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Sexual Precocity in a 16-Month-Old& V$ K" K1 K' `9 M9 q- P9 d7 O$ I
Boy Induced by Indirect Topical
# o8 c/ a4 E, lExposure to Testosterone; o) p" h/ y! J# H" ^
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) W' W3 e# W2 p6 r5 Y. C
and Kenneth R. Rettig, MD18 v5 I6 o& e) B7 H8 }4 G
Clinical Pediatrics
( V! q& i$ g2 W& {5 ?! _Volume 46 Number 6
$ |( k$ x9 I/ m/ z: \+ l' jJuly 2007 540-543; g+ c4 X: M u! e( y
© 2007 Sage Publications7 X$ f' g9 N* F( `4 E" d
10.1177/00099228062966510 E& v* S( P* h0 ^ q
http://clp.sagepub.com/ [7 t/ a( ?) I3 [6 s3 f- ~
hosted at
% J& u1 M3 a6 T' I8 P/ g6 bhttp://online.sagepub.com
8 J+ ?; a: ] j8 ^3 mPrecocious puberty in boys, central or peripheral,
* \& p; T% P# \6 ]( {6 I: {is a significant concern for physicians. Central
]2 K2 u- u0 H: t& { N% V, Sprecocious puberty (CPP), which is mediated3 G5 u+ E |3 ?/ R6 O9 i2 F
through the hypothalamic pituitary gonadal axis, has
% @$ O: W# S/ Q& ea higher incidence of organic central nervous system
, \" @! o4 E: M, w+ zlesions in boys.1,2 Virilization in boys, as manifested
% v+ Q; ]3 M i0 A1 M1 T3 u, w( wby enlargement of the penis, development of pubic: j1 i& O, C' `
hair, and facial acne without enlargement of testi-' h" C8 K- `, @4 u5 c
cles, suggests peripheral or pseudopuberty.1-3 We
+ S$ |$ |' n. f: \$ M& n8 X7 d8 treport a 16-month-old boy who presented with the( ~( `- V$ h7 a3 l1 }. v& Y
enlargement of the phallus and pubic hair develop-6 k" B7 ~$ N2 |' S, n
ment without testicular enlargement, which was due* n, u2 W0 C5 Q
to the unintentional exposure to androgen gel used by
1 O- |! X6 N7 Z% ]% b$ Ithe father. The family initially concealed this infor-
0 }+ ] @. i4 o+ @' @# v' d! Emation, resulting in an extensive work-up for this i& B! g# n! r- C
child. Given the widespread and easy availability of {) i. [* ?5 a
testosterone gel and cream, we believe this is proba-
9 e/ H$ J; K4 n4 m' o( h6 S! Ubly more common than the rare case report in the ]' Y, ]2 Q4 h1 G5 s. b! p
literature.4" j1 k: f y) y, s& }" w
Patient Report% Z+ s8 x F2 f+ q% p" g9 k
A 16-month-old white child was referred to the4 F- O& T4 t. `1 I
endocrine clinic by his pediatrician with the concern
, ?0 F- v/ G7 m" H, {2 L; D+ Dof early sexual development. His mother noticed" h; K+ {( W* d' k6 f* D
light colored pubic hair development when he was
! o# m; ?9 o1 }- M0 lFrom the 1Division of Pediatric Endocrinology, 2University of3 P0 ?# I2 Z+ P/ Y! u
South Alabama Medical Center, Mobile, Alabama.
