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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old
, A5 S2 h; {8 pBoy Induced by Indirect Topical
: [  j: E/ j9 k, K! z# uExposure to Testosterone) |8 K+ O! c3 G. r8 t9 t* Q0 P7 K4 d) e9 `
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 T2 g  y. J( d; ?8 M; Iand Kenneth R. Rettig, MD1
! `, b6 j! K" ?% b- EClinical Pediatrics9 |' A0 A, C  N
Volume 46 Number 6
% H9 g, f( C: E( pJuly 2007 540-543$ K# o7 |+ {: z
© 2007 Sage Publications
' v6 z" c0 j" ?! J$ R10.1177/00099228062966513 g) ^$ ?" K4 T" Y* M% I: z( |/ P
http://clp.sagepub.com2 f! j" V( D2 R2 `7 o
hosted at
: U6 ^8 g9 W3 ^+ thttp://online.sagepub.com' k- V2 \7 N4 T& U8 w
Precocious puberty in boys, central or peripheral,  Y+ y, l# u6 t. b. E- j
is a significant concern for physicians. Central# Q! K9 w+ C7 x; ]- V7 o) _
precocious puberty (CPP), which is mediated
  z6 V! {8 Q3 d$ f3 T# Nthrough the hypothalamic pituitary gonadal axis, has8 P* l* L, H9 [9 I( x+ F$ q( n8 i$ H
a higher incidence of organic central nervous system% v! z3 h# U! f
lesions in boys.1,2 Virilization in boys, as manifested' w$ a. \/ l' a
by enlargement of the penis, development of pubic- X* c# a8 Z2 `0 b3 o0 t
hair, and facial acne without enlargement of testi-$ X9 [" Y0 a8 J7 |. ~  m
cles, suggests peripheral or pseudopuberty.1-3 We4 }7 G; D3 Z2 ~0 g
report a 16-month-old boy who presented with the2 }- l# n" Q7 J  O7 B' l
enlargement of the phallus and pubic hair develop-" c) h3 I) p5 k6 F6 ?$ P
ment without testicular enlargement, which was due; |! x4 H$ q! d4 x
to the unintentional exposure to androgen gel used by7 i* m- F3 @# U5 E  b
the father. The family initially concealed this infor-+ y$ t* N2 q7 M. ^
mation, resulting in an extensive work-up for this/ e0 q' h) [6 Y1 Z! X8 c& v( }1 D
child. Given the widespread and easy availability of
8 Q" p5 K3 B( {6 d  b% q& A) ctestosterone gel and cream, we believe this is proba-0 \5 T, R# o$ B' R$ y& r
bly more common than the rare case report in the- j# f. ~( K' v" u( [' d
literature.4
$ Z) S8 \  L3 [Patient Report# V) l# M  z$ P, F. d, q8 a
A 16-month-old white child was referred to the7 r# r4 |* n: E" T2 a+ j- T
endocrine clinic by his pediatrician with the concern
! F( @, P; M0 q) {! Sof early sexual development. His mother noticed$ {& P0 H$ }8 V; M0 m+ Y
light colored pubic hair development when he was
0 Q3 x9 F* C- u7 J/ c. hFrom the 1Division of Pediatric Endocrinology, 2University of
9 o6 f! r- z! G6 ~3 r" g9 YSouth Alabama Medical Center, Mobile, Alabama.- @' Q  f" T6 T6 \, H0 x- s
Address correspondence to: Samar K. Bhowmick, MD, FACE,$ |& y/ E) H2 e# s- w
Professor of Pediatrics, University of South Alabama, College of3 Z0 c" \7 x+ x( E* o3 S
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 R* z* L. Q% u( t) [7 Je-mail: [email protected].: y$ I; C5 H. U( n' r- v% Y5 R! j  c$ j
about 6 to 7 months old, which progressively became5 W+ b5 Y; d1 N
darker. She was also concerned about the enlarge-
4 J% w. r) Q6 J/ T/ Fment of his penis and frequent erections. The child! H) K" `* w0 t& v, y8 W
was the product of a full-term normal delivery, with
: T/ @" e/ l5 U# ea birth weight of 7 lb 14 oz, and birth length of& |: F0 u! j& Z/ ]4 W
20 inches. He was breast-fed throughout the first year- \+ @4 A  \# M4 S
of life and was still receiving breast milk along with
4 N1 Z/ Q  L, C% g( y; |solid food. He had no hospitalizations or surgery,
7 ~/ t: g' h  ^( A' dand his psychosocial and psychomotor development
6 J: ~, K8 E. V$ u# ]was age appropriate.
) i% d' E) T2 i) M' nThe family history was remarkable for the father,
& G+ u7 C' W. }- D( S" Ywho was diagnosed with hypothyroidism at age 16,( x1 Q1 C* S7 a. ~) ~; [
which was treated with thyroxine. The father’s
' D# I& \1 I' y- Bheight was 6 feet, and he went through a somewhat+ p( @  R: e6 G- K  w2 T: u( Y
early puberty and had stopped growing by age 14.
% e1 B3 f- z0 R, H( C6 V7 ?, B' `The father denied taking any other medication. The
% u3 b+ W: R9 _child’s mother was in good health. Her menarche
0 s& B/ L3 z8 ]8 }8 O0 X" Swas at 11 years of age, and her height was at 5 feet9 O1 T7 M: F' P& M8 B
5 inches. There was no other family history of pre-$ o* }8 y" K0 u* s
cocious sexual development in the first-degree rela-, u; P$ `1 c# y, N, S
tives. There were no siblings.
