- 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
1 D$ ^) e8 u. |5 |. w3 `Boy Induced by Indirect Topical2 Z$ p8 r. [# Y% _; E# I
Exposure to Testosterone% g0 K! M. U1 p7 e4 i9 y% E1 Q7 b
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# S0 P& k: O7 q8 Nand Kenneth R. Rettig, MD1% }3 F- \3 E0 C- x
Clinical Pediatrics" j/ `4 G2 c' D4 X
Volume 46 Number 6' z2 p$ I2 B1 f! S' M: S) |' W
July 2007 540-543
& O& s' l# s4 v T; j© 2007 Sage Publications
6 H+ h8 T, y( ]* t10.1177/0009922806296651
3 f4 b0 i) e' F/ ohttp://clp.sagepub.com6 N& z+ M5 M- [5 n8 o) l
hosted at' E9 {( u: ]& X1 G: z$ y) t
http://online.sagepub.com
6 R1 z# j1 j( |4 h- EPrecocious puberty in boys, central or peripheral,1 L4 c3 ]; X8 x& F1 A4 m% G
is a significant concern for physicians. Central
/ X) g; x6 j/ X z! Q% @8 xprecocious puberty (CPP), which is mediated5 d e! P, \- n' ~
through the hypothalamic pituitary gonadal axis, has3 c, J8 E) O3 @- ^* ]$ j
a higher incidence of organic central nervous system
7 F- I5 a+ N# U5 ^7 y' P8 }lesions in boys.1,2 Virilization in boys, as manifested
+ ?( [5 F5 e' i6 A# _: bby enlargement of the penis, development of pubic
0 C- d3 h& p; x2 ?hair, and facial acne without enlargement of testi-
n; g5 ^1 b6 o! acles, suggests peripheral or pseudopuberty.1-3 We
* [9 p( m8 Y( }2 ^- l* freport a 16-month-old boy who presented with the
7 L; K3 ?; W" r+ G' |7 `enlargement of the phallus and pubic hair develop-7 o8 N+ o: c$ l9 v: x" ?
ment without testicular enlargement, which was due
# `4 ^' v9 l. y* w- Kto the unintentional exposure to androgen gel used by
- X5 {3 E& g( A- C0 v: I5 h% _0 Vthe father. The family initially concealed this infor-* Z" M; J2 u+ V+ d
mation, resulting in an extensive work-up for this: k3 V+ `! c+ {7 q- a# c) l# ~9 B- u
child. Given the widespread and easy availability of/ ?: \+ ^6 s- F v
testosterone gel and cream, we believe this is proba-
" Z6 ?2 y+ s% R5 b+ o+ @bly more common than the rare case report in the
) B# C$ ~0 _! y- Wliterature.4
' G0 S7 H1 ] L1 QPatient Report+ `# ~( K* R/ b
A 16-month-old white child was referred to the
+ D) o# k1 Y/ t# kendocrine clinic by his pediatrician with the concern( f4 R9 M6 U3 c6 m# i) ?) [
of early sexual development. His mother noticed
, N# O* @0 D" B: n; r7 Hlight colored pubic hair development when he was; b( e; B* b; X C3 f( W. b2 Y% ^
From the 1Division of Pediatric Endocrinology, 2University of
: P9 u) k v) w& e% O0 { G+ oSouth Alabama Medical Center, Mobile, Alabama.
+ e& k7 }* V, w" @; L% t p# aAddress correspondence to: Samar K. Bhowmick, MD, FACE,& T8 a8 U/ a8 _- P# H
Professor of Pediatrics, University of South Alabama, College of
& T% j4 O& N) OMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297; b9 j5 n, r9 z# X/ ]7 E
e-mail: [email protected].
