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Sexual Precocity in a 16-Month-Old: H' Y$ p) o1 H/ I2 b8 v
Boy Induced by Indirect Topical
8 u: i6 l( h/ _8 v& bExposure to Testosterone7 H, [; c" `! P/ {' f5 j
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% B) Y9 j8 L, O# fand Kenneth R. Rettig, MD11 O; ?3 {0 Z+ [9 U4 b# E
Clinical Pediatrics
. ^ x$ B _* v. @Volume 46 Number 6" m. l) t2 C. @( J: L l; u7 S! `
July 2007 540-543( m5 B( e" f$ l7 U
© 2007 Sage Publications
8 D4 Q, z* t+ e1 ?# l10.1177/0009922806296651
, k* Z$ w9 ?) Q; q! j# ?http://clp.sagepub.com, A& x6 V+ G$ b) h6 g
hosted at
; r6 b0 i* Z5 ?% A& m, P2 G( whttp://online.sagepub.com) x" A5 A$ m2 x4 ?9 y x+ H; _
Precocious puberty in boys, central or peripheral,8 T. U8 z7 _% o+ o' f
is a significant concern for physicians. Central( r- {' H: l; u2 c
precocious puberty (CPP), which is mediated. M* F6 v* L/ F
through the hypothalamic pituitary gonadal axis, has, t6 X U) x/ d% x( X8 N
a higher incidence of organic central nervous system% `: Z8 W, v2 O; N( Q2 S
lesions in boys.1,2 Virilization in boys, as manifested
, O$ `5 l/ O0 K, t0 Xby enlargement of the penis, development of pubic
' Z$ Y% h( q4 p5 ehair, and facial acne without enlargement of testi-8 L( m" v% Y/ i! h4 Q% N* x
cles, suggests peripheral or pseudopuberty.1-3 We
, f$ a! C2 }1 U% N$ J* N Creport a 16-month-old boy who presented with the
3 A: L2 S5 K6 ?7 B# u- R( D% Y, senlargement of the phallus and pubic hair develop-0 k$ q5 ~+ u$ s, V O
ment without testicular enlargement, which was due
1 W0 M' j& G# b6 N9 n9 v5 n: Xto the unintentional exposure to androgen gel used by
, B! }' w4 V+ M; K$ A2 Gthe father. The family initially concealed this infor-
! z" a1 y4 v/ |. E: S- \% I2 ymation, resulting in an extensive work-up for this3 _% M; g/ K5 k5 B" i6 r
child. Given the widespread and easy availability of- V7 @$ J& H% e( I. X8 A
testosterone gel and cream, we believe this is proba-
. G$ S/ Y) q! a) z1 b hbly more common than the rare case report in the1 I( @& p; `6 b3 K% J4 `
literature.4
3 M$ x4 I- i/ j7 S7 r% HPatient Report
4 T& d8 m- _9 w1 YA 16-month-old white child was referred to the
4 d( t# q9 H& F4 Mendocrine clinic by his pediatrician with the concern
$ v8 S. e9 G; f, ?8 R8 G' p' Nof early sexual development. His mother noticed
6 B& I9 S( A6 [ O6 ^# Glight colored pubic hair development when he was& T9 s: A# b/ Q' M
From the 1Division of Pediatric Endocrinology, 2University of0 j- `7 Y- ?: v' a4 d. B
South Alabama Medical Center, Mobile, Alabama.