' n9 d1 f" b: }' A6 l0 N: IPhysical Examination+ U8 e1 j2 p! l: Z) Z8 E0 e
The physical examination revealed a very active,9 ?, _; g! A6 S: `0 ?
playful, and healthy boy. The vital signs documented
$ \: \2 ^9 X" ya blood pressure of 85/50 mm Hg, his length was, b; L1 P+ o# ^! [) D
90 cm (>97th percentile), and his weight was 14.4 kg3 c' O4 b: _% v$ N$ @2 |" c' p
(also >97th percentile). The observed yearly growth
3 {- p$ n7 A, k1 ?5 i) z4 Mvelocity was 30 cm (12 inches). The examination of/ f4 ~& O0 E) V! P$ d5 r( _
the neck revealed no thyroid enlargement.' S& W3 X) C; @5 B2 f/ u
The genitourinary examination was remarkable for
# k' Y7 A( e0 O( t8 V: Ienlargement of the penis, with a stretched length of2 B0 |, k( }, ]/ B4 p% Y
8 cm and a width of 2 cm. The glans penis was very well
& }5 @& B* {/ ?1 Y" T2 y2 \developed. The pubic hair was Tanner II, mostly around" N& K( s8 i" s6 `9 J1 H
540
8 }# {! G  E9 Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 s5 z8 |# f; E0 I# g1 y- C9 H
the base of the phallus and was dark and curled. The& f1 T+ a- [7 m% M  A* n
testicular volume was prepubertal at 2 mL each.3 @( w& j( x2 _' o. i0 y
The skin was moist and smooth and somewhat
0 g. A: P; n+ O$ ioily. No axillary hair was noted. There were no/ ?; K6 l) N' ~# D) p" h, o2 ~  H# H9 }
abnormal skin pigmentations or café-au-lait spots.
$ D5 |! P+ {+ Y; {' L0 Y6 y% JNeurologic evaluation showed deep tendon reflex 2+' L  E, l; ?  Z
bilateral and symmetrical. There was no suggestion# G; E/ K8 H  ^9 j, n/ L
of papilledema.
: |/ {+ q3 z/ s9 ]: t1 J/ yLaboratory Evaluation
8 s, s' y; _+ lThe bone age was consistent with 28 months by
8 x. F( B+ j, ?6 `  vusing the standard of Greulich and Pyle at a chrono-4 i# T* _2 [% N+ p1 P
logic age of 16 months (advanced).5 Chromosomal  n. e) c6 v. V! E/ X
karyotype was 46XY. The thyroid function test
: S' D5 k9 q2 C" d& Jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-% q. m/ _8 _" N+ x& [5 a) P7 E3 s
lating hormone level was 1.3 µIU/mL (both normal).
1 j, I  h" N, Y& MThe concentrations of serum electrolytes, blood+ m9 c2 o4 A! I
urea nitrogen, creatinine, and calcium all were
* p! M# E  Y! P3 m$ vwithin normal range for his age. The concentration
3 ]7 |( `& q- p0 s  e& wof serum 17-hydroxyprogesterone was 16 ng/dL
2 J" d3 S" J; d2 J$ j/ n7 j(normal, 3 to 90 ng/dL), androstenedione was 20( [* ^! T3 {: t( [1 S
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
% F' y3 s- k  Q. {* n4 nterone was 38 ng/dL (normal, 50 to 760 ng/dL),# D4 w: a& P2 M. _7 }' ]+ K
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
- h$ z" z! M1 A+ u/ Z  h49ng/dL), 11-desoxycortisol (specific compound S)
8 _6 @/ W; U; k' M4 awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' H/ {' k6 T* q/ ^! Y) g- ftisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total  J: i, x9 X  Y3 x% f7 L- x
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ Q9 T* n0 l: R1 [  s* Tand β-human chorionic gonadotropin was less than
$ z) q2 [. ]- Q/ b3 n* ^0 p5 mIU/mL (normal <5 mIU/mL). Serum follicular: ?* m: Z( p  H
stimulating hormone and leuteinizing hormone; x& n" h1 \" V5 O  @# f5 Y
concentrations were less than 0.05 mIU/mL
) m: S7 z  M5 o' K( Q3 i# r(prepubertal).. t# T7 e  i/ N
The parents were notified about the laboratory1 W: ~6 i0 D  D; h  }4 A; p/ y9 S
results and were informed that all of the tests were
! [1 u$ y( `& O3 V% [8 l9 [4 `normal except the testosterone level was high. The
+ r( g9 J$ E9 n4 N, J/ i4 Ffollow-up visit was arranged within a few weeks to
% |4 a$ P9 ?% X7 i4 Yobtain testicular and abdominal sonograms; how-! M* Q1 x& Y8 v4 o
ever, the family did not return for 4 months.
' _3 }# [5 `: o: {, U* uPhysical examination at this time revealed that the
. [, i4 Y( y  _9 A6 o# p- cchild had grown 2.5 cm in 4 months and had gained
( L& p  }& m) U& b2 kg of weight. Physical examination remained) x, j/ K- |  K6 r& m
unchanged. Surprisingly, the pubic hair almost com-7 T8 x- d# h# u$ F9 ^2 e
pletely disappeared except for a few vellous hairs at
8 W0 m" e' p/ x% a0 r4 e8 Athe base of the phallus. Testicular volume was still 2# e! J/ d. T/ f7 c9 `0 m
mL, and the size of the penis remained unchanged.
5 o& y! A" g* P9 s! s: |4 RThe mother also said that the boy was no longer hav-
& \/ b+ R. ]/ f8 n5 ling frequent erections.* H2 U, R5 i, e% h. u$ J
Both parents were again questioned about use of
! v6 G1 W) h6 l: `: R* }any ointment/creams that they may have applied to1 y! c2 R+ B. a& p- @: u
the child’s skin. This time the father admitted the% O, v, x8 X+ W: Q$ G# G
Topical Testosterone Exposure / Bhowmick et al 541
% j7 G6 O4 r( E; N4 u$ Wuse of testosterone gel twice daily that he was apply-8 V( r6 x6 i8 R3 m" N" _8 Z
ing over his own shoulders, chest, and back area for
* J! `6 w6 z5 M2 L1 v3 Q- la year. The father also revealed he was embarrassed2 C. Q8 q* B6 l2 W6 Y  P+ o1 [
to disclose that he was using a testosterone gel pre-( _' c8 \* u; X8 n
scribed by his family physician for decreased libido- \0 o+ f7 ?3 K2 O8 z* X4 q( f2 `+ S
secondary to depression.
