- 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
& j3 R5 r# a3 t" h# y" I1 X) J& xBoy Induced by Indirect Topical
( h+ b8 @6 {/ lExposure to Testosterone
7 S z/ o) g/ x- U0 ESamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 K" h0 G f, P; v5 o5 i8 J0 U
and Kenneth R. Rettig, MD1
# h. L" c9 C3 `2 g! W- cClinical Pediatrics
- g: E+ m6 f& e( `/ f4 x0 DVolume 46 Number 6
) M; A M9 d: z3 [+ J& JJuly 2007 540-543& e n4 K9 t$ e9 f1 [2 B$ W/ q
© 2007 Sage Publications
0 ^( u' h( Q+ b* ?3 Z10.1177/0009922806296651
% ^$ c, C3 W# X1 {: nhttp://clp.sagepub.com' n+ P7 z& e) k# a
hosted at) u8 ~3 T- J* }6 I7 ]
http://online.sagepub.com
& k% i! @) ?3 l" SPrecocious puberty in boys, central or peripheral,7 ?, _, s3 c; l0 W) H4 Z6 N+ [
is a significant concern for physicians. Central
( X5 m4 t( |+ ]$ wprecocious puberty (CPP), which is mediated# b) J1 x0 X3 G2 k; ]! y. F
through the hypothalamic pituitary gonadal axis, has& |- P) }) P( t; o1 F! R7 N6 u
a higher incidence of organic central nervous system% x. T9 \/ M9 Z J6 o
lesions in boys.1,2 Virilization in boys, as manifested
! A; s( X/ i. T9 l& O1 m! m0 Sby enlargement of the penis, development of pubic1 B2 Q ~1 X) ?$ a! G! k4 g0 p# j
hair, and facial acne without enlargement of testi-9 U. {' S. e% y
cles, suggests peripheral or pseudopuberty.1-3 We
. m& K/ I+ M( U6 Y$ m8 [6 Breport a 16-month-old boy who presented with the
0 F' Z' \1 @* E! }+ F/ Kenlargement of the phallus and pubic hair develop-' a4 q8 h( u1 k, S5 u' t
ment without testicular enlargement, which was due
& z- n# l- R: q! X; P( s$ b6 rto the unintentional exposure to androgen gel used by7 R; ]+ q5 S" [9 ~$ ?0 H
the father. The family initially concealed this infor-
4 D; x' h4 ~# r+ o2 `5 q8 umation, resulting in an extensive work-up for this
* T3 E1 P1 R: N0 k1 Dchild. Given the widespread and easy availability of
8 C+ W' ?8 f) O0 i, \: E h* @8 a5 etestosterone gel and cream, we believe this is proba-
2 S; l' l k- k! K% `bly more common than the rare case report in the( O9 |3 p" K( X D; g
literature.4
* _, c5 p6 L( [6 \! APatient Report4 x; B6 @2 q9 A
A 16-month-old white child was referred to the
% L& Y) Q3 v# ^3 s1 u& l! M7 B$ @endocrine clinic by his pediatrician with the concern
4 ^. P2 [: A3 P" Gof early sexual development. His mother noticed
. c6 @9 ^+ M2 q! I: `. w! ?. alight colored pubic hair development when he was2 k$ P$ n5 @5 B2 W4 d. ~2 y
From the 1Division of Pediatric Endocrinology, 2University of
: L1 G$ c3 Q9 y. _1 i) w1 P ASouth Alabama Medical Center, Mobile, Alabama.
3 g7 Z0 X/ x1 r6 _0 zAddress correspondence to: Samar K. Bhowmick, MD, FACE,
+ c; g7 b, Y. J* s8 I# X2 E+ | `Professor of Pediatrics, University of South Alabama, College of
: c- ^4 O/ |+ z8 i& mMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% P: ?$ T' m# d1 D9 V; E# H
e-mail: [email protected].
