- 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 03:25:35
|
顯示全部樓層
Sexual Precocity in a 16-Month-Old P) [/ m% X s% r6 Q ?: o$ D
Boy Induced by Indirect Topical9 K3 u9 H1 r- j* [
Exposure to Testosterone! q3 Y) Q1 ?* @
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: r0 p7 J: ]! D- y( H+ L, r. Gand Kenneth R. Rettig, MD1+ K q4 f( b7 R: j Q1 w9 e
Clinical Pediatrics- O. @' r* X5 R0 |) p- Q
Volume 46 Number 6 _8 {1 m, c7 l' N0 U2 D
July 2007 540-543, e0 [ \5 ?9 k# V
© 2007 Sage Publications
* Y5 x$ |( @+ u( N$ Y10.1177/0009922806296651
7 z$ Q: P+ q3 J) d: |* o6 dhttp://clp.sagepub.com
8 F N% B1 ~5 X: \$ ?hosted at
2 J! f) s: h" E' r7 Z2 j6 t. T0 d) \http://online.sagepub.com
8 ]' n) u1 G6 B& p% c% f8 lPrecocious puberty in boys, central or peripheral,* K! u3 h. B$ |. j6 n. R8 z+ r% U* b
is a significant concern for physicians. Central" r6 H# @. \1 q; i: D' Q: M2 L4 g
precocious puberty (CPP), which is mediated
4 b7 L& E; `6 a1 |6 m1 Q& C0 B7 pthrough the hypothalamic pituitary gonadal axis, has
0 ]' H- l( N o% D1 u4 j" C, @+ [a higher incidence of organic central nervous system
# t0 A# w% T) `( L0 A9 s) Rlesions in boys.1,2 Virilization in boys, as manifested
7 \% h7 ^# {7 h' l. r7 Tby enlargement of the penis, development of pubic3 S! m6 d c9 [
hair, and facial acne without enlargement of testi-6 D1 J) e, C5 {2 `
cles, suggests peripheral or pseudopuberty.1-3 We
6 }$ u( a) ~, q( d. |$ A sreport a 16-month-old boy who presented with the
3 W5 Z2 [# n& K6 |& Kenlargement of the phallus and pubic hair develop-
5 J, f" ?5 c- i' M) P3 ]9 pment without testicular enlargement, which was due
- C4 i& F6 D' H+ M- W2 Yto the unintentional exposure to androgen gel used by
+ x: a. F4 ]$ L0 e5 Q( Sthe father. The family initially concealed this infor-
1 o5 m9 U7 u9 H+ e p' lmation, resulting in an extensive work-up for this
2 o0 M( e) d5 @4 }/ K* \child. Given the widespread and easy availability of2 O1 l. f j; z# S1 G! P: [
testosterone gel and cream, we believe this is proba-$ F; N5 `5 w0 i2 d5 y% Y! |( \8 @
bly more common than the rare case report in the
0 T6 f6 {8 A7 y, j7 T5 H/ Oliterature.4
: }: _/ i- Q& H) G% zPatient Report
8 j) E0 l) x" m& S7 _; F. F& S. y& ], eA 16-month-old white child was referred to the' E0 M3 b+ j, j7 j( D% r3 m) t
endocrine clinic by his pediatrician with the concern0 W% t1 L: H) U' ]/ A0 k
of early sexual development. His mother noticed9 ]: @/ G. y6 ?2 y1 N: d
light colored pubic hair development when he was9 F. \9 S5 ~$ }/ A0 i- c. t/ a2 o
From the 1Division of Pediatric Endocrinology, 2University of6 `# _! Q1 A: T& h( V, r4 I% w9 k
South Alabama Medical Center, Mobile, Alabama.% X+ V6 @0 L* X
Address correspondence to: Samar K. Bhowmick, MD, FACE,
, c6 ^0 w0 p; DProfessor of Pediatrics, University of South Alabama, College of
6 w9 `* m& d! y/ D, U- E F$ pMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. m4 n# |0 o7 Y% a3 J/ e% ie-mail: [email protected].
