- 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-Old3 _; z8 C( ]" S. N+ |
Boy Induced by Indirect Topical
( \ t; y2 L% p. F, c* Q% qExposure to Testosterone
% T+ q$ W% @$ W* A7 M7 nSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! X+ ^/ d% E, Hand Kenneth R. Rettig, MD1
0 O" j& T; q# b. tClinical Pediatrics$ X+ c5 c; W. w# p
Volume 46 Number 6
. H6 q7 ?# [" \1 ]; f9 @: TJuly 2007 540-543
% u( s( u* r( e© 2007 Sage Publications
. X% X; {+ x8 G$ `10.1177/0009922806296651# J- M; a5 g: r! z" ~, Z
http://clp.sagepub.com! M' P! q7 N* M. f: J" D6 e
hosted at
* s5 x& j! u& J2 O6 {: h5 E# _http://online.sagepub.com
3 t! v! V* F8 A* {: |4 cPrecocious puberty in boys, central or peripheral,
$ @- t9 s$ [/ G9 His a significant concern for physicians. Central0 i# E, l2 I6 ~. m0 ^. F% |; g
precocious puberty (CPP), which is mediated% G, v- P, \, [ a- c1 N
through the hypothalamic pituitary gonadal axis, has
9 n! j) }3 o j: v+ [/ ya higher incidence of organic central nervous system2 O2 |& ^0 e @/ D: ?, Q ~' _5 Z
lesions in boys.1,2 Virilization in boys, as manifested
6 F+ C( Z9 \+ K1 h. ` O4 F2 Uby enlargement of the penis, development of pubic
3 f: o/ [$ \; r, j$ v. Phair, and facial acne without enlargement of testi-% o! F; F/ w3 p. I j1 B$ g
cles, suggests peripheral or pseudopuberty.1-3 We
2 {; p' V" y* B- Breport a 16-month-old boy who presented with the
# J( `! S4 N5 t/ S, @enlargement of the phallus and pubic hair develop-
3 u0 x5 o I6 G) @ment without testicular enlargement, which was due; u T' I; z3 r; w$ E
to the unintentional exposure to androgen gel used by( n/ v) R) k- c
the father. The family initially concealed this infor-
% z. `7 q8 p# U9 Z6 J( ^- emation, resulting in an extensive work-up for this5 G. o6 e. ?3 Y/ O, P( Z
child. Given the widespread and easy availability of8 e7 j6 n' m9 W& c4 R( M, y
testosterone gel and cream, we believe this is proba-
1 Y- d) _2 @) W) lbly more common than the rare case report in the
$ D* n9 f. U+ E6 N* k5 q1 l% iliterature.4
! e: O/ `0 G0 I: O) q4 ^Patient Report' I; M5 w/ j6 f$ D$ L, A- ^! J' Z" t
A 16-month-old white child was referred to the/ j% b5 d" o& o7 d0 k) Z: Y, c% j( {
endocrine clinic by his pediatrician with the concern
7 b* L5 d' F/ S4 A; p6 e) dof early sexual development. His mother noticed2 s: m/ a* q. o7 O
light colored pubic hair development when he was+ F, {4 W3 ~7 b- V- m
From the 1Division of Pediatric Endocrinology, 2University of* M5 F/ Z5 E3 G
South Alabama Medical Center, Mobile, Alabama.
' i! ]1 \3 x% @0 S. D7 ~Address correspondence to: Samar K. Bhowmick, MD, FACE,- `2 G5 L" Z; f" d4 ^
Professor of Pediatrics, University of South Alabama, College of* @: C) J: o& C- U1 x4 i
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 @0 a% F! ?" s7 E) n# \# K0 me-mail: [email protected].
