- 註冊時間
- 2023-5-6
- 精華
- 在線時間
- 小時
- 米币
-
- 最後登錄
- 1970-1-1
累計簽到:5 天 連續簽到:1 天
|
發表於 2025-1-4 03:27:02
|
顯示全部樓層
Sexual Precocity in a 16-Month-Old
4 w3 l$ U; c& q, u2 VBoy Induced by Indirect Topical
& P% u: H. w+ O( o% m" RExposure to Testosterone
9 m! h7 {8 z# L" o) iSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- l/ M( i6 c+ `4 ]
and Kenneth R. Rettig, MD1
0 o3 A0 y1 n V a" f; ?Clinical Pediatrics6 x( I7 H) @- w. W1 D8 {
Volume 46 Number 61 u* R+ j/ y: t1 e
July 2007 540-5431 ~9 f S1 M; H: G$ c
© 2007 Sage Publications- ~' \ ~" W# P$ G% v/ R' J) v
10.1177/0009922806296651: f, L3 a" M" F* e9 E0 w# G
http://clp.sagepub.com5 t% i/ h' S/ w2 Z* V3 a: v- q
hosted at
3 F& c& W, Y; h; N: _: fhttp://online.sagepub.com$ Y0 y/ I% b" [. ?+ `8 l" i
Precocious puberty in boys, central or peripheral,7 r+ b2 _: [! u0 D& F. R1 x5 _
is a significant concern for physicians. Central; c1 B1 Q+ V- n0 K: }# T! `
precocious puberty (CPP), which is mediated: F* V8 L0 O) |" ]+ w
through the hypothalamic pituitary gonadal axis, has4 P, h3 U; u$ j1 H6 `) H
a higher incidence of organic central nervous system/ v" @) q6 q9 d( ^: w* p
lesions in boys.1,2 Virilization in boys, as manifested0 j8 |6 s; v5 e9 i- j- ^& `6 E
by enlargement of the penis, development of pubic
) N/ o' |2 G8 F* L7 k$ Dhair, and facial acne without enlargement of testi-
5 M% m" [# p D) T3 |. vcles, suggests peripheral or pseudopuberty.1-3 We
2 o, }; p3 o7 x! k2 d Y/ V* hreport a 16-month-old boy who presented with the
, d6 _- J4 k1 r$ M/ E8 D. v' denlargement of the phallus and pubic hair develop-) O+ J. I; R o! m
ment without testicular enlargement, which was due* s/ q: ?. Q9 f& u0 f
to the unintentional exposure to androgen gel used by
" M8 B/ p* e' rthe father. The family initially concealed this infor-8 L" S0 o% p' n2 g$ ~* d& w
mation, resulting in an extensive work-up for this
1 i5 e" V4 k: Pchild. Given the widespread and easy availability of5 {& I- C; ~1 H5 c/ a
testosterone gel and cream, we believe this is proba-7 d0 Q' l) d8 u. r# Z
bly more common than the rare case report in the
. Q; I ?" T3 Z/ D; {+ j+ I% nliterature.43 W* j* M- D0 ^1 Z" b7 K! p2 J7 w
Patient Report2 V) O- v6 m" w" s: p
A 16-month-old white child was referred to the
4 R% q) e e( nendocrine clinic by his pediatrician with the concern
, i- g$ B) j( A& }* oof early sexual development. His mother noticed: \' r: ~& i B3 H" @. l' v, T
light colored pubic hair development when he was
) }* x5 w8 p4 C7 K% M @& YFrom the 1Division of Pediatric Endocrinology, 2University of
l5 K2 o9 z6 E0 e# p6 y& lSouth Alabama Medical Center, Mobile, Alabama.. w0 J- d& D2 O! _
Address correspondence to: Samar K. Bhowmick, MD, FACE,. ^$ ] \! F5 N, [5 s. b
Professor of Pediatrics, University of South Alabama, College of
- s4 j% [+ K/ I' ]5 [Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 @& u% V/ e9 X1 w1 g, \; v1 |8 e
e-mail: [email protected].
