- 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
; |, `6 ?* ~$ g+ c( {) F( pBoy Induced by Indirect Topical1 U- v4 x, l" v4 }+ I' ?) E
Exposure to Testosterone
- c. |+ s3 ~4 e6 {& LSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. \: f3 {! n: U& n- @: tand Kenneth R. Rettig, MD10 y( o+ X4 t2 g5 u3 x) E2 T% _
Clinical Pediatrics
. k) J5 c' j1 V, u. }Volume 46 Number 6
% _3 Z& I/ R- \" r# \0 C cJuly 2007 540-5438 F J! q' v" n0 D' |
© 2007 Sage Publications
2 \3 _/ j' J- q& J3 B- U10.1177/0009922806296651
n! @2 @2 k- F ?# ^http://clp.sagepub.com. ?3 j) ^4 z, X
hosted at' n/ U5 q+ d5 ?- Z: n1 n; h: B
http://online.sagepub.com
! t0 y: n$ ~& g3 Y8 u; v4 iPrecocious puberty in boys, central or peripheral,
& l5 a7 q9 F) h* C |" fis a significant concern for physicians. Central
# ?7 N* _) A5 Z# Q) z. o4 Hprecocious puberty (CPP), which is mediated7 V; t$ |2 L7 m
through the hypothalamic pituitary gonadal axis, has* O" J" D: X$ N T( ?) G
a higher incidence of organic central nervous system
) l: a$ t6 F% u' a( ?5 Ilesions in boys.1,2 Virilization in boys, as manifested
1 p* k3 _5 Y& o& q( u4 ]by enlargement of the penis, development of pubic
a0 c' c6 @* Phair, and facial acne without enlargement of testi-4 C9 e/ x. a" p! j0 u) z, Z: @% U
cles, suggests peripheral or pseudopuberty.1-3 We5 w: n0 p; M, F3 G1 H; z9 S( I
report a 16-month-old boy who presented with the) r M1 u y9 s X) X+ G: T
enlargement of the phallus and pubic hair develop-
7 ^8 | E( A+ X9 n3 M* sment without testicular enlargement, which was due5 m/ n2 n* m3 R2 M* y1 z
to the unintentional exposure to androgen gel used by8 [: F6 d+ N1 c7 a
the father. The family initially concealed this infor-
7 B$ V! j4 l# K! k- Smation, resulting in an extensive work-up for this
2 `8 g) P3 l" N5 O. U# hchild. Given the widespread and easy availability of
6 l- E: L8 M* G% B! ~! mtestosterone gel and cream, we believe this is proba-
3 ?6 W2 A( C( u2 w8 Q0 t& kbly more common than the rare case report in the- B( ?* B( k( D8 B
literature.4# d3 Q9 r) P0 D8 {5 k# ?/ P
Patient Report5 g i- r6 E* S! {1 m; K" I
A 16-month-old white child was referred to the% z0 x- K3 R8 p* ^+ s" d8 O- m
endocrine clinic by his pediatrician with the concern a0 C9 j, s. {( t1 w
of early sexual development. His mother noticed
; S/ N, [% k% \" c7 Q2 Y3 dlight colored pubic hair development when he was$ B: _& u5 K+ U4 ?; p
From the 1Division of Pediatric Endocrinology, 2University of& ?8 u( s7 g9 ^ i1 C
South Alabama Medical Center, Mobile, Alabama.
