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Sexual Precocity in a 16-Month-Old
4 X- T" R0 ?, a. JBoy Induced by Indirect Topical
4 j6 P7 _; V, g) R2 U' WExposure to Testosterone1 S: a. M: y9 a. q" i
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( F3 p# C3 @" C$ [" o% ]1 Rand Kenneth R. Rettig, MD1: G% ^9 l$ v. X+ {: r$ w' c& J
Clinical Pediatrics
- ]$ Y) I2 x6 \: RVolume 46 Number 6( w5 k; s/ W9 P# ~2 Y
July 2007 540-5435 ~% d1 F* G$ }- z4 r$ c- g1 S
© 2007 Sage Publications0 |6 x. J/ N/ E8 [# T1 @3 y
10.1177/0009922806296651' |5 j. b1 u! c& w
http://clp.sagepub.com
; O: F6 e8 c5 N" t n$ b) u3 \- Yhosted at; j* K/ \+ x0 l, G: i+ K8 g) d2 Y6 X
http://online.sagepub.com
3 [5 E# m8 t# ^Precocious puberty in boys, central or peripheral,/ z% L5 z4 ~/ E* c% `: P& D# G1 d# ~$ j
is a significant concern for physicians. Central
+ D9 I* @% I$ V3 k; `precocious puberty (CPP), which is mediated
; x) B' K+ ]$ b O* ithrough the hypothalamic pituitary gonadal axis, has$ q- w( M" i* C4 m4 t
a higher incidence of organic central nervous system
g+ A$ l5 M2 R& }lesions in boys.1,2 Virilization in boys, as manifested+ L) T! p9 [ [$ O/ F4 d
by enlargement of the penis, development of pubic
X) Z1 ~* X0 ~' s2 jhair, and facial acne without enlargement of testi-
9 m0 `$ ^5 ^" n; h/ w/ c3 mcles, suggests peripheral or pseudopuberty.1-3 We+ ^" p+ ?+ [( }/ q+ G. l% E: i
report a 16-month-old boy who presented with the
1 e7 F/ g6 J6 R3 B; i$ k, tenlargement of the phallus and pubic hair develop-
" X- w1 `& J3 k3 Y0 v Ument without testicular enlargement, which was due0 W8 p3 a. T8 f' ?; w; |# O3 w! A
to the unintentional exposure to androgen gel used by- e2 A, ?) o. P. q3 w' H/ [
the father. The family initially concealed this infor-
1 r8 q- O D0 K3 d& D% r" ]) dmation, resulting in an extensive work-up for this
! O9 l; H9 L" M/ |child. Given the widespread and easy availability of) D3 Z; ^$ p C& Q# A
testosterone gel and cream, we believe this is proba-3 t Y3 `% t# w8 l
bly more common than the rare case report in the
2 c( J! j, ^( C' f4 ]literature.4
5 n# A8 L3 ?/ h" H. m2 S! DPatient Report6 b' E7 K$ k0 V' Y2 m8 A( D
A 16-month-old white child was referred to the' [ j5 B9 D8 O
endocrine clinic by his pediatrician with the concern% ~: a4 }0 D8 c+ A( f* i3 T6 |
of early sexual development. His mother noticed
) ^" _6 h4 d( x" Ulight colored pubic hair development when he was5 f7 X4 x, F- ]+ ? v1 v/ K
From the 1Division of Pediatric Endocrinology, 2University of
" {7 a0 Z7 r6 Q7 b& O) ^! [South Alabama Medical Center, Mobile, Alabama.2 Q$ f4 d Q. S+ U/ w8 G
Address correspondence to: Samar K. Bhowmick, MD, FACE,
3 | O' a/ y$ \; g' NProfessor of Pediatrics, University of South Alabama, College of
; E3 v8 V1 y; |# H" P6 oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; e- @# X1 V8 p( B s1 H ue-mail: [email protected].4 y+ m1 V5 \7 P8 _0 K5 q* ]% Q
about 6 to 7 months old, which progressively became9 c# g! a' T2 `& k1 O: y# [" g
darker. She was also concerned about the enlarge-
5 `" I" L1 L" \+ Gment of his penis and frequent erections. The child' F( ]/ M. l: q0 C" O7 F8 Z
was the product of a full-term normal delivery, with
5 |7 y0 ]+ y0 Y: q9 B/ B7 Da birth weight of 7 lb 14 oz, and birth length of
: Y* B7 ^2 ~) X4 E, @0 W+ a+ Z. d4 l20 inches. He was breast-fed throughout the first year7 b2 K, Y9 X* z' K2 m; _4 K
of life and was still receiving breast milk along with
* f! |6 f( @/ S- N! ~& B) Xsolid food. He had no hospitalizations or surgery,* Q! `1 h% ?3 g5 B) y N( H/ [
and his psychosocial and psychomotor development
$ L. w3 X: C; c5 owas age appropriate.