2 z# d7 @& `" D+ ]8 |# Z0 M1 jAddress correspondence to: Samar K. Bhowmick, MD, FACE,; j! t8 g4 i5 E% W' y4 ]
Professor of Pediatrics, University of South Alabama, College of
* ^% q' B0 T8 ~' R |0 ~5 f. VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ ~( W: u, w. a8 S+ y# le-mail: [email protected].4 M, _# a5 ^# }" x+ s. u
about 6 to 7 months old, which progressively became( G$ j/ K9 f; o8 [) B6 q& @
darker. She was also concerned about the enlarge-7 k! T; g+ t( Y: z( k
ment of his penis and frequent erections. The child5 z% s& T: A" d! C8 u9 t
was the product of a full-term normal delivery, with
7 Z7 a# `+ n, j0 Qa birth weight of 7 lb 14 oz, and birth length of
# C2 ^( x% Q0 b4 c0 ~20 inches. He was breast-fed throughout the first year' e4 W9 ^' n( F. `# @
of life and was still receiving breast milk along with0 J% H1 s" |6 p/ _; C
solid food. He had no hospitalizations or surgery,
" Z6 s) y" r8 K, n! Band his psychosocial and psychomotor development
' q) y5 ~$ E3 `' i8 m9 ~was age appropriate.. f1 q- [, ?0 L8 X- @/ ~, H1 D4 Z, b/ h
The family history was remarkable for the father,- H# u$ D1 O; B0 V6 u
who was diagnosed with hypothyroidism at age 16,8 E1 N& k: b; d/ N( P
which was treated with thyroxine. The father’s
8 w5 \$ {2 h3 xheight was 6 feet, and he went through a somewhat
- B5 h) C# `) G) L7 s( f# learly puberty and had stopped growing by age 14." _4 m0 }/ x* {* R2 n6 A
The father denied taking any other medication. The
, {- F$ |; N5 `& G8 Y( w# i+ ychild’s mother was in good health. Her menarche M' V; |9 x1 c/ ^/ J
was at 11 years of age, and her height was at 5 feet8 y" W7 a8 H; S- [/ t$ h2 _
5 inches. There was no other family history of pre-( K3 S* O- I( u5 U
cocious sexual development in the first-degree rela-! A7 m B5 R. c) L1 T; T3 P5 f/ ]
tives. There were no siblings.
' f! T9 V; B$ Y; g& bPhysical Examination
; E. K5 W+ @& r) j- A' w9 wThe physical examination revealed a very active,2 L& s2 p9 V8 z0 Z" F+ M. h
playful, and healthy boy. The vital signs documented
# G" P+ b( R k/ c+ Fa blood pressure of 85/50 mm Hg, his length was* r; s: [- `: H3 @' `
90 cm (>97th percentile), and his weight was 14.4 kg
" Z* t/ H2 @+ f0 V0 H' c(also >97th percentile). The observed yearly growth
4 y4 b' B' k( O& i/ r8 Kvelocity was 30 cm (12 inches). The examination of& f. W6 u5 Y+ n5 X6 h
the neck revealed no thyroid enlargement.% e0 L7 c. n* Y# p! ]& s, S5 G
The genitourinary examination was remarkable for: V# P6 Q. [+ T7 A: u7 S3 I# S
enlargement of the penis, with a stretched length of
% Z% r' H2 _+ q' {4 v% O) E8 cm and a width of 2 cm. The glans penis was very well1 M6 X, m6 I1 k6 q9 J! @0 z6 ]
developed. The pubic hair was Tanner II, mostly around. v4 D4 J6 s$ P; i# `, D( o
5403 e& z" h2 F6 z {& K. W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: }3 s _7 k3 T9 [' T
the base of the phallus and was dark and curled. The
$ Q$ c. B) Z; |7 R& }1 l3 @# Stesticular volume was prepubertal at 2 mL each.
! \4 S ]5 b# U( n: `1 }4 N0 ]5 U/ J; V1 FThe skin was moist and smooth and somewhat* J+ L( \) N3 a; y
oily. No axillary hair was noted. There were no& n# e! J% C L8 \6 \" L- `) Z
abnormal skin pigmentations or café-au-lait spots.
! B4 A7 j+ p" {* ENeurologic evaluation showed deep tendon reflex 2+
9 g, c! B$ W% C Gbilateral and symmetrical. There was no suggestion$ k z4 F! u6 B0 E, \+ I
of papilledema.
