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Sexual Precocity in a 16-Month-Old
' i+ M* d' m3 S# OBoy Induced by Indirect Topical' ?2 P* L, y4 j* d
Exposure to Testosterone# @, u7 [7 R' H- }) P* u
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2# B1 a2 j1 d$ t/ `
and Kenneth R. Rettig, MD1
3 o2 F. V5 f4 D9 J" MClinical Pediatrics2 C. T- D, T+ X' X( h
Volume 46 Number 65 F% {& S3 [0 C7 j1 I. ^7 @. v3 X
July 2007 540-543
& l% g' p4 `. G5 S© 2007 Sage Publications
5 K; _; U" A, p$ I, G, d10.1177/0009922806296651
4 j3 q" ~' O( Lhttp://clp.sagepub.com/ C1 I; u0 X& b- {0 Y( i0 J' T ?
hosted at
n1 f; V/ e. X, l, u% P+ yhttp://online.sagepub.com
# [! S9 r0 b! N2 A) m" |5 A) @Precocious puberty in boys, central or peripheral,2 F9 ^; I0 n' x. J3 {
is a significant concern for physicians. Central
/ Y$ Q. O4 W6 [precocious puberty (CPP), which is mediated
+ Y% X$ |- M! v2 [$ g+ K9 m3 cthrough the hypothalamic pituitary gonadal axis, has. R4 O8 z7 c6 O6 f
a higher incidence of organic central nervous system. z- f, Q" Y! E
lesions in boys.1,2 Virilization in boys, as manifested
P* s `1 u/ J% g9 t0 y! X- _, oby enlargement of the penis, development of pubic/ p; Q1 {" B0 F* B% o8 Y5 k( x
hair, and facial acne without enlargement of testi-9 J6 p. _2 l' t
cles, suggests peripheral or pseudopuberty.1-3 We' X2 u2 Q$ J* t6 F# ?8 J
report a 16-month-old boy who presented with the
! a' i: t0 Y2 _" e: r2 `& C; qenlargement of the phallus and pubic hair develop-/ Y+ ^. ~1 i! s5 {
ment without testicular enlargement, which was due; L% t" g; m4 |! d1 a ?) w* O: @" X
to the unintentional exposure to androgen gel used by7 s" O8 c8 b. h
the father. The family initially concealed this infor-9 `4 A! N8 ~. p3 e0 l& [
mation, resulting in an extensive work-up for this
' ?# E$ T# ^5 V% K% cchild. Given the widespread and easy availability of) _ a! U2 Y; a( G$ o
testosterone gel and cream, we believe this is proba-
; h' Y }; T: ^, Zbly more common than the rare case report in the' r2 `: Z& l$ r2 U) ~5 U) U; e4 Q
literature.4
: s/ a: B8 H; Y+ t7 O* W" p* q' YPatient Report- M% m8 {$ S! s
A 16-month-old white child was referred to the
! H) I' ^4 s; s2 |+ }3 Lendocrine clinic by his pediatrician with the concern' W! w$ r3 v2 U
of early sexual development. His mother noticed
1 o: y! l' z1 P; C& [3 v1 {. elight colored pubic hair development when he was, d& h+ |! s( K' _" j0 p/ u
From the 1Division of Pediatric Endocrinology, 2University of3 Q% ?6 d5 O m8 H4 Y
South Alabama Medical Center, Mobile, Alabama.
