- 註冊時間
- 2023-5-6
- 精華
- 在線時間
- 小時
- 米币
-
- 最後登錄
- 1970-1-1
|
發表於 2025-1-4 03:27:02
|
顯示全部樓層
Sexual Precocity in a 16-Month-Old
2 q* m2 m3 ~6 r I3 _: rBoy Induced by Indirect Topical# k# M- y% n: {- a0 ]
Exposure to Testosterone
, ^3 k1 _ G \, n7 ~0 T3 fSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ G$ \4 x9 n! c' iand Kenneth R. Rettig, MD1( [; x9 p0 G9 o, F" q
Clinical Pediatrics
& D' k9 X# n r7 {Volume 46 Number 6
5 l5 l5 r" j7 ^& k& EJuly 2007 540-543% z2 Z, z% U3 O
© 2007 Sage Publications$ [$ {! q# {( `. d) t& [
10.1177/0009922806296651
. O% U, j; h; _http://clp.sagepub.com& |& Y( d- B& Z8 n
hosted at
5 c. m, K0 K1 z/ b. Xhttp://online.sagepub.com
6 L" u$ X5 w: y$ l2 tPrecocious puberty in boys, central or peripheral,
2 m8 @# q& r8 X) l% V! b& sis a significant concern for physicians. Central5 Y3 ]7 ^: ?& S6 ]- L: B
precocious puberty (CPP), which is mediated" F& ]2 y4 S0 n
through the hypothalamic pituitary gonadal axis, has
/ Y- [, W* b- T+ ?a higher incidence of organic central nervous system
( B& s& w, {2 klesions in boys.1,2 Virilization in boys, as manifested
# [& @- F1 D" j- ~6 {by enlargement of the penis, development of pubic
/ n) X) [7 M4 @+ _6 \6 H+ a/ ehair, and facial acne without enlargement of testi-8 J% r. { k: U/ q0 ~% r
cles, suggests peripheral or pseudopuberty.1-3 We
+ P2 T9 u: ~# S7 m Z' [( greport a 16-month-old boy who presented with the
( X ~0 l9 G( b# e Benlargement of the phallus and pubic hair develop-
/ }2 {& M# [7 o9 j9 f7 m: zment without testicular enlargement, which was due
7 p: _1 P, j) }# K$ `' k4 Jto the unintentional exposure to androgen gel used by m: A9 n# d7 O/ J0 E- p1 n' T& M; @( f1 u2 z
the father. The family initially concealed this infor-3 h' E9 t/ s5 [; N* g1 B6 y" Z
mation, resulting in an extensive work-up for this. E6 i2 _6 d! j( Q* V
child. Given the widespread and easy availability of" w! u+ }) J9 k: C: s% B& i
testosterone gel and cream, we believe this is proba-
$ w2 l4 a( V% u w2 i6 Ebly more common than the rare case report in the
6 v5 ]# U# l: _ m* X! x6 Pliterature.4
$ _# k9 a E& zPatient Report. x, t2 i6 Y% `5 O0 c! U
A 16-month-old white child was referred to the/ E+ e' i& U# ~8 k7 ]
endocrine clinic by his pediatrician with the concern
; b0 M) l. W- g8 E x% tof early sexual development. His mother noticed! G! B/ I, Q& ^5 D
light colored pubic hair development when he was
3 A6 ~, b& ?9 e1 j5 {4 ^' M* {8 SFrom the 1Division of Pediatric Endocrinology, 2University of0 W( I+ `% C2 M
South Alabama Medical Center, Mobile, Alabama.0 @, y) W- P/ F3 b3 [( c+ ^
Address correspondence to: Samar K. Bhowmick, MD, FACE,, m" `/ \/ X' H: [" g. ]
Professor of Pediatrics, University of South Alabama, College of
9 H9 D, O' S7 V3 |Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 ^& f: Z% i+ ?, [6 z+ g; Z& n9 A
e-mail: [email protected].7 f. m3 Z7 Q6 h, V' D; W1 G5 D
about 6 to 7 months old, which progressively became( a% Y# t0 u" Z7 i F5 p+ o# K
darker. She was also concerned about the enlarge-
: c! |, f$ R% P& ? Z2 g; o3 Mment of his penis and frequent erections. The child1 C4 V* f; g5 r) E) D
was the product of a full-term normal delivery, with' E! P7 v4 p5 \# o! q$ v6 l! f' W8 h
a birth weight of 7 lb 14 oz, and birth length of
0 | h9 ^. x5 y- N' Z20 inches. He was breast-fed throughout the first year
3 m# u0 C2 S. C4 {' s" Oof life and was still receiving breast milk along with9 l+ M5 e& y' h$ d2 p" [- m3 X
solid food. He had no hospitalizations or surgery,
/ w1 G* G& O2 @! i: \) Y+ gand his psychosocial and psychomotor development S& V3 p* S @4 g% _" i7 d: u2 v
was age appropriate.
