- 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
" l4 E3 F* s2 w" O; E4 b: _Boy Induced by Indirect Topical2 x& f: v5 a- p3 ?3 Z
Exposure to Testosterone
: Z, s- i, n5 W+ E; S5 pSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: h+ W, O" P' ~ d& R+ \and Kenneth R. Rettig, MD1% s6 w& V; t, x" X D [5 q
Clinical Pediatrics
& n& N* R# \8 z' b2 G2 ^Volume 46 Number 6; V; X+ v1 S) @0 H' H3 g
July 2007 540-5434 z( ^4 \3 m: {. V0 }, n3 o
© 2007 Sage Publications" K$ Z0 A/ B/ ]. B+ t0 _2 t/ F/ Q% @2 @
10.1177/00099228062966513 ~& @& K* o+ e# f* x
http://clp.sagepub.com5 Y+ N& X+ d. e8 g: j4 [
hosted at
5 q2 }) i- C' g# C. s, P+ ohttp://online.sagepub.com& x$ J, P" M9 G7 V I
Precocious puberty in boys, central or peripheral,& H/ |( r3 a1 n$ G
is a significant concern for physicians. Central( H" M9 ~: b1 f5 ^2 p4 `
precocious puberty (CPP), which is mediated# K5 ?7 [ k- P- w' E
through the hypothalamic pituitary gonadal axis, has
! {, {& t8 X9 T! [2 v+ Ra higher incidence of organic central nervous system9 z2 C- Q2 A$ x& N" d0 q2 q
lesions in boys.1,2 Virilization in boys, as manifested' d( A& K! [* i9 V, A
by enlargement of the penis, development of pubic5 f/ R/ a; E* ~! q/ S# p3 u) E5 F, G J
hair, and facial acne without enlargement of testi-% d* U4 g/ }% t4 \! f! ^4 I2 O
cles, suggests peripheral or pseudopuberty.1-3 We
/ j# N# X' B) Mreport a 16-month-old boy who presented with the3 j I0 g0 b# c% d/ B
enlargement of the phallus and pubic hair develop-. k5 y0 p; M `5 W1 L
ment without testicular enlargement, which was due, [/ H4 e) z7 A C% _& Z$ m
to the unintentional exposure to androgen gel used by- P: c( g \4 T( M6 ^) Z0 {
the father. The family initially concealed this infor-
9 ]! ?/ q' X6 U$ d$ r. Pmation, resulting in an extensive work-up for this! d `; b& v% q8 h, h
child. Given the widespread and easy availability of
0 y8 C) e5 u. w2 l; ~2 |testosterone gel and cream, we believe this is proba-
; B8 {+ w" k1 l2 c; v& dbly more common than the rare case report in the' {; w$ [* E. O3 n- q& u4 S; o
literature.4
8 R" K5 v8 k$ iPatient Report% f ^' @8 o: B+ y' Y/ o4 U+ d
A 16-month-old white child was referred to the% h7 e0 ^- I: c" E
endocrine clinic by his pediatrician with the concern
9 [# W! u# Y. j3 _of early sexual development. His mother noticed) t0 l: G, O1 g1 a5 M/ b
light colored pubic hair development when he was9 T0 g8 P' O, N( W* r" \, Z
From the 1Division of Pediatric Endocrinology, 2University of- g- c+ r! {& A; ~0 N0 Q+ l
South Alabama Medical Center, Mobile, Alabama.