7 K7 h2 C U$ K( ]Address correspondence to: Samar K. Bhowmick, MD, FACE,2 n- T4 L4 u, j4 t
Professor of Pediatrics, University of South Alabama, College of( R$ O; S& C' G8 D' Y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
% f- w4 X& W+ Y" `# _( x6 Ge-mail: [email protected].7 O5 B4 {- x: a, g9 f$ j' {, R
about 6 to 7 months old, which progressively became
4 {7 `, \2 Y4 @: d& P9 G! Xdarker. She was also concerned about the enlarge-* v% ^3 Y6 E5 v
ment of his penis and frequent erections. The child
4 ?5 r2 {6 L! m. X$ o! V" L& m' cwas the product of a full-term normal delivery, with+ p* a. A$ M) d8 z9 S. ~$ I8 h2 {
a birth weight of 7 lb 14 oz, and birth length of( W! F h1 J2 g9 J _! L" {
20 inches. He was breast-fed throughout the first year
) ?' m1 Z% v7 T8 \, Eof life and was still receiving breast milk along with6 T0 Z. u& T5 ^3 y% O) x' C. j/ J; \
solid food. He had no hospitalizations or surgery,5 ^5 r7 y' J: p) l- ]
and his psychosocial and psychomotor development
% G1 X7 G) q! ~$ ?/ t8 owas age appropriate.8 N% g& q4 ]$ q8 j; m \
The family history was remarkable for the father,
! M5 S/ u; y% d9 D' lwho was diagnosed with hypothyroidism at age 16,
4 {0 O) P1 D, x" P2 }4 v/ R: j- w" ]0 Iwhich was treated with thyroxine. The father’s4 ]- t* P( I' h5 Z% V" z
height was 6 feet, and he went through a somewhat) G: j7 k7 o/ w- I" }
early puberty and had stopped growing by age 14.* X) X+ h% G9 D$ f$ j s' o
The father denied taking any other medication. The
. s% _4 ]: G8 }0 }, U& f7 Schild’s mother was in good health. Her menarche
& D) r! h/ S( y: B! u4 \was at 11 years of age, and her height was at 5 feet" m: L# a$ l& N1 I7 O" D1 D/ B
5 inches. There was no other family history of pre-
- |5 M' O& x4 Z/ H9 o1 bcocious sexual development in the first-degree rela-/ s% m6 z. ^( s$ @/ e5 f
tives. There were no siblings.
' r0 D: c# F& y& p6 vPhysical Examination' ? x. L7 E' [% \
The physical examination revealed a very active,: d' @& b; t/ Q0 M
playful, and healthy boy. The vital signs documented4 F- S g( ?7 } {' z9 u
a blood pressure of 85/50 mm Hg, his length was
7 \6 G5 m/ F" w- m+ |1 P/ h90 cm (>97th percentile), and his weight was 14.4 kg- O6 }: h. Z- \: G3 ]# a8 e; o! i
(also >97th percentile). The observed yearly growth
+ E' ~: e0 w% R) X2 i/ Ovelocity was 30 cm (12 inches). The examination of+ G% _9 u% |2 j/ B/ b& J
the neck revealed no thyroid enlargement.7 U( B- u- [! X$ S r# k- V6 N# u
The genitourinary examination was remarkable for/ X# d' d4 Y9 R* n5 o0 x
enlargement of the penis, with a stretched length of
; \) L1 |1 k; k" y: g- A8 P8 cm and a width of 2 cm. The glans penis was very well7 `* p0 w h1 s- Q6 B; i
developed. The pubic hair was Tanner II, mostly around
; C8 d1 Y- v2 F, n" d540
+ q# S+ @6 Q- j. \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& I/ w6 o! o$ V! K5 a! gthe base of the phallus and was dark and curled. The$ u! _& K6 P) {- b, ?7 k* f$ V
testicular volume was prepubertal at 2 mL each.* J% a- M+ q1 j2 V
The skin was moist and smooth and somewhat
; _1 }4 D/ e7 h! c7 @% R4 t! J3 W- Eoily. No axillary hair was noted. There were no, p. J) ]# u# }9 f. B' Q2 } t
abnormal skin pigmentations or café-au-lait spots.; G* L5 L, w- f, Q0 G' `! v* K1 M
Neurologic evaluation showed deep tendon reflex 2+, i9 E, ]; J& D& H0 d+ x" ^
bilateral and symmetrical. There was no suggestion/ i0 [% T& n$ K, ]" O7 c
of papilledema., J% w* a- H) f! s% i0 N8 D
Laboratory Evaluation k0 |; w* F" L) b% O/ ~+ }0 h+ _' ]