9 a) t1 T/ ?5 M& p: MThe child slept in the same bed with parents.
; m& e4 m2 o: |8 x* |+ sThe father would hug the baby and hold him on his
% w8 Y5 n$ ^* O/ n3 rchest for a considerable period of time, causing sig-% a& b; p8 L' b  M1 [7 T
nificant bare skin contact between baby and father.& u' {0 [# {; O0 a0 z9 a; }
The father also admitted that after the phone call,
: k. H8 p$ V2 L) zwhen he learned the testosterone level in the baby
6 [/ o" @5 x8 B: \2 x& G: \was high, he then read the product information0 r8 _  G' O% j: _- }
packet and concluded that it was most likely the rea-' q- ~/ W: v1 N
son for the child’s virilization. At that time, they
: b. J  d8 g* cdecided to put the baby in a separate bed, and the
- b2 n/ `* \6 n4 f3 R$ E  P2 b( |father was not hugging him with bare skin and had
. y2 P" M9 |  u$ H# S1 k; \' L% fbeen using protective clothing. A repeat testosterone
4 L. _# p, m/ Wtest was ordered, but the family did not go to the
1 I' q/ `, T, Q# _7 q4 f* Klaboratory to obtain the test.
* U3 g7 B" A- P% `2 B$ p& h! wDiscussion
3 U6 Z& {$ V" f% V) P& x1 ?; D1 MPrecocious puberty in boys is defined as secondary
6 q- t: h% Z( }$ f  bsexual development before 9 years of age.1,4# t1 D, l" p0 S1 s
Precocious puberty is termed as central (true) when
. H+ {  @( b  @. q) V+ Xit is caused by the premature activation of hypo-% Q2 W  p. F; U* v! C4 M- N
thalamic pituitary gonadal axis. CPP is more com-- @& r0 S5 e$ B& R* V5 y: L- m4 k
mon in girls than in boys.1,3 Most boys with CPP5 Z" ^  ^$ f8 Z. K; R" {
may have a central nervous system lesion that is' ]0 P. k( f& V+ t9 W9 G/ B8 ?
responsible for the early activation of the hypothal-
5 v) m# g3 v9 P' R0 C/ C0 xamic pituitary gonadal axis.1-3 Thus, greater empha-) b8 }& N  @4 m- s" U
sis has been given to neuroradiologic imaging in' d$ U' y; B+ P
boys with precocious puberty. In addition to viril-
" X7 ~8 R  F/ t2 F& G" mization, the clinical hallmark of CPP is the symmet-
- K, h5 H+ g! q, grical testicular growth secondary to stimulation by
5 `* @. [- l- `gonadotropins.1,3
% y9 N1 h' A  J$ L# s7 E% c: ZGonadotropin-independent peripheral preco-
/ @, O! z" W7 mcious puberty in boys also results from inappropriate
8 s' b  H* S, W% v  ?( _3 D5 zandrogenic stimulation from either endogenous or
1 X0 e2 A. `3 D2 ?. M7 oexogenous sources, nonpituitary gonadotropin stim-9 p, z1 Z" j; j: r1 m! C
ulation, and rare activating mutations.3 Virilizing
; F( T% T6 ~" v, _congenital adrenal hyperplasia producing excessive
0 @; E& ^$ n5 R/ x0 j; ]0 D- |) Z& Qadrenal androgens is a common cause of precocious* ]1 D. l: ?5 l  j/ I6 O
puberty in boys.3,4
8 d) B3 Z5 m3 H$ Y- kThe most common form of congenital adrenal: c4 f4 U; q4 J* Y- X& \  S
hyperplasia is the 21-hydroxylase enzyme deficiency.
8 z7 D: W9 i/ R3 @, ~* S; I. F/ yThe 11-β hydroxylase deficiency may also result in
, K5 O* b% n0 cexcessive adrenal androgen production, and rarely,
/ k+ ~5 b: F% ian adrenal tumor may also cause adrenal androgen) a3 T7 C3 o) h, ~: M
excess.1,3
2 j2 ^" o1 p4 r, W( |9 k5 R. j5 K) Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: ^, C* O  @4 d. ~2 G
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 M- }5 m/ f7 `0 y5 lA unique entity of male-limited gonadotropin-
- s% |( s6 D, v, o" mindependent precocious puberty, which is also known9 o$ e* |7 n% N
as testotoxicosis, may cause precocious puberty at a7 K6 t4 b; \3 M( z# [
very young age. The physical findings in these boys
7 m9 ^2 j% h8 [# swith this disorder are full pubertal development,1 _- R: X% [- ]/ Q$ }8 I
including bilateral testicular growth, similar to boys, A& ~' l$ I4 w, V0 s
with CPP. The gonadotropin levels in this disorder! ?- i5 U/ ?/ `. q7 d
are suppressed to prepubertal levels and do not show
9 Q# `. m. D, Tpubertal response of gonadotropin after gonadotropin-7 Y& ~) W+ u9 x; w9 \9 K) _
releasing hormone stimulation. This is a sex-linked) s7 `: j' _& T9 o/ P% d, ]# Z
autosomal dominant disorder that affects only
' Y3 i3 u, }" s; E8 p! m( Wmales; therefore, other male members of the family
9 e# g% k4 e+ F8 smay have similar precocious puberty.3
; E/ O5 C7 r# m' t8 h* A4 m  kIn our patient, physical examination was incon-
/ A8 L3 J4 G2 q9 Z8 Dsistent with true precocious puberty since his testi-
( H( V8 m8 T) p- M% t7 i2 Ycles were prepubertal in size. However, testotoxicosis9 _; m  t# A4 e
was in the differential diagnosis because his father, L, [- Q6 n" D/ T
started puberty somewhat early, and occasionally," d* M: E% e( |1 h
testicular enlargement is not that evident in the
/ G& N! e5 s7 Y4 K, i9 [/ ?9 Vbeginning of this process.1 In the absence of a neg-
& f& |; }, J! z+ cative initial history of androgen exposure, our5 E5 g! x& o8 G) T- |: q1 ?