% x% z7 m# O" _* LAddress correspondence to: Samar K. Bhowmick, MD, FACE,
$ ^1 k8 j3 n9 O8 L3 p% S3 VProfessor of Pediatrics, University of South Alabama, College of
) P5 ?$ e+ b/ l: ^Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. ]$ v0 ~; E" U/ c
e-mail: [email protected].& [0 J" `) f: F6 c/ B8 _
about 6 to 7 months old, which progressively became
6 ~) }; }! H- W; |" Pdarker. She was also concerned about the enlarge-
$ a1 N: n! h& x: Q1 D$ u2 z# Vment of his penis and frequent erections. The child
5 @: } K$ p: E2 u' Q1 R: mwas the product of a full-term normal delivery, with v% y3 |" V! G4 R9 i5 O/ S
a birth weight of 7 lb 14 oz, and birth length of
% n! e) D3 |, Y) w; A# K1 [! o9 p20 inches. He was breast-fed throughout the first year
# j( q2 g8 q$ s# Gof life and was still receiving breast milk along with& m4 g+ g1 b( p" Y
solid food. He had no hospitalizations or surgery,, @- \6 l7 _" ^- `6 E9 r
and his psychosocial and psychomotor development( C& K R& P! Y: D) P
was age appropriate.* F& v& W! J0 m/ Z
The family history was remarkable for the father,
: o: x6 Z* a q+ l+ j Jwho was diagnosed with hypothyroidism at age 16,5 f% o, j; v; f) o" w8 a8 ]& H1 @
which was treated with thyroxine. The father’s3 f/ S5 h7 u" v4 E4 I4 f0 a8 P
height was 6 feet, and he went through a somewhat. R& `: _! P/ B! L1 A9 ~
early puberty and had stopped growing by age 14.' d. ^7 e6 H2 J6 C% M1 c& T6 O3 A
The father denied taking any other medication. The9 v9 ^, A( }. m i5 L6 v z! r/ o+ }- ]
child’s mother was in good health. Her menarche
+ S# G! V' e: R5 ]1 J% [was at 11 years of age, and her height was at 5 feet8 ^* Q/ D4 `( X. f: g5 u
5 inches. There was no other family history of pre-
* r. S8 R" f$ n0 ?* {! X+ fcocious sexual development in the first-degree rela-1 |0 J- g3 t* ~/ [4 G
tives. There were no siblings.
4 @: d6 M9 `6 M! n" K" C$ KPhysical Examination
+ V6 ^& P, t. O2 r0 m( q! z1 @The physical examination revealed a very active,( D- V( ]% k% {' |$ a. ]
playful, and healthy boy. The vital signs documented
+ p' D/ W- f k$ B. Ra blood pressure of 85/50 mm Hg, his length was2 l x6 ^6 _" ^5 n
90 cm (>97th percentile), and his weight was 14.4 kg% P* R- j1 x* n9 B7 g$ e) m. {" q" d
(also >97th percentile). The observed yearly growth
. \% f6 h/ w- n- [velocity was 30 cm (12 inches). The examination of1 }% T+ l+ x9 b4 L% ]
the neck revealed no thyroid enlargement.
3 j" l; Y8 m% |; wThe genitourinary examination was remarkable for/ m2 q( `/ V% s
enlargement of the penis, with a stretched length of
5 X, B0 P+ p' M6 V! s' J1 b. ^8 cm and a width of 2 cm. The glans penis was very well- A; ^: G& C6 X7 u+ z3 H4 U
developed. The pubic hair was Tanner II, mostly around. d; P9 f3 ^" o
540
: N Y9 _* N# A! aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 O3 }/ l4 [' \. Y5 ]8 v. O* {/ ^ ^the base of the phallus and was dark and curled. The6 U" V& Z; x! Z' ~/ h8 }' Z
testicular volume was prepubertal at 2 mL each.
( c9 u7 p, Y: N. Z% sThe skin was moist and smooth and somewhat2 z9 h$ ?. k9 _! {9 [
oily. No axillary hair was noted. There were no# o- |4 m e, _+ X# \7 `" ?
abnormal skin pigmentations or café-au-lait spots.1 x, A" Q/ |* Y5 w# M$ \, o
Neurologic evaluation showed deep tendon reflex 2+8 k+ V: h5 c( L# M. ]1 t( U) B V) L
bilateral and symmetrical. There was no suggestion
6 d2 |. d6 P% q, M/ v. G7 b' Vof papilledema.
3 ?( n+ M: B: K8 g2 ULaboratory Evaluation
9 t- u7 o6 M' S7 mThe bone age was consistent with 28 months by' ]7 w$ }8 P5 o1 X6 y
using the standard of Greulich and Pyle at a chrono-* e9 m. |, v1 V$ I1 x
logic age of 16 months (advanced).5 Chromosomal2 r$ L4 q+ h# r! b" |: C
karyotype was 46XY. The thyroid function test
% a1 X$ r* I8 {9 ?showed a free T4 of 1.69 ng/dL, and thyroid stimu-
" d0 a2 w2 z" e1 Nlating hormone level was 1.3 µIU/mL (both normal).