! F! Y* V2 I1 b& UThe family history was remarkable for the father,
3 j3 P5 g5 U" O2 x0 @. H/ X( h) ?who was diagnosed with hypothyroidism at age 16,
, C$ D+ e* L4 r P) _' A: _which was treated with thyroxine. The father’s% p" U0 q1 E1 @- j9 u8 R
height was 6 feet, and he went through a somewhat
8 X% a: t" k/ x- ^7 B3 ^" bearly puberty and had stopped growing by age 14.
; O3 M& G) W; y. tThe father denied taking any other medication. The/ y- l+ ^$ J, x9 S" \
child’s mother was in good health. Her menarche4 ]! z( b& f' t0 W* M
was at 11 years of age, and her height was at 5 feet
5 S! Y e B- R, n* G1 a5 inches. There was no other family history of pre-% V* L. F7 K' c/ E/ W
cocious sexual development in the first-degree rela-# o6 v6 K& z3 C) ?2 }1 ^# J
tives. There were no siblings.' H- N# Z9 A9 r5 M S2 T
Physical Examination
" F: M# Y. W' i8 p" O8 Q* sThe physical examination revealed a very active,' x* J H$ D1 n" f1 t- ^" A& s9 \
playful, and healthy boy. The vital signs documented* n* Y7 E$ a2 j1 \9 h. `
a blood pressure of 85/50 mm Hg, his length was
. ~( q: J' C- E& l90 cm (>97th percentile), and his weight was 14.4 kg, C3 [( \( w% c* F
(also >97th percentile). The observed yearly growth
9 ^6 V# J% q/ j7 |/ Z7 {& Pvelocity was 30 cm (12 inches). The examination of
% e7 u1 F2 v5 W% y# {, a% Nthe neck revealed no thyroid enlargement. M$ x3 _; H0 O/ @2 f3 x6 J% ~3 y
The genitourinary examination was remarkable for
- @2 X- E( x* n2 q; fenlargement of the penis, with a stretched length of
% y. w& }! B, Y8 cm and a width of 2 cm. The glans penis was very well
- n, G$ n5 f. z) q& \, Vdeveloped. The pubic hair was Tanner II, mostly around# F3 p R6 A$ T
540
& q t" O( x2 a2 V- ]$ O1 }# cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' K9 C: X, L0 _5 J' ]the base of the phallus and was dark and curled. The
; d) i( S, Q- Q( E Ztesticular volume was prepubertal at 2 mL each.) F# `, `, E" w1 }
The skin was moist and smooth and somewhat0 \% }( I% w5 W- \' d! S" w4 y
oily. No axillary hair was noted. There were no
: P. J. H7 S1 s k; T/ P. w, sabnormal skin pigmentations or café-au-lait spots.