biggest concern was virilizing adrenal hyperplasia,- ~: f- Q7 b9 Y/ J8 p8 O
either 21-hydroxylase deficiency or 11-β hydroxylase
) X4 i9 k+ I1 r" X- u+ N  R0 I7 wdeficiency. Those diagnoses were excluded by find-
5 I, m( _1 d0 W8 @ing the normal level of adrenal steroids.
0 N$ k/ y" g+ YThe diagnosis of exogenous androgens was strongly
  U9 `  t. r# b2 |# Q& h% Xsuspected in a follow-up visit after 4 months because
4 e6 u, N- \! `+ [. ^' ~+ G4 e/ Gthe physical examination revealed the complete disap-
1 {+ r+ g" A% S7 z; f" spearance of pubic hair, normal growth velocity, and
% j3 Q- H" ~9 f* Z* n9 w1 ydecreased erections. The father admitted using a testos-
" r1 T1 r# D( O8 S; e. P) d/ c+ tterone gel, which he concealed at first visit. He was! K0 X+ Z( [# e9 k; W
using it rather frequently, twice a day. The Physicians’
3 B1 I; [& w* j1 C) D* w9 CDesk Reference, or package insert of this product, gel or
! s7 p/ t! F2 B1 ]cream, cautions about dermal testosterone transfer to0 @* x7 S, W6 Y9 e' W
unprotected females through direct skin exposure.
% t/ {3 i% T4 s+ n+ T3 YSerum testosterone level was found to be 2 times the
$ m" x: W: y7 g! kbaseline value in those females who were exposed to
, z  N* f: ?' v  weven 15 minutes of direct skin contact with their male
! b7 p1 n4 k2 V. m" z9 ]4 Vpartners.6 However, when a shirt covered the applica-
4 c$ D7 M+ d8 k( D# m' y. Ztion site, this testosterone transfer was prevented.
6 R: a( P6 C" L* {8 Q5 wOur patient’s testosterone level was 60 ng/mL,
" ]4 H0 P9 B: Z; lwhich was clearly high. Some studies suggest that
: c1 `- P2 I0 \7 I; G6 |dermal conversion of testosterone to dihydrotestos-
, |9 @! S# j5 e+ w1 rterone, which is a more potent metabolite, is more/ e  |- ]  Y4 u, Q! \
active in young children exposed to testosterone
8 `, c* I; N8 g9 ?% ~( ^$ texogenously7; however, we did not measure a dihy-
: ]" z6 X/ T9 H( A, cdrotestosterone level in our patient. In addition to1 t7 |/ c% |" ?. d! }
virilization, exposure to exogenous testosterone in
! K7 }$ r, K0 I# A! V* Ochildren results in an increase in growth velocity and0 h; E' j$ @$ X4 o5 H- O$ I2 o( _
advanced bone age, as seen in our patient.
/ [: X( k) K1 P& ?0 [" ~6 d" ?The long-term effect of androgen exposure during
6 A- {* C2 G: X' p- \5 wearly childhood on pubertal development and final
- S" u5 g$ }1 O6 j; p3 `9 [adult height are not fully known and always remain
6 t8 E4 d1 h3 pa concern. Children treated with short-term testos-
! J) Z$ K* d$ g1 Y5 D" `terone injection or topical androgen may exhibit some
# s3 g( g1 I9 \) \2 uacceleration of the skeletal maturation; however, after
6 J5 P- X6 t( @cessation of treatment, the rate of bone maturation
: V) ^& a2 b: |# u4 T4 [decelerates and gradually returns to normal.8,99 ^- m% C7 ]# e8 H
There are conflicting reports and controversy
. S5 V2 a8 h$ yover the effect of early androgen exposure on adult
* w; S: A! T9 _5 fpenile length.10,11 Some reports suggest subnormal1 V+ e/ N1 R2 y. v( h+ C
adult penile length, apparently because of downreg-! q) N8 h5 t6 o/ o8 M" Z7 b: Q1 y
ulation of androgen receptor number.10,12 However,
; I! U+ f% Q' l  Y/ ?Sutherland et al13 did not find a correlation between, l8 B6 m8 A/ B1 x+ E
childhood testosterone exposure and reduced adult
2 `2 x0 k$ M1 v6 Cpenile length in clinical studies.6 }2 J* \5 K' O1 _- f; r
Nonetheless, we do not believe our patient is$ ?+ n; b& T! I% A! \9 o: F
going to experience any of the untoward effects from) m. m5 ?1 v4 e4 S/ c
testosterone exposure as mentioned earlier because& t7 Y4 h9 S0 [- V& T
the exposure was not for a prolonged period of time.
% L. H7 o9 Y( _- B) R& x6 tAlthough the bone age was advanced at the time of/ K0 r5 h+ ?  z2 y# F
diagnosis, the child had a normal growth velocity at2 ^) Y& a- K) e& Z3 ~- S6 C1 }
the follow-up visit. It is hoped that his final adult- w8 _8 p( y& W. Y7 s6 K
height will not be affected.