1 @- `0 t. X) U. o. u4 Dabout 6 to 7 months old, which progressively became2 @. e2 ^% ~; m7 v
darker. She was also concerned about the enlarge-
) N# w4 Q- B: I3 o- F$ Z( iment of his penis and frequent erections. The child
$ O, J' R/ ~' d$ T1 \) z/ Y8 D$ Bwas the product of a full-term normal delivery, with
7 ` ` L. R9 H! B! sa birth weight of 7 lb 14 oz, and birth length of
: E* ` O+ z) A: W20 inches. He was breast-fed throughout the first year
0 D ^$ W- E6 l% Z- Zof life and was still receiving breast milk along with
b$ Y6 M, F( a7 @# T& \solid food. He had no hospitalizations or surgery,5 ~8 B7 v8 i" q3 M% A, e, \7 b1 w3 o
and his psychosocial and psychomotor development; g; ?7 [6 z& H9 A( c- k2 \
was age appropriate.
2 X$ Y- f; A+ {The family history was remarkable for the father,
9 e) T/ `7 \; T9 Uwho was diagnosed with hypothyroidism at age 16,7 M' T; ~: ]1 N8 g$ M. K( }/ [
which was treated with thyroxine. The father’s
i! r( R) |- c! P" `4 ]height was 6 feet, and he went through a somewhat
' b# t$ p7 [: s" bearly puberty and had stopped growing by age 14., C" C! q3 v3 N$ O2 c
The father denied taking any other medication. The
/ k" q# I& l4 R# m; B1 |child’s mother was in good health. Her menarche
% Q, i' L6 q" j) uwas at 11 years of age, and her height was at 5 feet
/ o+ }. \+ Z5 S" T4 \2 _8 K5 inches. There was no other family history of pre-
j; e# P/ F; ccocious sexual development in the first-degree rela-
# U+ _' _& \2 i) ?tives. There were no siblings.
2 c, j0 R, v' k( r4 ?9 q( CPhysical Examination5 j9 K4 G3 M% B6 N5 R4 a
The physical examination revealed a very active,9 l" K+ T, ?* V) |* M. |
playful, and healthy boy. The vital signs documented5 h: X5 X4 t% o4 F5 ]1 x
a blood pressure of 85/50 mm Hg, his length was
1 n0 x0 l3 T( }3 P90 cm (>97th percentile), and his weight was 14.4 kg# o' n8 C. E/ I+ ^, l- ]3 m* h! Y6 V
(also >97th percentile). The observed yearly growth/ K" E0 w2 F9 l' V$ d
velocity was 30 cm (12 inches). The examination of: C5 p6 s- l' X& b/ i: T
the neck revealed no thyroid enlargement.
+ t( O5 [ Y: U7 A" r4 C8 T% J* {The genitourinary examination was remarkable for6 y6 q3 }4 m0 i0 s* G' S9 S
enlargement of the penis, with a stretched length of
0 o0 o* ~; O8 j; g! \/ N. T8 cm and a width of 2 cm. The glans penis was very well0 Y' R+ E' P# t1 k4 @' X/ L9 r8 L
developed. The pubic hair was Tanner II, mostly around4 T8 M$ w* l X, \
5405 m5 q3 p- W1 d H, O5 S
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: U- Y9 S; l( R; {the base of the phallus and was dark and curled. The' s8 n3 s2 {, p7 i
testicular volume was prepubertal at 2 mL each.
3 }& r6 U- {( X+ |The skin was moist and smooth and somewhat
0 f7 z$ n) b- u! S' O3 N1 poily. No axillary hair was noted. There were no- c+ r# |2 w# T+ `2 k, C/ o
abnormal skin pigmentations or café-au-lait spots.
3 Y6 u* `) ]7 }( u7 }9 [4 E2 J$ P# r' w) INeurologic evaluation showed deep tendon reflex 2+" q' U$ f8 H/ b9 z1 G7 N8 r- d
bilateral and symmetrical. There was no suggestion% {5 E3 S" k& C: J4 r' ?# }1 S
of papilledema.
% s$ ?5 ~: L5 jLaboratory Evaluation
4 ^ T% h+ c' V' l* N3 dThe bone age was consistent with 28 months by
* r: E* o) j1 [1 b/ Musing the standard of Greulich and Pyle at a chrono-% q1 J0 |, h. m4 Y- H: D3 b9 X
logic age of 16 months (advanced).5 Chromosomal
" a9 i+ u5 }: I) A: R/ u/ Bkaryotype was 46XY. The thyroid function test; Y1 K2 R8 m0 _+ r3 \ e
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 I$ E8 g" R4 t0 F
lating hormone level was 1.3 µIU/mL (both normal).