: W9 G3 A2 N1 Yabout 6 to 7 months old, which progressively became9 ^% h9 N: t& o+ x4 q. G
darker. She was also concerned about the enlarge-4 L0 r! o) d9 i" G( u6 d
ment of his penis and frequent erections. The child
% \2 F( v3 ^$ h; v; W( pwas the product of a full-term normal delivery, with( W' j- A3 m- n3 s7 B4 |
a birth weight of 7 lb 14 oz, and birth length of; S8 t- u+ @4 H7 n% R/ {+ P
20 inches. He was breast-fed throughout the first year
" ^( b0 M3 x4 h& U9 H7 Jof life and was still receiving breast milk along with0 _3 c7 T8 H: y$ d/ x
solid food. He had no hospitalizations or surgery,
" {8 _, I. K; M c# s' D' }and his psychosocial and psychomotor development
- A& D; o' e6 }5 twas age appropriate.
! V7 y$ V8 ]" g' {: PThe family history was remarkable for the father,4 I& ~2 _) x; R5 k
who was diagnosed with hypothyroidism at age 16,
( O* e. m0 w/ b8 ]/ R r( |which was treated with thyroxine. The father’s7 L3 N' M+ y& ]4 {( n8 }$ s* ~
height was 6 feet, and he went through a somewhat
* T) `) \! h8 m& m, ], kearly puberty and had stopped growing by age 14.
5 e/ _0 y+ z3 n" y( eThe father denied taking any other medication. The
0 K7 ?. |# j0 }6 Echild’s mother was in good health. Her menarche
1 a1 Y3 ]; s: s6 V9 Iwas at 11 years of age, and her height was at 5 feet3 m0 {9 F5 F1 _8 U
5 inches. There was no other family history of pre-; W- v1 V( R$ ?3 \
cocious sexual development in the first-degree rela-* W" N# S" \9 b6 b# u* k) P5 z
tives. There were no siblings.( q& Y u5 o, N9 o$ P5 q- i
Physical Examination
8 y- w- l7 }7 p3 g" G2 b' N7 n5 D8 cThe physical examination revealed a very active,
. f4 \+ ^5 C) E- R0 Q% Aplayful, and healthy boy. The vital signs documented
' w6 {" K# H1 o z0 b' @: ]a blood pressure of 85/50 mm Hg, his length was- x" |- C+ T3 A' N
90 cm (>97th percentile), and his weight was 14.4 kg
6 |6 Q$ H1 t: _5 x(also >97th percentile). The observed yearly growth
1 @2 c, g- B4 f% W! P) Ivelocity was 30 cm (12 inches). The examination of" N0 ~" y8 c# j0 w B& h" D
the neck revealed no thyroid enlargement.
5 x6 h& {5 h9 F: n1 k( ]/ e' YThe genitourinary examination was remarkable for
1 Q: n, @) {/ @+ e5 renlargement of the penis, with a stretched length of
" B# x# W6 f& ]; D* A8 cm and a width of 2 cm. The glans penis was very well+ y' v' I- |) E' E' z$ e0 P+ {1 ~$ }
developed. The pubic hair was Tanner II, mostly around
1 d+ g" {0 F. n* @6 R1 g) f540
, O- x- D! T% w* ^4 [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 Y0 e) F0 |5 f' t( |. f$ s) z) `the base of the phallus and was dark and curled. The
0 T% I" L% V, V0 j3 |; l5 Ctesticular volume was prepubertal at 2 mL each.
1 e1 z- V8 @& [The skin was moist and smooth and somewhat
1 a8 \# D# {9 L o! Zoily. No axillary hair was noted. There were no/ O0 i% [! q8 E% K+ s
abnormal skin pigmentations or café-au-lait spots.& l, M; ~; v- K5 c
Neurologic evaluation showed deep tendon reflex 2+
& L; t& Q/ F$ S7 Obilateral and symmetrical. There was no suggestion* ?) v) a% h" Q0 L1 z
of papilledema.