& C" O, d& y5 j. k, e1 DAlthough rarely reported, the widespread avail-# U7 ]4 N, g: n, }: z( S, P5 k
ability of androgen products in our society may
) Y# {% x2 p8 K+ tindeed cause more virilization in male or female! O& H  n* B" M8 p+ w
children than one would realize. Exposure to andro-: s- E  U. b3 z: E9 u2 h. f
gen products must be considered and specific ques-
6 P+ R* q, n3 T+ c* \5 Wtioning about the use of a testosterone product or
# L. Y$ M1 V' Mgel should be asked of the family members during- \0 B8 D" w1 X8 F* j& I
the evaluation of any children who present with vir-
; j8 k- I* Z% O5 f- `4 xilization or peripheral precocious puberty. The diag-
0 P" [5 B9 Q, y) ]" O; Bnosis can be established by just a few tests and by1 @( Y* _7 P$ B7 B  u1 [- m
appropriate history. The inability to obtain such a$ z- e% K  G% P# \8 m
history, or failure to ask the specific questions, may
# R9 l7 _% r$ F3 e$ ~result in extensive, unnecessary, and expensive
* g5 ~1 s  \* X  Zinvestigation. The primary care physician should be
" L/ J" W/ o* ]! Naware of this fact, because most of these children2 B5 x! y, D" b
may initially present in their practice. The Physicians’6 W( g3 q1 w: ?  t% v$ f9 l6 B% \
Desk Reference and package insert should also put a* b% f4 H& I  u; O/ u9 n
warning about the virilizing effect on a male or) m8 `9 @+ V: |4 _  n4 P! b' r
female child who might come in contact with some-
9 ^0 s1 J* ?/ G* h: m$ qone using any of these products.
7 v0 T2 M5 G& K; v  i+ aReferences
5 P2 M, v% a4 ^% U! P# j# ?+ B1. Styne DM. The testes: disorder of sexual differentiation
* @5 u4 K5 A0 k8 U- i* t& b- jand puberty in the male. In: Sperling MA, ed. Pediatric0 E/ Q  i% E3 j
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( _0 E8 [* ]  N6 _. Y# v& p0 e  s
2002: 565-628.* ?+ |/ f3 c) g2 p7 R
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) l$ x6 q0 q, r( o) p. L0 k
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
7 A! P0 T/ B- h5 S5 g9 M# `7 a  FBoy Induced by Indirect Topical
  ?  m( \% B; Q% r% e& D: U' jExposure to Testosterone
' f$ }8 F2 Y0 Y0 TSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 |9 q  i# B# d9 \0 Y! Q9 w" T) A
and Kenneth R. Rettig, MD1: f& u  [3 {* t  T
Clinical Pediatrics: `  e" a8 S  \/ ?9 D9 m
Volume 46 Number 6
0 o3 e  v  {; i  T/ fJuly 2007 540-543
. _4 o. r, U6 U7 r! R6 ?# ?© 2007 Sage Publications
7 @- t! t# R5 q; T' y10.1177/0009922806296651
0 Y, J& L& k. t5 ?: Q5 E0 bhttp://clp.sagepub.com
) K. }, T7 Q, G5 M9 C. Y3 A/ n) Rhosted at
. b/ F' @" K4 lhttp://online.sagepub.com
2 E: G9 y3 r  s- P( r, tPrecocious puberty in boys, central or peripheral,
9 j+ `# _3 x, e0 Y7 z1 W* {) Q6 eis a significant concern for physicians. Central
. |" p1 W6 r9 _* E7 J1 u% uprecocious puberty (CPP), which is mediated$ G1 y% ~7 ?7 h! |
through the hypothalamic pituitary gonadal axis, has1 e6 H$ s' X+ S: x0 g0 _# o
a higher incidence of organic central nervous system: X/ L3 G& c+ r8 b  k9 ?
lesions in boys.1,2 Virilization in boys, as manifested& n" H- X) t" ^- e) G0 o
by enlargement of the penis, development of pubic
) Y& M- D5 {6 V( f4 A6 Xhair, and facial acne without enlargement of testi-
1 Z& H# n; q. _$ ycles, suggests peripheral or pseudopuberty.1-3 We
# \4 w! O+ S( h# rreport a 16-month-old boy who presented with the
- ]/ W4 u) _& i8 W' lenlargement of the phallus and pubic hair develop-
6 P, o! O( S$ F# Ement without testicular enlargement, which was due$ Y" ?0 T  k% o$ H0 `7 l
to the unintentional exposure to androgen gel used by
% K& p  `5 Y' ]( ithe father. The family initially concealed this infor-
2 p! m% I5 l8 d8 ^+ [: qmation, resulting in an extensive work-up for this+ J4 X6 Q, l& x5 T9 t2 ^( F
child. Given the widespread and easy availability of
, y# B& ]+ t& a0 ^testosterone gel and cream, we believe this is proba-
9 n" ~' s& B7 j4 tbly more common than the rare case report in the* v2 x1 I0 D) E. r, I" H9 K4 r, X
literature.4, u/ |. i- k& V5 F  N, o" e
Patient Report; g1 }6 L) y1 \  [1 c
A 16-month-old white child was referred to the
8 v2 l+ g3 c  L/ T+ q$ Nendocrine clinic by his pediatrician with the concern
4 _" s  U6 w( x% O4 hof early sexual development. His mother noticed
. @, d0 t6 g) Q2 d# Mlight colored pubic hair development when he was
% B# R  H3 M  k4 [9 ]& i" g8 t4 y# H5 CFrom the 1Division of Pediatric Endocrinology, 2University of+ T' W1 P$ A1 |2 C, X& b: g
South Alabama Medical Center, Mobile, Alabama.
, j( E$ F1 O% j% b  [2 LAddress correspondence to: Samar K. Bhowmick, MD, FACE,
! s& x% ~; ]% b, e5 X% nProfessor of Pediatrics, University of South Alabama, College of
$ @2 V. n0 g: t( eMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;: G" a% c0 I6 V0 r; r; t
e-mail: [email protected].8 @' |3 l' W1 d( R
about 6 to 7 months old, which progressively became
; p' y2 B. u! n5 Sdarker. She was also concerned about the enlarge-% v2 m0 {) C6 R$ C
ment of his penis and frequent erections. The child. c* E% J% r. I% K
was the product of a full-term normal delivery, with
% v2 I; j  I0 a9 p, v. Ua birth weight of 7 lb 14 oz, and birth length of) b. H7 p3 j7 D+ d7 W# e9 U( C
20 inches. He was breast-fed throughout the first year
1 `% c0 {- A+ y+ ~3 T. P: lof life and was still receiving breast milk along with% z6 Z4 A; E1 O6 J7 |$ I, h2 |
solid food. He had no hospitalizations or surgery,: w  n' ?0 R0 G0 |- o2 N
and his psychosocial and psychomotor development: ~% Q1 ?7 n- M8 ]& m! Z; ^
was age appropriate.* {- b2 a* K" \2 y( Z) d' l
The family history was remarkable for the father,
) |6 V. P, X. K. [. \1 uwho was diagnosed with hypothyroidism at age 16,
+ e+ \+ f* E- J) W' Q% f! Xwhich was treated with thyroxine. The father’s
: x* ~# e& u% l. w4 \( d+ Y: hheight was 6 feet, and he went through a somewhat" u" x# s8 @, N( R4 n
early puberty and had stopped growing by age 14.
