- 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
/ d; Z8 {2 W% t( _3 H( p' x. qBoy Induced by Indirect Topical- M C7 H9 _% ?( K8 F
Exposure to Testosterone
) S1 J! ~4 ~$ S f8 i, QSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 L o1 S! ]1 r5 e6 H
and Kenneth R. Rettig, MD1" Q) M: |* l" ?& K X
Clinical Pediatrics
( H; |6 t( J% C( |8 F2 I' |! eVolume 46 Number 65 n" U, H& ^9 s6 N0 {
July 2007 540-543
4 o0 p( i& b4 |( n2 z3 C© 2007 Sage Publications5 k, y! [8 i8 C! S
10.1177/00099228062966516 Q' G# S: K2 w( t0 m B4 t
http://clp.sagepub.com7 [% Q5 R- s) E" M; S3 I3 ?
hosted at
4 |' s( X, `7 W! r. t8 Shttp://online.sagepub.com4 _& j3 G2 G& h% e
Precocious puberty in boys, central or peripheral,# P1 U- C; D$ Y2 Z+ g$ }& u" i
is a significant concern for physicians. Central$ N- r$ w2 I8 p: }, R
precocious puberty (CPP), which is mediated
+ O% {& X' ~" r* m* `# tthrough the hypothalamic pituitary gonadal axis, has
. G: a: d# B) D2 Y% J8 xa higher incidence of organic central nervous system
; ?0 y O5 F7 C( o8 B- b9 alesions in boys.1,2 Virilization in boys, as manifested$ d, m K/ p* h. p. L3 u" h
by enlargement of the penis, development of pubic
4 D& N ^; R. [- Y2 A0 \; n. Lhair, and facial acne without enlargement of testi- D [4 u5 g* s" `7 { T
cles, suggests peripheral or pseudopuberty.1-3 We9 k* i* X5 u: q
report a 16-month-old boy who presented with the# \+ v5 h3 Y) L" Z1 X1 D
enlargement of the phallus and pubic hair develop-
3 x6 i! p: f5 h7 t. Nment without testicular enlargement, which was due
6 y1 P0 V! t# L; d7 W9 Mto the unintentional exposure to androgen gel used by
7 p8 R5 H+ Q, o! Gthe father. The family initially concealed this infor-/ `' U$ _ l- f; A) d8 y
mation, resulting in an extensive work-up for this1 Z% }& U. C* d1 t5 \3 W/ j2 z
child. Given the widespread and easy availability of
. S: C5 C6 f* Y) ]8 D9 gtestosterone gel and cream, we believe this is proba-0 Q* _; }' a$ h! O, S+ @6 Q
bly more common than the rare case report in the
' I; c. C: [* ~2 u; pliterature.47 T9 \. @3 b0 y: ?
Patient Report
3 S. o6 j4 h) B" m* t) e* w, @! xA 16-month-old white child was referred to the
$ M4 G, |6 E8 F1 Z% s/ i9 t2 V& hendocrine clinic by his pediatrician with the concern$ N2 R* a6 t r5 i4 G; ?
of early sexual development. His mother noticed$ M* n: Q# }. A" N( e. j; R- n
light colored pubic hair development when he was
: W5 Q0 m1 @) I. R% `" c( P9 s! LFrom the 1Division of Pediatric Endocrinology, 2University of8 \4 A6 p. u# j/ S3 S# ]
South Alabama Medical Center, Mobile, Alabama.+ `7 k( e8 e: f7 Q' z0 \3 B! o
Address correspondence to: Samar K. Bhowmick, MD, FACE,$ _& `0 f& F( [2 s$ Z; x
Professor of Pediatrics, University of South Alabama, College of: A1 D8 Q/ b" ?( T( |; r6 G4 s
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ O, ]# O! C% E2 t/ l/ H
e-mail: [email protected].