# N5 { c7 [0 u- n" k( kabout 6 to 7 months old, which progressively became7 h/ v5 L" _- B8 |. @6 C3 _
darker. She was also concerned about the enlarge-
1 s/ c$ m- K: R0 s5 Hment of his penis and frequent erections. The child4 P$ T+ Z7 c- T5 q6 f; a
was the product of a full-term normal delivery, with9 A4 M8 T+ K; S! I3 l8 J
a birth weight of 7 lb 14 oz, and birth length of
% ~( n$ ~* `* m7 l! O6 {- L/ a20 inches. He was breast-fed throughout the first year
- f$ m, G" P& [: F( Z; hof life and was still receiving breast milk along with' Y' s6 A! Z4 A! |
solid food. He had no hospitalizations or surgery,
* F+ q( Y- l6 Hand his psychosocial and psychomotor development
) m/ E# g3 Q5 X& |# twas age appropriate.+ q. Y t2 S& |3 l9 R u3 g
The family history was remarkable for the father,! ^4 P. {2 |/ b
who was diagnosed with hypothyroidism at age 16,
1 g5 W0 V/ Q; V2 w6 }( Ewhich was treated with thyroxine. The father’s0 f4 B! ^0 Y1 w5 N- f) ?
height was 6 feet, and he went through a somewhat# j) N$ R! S6 u* q% S# V) V
early puberty and had stopped growing by age 14.8 T" `3 ~/ x) c O) ^
The father denied taking any other medication. The" b5 } f% b) X5 C1 z* a3 a
child’s mother was in good health. Her menarche# k) P F# \4 O3 O" F8 J
was at 11 years of age, and her height was at 5 feet0 G8 S1 V! H- ?8 B$ e# J( s
5 inches. There was no other family history of pre-7 C. ^1 @% E3 w
cocious sexual development in the first-degree rela-' a) x/ p! W, i, a3 _6 [: C% d1 Y
tives. There were no siblings.
* p: l0 x) W. _# ?% sPhysical Examination
, e6 D3 `4 W, l: g% R, B$ lThe physical examination revealed a very active,* V0 s5 x }) |3 E
playful, and healthy boy. The vital signs documented
1 U: x; w1 G3 Z' q" U0 pa blood pressure of 85/50 mm Hg, his length was8 x0 C3 _0 E9 ]! |7 l
90 cm (>97th percentile), and his weight was 14.4 kg
1 a" _5 `* h. w9 }7 u; l(also >97th percentile). The observed yearly growth: K# y+ @! f; d- h1 i6 y8 a* y
velocity was 30 cm (12 inches). The examination of4 A/ B" D2 c+ n
the neck revealed no thyroid enlargement.# u2 l6 v: }7 c# {9 ]
The genitourinary examination was remarkable for
6 d! x, G7 l. v w& j3 }enlargement of the penis, with a stretched length of& B. u& K; f' `& d
8 cm and a width of 2 cm. The glans penis was very well" p& I$ C" M4 A% u* y6 e2 s" _
developed. The pubic hair was Tanner II, mostly around M( j& E! J+ U; L8 g
540
0 w; d. z W9 x) l# Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. p' j8 s& E, J/ |9 A) ~% M
the base of the phallus and was dark and curled. The) B9 f) L4 Y7 D6 c8 J2 I6 S$ W
testicular volume was prepubertal at 2 mL each.
& J) `' o2 j2 r! L1 DThe skin was moist and smooth and somewhat
% A$ Z) H3 m3 W, @) F: Zoily. No axillary hair was noted. There were no
$ T2 ~+ \% t9 K8 W: F; v6 w& q& A% Labnormal skin pigmentations or café-au-lait spots.
9 ]8 Q% P& p5 ?$ f2 ?% O0 GNeurologic evaluation showed deep tendon reflex 2+, D. p8 {) d% _0 D. {
bilateral and symmetrical. There was no suggestion
" n- ^2 o! F- B0 _of papilledema.: a- q# T3 U2 w/ ^5 M" B: I
Laboratory Evaluation
$ u/ a8 z$ b* ]* E0 S) ~$ ?7 XThe bone age was consistent with 28 months by
$ c6 g) E% z: ~; nusing the standard of Greulich and Pyle at a chrono-
$ \( B7 Q3 w+ J$ {+ |% @/ m ]1 Klogic age of 16 months (advanced).5 Chromosomal
, j' i, @, R+ rkaryotype was 46XY. The thyroid function test
, q3 O+ _( N1 ], O! K0 `; |8 N, s2 }showed a free T4 of 1.69 ng/dL, and thyroid stimu-
* e, f4 R& L b. c8 dlating hormone level was 1.3 µIU/mL (both normal).