! j' D- @5 r4 Q$ n8 w& S) A+ {Neurologic evaluation showed deep tendon reflex 2+
, y# }2 x- J/ wbilateral and symmetrical. There was no suggestion
7 U+ w, m' X9 C; N* U# v* ?of papilledema.
& d" n; G/ J6 _, K! ZLaboratory Evaluation- y4 f) _- Y5 E3 _
The bone age was consistent with 28 months by
+ g! h4 n c9 X) r% m% jusing the standard of Greulich and Pyle at a chrono-3 ?3 r. U$ @1 h d# o/ L- f8 U4 j
logic age of 16 months (advanced).5 Chromosomal1 M: I r' \4 N, u. {9 w) t
karyotype was 46XY. The thyroid function test
: K- }5 e! ?/ _- H: |1 Ushowed a free T4 of 1.69 ng/dL, and thyroid stimu-
N4 n: C8 d9 C _# b2 X9 Plating hormone level was 1.3 µIU/mL (both normal)., F, V7 W& j/ _4 v8 f2 p5 S
The concentrations of serum electrolytes, blood- @ v$ {+ O. o+ L, }/ i; U
urea nitrogen, creatinine, and calcium all were9 t; a7 ?$ [/ b1 ?! D2 H
within normal range for his age. The concentration
9 Z$ J! x4 s3 B* E' K, Nof serum 17-hydroxyprogesterone was 16 ng/dL& l' D8 {9 O5 r9 F1 U
(normal, 3 to 90 ng/dL), androstenedione was 20$ Q. K) _0 E6 x8 F! A6 ?: B9 q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
# [2 r& C5 G, Hterone was 38 ng/dL (normal, 50 to 760 ng/dL),' [8 c$ M6 B0 V) ~! z+ x$ _9 i1 @" H
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
& [) Q6 J! d: n( i9 F0 B9 G& _49ng/dL), 11-desoxycortisol (specific compound S)
. Q! d" J0 b' b8 ?& \ Mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-& V, M% f" s! \8 j4 C
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 O0 g1 M+ N1 a/ ?# utestosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ D% S1 Q+ P& S
and β-human chorionic gonadotropin was less than
' z4 C- @9 ^" y+ g3 v5 mIU/mL (normal <5 mIU/mL). Serum follicular
1 s$ v4 L+ ~" Y2 j% f! tstimulating hormone and leuteinizing hormone
, w% Y; Z) P& Vconcentrations were less than 0.05 mIU/mL
$ K. j* b) s* _" F: x(prepubertal).
9 E! O& o5 w. Z: p, F) xThe parents were notified about the laboratory2 S" q& e w: {& |+ C
results and were informed that all of the tests were
% x5 A+ n; ^0 z5 pnormal except the testosterone level was high. The) I/ q9 [; ~- I% }4 B, \4 `
follow-up visit was arranged within a few weeks to/ ? o- d. }& @: h/ n) O% E
obtain testicular and abdominal sonograms; how-
) |/ ]& e' w6 }6 U: i" k& wever, the family did not return for 4 months.
6 F3 g, ?. X* S1 h: ^- E; \Physical examination at this time revealed that the, ^. i, ?0 P3 f5 w/ o
child had grown 2.5 cm in 4 months and had gained+ x0 `' h- e. \& Y$ m; r) t. W
2 kg of weight. Physical examination remained8 a( [ [5 _1 q2 |
unchanged. Surprisingly, the pubic hair almost com-
' }0 S' K: T, I, C4 ?9 } B7 spletely disappeared except for a few vellous hairs at& K! c( u: }# ?/ ?, \1 H
the base of the phallus. Testicular volume was still 26 ]# t8 V. i$ Q$ V
mL, and the size of the penis remained unchanged.' }( ^+ ~. R% H$ J( M
The mother also said that the boy was no longer hav-- o/ W* s6 I9 D; h
ing frequent erections.
( |0 b: k$ p& I, O: fBoth parents were again questioned about use of
' G* T( U+ ]3 D" H' Jany ointment/creams that they may have applied to R* A: c6 b4 m
the child’s skin. This time the father admitted the* s3 j! t% ?+ G0 e9 A
Topical Testosterone Exposure / Bhowmick et al 5411 c, `& c3 J2 {- N
use of testosterone gel twice daily that he was apply-- M, y' Z% | c [' `
ing over his own shoulders, chest, and back area for0 r9 ?# o& u" J* m- s8 R
a year. The father also revealed he was embarrassed
( b; I2 C, Z4 x% c* ?) ]$ u0 ito disclose that he was using a testosterone gel pre-
: D$ v) V. d# H; C' |" pscribed by his family physician for decreased libido+ b* B# T! {! ?5 ]2 f
secondary to depression." I3 I- i+ s- u% j
The child slept in the same bed with parents. Y, M( n# S0 q
The father would hug the baby and hold him on his3 [6 i" h4 s/ \. `4 C- C2 v
chest for a considerable period of time, causing sig-. {; ]* A/ W) ^0 V
nificant bare skin contact between baby and father.
