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Sexual Precocity in a 16-Month-Old
" N! B! c" F+ Y6 X) o0 Q9 D8 iBoy Induced by Indirect Topical
0 g6 l& D9 y2 D' v1 h0 oExposure to Testosterone
3 c3 L7 h# I# R/ w/ YSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. L4 r* g2 r8 L1 ]! ^
and Kenneth R. Rettig, MD1. b5 d5 x5 M; M' i* H6 a4 K$ b
Clinical Pediatrics s }+ y4 R+ F7 K7 \: @9 M
Volume 46 Number 6
) {3 [+ k. H, UJuly 2007 540-5431 ^2 {' D j5 T6 z0 D
© 2007 Sage Publications
; a3 N1 W& x; T x6 b8 O10.1177/00099228062966510 G0 l* P2 ]1 b9 Z9 p; _; Y# L
http://clp.sagepub.com
) G1 ^* n. ]+ y# U+ Phosted at
, d P+ B& x' F/ |) xhttp://online.sagepub.com: X/ @+ w {3 y' J
Precocious puberty in boys, central or peripheral,
3 V1 N+ j8 _) [! Yis a significant concern for physicians. Central
' V' v% c6 I" Z- t5 v) cprecocious puberty (CPP), which is mediated5 P. I5 n2 E: [) {
through the hypothalamic pituitary gonadal axis, has
6 ^+ S) q2 K' B% `a higher incidence of organic central nervous system# ^, x" ~0 q6 X( w g8 o& u
lesions in boys.1,2 Virilization in boys, as manifested+ T3 K! y8 q8 y% U& [+ T0 W7 Z
by enlargement of the penis, development of pubic
" X3 M, u7 T! J1 Phair, and facial acne without enlargement of testi-
: _: n9 u' e4 D! Mcles, suggests peripheral or pseudopuberty.1-3 We' k; J+ i0 I/ e' r& B6 U$ `
report a 16-month-old boy who presented with the# \$ s+ O% y/ o% o& r
enlargement of the phallus and pubic hair develop-/ P8 `9 d7 v) [
ment without testicular enlargement, which was due3 x' C! t" i# q2 B7 y" K
to the unintentional exposure to androgen gel used by, {, H' G# u1 b
the father. The family initially concealed this infor-6 u6 ?* K/ x A+ u
mation, resulting in an extensive work-up for this. `/ W: z0 t% k
child. Given the widespread and easy availability of3 i1 Q. K* w0 O, G
testosterone gel and cream, we believe this is proba-% i9 { h9 S6 c
bly more common than the rare case report in the8 ]+ O3 z) B3 u2 m9 T6 i8 ^2 o0 j3 {
literature.4
5 B8 ]8 z' r# u G$ T# Y5 YPatient Report7 ]& ]: E5 }' Y- }% [
A 16-month-old white child was referred to the# y9 j; O' U. o/ ~) c6 L
endocrine clinic by his pediatrician with the concern. k4 |1 }* j4 o% w+ s, Z) e# O
of early sexual development. His mother noticed! v( U3 m8 g H3 T; X
light colored pubic hair development when he was* j! G5 O8 O3 m8 p* d
From the 1Division of Pediatric Endocrinology, 2University of
4 \+ L2 `4 \) J G4 FSouth Alabama Medical Center, Mobile, Alabama.
; j: @) R# b1 I4 e7 I8 e0 ?9 UAddress correspondence to: Samar K. Bhowmick, MD, FACE,
2 _& [- O$ @ k3 c( _Professor of Pediatrics, University of South Alabama, College of
' R0 i4 z1 c& z" M( VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, k0 M" u) e4 l! }% V2 Q( X
e-mail: [email protected].
' |) R- N- m$ T- G# \5 Vabout 6 to 7 months old, which progressively became8 U, C" e- y4 @- `, m
darker. She was also concerned about the enlarge-- G% \3 k8 b( c9 l$ k
ment of his penis and frequent erections. The child. }. q9 R5 S! Q/ @
was the product of a full-term normal delivery, with
; u( w5 p0 E; k2 s- L+ O6 o9 Q+ b1 Ea birth weight of 7 lb 14 oz, and birth length of
2 j3 z& A- T* G! p4 ~ d- i7 s; w$ j20 inches. He was breast-fed throughout the first year
5 i2 Y1 U- v" D3 D4 @of life and was still receiving breast milk along with; l1 ?, f2 N h( r
solid food. He had no hospitalizations or surgery,0 F3 K: ~4 H: A: a
and his psychosocial and psychomotor development
2 k4 n' z6 o Iwas age appropriate.