) o& b6 ~2 ]" B7 P* g* zLaboratory Evaluation+ }% s3 o0 S$ U9 n9 x. t: ]9 f6 g$ L
The bone age was consistent with 28 months by
) ~) s2 \* V" ^2 f* R; t. Dusing the standard of Greulich and Pyle at a chrono-/ l0 r+ q/ `5 T5 f+ p
logic age of 16 months (advanced).5 Chromosomal
% l: A0 y$ k4 {( U/ F6 akaryotype was 46XY. The thyroid function test
2 A8 K; s+ M# S/ h3 v) }showed a free T4 of 1.69 ng/dL, and thyroid stimu-) l" `1 Q9 R; a2 n1 K
lating hormone level was 1.3 µIU/mL (both normal).6 B& C: W7 n8 ]3 O8 l
The concentrations of serum electrolytes, blood
' x9 {( j. q, T2 B4 f( A2 Surea nitrogen, creatinine, and calcium all were
$ j; q4 c" ]) F4 _0 C3 zwithin normal range for his age. The concentration
# Y2 Q4 K, Y3 e# {of serum 17-hydroxyprogesterone was 16 ng/dL
0 K( n+ U4 h* s/ p" {0 L& W# b(normal, 3 to 90 ng/dL), androstenedione was 205 S8 }9 M5 c, Q; x5 [, L) w, h
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-. o) Z* i6 H8 |; T3 p
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
* Y, p7 ?8 x% Sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to4 @ [. N2 ~6 Q* k" f+ @
49ng/dL), 11-desoxycortisol (specific compound S)2 O+ b5 I3 u5 O. }3 `
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, l; G3 T, @% F* c0 Wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, A* i( I Q1 S9 F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),) e3 w, a- o) C4 z$ M& q
and β-human chorionic gonadotropin was less than* [- v' E( B8 c2 V
5 mIU/mL (normal <5 mIU/mL). Serum follicular" [( k+ }/ ?# O3 T. o S
stimulating hormone and leuteinizing hormone8 I& ?7 r$ H( [4 {! i
concentrations were less than 0.05 mIU/mL
# t0 N9 a! ^/ \7 N- m9 |+ D1 B- V(prepubertal).
* X8 S, Z# S5 } t+ M3 i! bThe parents were notified about the laboratory8 u/ t9 H- i: X6 d* n! o! H6 Q
results and were informed that all of the tests were& T7 H# ?4 l3 q# a1 j
normal except the testosterone level was high. The
- _3 b% I# k) E& s# C5 T6 i5 g2 vfollow-up visit was arranged within a few weeks to
6 P/ _' ~/ S4 A: x+ ^9 G& o1 x: Kobtain testicular and abdominal sonograms; how-
+ ~( Z2 j0 V" Vever, the family did not return for 4 months.$ U5 ]4 J- b8 n: G. S: p% G d
Physical examination at this time revealed that the( ~6 W' P8 D0 `% g
child had grown 2.5 cm in 4 months and had gained
. b0 g. W4 r+ m, Y5 _6 e2 kg of weight. Physical examination remained
# t! L2 n* X f/ @5 K! ^, ~( Vunchanged. Surprisingly, the pubic hair almost com-& z+ n- v/ a. t, I# E
pletely disappeared except for a few vellous hairs at
- j, y$ G& Y4 g5 y7 Dthe base of the phallus. Testicular volume was still 2. w3 w0 v, V& Y- @ Y
mL, and the size of the penis remained unchanged.% J! e! T- X% z' ~) T
The mother also said that the boy was no longer hav-
% A& J8 V: Q* [. ying frequent erections.
7 I) c' H3 s, Z3 T+ u" [Both parents were again questioned about use of6 w Q- R0 B: [0 k/ \5 `1 \, ^
any ointment/creams that they may have applied to. `- k- W* \0 j" q. L) ]
the child’s skin. This time the father admitted the
5 g4 P; o' S6 ~) q% q. bTopical Testosterone Exposure / Bhowmick et al 541
: w# P8 Z, i& z- luse of testosterone gel twice daily that he was apply-! f8 h/ |8 U) |4 D0 O4 C
ing over his own shoulders, chest, and back area for, X! l, U0 F$ L t* B% V
a year. The father also revealed he was embarrassed
' {* l$ d) s4 F9 g- U8 _7 fto disclose that he was using a testosterone gel pre-2 }( p/ T6 z$ ?; z0 \) A. \
scribed by his family physician for decreased libido- v8 Z+ B5 T% {2 Y
secondary to depression.
/ H, X% [) Z4 R2 eThe child slept in the same bed with parents.5 E( V5 |/ r% x' t' |/ ^: M
The father would hug the baby and hold him on his" q8 P2 A& y0 X+ h3 X
chest for a considerable period of time, causing sig-
4 t" R+ ~$ B) ^: a$ {* Anificant bare skin contact between baby and father.' `( @; }' ?7 Z4 t* z
The father also admitted that after the phone call,6 R/ s/ Z5 R/ ]4 g3 \, R( B7 Y
when he learned the testosterone level in the baby9 r. b [( k5 Q0 t7 s2 v2 V
was high, he then read the product information C1 f7 g# `+ [2 @
packet and concluded that it was most likely the rea-1 t8 e" n$ ]6 E) y$ t8 e# P* H
son for the child’s virilization. At that time, they
4 `* r) {- a5 M$ tdecided to put the baby in a separate bed, and the- i z, j, j$ k" {1 G
father was not hugging him with bare skin and had
3 D* f. K3 G9 B: \8 n7 xbeen using protective clothing. A repeat testosterone4 E' `- k! j, E" w% w* D7 j( O
test was ordered, but the family did not go to the: |7 [7 C2 X( G' ?# a
laboratory to obtain the test.