; ]; N" ~$ M+ ]9 q6 N6 s: S9 kabout 6 to 7 months old, which progressively became8 L) f1 Z) [) A0 _0 @
darker. She was also concerned about the enlarge-
% a8 w- {' [% b; w5 l7 k% bment of his penis and frequent erections. The child; J2 `+ u- O1 P; }4 C
was the product of a full-term normal delivery, with
. I6 i# ~7 o# [8 ra birth weight of 7 lb 14 oz, and birth length of5 k3 U9 }' K8 ?0 ~) W% |, h% R
20 inches. He was breast-fed throughout the first year2 d6 n5 S* x l# O9 z, ^
of life and was still receiving breast milk along with& O1 g0 N7 [1 o7 L2 t/ ^$ ?
solid food. He had no hospitalizations or surgery,/ f' s* c: H% Q! r; c& v8 Y
and his psychosocial and psychomotor development% { Q. [+ b. o4 R5 ^! r
was age appropriate.
3 @& Z) E8 T6 }8 tThe family history was remarkable for the father,; F0 H! G# ^) r/ ]# ]: e% d5 w
who was diagnosed with hypothyroidism at age 16,
$ ^7 C6 t$ t9 ~: G) `, Twhich was treated with thyroxine. The father’s" f; D, l" w6 Q+ P( y& F
height was 6 feet, and he went through a somewhat% e7 @/ `5 g( ^' P9 E
early puberty and had stopped growing by age 14.
: J/ s5 N; R1 C- o5 |1 j' I3 F! cThe father denied taking any other medication. The
f3 [2 f7 Y. D" I, C. schild’s mother was in good health. Her menarche' ]+ Y$ K5 h; |( E- {: i+ S, a7 P
was at 11 years of age, and her height was at 5 feet! ^3 a& v* b) A8 L: N# K5 Y8 x
5 inches. There was no other family history of pre-6 `. F2 r: z$ w! ?7 i. g6 c
cocious sexual development in the first-degree rela-
9 q- a! T! v# z9 I* E/ Etives. There were no siblings.7 l+ a/ ?8 q1 O @
Physical Examination+ d3 K, F& n: `# E
The physical examination revealed a very active,# d1 t- Q3 c6 Y6 a% E, [
playful, and healthy boy. The vital signs documented
+ \% J7 R* h5 C g+ o' ma blood pressure of 85/50 mm Hg, his length was; P2 n7 k! r1 `+ Q7 i: j" x/ E
90 cm (>97th percentile), and his weight was 14.4 kg
3 u" w, J6 c0 \7 f. b4 K(also >97th percentile). The observed yearly growth
: }/ l# s, K* L2 j% Qvelocity was 30 cm (12 inches). The examination of% q; k! [8 M; H9 K5 M
the neck revealed no thyroid enlargement.+ }! D5 v' R! a2 y
The genitourinary examination was remarkable for7 ~0 o+ Q5 x: }5 t4 ^
enlargement of the penis, with a stretched length of1 ~# a, |( j& D- f% h3 C
8 cm and a width of 2 cm. The glans penis was very well) V$ [' ~& @5 i6 a& t
developed. The pubic hair was Tanner II, mostly around2 y# h+ c5 x9 D' b7 x; O7 b
540
$ u8 Z7 k5 t0 R8 v# X$ Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 T. ~( x7 a$ O3 ]$ O$ D( {9 `the base of the phallus and was dark and curled. The
' v: P+ i3 D6 W0 {8 `- Ltesticular volume was prepubertal at 2 mL each.
- x' a) T+ d9 Q& m, s, ]. \8 ^4 Q( R- IThe skin was moist and smooth and somewhat
( c) F- F! u/ Y, {9 m! W- Uoily. No axillary hair was noted. There were no
' s; W e9 q5 d, D( Babnormal skin pigmentations or café-au-lait spots.
. ]; n4 k4 @7 p9 N" BNeurologic evaluation showed deep tendon reflex 2+- W% @' u" [: R _+ {( Z
bilateral and symmetrical. There was no suggestion
4 d P4 n7 t& K& U+ Oof papilledema.
$ i/ M( P' Z* B0 {8 a% `Laboratory Evaluation# z: h. Y8 O- _5 M
The bone age was consistent with 28 months by& ?+ K6 p$ m0 t& y9 Y9 N
using the standard of Greulich and Pyle at a chrono-
! `% z" ?9 P7 ^5 w' Qlogic age of 16 months (advanced).5 Chromosomal& D( B: m* ?/ |4 \: A# h
karyotype was 46XY. The thyroid function test
" V9 l+ q" V5 w7 ]! L8 P- Y0 lshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
D+ A7 i! Z y8 M! y6 w' k# O& klating hormone level was 1.3 µIU/mL (both normal).