& b6 N( q& H0 N X. DThe family history was remarkable for the father,
2 a" |/ E8 G) a& C3 X" Fwho was diagnosed with hypothyroidism at age 16,
& \) S+ X6 B, p( Rwhich was treated with thyroxine. The father’s
* X! s3 S( s! ^, S8 s% gheight was 6 feet, and he went through a somewhat
; {; A3 i' J, cearly puberty and had stopped growing by age 14.; w9 y# `3 u- i
The father denied taking any other medication. The
N/ S) {4 k$ T' p7 ~child’s mother was in good health. Her menarche
2 X* D! D+ J5 S7 m3 b) w6 g( Qwas at 11 years of age, and her height was at 5 feet
4 K* K. J5 d9 f8 y, {; ^5 inches. There was no other family history of pre-
_! A& r( z% l7 Vcocious sexual development in the first-degree rela-. E1 Q% B. H) z @" G+ y& ~
tives. There were no siblings.
; Q3 L$ i( p) B& {& T! vPhysical Examination1 y7 _& n8 i& B
The physical examination revealed a very active,& S5 P" @2 f; ?+ @
playful, and healthy boy. The vital signs documented0 j( g. G! R1 z' _6 @/ n2 ^
a blood pressure of 85/50 mm Hg, his length was
# ]% J1 f/ B2 @8 }6 ~- F/ N4 s90 cm (>97th percentile), and his weight was 14.4 kg
) M( H6 b+ y! b5 m: z. @5 W(also >97th percentile). The observed yearly growth$ q6 [1 l' S1 x8 x% `
velocity was 30 cm (12 inches). The examination of+ K8 n7 Y2 w6 l2 v
the neck revealed no thyroid enlargement.2 W. x) W2 B* t/ x7 h( L
The genitourinary examination was remarkable for6 s( l5 j' f1 y; Z' j
enlargement of the penis, with a stretched length of- k1 ?4 C$ I. p& [2 [4 O4 b9 B% W7 R
8 cm and a width of 2 cm. The glans penis was very well# g( b5 q6 G. I' y& A
developed. The pubic hair was Tanner II, mostly around' K) n+ o$ V& f8 h6 a& D
540
7 f: f. V$ i8 ~$ T% Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* v, l1 c' e A. j! Ythe base of the phallus and was dark and curled. The2 I1 u+ g: B1 B7 t3 J$ P+ j
testicular volume was prepubertal at 2 mL each.
! [. @! y" ?4 y+ `The skin was moist and smooth and somewhat
2 \, A# n2 R+ f/ P/ j1 Loily. No axillary hair was noted. There were no" L0 B9 ]. p8 _* X. A
abnormal skin pigmentations or café-au-lait spots.
( C# u+ o! r. C& e/ ~& MNeurologic evaluation showed deep tendon reflex 2+
6 O- \; H3 M7 `' x- Ubilateral and symmetrical. There was no suggestion: X3 S% V8 w4 F& J) H( @1 P
of papilledema.5 G7 g5 I0 d* i0 j% r8 B* F( A" _# {
Laboratory Evaluation
, k/ p H5 `( c7 R$ j7 jThe bone age was consistent with 28 months by7 _. N, v$ g- Q! T4 @: R
using the standard of Greulich and Pyle at a chrono-1 E/ D; E2 C1 {4 ]9 d8 [: j7 d& q
logic age of 16 months (advanced).5 Chromosomal
( B1 J9 D# P) C& D W; L2 A0 ikaryotype was 46XY. The thyroid function test
2 L' Q$ f' h/ f) j) V! yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-0 Z% [' l) B! f' e3 v
lating hormone level was 1.3 µIU/mL (both normal).