6 t; X% d0 ^* g) M6 V' n0 }9 |" D$ s8 Y/ ZDiscussion
$ o) T% c" z( U9 J- @: T7 e& ^Precocious puberty in boys is defined as secondary
4 k2 D- F Z0 y( O1 a# X( Fsexual development before 9 years of age.1,4
# {! K) H/ J A8 l6 S9 {Precocious puberty is termed as central (true) when
6 d6 Y( Z7 {: u4 C: J$ Q' Oit is caused by the premature activation of hypo-
/ |% B! T& ~0 ^5 Z' D% X- ?8 Y& Ethalamic pituitary gonadal axis. CPP is more com-/ L ~" x5 Z% Z9 i( e! F) \; f
mon in girls than in boys.1,3 Most boys with CPP& `# @, U, G$ a1 m! @0 n
may have a central nervous system lesion that is
. a4 i1 o' G& f6 {1 \responsible for the early activation of the hypothal-
' O5 q% ~+ h: g s7 x8 _amic pituitary gonadal axis.1-3 Thus, greater empha-- r' G4 @( u7 u. r5 U' Q
sis has been given to neuroradiologic imaging in- b0 I2 L% s9 }3 e# D8 d
boys with precocious puberty. In addition to viril-1 W5 S/ R1 E) x) O: l6 S
ization, the clinical hallmark of CPP is the symmet-
5 U% p3 A5 w5 Arical testicular growth secondary to stimulation by
! p4 E2 v& b6 z9 vgonadotropins.1,3
# q3 t5 O4 x+ {. m2 B7 f$ vGonadotropin-independent peripheral preco-
( \9 U* |6 C! n! Hcious puberty in boys also results from inappropriate8 v+ K4 L% M$ f! R2 `6 z: X* f( l
androgenic stimulation from either endogenous or
/ b8 U( j2 G4 ?" G5 |exogenous sources, nonpituitary gonadotropin stim-
$ g! T% ]9 o+ b9 I# b. ]; Vulation, and rare activating mutations.3 Virilizing
! G5 M2 T% u! f8 \8 B0 G" G& h; @" Icongenital adrenal hyperplasia producing excessive
2 |1 t: |- S6 L5 h2 C2 Y% ^/ Kadrenal androgens is a common cause of precocious
4 c3 {5 w% F- c# z7 vpuberty in boys.3,4
: ^; z# J/ t8 u! s9 mThe most common form of congenital adrenal
* q9 V3 P- }" Y3 E/ rhyperplasia is the 21-hydroxylase enzyme deficiency.$ l1 \/ W; e; }+ n
The 11-β hydroxylase deficiency may also result in
+ L9 ]( \8 G9 O$ X0 Gexcessive adrenal androgen production, and rarely," e. O$ }- W; y4 ^1 x( r
an adrenal tumor may also cause adrenal androgen
- j" d( o/ I) o8 hexcess.1,3
7 z$ _# q/ z: T# n" G( Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ N) w0 W. D2 l) q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& U8 U* [( W- [# fA unique entity of male-limited gonadotropin-' K0 X1 B/ ^8 e8 a
independent precocious puberty, which is also known: U2 q9 S' F6 j) G
as testotoxicosis, may cause precocious puberty at a
. b* h; j( Z: m. Gvery young age. The physical findings in these boys
; a1 P: F/ f0 I8 Twith this disorder are full pubertal development,
8 `7 ~8 W6 L+ G8 q9 b+ @/ Q8 H' Jincluding bilateral testicular growth, similar to boys
& P# ?7 C6 Y" swith CPP. The gonadotropin levels in this disorder9 E: p5 D+ p' D0 c
are suppressed to prepubertal levels and do not show- _& j+ _1 ^6 X3 M8 }( y
pubertal response of gonadotropin after gonadotropin-2 t" ^: l' L6 h5 v( {
releasing hormone stimulation. This is a sex-linked
! o3 E3 w! `/ r9 F3 Wautosomal dominant disorder that affects only