2 B/ F3 _6 a# H& ~( f3 z7 S Eabout 6 to 7 months old, which progressively became0 N& K% m0 \( Y* @: k. c
darker. She was also concerned about the enlarge-4 L8 x) A/ \9 u T7 ?1 Y1 {0 K; B# g1 F
ment of his penis and frequent erections. The child
0 M# g0 X1 d6 Ewas the product of a full-term normal delivery, with
2 c- t3 b$ C( i3 I- y# @% ea birth weight of 7 lb 14 oz, and birth length of0 [* i% l/ e7 {0 M6 i9 b9 E
20 inches. He was breast-fed throughout the first year
, J9 w$ O* Z# X% m3 l# f1 Sof life and was still receiving breast milk along with" S4 v- U8 I( x; h6 A3 F# E$ `
solid food. He had no hospitalizations or surgery,
% Y( A$ L ?7 ?5 jand his psychosocial and psychomotor development* g' j# _" O) w1 [2 r& W
was age appropriate.. m4 f. [5 h5 e* F) ^+ M
The family history was remarkable for the father,3 f8 l& A" M! N3 `8 F, I4 o3 K
who was diagnosed with hypothyroidism at age 16,( X0 T: y4 x/ J
which was treated with thyroxine. The father’s ^5 o4 h G, l1 D
height was 6 feet, and he went through a somewhat
' J8 ]8 x4 C7 Z+ h' a) S N5 i0 @early puberty and had stopped growing by age 14.
) O8 p! R ?- m. C5 V6 BThe father denied taking any other medication. The4 ~/ `" ^' \+ O. V _# r
child’s mother was in good health. Her menarche5 r+ I: U1 e; |! L
was at 11 years of age, and her height was at 5 feet- H9 j* [0 s9 `7 U: k' R6 E$ f
5 inches. There was no other family history of pre-2 y4 t" W4 J% d$ @% o1 U
cocious sexual development in the first-degree rela-: j* N0 ], y1 L, n
tives. There were no siblings.
l# [: ~ D& x/ B9 ]. TPhysical Examination
7 v, I" }: Z7 n4 Q- |# O: gThe physical examination revealed a very active,
& K8 \. q1 N4 E% V7 m- Q' p, aplayful, and healthy boy. The vital signs documented9 N% y) e( v) G `+ l4 c! Y( ]
a blood pressure of 85/50 mm Hg, his length was# i" c8 j$ x3 l4 @/ M- v1 f/ Y
90 cm (>97th percentile), and his weight was 14.4 kg
8 l( V. c; i# X' K6 I(also >97th percentile). The observed yearly growth
) ?3 j6 `! Z0 S/ [% Hvelocity was 30 cm (12 inches). The examination of8 O2 f) G( c2 ?# c }4 q! `5 O& W
the neck revealed no thyroid enlargement.+ H6 ]# s$ I9 k) ~) P( A$ I* |% y
The genitourinary examination was remarkable for
' u2 o$ ~- X$ u+ a/ p& W* benlargement of the penis, with a stretched length of
' h- V9 W' d. C5 S8 cm and a width of 2 cm. The glans penis was very well
! Q: e- ?/ b7 M$ j7 i1 Wdeveloped. The pubic hair was Tanner II, mostly around
2 ]0 M! ?) y3 k' V4 M' ?: m9 G540* V4 l6 x, O) ` t6 r3 ?: E: F- H( g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. ^+ ]9 I/ I. u
the base of the phallus and was dark and curled. The1 j' H# V* ^' M7 H: L {
testicular volume was prepubertal at 2 mL each.
5 T6 H5 G% k; ~: e4 k* u. eThe skin was moist and smooth and somewhat) s5 ]6 [8 a. K+ s+ U; S
oily. No axillary hair was noted. There were no2 s" W8 S: f, R5 ]4 N
abnormal skin pigmentations or café-au-lait spots.4 f r9 z6 i3 n4 L: w7 s# l
Neurologic evaluation showed deep tendon reflex 2+
1 U: S+ F$ X2 D! F( n( K' }/ n1 {' m' Cbilateral and symmetrical. There was no suggestion9 m9 L1 ?1 D2 m( n7 }. g
of papilledema.
. f! [* x. m) V5 ^# T4 X( r' gLaboratory Evaluation
6 u- a- ~5 t. W2 Q/ pThe bone age was consistent with 28 months by5 \+ f! }6 h) n* D5 }: d
using the standard of Greulich and Pyle at a chrono-" \) o% P6 d+ A8 N. i4 _0 C8 t