- l/ O+ a. L. f' L; |Address correspondence to: Samar K. Bhowmick, MD, FACE,% \6 I1 @. D: U) |
Professor of Pediatrics, University of South Alabama, College of7 f- @ k, ], s( i4 j) \2 b
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" L9 C5 g* t$ Y5 F
e-mail: [email protected].5 b" j* \" U- }* P. }
about 6 to 7 months old, which progressively became7 r B7 D/ [" {2 v/ e$ _
darker. She was also concerned about the enlarge-
4 o( R! S; c' P y6 G, O5 w* c+ ^ment of his penis and frequent erections. The child
! `' H1 O' Z( e0 {0 r7 pwas the product of a full-term normal delivery, with
y6 l# G9 B# V: C! j( Xa birth weight of 7 lb 14 oz, and birth length of
5 f" o8 b" b- |( c# v; J20 inches. He was breast-fed throughout the first year
( K6 w; o/ q ]7 K, {8 l/ _! Kof life and was still receiving breast milk along with6 x& k" i. h2 }# s7 J
solid food. He had no hospitalizations or surgery,* N7 ^! D6 Y) q+ x2 A' g9 s
and his psychosocial and psychomotor development
! [$ m8 J) s" d5 q$ dwas age appropriate., ]) l$ R. E7 x1 U+ G
The family history was remarkable for the father,
$ ^$ p/ x4 ]8 N6 m! C9 gwho was diagnosed with hypothyroidism at age 16,4 v7 w' U- [5 N' X
which was treated with thyroxine. The father’s
1 w3 n: h/ E2 s' [2 zheight was 6 feet, and he went through a somewhat! T$ Y2 n5 E0 h( M5 c& P6 U
early puberty and had stopped growing by age 14.3 N8 l" o6 T2 e7 x/ j% w
The father denied taking any other medication. The. z" S: y3 ^; g f
child’s mother was in good health. Her menarche f/ o- s) U, z) a7 @
was at 11 years of age, and her height was at 5 feet& I( B# t1 S. E+ ] |2 _9 j
5 inches. There was no other family history of pre-& V* x0 p7 z9 h$ Z' N' [- ~) K
cocious sexual development in the first-degree rela-
, o, A0 W3 j. d r8 }5 a+ r% G# @2 ~tives. There were no siblings.. X- ]; H. q6 m) A' ~
Physical Examination8 [" K3 h* Q- R
The physical examination revealed a very active,7 g0 Z- e6 ~' V; ?; x6 `( k
playful, and healthy boy. The vital signs documented
; G9 n& d0 W$ u; za blood pressure of 85/50 mm Hg, his length was
8 r& E: b) {: } y* U# ^% T8 m2 d90 cm (>97th percentile), and his weight was 14.4 kg
$ Z" n, p: m& ^1 H(also >97th percentile). The observed yearly growth E) Y) G0 k' D( R V$ [! k( i+ \
velocity was 30 cm (12 inches). The examination of" S: N0 I: s; s* r, g" S
the neck revealed no thyroid enlargement.
/ _6 I# q4 l, A9 p$ l3 [The genitourinary examination was remarkable for1 [: L& }7 R8 A$ J6 {6 Z( y) V3 `1 X
enlargement of the penis, with a stretched length of4 _0 t8 s2 ^8 X+ X; t1 A( v
8 cm and a width of 2 cm. The glans penis was very well! j$ k2 `5 L, r) M0 x
developed. The pubic hair was Tanner II, mostly around
' `. V A$ H" Z! [; g7 p540
7 T0 [% M7 A0 _# N4 Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 I, P& q" }) m1 T6 k; x u5 ?
the base of the phallus and was dark and curled. The; o4 t {1 u9 K7 J1 ~
testicular volume was prepubertal at 2 mL each.. m$ z' {/ M3 \2 S; N
The skin was moist and smooth and somewhat
' x/ q& T4 v% U; u3 T0 H% A2 _9 noily. No axillary hair was noted. There were no# b$ m( k7 p1 ]: j% P: P3 l
abnormal skin pigmentations or café-au-lait spots.
% \- m. O, p a8 xNeurologic evaluation showed deep tendon reflex 2++ ?4 ?. N8 P& u7 M
bilateral and symmetrical. There was no suggestion
% {; \8 Z/ R( D, s2 c: \of papilledema.7 }, S1 `8 H9 \6 R X1 g& i. L7 W3 [
Laboratory Evaluation
3 Z& M% l; x6 A% A+ T2 NThe bone age was consistent with 28 months by
2 H' ^# z9 P2 B ?( n4 L( ~using the standard of Greulich and Pyle at a chrono-
, f T% M) G( a; s- mlogic age of 16 months (advanced).5 Chromosomal
/ M) W) f' x3 zkaryotype was 46XY. The thyroid function test
7 O# p3 R3 c) {showed a free T4 of 1.69 ng/dL, and thyroid stimu- B; c8 W. g* ^' s
lating hormone level was 1.3 µIU/mL (both normal).