) g6 W6 Z! K5 \1 b+ z7 m) qLaboratory Evaluation
# @& P2 A/ a# |% }- [( `* VThe bone age was consistent with 28 months by6 W6 a9 \( Q) H1 D) Q. u
using the standard of Greulich and Pyle at a chrono-( u* O& p k4 ^, g4 ?3 k4 w$ V( J
logic age of 16 months (advanced).5 Chromosomal" ?3 k* A( K# G1 ]8 h
karyotype was 46XY. The thyroid function test/ `( g) H V- e! _/ I
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 F* [4 N& b8 [: e- j3 A0 |lating hormone level was 1.3 µIU/mL (both normal).6 f3 Z# N# K) Q9 A5 a( R, o
The concentrations of serum electrolytes, blood
9 D( B9 d9 ^6 P8 Qurea nitrogen, creatinine, and calcium all were
; P+ b( N3 S, C! ^/ fwithin normal range for his age. The concentration) ^! m7 u/ d0 g$ S& R* v
of serum 17-hydroxyprogesterone was 16 ng/dL" w9 P( p# h! e
(normal, 3 to 90 ng/dL), androstenedione was 20, B+ u" `: ^6 A) J' s8 Q6 c# {
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ ]; ]2 s- p# g; ]" d; s# L
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
& A5 `. z- l* R; r1 Adesoxycorticosterone was 4.3 ng/dL (normal, 7 to) B7 _) M; f/ H t# T7 Y) v
49ng/dL), 11-desoxycortisol (specific compound S)* l% s8 d' T, t. A# W# `9 R
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ y$ M/ y2 `9 |1 k- B9 Stisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* P5 t" y/ g0 ~, ~$ o4 Y% V3 c
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 W2 d/ r0 P' ]5 E
and β-human chorionic gonadotropin was less than0 [ W0 f1 I% ~0 G! y; Z* r
5 mIU/mL (normal <5 mIU/mL). Serum follicular' W; { R# o5 w/ `5 I
stimulating hormone and leuteinizing hormone
2 y5 H( a7 v7 q% }( V* vconcentrations were less than 0.05 mIU/mL
, C/ K* o+ ]6 ~(prepubertal).
( ~7 I. d, t+ O7 X; CThe parents were notified about the laboratory
7 |0 B9 {, z7 b/ j, M1 wresults and were informed that all of the tests were
; z5 L1 ]. H9 }" j; u, Vnormal except the testosterone level was high. The
% O9 W, w+ N9 p, S+ P1 Z) Efollow-up visit was arranged within a few weeks to
: q7 M; b3 D$ A, J7 Tobtain testicular and abdominal sonograms; how-' ~0 V, \3 W4 ?3 y. w( J
ever, the family did not return for 4 months.
, C) ?8 b2 H2 P- ]: F. M! v7 rPhysical examination at this time revealed that the
$ E4 t- I! ]1 B% H: o( Y( o zchild had grown 2.5 cm in 4 months and had gained# s' ^( z2 H& F: Q0 c
2 kg of weight. Physical examination remained! a- W/ r% {- e. a% m
unchanged. Surprisingly, the pubic hair almost com-9 v4 r9 ]% ~* Q0 H8 x
pletely disappeared except for a few vellous hairs at
6 P' s5 F: o( W! N' wthe base of the phallus. Testicular volume was still 2 ?7 e0 j6 D: w( [) w
mL, and the size of the penis remained unchanged.7 {+ f! O. U: c" A8 [
The mother also said that the boy was no longer hav-1 Q9 Z% E; @ o# d
ing frequent erections.
) V! O0 Z$ ^. rBoth parents were again questioned about use of
$ G! v) j f" |9 a$ Nany ointment/creams that they may have applied to5 Z2 K- S0 Z" ~' C
the child’s skin. This time the father admitted the1 W, G) M- i+ z, P
Topical Testosterone Exposure / Bhowmick et al 5410 [1 a) h* {/ x0 N5 o; F& R2 c) {
use of testosterone gel twice daily that he was apply-( K, Z8 q/ U6 H4 _# W& m; j
ing over his own shoulders, chest, and back area for% |& K: r0 b# y; ^3 ]7 r
a year. The father also revealed he was embarrassed
8 H6 V5 y4 O4 Jto disclose that he was using a testosterone gel pre-
- d- c6 S% U% E' o9 S. D' n# M5 i" Zscribed by his family physician for decreased libido6 ?% l0 Q. T- H, f0 p" W# L
secondary to depression.
& _" o* q' s$ ]! a. B8 J4 fThe child slept in the same bed with parents.4 l, ^, D1 c* c3 n4 D! O
The father would hug the baby and hold him on his
1 M n5 X( L# ?: c% Q6 z' H* fchest for a considerable period of time, causing sig-
i* y4 }3 M: }$ Qnificant bare skin contact between baby and father.