% M# b/ f7 a k3 w3 g9 P) a$ c* Tabout 6 to 7 months old, which progressively became
0 b+ e" {$ s, J) F% N2 Ddarker. She was also concerned about the enlarge-+ W, v B' ~: B* F: G
ment of his penis and frequent erections. The child4 ^* B7 v" y% C& f' b
was the product of a full-term normal delivery, with
+ q6 \& L N/ W$ V, aa birth weight of 7 lb 14 oz, and birth length of k: Z8 o! G/ R# G) K; b
20 inches. He was breast-fed throughout the first year% ]4 i9 e7 q# ^ O8 S9 Z
of life and was still receiving breast milk along with
; K3 u# Z3 [, P7 I$ X6 W+ |/ M- gsolid food. He had no hospitalizations or surgery,
' V K' l9 i# [' Q. B/ }( tand his psychosocial and psychomotor development
1 M7 p b( L2 s% W' } Swas age appropriate.
# B% D, \3 _, w0 R" B7 ?The family history was remarkable for the father,
3 k3 @- T" p$ A* s$ Y6 K2 a' D/ r7 uwho was diagnosed with hypothyroidism at age 16,
# U: e( S: e& f/ m! ywhich was treated with thyroxine. The father’s! S ~6 s% @, l5 l4 B' w
height was 6 feet, and he went through a somewhat
: r3 ?7 S. G. ?. q. b. bearly puberty and had stopped growing by age 14.9 F7 g, q; y) [8 K
The father denied taking any other medication. The
: c1 a5 ]' k2 {2 B5 [4 n9 m9 uchild’s mother was in good health. Her menarche% x2 J# J0 Q4 X" q( J: ^
was at 11 years of age, and her height was at 5 feet
1 X; v, p& c6 N; ?' J# A9 @5 inches. There was no other family history of pre-- w, N. _/ @) s% f5 j* Q
cocious sexual development in the first-degree rela-
$ a/ J1 V4 L& C2 \7 {tives. There were no siblings.
5 G* _5 J- c4 q% bPhysical Examination
& ~, r5 m8 `2 t5 qThe physical examination revealed a very active,$ Q4 P e8 ^) ], L' r! D( J
playful, and healthy boy. The vital signs documented
+ @1 R3 K! J% }) Ha blood pressure of 85/50 mm Hg, his length was" z% ]$ o+ t( P4 O: c9 F
90 cm (>97th percentile), and his weight was 14.4 kg
& c# }+ T! l9 a \- Q8 [) k(also >97th percentile). The observed yearly growth. K: y9 j; k1 P* X
velocity was 30 cm (12 inches). The examination of! u, L( I& u# b+ z' Q9 I
the neck revealed no thyroid enlargement.
% M: @% A9 ]& M2 L* pThe genitourinary examination was remarkable for
8 h# s2 c3 t& O/ o7 [+ Menlargement of the penis, with a stretched length of/ T, j% I' }" J% s- d* u
8 cm and a width of 2 cm. The glans penis was very well; ~4 `$ F! d! D! ^" n- f8 Q
developed. The pubic hair was Tanner II, mostly around
3 x% q8 s: P: G/ C! q5404 ?4 A1 ~- V! y8 W, e( H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; ]' Z" T* Y! Y5 p8 Bthe base of the phallus and was dark and curled. The& l7 E4 a2 `, q" ?8 K. |% i# u
testicular volume was prepubertal at 2 mL each.
; ^, k) g- n2 D7 M j) FThe skin was moist and smooth and somewhat
, S5 v; h( h" n! s0 b- Ooily. No axillary hair was noted. There were no
$ q. [2 w3 U* P8 n* y. {4 |' @abnormal skin pigmentations or café-au-lait spots.- h! M1 M* ~- K% a% P
Neurologic evaluation showed deep tendon reflex 2+4 X* [0 p1 J8 M6 g
bilateral and symmetrical. There was no suggestion- R3 g; r3 G+ {$ {' A5 U" f" x
of papilledema.
$ f5 J0 q) }" `9 ~" VLaboratory Evaluation1 W/ s, I& k& P2 w, [9 `0 R% w
The bone age was consistent with 28 months by7 h' Z5 h; z* ~& f! E" [9 Q
using the standard of Greulich and Pyle at a chrono-2 U$ h4 w1 B; _+ s- y- z
logic age of 16 months (advanced).5 Chromosomal
! }5 r- q! t% |; V4 R. |karyotype was 46XY. The thyroid function test' d' U: B/ B+ d M$ Z1 S L, j+ r
showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 s4 r" \! [- L5 o0 d
lating hormone level was 1.3 µIU/mL (both normal).