The bone age was consistent with 28 months by
6 h6 @. u, Y' i* n6 M! X, V7 Xusing the standard of Greulich and Pyle at a chrono-" T8 i0 O/ Q" w6 l. C* |
logic age of 16 months (advanced).5 Chromosomal
: \4 f9 i3 m' j! r: D. N. }karyotype was 46XY. The thyroid function test
, {: ~- P$ _* w+ Xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-6 n2 l1 o h& T+ V1 ]8 G
lating hormone level was 1.3 µIU/mL (both normal).# i3 n( N3 v8 k* W! W1 X
The concentrations of serum electrolytes, blood
3 F. y8 o8 K9 X6 f3 y( B7 vurea nitrogen, creatinine, and calcium all were
! k, p1 [/ i0 X8 w, z. P* q1 swithin normal range for his age. The concentration2 w8 z( q( n1 }. T
of serum 17-hydroxyprogesterone was 16 ng/dL
! b) @- U. y Y2 p& B) V(normal, 3 to 90 ng/dL), androstenedione was 20/ {# C2 e' C2 G/ Y
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 g, ^9 j; _3 }7 V8 c9 h {9 q
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
: |" {# I1 @" Q! [+ |& D, V. Kdesoxycorticosterone was 4.3 ng/dL (normal, 7 to6 @, F8 ^0 _' V3 S, m f; x
49ng/dL), 11-desoxycortisol (specific compound S)
- L, f$ g9 O. owas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 s, n6 _( T8 }8 `5 [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 _6 m$ N6 V8 V% o
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& e6 E- M& ?& d% [3 }( Sand β-human chorionic gonadotropin was less than, r2 }1 ~9 d8 Z( j1 Y7 g
5 mIU/mL (normal <5 mIU/mL). Serum follicular; t8 ^% q5 A! i7 ~& h/ w
stimulating hormone and leuteinizing hormone
5 v6 V7 m6 [, a- r+ d# H; vconcentrations were less than 0.05 mIU/mL& g) c9 F3 x) o3 L( [, l
(prepubertal).
9 k/ c. e; ^2 N' m; G* sThe parents were notified about the laboratory8 w* p, V2 K, g) p) K5 b. s, Q
results and were informed that all of the tests were' [% X- T7 x8 `7 G i7 E: z6 I- L7 J/ p# j
normal except the testosterone level was high. The
0 J# y# }7 N: u% `' r9 cfollow-up visit was arranged within a few weeks to" x8 n; T" ?4 q6 G
obtain testicular and abdominal sonograms; how-
6 }0 t. G0 ]' e. q+ I+ T$ u$ O+ _. Xever, the family did not return for 4 months.
' o' W* e) M0 e1 ZPhysical examination at this time revealed that the; z4 w( q6 m7 h# O
child had grown 2.5 cm in 4 months and had gained0 s- t( A, K$ a4 G2 k
2 kg of weight. Physical examination remained& g8 Y! [7 h. ], s' H& C9 V
unchanged. Surprisingly, the pubic hair almost com-
& H+ B" n) N; U2 k/ u8 b' W" @pletely disappeared except for a few vellous hairs at
* v x1 `, C8 n; gthe base of the phallus. Testicular volume was still 2
4 [) P4 _# q3 j+ F' LmL, and the size of the penis remained unchanged.
) o! g8 |. _7 D. Z) I/ C- W4 F! B0 fThe mother also said that the boy was no longer hav-
) f( Z3 G/ y' F" P5 i! ding frequent erections.
9 U, N4 k: a6 [2 A bBoth parents were again questioned about use of( v# O- N; n1 ?3 A) L
any ointment/creams that they may have applied to; R2 ^) A; s+ r2 h! z
the child’s skin. This time the father admitted the
& v" v5 S& Q) }3 a; b. QTopical Testosterone Exposure / Bhowmick et al 541 i' Q' Y1 P1 }
use of testosterone gel twice daily that he was apply-: C U- E2 q. |) _% W
ing over his own shoulders, chest, and back area for* B# [; h& h5 N3 r4 f! _7 }
a year. The father also revealed he was embarrassed
! h9 q( a1 a; Y# W7 vto disclose that he was using a testosterone gel pre-4 U, N* a# c& J/ o
scribed by his family physician for decreased libido% ]& q, d& b$ J: K/ e
secondary to depression.( s* h' a- o+ o4 ^; ?& m5 ^
The child slept in the same bed with parents.