+ Q! y, v9 ~7 k/ s( N0 uThe father also admitted that after the phone call,
3 D- Z; k+ R7 Z& P+ awhen he learned the testosterone level in the baby# ]3 ]% ~: Q- h9 u
was high, he then read the product information
% X: E% U) B9 B5 W5 T9 ]1 Kpacket and concluded that it was most likely the rea-
( C# E% l6 @$ u& _: s3 O2 eson for the child’s virilization. At that time, they
, s- Q- j) ^: m* Qdecided to put the baby in a separate bed, and the* k3 |& [4 c; G4 }5 F3 X; q0 Q
father was not hugging him with bare skin and had. h# ^4 u. j. g5 L# S5 U
been using protective clothing. A repeat testosterone
! y m8 K6 e @" btest was ordered, but the family did not go to the1 y! o& ?" J! \5 n& V
laboratory to obtain the test.& B& l7 z0 p, i) {! V+ A7 F
Discussion
, p U4 t' J- j3 _) lPrecocious puberty in boys is defined as secondary% f3 w6 |3 ~' \* M7 L
sexual development before 9 years of age.1,4 \$ f+ R1 M% a, U H
Precocious puberty is termed as central (true) when$ R4 y7 V! j5 T
it is caused by the premature activation of hypo- A: l9 t' S! C" g( y
thalamic pituitary gonadal axis. CPP is more com-: N" R1 X" ? S" T/ h8 w
mon in girls than in boys.1,3 Most boys with CPP) M; T& M. b& T3 q
may have a central nervous system lesion that is
% f7 v, G: ?5 l; g, n) Eresponsible for the early activation of the hypothal-5 @6 E8 x J% } p2 s! z- [
amic pituitary gonadal axis.1-3 Thus, greater empha-
6 \" d$ T9 ]3 C& w4 }7 j2 csis has been given to neuroradiologic imaging in. p+ n$ Q: y3 o
boys with precocious puberty. In addition to viril-: _% s' L) Z9 y
ization, the clinical hallmark of CPP is the symmet-
$ s+ P3 ?% ~) I6 c# ?rical testicular growth secondary to stimulation by
( o, ~6 h+ q1 R% Qgonadotropins.1,3# A3 B5 V6 U; ~$ G) k+ h% b- z8 j1 d
Gonadotropin-independent peripheral preco-
# T0 N, {! ~6 t; T7 ycious puberty in boys also results from inappropriate/ u2 s/ H- G, f! b
androgenic stimulation from either endogenous or
6 K+ Z$ c; D' dexogenous sources, nonpituitary gonadotropin stim-/ J; ?3 |3 r& s7 T2 `8 x
ulation, and rare activating mutations.3 Virilizing, e+ F. r) b0 s" N8 M: o
congenital adrenal hyperplasia producing excessive: T# {: o/ K2 r: R1 L6 N( E' Q
adrenal androgens is a common cause of precocious
0 ?5 \: E( ?% ^! W" Rpuberty in boys.3,46 ` f A. ]* {. c7 X
The most common form of congenital adrenal6 u( r5 Q6 s' A3 S* F, i
hyperplasia is the 21-hydroxylase enzyme deficiency.
: x# Z* j; Y, S* f. v: u$ sThe 11-β hydroxylase deficiency may also result in0 h, e. j( y9 I5 X2 ^; u
excessive adrenal androgen production, and rarely,
$ |4 a7 z" R/ r/ r. yan adrenal tumor may also cause adrenal androgen
: t# h/ l/ a3 `; g2 _; u6 Kexcess.1,3
k& O t ~( u3 j2 zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 {4 ^; ?/ e; y* z542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 ]; ?: c9 ^0 X
A unique entity of male-limited gonadotropin-
# Y2 o c1 |) a8 f7 z0 ?independent precocious puberty, which is also known
! o4 @1 M1 ^" ~6 J" }2 cas testotoxicosis, may cause precocious puberty at a
4 i0 T3 w: L) i* W! overy young age. The physical findings in these boys
9 T) `" l! r Dwith this disorder are full pubertal development,: N, |8 b* V2 ]1 U/ H5 l
including bilateral testicular growth, similar to boys
! l; I5 S) j! x2 X. gwith CPP. The gonadotropin levels in this disorder0 {* w' H3 d0 }( y
are suppressed to prepubertal levels and do not show6 ]4 i+ E1 S5 K% I" f
pubertal response of gonadotropin after gonadotropin-
6 V# v8 t' a+ ?/ h5 kreleasing hormone stimulation. This is a sex-linked
$ q0 s+ z% r; F" e8 K; y7 Q' ?! z: Iautosomal dominant disorder that affects only
( T* S& j0 c( t% s3 hmales; therefore, other male members of the family
# P5 t! O+ r8 d) Q1 fmay have similar precocious puberty.31 q" Z$ G J3 q4 i! I3 g
In our patient, physical examination was incon-
7 P! l9 y$ d( z6 C. L0 Y Isistent with true precocious puberty since his testi-
1 N @- F1 f) X3 y! Scles were prepubertal in size. However, testotoxicosis
6 z1 W+ s: x* o: U8 }0 Jwas in the differential diagnosis because his father
( |0 c: K( x( i+ E" Kstarted puberty somewhat early, and occasionally,6 A) Q* L1 i$ f% @5 o$ ?
