow-up visit was arranged within a few weeks to
5 E% C8 v8 H3 O* M; d% c" Tobtain testicular and abdominal sonograms; how-
% U5 @2 U9 y( f2 e/ Tever, the family did not return for 4 months.
/ d; a- L4 N) x2 t4 `2 GPhysical examination at this time revealed that the
/ E% K+ ?9 l' K: _$ \2 Dchild had grown 2.5 cm in 4 months and had gained
5 M9 K7 K1 K, |* W2 kg of weight. Physical examination remained0 {! V& K( H- P1 u+ Q- P4 v" U
unchanged. Surprisingly, the pubic hair almost com-5 O$ e J9 R" F: Z8 F
pletely disappeared except for a few vellous hairs at( s- H" z9 z' Z9 R* g, E; f
the base of the phallus. Testicular volume was still 2
4 W7 a ]$ M. u( WmL, and the size of the penis remained unchanged.% b% r- s! b3 \ e4 ^% }, D
The mother also said that the boy was no longer hav-$ m5 {) H: r; U7 g7 @' K/ T; q# a6 r
ing frequent erections.
3 Y* x4 t+ S9 `9 X' ^. VBoth parents were again questioned about use of
" u" C; B" d) t vany ointment/creams that they may have applied to0 z& F: `7 Z2 F2 G! R7 L
the child’s skin. This time the father admitted the
& }( O, a' b8 p4 ~$ q2 ^% oTopical Testosterone Exposure / Bhowmick et al 541
3 Q H1 m. D& Buse of testosterone gel twice daily that he was apply-
- W, l0 _4 m( p% r2 e, uing over his own shoulders, chest, and back area for+ O! e7 Z2 P! a, K1 _+ e/ E# e' b
a year. The father also revealed he was embarrassed
; {' ^9 }0 x; \- i$ p! lto disclose that he was using a testosterone gel pre-
# m) P* Q) w( J9 Mscribed by his family physician for decreased libido3 r: {, b; o: P- P2 j
secondary to depression.& _7 {3 ^8 u5 D$ K% ?
The child slept in the same bed with parents.
) m- m: g- Q o( r) Q. d# G1 f7 @The father would hug the baby and hold him on his
; B, X4 O5 I6 G7 \, _- _0 {$ C: i# Qchest for a considerable period of time, causing sig-- |& v* @& n4 s# `' @2 z$ O4 [0 n
nificant bare skin contact between baby and father.( W! q+ ~' c2 S
The father also admitted that after the phone call, T$ t- e. ^/ d* q8 p6 a
when he learned the testosterone level in the baby! \( C" I1 b7 R' n9 c$ O% z
was high, he then read the product information. O* n( c0 X/ V! _: v
packet and concluded that it was most likely the rea-
" ]7 l$ r, G2 n- E4 bson for the child’s virilization. At that time, they
# I$ @* F% i7 p/ e" ldecided to put the baby in a separate bed, and the
9 t: R9 K- t" [6 r/ gfather was not hugging him with bare skin and had
" S( G" Q% C9 L( ^3 @5 n0 p+ Ibeen using protective clothing. A repeat testosterone
) L. ~7 a, y6 m7 z' g0 b$ W9 ttest was ordered, but the family did not go to the
: \1 \% F* Z8 ^+ q! Xlaboratory to obtain the test.# C* r* f- C F; c: {
Discussion3 @) c* w; c7 t8 N* q3 h0 f
Precocious puberty in boys is defined as secondary
' F' y- v6 N8 x* Q9 Asexual development before 9 years of age.1,4* l4 g, e2 a; A G9 l7 Q( L
Precocious puberty is termed as central (true) when) ?% R( B7 z! E7 t- X* o
it is caused by the premature activation of hypo-7 B3 y( I2 ^8 @8 i2 C* _
thalamic pituitary gonadal axis. CPP is more com-
" v; F% m. H7 |' dmon in girls than in boys.1,3 Most boys with CPP( y G7 J. n: z, l- z" |) n3 t; ?