+ A' D8 b1 J2 a* j+ V: uThe concentrations of serum electrolytes, blood0 F* t. d! z2 N3 ]9 w% Z' r/ S
urea nitrogen, creatinine, and calcium all were7 [9 _8 V0 y3 d
within normal range for his age. The concentration9 y' T% p6 j. B- p6 M) m+ z' a
of serum 17-hydroxyprogesterone was 16 ng/dL
8 E/ a7 c- E) `% A1 I9 e2 v(normal, 3 to 90 ng/dL), androstenedione was 20: | o" @ K8 y( M m
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& E8 J/ X: b; B/ E) c, W9 ^9 X
terone was 38 ng/dL (normal, 50 to 760 ng/dL),! F$ }/ C! \* u
desoxycorticosterone was 4.3 ng/dL (normal, 7 to$ d+ n& w% U, [( O! k4 q8 j
49ng/dL), 11-desoxycortisol (specific compound S)
# ^! L, q' i7 b# r+ c1 bwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, f3 V# X+ \! V/ \! z3 ?4 x
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 x" Q8 T' I% _% F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, V2 P* ^; ?* r0 x! d; b, h
and β-human chorionic gonadotropin was less than
0 c4 @. w' t% d5 mIU/mL (normal <5 mIU/mL). Serum follicular9 ]" X R9 R' l8 k; |% g& ?; ^7 h
stimulating hormone and leuteinizing hormone& D# F# e$ c8 x n0 A U, G/ |5 _/ v
concentrations were less than 0.05 mIU/mL
1 _& t! N/ G3 e( r( w(prepubertal).3 D/ o! R( h' _2 J# l) H
The parents were notified about the laboratory) I0 d# E: F9 v1 l5 k
results and were informed that all of the tests were5 s$ _. R0 n$ S2 u6 l! G
normal except the testosterone level was high. The8 L) ]! K6 j$ [( U* F
follow-up visit was arranged within a few weeks to4 G9 d5 n9 q8 X4 V
obtain testicular and abdominal sonograms; how-
; j+ n a' }4 L5 d2 Aever, the family did not return for 4 months.5 L6 K! Y1 r( K( T2 z f0 |
Physical examination at this time revealed that the7 a2 o4 A% Z2 f, }4 s
child had grown 2.5 cm in 4 months and had gained
4 g1 J/ F& `# P3 k$ g% Q: y( O# Y+ a2 kg of weight. Physical examination remained
& f- g* u1 y1 z6 S( a- tunchanged. Surprisingly, the pubic hair almost com-( t6 [7 u) I+ F( t( n
pletely disappeared except for a few vellous hairs at
8 k) q1 w7 g. N0 ~4 w0 x1 I8 Rthe base of the phallus. Testicular volume was still 2* j( A: u! C3 n* A3 I$ W1 W
mL, and the size of the penis remained unchanged.
1 L* j3 r j7 Q* v4 `/ X6 {) v u/ UThe mother also said that the boy was no longer hav-
! R7 \0 z1 Q6 _: n+ ~# king frequent erections.
% P0 h' E+ G0 t% ? X0 p3 k+ ]/ ^Both parents were again questioned about use of
+ Y. E9 o! z! `: F' b0 dany ointment/creams that they may have applied to
5 i- L0 { f! S; [the child’s skin. This time the father admitted the
; ` h# W1 a4 B _Topical Testosterone Exposure / Bhowmick et al 541
: m% x; M0 x4 j1 O- ~use of testosterone gel twice daily that he was apply-2 f: Q0 C4 K& t1 V
ing over his own shoulders, chest, and back area for7 ~1 I# y5 B1 J1 G; q
a year. The father also revealed he was embarrassed
- d# H: `5 |9 K* q5 cto disclose that he was using a testosterone gel pre-& b0 O' I# c1 r3 i1 @* m
scribed by his family physician for decreased libido( A( P! J, n3 K7 W* K$ Y4 ~
secondary to depression.; m$ y+ \- A6 J2 l+ `- h
The child slept in the same bed with parents.