9 Y( I" F) M$ @3 A+ p6 tThe concentrations of serum electrolytes, blood
5 i3 V1 Y) o0 _' j- ]% o. Hurea nitrogen, creatinine, and calcium all were
8 W" I) a/ z% W5 w5 }( ]within normal range for his age. The concentration$ Q9 z& Q* ~; s1 F
of serum 17-hydroxyprogesterone was 16 ng/dL4 _3 J- I0 ^" C1 @1 Q. Q4 w/ h$ U
(normal, 3 to 90 ng/dL), androstenedione was 20
3 t9 n# |& ~- \0 rng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& B/ T5 t5 ` F$ B( L# Q3 G
terone was 38 ng/dL (normal, 50 to 760 ng/dL),4 E' r) S! Y; G; |8 P7 n
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 x2 q7 R0 y2 ~; x49ng/dL), 11-desoxycortisol (specific compound S)# ~/ x% O4 [) b# d
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! g( `# O6 X1 F$ R( d. x
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ a' p# Z/ \" T& j! \
testosterone was 60 ng/dL (normal <3 to 10 ng/dL), H H9 b' j7 y% N
and β-human chorionic gonadotropin was less than
) e K& }. r( ^0 q1 j! D5 mIU/mL (normal <5 mIU/mL). Serum follicular2 \; _4 h3 W+ U) p3 x+ E. r" f
stimulating hormone and leuteinizing hormone
4 U& v1 q% p" s- T' z, gconcentrations were less than 0.05 mIU/mL
- l$ O1 _# [. }! M& r* A(prepubertal).
5 }/ _1 {1 ]% s; w$ t8 XThe parents were notified about the laboratory
6 W3 q6 A. ]+ P+ j/ lresults and were informed that all of the tests were
1 r) E' a8 z4 c. d2 @6 e, }( B: \normal except the testosterone level was high. The
" P- c+ b$ L6 F. g: W. sfollow-up visit was arranged within a few weeks to' r3 c8 c0 A% s
obtain testicular and abdominal sonograms; how-; z; `! m) z- q9 q' N: z/ {
ever, the family did not return for 4 months.; S7 y( |7 g8 c; B" W
Physical examination at this time revealed that the
* o2 I/ ~% w/ G9 ~child had grown 2.5 cm in 4 months and had gained" J$ t- Z/ o2 }' D- X
2 kg of weight. Physical examination remained
* @5 }- J, z6 Runchanged. Surprisingly, the pubic hair almost com-
+ f6 y2 C) W- }! Y* `! vpletely disappeared except for a few vellous hairs at' Q$ [+ X: S1 n& z3 q( E
the base of the phallus. Testicular volume was still 2* N' q6 M Z) |0 h7 d# F* R
mL, and the size of the penis remained unchanged.6 K0 z; N: L0 {! T) ^
The mother also said that the boy was no longer hav-+ C7 u% [% O7 A
ing frequent erections.' q& G' N8 f# K) O
Both parents were again questioned about use of/ I; m- S# E" [' b
any ointment/creams that they may have applied to4 d: d8 ?+ e) O( S- l; u! {: m) ^
the child’s skin. This time the father admitted the A* N+ Y3 M9 g9 [- M/ U/ R8 j3 N9 B- j
Topical Testosterone Exposure / Bhowmick et al 541
. p- j3 t+ R, Y4 J4 Wuse of testosterone gel twice daily that he was apply-
5 P& X E4 r0 F, r2 O {7 Cing over his own shoulders, chest, and back area for
( l$ n8 `# B* `, W( i) c9 K! K# ]a year. The father also revealed he was embarrassed2 w: P" s) P/ M1 `/ J, `
to disclose that he was using a testosterone gel pre-
i# L, x9 d+ E( E5 z' hscribed by his family physician for decreased libido% i5 x! l+ k1 N! b$ W7 ?, m
secondary to depression.
9 y0 K) J1 Y* q0 E, ?/ SThe child slept in the same bed with parents.
( j! u4 _) J/ e8 a) ?7 BThe father would hug the baby and hold him on his
% h5 F% R0 g+ d m5 Fchest for a considerable period of time, causing sig-0 E/ U' ?$ d5 D/ A
nificant bare skin contact between baby and father.# K8 T) U4 d$ o2 Z/ x* s% B( k
The father also admitted that after the phone call,' L; u0 }6 r' V9 O9 G
when he learned the testosterone level in the baby
5 Q7 j- P5 |! r4 V6 C/ Iwas high, he then read the product information
5 P; ?3 T5 o2 L) X8 Gpacket and concluded that it was most likely the rea-
0 R2 \: S8 e' Q/ ~, _son for the child’s virilization. At that time, they: }' W6 c& I* k9 Z5 `) `7 }! a
decided to put the baby in a separate bed, and the7 M5 K: }' [( J$ N( ], A! d
father was not hugging him with bare skin and had1 t! A& L ?3 u! p ^0 m
been using protective clothing. A repeat testosterone
2 h- e5 ]( v1 r1 Htest was ordered, but the family did not go to the
" |) w" \0 g- u% j* ]laboratory to obtain the test.