& j9 C) N& J& J+ C. Y( k; j* B, Jmales; therefore, other male members of the family# _0 s- S4 ]1 w1 V; k5 h5 m
may have similar precocious puberty.3 M* p* [ z1 \$ F
In our patient, physical examination was incon-
/ G1 l* h3 H! I7 _/ y8 Ysistent with true precocious puberty since his testi-
i$ R. ~! b* ]5 M! @! jcles were prepubertal in size. However, testotoxicosis
# m4 T: O% Y, t( hwas in the differential diagnosis because his father0 K, K5 z# S5 ~" Q* e1 P; _8 Q
started puberty somewhat early, and occasionally,
( ^$ `* L. f; K: Ktesticular enlargement is not that evident in the( @3 A0 X0 X, `3 n
beginning of this process.1 In the absence of a neg-
: E# V& c' W% Q9 F! mative initial history of androgen exposure, our
5 a4 p) G: i1 ]. k7 k" xbiggest concern was virilizing adrenal hyperplasia,
. b# t& u0 W G8 {6 h U2 zeither 21-hydroxylase deficiency or 11-β hydroxylase( `7 z% j. g0 s% J" P( k& ?. d
deficiency. Those diagnoses were excluded by find-
" d3 z/ _) U6 ^ing the normal level of adrenal steroids.
$ Z" F0 \. G2 Z+ Z; V7 l1 p# b7 eThe diagnosis of exogenous androgens was strongly
& z! j+ R! t4 ?suspected in a follow-up visit after 4 months because" N2 U9 F; t3 H! Q e C. U
the physical examination revealed the complete disap-
( z9 {4 A) d* N7 [9 ^/ g# p3 ipearance of pubic hair, normal growth velocity, and
& }6 N& s d; Pdecreased erections. The father admitted using a testos-
* d. _. y9 f! K* Eterone gel, which he concealed at first visit. He was1 V( x# }8 [% u, E" B$ |% b2 b
using it rather frequently, twice a day. The Physicians’( ~! Z1 [* d# M8 G# \: y @: m
Desk Reference, or package insert of this product, gel or+ ^5 v) L6 \- S" @0 Q* p; `: t3 C* X
cream, cautions about dermal testosterone transfer to
3 m F# b: C# d( t' \3 dunprotected females through direct skin exposure.
% _, }# v; ~! j! j; G+ u4 PSerum testosterone level was found to be 2 times the) Q) ?* W, ~! R# L; G
baseline value in those females who were exposed to2 J9 t- u7 C8 H) Z6 C, d# \
even 15 minutes of direct skin contact with their male# F9 Y$ d* G2 v& M% Y# ]: O
partners.6 However, when a shirt covered the applica-
+ M" `( @0 G' G8 |4 ?1 _tion site, this testosterone transfer was prevented.$ W3 _9 @3 |9 u4 U6 W( e
Our patient’s testosterone level was 60 ng/mL,
5 m% E6 q+ X. l8 K1 N3 g' o0 T6 owhich was clearly high. Some studies suggest that. [3 @% e9 i2 B: X4 d4 I9 O4 N
dermal conversion of testosterone to dihydrotestos-
6 m$ C5 r4 U' n1 }terone, which is a more potent metabolite, is more3 P4 o5 P' q2 \9 R) a
active in young children exposed to testosterone4 |5 x2 T L0 W# M& d: f
exogenously7; however, we did not measure a dihy-
3 L3 I. U& f, s! K# e: I) Q7 Vdrotestosterone level in our patient. In addition to
* _2 B: P5 }0 e8 c6 E# S5 w% Xvirilization, exposure to exogenous testosterone in( ]! A& A+ O/ n: m, {3 g- y
children results in an increase in growth velocity and4 F1 G( [3 j4 `: t: y8 U/ j
advanced bone age, as seen in our patient.
