- 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" C0 R% O9 @! E1 {9 f' @
Boy Induced by Indirect Topical/ E9 G6 |! Y. j4 ~8 P3 v$ x
Exposure to Testosterone0 X+ c, E3 N0 |1 ]
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 y; x5 H2 [0 p2 Y
and Kenneth R. Rettig, MD1
6 V! |4 e \; m5 M' ?Clinical Pediatrics8 o7 C: _# l2 j2 ? J5 }6 n
Volume 46 Number 6
$ V- z, U6 J$ v+ {3 u) NJuly 2007 540-543
* S7 Z" G$ k6 Z* Y© 2007 Sage Publications
. W. K) S; {% c10.1177/00099228062966518 q8 o/ j& E' U; O M3 v
http://clp.sagepub.com
- y9 T( f8 C5 Bhosted at; m; a/ g/ r6 j0 D7 Q
http://online.sagepub.com
( t" j& c, y, `Precocious puberty in boys, central or peripheral,
% X+ B, h5 }- M+ D! k) B* Wis a significant concern for physicians. Central
: s2 L$ R/ c+ a; ?precocious puberty (CPP), which is mediated$ y& P3 t& i3 P, Z5 y5 ~# n
through the hypothalamic pituitary gonadal axis, has1 I1 z4 z3 m2 T1 `7 W" U
a higher incidence of organic central nervous system
( C7 a* \! A7 u1 H+ P% D' a, ?lesions in boys.1,2 Virilization in boys, as manifested# Z4 g& S# K2 O+ c f4 X
by enlargement of the penis, development of pubic
- r5 u' I- t, ? S: K7 S2 @hair, and facial acne without enlargement of testi-
6 J. w/ F P1 _. ocles, suggests peripheral or pseudopuberty.1-3 We2 M! r/ l& A3 x4 t% t" `( E
report a 16-month-old boy who presented with the4 C' B# Y$ g5 e0 D
enlargement of the phallus and pubic hair develop-
$ d* o( H1 M+ r# G) Q- Z; Cment without testicular enlargement, which was due
+ `/ t& }$ J/ ito the unintentional exposure to androgen gel used by) ], z' Y3 B9 q0 v0 U
the father. The family initially concealed this infor-
: i5 a! Z1 Y' A+ g1 A, G. fmation, resulting in an extensive work-up for this0 R% K9 U# E6 Z/ H
child. Given the widespread and easy availability of
. H! x8 d8 \: G: g. F r. Ftestosterone gel and cream, we believe this is proba-& `, o9 z T4 f9 a3 r; H/ K) c' z2 V
bly more common than the rare case report in the
, N4 r2 M f& Vliterature.4" V; |7 S" d9 l9 Y) E8 g
Patient Report" T/ o+ {/ F9 ^
A 16-month-old white child was referred to the, k) f2 [0 o2 ?$ l' g
endocrine clinic by his pediatrician with the concern
* z4 ` V& }' L- k4 Yof early sexual development. His mother noticed
! N! x- I/ E, O: E6 m; b# M, G) ~light colored pubic hair development when he was: j0 n8 f0 z0 I4 g/ j
From the 1Division of Pediatric Endocrinology, 2University of
9 j+ \7 h, ]# V7 W8 hSouth Alabama Medical Center, Mobile, Alabama.; E+ d. p, a1 O2 i- f9 i
Address correspondence to: Samar K. Bhowmick, MD, FACE,, S" s/ Y! n/ `& i# {+ D3 B
Professor of Pediatrics, University of South Alabama, College of3 y+ ~% j m/ ?. y, {& t8 J
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 j' X( [+ w/ v( Qe-mail: [email protected].
4 O1 ~$ i$ j" U! j- R$ ~' F/ Babout 6 to 7 months old, which progressively became+ E9 A& l' x3 X6 E& G
darker. She was also concerned about the enlarge-: G8 e* O# K. L1 y5 e- E7 O( e
ment of his penis and frequent erections. The child
7 d# H, s& p) fwas the product of a full-term normal delivery, with
! J/ A- }0 P+ J9 B; z0 Y! G8 Va birth weight of 7 lb 14 oz, and birth length of% D- u! h. I9 B
20 inches. He was breast-fed throughout the first year
5 Z1 P. t6 f( {' h5 Rof life and was still receiving breast milk along with
, |; z; p# Z7 v' v, _6 tsolid food. He had no hospitalizations or surgery,
0 A, d3 L5 _6 K% ^" x g' ]3 _- oand his psychosocial and psychomotor development/ D- f: U7 ]$ b* G6 B* H
was age appropriate.