; J7 E% Z" V! p6 g4 ^8 dThe father would hug the baby and hold him on his
- T+ l% |4 p$ Q$ }- h& Hchest for a considerable period of time, causing sig-
9 T6 J2 Z- _- Y3 W$ A. hnificant bare skin contact between baby and father.
& ]7 N: v& U* _- K" @$ f6 nThe father also admitted that after the phone call,: u: l! k1 d& V5 I( r
when he learned the testosterone level in the baby
! _8 G! D7 p9 w/ D+ J4 F/ ?was high, he then read the product information
# h% `; y: [3 ]9 F1 Tpacket and concluded that it was most likely the rea-- d* |8 ]6 A) ? y
son for the child’s virilization. At that time, they
6 I! ^8 V* V! w- x! cdecided to put the baby in a separate bed, and the0 u& Z: Z) L! T& t, I: V8 D( |
father was not hugging him with bare skin and had
! O0 i. H/ r: y2 P" cbeen using protective clothing. A repeat testosterone
3 X7 w" Q6 `% h5 h' G2 t0 itest was ordered, but the family did not go to the0 b6 a2 Y8 f+ @* [; R4 h( S
laboratory to obtain the test.
L) k. `7 Y7 G% d- f8 D2 @Discussion
2 g; Y! f( n# r" T {Precocious puberty in boys is defined as secondary, }0 q+ h5 A$ w$ l% M: H, s
sexual development before 9 years of age.1,4: a& y6 C+ V4 r m9 I0 O
Precocious puberty is termed as central (true) when
" T! R( n# v) C! C+ ]1 p3 H5 Pit is caused by the premature activation of hypo-; \- n9 W: F2 S. M& w3 a
thalamic pituitary gonadal axis. CPP is more com-
1 h# C* Y9 `7 b9 J8 U) A# }) H, [mon in girls than in boys.1,3 Most boys with CPP8 @- T% I6 S# C; Z
may have a central nervous system lesion that is
% {. G: J6 P7 \* C; q* Z) Aresponsible for the early activation of the hypothal-, f; A% {6 j* R8 O
amic pituitary gonadal axis.1-3 Thus, greater empha-
( j' Z, C& N1 l9 Y4 n& I0 q; Fsis has been given to neuroradiologic imaging in& f: O N6 K. c# g8 m i8 _0 H& l
boys with precocious puberty. In addition to viril-
4 J: `9 O2 p# Hization, the clinical hallmark of CPP is the symmet-( \7 M$ d2 Q3 l
rical testicular growth secondary to stimulation by4 [; i+ E9 E' L
gonadotropins.1,3
# i" j9 n' e( x7 w: q' n- \7 [Gonadotropin-independent peripheral preco-
" I C7 q/ \& k4 f/ Mcious puberty in boys also results from inappropriate- a P5 b& m, C+ |3 V: ]# T C
androgenic stimulation from either endogenous or/ E, l% [; t! h2 r% ` d; \1 L
exogenous sources, nonpituitary gonadotropin stim-8 R& ]5 h9 B1 W0 ]
ulation, and rare activating mutations.3 Virilizing
: o9 B' Z' v0 O" W' @, ]. wcongenital adrenal hyperplasia producing excessive
8 m. w1 E& B. Y% N- ~& p. yadrenal androgens is a common cause of precocious, N$ g+ A) v1 r# A9 F5 J e! G' Z
puberty in boys.3,4
) p( l7 v/ ~1 y$ [The most common form of congenital adrenal
* [* d- `/ ?7 Q' v& p) s' v2 Yhyperplasia is the 21-hydroxylase enzyme deficiency.