; H' i; L5 q. [- X% i, E( a; RThe family history was remarkable for the father,) G1 i' ]% V3 C/ c. g
who was diagnosed with hypothyroidism at age 16,9 G+ }! l% H( V4 C" P* A
which was treated with thyroxine. The father’s% c3 r X' b# h4 a% z
height was 6 feet, and he went through a somewhat
4 T9 E7 L; ]2 k8 C9 M! Oearly puberty and had stopped growing by age 14.
P5 V1 W' }) r4 \The father denied taking any other medication. The& X. U* I( {$ i6 n
child’s mother was in good health. Her menarche
, C$ D& i5 v& T$ o. H- Awas at 11 years of age, and her height was at 5 feet
$ e1 R* @- A4 y. ~' e( [5 p5 inches. There was no other family history of pre-; h$ T! m( H& n4 d
cocious sexual development in the first-degree rela-5 i$ [1 p0 W& G& Z' d# P
tives. There were no siblings.
* B" m! v3 G, O8 X$ `9 PPhysical Examination. b% Q4 t; t+ O( s V
The physical examination revealed a very active,. U" R, c$ ]- U4 ^0 u8 n
playful, and healthy boy. The vital signs documented
4 y2 O( V( `5 @& k6 E" B2 T* d' ^a blood pressure of 85/50 mm Hg, his length was6 l& v0 O+ I u% }
90 cm (>97th percentile), and his weight was 14.4 kg
7 J' F2 A. r9 [(also >97th percentile). The observed yearly growth
! n/ G; ?' A. T0 mvelocity was 30 cm (12 inches). The examination of
( i4 j# J" x* x% Y' othe neck revealed no thyroid enlargement.
$ W# O4 k; `! H# q. X( U7 qThe genitourinary examination was remarkable for" ` P. ]7 s Z; u0 Z
enlargement of the penis, with a stretched length of0 ^& T) S+ Q* }( y; M2 I
8 cm and a width of 2 cm. The glans penis was very well
9 G- @' N; p, X5 j& @: b) s- P$ Rdeveloped. The pubic hair was Tanner II, mostly around
8 d2 p8 ^ i! @4 p5406 ?, N. x( P( b3 |) r h; ~' r2 y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, |/ M. T& \* j
the base of the phallus and was dark and curled. The
' ^1 t; ^* T {, I$ y4 ]. H5 _# B8 z" ptesticular volume was prepubertal at 2 mL each.) E6 u5 p+ O( X' m
The skin was moist and smooth and somewhat
! ?; }! i& y$ b2 x( k# roily. No axillary hair was noted. There were no
6 h6 {" W6 k; a9 cabnormal skin pigmentations or café-au-lait spots.7 H* y# a2 ~, t+ ^6 n4 ^
Neurologic evaluation showed deep tendon reflex 2+
9 P: Q7 g+ F: ?3 e" Wbilateral and symmetrical. There was no suggestion
: Y. Y8 b1 ~! I* Z6 Iof papilledema.6 k5 n% t& n L6 a
Laboratory Evaluation* Q( |( U$ T% X4 l
The bone age was consistent with 28 months by
$ s; l6 L5 C) j' h0 _- jusing the standard of Greulich and Pyle at a chrono-% d9 ]" m0 i5 k' A# X6 u/ Q
logic age of 16 months (advanced).5 Chromosomal
3 s* O( m9 Y+ {5 H& m8 j9 Jkaryotype was 46XY. The thyroid function test0 H S$ K( @/ F; O0 w7 E
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 }+ E* S. [( S' `. jlating hormone level was 1.3 µIU/mL (both normal).% |5 q5 W1 O% B! I6 k" |3 G
The concentrations of serum electrolytes, blood, l$ j( N% _$ H8 x: {
urea nitrogen, creatinine, and calcium all were