may have a central nervous system lesion that is, J" J0 e! V* f% Y7 ?5 y
responsible for the early activation of the hypothal-8 v& g7 p2 ]2 Q7 l9 X- Y' C, q
amic pituitary gonadal axis.1-3 Thus, greater empha-
% r$ }; Z( a8 T& Qsis has been given to neuroradiologic imaging in
2 n% f5 ~6 A7 P0 P% `+ H8 V+ Dboys with precocious puberty. In addition to viril-" \+ Q/ L* p9 i: ?
ization, the clinical hallmark of CPP is the symmet-
" q/ m' I, S! O5 ?" Srical testicular growth secondary to stimulation by
) W6 }* W" z, W% p; ~) {8 E3 ?gonadotropins.1,3$ ]$ V$ H# Y0 ?, F
Gonadotropin-independent peripheral preco-0 L; [- d+ S: e+ {) [
cious puberty in boys also results from inappropriate- y @! k* J+ W2 g$ ^
androgenic stimulation from either endogenous or5 j8 N% ]0 V: \# l. s; m- ?: U" }
exogenous sources, nonpituitary gonadotropin stim-$ X2 ]$ M: ^8 @+ D a
ulation, and rare activating mutations.3 Virilizing8 @9 d1 J- v& q+ ? C4 s
congenital adrenal hyperplasia producing excessive. g4 u! S0 p: \8 H6 ~" |0 P$ Q( a
adrenal androgens is a common cause of precocious& P- J& U6 k h' h; P0 o
puberty in boys.3,41 o+ |4 |4 F% p! s5 Y
The most common form of congenital adrenal4 m% b1 ~3 \: t+ \1 M' b0 P% Y
hyperplasia is the 21-hydroxylase enzyme deficiency.
% i" W" U, ^" f8 N" W% NThe 11-β hydroxylase deficiency may also result in
; t6 \$ A1 P3 a5 kexcessive adrenal androgen production, and rarely,* Z$ y( J( {9 u$ i0 }; }
an adrenal tumor may also cause adrenal androgen
$ B- M* v% \/ P' h1 kexcess.1,3) B" \" ~ H" |- N& O9 ?
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 b0 B- N( w" m0 {0 h) U4 u2 `542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 h; f c, j1 |- S: [- Z B, @
A unique entity of male-limited gonadotropin-4 @3 n! t# o6 D I
independent precocious puberty, which is also known
: T& B5 [3 n7 D8 @- das testotoxicosis, may cause precocious puberty at a
) ] {/ Y3 `( c% ?0 Tvery young age. The physical findings in these boys
! H$ x! L% e; }, Zwith this disorder are full pubertal development,$ P9 H2 P ^- t% w: E8 s7 I
including bilateral testicular growth, similar to boys, ?, |5 t! H2 H2 c- J4 Q
with CPP. The gonadotropin levels in this disorder
% W2 ]5 d$ S- d6 Eare suppressed to prepubertal levels and do not show
' X" [$ A' ~/ W+ T, ^8 Lpubertal response of gonadotropin after gonadotropin-
8 z" D" V: H, I) p( qreleasing hormone stimulation. This is a sex-linked
1 q2 W9 V- f2 H/ L3 `- q& A2 bautosomal dominant disorder that affects only
0 e5 F; }2 b1 ?$ b. \males; therefore, other male members of the family
' h1 e, Y* y- r* R# N2 Y1 xmay have similar precocious puberty.3' G: Y) S: _7 V( _8 m! ]/ n$ o
In our patient, physical examination was incon-% a0 j5 P4 B# h* T2 L0 ^6 `
sistent with true precocious puberty since his testi-
* ?7 l! L/ u1 Z$ S. [: rcles were prepubertal in size. However, testotoxicosis
5 ~" K" l; M; |2 vwas in the differential diagnosis because his father7 r7 V8 C9 q: X3 V) r* L
started puberty somewhat early, and occasionally,
3 V, A5 N% D# o7 S1 g; R+ W2 Qtesticular enlargement is not that evident in the1 Z- f7 E; N: G$ l" ]) L+ E
beginning of this process.1 In the absence of a neg-
6 l s- A, |3 R, s& J8 o% I4 Uative initial history of androgen exposure, our
+ d% d8 Q# [; i: |* dbiggest concern was virilizing adrenal hyperplasia,' ^" k* h% q' N+ Z( D' D9 ?1 Z