$ W2 P; ]" q9 |, J2 L2 d- p& W, oThe concentrations of serum electrolytes, blood
5 L& x6 e0 j# |5 |/ O' purea nitrogen, creatinine, and calcium all were
5 n5 y/ A. ]4 f. Z) u# C5 G: Mwithin normal range for his age. The concentration
2 c# X! J4 R+ L$ |4 E3 Qof serum 17-hydroxyprogesterone was 16 ng/dL; t; v. U1 k# l( ^
(normal, 3 to 90 ng/dL), androstenedione was 20
/ p1 x; o+ i" o8 i$ n$ W$ e8 F) bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, h+ K5 F2 F% p7 z3 gterone was 38 ng/dL (normal, 50 to 760 ng/dL),
V4 P' h9 U7 z4 U5 |" X: tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to* y' V" q# K" _; H# Z& ^' a' u
49ng/dL), 11-desoxycortisol (specific compound S). r+ q2 _6 `6 x$ }6 F
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-$ K4 Z* e4 _0 w& d4 T
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% X. E) U+ [; y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL)," M, \( {& L4 Z. h+ _1 [
and β-human chorionic gonadotropin was less than
# g. t6 X) D- v5 mIU/mL (normal <5 mIU/mL). Serum follicular! v3 N+ z9 j# k6 w0 ^
stimulating hormone and leuteinizing hormone% d' S+ l# E" l- u: I; X$ d
concentrations were less than 0.05 mIU/mL
# T0 p( a8 d R(prepubertal).
6 n" C I4 d w9 uThe parents were notified about the laboratory+ v( r9 a# Z) r$ R( J$ J4 R
results and were informed that all of the tests were3 ?# H, Q4 J. J0 ?9 {, n9 y% Z
normal except the testosterone level was high. The: a( ]: Z: J1 X. X/ J k; ~
follow-up visit was arranged within a few weeks to1 t- Z$ }0 e( j4 A
obtain testicular and abdominal sonograms; how-
$ x8 Q! I+ L7 Y4 d4 Gever, the family did not return for 4 months.- P5 f9 f# P# ~6 [5 K: n# ]
Physical examination at this time revealed that the9 V! R+ i, t' w% h: L' c# T
child had grown 2.5 cm in 4 months and had gained
w, n7 s* ^' ?" E* i W2 kg of weight. Physical examination remained
: r, q& T, @( Y% Z) p- H7 ?0 Lunchanged. Surprisingly, the pubic hair almost com-$ [3 U2 y9 B5 E
pletely disappeared except for a few vellous hairs at
7 }0 H" R( R/ N2 \4 n; i1 k9 dthe base of the phallus. Testicular volume was still 2
9 O7 ^/ o0 R d# s% H/ [* qmL, and the size of the penis remained unchanged.
& @" u( L, t- j/ C- ]8 DThe mother also said that the boy was no longer hav-0 @; U$ Q6 a) u; q$ o) y
ing frequent erections.$ M2 [# P2 w1 O5 B! g* x
Both parents were again questioned about use of% o- U' W# _: N, {# Y
any ointment/creams that they may have applied to$ O4 o9 r5 ]% K! W
the child’s skin. This time the father admitted the7 e M: q8 u9 N5 U# S% ^% [
Topical Testosterone Exposure / Bhowmick et al 541
4 E3 [" l9 l0 |1 q& P$ Cuse of testosterone gel twice daily that he was apply-
8 A- p0 T" j8 T; l- D' m+ uing over his own shoulders, chest, and back area for+ y% @; p4 |7 }' Q% N
a year. The father also revealed he was embarrassed
6 z- a5 g. W4 x8 Q% _: U7 L# w: wto disclose that he was using a testosterone gel pre-2 ^+ g* T% S+ H! { R0 k* @
scribed by his family physician for decreased libido# a& ]3 g- j7 [% M/ Q+ k8 G o
secondary to depression.7 V" V4 F1 x3 k" O
The child slept in the same bed with parents.