' j- U+ m- `! X- T/ {" y5 QThe concentrations of serum electrolytes, blood
" P- g% _1 {* F. W V) burea nitrogen, creatinine, and calcium all were" J% P8 N. F1 M$ y6 s7 B. J
within normal range for his age. The concentration
/ G+ X3 O% M# X' {) Zof serum 17-hydroxyprogesterone was 16 ng/dL5 K6 b3 g: K- x9 B0 |1 ?/ t& S
(normal, 3 to 90 ng/dL), androstenedione was 20
. H5 C1 y$ E5 `/ L0 V4 C" a# zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) Q4 I' {( q% ]& \3 Mterone was 38 ng/dL (normal, 50 to 760 ng/dL),$ u8 F; T1 d8 u6 e y: H/ P
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
- F7 w, U' n8 ~ g49ng/dL), 11-desoxycortisol (specific compound S)% W3 p; e+ s: [2 d5 [/ ?1 r
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
/ w" `7 }! [0 N& _6 w+ P- m$ J5 @0 mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: M3 U# B) Q) P5 Z: M9 p6 F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
. B, u! U( j* [1 |! Q$ }0 p+ Fand β-human chorionic gonadotropin was less than
4 y2 y- l/ w$ t. z3 _* E5 mIU/mL (normal <5 mIU/mL). Serum follicular; K6 _ G J F8 \$ ?: L8 G7 M
stimulating hormone and leuteinizing hormone
0 O V) }$ K* |5 pconcentrations were less than 0.05 mIU/mL
/ t2 R2 B! ]3 N6 k' Y" K* V* M. M( ?(prepubertal).& o& O% Y4 p2 m, F% h7 U' |
The parents were notified about the laboratory
7 W2 T! @5 s9 G! ]8 P6 M2 q8 c" R& Vresults and were informed that all of the tests were: A1 D# L: b* V# z
normal except the testosterone level was high. The
# Z: _; `" ~. n4 @2 v: j+ O# i% Jfollow-up visit was arranged within a few weeks to
' U I. b# G* A& [( Kobtain testicular and abdominal sonograms; how-
: H8 S4 [0 u& L3 n9 M" R# Oever, the family did not return for 4 months.8 e/ H3 M; ?. l+ U) P$ r
Physical examination at this time revealed that the# |- w8 Z. K) d# i
child had grown 2.5 cm in 4 months and had gained
6 z5 x1 }' }/ p! R6 W% c9 s; f- I5 W2 kg of weight. Physical examination remained! A% Y, Q/ a I* r
unchanged. Surprisingly, the pubic hair almost com-, m: N; u, M+ l$ o8 e
pletely disappeared except for a few vellous hairs at: W+ u9 V. [7 q7 N* X% H
the base of the phallus. Testicular volume was still 27 Y3 K$ P9 X) g9 I3 A: y
mL, and the size of the penis remained unchanged.6 k: J+ z, h% [: B
The mother also said that the boy was no longer hav- J0 T9 {. L4 j$ g) i I
ing frequent erections.
/ R2 a2 P- r5 q, L) T5 ABoth parents were again questioned about use of
' b1 s3 Y! u, V+ O5 Cany ointment/creams that they may have applied to7 k' W( e6 I5 I. X- [: d1 v/ D& q
the child’s skin. This time the father admitted the' {- l0 l( t, }9 W
Topical Testosterone Exposure / Bhowmick et al 541# |/ t. o1 S" Z6 U/ Q% S' E, \
use of testosterone gel twice daily that he was apply-/ [: y: p( p; W1 I
ing over his own shoulders, chest, and back area for7 D8 U- P6 Q9 Q/ F, _, T
a year. The father also revealed he was embarrassed
# K! d* j q' }0 X4 a& W( ~" [6 dto disclose that he was using a testosterone gel pre-! Y& h7 U3 Y. F7 z
scribed by his family physician for decreased libido
' d0 z+ `+ K% csecondary to depression.
, u" j: Z. m2 F0 I! @, _0 b, pThe child slept in the same bed with parents.3 ^# L% g; b$ v; B( @
The father would hug the baby and hold him on his9 ~6 V1 M; N. X/ k, B( E
chest for a considerable period of time, causing sig-" C: s# M3 P5 Z/ l
nificant bare skin contact between baby and father.