% |' e* G( ~& x" ? ]: f: Dwithin normal range for his age. The concentration: |0 H, J# c, o' K/ M( F* V* B0 a
of serum 17-hydroxyprogesterone was 16 ng/dL
- Q8 \+ t2 T" _& L$ Q(normal, 3 to 90 ng/dL), androstenedione was 20: L' p1 L' r- X# a$ b$ M$ x
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-5 J8 @2 b, U2 `& I( t2 m
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 o# E1 D! `( L7 _' h; ^4 [/ Z2 Cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to2 Q/ Q( _* M# ]% D n
49ng/dL), 11-desoxycortisol (specific compound S)
" {8 N1 Z5 I* g2 o/ Wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 q& n* M2 r: t, C9 f$ V) m3 w9 Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 ~: o( R7 F- d+ O" W6 dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ `% j& [" @4 f- X$ ~5 u) z* sand β-human chorionic gonadotropin was less than0 o$ D) b5 K: \# f
5 mIU/mL (normal <5 mIU/mL). Serum follicular
% D3 f5 |# s s8 }" ^6 wstimulating hormone and leuteinizing hormone( e" X1 C l, R
concentrations were less than 0.05 mIU/mL [6 b$ `" ]. z7 Z5 r
(prepubertal).
; t, `1 f! D8 F5 ^9 g }8 G! ^The parents were notified about the laboratory7 s. h& ~. z% ~7 m9 f# u
results and were informed that all of the tests were# T. H$ U5 I3 c4 s) b. r) r
normal except the testosterone level was high. The
1 e) T* M3 k* V/ ]# V' [$ T9 Ofollow-up visit was arranged within a few weeks to
& R' b! F1 _1 J% f$ e+ uobtain testicular and abdominal sonograms; how-. x! h9 Y) }0 ~# ?' W/ C# c
ever, the family did not return for 4 months.
4 P. }# u( \7 V* LPhysical examination at this time revealed that the4 _$ i* \8 u( t
child had grown 2.5 cm in 4 months and had gained
) Q* Z6 A, h3 F1 U2 kg of weight. Physical examination remained
]4 p" \) V! Dunchanged. Surprisingly, the pubic hair almost com-9 C& Q* p0 z) g2 z
pletely disappeared except for a few vellous hairs at
/ i8 J, k7 A F& j% Nthe base of the phallus. Testicular volume was still 27 X6 d3 m. b7 D1 B
mL, and the size of the penis remained unchanged.
+ R" C `- h% u- n+ v+ X' G# YThe mother also said that the boy was no longer hav-$ E" n4 f! a3 Q+ R" B) J3 N$ E
ing frequent erections.
$ s3 @% x8 d2 @/ u. _Both parents were again questioned about use of3 \" B/ z, P1 X Z- a
any ointment/creams that they may have applied to" E# O: g4 h3 r: U L
the child’s skin. This time the father admitted the
* f; ^: O6 V9 l& ~% L$ DTopical Testosterone Exposure / Bhowmick et al 541
! S4 L) X0 L# o" Q+ I, z* Ouse of testosterone gel twice daily that he was apply-, w6 |& I) t+ \0 y/ m4 O
ing over his own shoulders, chest, and back area for/ k1 g3 l6 [, X
a year. The father also revealed he was embarrassed
2 Z% t- @" n& h0 O4 u. _- h: qto disclose that he was using a testosterone gel pre-
- K/ `5 h8 X; {+ U% p) vscribed by his family physician for decreased libido- h+ X* W/ w1 J% b
secondary to depression.