7 u5 r* |1 V' W" |! kThe father denied taking any other medication. The
. ~  ]. c3 l' {" C9 bchild’s mother was in good health. Her menarche
4 i3 y- u( [5 ?4 g- o. y! qwas at 11 years of age, and her height was at 5 feet- n& O. P; L6 h7 ]& q9 L
5 inches. There was no other family history of pre-
' ~% F/ Z6 ^3 X4 O7 ycocious sexual development in the first-degree rela-. Q& B; T! M' P6 s
tives. There were no siblings.: \( @0 f2 K0 h, s' p* c6 t
Physical Examination- L& R  S/ s# |6 w* V1 a6 ]; h
The physical examination revealed a very active,( j% T8 \* j/ V! ^3 p% [, L! P) m' X
playful, and healthy boy. The vital signs documented
0 c. H, D  m) `% Ya blood pressure of 85/50 mm Hg, his length was* Y6 M+ G8 H- o3 j
90 cm (>97th percentile), and his weight was 14.4 kg
5 o  Q" T6 k$ v* {* ^3 n(also >97th percentile). The observed yearly growth
8 X* J. \6 n4 H* qvelocity was 30 cm (12 inches). The examination of# X6 N- ^- _$ S0 ]
the neck revealed no thyroid enlargement.
/ s2 H; f) F+ D2 `' h3 ~: SThe genitourinary examination was remarkable for
# O2 y- d+ k6 {/ M! M1 uenlargement of the penis, with a stretched length of
6 |; n* e9 n" k. [/ g- u8 cm and a width of 2 cm. The glans penis was very well2 O3 h: v6 s' F& A: c) O* J7 V9 j% F
developed. The pubic hair was Tanner II, mostly around; D$ w( ~; k3 I% N( ]
5402 K+ o  J7 |, c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' n% q  }6 b) ?4 \2 Y! {- g7 W9 ]
the base of the phallus and was dark and curled. The( l" G# H" s$ }) F$ F: r7 e
testicular volume was prepubertal at 2 mL each.
: S( T( i5 ?* Z! t; KThe skin was moist and smooth and somewhat
1 g5 M$ P/ f7 C3 d" W/ Noily. No axillary hair was noted. There were no
3 E3 {: k7 F+ [3 Q3 l- B7 oabnormal skin pigmentations or café-au-lait spots.% h$ L3 N* d% _0 C: J9 k
Neurologic evaluation showed deep tendon reflex 2+
3 P+ M: I5 i  o5 k# ?# _6 sbilateral and symmetrical. There was no suggestion  d! U7 w* Z& O) P: G6 r+ b4 z
of papilledema.7 c0 M4 ~  d0 ^% I9 B! j4 `
Laboratory Evaluation) t$ \! I* f1 P+ W% w6 \. ]
The bone age was consistent with 28 months by  `2 ~1 v5 z  G- l3 Z
using the standard of Greulich and Pyle at a chrono-2 s( x" {0 l* u' S5 v8 w6 c
logic age of 16 months (advanced).5 Chromosomal
# {& R4 k! X+ k9 Gkaryotype was 46XY. The thyroid function test
, e: e* W; b- }1 l3 `7 ^" vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
& m7 S- h: k- A  C4 ]5 P" z8 plating hormone level was 1.3 µIU/mL (both normal).2 t9 Q; ?: x" j5 U3 p) |
The concentrations of serum electrolytes, blood% L# S, O6 b1 Q
urea nitrogen, creatinine, and calcium all were' K* H3 M; h& b
within normal range for his age. The concentration
( u$ U) q) A9 N+ [2 dof serum 17-hydroxyprogesterone was 16 ng/dL; p* \+ }. t$ _6 y7 T) f5 z* r$ H3 {
(normal, 3 to 90 ng/dL), androstenedione was 20' n' U' q4 R( o9 g; \0 b0 _
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 K, F5 x. H* Dterone was 38 ng/dL (normal, 50 to 760 ng/dL),- n8 j, \) Z8 C) Q" _5 A) K! ?' O
desoxycorticosterone was 4.3 ng/dL (normal, 7 to0 c, a0 @, q& y! E8 a
49ng/dL), 11-desoxycortisol (specific compound S)
- U, b* J2 U1 Y6 U2 T5 t8 n) Lwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& {' ?( y7 u0 \: f- F+ {tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* @9 J$ N& Z! I. O1 Z( t- L
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! a. p& ^. U% Zand β-human chorionic gonadotropin was less than
0 J) r+ h. t* M& {+ n9 P: b( q$ @5 mIU/mL (normal <5 mIU/mL). Serum follicular+ X) [1 Y! Y9 ~* s4 z% T
stimulating hormone and leuteinizing hormone2 G8 l$ h" E1 Z7 `; f4 y( N
concentrations were less than 0.05 mIU/mL
7 u8 ?- x$ b' J  B! t+ P) n(prepubertal).+ j5 y& ^! X" P/ b" r" O
The parents were notified about the laboratory: h8 k8 z- |" R/ x5 u
results and were informed that all of the tests were
  c+ p: Y- e$ t' I; cnormal except the testosterone level was high. The2 {( }* g+ y8 c6 F- A5 \
follow-up visit was arranged within a few weeks to% k- r. M3 {1 S6 e% R7 M4 g- T! g
obtain testicular and abdominal sonograms; how-
; t. c: M) E' `$ l9 _3 z1 d* Gever, the family did not return for 4 months.