either 21-hydroxylase deficiency or 11-β hydroxylase
5 Y( |/ T* ]/ t; {deficiency. Those diagnoses were excluded by find-
" s/ x" e3 c* G3 _ing the normal level of adrenal steroids. R1 O B) a! ^( q
The diagnosis of exogenous androgens was strongly- O2 v0 V ]7 U$ m& G
suspected in a follow-up visit after 4 months because2 A$ b" z; a5 g! x/ w( k
the physical examination revealed the complete disap-
' M5 s d2 x( }# J. m1 spearance of pubic hair, normal growth velocity, and
) Z2 U& Z1 o2 H4 \6 `3 C s4 ^* }decreased erections. The father admitted using a testos-3 J7 a$ n! q S9 n: v
terone gel, which he concealed at first visit. He was
H) H4 j% Y9 t' Musing it rather frequently, twice a day. The Physicians’% t8 s: K0 F" k( X5 H/ [
Desk Reference, or package insert of this product, gel or
( h1 W* |) z* j% @1 ]cream, cautions about dermal testosterone transfer to
5 ~8 n) d1 v2 M$ C* A6 Z9 x- \ munprotected females through direct skin exposure.3 H: a% _4 \& v* x, s$ Y0 M8 S
Serum testosterone level was found to be 2 times the
5 |# y% J6 |7 e# k) `7 P( \baseline value in those females who were exposed to
3 f, |) I2 `9 g! @1 M) ^even 15 minutes of direct skin contact with their male
# V% ?: S; G! h& X% H6 q8 I8 vpartners.6 However, when a shirt covered the applica-
6 k* u7 l9 Z* q O0 ?tion site, this testosterone transfer was prevented.
, } @, \% o( d7 n, u6 O$ x! oOur patient’s testosterone level was 60 ng/mL,
. y9 N: |% G9 o9 Y, J/ _( ]which was clearly high. Some studies suggest that
+ m' H; I: J2 d, h; U1 h1 @1 edermal conversion of testosterone to dihydrotestos-$ e; i& H3 P m) @) M( n6 i7 ]
terone, which is a more potent metabolite, is more- \1 y$ S) J# e4 d9 M* P
active in young children exposed to testosterone. c e* `; v: c2 t6 q1 o$ ^8 f. U n
exogenously7; however, we did not measure a dihy-9 @+ F: l4 s- u
drotestosterone level in our patient. In addition to
; z* a& R2 h& i7 Evirilization, exposure to exogenous testosterone in1 C% P0 c/ M* I) x, Q; _8 n0 I
children results in an increase in growth velocity and
3 Z' L6 E( @4 x2 h$ e0 ladvanced bone age, as seen in our patient.$ O! |0 Z N# A/ q
The long-term effect of androgen exposure during9 J0 {( O6 y8 P( t( n. U1 V
early childhood on pubertal development and final
/ ^2 F- q# A3 C' G7 N- B6 }% R! hadult height are not fully known and always remain
/ L$ N8 n* v$ f1 fa concern. Children treated with short-term testos-
) y c; n& |5 j" ]# a' Pterone injection or topical androgen may exhibit some) t$ f" \& b+ ]1 O/ F A
acceleration of the skeletal maturation; however, after
0 U* i/ ~/ ]8 F2 E/ ^5 Scessation of treatment, the rate of bone maturation
& ?+ R5 G' {, B* }# P+ u, ]/ edecelerates and gradually returns to normal.8,9
* l3 ^9 h( d/ v0 GThere are conflicting reports and controversy
! g& i' l5 r# E2 V3 {2 L- @, cover the effect of early androgen exposure on adult
. l8 t$ O, C! m' n& {penile length.10,11 Some reports suggest subnormal
1 {" M4 `, j, uadult penile length, apparently because of downreg-
; [+ p) L, v. o0 j. e" c2 Xulation of androgen receptor number.10,12 However,. |& [ c) _ i; P
Sutherland et al13 did not find a correlation between
# K. [) w9 c5 E8 ~childhood testosterone exposure and reduced adult
$ U/ ^2 U; g' [( h' ~+ U. Dpenile length in clinical studies.