$ c4 {* N' `' JThe concentrations of serum electrolytes, blood/ U6 n9 Z/ V) w- j
urea nitrogen, creatinine, and calcium all were
; d" E2 p3 o' Pwithin normal range for his age. The concentration/ P# y" i0 X( N7 H5 @
of serum 17-hydroxyprogesterone was 16 ng/dL( Y2 [+ ~: I2 J
(normal, 3 to 90 ng/dL), androstenedione was 20# K, A3 q- T1 g' e* b# |' ]
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# L- E, E- Z1 p8 B% C# t3 e
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 i6 E6 [ S& ?$ u# e3 ?desoxycorticosterone was 4.3 ng/dL (normal, 7 to6 H7 [* K& e- Q5 U5 E
49ng/dL), 11-desoxycortisol (specific compound S)+ w. R4 [ C# _) p" ]
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* z+ y6 ]1 i9 w5 L3 C/ r, p" Y
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
6 v5 v: o; ]6 `. Z9 R8 ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" [/ K! h8 O: I. E: h& A9 q5 Oand β-human chorionic gonadotropin was less than
Y+ W* f9 q/ o) P' Y& E% X5 mIU/mL (normal <5 mIU/mL). Serum follicular8 F, G/ Q* J$ z, z
stimulating hormone and leuteinizing hormone
8 o2 c+ |0 D& p9 M/ u/ `% cconcentrations were less than 0.05 mIU/mL
, T# t2 N# d. j- c3 M9 f(prepubertal).+ U. o" d( @3 E! |
The parents were notified about the laboratory
$ G3 L* i. p0 l8 t- p+ Eresults and were informed that all of the tests were: Q, |4 s" _0 @5 Z
normal except the testosterone level was high. The
) v( f% P/ ?1 z6 Dfollow-up visit was arranged within a few weeks to
- V! Y; `7 @* Nobtain testicular and abdominal sonograms; how-6 y, `5 b; z4 A U) W' R% O4 L2 ~
ever, the family did not return for 4 months.
5 I o. K) Q5 o" @7 LPhysical examination at this time revealed that the L# f3 A& `, D. |( o9 T) t! f
child had grown 2.5 cm in 4 months and had gained
% m3 z) H! D6 u! d+ L: b5 b& h5 }2 kg of weight. Physical examination remained% L6 t) k8 \2 t# S/ k& L8 z
unchanged. Surprisingly, the pubic hair almost com-& \: E8 k( ?7 y/ S% N2 ^8 ^
pletely disappeared except for a few vellous hairs at
; r$ Z6 q+ p. L5 l1 ^; Pthe base of the phallus. Testicular volume was still 2' o. @) ~. C8 Q3 l
mL, and the size of the penis remained unchanged.; U( ^" ^# U; ^& v
The mother also said that the boy was no longer hav-) m! S3 Z \" c8 q3 i
ing frequent erections.( y w( W1 Z9 K6 ?4 q3 _- a. R* L
Both parents were again questioned about use of) S3 u( @. K" I! |* q4 g# O4 e
any ointment/creams that they may have applied to0 _/ S; b# {: R
the child’s skin. This time the father admitted the- O7 Y3 K7 {) e4 n" g6 L
Topical Testosterone Exposure / Bhowmick et al 541
* {$ r8 [ {5 f2 s! j" Nuse of testosterone gel twice daily that he was apply-
7 W0 p, u( i0 p2 Ting over his own shoulders, chest, and back area for8 @7 T6 u$ n q) }" T- ]5 r, Q i
a year. The father also revealed he was embarrassed+ F+ `; |3 H. W( D, M; q
to disclose that he was using a testosterone gel pre-
+ j) @/ b! y. i+ {scribed by his family physician for decreased libido
+ s' V- t0 l7 B% ^( ksecondary to depression.
2 _( o5 L7 ^ q; ?3 F& vThe child slept in the same bed with parents.
) X: c# F+ Y0 ~# `2 KThe father would hug the baby and hold him on his
' V6 l6 i% a' Pchest for a considerable period of time, causing sig-0 v& E4 F% `4 E
nificant bare skin contact between baby and father.* \# l$ {& [0 p) X
The father also admitted that after the phone call,
+ z8 B! ^2 r3 Cwhen he learned the testosterone level in the baby
( X+ {' a' ^- I; v" uwas high, he then read the product information
4 M9 P# B; s" w+ T$ Wpacket and concluded that it was most likely the rea-
8 b+ X) x, D- k- X, F& uson for the child’s virilization. At that time, they6 d6 x9 i9 ~/ ]( V ]
decided to put the baby in a separate bed, and the: l- j& i' ?) b. K, p5 t
father was not hugging him with bare skin and had: B5 V6 w2 W6 `& ?2 U: w$ d
been using protective clothing. A repeat testosterone4 y3 H( G" O; k0 q% v" W
test was ordered, but the family did not go to the& C+ [" c# @8 |" e. d9 _
laboratory to obtain the test.