$ b2 G* A, y5 l$ o' Z. N0 EThe child slept in the same bed with parents.; s& o( c: b# q7 |/ H8 Y" K
The father would hug the baby and hold him on his
; t1 E/ y: _; ~% \" S9 schest for a considerable period of time, causing sig-, Y- A5 M+ [/ y2 e
nificant bare skin contact between baby and father.$ w; C9 R l/ `' A! q" K+ ?5 a: Y" x
The father also admitted that after the phone call,
4 i& s" `+ f# p: ?when he learned the testosterone level in the baby
# \2 O4 U+ ]. K3 ^" bwas high, he then read the product information
5 ]& M9 m, [: S- o8 ppacket and concluded that it was most likely the rea-% c/ m( T6 J; M" D
son for the child’s virilization. At that time, they
3 k& u5 i6 `: o2 ~$ c2 kdecided to put the baby in a separate bed, and the$ p! g- G% {1 p8 ?
father was not hugging him with bare skin and had
$ D( g$ S$ |9 \( O& W' X6 r6 P, c; Ubeen using protective clothing. A repeat testosterone0 x/ V |+ [1 |2 y! V' O/ \
test was ordered, but the family did not go to the
, f5 I+ s; C) s. _$ h& llaboratory to obtain the test.: `; s! ?- v2 t, P
Discussion! g, e0 C, s/ E( N9 E2 x
Precocious puberty in boys is defined as secondary
( ^- Q5 {/ j3 v2 \5 A% dsexual development before 9 years of age.1,4
" z+ N9 g/ g- O: J9 @Precocious puberty is termed as central (true) when
! ?, ?1 t8 C8 B/ H: H2 ait is caused by the premature activation of hypo-! r% w. e! e6 X1 z% F' B$ L% i
thalamic pituitary gonadal axis. CPP is more com-: f+ I9 R" r. i
mon in girls than in boys.1,3 Most boys with CPP
p! o& c' e. c: e& v) F# A5 Jmay have a central nervous system lesion that is) E! X7 D5 ?( R' i/ K# R
responsible for the early activation of the hypothal-
; [8 D+ Y' s2 Gamic pituitary gonadal axis.1-3 Thus, greater empha-" Y* t/ f2 r ]+ P3 ?- G
sis has been given to neuroradiologic imaging in+ I; h$ ~* |2 ~$ r: b1 B: O/ O
boys with precocious puberty. In addition to viril-& K+ r( j( F6 r8 z3 ^. F
ization, the clinical hallmark of CPP is the symmet-" A' \' S) F; [7 l1 F5 y
rical testicular growth secondary to stimulation by1 H1 m. }( J0 M: ^
gonadotropins.1,3
: D% W- g& E$ w1 ^. V6 ]Gonadotropin-independent peripheral preco-7 J: J7 V& I# v/ L# T: `: z
cious puberty in boys also results from inappropriate
8 a) G5 V" k4 r2 @( Candrogenic stimulation from either endogenous or
) c" d1 v/ n4 a4 R) D. |3 Fexogenous sources, nonpituitary gonadotropin stim-
8 B+ l/ u b, y: eulation, and rare activating mutations.3 Virilizing
' ?6 Z, U j" a. Z2 @, Ocongenital adrenal hyperplasia producing excessive$ N8 ~# {. W' H; J( M/ I7 P. o( w K
adrenal androgens is a common cause of precocious
) d4 Q- |; N9 ~1 G5 L& _& Y$ b }* kpuberty in boys.3,4
+ _. }( j- Q& k( T9 X3 ~) }1 SThe most common form of congenital adrenal" J" C& g3 _) h& L! ^
hyperplasia is the 21-hydroxylase enzyme deficiency./ F, o- s) b1 H9 C
The 11-β hydroxylase deficiency may also result in
) i0 K5 m( ]; I2 w! d4 u. X/ Yexcessive adrenal androgen production, and rarely,
& h3 f; ^2 W1 Fan adrenal tumor may also cause adrenal androgen
' P. A' }5 z, Q$ nexcess.1,3# h2 `6 A7 L5 x; K1 u8 h
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 P3 C; o3 u1 O542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
" x. E4 x. r! RA unique entity of male-limited gonadotropin-% e- Y2 G; E/ o" j
independent precocious puberty, which is also known
; U C6 x( v4 a% s8 [* \as testotoxicosis, may cause precocious puberty at a
W) E6 M+ c% g( h) S* v1 Gvery young age. The physical findings in these boys