* Z) K3 d! Y+ c) y' [The father would hug the baby and hold him on his$ f! F& d9 K* q' w; \- Y
chest for a considerable period of time, causing sig-9 l: J2 a& n( k" P+ U
nificant bare skin contact between baby and father.3 s0 w) w, r. `' E$ l: T8 ]
The father also admitted that after the phone call,
% e' i' [' c$ U# Kwhen he learned the testosterone level in the baby
& A0 d6 B: c4 N) G. w$ {$ Hwas high, he then read the product information
, {) q/ |4 I) I8 M' y5 l' g6 Bpacket and concluded that it was most likely the rea-
) p! ^' f; w; U' n, c5 Nson for the child’s virilization. At that time, they
/ \4 t5 Z- C- n6 I: l! Hdecided to put the baby in a separate bed, and the# X' U$ r# z1 K% o. l5 B% Y
father was not hugging him with bare skin and had
" V) a& N% G( Q0 Q8 W6 L, hbeen using protective clothing. A repeat testosterone
]7 R! Y2 R/ \: I2 E% ^test was ordered, but the family did not go to the
3 W6 J: j' S& E% ~5 p1 c0 k5 m% [+ i! claboratory to obtain the test.
' H+ j- i7 N& d+ h0 l! z* vDiscussion: O: E; W5 w6 w$ j* g2 G3 ?
Precocious puberty in boys is defined as secondary7 y) [: b* j1 g1 ?- O
sexual development before 9 years of age.1,4/ h; L- P5 M( j3 q# j! U( f& g- S
Precocious puberty is termed as central (true) when
. g7 i- e0 l3 a& Z: U( q' s7 eit is caused by the premature activation of hypo-
/ c2 X# S6 l' M; y& s7 Qthalamic pituitary gonadal axis. CPP is more com-
0 q% E! |9 Q9 R5 `mon in girls than in boys.1,3 Most boys with CPP+ s: ^) G9 {4 _0 w% m. ^% S
may have a central nervous system lesion that is
) }( A6 ?& G) w- H% J( l# Uresponsible for the early activation of the hypothal-
! ]- o- a% F* ?- k- \0 Q0 _amic pituitary gonadal axis.1-3 Thus, greater empha-
* o( g0 x1 a% ?' u. g) ]sis has been given to neuroradiologic imaging in
o! x3 g2 k5 w# ^4 z2 U% X/ _boys with precocious puberty. In addition to viril- U- i9 b \ v" w
ization, the clinical hallmark of CPP is the symmet-
. r6 [, s; J1 |3 Grical testicular growth secondary to stimulation by
, i% `3 |( T" T) Ygonadotropins.1,3
# R$ R( {( w5 N4 h0 W, ^Gonadotropin-independent peripheral preco-
+ B2 q' _) ?, _4 w, g' i( `& ecious puberty in boys also results from inappropriate
/ ]4 C( u6 Y( t$ ^/ w8 h; ~% L' V) Q0 yandrogenic stimulation from either endogenous or
5 X$ Y7 O" y- M+ @8 R2 w% _exogenous sources, nonpituitary gonadotropin stim-; { j# [8 i, b
ulation, and rare activating mutations.3 Virilizing: }/ ]( c9 V9 q4 ^
congenital adrenal hyperplasia producing excessive
5 o! r2 s" K- U" d+ z0 Y$ i' C: Yadrenal androgens is a common cause of precocious9 o! c7 K8 a8 s9 x