; g9 u8 e6 h' G6 r# a2 s0 O. [; lThe family history was remarkable for the father,2 _% A8 l( K* Y; F, ?" K
who was diagnosed with hypothyroidism at age 16,
% z4 v- U1 V$ D" p& \1 h- kwhich was treated with thyroxine. The father’s6 {. K/ r. v, R. R
height was 6 feet, and he went through a somewhat
S7 G# p* x' |) h9 `4 ~2 qearly puberty and had stopped growing by age 14.
) ?+ h% E2 y6 c- @. }& k: qThe father denied taking any other medication. The
- P6 g! Q# K/ v3 C$ m1 ~! C* `child’s mother was in good health. Her menarche
4 v9 J; q) j4 j5 W8 S7 bwas at 11 years of age, and her height was at 5 feet* Y8 w0 Z/ P% j+ Q
5 inches. There was no other family history of pre-
9 b: N, l/ y. I/ x1 ?; s. Qcocious sexual development in the first-degree rela-
" b5 e7 m! f7 ~/ X/ ]tives. There were no siblings.
; g Z3 D' {4 JPhysical Examination9 G s$ t( U7 A: W: N
The physical examination revealed a very active,
5 G' k1 j9 ]' p2 b/ Eplayful, and healthy boy. The vital signs documented2 }/ J# w& i: @2 z+ }1 M! S% @* V) g5 |
a blood pressure of 85/50 mm Hg, his length was0 h% m9 s/ L2 V' z8 F
90 cm (>97th percentile), and his weight was 14.4 kg: e; p4 K& O' }$ U0 |% W
(also >97th percentile). The observed yearly growth: U2 \ H: G2 h0 }* C
velocity was 30 cm (12 inches). The examination of
! D' d( c" y% f1 T3 @, I; ~the neck revealed no thyroid enlargement.
% \9 j- p- H7 p( Z1 m$ [- K& y4 oThe genitourinary examination was remarkable for* ]: `/ M5 ]4 n: X2 k8 T0 \
enlargement of the penis, with a stretched length of2 x) d$ [1 x# ]7 Z q: ?" ~2 ~, l& k
8 cm and a width of 2 cm. The glans penis was very well
! _( I% L2 m# K) x& bdeveloped. The pubic hair was Tanner II, mostly around
2 D. g Z' z" }& ]7 n8 ]3 L$ y7 r540
1 n- |- R B9 v) y) iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' g" x3 [3 e3 e9 Z) P6 p u/ Athe base of the phallus and was dark and curled. The; s) f* h* g5 `% j& e* |- L
testicular volume was prepubertal at 2 mL each.
b+ |/ k- e7 I2 RThe skin was moist and smooth and somewhat; M7 @' ^5 F q( c
oily. No axillary hair was noted. There were no. p! O0 _+ g. t% i% {
abnormal skin pigmentations or café-au-lait spots.
6 W& V' w3 z1 eNeurologic evaluation showed deep tendon reflex 2+
3 H+ m% C4 s$ A t4 @6 n+ z/ bbilateral and symmetrical. There was no suggestion; u1 ~% r Z% U0 Q' }' [
of papilledema.! }, n$ J/ o+ L5 H
Laboratory Evaluation4 g5 W. V/ q* c7 u7 Z7 w& o
The bone age was consistent with 28 months by& [- L! |# [& X7 j i
using the standard of Greulich and Pyle at a chrono-
$ B& ]$ ~& L+ \6 _, Ulogic age of 16 months (advanced).5 Chromosomal
: J# M' k) S# \, u k0 Akaryotype was 46XY. The thyroid function test
5 J b, i6 |: S( q3 Wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
L* t7 J( @. y P5 ?9 q; i) {! Jlating hormone level was 1.3 µIU/mL (both normal).