1 P% G# G2 m0 F6 HAddress correspondence to: Samar K. Bhowmick, MD, FACE,
* R" v. g, A; }. e# k* }% U" JProfessor of Pediatrics, University of South Alabama, College of/ e8 Y+ i8 |0 \- b; u
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- d) S M1 K6 Xe-mail: [email protected].2 d/ [% a* `6 l+ K5 }% K
about 6 to 7 months old, which progressively became
) ]. M U+ u3 Hdarker. She was also concerned about the enlarge-! K' i0 t" a0 g' K
ment of his penis and frequent erections. The child+ d- \' O$ i& W9 P3 b e, C
was the product of a full-term normal delivery, with! L6 e. _8 x" z( @! J; u8 M# n0 E, q
a birth weight of 7 lb 14 oz, and birth length of
$ J1 v% |( j: \0 w+ [20 inches. He was breast-fed throughout the first year0 M! Y- _9 m$ ~
of life and was still receiving breast milk along with
4 s; r) } ^1 Ksolid food. He had no hospitalizations or surgery,2 ^, ~, y c8 Y+ r5 i' l
and his psychosocial and psychomotor development
0 u3 J8 U; G* V9 f* G* R+ ?5 bwas age appropriate.6 |% K* h3 ~) A4 T% R3 a( b
The family history was remarkable for the father,
+ F& R7 b: b5 ^% s% ?1 k* N. Awho was diagnosed with hypothyroidism at age 16,, }( f9 ?1 Q& [+ Y% D+ p( }
which was treated with thyroxine. The father’s
5 `2 ~/ j, r+ R- R+ ?- p0 Hheight was 6 feet, and he went through a somewhat* W3 b0 p( H7 x. @- g
early puberty and had stopped growing by age 14.. B& R3 e! l: a; y4 A
The father denied taking any other medication. The
3 ?* k4 M8 `5 ~" H( Mchild’s mother was in good health. Her menarche1 j# p: x; _- r, m
was at 11 years of age, and her height was at 5 feet
, _$ R/ e) M# r5 s8 p0 L8 o5 E2 L5 inches. There was no other family history of pre-1 h* N, D- d, n# T% N& }& M
cocious sexual development in the first-degree rela-. P% O+ Y6 t/ l
tives. There were no siblings.4 W" U. S/ f5 G
Physical Examination j4 i( N9 ~8 C% k5 P, o( c3 _. I
The physical examination revealed a very active,
, M) P( Y9 i; `, I; u) yplayful, and healthy boy. The vital signs documented3 `2 q e/ ^, Z4 v! ?
a blood pressure of 85/50 mm Hg, his length was# {$ \: W0 C4 H
90 cm (>97th percentile), and his weight was 14.4 kg( c- `+ y. Y# c1 E8 j ?$ x
(also >97th percentile). The observed yearly growth: L! G- g: \+ o# k: } ?
velocity was 30 cm (12 inches). The examination of
% B3 i7 G. r1 {4 ^0 mthe neck revealed no thyroid enlargement.
/ M& q. J8 z ~! v eThe genitourinary examination was remarkable for0 Q' @1 C8 I7 l3 l7 O5 F9 B5 q
enlargement of the penis, with a stretched length of/ j0 w" h% g% c% B: _$ F- \
8 cm and a width of 2 cm. The glans penis was very well7 M, |2 X" Q3 L
developed. The pubic hair was Tanner II, mostly around
. F, q ^( W: C6 U! I! W) ^8 c5409 _! c4 K0 _3 @# S5 d5 @- X8 g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: Z! W# j6 c h9 t3 |0 d/ D) a0 xthe base of the phallus and was dark and curled. The* j2 @ n/ v4 [- u$ _5 {" U
testicular volume was prepubertal at 2 mL each.
! e0 W! H0 X0 \9 R) h1 vThe skin was moist and smooth and somewhat
6 o/ A+ V. |. A! X$ Poily. No axillary hair was noted. There were no
% E" X/ ^3 J1 x ]7 V! [9 zabnormal skin pigmentations or café-au-lait spots.
- e& W! A4 v7 e* v- xNeurologic evaluation showed deep tendon reflex 2+
- }6 h b* `: b! Hbilateral and symmetrical. There was no suggestion
$ {8 S& u( E1 i& I: tof papilledema.
& ?! x |) z* b3 _5 F" O$ XLaboratory Evaluation
- i- T5 t6 a* n' W+ K1 y' }- r- fThe bone age was consistent with 28 months by2 D+ [; A/ O, B
using the standard of Greulich and Pyle at a chrono-' p) _% e( t r0 V4 g
logic age of 16 months (advanced).5 Chromosomal
; u4 |0 s" [1 Q$ u6 R6 Skaryotype was 46XY. The thyroid function test. ?; i# J$ C; U5 G' B, i/ C
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 E& f) L/ [. _9 Z2 ]* }0 W
lating hormone level was 1.3 µIU/mL (both normal).