: t# m! x- l6 k7 S0 e( T8 VThe 11-β hydroxylase deficiency may also result in
1 ]8 [7 v3 p9 @4 yexcessive adrenal androgen production, and rarely,0 r& G9 u7 g4 i- x
an adrenal tumor may also cause adrenal androgen
2 x* N( F+ ?8 f/ M, sexcess.1,33 t4 W/ ]7 H- C& O) I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; ^$ o. O6 g/ e' ^( A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, s0 p# C1 E4 c5 ]9 F( l
A unique entity of male-limited gonadotropin-* O" |4 @' x ~9 q
independent precocious puberty, which is also known
3 d) h! r5 S, `, k) F, b4 \9 Jas testotoxicosis, may cause precocious puberty at a0 \/ c) _: @ L+ |0 d
very young age. The physical findings in these boys
& C& S2 E4 R0 s8 q) y; o2 u/ Pwith this disorder are full pubertal development,) C: c( d, }$ ?0 t% @. ]9 @
including bilateral testicular growth, similar to boys
# g6 D0 G1 k7 L% K- Xwith CPP. The gonadotropin levels in this disorder
2 V& r7 X, H7 S$ }" P) ^are suppressed to prepubertal levels and do not show
- u& m9 ^. j: B" U4 Dpubertal response of gonadotropin after gonadotropin-
6 O" }8 W# I# g- s0 areleasing hormone stimulation. This is a sex-linked; j! C. x) U- c( R' i
autosomal dominant disorder that affects only. Y, X- |- d; |
males; therefore, other male members of the family
% C' r/ X+ M3 \2 Umay have similar precocious puberty.3
! s1 p6 |! b" r9 mIn our patient, physical examination was incon-9 f* U5 O r/ o6 T. Y' H
sistent with true precocious puberty since his testi-
$ p8 L G) p; Y* Ncles were prepubertal in size. However, testotoxicosis
3 K! O) W9 v' e/ P! D+ g$ w: ywas in the differential diagnosis because his father, w8 d3 z0 \1 X D; ?
started puberty somewhat early, and occasionally,3 [# J. j6 B6 Y( s+ D% `
testicular enlargement is not that evident in the1 M% e( n% S' m# o4 _
beginning of this process.1 In the absence of a neg-
' |4 Y1 B' ?' s- t9 hative initial history of androgen exposure, our1 I9 r/ E6 E8 f9 z
biggest concern was virilizing adrenal hyperplasia, @7 ~5 V0 V* C' |- f
either 21-hydroxylase deficiency or 11-β hydroxylase! F7 w1 Q$ C4 D/ T" Y
deficiency. Those diagnoses were excluded by find-& B% k' I, R2 C! {& P! R* g
ing the normal level of adrenal steroids.; O r' n5 T% ~
The diagnosis of exogenous androgens was strongly" w2 Y; _ ]- S. O4 G+ v+ k
suspected in a follow-up visit after 4 months because
# m( }% m( i- q" [the physical examination revealed the complete disap-, j( e( C) W8 q3 \7 j
pearance of pubic hair, normal growth velocity, and
. c0 p) X( x3 u2 G( t# ?8 ddecreased erections. The father admitted using a testos-
) S; V) A- ]1 x9 k3 Y) bterone gel, which he concealed at first visit. He was/ Y* R" N. Z4 f/ j8 t
using it rather frequently, twice a day. The Physicians’
) Z& \8 h3 [7 g5 H# wDesk Reference, or package insert of this product, gel or
* l1 C, b6 R7 Q: [$ a1 S( O e( U0 vcream, cautions about dermal testosterone transfer to7 ?7 }8 K' m8 \! U( i
unprotected females through direct skin exposure.
# a3 |7 E8 U( Q+ i1 v' d) t. tSerum testosterone level was found to be 2 times the# C9 C( \# u7 g
baseline value in those females who were exposed to
* h/ c5 u3 U+ ^- C7 K0 m# |* B( teven 15 minutes of direct skin contact with their male# d% w! ]: x4 F* \
partners.6 However, when a shirt covered the applica-% }0 D" [3 U+ R1 m+ s
tion site, this testosterone transfer was prevented.
/ W4 X8 P+ q+ QOur patient’s testosterone level was 60 ng/mL,# j' t/ {; M- R7 F3 V+ q5 {& F
which was clearly high. Some studies suggest that
; {) M8 a/ |7 j( m# X7 D ^dermal conversion of testosterone to dihydrotestos-) R/ F. U6 {4 Z: e% D, u5 e0 q
terone, which is a more potent metabolite, is more
w( C7 M9 N% J2 ^/ R$ u+ W: tactive in young children exposed to testosterone8 w$ \0 I1 q7 M% M, o2 ]2 L9 C
exogenously7; however, we did not measure a dihy-4 v. {; X$ v: T) f( z
drotestosterone level in our patient. In addition to
& K3 Z: v: } ]- U1 |; jvirilization, exposure to exogenous testosterone in5 K# S: P Y, w* S" n' m5 `$ |# }
children results in an increase in growth velocity and
2 _9 f4 p0 U0 Q j: l3 x2 |* \advanced bone age, as seen in our patient.