* \: W5 G3 k' G, XThe father would hug the baby and hold him on his7 b6 h' y/ r! J2 j$ ]- V j* l# @
chest for a considerable period of time, causing sig-5 I+ X2 j8 u) K% b7 x l
nificant bare skin contact between baby and father., y9 ^/ E' K+ V. ]1 m3 y9 ]
The father also admitted that after the phone call,
9 p5 X' }+ X7 I2 ]when he learned the testosterone level in the baby
7 C/ {( |( L" Cwas high, he then read the product information- R, r7 |1 ?6 ]) J, ?) z3 ~! m e
packet and concluded that it was most likely the rea-
! }& i$ Z& ?+ _& V4 a' Yson for the child’s virilization. At that time, they
) Q& Q* s8 G3 g2 N# @5 cdecided to put the baby in a separate bed, and the
; g8 u& i/ H, y" cfather was not hugging him with bare skin and had
& h# c# U, D v. L$ Bbeen using protective clothing. A repeat testosterone5 G4 j. x! r* ?9 J0 e8 G/ x
test was ordered, but the family did not go to the3 G! j/ a; r6 q# M- G7 `7 S4 f9 D
laboratory to obtain the test.3 L R. a' ?2 u
Discussion
0 i, e8 ]* H0 ~Precocious puberty in boys is defined as secondary) ^% B% E3 X$ ]" i& a. A
sexual development before 9 years of age.1,4
$ p0 e5 W3 U: N/ HPrecocious puberty is termed as central (true) when9 D3 x: ~1 F, F# g( |+ R) D t
it is caused by the premature activation of hypo-
3 k- n/ c" K, nthalamic pituitary gonadal axis. CPP is more com-; W+ }" l7 [/ j; c
mon in girls than in boys.1,3 Most boys with CPP% y! U: ]1 Z+ T+ P% Q& s' ~
may have a central nervous system lesion that is
! R; A% ^ V' Y4 J0 o/ H1 G; kresponsible for the early activation of the hypothal-, f. y1 Z6 V: D
amic pituitary gonadal axis.1-3 Thus, greater empha-
" A+ x4 c; h" g/ \sis has been given to neuroradiologic imaging in
; G9 B: U/ s! @' x* g' }boys with precocious puberty. In addition to viril-! _2 E* M+ y. x
ization, the clinical hallmark of CPP is the symmet-
5 q; U1 e. i' Irical testicular growth secondary to stimulation by1 N( G' A' v6 m5 j% t8 z9 T' C
gonadotropins.1,3$ W+ g5 ~0 U9 \3 ?/ k
Gonadotropin-independent peripheral preco-$ u9 t# l2 j' o- k& c
cious puberty in boys also results from inappropriate Q/ v& k9 k7 z( V
androgenic stimulation from either endogenous or7 n8 y& Q" z! u8 Y$ \1 I
exogenous sources, nonpituitary gonadotropin stim-
- F8 _& s- ?5 ~' Q E+ B4 b3 _/ x& Z: `ulation, and rare activating mutations.3 Virilizing$ v' v# m4 [8 ~! h+ B$ q
congenital adrenal hyperplasia producing excessive/ R' t( Q8 ~; P5 b
adrenal androgens is a common cause of precocious# O/ B3 P3 I$ J- U- y
puberty in boys.3,4
8 r: ]3 |1 X0 R% SThe most common form of congenital adrenal1 R+ a" c% K6 ]3 F i" y
hyperplasia is the 21-hydroxylase enzyme deficiency.) h& w7 h. s) E0 d E' {4 Z" E1 ]' V
The 11-β hydroxylase deficiency may also result in
# t8 C9 H) S4 P ]5 E% o8 Hexcessive adrenal androgen production, and rarely,
( n, q2 E( ?+ _! Yan adrenal tumor may also cause adrenal androgen$ N: w6 l4 M6 t+ V1 E, I1 d
excess.1,3) l6 |8 _, l7 o, P. i
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ |" A% t# k* _$ |# E* _) P; a542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
* e5 Z" L7 q7 D1 ` j+ SA unique entity of male-limited gonadotropin-
1 ~2 H6 b. m% _1 P: Rindependent precocious puberty, which is also known
7 z* l" i4 q' p; ?; g( i8 Jas testotoxicosis, may cause precocious puberty at a
0 t$ M4 Y7 q+ ? C1 V- I% Jvery young age. The physical findings in these boys( u# Z3 N2 E( p( i1 [3 _: a' A5 ~