puberty in boys.3,4
" W9 G7 X% e. nThe most common form of congenital adrenal
4 J7 a/ q" z* E9 dhyperplasia is the 21-hydroxylase enzyme deficiency.
/ [& U" d3 f4 ^6 [' z0 j6 @/ d5 U! kThe 11-β hydroxylase deficiency may also result in0 M- o2 |4 P. s+ ~7 ^
excessive adrenal androgen production, and rarely,' |) [, w' Q, h- D& w6 I3 @* a7 s& O
an adrenal tumor may also cause adrenal androgen# z' v9 m# T) W4 M* |. f# M
excess.1,3
$ E# g8 `, z, cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 p2 k/ t: b4 Z |2 T5 E/ ?" U& q& j542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 Q. r. @& ?6 A: p" c+ b# Z# k
A unique entity of male-limited gonadotropin-
, i0 \8 a8 K N& e% x* o% v8 F: y6 Uindependent precocious puberty, which is also known
; F& t; R E7 {, zas testotoxicosis, may cause precocious puberty at a
; k* M W1 q5 X4 D$ X9 ]3 ^very young age. The physical findings in these boys
) [3 D+ E9 C( bwith this disorder are full pubertal development," l" ?/ u$ X; {
including bilateral testicular growth, similar to boys- J1 V* O# y" ^: S; _! c9 X. j2 a
with CPP. The gonadotropin levels in this disorder( Q" G' x! A- v; \4 o6 F8 b- t9 _
are suppressed to prepubertal levels and do not show
M% |$ b3 Q' ^5 U& U% T/ |9 J% ]pubertal response of gonadotropin after gonadotropin-7 N) J, ~( V6 m3 }+ d
releasing hormone stimulation. This is a sex-linked
' A7 \2 M+ U) _1 Q7 B# ?autosomal dominant disorder that affects only& c" @( _: B* C( W0 |( f. M8 L
males; therefore, other male members of the family
: a) }! f# w0 V8 y/ n( d' }" h' fmay have similar precocious puberty.3
: f: S3 r% Z: Y: D" T# g1 AIn our patient, physical examination was incon-
3 R ~6 U3 l- k* L- m; Psistent with true precocious puberty since his testi-# J6 K, w. |* o' a/ V9 g
cles were prepubertal in size. However, testotoxicosis+ h# R5 i$ J' W9 v, d4 D
was in the differential diagnosis because his father
: e. [' z {7 s, Vstarted puberty somewhat early, and occasionally,
; C: q. \# d- B* c, Ttesticular enlargement is not that evident in the# P) E2 D- z Z$ ^) M1 v8 i
beginning of this process.1 In the absence of a neg-
! E; N0 W5 j* zative initial history of androgen exposure, our
! E( T2 v5 L% w1 W/ t2 gbiggest concern was virilizing adrenal hyperplasia,3 @5 c9 l, o. m. c1 m/ a9 I) y
either 21-hydroxylase deficiency or 11-β hydroxylase" U/ Z0 r: J# q
deficiency. Those diagnoses were excluded by find-
4 ~" ^: n) f" E9 L) @+ `ing the normal level of adrenal steroids.
8 O! `8 ^1 I( H$ k$ kThe diagnosis of exogenous androgens was strongly
- s3 x' I0 {0 Z; bsuspected in a follow-up visit after 4 months because
' L j4 @5 K4 y" @* nthe physical examination revealed the complete disap-
9 G9 o, ~: x6 U# Y2 {4 o0 X1 cpearance of pubic hair, normal growth velocity, and
+ d8 |' v0 ~% W c0 E; o. k4 f0 hdecreased erections. The father admitted using a testos-/ {7 c% q* W( n1 N- J
terone gel, which he concealed at first visit. He was
8 |1 F5 c; m+ L2 j1 husing it rather frequently, twice a day. The Physicians’
+ [, x( H& @. q$ N5 v* yDesk Reference, or package insert of this product, gel or
7 u) \7 o" ~- }cream, cautions about dermal testosterone transfer to
% N/ v p3 L. Dunprotected females through direct skin exposure.8 E+ ^* z* F" E, o" A7 r9 Q9 k& @+ L
Serum testosterone level was found to be 2 times the
4 e' _# [. [% L& abaseline value in those females who were exposed to' a$ j+ C$ j. R P* d+ J
even 15 minutes of direct skin contact with their male
! ~& A+ g/ Q8 j j2 Y) \partners.6 However, when a shirt covered the applica-
5 }& d& X' h$ X( t) }( Otion site, this testosterone transfer was prevented.7 }! ~" ~0 F8 [+ ?