5 V# t: ^6 R4 |: p: e! v; v1 CThe concentrations of serum electrolytes, blood
2 e8 d1 p5 Z+ ]8 ourea nitrogen, creatinine, and calcium all were# w3 ?; p- Y2 c9 k# e
within normal range for his age. The concentration
9 x1 X- r* y" _1 J5 ~of serum 17-hydroxyprogesterone was 16 ng/dL
7 q( p7 s1 D( Q: `* y) q(normal, 3 to 90 ng/dL), androstenedione was 20
8 R$ E7 ^' Z/ x" E# rng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: H( [7 o% X: ^. J2 {
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
| h" _% [% ^& v+ _! c4 edesoxycorticosterone was 4.3 ng/dL (normal, 7 to( S7 e5 u; F" Y- \8 s. R$ _
49ng/dL), 11-desoxycortisol (specific compound S)
4 T$ a0 F: m6 ]! }# h( K4 ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
`" D% Y' m: Y; k: Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
' @/ h: `( U' btestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
3 b, J8 _/ k* x6 {and β-human chorionic gonadotropin was less than
; f$ U' f; J p# e: y# ?, {5 mIU/mL (normal <5 mIU/mL). Serum follicular Z$ `. ]3 j! K6 S$ G, e6 N5 s# v
stimulating hormone and leuteinizing hormone
7 }% _' H& G. g4 C1 N! Nconcentrations were less than 0.05 mIU/mL
+ d/ X3 Q& D% H- e7 q(prepubertal).
1 k. a( W/ ?- s+ r, N! y, y# DThe parents were notified about the laboratory
8 ?: q: I! l4 ?* Gresults and were informed that all of the tests were
7 l4 o1 n% a, t3 O) m6 l' Y; o: @normal except the testosterone level was high. The
$ S' R4 t' s1 F- gfollow-up visit was arranged within a few weeks to& u& ]- j8 F5 ]
obtain testicular and abdominal sonograms; how-
* L& P" M1 M4 T# W# jever, the family did not return for 4 months.8 x* t) S1 G4 k$ X& \" P. s
Physical examination at this time revealed that the# S7 W; a7 e& ?
child had grown 2.5 cm in 4 months and had gained8 }3 T" D) k8 q! p* b8 [
2 kg of weight. Physical examination remained
" @& B2 L+ g) m, J" f: runchanged. Surprisingly, the pubic hair almost com-
/ e3 G. ?4 |5 U( u+ m# rpletely disappeared except for a few vellous hairs at/ \# |* D5 _: G5 T; L9 x
the base of the phallus. Testicular volume was still 2. ?0 x. O$ F& u; y
mL, and the size of the penis remained unchanged.
; {* O0 |5 O$ z! P2 }; \& rThe mother also said that the boy was no longer hav-
+ ]3 v3 ^ y5 q( sing frequent erections.
: ^+ V! U8 ~* {; eBoth parents were again questioned about use of" a, P- S, K4 ?) x \
any ointment/creams that they may have applied to
) o% w) ~0 Y$ K+ A. k: Qthe child’s skin. This time the father admitted the
9 y2 V' {- r- s$ E5 PTopical Testosterone Exposure / Bhowmick et al 541" i) a5 H) z0 j
use of testosterone gel twice daily that he was apply-
2 x0 i0 @. D2 Y+ l6 k5 Cing over his own shoulders, chest, and back area for
5 w' ? _1 R* O9 q3 Wa year. The father also revealed he was embarrassed& J7 g$ J" S- w: c# o9 [3 t+ Q7 O' N
to disclose that he was using a testosterone gel pre-3 t! I# F2 {8 E; N# |3 A# d+ k
scribed by his family physician for decreased libido4 \$ a. y+ _& p- P
secondary to depression.: P% c ^% F5 Y6 X* j- S
The child slept in the same bed with parents.
: M% g, |9 {& R; E: K, T1 z$ K6 \The father would hug the baby and hold him on his
! h( U1 I4 \4 E5 _" \! xchest for a considerable period of time, causing sig-1 H( k# u; e, L/ x4 m8 F: A1 x
nificant bare skin contact between baby and father.
; @9 E8 @0 W0 @9 | W6 p9 EThe father also admitted that after the phone call,
. r# C: L+ C3 G. ^8 V% h4 ~# C6 Nwhen he learned the testosterone level in the baby
2 U) m; J. Z1 P6 K4 p( |3 k7 Z9 swas high, he then read the product information
* J& u0 l) b, |9 {, n$ d3 `+ Dpacket and concluded that it was most likely the rea-" G- N7 B2 Z3 @) r: H) a. e" T7 c
son for the child’s virilization. At that time, they
q8 W1 z% h4 `3 Ydecided to put the baby in a separate bed, and the5 W% \2 l5 C4 |. Q, K6 d; N, F) ^2 e
father was not hugging him with bare skin and had7 u* }, @2 ?2 I+ L! A8 @
been using protective clothing. A repeat testosterone- D; @, J; W8 j! J9 \$ F
test was ordered, but the family did not go to the9 A' V7 h, H F( ^, m
laboratory to obtain the test.