: A1 u* H/ x- I: K. @& x% ^! V: DThe concentrations of serum electrolytes, blood$ }0 ?* K7 P. Y! f6 a9 X
urea nitrogen, creatinine, and calcium all were, B- s( I) N+ B5 E! a
within normal range for his age. The concentration# a" O4 C1 B+ K5 d) o' `1 U" y
of serum 17-hydroxyprogesterone was 16 ng/dL
& Z1 ]! ~% k* U& z(normal, 3 to 90 ng/dL), androstenedione was 20
" c8 H' ]7 U+ {% M2 ~, ?2 wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* I3 L, k1 y, t% U, Q7 f9 V6 o
terone was 38 ng/dL (normal, 50 to 760 ng/dL),$ r: \! A! e i" D
desoxycorticosterone was 4.3 ng/dL (normal, 7 to, `# n* K1 X* q" j9 h% S
49ng/dL), 11-desoxycortisol (specific compound S)
: D- u6 w6 G& U+ p: E' Gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: w3 l, ~% S, p+ h3 y4 j& Z5 _( P
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 R; r$ o- _" Z0 @testosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ A. t$ J, V* j1 g4 ]2 L. W: i R
and β-human chorionic gonadotropin was less than* [2 s' w% y. v( K' ^4 l4 ~: U, ^
5 mIU/mL (normal <5 mIU/mL). Serum follicular. E- D; {: o& ?/ S, B# B7 K D# e" K
stimulating hormone and leuteinizing hormone
# K# w0 T) d# j: A6 {concentrations were less than 0.05 mIU/mL. F9 c( Z2 g; Y4 H
(prepubertal).3 |# c9 ]0 q3 M" P$ d( s# P$ D
The parents were notified about the laboratory
8 c* T3 M$ n3 p6 G9 K, E3 Iresults and were informed that all of the tests were7 U/ b' ?3 E/ W; a# x7 H B
normal except the testosterone level was high. The
( Y8 ^5 v* }( Efollow-up visit was arranged within a few weeks to: F3 n1 N$ L4 `
obtain testicular and abdominal sonograms; how-
5 U4 q; l2 S# t3 j7 S* wever, the family did not return for 4 months.
2 @$ E E. C" l0 MPhysical examination at this time revealed that the5 J- Z' z# A( h& M$ R; h
child had grown 2.5 cm in 4 months and had gained
, j) _1 J" Y; E/ J8 N2 kg of weight. Physical examination remained
5 L2 e- ?/ H- t# L& Eunchanged. Surprisingly, the pubic hair almost com-
; e3 P0 [9 _% npletely disappeared except for a few vellous hairs at
2 }5 @9 d0 F3 Sthe base of the phallus. Testicular volume was still 2
# Z3 G) ~# N6 ?% ?: v, ^4 XmL, and the size of the penis remained unchanged.
" C3 S! I3 P! r. p4 YThe mother also said that the boy was no longer hav-' r7 z3 B' J: z7 o8 t: ^, j; y* q
ing frequent erections.
+ L2 \$ n# | f+ Q/ b* }Both parents were again questioned about use of# W8 x: b2 N' w% w
any ointment/creams that they may have applied to) Y4 N7 h+ Y0 E- s* m2 ^
the child’s skin. This time the father admitted the% |( y: S2 U+ W3 p0 z# d- ]4 c* g
Topical Testosterone Exposure / Bhowmick et al 541
1 r2 z! b/ m6 _; m) y; ?4 Wuse of testosterone gel twice daily that he was apply-
! S, x( ]: V% f$ H8 d( Xing over his own shoulders, chest, and back area for
# n; `* b- ]: g! p# h. g! W ya year. The father also revealed he was embarrassed [, b" C& y _
to disclose that he was using a testosterone gel pre-. R# H+ o; _ K6 V
scribed by his family physician for decreased libido0 Y5 f/ `6 |) u2 C; l; M
secondary to depression.
( U0 X8 U% f# ^- b1 |5 YThe child slept in the same bed with parents.