2 S2 w6 N1 Q1 h( nThe concentrations of serum electrolytes, blood
2 }8 z) m0 `, s0 B- o. G) v lurea nitrogen, creatinine, and calcium all were2 R* c) \4 A" \& R& m, x4 r
within normal range for his age. The concentration! [1 n: }: Y. x9 g0 l" [# ]; ?
of serum 17-hydroxyprogesterone was 16 ng/dL
" z$ v7 l& I9 A# j(normal, 3 to 90 ng/dL), androstenedione was 20
5 V; W+ u/ S. _" mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 G9 @& |0 @/ D2 J2 x
terone was 38 ng/dL (normal, 50 to 760 ng/dL),. W' V1 u: B% p7 V! T
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 g$ l, ]8 S8 j; L% e49ng/dL), 11-desoxycortisol (specific compound S)
; T3 I, l6 p: y6 G, ]was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" \9 w' H, l4 O( K
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
9 R: i: ?- c* h& ?testosterone was 60 ng/dL (normal <3 to 10 ng/dL),4 W1 ]" @9 {/ d% n8 Y+ d% ~9 _
and β-human chorionic gonadotropin was less than1 s6 q; ]5 g) U+ J( i, N/ ^
5 mIU/mL (normal <5 mIU/mL). Serum follicular
" Q& q) o; A, f9 a* k" a* Istimulating hormone and leuteinizing hormone2 C! O/ v' G! s n
concentrations were less than 0.05 mIU/mL
7 e/ N: x" u+ L4 J2 E/ J! y+ l' e' P(prepubertal).- I6 S/ M) a: W. U
The parents were notified about the laboratory
6 L, ?6 [4 l% n2 m& P, Q( yresults and were informed that all of the tests were/ x9 @" ^+ M" t1 n9 A" b3 g% e: y
normal except the testosterone level was high. The
; z) b) `8 s' }: H' w% lfollow-up visit was arranged within a few weeks to
0 F* m5 H* k% T% f# v& u9 Xobtain testicular and abdominal sonograms; how-
2 s* T( o2 w- J& Y4 V" cever, the family did not return for 4 months.: h; H4 \$ R7 C( w h3 y
Physical examination at this time revealed that the2 L9 M' k# g% T6 A* Q) y) A
child had grown 2.5 cm in 4 months and had gained
( U/ B0 B4 k" G2 kg of weight. Physical examination remained
D% }2 M6 X5 V _5 _unchanged. Surprisingly, the pubic hair almost com-. F* ]. {: ?" E: Z/ @6 ^
pletely disappeared except for a few vellous hairs at
9 B6 a& S! T3 {' u9 Lthe base of the phallus. Testicular volume was still 29 b: g [. T$ x; B
mL, and the size of the penis remained unchanged.' [5 `2 B4 Q. K" B7 G# [
The mother also said that the boy was no longer hav-
+ X& t5 @: a; t3 Xing frequent erections.- R# I. g9 [) r% A
Both parents were again questioned about use of- d0 L7 W9 M, V& L" k2 w2 J
any ointment/creams that they may have applied to _2 {0 U% Y- N: |. N; i6 ~
the child’s skin. This time the father admitted the
0 Q, H7 k+ B' f* f* ^" LTopical Testosterone Exposure / Bhowmick et al 541
# Z6 v9 n. E) B9 Iuse of testosterone gel twice daily that he was apply-2 {7 R" }' I, b, Q$ n- u" G
ing over his own shoulders, chest, and back area for
( ?) L2 U8 T3 k; l# E F8 h3 _/ ya year. The father also revealed he was embarrassed
. u. v+ b( Y3 j2 ^to disclose that he was using a testosterone gel pre-4 [) [* D# J$ d2 B5 A
scribed by his family physician for decreased libido: D8 g! ~) X& s$ h1 @# r5 ?/ C
secondary to depression.
1 K! e/ N" Z$ w( ]: fThe child slept in the same bed with parents.
& k( v$ M. J* ^* g, W* aThe father would hug the baby and hold him on his Q2 [4 e$ i8 t S" x
chest for a considerable period of time, causing sig-
* G' U4 l3 Q* H8 M u! _nificant bare skin contact between baby and father.