1 |0 T ~; c! C z5 C0 X" IDiscussion# R: v f S. z7 Z7 H: a
Precocious puberty in boys is defined as secondary
- ^9 y2 M: u7 K3 o! A& ~sexual development before 9 years of age.1,4: f9 Y0 ~$ M& B% ^! a
Precocious puberty is termed as central (true) when/ T( y9 V8 B2 s6 S( g1 B! g
it is caused by the premature activation of hypo-
) ]3 {9 f4 m2 {4 t" R$ jthalamic pituitary gonadal axis. CPP is more com-0 P' H. @( ~0 d0 c+ ^
mon in girls than in boys.1,3 Most boys with CPP
+ ^' u$ q) R# e7 x. o/ {, E- Kmay have a central nervous system lesion that is
5 G; ?/ X' b0 W0 M2 U( v' E( L" Bresponsible for the early activation of the hypothal-
r$ }* J6 z) y3 c' t @amic pituitary gonadal axis.1-3 Thus, greater empha-
& k6 U" f1 P/ F/ N4 O& asis has been given to neuroradiologic imaging in
( ^ q2 `& Z3 [. ?boys with precocious puberty. In addition to viril-
" ^6 Y/ H/ K, C4 y$ f6 }ization, the clinical hallmark of CPP is the symmet-! Y9 E6 G! B4 ?/ Z
rical testicular growth secondary to stimulation by# V8 z- R; [: V8 V. ?/ i; c5 x
gonadotropins.1,3
$ G1 q! m$ l$ Y) |Gonadotropin-independent peripheral preco-* N. y& R7 i u# r* t. b$ D' E4 l* [
cious puberty in boys also results from inappropriate
2 L G5 k7 [/ ]1 X- N7 M/ J$ tandrogenic stimulation from either endogenous or2 {# ^& T8 ~$ m% s
exogenous sources, nonpituitary gonadotropin stim-3 _1 y2 @% c* ^* @1 d; J
ulation, and rare activating mutations.3 Virilizing5 g% z2 Q0 z1 I, c7 ?% O- H
congenital adrenal hyperplasia producing excessive8 q9 Y$ D% J- S
adrenal androgens is a common cause of precocious! q, B$ E. g T' S, B$ g- G8 Q" M
puberty in boys.3,4
1 G3 B: T& y) r2 f! ]The most common form of congenital adrenal' }+ \ w# f) r! R: \, b
hyperplasia is the 21-hydroxylase enzyme deficiency.
% `, _$ w% D d R% U9 |$ UThe 11-β hydroxylase deficiency may also result in+ X3 X; ?) O. L) p" E6 O
excessive adrenal androgen production, and rarely,
' t$ Z6 o- ?& h. X5 u+ ?5 L; Can adrenal tumor may also cause adrenal androgen' R. e4 N$ s: ?& g# N$ Z3 t; T
excess.1,3
# t% Z" O, F% _0 i/ oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, V0 o6 `. t/ u- r3 o( I
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007% M; G# f' {) U
A unique entity of male-limited gonadotropin-
! E' @+ {, [' i2 Y' S* g7 zindependent precocious puberty, which is also known1 q2 q* {9 i7 q% |1 s
as testotoxicosis, may cause precocious puberty at a# Z1 A3 u4 T' s
very young age. The physical findings in these boys
/ r$ j l+ B% Owith this disorder are full pubertal development,( r. N; Q4 a1 p6 m5 m6 y6 s
including bilateral testicular growth, similar to boys
) U1 `* e4 j) F4 S* o) p5 B/ N+ K/ Gwith CPP. The gonadotropin levels in this disorder
7 H2 |( D4 J- W) L S1 fare suppressed to prepubertal levels and do not show
, R. s) F7 B4 ~6 Q4 |9 f0 spubertal response of gonadotropin after gonadotropin-
" K! z6 x6 P5 @/ ~, o# qreleasing hormone stimulation. This is a sex-linked! |, h2 I5 r1 t3 \
autosomal dominant disorder that affects only