2 |+ t4 v" s$ [* i" \' YThe concentrations of serum electrolytes, blood
* @$ _; o' Y! ^4 Purea nitrogen, creatinine, and calcium all were u, s9 H1 q u; L
within normal range for his age. The concentration1 X& n( n1 b' n
of serum 17-hydroxyprogesterone was 16 ng/dL
/ C" n' K. j6 b; @( |+ M! Q(normal, 3 to 90 ng/dL), androstenedione was 20
# s$ M0 ~. p3 W8 r. |2 }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ J9 Z( q6 u( S E2 k$ c4 k# [
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
$ U6 z5 I- |7 r- x i" f; Ndesoxycorticosterone was 4.3 ng/dL (normal, 7 to/ w2 }/ _$ N% ?
49ng/dL), 11-desoxycortisol (specific compound S)+ V: a# C2 J+ P" b7 M/ e5 N( \
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 t4 }, ^5 s# f* \0 p
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 G; _2 l. @# j# a; M& F; [3 S0 N3 ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 x4 U9 x2 N) u& i% E2 p1 eand β-human chorionic gonadotropin was less than
& m/ I0 L5 n. R5 mIU/mL (normal <5 mIU/mL). Serum follicular5 |+ g! ~: p2 H9 T5 f
stimulating hormone and leuteinizing hormone& t3 X3 ~, M7 A \
concentrations were less than 0.05 mIU/mL
( R ^2 s* B* O(prepubertal).
( Z7 i6 g- D, ~ l, ?The parents were notified about the laboratory
# \8 R; L7 A8 f, L9 xresults and were informed that all of the tests were
8 X* W' T- w" F7 Pnormal except the testosterone level was high. The5 O* h- P/ P. { T9 I
follow-up visit was arranged within a few weeks to
8 r q6 s' g. l! ?6 z) w; o& tobtain testicular and abdominal sonograms; how-& M3 \# N& p1 M0 l) l
ever, the family did not return for 4 months.0 @) F# u% ]- @& y$ v' U+ V, x
Physical examination at this time revealed that the
+ f5 Q: t; s7 }# achild had grown 2.5 cm in 4 months and had gained
0 I$ l; J: Y* V( D* A6 |: A- u) x2 kg of weight. Physical examination remained3 i* X: {! t% c& ^: k
unchanged. Surprisingly, the pubic hair almost com-
6 @4 a% b! [- F! Zpletely disappeared except for a few vellous hairs at
/ l0 y K& T1 W* ethe base of the phallus. Testicular volume was still 2
% c0 k' I+ ?; ImL, and the size of the penis remained unchanged.
* M# K, f! @! |, z/ v& U* h2 RThe mother also said that the boy was no longer hav-4 V9 M; q) V9 T' b7 |
ing frequent erections.
; c; D6 b r/ D0 y& H2 k( ZBoth parents were again questioned about use of$ V0 O9 k+ ]4 ^5 p! H
any ointment/creams that they may have applied to/ F; V! [6 L' n. ^' P
the child’s skin. This time the father admitted the. v9 e1 G/ S- n% b
Topical Testosterone Exposure / Bhowmick et al 541
! }7 M P/ P9 d. R: K2 J3 Ruse of testosterone gel twice daily that he was apply-
" r! B3 F' q6 @8 H! king over his own shoulders, chest, and back area for
2 ?$ P- m, ^3 o2 va year. The father also revealed he was embarrassed6 U5 M- g* I) ~
to disclose that he was using a testosterone gel pre-# @$ x4 |5 c& N# u% K
scribed by his family physician for decreased libido
" w9 t5 p7 |3 b2 q: h4 k2 c9 _secondary to depression.' _% k: D8 a1 ]: o0 R, q
The child slept in the same bed with parents.6 b/ ]0 l) ^6 l# k. @8 b
The father would hug the baby and hold him on his
. m3 Q o, T) kchest for a considerable period of time, causing sig-6 C7 U6 ^8 i( f5 U( A0 I
nificant bare skin contact between baby and father.% T3 j9 J+ C+ Q
The father also admitted that after the phone call,
R1 X2 C$ j4 ^4 m( Pwhen he learned the testosterone level in the baby
3 e6 G/ o/ A# k; Y# O7 Nwas high, he then read the product information) Q! V; t* m$ }% s( Q3 w* S; J, N, K
packet and concluded that it was most likely the rea-
% b, B* l! X v$ h% W9 qson for the child’s virilization. At that time, they+ h* Z& D; P6 A, U! @- l8 Z
decided to put the baby in a separate bed, and the) T4 j. g! G8 R( j- ~* n
father was not hugging him with bare skin and had
7 g; \! l4 \1 ~$ ^! u4 @been using protective clothing. A repeat testosterone. j3 R( \' n* x9 N
test was ordered, but the family did not go to the' R2 R5 B2 ~( k3 s4 Z. W% B5 y+ l
laboratory to obtain the test.