0 R4 h- L3 t! |Discussion9 i- @6 o7 ~2 g" R9 Q
Precocious puberty in boys is defined as secondary
) I' a6 ?5 P& ]; G" ~( osexual development before 9 years of age.1,4
5 M/ p% j+ p: D! \8 {' x. IPrecocious puberty is termed as central (true) when
5 A0 W3 m8 Y% m; t% N( _' J$ W4 Vit is caused by the premature activation of hypo-, w: O$ ^* F: @$ C( J+ a
thalamic pituitary gonadal axis. CPP is more com-9 F, [# j. y! T; h5 c4 m/ [& e
mon in girls than in boys.1,3 Most boys with CPP
3 v4 m0 l# l; `" P" pmay have a central nervous system lesion that is$ W* i0 o y+ z2 X6 M2 e
responsible for the early activation of the hypothal-
6 n, m3 z) ~& t+ N2 Z( B' [: Q; [" D' Tamic pituitary gonadal axis.1-3 Thus, greater empha-( B" d9 `9 @5 j
sis has been given to neuroradiologic imaging in9 I" q1 V. I7 g
boys with precocious puberty. In addition to viril-- F( H2 {0 [" y* M8 H; s
ization, the clinical hallmark of CPP is the symmet-
* R& E' O; K* _/ a( ~6 ]5 q6 d$ Frical testicular growth secondary to stimulation by
( R9 _4 S8 Y4 X) ?gonadotropins.1,30 N& r* r! B- o. T$ m) e+ |
Gonadotropin-independent peripheral preco-
9 X- U6 {+ g! p7 M. O- ~8 E Bcious puberty in boys also results from inappropriate! Z* K8 ?. E$ b! b) \4 G
androgenic stimulation from either endogenous or
& d& Y" q6 }/ U0 j( }9 B4 V* Qexogenous sources, nonpituitary gonadotropin stim-! o- `" N5 s$ O3 q: c
ulation, and rare activating mutations.3 Virilizing
! ?, c. i6 G6 Lcongenital adrenal hyperplasia producing excessive) H O" F& C# L& H% a! x6 [
adrenal androgens is a common cause of precocious/ P5 t# _- i% s6 O% N% E
puberty in boys.3,4+ w1 G( ^9 L# E! n4 n8 ~: M
The most common form of congenital adrenal
: ` n. q! ]/ B0 s" S: |! Uhyperplasia is the 21-hydroxylase enzyme deficiency./ z$ y& w1 A! p9 J- a, R( b
The 11-β hydroxylase deficiency may also result in" b: `! u' o' _. e" q0 u
excessive adrenal androgen production, and rarely,9 ^9 \& m/ T+ m8 P8 x h
an adrenal tumor may also cause adrenal androgen @2 F$ @$ C' Y) _& ~3 D( L9 O
excess.1,3
/ {/ t; }; M% H* mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) c8 x) Q9 |+ [& u+ L& E542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! O$ K6 M& V% I" h
A unique entity of male-limited gonadotropin-
! {* z1 W$ J2 c" z& xindependent precocious puberty, which is also known, N% y! R# ^9 R2 Y. g
as testotoxicosis, may cause precocious puberty at a
6 {; a! \2 M' [+ m% }! H0 Qvery young age. The physical findings in these boys& ?" ]' S; p# \, X1 J) i
with this disorder are full pubertal development,' K3 O; L* s, I4 O" G' H/ D+ d
including bilateral testicular growth, similar to boys
: Z2 U- b" p' _with CPP. The gonadotropin levels in this disorder5 Y6 o0 Z2 J7 U# P# A4 b
are suppressed to prepubertal levels and do not show
5 Z- |8 A7 }8 p& s9 |. Hpubertal response of gonadotropin after gonadotropin-1 o: ]/ e4 Y ]& s( {, A9 G
releasing hormone stimulation. This is a sex-linked" N% N- T! E+ V0 G5 V6 e9 r7 S) H