3 `- M1 s+ X7 p) d4 F) yThe father also admitted that after the phone call,
5 {* U: N1 u P# [) @8 q8 Dwhen he learned the testosterone level in the baby0 n. m5 Y4 T2 f9 K
was high, he then read the product information9 p$ T1 g: ] H
packet and concluded that it was most likely the rea-
! ~7 k$ M0 {+ r# uson for the child’s virilization. At that time, they
0 i' y3 D5 H2 e7 Kdecided to put the baby in a separate bed, and the% z( Z# P4 K7 u. @8 u$ X
father was not hugging him with bare skin and had+ J J3 K4 a+ R1 B5 p) D
been using protective clothing. A repeat testosterone6 ~! ^3 F, q! H: K% z3 _8 u
test was ordered, but the family did not go to the* m3 h. j# q( G5 S
laboratory to obtain the test.
5 R( g5 p' U: C9 i e6 V* p+ T; nDiscussion% f6 L, t2 g- w5 _1 F3 K+ w5 X5 J
Precocious puberty in boys is defined as secondary
% H% \. e6 H+ I2 H& bsexual development before 9 years of age.1,4
+ k, Z$ N9 K1 m2 Y. D& \! WPrecocious puberty is termed as central (true) when
& Y: G7 _: t, z( Z c# rit is caused by the premature activation of hypo-
- W2 G6 W6 a7 N, Dthalamic pituitary gonadal axis. CPP is more com-
4 x! o; F+ Z/ }/ M! X/ ^" n% U7 cmon in girls than in boys.1,3 Most boys with CPP [3 p* I! h u6 `: z! R
may have a central nervous system lesion that is j+ X @( P5 k7 B
responsible for the early activation of the hypothal-6 P W7 R. f; y7 {, [( i( p9 w- V
amic pituitary gonadal axis.1-3 Thus, greater empha-) b* [0 L) o; l o6 K6 h3 r" j
sis has been given to neuroradiologic imaging in
/ S5 E# I- m, G# |8 Yboys with precocious puberty. In addition to viril-
: v3 l4 Q' W8 ~) W7 U6 Hization, the clinical hallmark of CPP is the symmet-7 w( Z+ Y& i- e. F
rical testicular growth secondary to stimulation by' X5 ?5 r' O9 U7 c2 U
gonadotropins.1,37 U! ~# ?9 |4 k8 ~
Gonadotropin-independent peripheral preco-
9 n( ~* w! ~6 E; n: n- Ccious puberty in boys also results from inappropriate
# p7 O3 t, X7 r" N" a8 wandrogenic stimulation from either endogenous or0 A. c* k8 b% v* [6 h# E2 V
exogenous sources, nonpituitary gonadotropin stim-
* f# j+ p- D' k3 dulation, and rare activating mutations.3 Virilizing
2 W& n* u) P; f: x' Mcongenital adrenal hyperplasia producing excessive; i8 R1 C; L( B K0 U+ R' G- E! }
adrenal androgens is a common cause of precocious/ O- |4 x& g+ p" O7 p7 k
puberty in boys.3,4
- l: ^3 |2 e5 `6 g( a, Q+ f9 RThe most common form of congenital adrenal
! Z* @) d6 C& ahyperplasia is the 21-hydroxylase enzyme deficiency.* }! q, U" r+ @! ~, D, l" g
The 11-β hydroxylase deficiency may also result in
2 d( v! g# R5 kexcessive adrenal androgen production, and rarely,
, F# l3 X2 C0 e" s* c$ O a- {& jan adrenal tumor may also cause adrenal androgen1 x0 u! ?- b, T0 R. h$ Q+ `
excess.1,3
0 N: c1 e; @4 y4 \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 Y0 n8 M4 f5 i" K& E+ W4 m
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. U" Q: j6 W. w
A unique entity of male-limited gonadotropin-7 G2 M. Y6 e7 N
independent precocious puberty, which is also known6 J! q( m) c7 Y$ n
as testotoxicosis, may cause precocious puberty at a _6 x2 |$ ]# s) Q! G( [
very young age. The physical findings in these boys N- X s" s1 u/ d; d
with this disorder are full pubertal development,
' V4 m9 U8 K% C( }+ aincluding bilateral testicular growth, similar to boys0 `. @; M. ^3 n: B* g! O9 |
with CPP. The gonadotropin levels in this disorder0 _% [$ O% W# V- X3 D# W- s