Our patient’s testosterone level was 60 ng/mL,( @ e" y( c7 D+ A: K
which was clearly high. Some studies suggest that' A3 S* R) J- ?( X% u6 j9 W- I
dermal conversion of testosterone to dihydrotestos-/ }: O6 t( i" R9 E; V( l# D) T% Y
terone, which is a more potent metabolite, is more
8 z' d! C# M8 K5 eactive in young children exposed to testosterone* x) i2 N5 p& Y, d4 g: c
exogenously7; however, we did not measure a dihy-
1 v! x0 i$ q% _, i# d* }! W+ Edrotestosterone level in our patient. In addition to
8 s3 q/ U; V8 x7 P! c1 Gvirilization, exposure to exogenous testosterone in# v% x: {% {8 l9 A# e( H
children results in an increase in growth velocity and
+ v/ V4 \" V+ F: |- U* Gadvanced bone age, as seen in our patient.5 q* i+ A' {/ D5 j3 y1 W0 e
The long-term effect of androgen exposure during
6 Q2 ^! N0 q) d' Iearly childhood on pubertal development and final
" s. ?% g3 q0 D% J/ Hadult height are not fully known and always remain1 o0 E9 U& ~9 T: g1 t
a concern. Children treated with short-term testos-
4 l+ G: F- j; p& b$ O& E& Iterone injection or topical androgen may exhibit some9 s7 k5 N9 ]+ `
acceleration of the skeletal maturation; however, after, C4 |! M9 N5 X& ~ E* Y2 I
cessation of treatment, the rate of bone maturation, V- _ M/ K; G; d2 ~
decelerates and gradually returns to normal.8,9
& q+ A! X8 p% c- a2 k$ q$ C+ y4 ZThere are conflicting reports and controversy s# R$ N6 G6 J; t
over the effect of early androgen exposure on adult8 z8 B a% \# k1 Z- n) ?4 A9 K8 }* f
penile length.10,11 Some reports suggest subnormal4 H( q- U! c; j9 N' s1 I9 X/ v7 u
adult penile length, apparently because of downreg-
( @3 Q9 Y, R8 u0 \. |ulation of androgen receptor number.10,12 However,% R' V0 U: I' X, }# v- Q' d- M
Sutherland et al13 did not find a correlation between
, F% i% H* @4 _childhood testosterone exposure and reduced adult. Q4 b) t+ n6 _3 V: z4 T, W. E
penile length in clinical studies.( S* q Y* W: Q1 X: P- k$ y3 m" r
Nonetheless, we do not believe our patient is
) k% ?6 B+ e7 mgoing to experience any of the untoward effects from9 J0 ?; E. [; t/ a* `' {5 y
testosterone exposure as mentioned earlier because& P6 w- p/ S$ G) ?- w7 Q7 y: R
the exposure was not for a prolonged period of time.
7 ?- I: w' M# F+ f MAlthough the bone age was advanced at the time of
i9 u6 E# u5 X+ X, s% zdiagnosis, the child had a normal growth velocity at3 s/ z4 ?! x5 X9 Z6 h; U
the follow-up visit. It is hoped that his final adult& i; |* z7 i G
height will not be affected.
: h8 }1 B4 J/ u$ Q3 uAlthough rarely reported, the widespread avail-
4 v/ x4 v& m H6 V. j5 I% wability of androgen products in our society may
4 u0 ?- o$ |) y$ G/ windeed cause more virilization in male or female* H' v! `& P4 O5 u
children than one would realize. Exposure to andro-4 t. A9 z! G! T3 u
gen products must be considered and specific ques-& Q9 t( C* }! L
tioning about the use of a testosterone product or
- q8 k% D9 [$ P8 G) E8 agel should be asked of the family members during
/ k- I* E( o7 b' _# `7 jthe evaluation of any children who present with vir-
6 N0 H; l. y: v* C. j% G7 E& Yilization or peripheral precocious puberty. The diag-
* \4 B+ r$ }# G* `nosis can be established by just a few tests and by% m- k& }, m7 s, i Y( r" p
appropriate history. The inability to obtain such a
; t0 w" V5 C1 G4 i# x: d& xhistory, or failure to ask the specific questions, may+ X& G! h& W% _ ?6 q
result in extensive, unnecessary, and expensive
/ v9 k0 D* t) F8 |( uinvestigation. The primary care physician should be
$ @# e. P* Y% I; t' o3 B9 I0 N- Uaware of this fact, because most of these children! G) g4 t1 |. ^( O- w9 i, d, P
may initially present in their practice. The Physicians’
7 v! w3 p# @+ u8 t! VDesk Reference and package insert should also put a3 M: Z% |1 W: [' F) i" O
warning about the virilizing effect on a male or
4 t2 Y+ t' l2 @female child who might come in contact with some-
7 \! }/ f+ T0 R3 J7 T, hone using any of these products.# s+ K& H7 m1 j0 T
References+ Z3 q5 ~8 I7 w+ T9 X$ S
1. Styne DM. The testes: disorder of sexual differentiation9 g5 a+ w3 X1 u3 h) L5 b
and puberty in the male. In: Sperling MA, ed. Pediatric/ l% F: p- |( |# h6 z6 R
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" F+ Y6 r$ {/ P& T6 a# D6 v
2002: 565-628.
% @1 |/ p& |1 R0 q0 j1 ]2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 i* J* a8 ?9 Z8 a5 G# P: i( U8 m. Zpuberty in children with tumours of the suprasellar pineal |
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