, q! z8 j- J$ d, N3 G f6 T0 O/ O) _The father also admitted that after the phone call,% {& m# [2 u2 X- v- L
when he learned the testosterone level in the baby( h6 i# ~$ w- c) \2 C
was high, he then read the product information
3 `6 G3 w* @7 n/ p2 P" o* Wpacket and concluded that it was most likely the rea-: o9 `; y X$ X; L) m$ j% F2 c) h
son for the child’s virilization. At that time, they- ]* y# Q8 D, q& X
decided to put the baby in a separate bed, and the
5 M* |* W. \$ Dfather was not hugging him with bare skin and had. J+ k% k* [$ S
been using protective clothing. A repeat testosterone6 O4 `$ K8 y( Y: G
test was ordered, but the family did not go to the( `5 b. O$ [8 c1 d# I) F
laboratory to obtain the test.
' ~$ B9 H, W, u% wDiscussion" u) v" g1 o [" q, V9 U1 n
Precocious puberty in boys is defined as secondary
( ]3 F6 S, A+ d0 hsexual development before 9 years of age.1,47 V( z5 P/ S$ M- U
Precocious puberty is termed as central (true) when
% N2 F0 r, v1 o1 r0 X* @; pit is caused by the premature activation of hypo-
' ]' @4 H# a* [1 Vthalamic pituitary gonadal axis. CPP is more com-8 _$ m( x: Y9 m; t) G
mon in girls than in boys.1,3 Most boys with CPP. d4 w/ G( W! ~% e- y0 ^" k
may have a central nervous system lesion that is+ F+ I) o7 p0 B. X5 x& g% e
responsible for the early activation of the hypothal-
0 E7 U- D/ D0 }amic pituitary gonadal axis.1-3 Thus, greater empha-
" y% e' e2 M2 ~sis has been given to neuroradiologic imaging in1 D+ ?. Q$ w, `4 G0 F r: O
boys with precocious puberty. In addition to viril-
/ ]) F8 {$ D: _) V0 `ization, the clinical hallmark of CPP is the symmet-# ?9 g' S, ~% n" M2 o; f7 t' ^
rical testicular growth secondary to stimulation by
4 |1 m b: H$ d" }4 k% m/ h7 Kgonadotropins.1,3
6 ?) R' J) Y6 a. y7 H. Y/ jGonadotropin-independent peripheral preco-0 j" W0 K2 B; u0 A
cious puberty in boys also results from inappropriate% P3 }7 @8 _3 T& S1 V
androgenic stimulation from either endogenous or0 o% F* H" a& L7 L: x
exogenous sources, nonpituitary gonadotropin stim-
% P* P3 ]3 U( S h5 X0 U; H, ]ulation, and rare activating mutations.3 Virilizing1 ^; e& q9 `+ a! c8 X8 A. A1 V
congenital adrenal hyperplasia producing excessive
) C6 v$ x, w2 i) _4 k* ~adrenal androgens is a common cause of precocious
4 o P% W1 F" m$ y: N! ?puberty in boys.3,47 O8 _2 [4 P$ Q3 c/ w7 N4 G
The most common form of congenital adrenal, _# l, y; E$ c6 }4 \- r
hyperplasia is the 21-hydroxylase enzyme deficiency.
) o+ [9 I! T) N: f: L8 CThe 11-β hydroxylase deficiency may also result in
S6 Q2 m5 A. Z9 U! jexcessive adrenal androgen production, and rarely,% {0 M6 ^1 w) F) f% f% l6 m5 w* C
an adrenal tumor may also cause adrenal androgen
3 w7 Q" c1 I* N5 t# G" ]) b0 Nexcess.1,3
, \. H* O3 I0 \& lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' q" _2 p4 C5 ]4 S6 {" U542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
y" [* m! K$ I8 E3 rA unique entity of male-limited gonadotropin-
/ V- J+ V5 d& E& H; a7 v+ k3 Tindependent precocious puberty, which is also known
& B# W5 G+ r9 |$ Y b" i: Uas testotoxicosis, may cause precocious puberty at a' _% \5 T$ g4 G7 ~. F; |! u
very young age. The physical findings in these boys8 P+ O! a) Z* O' G1 K* t! B# H
with this disorder are full pubertal development,
2 x2 O U6 w5 x0 D* n2 f* e( [including bilateral testicular growth, similar to boys
0 g3 c: L5 T& e; y$ v1 W7 Hwith CPP. The gonadotropin levels in this disorder
; ~1 J' `3 a6 h8 Jare suppressed to prepubertal levels and do not show
( n. p- a% e: X3 ^* k9 [: t$ A9 F& spubertal response of gonadotropin after gonadotropin-