\( Y: t$ {) xThe long-term effect of androgen exposure during
& `! R5 O; @. pearly childhood on pubertal development and final: A. h) \0 f0 I! }) Y- T+ X
adult height are not fully known and always remain: c1 w1 _# K0 e2 b. P3 \
a concern. Children treated with short-term testos-
* L; Y# O8 ]6 e" [; m/ kterone injection or topical androgen may exhibit some
6 ]5 Y, H2 G8 D8 a9 C; l: l/ E3 V! vacceleration of the skeletal maturation; however, after& F4 U2 i8 ~9 P! S7 S
cessation of treatment, the rate of bone maturation7 k3 @ [% e9 K1 k4 ]% [
decelerates and gradually returns to normal.8,9
, z" r' ?# Z( |& G) d% rThere are conflicting reports and controversy6 [* `4 P) W% d9 l# [. X
over the effect of early androgen exposure on adult
: h, O( v* g4 A5 E3 L3 Z1 X: wpenile length.10,11 Some reports suggest subnormal2 M/ \. ` @5 o* i
adult penile length, apparently because of downreg-
0 {" [. q$ q& w u; Q0 \6 tulation of androgen receptor number.10,12 However,' N2 O- o0 Y, N* B0 m3 A& h
Sutherland et al13 did not find a correlation between9 V' D" k( r3 D- u4 x# i
childhood testosterone exposure and reduced adult$ C0 w" y& C& Z: f* ?+ }6 k- w0 y/ ]
penile length in clinical studies.) u' O. ? O, k# W7 S5 m
Nonetheless, we do not believe our patient is
' B# p/ @' q1 j! a) Hgoing to experience any of the untoward effects from" }- ?0 ]: u4 O0 f
testosterone exposure as mentioned earlier because, `" @# ?( ^5 j( z7 o
the exposure was not for a prolonged period of time.! r) |2 O% J" Q7 f0 D, f& s
Although the bone age was advanced at the time of# t8 w4 t$ Q- v) n( Y8 U/ E
diagnosis, the child had a normal growth velocity at, N# j, a" L9 X* b) V3 z
the follow-up visit. It is hoped that his final adult+ U6 o3 w1 L+ o7 z2 }; {4 v
height will not be affected.
# z7 n$ M% r9 g' q: _9 U4 mAlthough rarely reported, the widespread avail- i5 K4 I/ c; g/ b* Q: r, _
ability of androgen products in our society may
7 H- h% i' ^- R8 {6 h- x- \( Uindeed cause more virilization in male or female% d3 m& |% }2 s* {8 _$ K7 P
children than one would realize. Exposure to andro-
4 k4 ]! B/ i5 O# @) h+ Ngen products must be considered and specific ques-* Q [. A8 M" E9 ?
tioning about the use of a testosterone product or6 O* u9 F# K2 a x# l9 f
gel should be asked of the family members during: o$ c# d) L3 I
the evaluation of any children who present with vir-: O1 `) y' b/ g a; U6 d- [
ilization or peripheral precocious puberty. The diag-
3 G! q9 m: P8 W# S9 E' _; hnosis can be established by just a few tests and by `# Y" j% ^2 u7 _
appropriate history. The inability to obtain such a
. [5 }6 ]2 D7 w* H, Ohistory, or failure to ask the specific questions, may
( v" |, o- u) S! ^- m) tresult in extensive, unnecessary, and expensive9 _+ C& e" m0 J( H
investigation. The primary care physician should be
! x6 P7 W x" s+ faware of this fact, because most of these children
, |- |7 J9 C' ]; d0 _; Imay initially present in their practice. The Physicians’' x2 M X% Q; I& I6 k" m
Desk Reference and package insert should also put a
2 t8 h0 ~! k% M3 ^. Ewarning about the virilizing effect on a male or
+ E3 Y6 I0 V! }/ L. W1 Ufemale child who might come in contact with some-
; P, v0 y% s; V% s9 Q4 M" Aone using any of these products.. Y) b/ u0 O- m% U' @0 z/ t2 y
References
+ N2 t. F8 h- u3 E8 b1. Styne DM. The testes: disorder of sexual differentiation1 U0 v9 B3 n: i# C. J
and puberty in the male. In: Sperling MA, ed. Pediatric5 I" `, M4 c: n- Q# |
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
z6 h- `/ B2 i' L9 C* i2002: 565-628.
" q9 C, V% d( E8 \" U2 e0 Y* D5 y2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: [& L$ C7 M; O/ ~% _5 jpuberty in children with tumours of the suprasellar pineal |
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