are suppressed to prepubertal levels and do not show' `4 q D# v/ v; J4 h! k/ {1 Q" w
pubertal response of gonadotropin after gonadotropin-% X6 o4 Q6 ^( W4 h1 o
releasing hormone stimulation. This is a sex-linked* @7 y; O+ O' |" w
autosomal dominant disorder that affects only) C% F% a+ U3 o+ O
males; therefore, other male members of the family
! o e% e* H" {" Y+ _% e+ dmay have similar precocious puberty.3
9 [7 p7 f% c/ P" L% l, D$ GIn our patient, physical examination was incon-
2 c7 T* E$ M" t( msistent with true precocious puberty since his testi-' j9 y, e( Q5 Y( A8 O
cles were prepubertal in size. However, testotoxicosis
: ^/ _# I0 |$ `8 N1 |% S: Xwas in the differential diagnosis because his father4 |+ P$ M! S, U- \6 q
started puberty somewhat early, and occasionally,) K) p% Y% e" O! u! F4 j
testicular enlargement is not that evident in the
! m- U" c% C6 D6 wbeginning of this process.1 In the absence of a neg-
# L3 G. Y b) v( B2 R5 p1 dative initial history of androgen exposure, our
% w/ B- a) ?' \/ Y( _! gbiggest concern was virilizing adrenal hyperplasia,& z% e5 j; W! m3 F9 Y- u7 ~% z3 x6 ^
either 21-hydroxylase deficiency or 11-β hydroxylase$ D0 S$ ~$ M( G o; I
deficiency. Those diagnoses were excluded by find-- R( N4 N/ @0 A+ t9 I2 T& `- D
ing the normal level of adrenal steroids.2 x5 N- s, O' d8 s+ R% V k
The diagnosis of exogenous androgens was strongly8 r! D5 [( z5 K4 ]5 O! y
suspected in a follow-up visit after 4 months because
, z& D% P, q7 K' O3 d1 Nthe physical examination revealed the complete disap-/ Y7 j q+ a* P! a2 ?1 P
pearance of pubic hair, normal growth velocity, and6 K* ^4 L7 W$ p! I/ s
decreased erections. The father admitted using a testos-
8 r1 Y' N# D. J6 _4 b# b: gterone gel, which he concealed at first visit. He was5 s1 n8 L" E# u
using it rather frequently, twice a day. The Physicians’7 x k |$ R- n/ r: ?0 B
Desk Reference, or package insert of this product, gel or8 e1 [, ~. C& g( w! Q3 d: ]
cream, cautions about dermal testosterone transfer to
1 H2 b* G3 t! M" Funprotected females through direct skin exposure.
7 K& u1 t9 _0 x5 Z- N) y$ LSerum testosterone level was found to be 2 times the
: [2 s& ^3 k) {6 _baseline value in those females who were exposed to8 U+ q: B4 @0 L
even 15 minutes of direct skin contact with their male
- ^2 S& x$ I5 m, O- S5 O9 l3 upartners.6 However, when a shirt covered the applica-& \) ~, b$ p* P5 w0 P$ y' h% A/ H
tion site, this testosterone transfer was prevented.: T* l3 B! R, p
Our patient’s testosterone level was 60 ng/mL,
! X4 \) D7 \) q0 l% o4 |: `which was clearly high. Some studies suggest that
# g2 T+ P) k( B. j/ Bdermal conversion of testosterone to dihydrotestos-
, \( s6 a0 I' @terone, which is a more potent metabolite, is more3 Y) B) X; p4 B' n1 _) ~
active in young children exposed to testosterone/ ^! t( _% X1 D
exogenously7; however, we did not measure a dihy-
. ]+ K- l3 [* O5 Tdrotestosterone level in our patient. In addition to4 s' k% f1 d1 @, V1 U, l7 p
virilization, exposure to exogenous testosterone in" H) n" P( ]0 `3 }) y1 M
children results in an increase in growth velocity and. W& ?4 i% b! R& D- D
advanced bone age, as seen in our patient.# C2 G* N z$ i; N$ m- |
The long-term effect of androgen exposure during* E8 ~% t0 O/ a
early childhood on pubertal development and final0 N- | w! D) ~7 ~( G: G* I
adult height are not fully known and always remain