5 E, W6 ^" |: ]1 dDiscussion
! p! e$ v5 r4 f/ V3 lPrecocious puberty in boys is defined as secondary
8 }3 [7 l: x$ ?4 n/ hsexual development before 9 years of age.1,49 d; o- S h0 J5 q' P* O
Precocious puberty is termed as central (true) when
& D: `! I$ P V# U7 Git is caused by the premature activation of hypo-- w: Q' r3 g& P j( N) B/ }
thalamic pituitary gonadal axis. CPP is more com-
, S9 X1 n, g1 R3 q; _mon in girls than in boys.1,3 Most boys with CPP
# y: L T( r% x: W: ?; q- Rmay have a central nervous system lesion that is
/ N6 k7 }5 W" Z( vresponsible for the early activation of the hypothal-& O: f/ Z# K J# x7 b1 D2 }
amic pituitary gonadal axis.1-3 Thus, greater empha-
$ z% A1 B' }$ |! }& E, Ssis has been given to neuroradiologic imaging in
# |) Z$ U3 [7 U: F0 O3 D' J* h1 ]boys with precocious puberty. In addition to viril-* P5 d5 M+ R) L, s/ l' ?
ization, the clinical hallmark of CPP is the symmet-6 F8 D8 U( C6 [9 E) `8 _ G
rical testicular growth secondary to stimulation by; _& M: f7 I2 [
gonadotropins.1,3: X7 X# r; H/ H3 F" a( i ?
Gonadotropin-independent peripheral preco- P. I/ J* B# L" a' G
cious puberty in boys also results from inappropriate
# S! A) Z( |2 T, B8 l0 r" C0 tandrogenic stimulation from either endogenous or( W4 V7 l U! ]! d% w4 a& r* G
exogenous sources, nonpituitary gonadotropin stim-5 K) g* K% X) ^' {) j; f# P @
ulation, and rare activating mutations.3 Virilizing6 I8 V6 T' }6 Y; c7 Y$ Y
congenital adrenal hyperplasia producing excessive
6 |- X, F, t* j$ X' x2 {: k- G7 xadrenal androgens is a common cause of precocious( t5 I+ b4 ~2 @0 v7 e) }
puberty in boys.3,4, Q3 h4 j$ r$ n$ ^( ]' F
The most common form of congenital adrenal
; `; s9 q# s; X2 G* r& J& ?* Rhyperplasia is the 21-hydroxylase enzyme deficiency.) y+ V5 k$ u" C1 _! p
The 11-β hydroxylase deficiency may also result in4 X! e$ ~0 z8 P: F. k% G
excessive adrenal androgen production, and rarely,
" Q& U9 H/ n$ a% @3 J8 s* {an adrenal tumor may also cause adrenal androgen. d, _+ g9 }4 G5 |
excess.1,3+ F+ t* A. u7 m
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ ]( |2 O" K9 i$ A- f+ a) \, s
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 Q$ E& P4 |* F1 ~5 B( D! H8 FA unique entity of male-limited gonadotropin-" _( k/ ?( K3 M+ T4 Z
independent precocious puberty, which is also known
) u/ d' m1 l: E% ~! J; L: _as testotoxicosis, may cause precocious puberty at a3 @/ _' u% [! Q+ {& ?. W K
very young age. The physical findings in these boys$ @- r6 E( a* Y3 r1 n: X% ^
with this disorder are full pubertal development,
* M( g8 K m7 c2 W9 z; _including bilateral testicular growth, similar to boys
3 A) A8 p$ y( `/ v$ U3 D* A/ T$ m4 L3 f$ Hwith CPP. The gonadotropin levels in this disorder
5 d) n2 S, r% M% care suppressed to prepubertal levels and do not show
x5 ]/ L; f" l1 Y9 f+ s( gpubertal response of gonadotropin after gonadotropin-
% z |9 `% P; O9 p- }8 treleasing hormone stimulation. This is a sex-linked$ {- o. u4 e, K% Q. e8 T. b
autosomal dominant disorder that affects only
8 y6 R+ ]1 z3 f, x$ g3 f6 \males; therefore, other male members of the family
! ~3 M* D9 _% W5 o( S* Amay have similar precocious puberty.3
- w! Y0 {$ u7 b! B+ Y( r' n2 s$ |; }In our patient, physical examination was incon-