% r4 d& X  ^6 g; S! q2 ZPhysical examination at this time revealed that the
: j8 F/ Z' ?0 ~- d3 {$ bchild had grown 2.5 cm in 4 months and had gained
9 B0 f; H0 M( j% x2 kg of weight. Physical examination remained8 n, `$ {+ w5 b6 H
unchanged. Surprisingly, the pubic hair almost com-
& [  D* b, [5 U1 xpletely disappeared except for a few vellous hairs at
" @8 ]$ g# N6 mthe base of the phallus. Testicular volume was still 2& [! e/ W+ O7 h! |. R2 Y+ T+ f
mL, and the size of the penis remained unchanged.- u& ?: x% o7 E) C2 l7 s8 D
The mother also said that the boy was no longer hav-, d1 h+ G: o& D  T7 l
ing frequent erections.
- A/ p, |' K+ ?# {6 g2 ]  XBoth parents were again questioned about use of
9 d7 V$ @- S, s( d" c& `* T, Iany ointment/creams that they may have applied to& O; X, c' `. N) [
the child’s skin. This time the father admitted the: p6 O* S( X# A" l, I+ s
Topical Testosterone Exposure / Bhowmick et al 541
& }+ R: e3 ^7 {0 z6 ^( m+ buse of testosterone gel twice daily that he was apply-' ^% Q' p% ^0 |- r( X, e$ }
ing over his own shoulders, chest, and back area for/ ?% E1 w; ~1 n
a year. The father also revealed he was embarrassed- N3 z: d7 v+ P, N4 ^' [
to disclose that he was using a testosterone gel pre-
- Q# s9 Y7 d6 X) F8 Oscribed by his family physician for decreased libido1 x# h% |  L3 K/ w1 A
secondary to depression.
; S6 N, |  L6 P9 [3 vThe child slept in the same bed with parents.
, C- V+ h" [3 d% u1 ~$ ^The father would hug the baby and hold him on his7 Z, K7 l; Q4 h1 W# `
chest for a considerable period of time, causing sig-
% I& B8 [7 P5 e3 j0 Fnificant bare skin contact between baby and father.; r& x* H  k3 _$ Z
The father also admitted that after the phone call,# \4 k0 Q& w9 z. p1 O" a
when he learned the testosterone level in the baby, c! j6 z+ u% f# L
was high, he then read the product information
* C3 s/ [1 z' Q* Q1 J4 F: G+ b0 Epacket and concluded that it was most likely the rea-
6 G6 S3 v8 w) H- R, e- g' T' p4 Kson for the child’s virilization. At that time, they- K& H& A  k4 q& K( v. Z
decided to put the baby in a separate bed, and the9 ?8 l9 n/ b! g5 F- N
father was not hugging him with bare skin and had
0 D, X; K8 v$ B& A; [! cbeen using protective clothing. A repeat testosterone" ~0 k  a) Z# j+ v8 \
test was ordered, but the family did not go to the  z+ p) E5 C$ |2 ]) Q0 ?
laboratory to obtain the test.
- f1 `5 Y7 S- m4 `, ~2 Q  i. A& ADiscussion
; s% p# r) Y1 ~+ y+ H  }Precocious puberty in boys is defined as secondary% @0 W3 R7 s4 G* m( w8 \
sexual development before 9 years of age.1,4
" D4 k" L' ]2 Y" iPrecocious puberty is termed as central (true) when1 U! C0 L. ^/ m7 U/ t+ f
it is caused by the premature activation of hypo-, D5 Y. V* A/ C) ~$ o
thalamic pituitary gonadal axis. CPP is more com-
6 ~+ T" r$ Y: t9 N$ @4 F! g4 w1 v) Mmon in girls than in boys.1,3 Most boys with CPP: Q" [( ~+ i- Z
may have a central nervous system lesion that is
$ @/ L! w% K, t3 lresponsible for the early activation of the hypothal-
  H: S& F( A8 f' s8 E8 H3 d1 Famic pituitary gonadal axis.1-3 Thus, greater empha-
$ p: h0 ]1 {8 tsis has been given to neuroradiologic imaging in
% m/ i! [8 ]  w; t/ y# ~boys with precocious puberty. In addition to viril-$ X! J! l  Y3 N& F# Z  k
ization, the clinical hallmark of CPP is the symmet-
- t4 K. w2 d. B) ~8 B' U2 q2 t7 o: vrical testicular growth secondary to stimulation by9 I4 S9 H# r+ U: B( `1 i
gonadotropins.1,3
# o" ]/ V* E# Q) g9 P! WGonadotropin-independent peripheral preco-/ F4 Y& N) J" W
cious puberty in boys also results from inappropriate  \2 d0 Z2 F' o! H( n0 j5 A0 k
androgenic stimulation from either endogenous or  T4 O* W/ ~3 }/ r" G
exogenous sources, nonpituitary gonadotropin stim-/ h! ~) `  q5 P1 S, G' k
ulation, and rare activating mutations.3 Virilizing- b9 S1 h8 L  ?