logic age of 16 months (advanced).5 Chromosomal' u" N% v6 f: s+ w( \) M
karyotype was 46XY. The thyroid function test; M! s8 | h" k* {6 d! J
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
7 P1 X6 K6 L* y/ |lating hormone level was 1.3 µIU/mL (both normal).
6 Q/ m# ^# ~. Z8 cThe concentrations of serum electrolytes, blood
- j* [+ b. { `4 r7 {+ _urea nitrogen, creatinine, and calcium all were
+ x6 K8 ~1 w2 \% D, Kwithin normal range for his age. The concentration5 b: B) }- Y4 V9 y( G e" @
of serum 17-hydroxyprogesterone was 16 ng/dL
5 ]( h( m2 r: I7 p4 d(normal, 3 to 90 ng/dL), androstenedione was 20) h- O- i$ y# F% l
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 t2 y) ?, _, T+ |terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. J9 o! c) {/ `: O& a2 S* Hdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ ]7 W* q; m# D7 j# h! a0 ^49ng/dL), 11-desoxycortisol (specific compound S)
# \) v6 q! P) ?/ kwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-+ E% r) L, D" i) ?: w7 ?
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% C ?( n4 r! h" U5 n
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 p- |! s5 Z8 \" e7 T8 Iand β-human chorionic gonadotropin was less than
1 r8 u$ l8 B* {6 j5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ v n. v# Q) E9 H5 ^stimulating hormone and leuteinizing hormone, d" Y" e g) l) D: X
concentrations were less than 0.05 mIU/mL
, _" N& j0 e* v: m1 u0 y(prepubertal).
( m" i5 V2 W7 |7 P$ S# N$ LThe parents were notified about the laboratory% W0 C' |, L1 L0 f! B
results and were informed that all of the tests were
& q6 g4 H' e; v; Inormal except the testosterone level was high. The3 U3 v9 A4 X2 S- Q) S/ L- I2 a8 ?
follow-up visit was arranged within a few weeks to
3 F, j; [$ H0 |5 S* _' u5 Aobtain testicular and abdominal sonograms; how-
# b c$ P5 y0 W: T" T( Z8 Qever, the family did not return for 4 months.! h2 A* [( Z* F2 Z* e; |
Physical examination at this time revealed that the
) {, s6 K: H5 |; F, Nchild had grown 2.5 cm in 4 months and had gained
4 c, n! I: o' l! g$ G. D! L+ \& p2 kg of weight. Physical examination remained: U: W# z- S; \( d9 H0 W% i
unchanged. Surprisingly, the pubic hair almost com-
: W- \; d0 M2 k+ y! m, }! Gpletely disappeared except for a few vellous hairs at
8 E$ K& O* I _0 g. _& qthe base of the phallus. Testicular volume was still 23 K+ |/ r/ v# s
mL, and the size of the penis remained unchanged. h: F6 R5 o% W$ f
The mother also said that the boy was no longer hav-1 \; D% g* [" E. ~
ing frequent erections. E4 I* @( i) I8 c# v, u
Both parents were again questioned about use of0 ], C2 y+ R, }9 _) d8 h8 n
any ointment/creams that they may have applied to
6 ]% T: v/ D( k- p {% R3 O3 gthe child’s skin. This time the father admitted the
" m5 V: i$ T- @' `6 a3 ATopical Testosterone Exposure / Bhowmick et al 541
1 m" ?5 q2 V! n. K# {% ]use of testosterone gel twice daily that he was apply-6 d( C( D& g) V" s
ing over his own shoulders, chest, and back area for
8 A& V% |" Z* d; U4 Sa year. The father also revealed he was embarrassed- K) h% H# Z1 |& r ~. r
to disclose that he was using a testosterone gel pre-
I" b% z, s' ]1 T) Fscribed by his family physician for decreased libido6 V1 ]% \9 @! }6 K9 D1 v+ @
secondary to depression.1 k" R1 \! y0 i- H( H' [7 f& W4 h1 n
The child slept in the same bed with parents.
) r6 z( A4 o9 @( i, d& wThe father would hug the baby and hold him on his0 ]" u, M3 u# l5 B7 X* c
chest for a considerable period of time, causing sig-7 r% x& d6 V6 I( J: A+ y! K
nificant bare skin contact between baby and father.