$ y: ?4 ~/ b0 W% W0 c9 \* Lsistent with true precocious puberty since his testi-
% n, Q- }6 G3 K2 j7 E; d0 Bcles were prepubertal in size. However, testotoxicosis% G9 Y* H) |$ ?0 n. C2 a6 g, k7 Q
was in the differential diagnosis because his father" C( [8 [* J! Y8 R2 z
started puberty somewhat early, and occasionally,! l' [ ]/ Q$ x5 U
testicular enlargement is not that evident in the
9 |- ]9 A* S/ R: Cbeginning of this process.1 In the absence of a neg-
' z( ^. v; u6 ~ative initial history of androgen exposure, our
' x9 s( ?1 D0 h8 I+ q/ I" Xbiggest concern was virilizing adrenal hyperplasia,
* l* Z% Y, I2 `+ teither 21-hydroxylase deficiency or 11-β hydroxylase
7 s6 L+ T5 s9 ]deficiency. Those diagnoses were excluded by find-$ I, W) f" F$ T( I9 g9 p2 P: G
ing the normal level of adrenal steroids.
: y) B3 y/ M6 q: i) |The diagnosis of exogenous androgens was strongly$ \# b; o+ o/ G7 M3 V2 U) t
suspected in a follow-up visit after 4 months because
8 t. ?6 \3 ^9 A$ b/ P) O; f8 }the physical examination revealed the complete disap-
! ?9 Q0 e8 F3 G$ A; H- ^9 ?pearance of pubic hair, normal growth velocity, and
$ i r+ r: E4 j9 y9 \& ~7 ~8 Gdecreased erections. The father admitted using a testos-
- F) p: F; x) r2 V7 \" Xterone gel, which he concealed at first visit. He was
2 i, o; C! i0 l E A# susing it rather frequently, twice a day. The Physicians’
# I5 i7 s" l" z" ?0 a! RDesk Reference, or package insert of this product, gel or5 ?3 O, _0 `. V- z0 ?
cream, cautions about dermal testosterone transfer to
& l/ l7 q# |" @0 n7 E9 zunprotected females through direct skin exposure.' S& m! c: q2 l5 F' C- @. H/ r" D- z
Serum testosterone level was found to be 2 times the; L8 g$ `) [' h8 A U
baseline value in those females who were exposed to
c/ V1 U9 e- o1 w) |$ Zeven 15 minutes of direct skin contact with their male& K4 _7 p! n. H( } i @- z
partners.6 However, when a shirt covered the applica-
. ?5 B2 M/ _7 C3 G1 G! Q0 Z3 [tion site, this testosterone transfer was prevented./ E7 m) E; o& h0 Q5 S( r
Our patient’s testosterone level was 60 ng/mL,! j* r: N' ~0 P3 O$ C* N
which was clearly high. Some studies suggest that
4 ^- v" F) P# hdermal conversion of testosterone to dihydrotestos-
[% y) O+ t) M7 F' F0 A. bterone, which is a more potent metabolite, is more6 f7 y k+ ~; M4 K' f( r
active in young children exposed to testosterone2 {4 n* }- i3 c
exogenously7; however, we did not measure a dihy-
, P \/ q! x$ F6 q* V; Sdrotestosterone level in our patient. In addition to
( |+ ?( @5 H0 Y/ y: S9 [) z: Gvirilization, exposure to exogenous testosterone in
+ i& \7 b3 M, T2 B2 m5 echildren results in an increase in growth velocity and
. ~# U* o- g8 H, p% oadvanced bone age, as seen in our patient. V2 T" I1 w. ]" Q7 ~
The long-term effect of androgen exposure during
- T" Y# F9 W0 s& d0 `( \early childhood on pubertal development and final7 I( N6 o( i2 b; O/ p
adult height are not fully known and always remain
2 G& g# Q( b: q. Ma concern. Children treated with short-term testos-4 [6 ?; B. l I, T- `) N/ r6 x4 d% Z
terone injection or topical androgen may exhibit some
) n" `! u2 ]3 A% i! macceleration of the skeletal maturation; however, after% K; {/ K8 m; `& R$ {+ y! E