testicular enlargement is not that evident in the u1 d$ B4 L7 K$ ]" z5 a) v- \
beginning of this process.1 In the absence of a neg-
. l& G5 [1 x9 y' x5 G9 qative initial history of androgen exposure, our
0 \/ h5 L9 G8 o- A9 [7 y) j, [biggest concern was virilizing adrenal hyperplasia,, M0 T" m6 X3 B- s
either 21-hydroxylase deficiency or 11-β hydroxylase
) d) c% c7 K" B7 y& S! l2 q0 ~$ }deficiency. Those diagnoses were excluded by find-, V% u- N# b3 I9 J
ing the normal level of adrenal steroids.4 x% F$ R1 t+ u0 M7 @. ^, X
The diagnosis of exogenous androgens was strongly- j0 v4 N) c: \- X( r
suspected in a follow-up visit after 4 months because, A9 f) e- \2 x# ?, X# p1 ~
the physical examination revealed the complete disap-1 A7 }, _* \+ }% }/ k
pearance of pubic hair, normal growth velocity, and: J6 p/ G# h+ R, X+ v$ u. d
decreased erections. The father admitted using a testos-6 }. v( n4 }* ?( E# |
terone gel, which he concealed at first visit. He was
9 u8 M3 j7 s# S9 U! n& b! \3 ^# Jusing it rather frequently, twice a day. The Physicians’' Y- g( e. V5 V! F
Desk Reference, or package insert of this product, gel or
q& V1 U0 e2 t9 E7 |9 Lcream, cautions about dermal testosterone transfer to1 u2 r3 Q x9 i) t D' H
unprotected females through direct skin exposure.
+ F2 U/ r/ g- j7 J4 QSerum testosterone level was found to be 2 times the
' {( T1 R+ a$ {% nbaseline value in those females who were exposed to% ]- ?9 E4 J& Z5 [8 p/ W
even 15 minutes of direct skin contact with their male
1 @- G5 i) V) l( B0 t4 Opartners.6 However, when a shirt covered the applica-
0 ^# {3 V# g( f* Ution site, this testosterone transfer was prevented.( L, x3 y0 B2 C: z( n( X t% j
Our patient’s testosterone level was 60 ng/mL,* W( n Q# u& q, _
which was clearly high. Some studies suggest that
7 T3 B' y- c* i. j5 v( Idermal conversion of testosterone to dihydrotestos-
8 R b( N$ A& a8 p* F4 `terone, which is a more potent metabolite, is more) g& k1 o$ t6 O( q+ ~: W! z
active in young children exposed to testosterone
* S% h U* ?& E; ^% T! Lexogenously7; however, we did not measure a dihy-
* [; e9 Z: U! c0 W* x0 y" G! ]drotestosterone level in our patient. In addition to7 ]1 ~$ W5 b0 Y1 |, A
virilization, exposure to exogenous testosterone in7 G; k- Z' l: T% B, ]& u' P) E
children results in an increase in growth velocity and
! _2 z; v* V! V. \8 N; H( Jadvanced bone age, as seen in our patient.