" `' s) ]$ F$ C& `4 D; c& LThe long-term effect of androgen exposure during8 f+ u: @- M. N% ~, L: g
early childhood on pubertal development and final, r( |+ t" J+ K m. m
adult height are not fully known and always remain7 [4 ?, |' i0 Y; j
a concern. Children treated with short-term testos-
7 ]9 T, d3 Y& i" X/ a6 V" [terone injection or topical androgen may exhibit some
) H7 }+ f/ v$ g& X& ^: Aacceleration of the skeletal maturation; however, after0 M2 r9 h$ Q+ I1 `# g% O" u
cessation of treatment, the rate of bone maturation
6 T$ @) y" k! p! S- k2 \decelerates and gradually returns to normal.8,92 Y3 o4 F4 Y- j. Z) V
There are conflicting reports and controversy6 B# h g0 _; s
over the effect of early androgen exposure on adult) T8 r" |, T# V0 L) c
penile length.10,11 Some reports suggest subnormal& I1 D9 x) o6 A9 H' m
adult penile length, apparently because of downreg-
{ S5 L0 M; [* t% z4 Bulation of androgen receptor number.10,12 However,
5 n1 l5 ^/ e3 ?" nSutherland et al13 did not find a correlation between+ P0 u% O% C7 h n7 W4 Y$ @
childhood testosterone exposure and reduced adult
! @) y) U' c; O8 A# Ipenile length in clinical studies.
/ [+ F2 S& U1 o" r- kNonetheless, we do not believe our patient is/ _$ U# |& Q* J; j/ p0 v `
going to experience any of the untoward effects from- ~" E8 v% W0 y N( V! R
testosterone exposure as mentioned earlier because, m% N/ v) Y" p( G/ o; r
the exposure was not for a prolonged period of time.
( p7 c3 `4 e. v! gAlthough the bone age was advanced at the time of" ^# T1 L/ s; R
diagnosis, the child had a normal growth velocity at
4 U# T3 w* I6 bthe follow-up visit. It is hoped that his final adult: o+ Q" q1 t- l9 y H
height will not be affected.7 ?" j* K- o1 M$ _# O$ p, A
Although rarely reported, the widespread avail-/ U8 h3 T- X! N- H6 E* {
ability of androgen products in our society may' v4 j3 b0 U- n: j6 V
indeed cause more virilization in male or female
: p$ v: T \/ {* m# s# g8 Mchildren than one would realize. Exposure to andro-8 T1 \6 z# h( H! h3 i
gen products must be considered and specific ques-, A/ m5 f2 d" t" C
tioning about the use of a testosterone product or5 O0 V! K3 w5 }: L9 F
gel should be asked of the family members during' u; [3 l% H; T2 c; T! ]% K
the evaluation of any children who present with vir-, Q# O4 c. P6 C9 o2 d4 Z
ilization or peripheral precocious puberty. The diag-, _! ~5 A5 g; d+ j7 X
nosis can be established by just a few tests and by8 P1 z. U+ u6 O
appropriate history. The inability to obtain such a& g `8 E/ Q0 e( W
history, or failure to ask the specific questions, may8 L5 ?$ q' j* L" M8 n. }- v3 o
result in extensive, unnecessary, and expensive( D, P* f% j8 ^% Q3 v* m4 z% F% t
investigation. The primary care physician should be' P* l& n% G5 k. z3 d& u
aware of this fact, because most of these children* i. W; y: ~* S% d; |
may initially present in their practice. The Physicians’) G) k* b$ E+ v: r' N$ h; }
Desk Reference and package insert should also put a0 G( J" |% i" B! P/ I! {% m
warning about the virilizing effect on a male or. w6 Y/ ?; M. @( J0 Z5 N7 y- }7 Y
female child who might come in contact with some-
. g! \1 y! _' s! D" @one using any of these products.
+ l9 k5 E) Y6 c' R0 e* a) X7 Y0 nReferences
- b; ?" `" E! t2 N) w' d1. Styne DM. The testes: disorder of sexual differentiation% b# m! d+ f: U; _: } @6 X
and puberty in the male. In: Sperling MA, ed. Pediatric
: }7 C3 v3 w) fEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" T3 r6 o) R8 ]* Y2002: 565-628.
; ]8 v$ _; c; t, `9 ^, b, b# f+ y9 r% w2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% r X X7 S0 s% {" {, g# D& ~puberty in children with tumours of the suprasellar pineal |
|