0 N6 h3 t4 Q( p) CThe father also admitted that after the phone call,
* |, g& K* |% ]! L& D* owhen he learned the testosterone level in the baby0 O4 i. z4 C. D) k; D
was high, he then read the product information
/ y' a5 g, o& x+ Ipacket and concluded that it was most likely the rea-4 j& G7 r8 L1 B( Q8 T+ t
son for the child’s virilization. At that time, they
7 p/ ~) K- }8 t: ddecided to put the baby in a separate bed, and the
0 \8 M0 I7 L7 l' P% G8 N, S/ b% Mfather was not hugging him with bare skin and had
# k" V, g: `$ l, m, sbeen using protective clothing. A repeat testosterone6 r* w# Z# [+ u9 C% E+ C3 p' O
test was ordered, but the family did not go to the8 L: y; J" c* M
laboratory to obtain the test.0 z( h3 l2 s1 C
Discussion# Y9 w: A3 C4 j( e
Precocious puberty in boys is defined as secondary
: [3 } `( k6 ?7 z" P/ x nsexual development before 9 years of age.1,4' T8 |3 ^2 C. B% r
Precocious puberty is termed as central (true) when8 h- ] {8 z" y. R( g
it is caused by the premature activation of hypo-& E0 Q/ p1 h T$ Z% A3 h1 m( q$ J! {
thalamic pituitary gonadal axis. CPP is more com-
) `2 H* x9 p* r* C4 W7 dmon in girls than in boys.1,3 Most boys with CPP
. r: b4 s, y( j; z- d" `may have a central nervous system lesion that is
* i$ r, B1 w$ lresponsible for the early activation of the hypothal-# Z0 {) N9 ~# S" a/ t+ ?
amic pituitary gonadal axis.1-3 Thus, greater empha-
3 g4 _4 ]# A% b% d8 \sis has been given to neuroradiologic imaging in* A# Y! F3 p; q$ b& [3 l u, }0 f
boys with precocious puberty. In addition to viril-/ F, o+ c& A6 m+ G6 q" B
ization, the clinical hallmark of CPP is the symmet-3 c- `' w' }3 t. H2 ]
rical testicular growth secondary to stimulation by/ H0 U, h" c5 i/ x% l
gonadotropins.1,3
, n( u, D9 l/ u" dGonadotropin-independent peripheral preco- z+ j$ l$ Y' b+ [- U' u
cious puberty in boys also results from inappropriate
n w! O# O/ U# v: `' L5 a" U5 sandrogenic stimulation from either endogenous or
$ @% S& U* x& ~$ d' D! iexogenous sources, nonpituitary gonadotropin stim-9 k+ @$ R/ d6 [3 t
ulation, and rare activating mutations.3 Virilizing
. Y7 _1 w5 T$ a! \8 acongenital adrenal hyperplasia producing excessive
. l, b2 B4 j1 e* Y4 `% uadrenal androgens is a common cause of precocious
) Q3 Z) V, n! d, j$ F& F tpuberty in boys.3,4
7 k9 Y7 e# ^5 @- D) UThe most common form of congenital adrenal
6 ~! Q+ J$ `$ Z+ }6 p p, I5 F% dhyperplasia is the 21-hydroxylase enzyme deficiency.
# a b) L. R) c8 A" [% lThe 11-β hydroxylase deficiency may also result in
/ v6 K) s8 W. yexcessive adrenal androgen production, and rarely,+ T+ O( l& ~9 V* {
an adrenal tumor may also cause adrenal androgen- R, H* l" b/ i- q. c3 p% i, P
excess.1,3" x+ j2 b& G7 f* t. Y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ g4 S: |0 y, O) U+ ~542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ E" \; X7 @- V
A unique entity of male-limited gonadotropin-+ s3 g& k" J# a4 w/ e$ `
independent precocious puberty, which is also known
?, N7 K4 Y, g/ Ras testotoxicosis, may cause precocious puberty at a
$ Z. t1 x* z: d5 I9 Wvery young age. The physical findings in these boys
- q( T" X* A8 kwith this disorder are full pubertal development,, J$ ~! s* t2 {. h2 C$ u/ b
including bilateral testicular growth, similar to boys