/ l' T V7 H5 k; G; \: c5 N8 b# NThe father would hug the baby and hold him on his( Q, Z) Q( I! h, ~3 J
chest for a considerable period of time, causing sig-
; e, e( z8 }& d( I8 Z& V8 Jnificant bare skin contact between baby and father.5 A1 w0 ?" i5 V; U: |/ p
The father also admitted that after the phone call,
$ w" d: y( v- bwhen he learned the testosterone level in the baby
2 n& s% C$ U+ I# j* Hwas high, he then read the product information! Y: V* x* I0 u+ j! s
packet and concluded that it was most likely the rea-
& q1 L& }; ]9 json for the child’s virilization. At that time, they
! [9 @) K, C. N, k8 `decided to put the baby in a separate bed, and the/ l5 y+ ~0 L2 R1 ~7 N. H
father was not hugging him with bare skin and had1 Q1 `; K) D& k1 p$ T
been using protective clothing. A repeat testosterone1 _- M! U. b( V) I k# P
test was ordered, but the family did not go to the
6 x4 V8 e1 m1 L7 p0 Q/ vlaboratory to obtain the test.- E9 R0 L- c3 i1 Q
Discussion$ I" B: j2 L' [: {) {9 q& E
Precocious puberty in boys is defined as secondary$ }) w9 u5 d* M
sexual development before 9 years of age.1,4
?4 e$ Y+ R: _6 Q9 T% E) R( WPrecocious puberty is termed as central (true) when
' o! [7 |: t2 p- F( Pit is caused by the premature activation of hypo-& H# S8 b& ^) W! ?$ N
thalamic pituitary gonadal axis. CPP is more com-
* Z8 m1 H, ]1 M8 Q' Hmon in girls than in boys.1,3 Most boys with CPP
$ X t' k- A# k, @may have a central nervous system lesion that is! J# T6 R# ]9 ~( f. }. o' Z c
responsible for the early activation of the hypothal-
9 ^; c! ^/ ^) Z" D, n% Mamic pituitary gonadal axis.1-3 Thus, greater empha-4 v# |1 t; c" [' [# Z0 S4 k! d5 Y
sis has been given to neuroradiologic imaging in$ R0 h" j+ P, m
boys with precocious puberty. In addition to viril-
) g H% X! N! Kization, the clinical hallmark of CPP is the symmet-8 P' M8 C. ~4 z V6 b
rical testicular growth secondary to stimulation by
7 [( E0 K0 Y- O5 Bgonadotropins.1,37 f. I6 E$ S2 h& j
Gonadotropin-independent peripheral preco-
4 G% ]5 ], p1 P3 i) y Ycious puberty in boys also results from inappropriate
! p0 a5 [ h/ @0 Y2 xandrogenic stimulation from either endogenous or
& n6 Q# `4 g j. Z; r A+ J( X5 vexogenous sources, nonpituitary gonadotropin stim-8 y; @7 }4 @( _2 }
ulation, and rare activating mutations.3 Virilizing5 c9 m* r% H) Y( J; U4 o2 W; L
congenital adrenal hyperplasia producing excessive9 B. b$ R' v* |( i- s
adrenal androgens is a common cause of precocious" P3 n# Q" ]5 p& n6 U7 P0 O9 t
puberty in boys.3,4
: y! o* X3 N: ]4 p3 ]% qThe most common form of congenital adrenal( K5 C- ^* C- B+ ~* H5 m4 Q
hyperplasia is the 21-hydroxylase enzyme deficiency.( R3 i9 o* [5 P
The 11-β hydroxylase deficiency may also result in4 X! I8 y; G6 ~( d9 r' v
excessive adrenal androgen production, and rarely,. n- { P4 V g* G$ Z& F5 y7 {
an adrenal tumor may also cause adrenal androgen1 p, C. v3 \8 ?/ }- ]; P' ~5 T+ t
excess.1,3
. d( D& k6 o4 F0 {7 mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 _$ W( t; E6 w. W. s
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
# o8 b |: l7 g8 u5 b. }A unique entity of male-limited gonadotropin-
8 Y, K* W8 b* o3 {% _independent precocious puberty, which is also known2 C# i/ [( J% q. ^
as testotoxicosis, may cause precocious puberty at a
+ r! W& [0 j1 Overy young age. The physical findings in these boys
# l7 ~, Z- \' S( Awith this disorder are full pubertal development,
g, V6 R, a c! Q- e+ G, }! o5 iincluding bilateral testicular growth, similar to boys