- P) b' v0 y6 Q, g1 Kreleasing hormone stimulation. This is a sex-linked
& t' \/ N& G7 @; B/ I4 Sautosomal dominant disorder that affects only
4 _; t1 E% f/ W. t# r# Z- I6 G7 |males; therefore, other male members of the family3 H; O3 | |' R' S
may have similar precocious puberty.3
" s& l$ }1 }7 O9 n/ {* n+ YIn our patient, physical examination was incon-( n' j# Q2 G5 k" O+ F1 N% l* G; z
sistent with true precocious puberty since his testi-- M3 w2 ~/ ?1 |3 |8 s8 ~( J
cles were prepubertal in size. However, testotoxicosis) N5 i7 x1 j1 j/ U: R
was in the differential diagnosis because his father
9 F- f. \. q( A+ u" tstarted puberty somewhat early, and occasionally,
6 v; v7 S& }- E% S: z$ ^4 X1 Rtesticular enlargement is not that evident in the4 ]( G* ?9 Z2 k7 P" t# W6 S3 x; j8 w
beginning of this process.1 In the absence of a neg-3 C& K1 [& F% N0 I) {: S! b
ative initial history of androgen exposure, our
& { S7 J) m9 bbiggest concern was virilizing adrenal hyperplasia,! }% }) ^3 U. D$ V# P! |: n$ u$ I+ A6 O
either 21-hydroxylase deficiency or 11-β hydroxylase
! d2 Q% D& s6 y& U ideficiency. Those diagnoses were excluded by find-
9 T# d, d( P+ s8 Ning the normal level of adrenal steroids.0 }( @/ `5 P* T H& Y4 }
The diagnosis of exogenous androgens was strongly3 b2 n/ \( e5 [
suspected in a follow-up visit after 4 months because5 w1 I: W6 S+ E9 ]: _" D* I
the physical examination revealed the complete disap-$ J% E0 `& i# a$ b
pearance of pubic hair, normal growth velocity, and
2 A/ N, D- w. \7 ?( adecreased erections. The father admitted using a testos-9 g1 D1 |8 [) o9 p6 z
terone gel, which he concealed at first visit. He was, O4 H. P5 Q& a) |
using it rather frequently, twice a day. The Physicians’
d+ N$ x+ z! W& X8 ]. ^9 c; BDesk Reference, or package insert of this product, gel or) O: Q$ ^: J/ ?" w$ t/ f O% z8 n
cream, cautions about dermal testosterone transfer to# d: [) L( Y1 T- i) C
unprotected females through direct skin exposure.
4 k* h" _! Q0 d+ W0 b9 F* xSerum testosterone level was found to be 2 times the; L# Z, f: b( t9 k4 L
baseline value in those females who were exposed to5 N) j6 @# J. g$ P
even 15 minutes of direct skin contact with their male
5 K' e" \0 d0 g @partners.6 However, when a shirt covered the applica-/ B: v* Q/ j, N+ G$ c
tion site, this testosterone transfer was prevented.+ x2 A) N: G. d6 H0 g
Our patient’s testosterone level was 60 ng/mL,
% d. h \/ L+ N# A# ewhich was clearly high. Some studies suggest that
& A' B( q& o) z" I! s" t8 a. hdermal conversion of testosterone to dihydrotestos-
& w( k$ n$ C6 m" x2 w2 T# t Gterone, which is a more potent metabolite, is more
) ~7 V( _% z/ _9 ]3 x7 gactive in young children exposed to testosterone
- v0 M) m7 D/ w9 nexogenously7; however, we did not measure a dihy-
( p. _" _; X$ x: W5 X9 ldrotestosterone level in our patient. In addition to0 w1 L4 b' ]/ x+ O0 N+ f
virilization, exposure to exogenous testosterone in% o9 R1 J! ?0 E
children results in an increase in growth velocity and( s& Q" A# T( u/ p1 D$ A
advanced bone age, as seen in our patient.! ~7 C. C5 ]: F0 w F- K r
The long-term effect of androgen exposure during
T0 R$ _4 v3 O2 g2 n1 ?6 y) jearly childhood on pubertal development and final
+ I* z( d4 A/ d, O4 m; k M# Radult height are not fully known and always remain5 r6 @# G$ _5 e7 J: v
a concern. Children treated with short-term testos- x) p' @1 G- _
terone injection or topical androgen may exhibit some
6 g2 V' n+ b& I1 G$ jacceleration of the skeletal maturation; however, after
9 q7 i1 G. N$ m5 M4 W1 hcessation of treatment, the rate of bone maturation- O* k) E* E8 ?