0 l" c8 z8 ]6 v2 pDiscussion) u2 D3 J% e' w# G" i
Precocious puberty in boys is defined as secondary
' ~/ e* ?$ Y4 V! I2 U. |sexual development before 9 years of age.1,4
, N: @0 U/ x/ B' V, g9 |4 ]( [ ZPrecocious puberty is termed as central (true) when4 P# a& z# ^, O' [* ^* g* |: k
it is caused by the premature activation of hypo-: t+ Q) o4 I1 A6 T
thalamic pituitary gonadal axis. CPP is more com-! f6 z2 @. a$ A1 g! z) X
mon in girls than in boys.1,3 Most boys with CPP+ [0 C# \% ]- U! J
may have a central nervous system lesion that is
9 \1 B; p+ s" _5 K. \$ Zresponsible for the early activation of the hypothal-! A& f4 `# q, D$ Y0 H; \) T' _
amic pituitary gonadal axis.1-3 Thus, greater empha-
5 P4 g( h3 ?/ l/ jsis has been given to neuroradiologic imaging in
( ]/ l6 c* e+ W# @( v& t/ f* y! J" iboys with precocious puberty. In addition to viril-1 Z: P$ g( u! G5 i
ization, the clinical hallmark of CPP is the symmet-
% `# _# A) M: s5 Erical testicular growth secondary to stimulation by. k. }: U' K4 i8 e$ P0 j/ |
gonadotropins.1,3
6 x; ]- ?- e% T, A+ GGonadotropin-independent peripheral preco-+ C u7 H3 _9 r
cious puberty in boys also results from inappropriate. z( j$ H# N7 g$ B8 u4 a
androgenic stimulation from either endogenous or
/ @1 S4 E+ e" E5 S0 T2 r5 l! sexogenous sources, nonpituitary gonadotropin stim-. @2 k8 A& u) W3 D- ?$ q0 l
ulation, and rare activating mutations.3 Virilizing
/ _) S' i, z/ z; g x, U* Qcongenital adrenal hyperplasia producing excessive
' s# ^5 l0 J% I3 r/ R& X6 `- w: C6 h& ladrenal androgens is a common cause of precocious
9 O3 B* u ?/ Y9 B/ y2 t {puberty in boys.3,4' N0 b8 [6 S, w% u! l8 p$ Q
The most common form of congenital adrenal
' `* K# _7 q" e y. h! {hyperplasia is the 21-hydroxylase enzyme deficiency.. U! u2 _# H' _4 S8 t# S
The 11-β hydroxylase deficiency may also result in
0 {4 S, y3 c V6 V* ~* O2 rexcessive adrenal androgen production, and rarely,: [2 g: J+ `$ X* s
an adrenal tumor may also cause adrenal androgen! z/ ] a+ H1 P
excess.1,3
* T, \( O- z- ^- f( pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& k. i. {8 `7 ^9 g9 o) T
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; j2 O. H2 v1 e" F% c* D6 c# \3 cA unique entity of male-limited gonadotropin-
" d1 M2 s0 N7 n0 i1 a+ p; Nindependent precocious puberty, which is also known6 X! k7 _2 d: ~- A7 c
as testotoxicosis, may cause precocious puberty at a1 j6 }3 ]) Y' {- T E
very young age. The physical findings in these boys. w0 H: r; u* B" y a4 L7 l
with this disorder are full pubertal development,1 z: P* T9 U8 H% t5 n
including bilateral testicular growth, similar to boys! z# v; R3 r$ e; z- k
with CPP. The gonadotropin levels in this disorder* t2 N0 t9 e$ V
are suppressed to prepubertal levels and do not show
" H2 l% H( O' o- I( a' z% Ppubertal response of gonadotropin after gonadotropin-
6 x6 d A0 o7 {6 e+ M5 w l e, u! J dreleasing hormone stimulation. This is a sex-linked