. n% \* `2 z$ o% ] U" i kwith CPP. The gonadotropin levels in this disorder
% y2 U+ F, N/ Y* Uare suppressed to prepubertal levels and do not show
( Y/ b" G% T$ J, f | dpubertal response of gonadotropin after gonadotropin-
$ Z- y; i. `- C8 i8 D4 Oreleasing hormone stimulation. This is a sex-linked
0 l# ]' O& I7 C! c6 ]; |autosomal dominant disorder that affects only
% {( \4 m9 ^% x7 r* V) K) `% Pmales; therefore, other male members of the family0 T$ _$ j' j4 ]" ]8 G
may have similar precocious puberty.3
6 U w+ f! E' a+ x1 @1 s% v7 [' YIn our patient, physical examination was incon-
- ^% O" {+ t7 H! d" a1 E' V9 r2 }* Gsistent with true precocious puberty since his testi-
A' c( K5 ^0 K3 `cles were prepubertal in size. However, testotoxicosis
! a1 w7 ]( U; h5 s# u" M3 N wwas in the differential diagnosis because his father
{, ~0 X8 d2 z/ p+ sstarted puberty somewhat early, and occasionally,
/ p. ^) M) ]" X: H2 Q& @testicular enlargement is not that evident in the
3 t+ h. M7 E' s$ _. v" \ [, ]& Sbeginning of this process.1 In the absence of a neg-
8 Z R/ L: X. z) g* j2 @" V$ {ative initial history of androgen exposure, our1 G: N0 @" U% Z! |
biggest concern was virilizing adrenal hyperplasia,! d: n$ v! \: I9 q. P1 w
either 21-hydroxylase deficiency or 11-β hydroxylase
0 N" V' i1 C, a( x1 k e edeficiency. Those diagnoses were excluded by find-! X a8 y1 C# {; g5 j+ X3 m4 ^
ing the normal level of adrenal steroids.
& s6 a8 @% L9 C" bThe diagnosis of exogenous androgens was strongly
8 B4 b* P- [6 T1 S0 d* Asuspected in a follow-up visit after 4 months because( V# M. K5 t' s; E3 J
the physical examination revealed the complete disap-
( B5 E7 @& j% [( tpearance of pubic hair, normal growth velocity, and, V' ?- d! r1 _! H
decreased erections. The father admitted using a testos-- t$ u6 x1 g$ u2 |) v- Y# a% L
terone gel, which he concealed at first visit. He was
: T8 A0 \9 ]! o9 n+ X0 Zusing it rather frequently, twice a day. The Physicians’
0 ?0 _' A. {' ?, |Desk Reference, or package insert of this product, gel or8 O. \8 Z1 b5 y* C0 [, N
cream, cautions about dermal testosterone transfer to
9 @. j. Z; u/ j% e& x' `unprotected females through direct skin exposure.. X( i' W9 e2 y" L2 i, |% n
Serum testosterone level was found to be 2 times the- `9 A) Z& y: U. W
baseline value in those females who were exposed to" h8 ^5 ]8 b6 a' U1 m' x
even 15 minutes of direct skin contact with their male
$ x8 _1 }/ \# Tpartners.6 However, when a shirt covered the applica-7 O7 e, V& k2 @
tion site, this testosterone transfer was prevented.
' |. w6 X- m D. {Our patient’s testosterone level was 60 ng/mL,
% N1 A5 N7 u C, Uwhich was clearly high. Some studies suggest that% H- ~7 s% p( o3 P: o' p+ v' C6 ~
dermal conversion of testosterone to dihydrotestos-
6 ?5 F( k* Z7 }6 e+ Y4 }5 xterone, which is a more potent metabolite, is more
" }% O0 Y' X' M6 C0 lactive in young children exposed to testosterone; A7 d1 X( u( S, d/ X4 V1 W
exogenously7; however, we did not measure a dihy-
" G3 S# e( d9 e$ A6 R; r* T& D9 \drotestosterone level in our patient. In addition to5 r: \( a! O( m) X" }+ V2 o2 {) K
virilization, exposure to exogenous testosterone in
- k6 Y0 S0 A" a' ^ x" q% ]; ychildren results in an increase in growth velocity and
8 K; T- y6 M/ `& N0 I5 radvanced bone age, as seen in our patient.) t, `* A Y' P' s5 }) \
The long-term effect of androgen exposure during% _5 P# {- A% Y7 e! s/ n: y
early childhood on pubertal development and final2 N% [; B* n8 U3 T4 v: o7 i; d1 Z. y. V
adult height are not fully known and always remain