cessation of treatment, the rate of bone maturation
- ^& U* X" |: a; ?decelerates and gradually returns to normal.8,9 G# A; m0 N! Q4 f/ a0 w' Y
There are conflicting reports and controversy% A+ Y6 Q1 Z# Z
over the effect of early androgen exposure on adult' J" e3 ]* b$ v4 w9 I! m
penile length.10,11 Some reports suggest subnormal
4 n! {$ G) W/ t' Xadult penile length, apparently because of downreg-8 W8 Z# N3 m2 i& K( p# y
ulation of androgen receptor number.10,12 However,
1 ^# v3 Q1 L: I" [! j* G2 |0 z6 sSutherland et al13 did not find a correlation between' D7 I1 X' `4 {3 ] V+ {/ Y
childhood testosterone exposure and reduced adult$ }: n4 P; L4 m/ }
penile length in clinical studies.; m/ \; _3 G' }! E' V! E* j
Nonetheless, we do not believe our patient is
( M; D8 y7 k* V- ~going to experience any of the untoward effects from
3 i* [! J0 }$ s8 q# U7 wtestosterone exposure as mentioned earlier because9 E% C* M, _2 D: }- w
the exposure was not for a prolonged period of time.
& T& h9 P9 r: z a: A/ n8 m$ c; PAlthough the bone age was advanced at the time of2 O: k* C1 {; O6 q
diagnosis, the child had a normal growth velocity at
2 G j6 q/ z0 b7 |, n2 Tthe follow-up visit. It is hoped that his final adult0 g4 U/ x. Y/ f) h
height will not be affected.% q; S5 ?) M/ a- o
Although rarely reported, the widespread avail-
& E' n8 ]$ Y, y& Y0 J5 W+ v0 Uability of androgen products in our society may
2 B0 t- }6 a% L. yindeed cause more virilization in male or female4 a, [, t1 x5 D9 w0 l3 A7 s
children than one would realize. Exposure to andro-
) \2 s$ C- G e0 g8 l1 y7 t( Ugen products must be considered and specific ques-
+ y4 V; M7 m# a, U2 I; Ktioning about the use of a testosterone product or% Q2 _( s9 w9 K5 Z3 B
gel should be asked of the family members during
- l# K& ~% u8 {, w) Y' Nthe evaluation of any children who present with vir-% B B; ~5 i% k% M6 Z
ilization or peripheral precocious puberty. The diag-
3 n# ^* \0 J" ]" Q8 o1 w/ Unosis can be established by just a few tests and by; T. t: ?6 N. Y3 @3 k( D
appropriate history. The inability to obtain such a
, e& L3 B0 [$ U+ a9 h" rhistory, or failure to ask the specific questions, may
* R- q6 W4 |& {result in extensive, unnecessary, and expensive
! X; t3 `. \& |3 uinvestigation. The primary care physician should be: c5 W" z! {3 h% g0 J+ S
aware of this fact, because most of these children
8 ?( B- W; X) g, E$ t. C$ e& P y2 Qmay initially present in their practice. The Physicians’
4 }$ I5 S1 D% \# Y1 wDesk Reference and package insert should also put a
$ y+ R: P; ~ }9 r1 O( E: Rwarning about the virilizing effect on a male or
4 b* E2 o7 d$ t/ Q* _# \$ A% Ffemale child who might come in contact with some-" p: e7 W. F [0 S$ [& l" V
one using any of these products.! @% K8 e% Y* p: Z+ N% a
References
; o$ h5 X3 W$ ~9 p' V, g1. Styne DM. The testes: disorder of sexual differentiation
) f% g- r+ R5 Sand puberty in the male. In: Sperling MA, ed. Pediatric) I4 R2 w' x, @4 D# K
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( v( D- a$ R* X( }! B' m. L' [7 h& j2002: 565-628. A4 c( J2 W1 j; B/ W; y {+ S
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; A8 o/ |; z. H) h3 r) D
puberty in children with tumours of the suprasellar pineal |
|