5 v! a5 K' [3 `0 k6 L4 _autosomal dominant disorder that affects only
, ~* a* p9 f$ S$ C! v d$ wmales; therefore, other male members of the family
- G& f1 i. O" |may have similar precocious puberty.3# I! V' m$ e" R( D5 }# Y/ t$ X2 ]
In our patient, physical examination was incon-8 j+ R! h2 j8 e* D) o: W
sistent with true precocious puberty since his testi-
3 I. p K% \; o4 U8 m& Ecles were prepubertal in size. However, testotoxicosis
' F6 r6 a, k6 swas in the differential diagnosis because his father2 e$ t0 w+ ]+ i' i- b
started puberty somewhat early, and occasionally,- y( f: a$ {2 @, O
testicular enlargement is not that evident in the' s% f: b, I5 _, m" v/ s
beginning of this process.1 In the absence of a neg- ?! h+ L3 z, X3 x- k5 K1 E6 c7 e
ative initial history of androgen exposure, our" N0 ^0 v# h$ ~$ @. |" A& Z- Y
biggest concern was virilizing adrenal hyperplasia,# r% v( l* ]+ \7 @; u" U4 c
either 21-hydroxylase deficiency or 11-β hydroxylase
! }7 P. ?, I; Ndeficiency. Those diagnoses were excluded by find-
, k' j$ j S# V8 k5 g5 e0 e ring the normal level of adrenal steroids.0 `- O% x: `/ s, U$ E' s9 X* q
The diagnosis of exogenous androgens was strongly7 P- R, q# z( u( C" N. O7 t2 {
suspected in a follow-up visit after 4 months because
5 C# R. o/ f Ithe physical examination revealed the complete disap-1 ]! m2 W# c8 @; P* X
pearance of pubic hair, normal growth velocity, and
/ B1 |, p- T2 J/ G8 G; {decreased erections. The father admitted using a testos-( w* e/ C8 s2 p. Z! O9 L
terone gel, which he concealed at first visit. He was
+ _8 x3 z/ N# Jusing it rather frequently, twice a day. The Physicians’
+ \3 ~' O5 |8 e/ V0 ZDesk Reference, or package insert of this product, gel or
/ c3 a( W. s; p8 m; k1 H' W: i# hcream, cautions about dermal testosterone transfer to
* f2 D& X; o5 K1 ~9 }; @unprotected females through direct skin exposure.& h- |4 M0 n/ I. A" m2 D, I
Serum testosterone level was found to be 2 times the
& c$ q" ?& Q$ ^. e5 k; a, y+ }baseline value in those females who were exposed to# @; k! f8 U' M* e2 I
even 15 minutes of direct skin contact with their male
: G; h9 @3 o- g! K+ ?- M3 k/ ]. qpartners.6 However, when a shirt covered the applica-) M( A8 E/ n1 `. }( i7 x
tion site, this testosterone transfer was prevented.0 P2 h' N) j9 w! ~7 o5 M! ~1 c0 M F
Our patient’s testosterone level was 60 ng/mL,
1 |; m( T3 s& |. wwhich was clearly high. Some studies suggest that8 Z, D8 [- ` B( a K
dermal conversion of testosterone to dihydrotestos-
1 Q2 i# [+ a2 N; F% nterone, which is a more potent metabolite, is more
1 ^" P8 p3 d/ X+ iactive in young children exposed to testosterone$ u4 q# j. a8 L. s
exogenously7; however, we did not measure a dihy-
0 N+ ^0 l0 y5 p6 P2 m/ Y2 G4 {drotestosterone level in our patient. In addition to/ t: E4 J, k% E
virilization, exposure to exogenous testosterone in+ X% r, d4 F4 W X8 ^* A
children results in an increase in growth velocity and
G& H5 _: r5 F& tadvanced bone age, as seen in our patient.