decelerates and gradually returns to normal.8,95 q& g$ B. A" ^" s4 M) J# N& ^$ H/ e
There are conflicting reports and controversy
( H0 c- y5 ]8 b0 ^0 }/ ^over the effect of early androgen exposure on adult
$ w" [- z3 e |- H6 a& o) W& [penile length.10,11 Some reports suggest subnormal! w. w- f3 z- t& U; g7 e5 s
adult penile length, apparently because of downreg-
! y" V. j6 A) M3 M+ b7 mulation of androgen receptor number.10,12 However,
* G( T% n' S" V0 k$ hSutherland et al13 did not find a correlation between2 h. @: t, m, @: g" i
childhood testosterone exposure and reduced adult
4 m' m4 \+ ~( ~5 W3 E& q# t3 Qpenile length in clinical studies.
6 w' j0 S8 p0 r o# z% WNonetheless, we do not believe our patient is( L3 V; M& A7 ]) Z+ I6 y
going to experience any of the untoward effects from2 A: ~7 r! G2 T: L- ?
testosterone exposure as mentioned earlier because3 x: ?3 E. o7 Q* J" A
the exposure was not for a prolonged period of time.) S* J4 F1 u ]# J, I$ O
Although the bone age was advanced at the time of9 @" j2 e' P b% K
diagnosis, the child had a normal growth velocity at
: O1 V! B7 \) `/ {) @1 l) Vthe follow-up visit. It is hoped that his final adult
8 N" }( Z+ A V6 b# ]/ J% r' B5 _height will not be affected.8 b# `. I5 l& j' I
Although rarely reported, the widespread avail-8 D- G9 H3 C$ Q8 w% F! B, ~
ability of androgen products in our society may2 ^3 e! X- d; P% f0 S) O
indeed cause more virilization in male or female: H$ g* }4 L3 B& I( _& `. o: X
children than one would realize. Exposure to andro-
7 f5 x0 x7 M: N0 wgen products must be considered and specific ques-
5 I. P$ O7 z. g2 wtioning about the use of a testosterone product or3 [' h8 D6 z0 n% T: a6 N
gel should be asked of the family members during
5 z6 C) N0 K$ @1 d! Y" C7 _% gthe evaluation of any children who present with vir-! `+ q6 W8 ~1 ]# ^
ilization or peripheral precocious puberty. The diag-% q6 P: ^# q Q3 k7 ~, `5 v
nosis can be established by just a few tests and by C4 Y- {2 r9 `5 p/ u, m8 I# u9 e
appropriate history. The inability to obtain such a
4 @# T- f( b" j; G+ u2 ` `history, or failure to ask the specific questions, may0 h# A. [! L4 j
result in extensive, unnecessary, and expensive% Y. F$ C3 ^/ h1 _' T" H, u3 U9 P
investigation. The primary care physician should be/ Y8 ^7 {' [, t! A- z9 n
aware of this fact, because most of these children8 e7 K+ P; J7 y, k7 t
may initially present in their practice. The Physicians’& P7 w2 g0 N: t" O
Desk Reference and package insert should also put a/ ^- t) H6 }* K+ I4 T
warning about the virilizing effect on a male or& z6 g+ v6 T4 S* u
female child who might come in contact with some-% S+ m9 c3 }: U, R$ Y# ]
one using any of these products.
, h. L+ e; l# CReferences% O% Z5 }1 V5 T7 O; n$ X
1. Styne DM. The testes: disorder of sexual differentiation
9 L* T8 M* L' s3 d0 I+ kand puberty in the male. In: Sperling MA, ed. Pediatric
0 f& {: _2 Y" v3 nEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 q* I. s: q" G8 p7 o+ L$ Y" _
2002: 565-628.
# W% {9 w; O5 Q. D& l) C2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 L T8 u5 X3 r; M& E
puberty in children with tumours of the suprasellar pineal |
|