4 B0 t H; M: _% G3 }5 B3 Y. }males; therefore, other male members of the family0 t/ j2 ?( v* W" H; w( c, e
may have similar precocious puberty.32 m) T/ z2 A; v1 U1 g- b
In our patient, physical examination was incon-
9 [1 ?7 i* f4 `# \2 q) z) ~4 ~sistent with true precocious puberty since his testi-) N# v3 Y! S' y5 X4 Z( V
cles were prepubertal in size. However, testotoxicosis- ^0 Z4 w @( L0 N9 ^8 z7 g
was in the differential diagnosis because his father
* R2 Y" g& x7 a; z1 R. z8 Q! zstarted puberty somewhat early, and occasionally,' r3 D( k* k% S' U# } w
testicular enlargement is not that evident in the: I) Z' _* v; j6 H) l
beginning of this process.1 In the absence of a neg-" d0 O3 p( D8 c$ b. m1 V, a+ R
ative initial history of androgen exposure, our
2 X7 j& q/ ]- [1 U6 Ubiggest concern was virilizing adrenal hyperplasia,9 ^( s" o+ S' D7 r( D( r0 R; ^
either 21-hydroxylase deficiency or 11-β hydroxylase
7 m# d/ I/ c+ d* t8 d$ T" xdeficiency. Those diagnoses were excluded by find-
0 k+ E* e( t) S4 B8 |ing the normal level of adrenal steroids.# m3 o8 c! E$ z8 c9 D' l
The diagnosis of exogenous androgens was strongly
* z* m, g. G. } E/ q4 fsuspected in a follow-up visit after 4 months because8 K# P% P: ?/ `2 Q; x* \
the physical examination revealed the complete disap-
3 B0 G; @9 g* @! B# ypearance of pubic hair, normal growth velocity, and
: X# y( J. c; {9 fdecreased erections. The father admitted using a testos-
, u4 d+ q/ H4 z8 G- lterone gel, which he concealed at first visit. He was+ Q7 B" @ Q+ p2 x% D
using it rather frequently, twice a day. The Physicians’) U! k8 I* }: L3 X
Desk Reference, or package insert of this product, gel or
- D9 p; A E2 W6 Q u. k+ D: Gcream, cautions about dermal testosterone transfer to
1 H8 t" I5 D4 s+ O' [unprotected females through direct skin exposure.
" l# @$ Q& a" K# y# R9 V0 y$ tSerum testosterone level was found to be 2 times the/ t8 \2 X& b6 t& o) v% U3 `9 C/ q
baseline value in those females who were exposed to
! K3 D0 J% J* Veven 15 minutes of direct skin contact with their male
5 j8 ?/ u% ^ l% I) mpartners.6 However, when a shirt covered the applica-
) \5 g, _& z! M7 j7 _3 b, ~9 }/ i& Ktion site, this testosterone transfer was prevented.8 R7 |5 C3 [; L, X/ t# B9 N1 w
Our patient’s testosterone level was 60 ng/mL,
: F! c$ }# G3 hwhich was clearly high. Some studies suggest that/ s6 O `& R. `( i V2 ]
dermal conversion of testosterone to dihydrotestos-
0 t3 b7 h9 o* r) ]; {- zterone, which is a more potent metabolite, is more o% v% {) f" N6 q- W8 \! M, }; d
active in young children exposed to testosterone
- P( V( \2 E4 g2 eexogenously7; however, we did not measure a dihy- J' z h. G- Q) i8 n8 {4 F
drotestosterone level in our patient. In addition to2 c4 I8 b: o$ Z6 o5 O
virilization, exposure to exogenous testosterone in
: F0 R0 L. x. F$ p4 h9 ?/ pchildren results in an increase in growth velocity and
" ?" I# G. [% uadvanced bone age, as seen in our patient.