- g- I$ z$ m# U S9 c! j. Qa concern. Children treated with short-term testos-
% F- \7 T' r9 W, Y# jterone injection or topical androgen may exhibit some+ A3 p' c# |" h- W( p$ l$ K7 {( E- x
acceleration of the skeletal maturation; however, after
. G' U1 } U. T- Ocessation of treatment, the rate of bone maturation; e( X, H ]5 o3 s3 P3 {
decelerates and gradually returns to normal.8,97 H" L) o7 N, m, V3 m+ n
There are conflicting reports and controversy
) P# V2 W- n7 V1 x) y& [9 ?over the effect of early androgen exposure on adult
6 V. L- E. q8 `) h" o0 [penile length.10,11 Some reports suggest subnormal
+ \- H) X! v8 x0 m# f7 }: Iadult penile length, apparently because of downreg-. y" s* @2 G+ r# k; M* F
ulation of androgen receptor number.10,12 However,
4 f# v) m) {5 A2 L5 ZSutherland et al13 did not find a correlation between9 h& G& B0 g u
childhood testosterone exposure and reduced adult0 P' o( A7 H& l1 L6 Q& j$ ]& f0 w
penile length in clinical studies.& s4 z& `1 Z$ p# V5 e
Nonetheless, we do not believe our patient is Z+ C% _. d1 H$ |% Q& O2 D( a& X
going to experience any of the untoward effects from0 T2 X3 u( |2 w0 |" j
testosterone exposure as mentioned earlier because% M F+ h8 _' y3 L$ |
the exposure was not for a prolonged period of time.
* P/ a8 q7 d7 R8 m# MAlthough the bone age was advanced at the time of3 i! G$ f' n+ O- W$ H3 d! } P
diagnosis, the child had a normal growth velocity at
% T# D$ f1 a% j( {, j0 wthe follow-up visit. It is hoped that his final adult
- d1 v9 }- K0 P6 T. ^height will not be affected.3 q; w, h5 p5 n3 Z
Although rarely reported, the widespread avail-( A. E2 O u) b: G- B1 l$ L
ability of androgen products in our society may; z5 H+ `9 I1 L8 i; r5 ~' ^6 O
indeed cause more virilization in male or female
, `. S4 G4 y# M8 lchildren than one would realize. Exposure to andro-
! C+ X7 p+ O! f7 E, Q" f) ~gen products must be considered and specific ques-1 H: y# ]/ ~! ?- g& i7 R" A& S6 ~) F
tioning about the use of a testosterone product or
7 v1 \0 K# i P* q d6 S* `gel should be asked of the family members during
) @) I! w% o& kthe evaluation of any children who present with vir-
; i) g7 ?" l* }3 T+ \- u) X9 O+ m; Eilization or peripheral precocious puberty. The diag-
/ [5 L8 Z) E) u9 Qnosis can be established by just a few tests and by. r1 T# @: [- R- R. G
appropriate history. The inability to obtain such a5 A% \+ ?* A) M3 J6 D5 ~
history, or failure to ask the specific questions, may, V# z4 p+ s. A; n/ w
result in extensive, unnecessary, and expensive
; r; N- _5 J+ e( z+ `* ~; }9 w; Sinvestigation. The primary care physician should be
/ ^3 h+ |( ] f( d9 l5 ] M& h2 Z- Raware of this fact, because most of these children
. @$ X+ e3 i3 V4 L4 Lmay initially present in their practice. The Physicians’
8 p+ t3 o1 J8 E2 f7 M D6 nDesk Reference and package insert should also put a
" X% t' n% D, o1 k' L6 m" e) e) Pwarning about the virilizing effect on a male or- W$ ]7 [ D7 J9 i) b7 E- C& d
female child who might come in contact with some-+ l* y H- v ]& F# H0 I( B
one using any of these products.) f `6 o1 E+ f' P# {0 A* Q" C, x3 x
References* Y8 Q; T! c( N" K$ f: B
1. Styne DM. The testes: disorder of sexual differentiation
% H; d/ X* u* h! pand puberty in the male. In: Sperling MA, ed. Pediatric
5 X6 ]' i" w+ h/ d$ I U' B1 BEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
a: r) h' l0 `+ d/ B2002: 565-628.4 o* W& g. V* O. }' _( e# V
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% R7 h1 F" C! o
puberty in children with tumours of the suprasellar pineal |
|