7 Y5 s' p7 A, h/ b [The father also admitted that after the phone call,9 j4 g& A" R; m% F3 D: j" k0 h
when he learned the testosterone level in the baby
8 |8 D9 l. z0 q0 C7 f+ n% p0 B* U' E1 vwas high, he then read the product information9 y( V& y6 {$ k# w/ O9 B
packet and concluded that it was most likely the rea-. n) D8 i7 s, ~9 a' t! P$ I
son for the child’s virilization. At that time, they. x8 K/ t8 ~, L. u: u: Z S
decided to put the baby in a separate bed, and the
3 Y7 S1 @( t" K/ T' lfather was not hugging him with bare skin and had2 x1 a6 w- Y" p$ o, u' Y
been using protective clothing. A repeat testosterone$ P8 i# T. U% T- W
test was ordered, but the family did not go to the
5 L; v* ?$ M. R. n- C; N( Ilaboratory to obtain the test.5 E0 L3 H; ]; r+ j1 C5 n
Discussion
% Z% v( f: O% l \$ Z1 a/ b {Precocious puberty in boys is defined as secondary/ ~5 V5 k2 D. F7 C1 M* n- o
sexual development before 9 years of age.1,4* k0 W. U$ x/ _9 D) c
Precocious puberty is termed as central (true) when
; ~7 v6 z( m# r, Nit is caused by the premature activation of hypo-) t4 q1 D6 P7 ]& R6 Q3 A! e
thalamic pituitary gonadal axis. CPP is more com- J, o* F* l0 i* _6 M; \1 J) I# ^
mon in girls than in boys.1,3 Most boys with CPP) K, v1 i/ z) ?% G
may have a central nervous system lesion that is! Y9 j& B r5 |/ }5 H0 M. K+ B
responsible for the early activation of the hypothal-
# X' f; A# h) A; C% Tamic pituitary gonadal axis.1-3 Thus, greater empha-
5 \: ^3 R+ }. Rsis has been given to neuroradiologic imaging in
. V; q& C6 B5 Y! rboys with precocious puberty. In addition to viril-
! J8 C: a+ O& F1 w: t. v' Wization, the clinical hallmark of CPP is the symmet-
# x* u* ~7 y1 h) |3 T, crical testicular growth secondary to stimulation by$ i2 J0 |; y* s, i3 x7 s6 f
gonadotropins.1,3( Q# o- j2 r: X+ q- d# c
Gonadotropin-independent peripheral preco-6 d" |; ]6 U! j
cious puberty in boys also results from inappropriate1 l* l3 G9 Y! Z) E& v
androgenic stimulation from either endogenous or1 y, ^' z% g$ n. k7 I
exogenous sources, nonpituitary gonadotropin stim-
( n h" J, W3 ~1 U6 h) o" ?; f" R1 xulation, and rare activating mutations.3 Virilizing$ V8 h1 q0 r9 l
congenital adrenal hyperplasia producing excessive+ Q$ ?& J' H8 o! _, l5 Y( ?0 c. F$ z
adrenal androgens is a common cause of precocious
1 R: g3 i3 Z5 l8 lpuberty in boys.3,4
2 p' ?1 `/ _7 \: T _! G' s" S; eThe most common form of congenital adrenal
8 v6 u# d2 S1 B% q: a, hhyperplasia is the 21-hydroxylase enzyme deficiency.