( e/ V+ n7 A, \; U* H" } w; BNonetheless, we do not believe our patient is* P5 u$ @* k+ Z6 f+ g/ i3 z- A9 O
going to experience any of the untoward effects from
+ V, V4 `! N/ i, m0 d) ^testosterone exposure as mentioned earlier because$ \) S1 W/ H0 O1 r: r7 }, `" t
the exposure was not for a prolonged period of time.
2 c2 [7 T0 S$ T( l0 WAlthough the bone age was advanced at the time of
' U4 g, `& S2 d; r4 Cdiagnosis, the child had a normal growth velocity at
4 t8 r' [! v h" N% F# x0 ]the follow-up visit. It is hoped that his final adult
5 L, ?+ u4 M) N7 Mheight will not be affected.3 _9 h$ j& p0 u! f
Although rarely reported, the widespread avail-
6 O: _: o' v, h0 Tability of androgen products in our society may' C/ I7 H; x2 A
indeed cause more virilization in male or female
. L' q' {% s% k0 U5 h2 Uchildren than one would realize. Exposure to andro-
' q0 Y0 y/ X" A. |4 s( Bgen products must be considered and specific ques-0 t1 o3 m! Y, x3 j8 M# S) X5 Y2 a
tioning about the use of a testosterone product or6 s- E( k' y$ o. S
gel should be asked of the family members during% L; R& [% }* k! M& k" y# ]
the evaluation of any children who present with vir-
+ L; n9 G" \* ^9 @ilization or peripheral precocious puberty. The diag-/ `- R* Z" Z, p1 J5 A. x0 ~
nosis can be established by just a few tests and by
/ {1 G7 f# m# u5 Y6 ~appropriate history. The inability to obtain such a
3 R# r3 w5 h/ c; u& t. jhistory, or failure to ask the specific questions, may
i9 H; Z( o. [2 ]5 Z0 qresult in extensive, unnecessary, and expensive$ C Q( I: F" [' _+ t6 {
investigation. The primary care physician should be
5 L6 W8 a# b% a% C( V( caware of this fact, because most of these children) F! { P1 V% ~
may initially present in their practice. The Physicians’
: h/ V9 V7 P" k( z) ?; cDesk Reference and package insert should also put a
1 Y; h1 ?$ k. _1 n5 ?1 uwarning about the virilizing effect on a male or7 A' h; s- X) X+ ]7 Z! ^
female child who might come in contact with some-
' I! _4 d# s0 j, I0 Cone using any of these products.
2 u5 X+ V) N' s1 y# WReferences2 {& {+ _0 x6 V2 [9 `& f9 Z" z1 L/ d6 q
1. Styne DM. The testes: disorder of sexual differentiation8 r2 H5 t( J, |6 t7 T( T; u# X
and puberty in the male. In: Sperling MA, ed. Pediatric
4 I( x0 d* p. I+ h, A" GEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! ~0 q; b5 N6 L- d. H9 w5 |2 E) W
2002: 565-628.
' F. H# E) O3 y" k6 M' a3 ^3 \2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious5 S6 @" u' D& F
puberty in children with tumours of the suprasellar pineal |
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