( p1 q, b1 L% oThe long-term effect of androgen exposure during
3 ]# J6 p& l( A6 B6 j- Cearly childhood on pubertal development and final
& i ]1 f( k1 [/ nadult height are not fully known and always remain
4 X! b' I, u# h. y+ za concern. Children treated with short-term testos-
, b6 ]$ M7 x6 k4 I& Gterone injection or topical androgen may exhibit some
( c* |$ L( N* v, o/ u# ^% Qacceleration of the skeletal maturation; however, after1 o$ T8 k6 v6 m
cessation of treatment, the rate of bone maturation
, F$ G+ g$ I8 u" A/ ?3 Edecelerates and gradually returns to normal.8,96 h* i, y: t. F. }
There are conflicting reports and controversy/ \2 i1 t* m2 k; R* L
over the effect of early androgen exposure on adult7 w6 O" ^5 _( J" w1 b' ^$ f
penile length.10,11 Some reports suggest subnormal
8 _7 T1 w/ c9 f0 p/ P/ ~5 I$ l6 ]7 jadult penile length, apparently because of downreg-
8 r& n& M; i$ h9 M8 @6 u/ iulation of androgen receptor number.10,12 However," h& t% K; ]9 O# G7 M; Z* B
Sutherland et al13 did not find a correlation between
2 ~4 U' i6 ^( g- `; h2 c; x4 ^childhood testosterone exposure and reduced adult, Q, J! {! E, F( q4 `9 D5 B' i2 n& w
penile length in clinical studies.8 O4 z6 J4 X+ ?; ^4 z
Nonetheless, we do not believe our patient is
1 j* O; E4 W) q' u9 }going to experience any of the untoward effects from) P5 D# @8 g" W( D7 w3 a
testosterone exposure as mentioned earlier because/ W' e* v4 \; D: }. U. T g# d* p
the exposure was not for a prolonged period of time.
% M. q5 n n8 U8 g" oAlthough the bone age was advanced at the time of& j! L- n& x! ~8 ~( Z4 G9 [# V" R
diagnosis, the child had a normal growth velocity at; Q B+ E( w/ O! D! k5 r" M
the follow-up visit. It is hoped that his final adult. F3 G8 G; W) A& r1 o( ?4 `
height will not be affected.5 ~. z* b1 M4 U& O9 t6 i
Although rarely reported, the widespread avail-5 y; {+ H2 l8 r, r, v. v/ L
ability of androgen products in our society may$ g" Y7 r& \, Z- |
indeed cause more virilization in male or female4 P2 I9 P. p) A& f* x- T& T; X
children than one would realize. Exposure to andro-4 a5 {& s) n9 T' d. J' e' Y) Y4 |
gen products must be considered and specific ques-2 N. }' R& r3 I5 M9 Y
tioning about the use of a testosterone product or
6 ^. R: b1 v. I6 U# }+ s1 E7 bgel should be asked of the family members during* X# m% P1 ~* j" C8 A0 g" K' _
the evaluation of any children who present with vir-- g: ]- z) \) n7 G- r4 b, u" i1 ]$ E
ilization or peripheral precocious puberty. The diag-) J5 }1 ?$ @) t, r
nosis can be established by just a few tests and by
6 R2 E: Y0 k* ]2 Q3 U. g- }3 Oappropriate history. The inability to obtain such a. L' J7 f2 X h- f8 B
history, or failure to ask the specific questions, may
% @3 c8 U$ { ]9 l( \result in extensive, unnecessary, and expensive
3 L9 B5 U7 R, h- ?& h S7 Sinvestigation. The primary care physician should be. t' L" j9 N; t% _! P. [4 c
aware of this fact, because most of these children
! L w3 c9 r9 ?/ [may initially present in their practice. The Physicians’
, H. a* T# c8 ]9 X# hDesk Reference and package insert should also put a2 f5 q; L3 W2 m% _. ?2 x* @
warning about the virilizing effect on a male or! a q6 j% O1 d1 N) F! }, x- D
female child who might come in contact with some-
" G8 K+ K( x% L g& cone using any of these products., N; ^& V5 d6 x V) r0 b. u1 q P; T0 Z
References
+ M2 t% V+ s2 z' A4 b' b) M% g1. Styne DM. The testes: disorder of sexual differentiation
# ` l! M0 e6 N2 vand puberty in the male. In: Sperling MA, ed. Pediatric+ l) i) ~- b: h& F' c
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ D4 M9 s# ~8 W' p( o; ?2002: 565-628.5 K4 f/ s1 }: U/ @
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! @& _1 O1 R) i W# N! [ e
puberty in children with tumours of the suprasellar pineal |
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