# ^9 a; x, S/ o' [3 J2 ca concern. Children treated with short-term testos-
- L) N3 ^; o% K7 }terone injection or topical androgen may exhibit some
5 w+ d# F6 Z/ ^1 r3 jacceleration of the skeletal maturation; however, after' G; h# q+ w3 ~
cessation of treatment, the rate of bone maturation
% A+ r2 P3 w0 j( m0 Cdecelerates and gradually returns to normal.8,9
0 Y0 A2 w; _9 fThere are conflicting reports and controversy
4 ] ] W0 H0 x3 r R8 P) Lover the effect of early androgen exposure on adult7 Y# b. `1 [% v/ C& l* j5 Q
penile length.10,11 Some reports suggest subnormal( n9 n ?# Z! t5 q/ H+ J
adult penile length, apparently because of downreg-
& g8 _& O( ?4 _( r0 f( uulation of androgen receptor number.10,12 However,7 P4 q3 a1 ?4 V+ Y
Sutherland et al13 did not find a correlation between* O7 a( ]& L) J
childhood testosterone exposure and reduced adult
% ]/ v9 D% ^: M2 H( I: s" h$ epenile length in clinical studies.; V! T- \* I7 X: @5 `
Nonetheless, we do not believe our patient is, F' u2 w. l' b9 w" t
going to experience any of the untoward effects from
+ u, n: C- V/ d7 U3 Etestosterone exposure as mentioned earlier because
5 m" S% l& R4 O& G: p) vthe exposure was not for a prolonged period of time.
9 c; l1 {+ h7 m8 @: lAlthough the bone age was advanced at the time of
) v% z/ N" k* \! B: @! c$ ~diagnosis, the child had a normal growth velocity at
% d4 a( X- U5 D& n' {' Pthe follow-up visit. It is hoped that his final adult/ w: i( w; \( ]' Q
height will not be affected.& o( J$ T3 I8 N/ r
Although rarely reported, the widespread avail-. S: S1 y. O8 ^9 r5 Z4 K
ability of androgen products in our society may6 z! ^# C. n& ?% [# n/ g O
indeed cause more virilization in male or female
, l: W& u) `5 _9 M+ t w3 @! Hchildren than one would realize. Exposure to andro-
7 |6 j7 ^, G* ?& B* ~gen products must be considered and specific ques-
+ T/ a5 L- q0 a9 Utioning about the use of a testosterone product or' q3 |2 t4 x f u9 ~
gel should be asked of the family members during% D$ J/ j) D. a3 b
the evaluation of any children who present with vir-
8 M% ^2 }5 a8 O+ [$ v% Uilization or peripheral precocious puberty. The diag- e: W2 C# E. V0 y1 e' l1 f' m
nosis can be established by just a few tests and by* U. W7 I" I' Q2 I
appropriate history. The inability to obtain such a$ m* K' _( w. h( D+ S; x' w
history, or failure to ask the specific questions, may! Z! s5 _' Q: _4 Q/ @' s0 t. `
result in extensive, unnecessary, and expensive
. C) O' R4 F; ^2 M4 linvestigation. The primary care physician should be
Z% s; m+ X L& ~aware of this fact, because most of these children
( |. W9 V5 j% ~may initially present in their practice. The Physicians’
' ]% `& y8 \, p" a5 m. ODesk Reference and package insert should also put a+ @% |, `4 `" j$ X
warning about the virilizing effect on a male or. P5 B+ S2 g& Z. q2 U1 n
female child who might come in contact with some-
1 |6 |# N$ S8 I" D8 |' yone using any of these products.0 n8 L5 X3 ]9 F! l; L5 Z
References/ J0 T! ]7 R K& r
1. Styne DM. The testes: disorder of sexual differentiation, S/ o& h* ~1 m W- x8 {: r Y- R: g) _
and puberty in the male. In: Sperling MA, ed. Pediatric/ [& `8 P& ~% p0 ~# t# B2 [$ d" P
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;9 v8 ^+ ?' S& p
2002: 565-628.) u) M8 e; |! b; s) i4 B) v5 k% y
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# T2 v7 g6 K$ K1 @( H. Y$ p
puberty in children with tumours of the suprasellar pineal |
|