: z6 ^. e, Y' v9 w, u0 O0 w8 wThe 11-β hydroxylase deficiency may also result in
+ m" G& |2 q3 z$ l- B! h/ fexcessive adrenal androgen production, and rarely,2 c% A- m# Z9 T& @- h* u2 u
an adrenal tumor may also cause adrenal androgen
9 o9 A3 w6 I) F; e% fexcess.1,32 N I! V: C0 ~2 A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* A' `+ ]5 K6 W9 T. k" U
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* r, f r0 B9 k7 O" y
A unique entity of male-limited gonadotropin-6 y7 k7 u1 ^' Z) c5 R8 n1 g, Y
independent precocious puberty, which is also known
1 Q' S" r" C) j7 }4 Vas testotoxicosis, may cause precocious puberty at a# w6 E; m1 s% Y3 |* ^, q1 G& L
very young age. The physical findings in these boys- @4 \* }* S2 r* r" _2 U# d
with this disorder are full pubertal development,
' I' L- Y- e; z/ W7 nincluding bilateral testicular growth, similar to boys+ c2 y0 L1 u4 j0 k2 ], `) G
with CPP. The gonadotropin levels in this disorder/ g: L! m4 d4 c
are suppressed to prepubertal levels and do not show( b- z" O3 x' `/ `
pubertal response of gonadotropin after gonadotropin-
# E2 U) \7 Q% Oreleasing hormone stimulation. This is a sex-linked
' ~/ c4 K ~/ O/ V9 f _autosomal dominant disorder that affects only
" F2 Q! u3 q: \5 Y3 lmales; therefore, other male members of the family
1 M( Q* M! @' [may have similar precocious puberty.3! C4 A! c$ Z5 p$ p [
In our patient, physical examination was incon-
# D& a1 O4 G( X* K* E$ Esistent with true precocious puberty since his testi-' `4 T3 I# ]8 L f. v$ ]
cles were prepubertal in size. However, testotoxicosis
8 e, T, P7 h$ y7 ]! [was in the differential diagnosis because his father: S1 ?& E0 Y2 p+ p$ Z9 E
started puberty somewhat early, and occasionally,, W! E4 s5 g$ F. @0 \
testicular enlargement is not that evident in the# n: K) O2 _0 s, h% T$ m W: ?# b
beginning of this process.1 In the absence of a neg-& Q: m4 K) x& F/ Z
ative initial history of androgen exposure, our' k, L) o8 H2 e" w6 _
biggest concern was virilizing adrenal hyperplasia,0 s$ q6 G! A7 u7 O0 D* I0 i
either 21-hydroxylase deficiency or 11-β hydroxylase( M2 `/ ]6 I, Z' r! a2 q
deficiency. Those diagnoses were excluded by find-8 S8 m! ?! z% u1 K) U$ m7 x
ing the normal level of adrenal steroids.& b' R" |* j' k& [% l
The diagnosis of exogenous androgens was strongly( M6 D$ k) A% v. }& L
suspected in a follow-up visit after 4 months because8 T: e+ C. i* \; I( U9 G$ s
the physical examination revealed the complete disap-( @8 g+ S. P( S' ]
pearance of pubic hair, normal growth velocity, and& t9 D6 _. L9 w# f6 L
decreased erections. The father admitted using a testos-
: }- _) A& [9 C% Aterone gel, which he concealed at first visit. He was
. G5 {, h+ _; g8 Y2 Cusing it rather frequently, twice a day. The Physicians’1 }% ]3 Z" j3 ?' M0 Q' l
Desk Reference, or package insert of this product, gel or
0 B" m( r, Q1 [% ocream, cautions about dermal testosterone transfer to k% I+ u8 {" I. H0 Z$ h) {4 w! N
unprotected females through direct skin exposure.
: u6 Z! b! K6 g, d$ _Serum testosterone level was found to be 2 times the
% p& D5 V" e2 O6 Y: Y# F9 sbaseline value in those females who were exposed to" j' m6 K9 u" K8 i/ q7 `
even 15 minutes of direct skin contact with their male
/ y9 w; O, f; T6 y! U1 S( Mpartners.6 However, when a shirt covered the applica-
* }- V- `8 A7 G& z. ^0 ?tion site, this testosterone transfer was prevented.
6 X: R9 C5 R$ Z' u. I3 \Our patient’s testosterone level was 60 ng/mL,
3 u0 m+ F+ I: n0 A* hwhich was clearly high. Some studies suggest that
' U) k( f) `& x+ N; ^dermal conversion of testosterone to dihydrotestos-. h# I/ z( h1 D4 |0 N+ v$ q
terone, which is a more potent metabolite, is more& Q, ^( Y' |6 E$ _& U( s
active in young children exposed to testosterone
7 y% ?* |$ T& D4 L3 U( nexogenously7; however, we did not measure a dihy-
3 ^' e, G8 u/ V2 a: A$ _& Mdrotestosterone level in our patient. In addition to0 @" y4 Q+ ^: w
virilization, exposure to exogenous testosterone in0 W% X/ c8 i5 Q
children results in an increase in growth velocity and
% B! x( B9 p. R d4 [advanced bone age, as seen in our patient.