autosomal dominant disorder that affects only$ I9 }8 Z$ t1 O" O$ R) h$ [
males; therefore, other male members of the family
, V6 a: @) L+ j e3 a1 v5 R+ tmay have similar precocious puberty.3
( l& p( ^* U1 N! j* S! IIn our patient, physical examination was incon-
0 k# z9 T9 ]( T3 `' Q4 osistent with true precocious puberty since his testi-
) x: c1 F' F; m8 T C3 hcles were prepubertal in size. However, testotoxicosis6 l9 F! h7 l" `* j0 C2 S( z0 X
was in the differential diagnosis because his father. d+ K7 V2 K# E- O% I
started puberty somewhat early, and occasionally,
) m) ~& Z( Y F. J" P4 ?8 Ktesticular enlargement is not that evident in the
7 Z) E: J! d7 P+ z% H# Ybeginning of this process.1 In the absence of a neg-
+ Q, P' l$ u( o# ]/ ^7 p6 q0 iative initial history of androgen exposure, our
- Q1 M3 O1 B6 M) Fbiggest concern was virilizing adrenal hyperplasia,/ W9 @. @. d: _5 r7 C( P$ V
either 21-hydroxylase deficiency or 11-β hydroxylase4 t- {+ \' H8 |& D8 F# ]
deficiency. Those diagnoses were excluded by find-
4 h# s- H8 l% s/ j+ y) M, d, ^0 h- hing the normal level of adrenal steroids.9 y; S9 {5 i- l; n$ {
The diagnosis of exogenous androgens was strongly/ e6 A6 y5 j! p* o$ p7 A
suspected in a follow-up visit after 4 months because- v# \$ J2 i: ~& G! A& a* x
the physical examination revealed the complete disap-) v- Z$ C2 i$ @* h6 w! a
pearance of pubic hair, normal growth velocity, and
5 F( U4 w* y2 |( tdecreased erections. The father admitted using a testos-5 ^, z2 f: h2 M6 c. }
terone gel, which he concealed at first visit. He was Z" i/ }3 j0 D4 w9 N
using it rather frequently, twice a day. The Physicians’
( `+ ~$ }0 d9 W2 d9 oDesk Reference, or package insert of this product, gel or) ~& b' E+ _) o$ R+ _% q
cream, cautions about dermal testosterone transfer to
: z" j% z" H# |9 \unprotected females through direct skin exposure.
9 b6 ^/ x0 {% ZSerum testosterone level was found to be 2 times the
; i0 E- Z+ C$ i' ~/ mbaseline value in those females who were exposed to
+ m$ y2 E1 r0 N' Ueven 15 minutes of direct skin contact with their male4 g! B! k$ t/ o7 F( ]/ d
partners.6 However, when a shirt covered the applica-
2 N# U- q' u: R9 V) a) J/ dtion site, this testosterone transfer was prevented.' L$ i, M' a7 @% ~" O [2 o. H8 T+ }
Our patient’s testosterone level was 60 ng/mL,
( s2 e% D! }0 G% }which was clearly high. Some studies suggest that9 z K! ?: s& E! i4 a" W( Q
dermal conversion of testosterone to dihydrotestos-
7 c& v. x: {/ u( c/ Fterone, which is a more potent metabolite, is more
' e$ M! o$ C: M5 Cactive in young children exposed to testosterone* M0 Q. H" X$ s1 P
exogenously7; however, we did not measure a dihy-
! l; o8 D. }) M8 E$ N4 Ydrotestosterone level in our patient. In addition to* w6 [# ]$ ~& e$ V& z" U
virilization, exposure to exogenous testosterone in
$ M3 M/ z$ C% e, L. N3 d9 s: `children results in an increase in growth velocity and
- ]) y6 k: s- J. G8 R+ qadvanced bone age, as seen in our patient.