with this disorder are full pubertal development,5 m3 X! E2 B( _% }
including bilateral testicular growth, similar to boys
) G2 Q9 V/ W$ |. v9 p4 Nwith CPP. The gonadotropin levels in this disorder
. k( L% x5 Y) B+ ?2 s4 ^! Gare suppressed to prepubertal levels and do not show
, F8 V) m: ^8 P3 Q" lpubertal response of gonadotropin after gonadotropin-1 [3 c+ G6 k4 |5 O( o
releasing hormone stimulation. This is a sex-linked
: w3 u0 r+ `$ Q" |autosomal dominant disorder that affects only
; a& i2 ~+ j$ lmales; therefore, other male members of the family
% j8 ]. f3 l( ~4 i) s8 a4 v8 \( Hmay have similar precocious puberty.3
. r6 f2 E r" T( i4 k+ x, G; TIn our patient, physical examination was incon-
. S1 q# I" O# B- G, w# H, usistent with true precocious puberty since his testi-. s4 w* ?" z+ M0 K
cles were prepubertal in size. However, testotoxicosis% R& j& I t8 _7 T
was in the differential diagnosis because his father
4 Y8 l% @. Y& l# @3 L- c5 estarted puberty somewhat early, and occasionally, A! P7 t) n- a" x
testicular enlargement is not that evident in the
# b. b* I7 e! Dbeginning of this process.1 In the absence of a neg-
% ^ V) m* Y5 u) V! @ative initial history of androgen exposure, our }9 ], x8 |' {% V
biggest concern was virilizing adrenal hyperplasia,) [# T9 s3 {! G) U, D
either 21-hydroxylase deficiency or 11-β hydroxylase
# J. {$ w4 J: f$ S H- t" r& Edeficiency. Those diagnoses were excluded by find-+ f+ q. d, O) o
ing the normal level of adrenal steroids.; |8 ], i4 L1 _ A. r
The diagnosis of exogenous androgens was strongly. O2 t7 u9 X( }! B% G4 d) f
suspected in a follow-up visit after 4 months because
/ r* J% Z) l7 |3 n! _( m' B# V& Xthe physical examination revealed the complete disap-$ q& g6 a" q3 G- a3 V! o1 c! e
pearance of pubic hair, normal growth velocity, and
+ K% V, S) ^# \/ j/ W1 _& B8 Tdecreased erections. The father admitted using a testos-
2 v5 @1 p) r+ U' Q4 \/ h& g9 j+ oterone gel, which he concealed at first visit. He was
6 X/ `; f. |& p; |using it rather frequently, twice a day. The Physicians’# k/ W+ Y. c2 f E$ `
Desk Reference, or package insert of this product, gel or/ L' ]# }, R& e8 o1 S7 U
cream, cautions about dermal testosterone transfer to
/ O5 c. s2 ^5 N+ }unprotected females through direct skin exposure.
/ F$ u4 N+ M; xSerum testosterone level was found to be 2 times the1 x3 x: `0 d v- _
baseline value in those females who were exposed to& S+ P1 X% J9 _& Q T! M( {
even 15 minutes of direct skin contact with their male$ v4 o7 _8 c$ |8 U
partners.6 However, when a shirt covered the applica-
; ]/ |0 x! P9 G E/ g1 l' ition site, this testosterone transfer was prevented.
5 z# O1 h) ^% V4 ~* tOur patient’s testosterone level was 60 ng/mL,
1 \+ q6 \) t) t5 g- h7 \which was clearly high. Some studies suggest that
9 i5 ~- U1 j* n) K$ [6 q0 N0 xdermal conversion of testosterone to dihydrotestos-. p9 n6 s# e) W! E1 S( Q
terone, which is a more potent metabolite, is more; R. c1 C* c9 P: v# P" P! O8 m
active in young children exposed to testosterone
$ w( m0 D# v& n; I, lexogenously7; however, we did not measure a dihy-
" m% T, @( E0 g9 z x& {% Kdrotestosterone level in our patient. In addition to- P, O5 u9 y9 f7 H- ^4 ~2 ]: L, J# U
virilization, exposure to exogenous testosterone in
; g1 K I7 T2 Achildren results in an increase in growth velocity and
3 x8 l- ?& s4 }! J8 L1 Xadvanced bone age, as seen in our patient.