2 R) E5 {9 s" h% KThe long-term effect of androgen exposure during
( n1 y" d b- r* s/ E6 o, kearly childhood on pubertal development and final
8 S- q2 [2 @. qadult height are not fully known and always remain6 v' S( D2 F+ g0 T3 E. R
a concern. Children treated with short-term testos-- r& b+ v+ [: G+ ?2 Y( v6 Z& s8 [
terone injection or topical androgen may exhibit some& E( r) ^1 Z9 {( T
acceleration of the skeletal maturation; however, after
: \7 _7 K$ E/ t+ ycessation of treatment, the rate of bone maturation
( M% ^: U$ f, y; y1 adecelerates and gradually returns to normal.8,9% Q w2 k" t9 a$ A j, W8 R9 m J- Q
There are conflicting reports and controversy
, ?# M: G, N/ z9 j* F! P! O: Zover the effect of early androgen exposure on adult
" c* T7 _) Z3 e, f, K; Rpenile length.10,11 Some reports suggest subnormal
" o2 H# [7 x% D/ Radult penile length, apparently because of downreg-! n/ N) B4 R* q$ ^) I
ulation of androgen receptor number.10,12 However,6 D- ^, \" `0 r' L
Sutherland et al13 did not find a correlation between! {) `! `. i$ k9 z5 Y( }# }8 a" A
childhood testosterone exposure and reduced adult) P1 V! [5 [) Z
penile length in clinical studies.3 p9 j1 a: E: S; a
Nonetheless, we do not believe our patient is/ y. ]: M5 @0 j+ \* K% W
going to experience any of the untoward effects from/ ]/ k1 g' f* a8 T1 D# p. {3 K5 D
testosterone exposure as mentioned earlier because
( }# Z A" i4 M3 Ethe exposure was not for a prolonged period of time.+ m1 u, P4 h$ U6 ]& e
Although the bone age was advanced at the time of9 J* j* x$ ~6 S! g) H
diagnosis, the child had a normal growth velocity at
2 N* _! h- b# \9 t7 m7 Sthe follow-up visit. It is hoped that his final adult
/ }) m1 X3 s( R. Aheight will not be affected.
. H6 Y! g; g) `! } h1 w4 UAlthough rarely reported, the widespread avail-3 A/ s* D8 R' z+ w
ability of androgen products in our society may
6 _2 n# G4 y% r. _# q4 ?7 Windeed cause more virilization in male or female
. f1 U/ H2 }2 i0 pchildren than one would realize. Exposure to andro-. L [, V& X& J+ a- a% }
gen products must be considered and specific ques-: O U3 v5 x/ O3 j$ y4 ^
tioning about the use of a testosterone product or0 u; G9 u- ~6 b3 N! O# v. x. M
gel should be asked of the family members during
$ D3 @+ U3 N9 k2 _/ \) Z& m/ Gthe evaluation of any children who present with vir-( \* _9 D" T/ [* V# e2 ~7 W) c
ilization or peripheral precocious puberty. The diag-$ ?, @6 `1 v" h0 d7 ~( p0 X7 s
nosis can be established by just a few tests and by/ ~' E7 i, Z8 m* c* C" J. T4 }7 q
appropriate history. The inability to obtain such a9 `1 u1 z% R- ?/ W" M9 \* N0 f% p
history, or failure to ask the specific questions, may
% E8 {# S, x& N5 @/ C- ]: Yresult in extensive, unnecessary, and expensive$ n: c, |* u* T8 A4 C3 d9 W' u7 ?
investigation. The primary care physician should be8 ?8 A1 P/ s+ N' K' E
aware of this fact, because most of these children
# S+ M. _0 T2 y2 d+ {; ]may initially present in their practice. The Physicians’
/ O$ Q+ P \- {6 V- Q$ }6 \& T3 a" ADesk Reference and package insert should also put a
( g. v6 R2 O, y2 T+ c& Vwarning about the virilizing effect on a male or
j7 u+ a6 }0 Z1 i( A; m' T' Ofemale child who might come in contact with some-* H5 ?8 y, e% f% e
one using any of these products.
3 m* c2 C4 M5 R; n! bReferences
' I7 v7 b7 j k: U1. Styne DM. The testes: disorder of sexual differentiation# Q, z& g) o- F4 a; J* ~
and puberty in the male. In: Sperling MA, ed. Pediatric. R! W, C* v6 ]- n- M
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 |0 \, u j/ `$ p2 b; T2002: 565-628., P: s3 ?' o" U" J- ?6 F
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 f! u& n( C7 j' V+ Cpuberty in children with tumours of the suprasellar pineal |
|