* h6 X, a8 \1 Y/ E2 Rwith this disorder are full pubertal development,, B2 n, C B. W% t7 k( s' S
including bilateral testicular growth, similar to boys
+ x/ ?+ b% V" U) kwith CPP. The gonadotropin levels in this disorder
+ |" s$ ^+ J0 ^" l3 K" Uare suppressed to prepubertal levels and do not show
( f& `! a- t% M$ Spubertal response of gonadotropin after gonadotropin-
6 A0 Z% Z0 i2 N7 `% `% X1 |7 ureleasing hormone stimulation. This is a sex-linked9 a0 A# ~% F. c5 i2 \! U2 ~/ |8 t
autosomal dominant disorder that affects only
" c# W3 l$ Q- y& k4 p6 Jmales; therefore, other male members of the family
( N1 I4 l$ S. p5 g" ~may have similar precocious puberty.3* u* l0 k4 N3 s9 | g& V3 f) t
In our patient, physical examination was incon-
0 E; O) `+ o$ o1 J# [* Vsistent with true precocious puberty since his testi-
8 |& R' M3 f, u+ r+ Acles were prepubertal in size. However, testotoxicosis# c! C/ g M/ @; F
was in the differential diagnosis because his father H. _$ e1 Y" [3 b/ Q7 ]
started puberty somewhat early, and occasionally,
/ s* t0 ?$ C- q. d6 b8 K; e3 Ttesticular enlargement is not that evident in the
% W; x. I l$ ~8 w% [( i) {beginning of this process.1 In the absence of a neg-
( h7 V" g& U+ t% o, @' @ative initial history of androgen exposure, our# C5 F }% r/ p3 }) H
biggest concern was virilizing adrenal hyperplasia,8 x! J9 e# B3 y0 e; ^
either 21-hydroxylase deficiency or 11-β hydroxylase: ~4 d$ X, u# Z- [
deficiency. Those diagnoses were excluded by find-( J" r {" S. A8 o$ M
ing the normal level of adrenal steroids." z; W) t9 K3 i5 _' L/ B
The diagnosis of exogenous androgens was strongly
3 e! x! S4 F: dsuspected in a follow-up visit after 4 months because
: ]7 L) a( l2 O2 ^! H5 Fthe physical examination revealed the complete disap-
|$ J- b( U% e2 a& h9 ~pearance of pubic hair, normal growth velocity, and
3 i$ M" c; X' H2 r" T" Idecreased erections. The father admitted using a testos-
0 A2 u1 P3 s) a$ P5 C3 b dterone gel, which he concealed at first visit. He was
+ ~, S' O! M- ]7 ^3 x# Jusing it rather frequently, twice a day. The Physicians’- n7 H" W& k n" Q
Desk Reference, or package insert of this product, gel or4 J# K. O! T' G% f7 M! {4 Y
cream, cautions about dermal testosterone transfer to, S5 H- q: v4 \2 {# x/ ?
unprotected females through direct skin exposure.
2 V/ }7 F' |* T: O: g+ ]% ESerum testosterone level was found to be 2 times the
% V) G' d9 N& x! a6 bbaseline value in those females who were exposed to$ r9 ~4 a. W* U5 a4 ^# z* G
even 15 minutes of direct skin contact with their male+ z; q2 r& T8 z# X% A4 F
partners.6 However, when a shirt covered the applica-
! L# o/ M/ a- f8 _5 P* Q1 wtion site, this testosterone transfer was prevented.' {# M2 l; P1 V: `; U
Our patient’s testosterone level was 60 ng/mL,
. ~9 `6 c! F8 \, A' I1 Uwhich was clearly high. Some studies suggest that
{- {+ [7 U' t! ? D, Q' C+ Ddermal conversion of testosterone to dihydrotestos-* O: {5 x' t# A% F4 E% c
terone, which is a more potent metabolite, is more4 {; W) i' q! e5 ]) s4 z$ l% z
active in young children exposed to testosterone" I2 S3 D) u& y* x! Y$ S, V6 ~
exogenously7; however, we did not measure a dihy-
3 f7 M" O5 Z E* [6 Ddrotestosterone level in our patient. In addition to
* k$ `6 s; h6 D* ^$ ]/ evirilization, exposure to exogenous testosterone in
! g ?, ^ _& t, x3 q+ l/ i# zchildren results in an increase in growth velocity and# @3 n8 y: K4 n' \$ u
advanced bone age, as seen in our patient.