7 H1 X7 F/ u2 ^( aThe long-term effect of androgen exposure during
. b8 t& x z# O i" [2 o* Mearly childhood on pubertal development and final
2 V) C/ ]3 C' y5 O, Z; U2 t+ Y9 Vadult height are not fully known and always remain' M5 B/ L0 }7 _; \
a concern. Children treated with short-term testos-; I: Y7 _, o1 b4 ^; c+ i! ]0 x
terone injection or topical androgen may exhibit some
* e) u( E+ g; q! Qacceleration of the skeletal maturation; however, after
& P! p2 j3 }8 M1 j* B) _cessation of treatment, the rate of bone maturation
+ {5 s- \1 \% O: {$ N+ I1 jdecelerates and gradually returns to normal.8,96 L, F1 f, o. L+ o8 H/ q
There are conflicting reports and controversy
) F `/ M# r, P1 A7 kover the effect of early androgen exposure on adult- Z% C, g) J) }/ [$ i* w S
penile length.10,11 Some reports suggest subnormal
" `3 |6 \0 F! |# cadult penile length, apparently because of downreg-' a5 w- d& t* _. y1 U, c' |
ulation of androgen receptor number.10,12 However,( f2 P4 q# g! ^
Sutherland et al13 did not find a correlation between1 R9 X2 q4 F5 e7 Q) Z% Y9 a
childhood testosterone exposure and reduced adult
) H2 z) @. _$ x6 ]2 ^/ L% Fpenile length in clinical studies.8 \& Y; l2 S5 I' Z+ H8 E
Nonetheless, we do not believe our patient is% _2 y/ T7 I+ K, R$ S
going to experience any of the untoward effects from
! e6 Q6 b7 P5 S' |$ h+ Y" Rtestosterone exposure as mentioned earlier because
( d- c$ A: j$ J7 }: d" Q6 nthe exposure was not for a prolonged period of time.9 s/ w5 f* ]4 q) P, Q4 s8 M9 I
Although the bone age was advanced at the time of
+ Z6 f0 K$ t- b6 y- M4 {) udiagnosis, the child had a normal growth velocity at
4 }& Y7 q0 j, [' K' h0 f/ E' wthe follow-up visit. It is hoped that his final adult8 c- n: C' W- h# [6 }& u6 W. W
height will not be affected.
" S' Q+ g e& f. kAlthough rarely reported, the widespread avail-
! v1 `8 u6 p* R# `) a4 sability of androgen products in our society may g% U; b, ~0 q9 Q5 G+ X# w/ ~$ y
indeed cause more virilization in male or female3 J; V/ g/ X9 p) z, \( V U- H
children than one would realize. Exposure to andro-
; d, I1 h9 c4 H m+ M; Ogen products must be considered and specific ques-
+ S4 A* n( d4 t6 o5 Stioning about the use of a testosterone product or3 D+ c& |6 i; U& M+ w
gel should be asked of the family members during# b* X' u% H9 [4 ? B" U
the evaluation of any children who present with vir-
& g2 V. n: ]9 A( Q- g7 @# N# o4 Bilization or peripheral precocious puberty. The diag-7 `$ {6 e& U+ M2 l' ?) u0 Z
nosis can be established by just a few tests and by, _ C$ z6 b" n; K9 }3 j5 @
appropriate history. The inability to obtain such a$ w5 e P. C4 X
history, or failure to ask the specific questions, may
+ g+ ^6 `+ \; ], `( y4 l; k. C0 x# z: aresult in extensive, unnecessary, and expensive
- n( z2 b4 e1 s- c+ m% q0 h0 @investigation. The primary care physician should be
1 ?/ x: n/ S" `& z6 o/ p) oaware of this fact, because most of these children* k& M# w% h5 q- f( q5 k# c
may initially present in their practice. The Physicians’
' D+ x, d E' [* K: GDesk Reference and package insert should also put a
$ ~% b( G" }' Cwarning about the virilizing effect on a male or
# \ |: y) I2 M' w% m5 e. d/ F. _female child who might come in contact with some-& O! q6 E, w4 [+ X
one using any of these products.+ c3 I8 H* `2 h9 `) u/ {
References& c: V8 i9 S" f' i8 q4 _
1. Styne DM. The testes: disorder of sexual differentiation
/ `% D; n/ Z$ n6 T$ g } }5 ]and puberty in the male. In: Sperling MA, ed. Pediatric; n# s) m% p9 e, f9 l9 |- S
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* S3 i* G6 H L
2002: 565-628.3 I! S# A, R& D
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 k* t. E. @9 o' j. a2 dpuberty in children with tumours of the suprasellar pineal |
|