, x5 t& q. Q' [7 M. C e; Y4 DThe long-term effect of androgen exposure during
5 K3 m) t/ q2 v" |/ T" t9 {early childhood on pubertal development and final0 g9 j- {2 _' B. w+ S% v4 c
adult height are not fully known and always remain
) s0 S# j# n1 ~2 {) Ba concern. Children treated with short-term testos-# c. w0 J+ S7 _& v* L# `, o+ l
terone injection or topical androgen may exhibit some8 i ?0 ?" B7 r4 c$ L0 y8 ~& O
acceleration of the skeletal maturation; however, after5 `% W/ a3 e3 t
cessation of treatment, the rate of bone maturation, ]0 H% D! z1 s3 l( G( I( }# o
decelerates and gradually returns to normal.8,9
3 `. g, F2 N& U2 w+ M$ o( vThere are conflicting reports and controversy; n" R- v5 j) I& q+ k0 T
over the effect of early androgen exposure on adult: y$ O5 C2 w* K
penile length.10,11 Some reports suggest subnormal
( R Q( V: X5 o, V( N1 Wadult penile length, apparently because of downreg- R5 w9 t! W! H6 U7 L# t; n
ulation of androgen receptor number.10,12 However,
2 H5 F0 l. M6 S2 B$ ]Sutherland et al13 did not find a correlation between3 R# ~7 Z1 I; E% c
childhood testosterone exposure and reduced adult$ i5 f* f K* l4 |1 J8 x% e g
penile length in clinical studies.
1 T# g& {( T5 R2 D" pNonetheless, we do not believe our patient is
. I5 F( N/ w7 x) ^1 m6 X3 wgoing to experience any of the untoward effects from) S* r1 X( ]" W, }8 h L) P6 ?( G
testosterone exposure as mentioned earlier because [. ~5 g( r5 ?' ~& r" _. E
the exposure was not for a prolonged period of time.
" }1 \, w% V) a" cAlthough the bone age was advanced at the time of. g* F% y+ {* P, f2 L
diagnosis, the child had a normal growth velocity at0 s# P5 H3 G$ S5 c
the follow-up visit. It is hoped that his final adult
5 H5 D# e; d. R: j& e+ bheight will not be affected.
, x% W m1 e% f, O# eAlthough rarely reported, the widespread avail-- c9 Y$ @! C* Z+ F( z# f
ability of androgen products in our society may
+ t: G$ j# q; `' H9 U+ E8 Findeed cause more virilization in male or female4 h% s; w: d& a7 ?0 u; e
children than one would realize. Exposure to andro-
5 `/ ]" F2 x, O, f5 Z: `! Agen products must be considered and specific ques-6 i; w2 V) E/ N8 ~
tioning about the use of a testosterone product or
/ T) e; l' g, Z. C, J! r$ Tgel should be asked of the family members during
# f" T J% ^8 G+ Kthe evaluation of any children who present with vir-' _: f; y2 a: E+ _. e: I/ R
ilization or peripheral precocious puberty. The diag-- b9 c* O% G. i! U3 B+ ]& O. E& j
nosis can be established by just a few tests and by: r1 r1 O4 j5 x% T9 ]+ ~
appropriate history. The inability to obtain such a n% a* X) S8 S# y
history, or failure to ask the specific questions, may
7 |7 n9 ]5 J; B: N% z, K5 Aresult in extensive, unnecessary, and expensive. H/ K c5 H3 L* j0 Z7 C2 R$ l$ {4 q
investigation. The primary care physician should be
; r& W1 }3 \7 p$ G6 I& O. maware of this fact, because most of these children$ o6 B4 j, }( J& }5 h3 Q. k* N
may initially present in their practice. The Physicians’
6 |& O# C8 U3 dDesk Reference and package insert should also put a3 v& ^, i, s& Y, W4 T9 r; m/ H) D
warning about the virilizing effect on a male or+ ?$ f; B: L( F: ^/ ~; a1 J! o% f" @
female child who might come in contact with some-% |1 h! |' `1 Q% f
one using any of these products.
6 ]( p, X8 }0 o7 X/ p: b" LReferences: i8 n6 ~2 c. P- g+ r8 p. a
1. Styne DM. The testes: disorder of sexual differentiation
- G. K; p" W8 s8 B1 wand puberty in the male. In: Sperling MA, ed. Pediatric% O* J6 X( w: R1 s \/ _
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;' O! E: o" E! p% n. {4 R
2002: 565-628.
, @! o/ B# N1 H1 g- E) Q2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% _( q8 f' E9 g1 apuberty in children with tumours of the suprasellar pineal |
|