8 s( e" D/ h5 H6 N1 \1 CThe long-term effect of androgen exposure during
2 z2 x' ]5 a! I2 A3 b; Eearly childhood on pubertal development and final
$ r! k% p i6 @9 Q. O- `- Fadult height are not fully known and always remain
' }& H& j! T4 T7 l3 N4 ia concern. Children treated with short-term testos-
: k. H6 r2 t2 A, j/ [+ g; |' D' Uterone injection or topical androgen may exhibit some
c6 q, K0 q$ Zacceleration of the skeletal maturation; however, after. X6 n& f [! e
cessation of treatment, the rate of bone maturation
' n2 g, v6 b5 c% H1 t5 T7 hdecelerates and gradually returns to normal.8,9
% |$ h) {2 G+ P0 N0 @# r* ]' OThere are conflicting reports and controversy. E1 L8 ~$ `; o; D# O! X4 a* L) ^8 _
over the effect of early androgen exposure on adult
7 z# z- {5 ?: a9 ^penile length.10,11 Some reports suggest subnormal
0 v* Z) b6 C0 I) uadult penile length, apparently because of downreg-! k+ Q* Y8 l0 @$ r/ Y
ulation of androgen receptor number.10,12 However,
* y) i2 L) M* p" z) g8 m3 BSutherland et al13 did not find a correlation between
9 u4 Z0 l3 Q1 fchildhood testosterone exposure and reduced adult
1 H, b- K2 y" q, a% cpenile length in clinical studies.
' {0 @, M6 l' W/ t7 k1 BNonetheless, we do not believe our patient is
% f7 x( w1 }- Igoing to experience any of the untoward effects from
0 b# E. H: P) r* h3 H Ktestosterone exposure as mentioned earlier because
! M3 B! B7 c, M3 Nthe exposure was not for a prolonged period of time.
; k) z" w8 { B8 LAlthough the bone age was advanced at the time of
# U) B, u! P9 B, Ldiagnosis, the child had a normal growth velocity at T! S. I% ~8 r0 `# Y+ M$ K0 }
the follow-up visit. It is hoped that his final adult9 P1 |1 P( F1 m, \
height will not be affected.# p9 {5 X3 A' F! u
Although rarely reported, the widespread avail-* R4 R1 E$ k: P5 d7 O
ability of androgen products in our society may- Y! E! l4 [9 c7 w: J$ J
indeed cause more virilization in male or female, a6 g: _( L4 E2 n& T6 p |
children than one would realize. Exposure to andro-1 ^1 e2 j0 M. k: t
gen products must be considered and specific ques-
1 t; z8 b8 j& ~8 J" i& z( {+ Ktioning about the use of a testosterone product or" |2 R* }+ G) D3 X8 G$ R( N, F
gel should be asked of the family members during( P6 \; F- F$ L% t; U- x0 s" w
the evaluation of any children who present with vir-6 C" s( S( O8 w' W% L4 z& x' }
ilization or peripheral precocious puberty. The diag-
$ D$ q" |4 a0 d* X, ~! j- L/ Z" r& enosis can be established by just a few tests and by
: z- G9 v$ ^8 |7 K) B; qappropriate history. The inability to obtain such a' U$ Q" F, A/ [$ W7 u3 T
history, or failure to ask the specific questions, may
, ]+ M( r+ J1 d! V M$ I1 \. aresult in extensive, unnecessary, and expensive
$ V8 ~4 f! W) W3 N3 ginvestigation. The primary care physician should be
2 @3 c2 @* M( Laware of this fact, because most of these children/ e" T' J4 ]( F2 d1 ^6 d. {
may initially present in their practice. The Physicians’
% C5 b( \$ N/ L" f1 d) D# fDesk Reference and package insert should also put a; W; g7 Z" O! c' N
warning about the virilizing effect on a male or
1 d7 a; {0 i& `' _6 V: F$ ifemale child who might come in contact with some-" ?# D$ Z1 `( o0 f
one using any of these products.+ k% \. h- g! T- w, U& J
References
1 l, Y% ~2 K& @* h* C8 X1. Styne DM. The testes: disorder of sexual differentiation
" [* ~/ @5 g% e! W* B4 _0 \, a- L) eand puberty in the male. In: Sperling MA, ed. Pediatric- k# M2 j& K& U- e- @3 G. @* |
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 m0 z4 g i; {; m1 ^- M
2002: 565-628.% n" O/ ?& d) D* s& L
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& y& [6 r) {4 u' \
puberty in children with tumours of the suprasellar pineal |
|