0 a4 L; k2 k6 W- d5 h& sThe long-term effect of androgen exposure during3 Z) t2 O+ P$ }" G% V
early childhood on pubertal development and final
! T) I: t5 l m$ Y- d( K( \adult height are not fully known and always remain: B: j) o4 q0 @$ A( e5 u: S0 D# i
a concern. Children treated with short-term testos-
0 s! _4 d8 {, I: \1 l1 U+ Jterone injection or topical androgen may exhibit some
4 ^& O: z s" Y7 C4 q! Tacceleration of the skeletal maturation; however, after( k6 |1 d* f0 r1 Z5 b8 k
cessation of treatment, the rate of bone maturation
9 A% i6 u7 Q3 e, a1 k+ mdecelerates and gradually returns to normal.8,9
. `% [3 Q% r( N4 _There are conflicting reports and controversy0 o! X$ ~# F' Y8 H& w! `2 Q
over the effect of early androgen exposure on adult
( c! j- o( p' \- W' Fpenile length.10,11 Some reports suggest subnormal& C- m, B u! t8 M* v" O3 c8 R
adult penile length, apparently because of downreg-% r, z, m G" b/ @/ V, o/ s
ulation of androgen receptor number.10,12 However,& |. c9 I0 m H& p. A3 U
Sutherland et al13 did not find a correlation between7 C: X) q- u5 i9 @5 ?3 ~9 R
childhood testosterone exposure and reduced adult* p, r7 s( S$ d2 e( s" Z
penile length in clinical studies., U' |& c& {9 F! {2 C
Nonetheless, we do not believe our patient is
2 g# v1 w1 V: Fgoing to experience any of the untoward effects from
& J, h" u2 A; b0 V* S6 m! y4 R# Btestosterone exposure as mentioned earlier because x x; H9 a% d! L) j2 H3 v
the exposure was not for a prolonged period of time.& J8 g5 ~3 C7 m( X* N3 _
Although the bone age was advanced at the time of. b: N ]" X' C; N9 U0 U* Y! p
diagnosis, the child had a normal growth velocity at+ U& o X& y! x7 U! d- Q* U) ^" |0 T
the follow-up visit. It is hoped that his final adult
- N4 f5 o" B5 ]1 bheight will not be affected.
' i5 z8 s; `& ?) l7 u. xAlthough rarely reported, the widespread avail-* o+ p8 J# e3 L
ability of androgen products in our society may
# b, }. \; p bindeed cause more virilization in male or female
1 }0 ~' P0 ]. t! J2 }8 Ychildren than one would realize. Exposure to andro-
7 ~0 \! P2 z/ f) a$ O* r& @) E7 ?gen products must be considered and specific ques-, w+ R" N1 E; G# P! c: d5 k
tioning about the use of a testosterone product or F! K# @; y6 Q T! I
gel should be asked of the family members during' Z+ {+ s- L0 G- w4 x8 ?
the evaluation of any children who present with vir-4 }! B* G/ M4 i2 t2 O
ilization or peripheral precocious puberty. The diag-3 D' M5 L4 j9 l) D/ N; t" i
nosis can be established by just a few tests and by0 j- u8 e9 W$ i" v# r! z1 U
appropriate history. The inability to obtain such a. p+ c" Y" u0 o- a! h2 u0 D
history, or failure to ask the specific questions, may% Z1 ^. D. i2 r/ @
result in extensive, unnecessary, and expensive
: p w4 J$ {- J' Yinvestigation. The primary care physician should be
9 Z0 ?2 K- a: x/ M+ oaware of this fact, because most of these children
0 x6 X: D9 m5 U* P* i8 |) W$ v+ `may initially present in their practice. The Physicians’2 b$ T2 e6 d" u: O, \# ^: Q c* n
Desk Reference and package insert should also put a: u* N2 f4 ] A( A1 j( c: S
warning about the virilizing effect on a male or
9 O( l7 Z' t- p* g* w( Yfemale child who might come in contact with some-, R3 N& q; ^2 {8 F1 K& p, }
one using any of these products." `% T7 r( Z' l) x
References J$ z5 x0 g) n9 Q, m9 z7 v! O
1. Styne DM. The testes: disorder of sexual differentiation; C% v6 U2 j: q7 j
and puberty in the male. In: Sperling MA, ed. Pediatric f6 j0 b' L2 T R- g
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& C/ R5 h5 P9 q# `6 b$ }5 u2002: 565-628.
; Q. F+ E) A* }7 D2 b2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 \8 e$ @6 j# j% T6 I, f
puberty in children with tumours of the suprasellar pineal |
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