/ X; u, Q! e6 R7 `) A$ mThe long-term effect of androgen exposure during3 I3 ~5 O" F. \2 [* s
early childhood on pubertal development and final
G1 l7 }' U8 u, K! ?adult height are not fully known and always remain
P4 }' W7 [4 B8 K" i; s5 ha concern. Children treated with short-term testos-" n9 h I6 B- l Q( `* A
terone injection or topical androgen may exhibit some" @; o; o8 d7 ~. Y
acceleration of the skeletal maturation; however, after
/ J% L8 {% M) F0 n$ p, bcessation of treatment, the rate of bone maturation( P' r! f5 p1 ?- A
decelerates and gradually returns to normal.8,9
6 _1 s7 [1 j* R3 m1 x1 V. y# SThere are conflicting reports and controversy
! p" q A. |: n5 E8 Sover the effect of early androgen exposure on adult$ y) m/ N5 g4 j: E
penile length.10,11 Some reports suggest subnormal
* r* G5 n+ ?' w) `( N9 e3 hadult penile length, apparently because of downreg-* _+ S! a' p/ n2 k
ulation of androgen receptor number.10,12 However,
. N( U1 n3 Z, z6 l: k& P0 ]Sutherland et al13 did not find a correlation between3 V! `% z. u) ~2 ]3 A
childhood testosterone exposure and reduced adult' T# L/ z; L: L1 w" T N* s/ C
penile length in clinical studies.- |) r, C0 R- T3 z
Nonetheless, we do not believe our patient is
1 z# P' P4 z! S Sgoing to experience any of the untoward effects from
* I2 t; i- o0 n* y( ptestosterone exposure as mentioned earlier because( `. Q5 h4 U9 U+ J4 m5 V# ]* d1 H
the exposure was not for a prolonged period of time.
8 v0 y4 b! L9 G5 aAlthough the bone age was advanced at the time of
$ h, V9 d$ E0 c% adiagnosis, the child had a normal growth velocity at
$ x& m' {( H& y% |( @the follow-up visit. It is hoped that his final adult
; r1 S8 _; T- aheight will not be affected.
6 @2 R, z) v/ G. r7 M3 bAlthough rarely reported, the widespread avail-8 @+ s* t1 G9 X4 z
ability of androgen products in our society may- Y0 B% G3 M: z$ q' V4 m2 n9 e8 s- D
indeed cause more virilization in male or female
& U! `5 F5 Q7 w$ ?children than one would realize. Exposure to andro-
8 \9 t5 o+ ^5 e# M+ Z! ?' ^& {" Cgen products must be considered and specific ques-
/ r, e. Y" G: C" M# x0 w3 \tioning about the use of a testosterone product or$ a" U* n/ b Y9 o }8 Q- s
gel should be asked of the family members during$ M8 u2 L2 {+ j' [. O
the evaluation of any children who present with vir-5 g' U, D, _- Y/ |" \
ilization or peripheral precocious puberty. The diag-! \- K0 S% f, X7 k( K! ]8 e& d1 r
nosis can be established by just a few tests and by
8 C# k/ d; }- {7 i& D5 ?7 kappropriate history. The inability to obtain such a! t' B2 ]4 Q( G& X
history, or failure to ask the specific questions, may
' ]# m. ]3 q; P1 Z4 nresult in extensive, unnecessary, and expensive
- z: a3 }9 @- `! minvestigation. The primary care physician should be2 k. o2 T0 [1 \# c c) n6 v. i7 G2 U9 Q! J; G
aware of this fact, because most of these children4 }! Y+ B+ ~ K0 ?+ M) g* x9 B S4 @
may initially present in their practice. The Physicians’% p) V0 G5 F; _8 O1 k/ ?4 H
Desk Reference and package insert should also put a/ E: v6 b1 ^: a1 ^, I5 y
warning about the virilizing effect on a male or
# N- ]8 s$ s0 W/ yfemale child who might come in contact with some-4 `2 g+ y" E4 a' D
one using any of these products.+ F$ z0 `6 K) C. n. c j3 w
References
; |. I4 a* x) }1. Styne DM. The testes: disorder of sexual differentiation1 E3 a! J$ v9 l0 G# _6 p x1 o
and puberty in the male. In: Sperling MA, ed. Pediatric
+ ^+ ^- v3 u; S; f! T; W/ {Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 p. F9 g- b0 x
2002: 565-628.6 m2 V. @$ }) ^$ I( I' @9 h' b( D
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 U( i* e8 ~5 s
puberty in children with tumours of the suprasellar pineal |
|