6 T6 d. z H1 |with CPP. The gonadotropin levels in this disorder( c7 c3 v* S; \9 @& Z
are suppressed to prepubertal levels and do not show
0 M2 g- r* Z) l! Apubertal response of gonadotropin after gonadotropin-
$ e V% e$ m9 k) `; Sreleasing hormone stimulation. This is a sex-linked$ P6 g; h C' N7 ]9 D
autosomal dominant disorder that affects only
# x- n) A# b7 G6 b/ n6 H3 [1 ~1 _8 k/ vmales; therefore, other male members of the family- R/ C9 _8 h$ V0 J. |
may have similar precocious puberty.3
. K- x) t) a- M+ n$ z$ W+ g4 Y/ MIn our patient, physical examination was incon-
3 X, d" D+ B: t' [2 _* Ksistent with true precocious puberty since his testi-8 K" [; V7 H, e6 ^, ~) T
cles were prepubertal in size. However, testotoxicosis
) T9 A |/ Y7 f3 lwas in the differential diagnosis because his father
- [8 h% T# T6 B; Z' ~" Y4 a4 e) estarted puberty somewhat early, and occasionally,0 W7 l1 f$ Y) W0 R. q, \
testicular enlargement is not that evident in the
/ j' @: C/ M+ X2 tbeginning of this process.1 In the absence of a neg-
8 Q/ E' ]( b v' z, N% Vative initial history of androgen exposure, our
$ p5 A0 Z# Q# @# ?+ [biggest concern was virilizing adrenal hyperplasia,/ z! Z. a6 a' W6 V$ }" r
either 21-hydroxylase deficiency or 11-β hydroxylase# i0 |, w$ V- E1 Q9 h6 X
deficiency. Those diagnoses were excluded by find-7 D* y$ F3 h' k
ing the normal level of adrenal steroids.3 J B3 d" g, f- v, a+ _6 c8 u
The diagnosis of exogenous androgens was strongly
3 u2 o+ q3 l" ~7 W5 w/ [* B" Csuspected in a follow-up visit after 4 months because
' g. ~' X: s5 z+ Vthe physical examination revealed the complete disap-
3 [6 f5 c% p3 N9 fpearance of pubic hair, normal growth velocity, and
- e- U2 P0 t& I$ W5 ]1 Hdecreased erections. The father admitted using a testos-: K- {/ i& }7 w; P& h _7 g
terone gel, which he concealed at first visit. He was9 |( b6 Q& `3 R8 g, l5 ?7 ^
using it rather frequently, twice a day. The Physicians’1 ^! Y9 K9 X/ d. ?; x( `$ _ K
Desk Reference, or package insert of this product, gel or
5 q$ o: `% B( K' f, o5 }" {. H9 K7 xcream, cautions about dermal testosterone transfer to
$ b5 ~2 \1 O& r9 q9 Y, ?0 f3 k) o4 hunprotected females through direct skin exposure.6 Y' n3 ^# n) T, E
Serum testosterone level was found to be 2 times the
% H: |4 x2 x7 ]! B# {" sbaseline value in those females who were exposed to" b$ m% k8 A/ u, ]/ Y0 m
even 15 minutes of direct skin contact with their male
- R9 t% _) m: e. R7 G+ ~# _partners.6 However, when a shirt covered the applica-
; ?: g0 b4 n1 D: e3 [$ f+ B% rtion site, this testosterone transfer was prevented.
5 T1 w* r) N5 aOur patient’s testosterone level was 60 ng/mL,- x9 ^3 ~; I, h, e
which was clearly high. Some studies suggest that
2 F+ e7 g8 T- D( S) x$ x2 b0 }& \dermal conversion of testosterone to dihydrotestos-# O( l k# `: i0 M5 f: C0 g& [
terone, which is a more potent metabolite, is more
7 |- p( F, \' H2 P, pactive in young children exposed to testosterone
+ I8 D" U# a: G2 [8 ^$ sexogenously7; however, we did not measure a dihy-. P% R# s0 e+ S! [# A1 P! r) J
drotestosterone level in our patient. In addition to
7 I9 y% ]$ {- {; D" dvirilization, exposure to exogenous testosterone in
3 ^( Z! l6 a$ e H5 o8 r0 Ichildren results in an increase in growth velocity and
( A$ w: |% P7 F. |* Z* z1 i# sadvanced bone age, as seen in our patient.
) z, k3 a( u, Q9 C3 e0 x/ JThe long-term effect of androgen exposure during, w3 O& ], n' I& |, e' ]
early childhood on pubertal development and final
b. o. P/ N- I: z+ X& Z$ fadult height are not fully known and always remain
8 C$ V+ N6 Q3 S2 a) Pa concern. Children treated with short-term testos-
+ ?% g) f0 _+ N: b% _& J0 Eterone injection or topical androgen may exhibit some" B! p6 `! d5 w+ }) d7 u
acceleration of the skeletal maturation; however, after
; h- s2 ]3 B/ k' n' O$ b! j! Ncessation of treatment, the rate of bone maturation
# n0 L7 l8 n ?decelerates and gradually returns to normal.8,9( X- V) V5 V' X! `. `- X
There are conflicting reports and controversy
' J8 p* Q7 _ w4 m5 N+ ~over the effect of early androgen exposure on adult
3 G# B5 Y# P- I) ]* T6 G0 bpenile length.10,11 Some reports suggest subnormal
; a3 N- |0 E% x0 F" I8 {7 \2 Hadult penile length, apparently because of downreg-
$ s) U1 @$ U6 b2 T6 t9 U! Q8 q6 v& Fulation of androgen receptor number.10,12 However,
& }' ~7 e: p" GSutherland et al13 did not find a correlation between5 H4 U- v# b! a
childhood testosterone exposure and reduced adult/ }. [. L9 e i& k+ h4 r
penile length in clinical studies.
+ s' x8 B7 Y3 l3 U1 YNonetheless, we do not believe our patient is# c+ L8 v7 d7 }* Z2 T" Y/ {' ^- T6 q
going to experience any of the untoward effects from! d5 x8 c$ k- x3 Z% B2 F3 S5 Q
testosterone exposure as mentioned earlier because1 ~$ U" A& K& w3 R0 Z6 L
the exposure was not for a prolonged period of time.
/ W! @# H! p2 ^* rAlthough the bone age was advanced at the time of7 J! Y# d' J+ }( j! ^0 u
diagnosis, the child had a normal growth velocity at
) }" e4 Y) {( m" @( j9 kthe follow-up visit. It is hoped that his final adult
z% J3 ^& w" qheight will not be affected.3 e0 i) e% k3 b/ k
Although rarely reported, the widespread avail-2 p$ V! G+ Q; t2 j+ |: p' C
ability of androgen products in our society may
4 \+ V6 S1 P y+ p" e1 Lindeed cause more virilization in male or female3 u9 Q1 x7 T7 y9 [& H; H. G
children than one would realize. Exposure to andro-. V& {! {6 g, m( |. a. a
gen products must be considered and specific ques-
# T% n9 y3 _+ S* w0 a. Vtioning about the use of a testosterone product or1 F1 `2 i, @3 H0 \- V
gel should be asked of the family members during
% I4 a2 c$ R7 S( mthe evaluation of any children who present with vir-
d3 W. p" s" Z* x# O% M% m: v& H$ Rilization or peripheral precocious puberty. The diag-
3 s" N$ q. A. Z& d& |( unosis can be established by just a few tests and by$ T2 e- @4 n* d- `7 B1 L% o
appropriate history. The inability to obtain such a
7 D p8 \5 s! F- e6 y3 n. zhistory, or failure to ask the specific questions, may' L; l/ A9 G/ `: i; O }) A
result in extensive, unnecessary, and expensive
! M: ^. X% h+ D* ^ D8 Z8 ninvestigation. The primary care physician should be; d4 K" d/ x) }4 ?
aware of this fact, because most of these children( ~" L. M$ t; U# j( f2 C W- @" G
may initially present in their practice. The Physicians’ s/ Y5 x( h# C( x' p7 M y/ {2 \2 F
Desk Reference and package insert should also put a( ^3 L: d1 _( }3 s& E" A
warning about the virilizing effect on a male or* E! J" B/ b# l7 y, p
female child who might come in contact with some-
: J; o; ?/ d% n ~: b8 M7 }4 z3 J' cone using any of these products.) Q8 O" X# B) Z( @) P6 {) l
References
; m) |' f5 V' x P. h5 h2 M1. Styne DM. The testes: disorder of sexual differentiation
+ R4 g, j+ }, e+ W; E3 R1 o9 \and puberty in the male. In: Sperling MA, ed. Pediatric
- u. e5 Y. ^ H f3 YEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( p& b) [2 n* ^! t
2002: 565-628./ [8 A& r) T9 v$ ~/ a4 M
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ r8 O2 o% V' w8 C5 g7 Kpuberty in children with tumours of the suprasellar pineal |
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