congenital adrenal hyperplasia producing excessive
, P6 k* y) Q: @# U) Madrenal androgens is a common cause of precocious
: s4 N/ v  V$ Vpuberty in boys.3,4
+ t2 C2 U9 ^- z; t( K: @The most common form of congenital adrenal
1 R+ e5 t9 S$ b+ }" ?, ihyperplasia is the 21-hydroxylase enzyme deficiency.7 t# y+ s0 }+ A# G
The 11-β hydroxylase deficiency may also result in
- Y& ^' f6 j) A9 C7 N6 s5 uexcessive adrenal androgen production, and rarely,0 ?* O' j+ J2 q' B( C
an adrenal tumor may also cause adrenal androgen
3 \6 J& |. E/ n; yexcess.1,3
8 p4 f- L" ~# Y6 Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ V5 f+ T6 U) d7 a542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- f# Y+ B$ I! T  @- ?& f) \( YA unique entity of male-limited gonadotropin-! z6 c( N- G/ G) S# s3 l  ]  U
independent precocious puberty, which is also known
! e7 c* A' L# i" ?+ zas testotoxicosis, may cause precocious puberty at a
- ?$ {* j/ R# ?, ~2 ?9 n4 Gvery young age. The physical findings in these boys2 e' `' L0 t; X6 w
with this disorder are full pubertal development,
7 v3 ~( q) O0 }+ R0 t: O' o+ Cincluding bilateral testicular growth, similar to boys6 Q( X% P; g. X
with CPP. The gonadotropin levels in this disorder8 i) x$ U; z; @% F; r# K
are suppressed to prepubertal levels and do not show
4 B/ o0 m8 B# V7 L4 apubertal response of gonadotropin after gonadotropin-
) Z/ g2 F! @! ]" C" }" Breleasing hormone stimulation. This is a sex-linked
8 @" y* d/ Q  ~# G1 Hautosomal dominant disorder that affects only9 t% E3 M7 v$ P2 O
males; therefore, other male members of the family* [$ M) Y1 |9 M3 Y& I1 }$ d
may have similar precocious puberty.39 ^" [4 b6 l; b; F4 F/ r
In our patient, physical examination was incon-
0 _7 F! Z. v0 d' Q5 d) l( bsistent with true precocious puberty since his testi-+ o$ X0 H( D" o6 [' s
cles were prepubertal in size. However, testotoxicosis9 [4 J0 i  b( N9 g! [5 e7 X
was in the differential diagnosis because his father  ]" ?9 {3 w3 p% Z# `6 D. p
started puberty somewhat early, and occasionally,+ K3 z7 f$ Z* J# `) Q
testicular enlargement is not that evident in the
+ z% f( o% @& I! }beginning of this process.1 In the absence of a neg-
: g  k- a& I$ u6 w! v: r# f3 F6 xative initial history of androgen exposure, our
: `4 X: s( g! q6 l7 m6 v! J1 z9 fbiggest concern was virilizing adrenal hyperplasia,
/ G: v1 r" ]" u  z9 a. x4 `either 21-hydroxylase deficiency or 11-β hydroxylase) l' L& q' _$ s, p! {
deficiency. Those diagnoses were excluded by find-
- N% e% @  C# l# z, {ing the normal level of adrenal steroids.
( G/ L( |! J4 k* cThe diagnosis of exogenous androgens was strongly
. m; f: @/ w* e1 ^1 xsuspected in a follow-up visit after 4 months because: }. O" |+ u4 u4 }
the physical examination revealed the complete disap-
" P: }! L* b* q. `pearance of pubic hair, normal growth velocity, and: E- O0 M7 ~7 U% ~0 v. h
decreased erections. The father admitted using a testos-! u, S* T, B0 r$ B$ `1 o7 y
terone gel, which he concealed at first visit. He was
/ d0 T5 c" L( k% F4 Eusing it rather frequently, twice a day. The Physicians’
# |' X# B: ?5 n0 P3 {$ Z# QDesk Reference, or package insert of this product, gel or- U9 J* ?- b7 h  K4 a. M. r
cream, cautions about dermal testosterone transfer to; d5 h: F5 s: S& ~
unprotected females through direct skin exposure.+ P! }$ ~# T! R3 ~4 A9 O
Serum testosterone level was found to be 2 times the* \6 g* L3 ], ]% T  Y$ s3 K  m5 i
baseline value in those females who were exposed to6 E- P( ?# P5 X: t7 ]
even 15 minutes of direct skin contact with their male; `6 t9 O7 e& ?) E) w7 X' }8 F; w8 L
partners.6 However, when a shirt covered the applica-
6 q& v" T# m* n: s  o' e! Ftion site, this testosterone transfer was prevented.& e+ [3 K4 n3 F( r
Our patient’s testosterone level was 60 ng/mL,
( u6 a1 z; F  k% Nwhich was clearly high. Some studies suggest that
! [5 d: j1 ~+ i% r, tdermal conversion of testosterone to dihydrotestos-" A$ z1 T% _( R+ ^$ p) m! v
terone, which is a more potent metabolite, is more
/ b3 g  v4 L& z/ g  }9 Uactive in young children exposed to testosterone
" D" T- d0 D6 Bexogenously7; however, we did not measure a dihy-2 ]( J7 W1 i3 e" G7 v% R
drotestosterone level in our patient. In addition to
& b& Q* T) p4 }virilization, exposure to exogenous testosterone in# y; X; O6 c- y' @2 I
children results in an increase in growth velocity and- J* L4 R2 \4 \; i
advanced bone age, as seen in our patient.
$ {! ?7 U" U& ~1 V* \( JThe long-term effect of androgen exposure during" e* k# E" I  b# j
early childhood on pubertal development and final3 K6 M1 H- }1 Z
adult height are not fully known and always remain1 y% E" Y; H: }' S5 v
a concern. Children treated with short-term testos-3 u( o5 i, k. U0 D% V4 `- h
terone injection or topical androgen may exhibit some
' M2 i3 a% P8 R, Y% W# l7 V! pacceleration of the skeletal maturation; however, after  P, L1 K, x& v
cessation of treatment, the rate of bone maturation
) v4 Y; d' g8 i% d1 ~decelerates and gradually returns to normal.8,95 D6 @6 J" p; s3 g9 }
There are conflicting reports and controversy
& m* F0 f1 |! O3 \6 ?over the effect of early androgen exposure on adult
" E8 N, l. R  M) G7 A( r4 L" dpenile length.10,11 Some reports suggest subnormal2 a* Y  N2 M( x% d& ~! O% r" p
adult penile length, apparently because of downreg-
' ?- E( ^& S) ?  p% mulation of androgen receptor number.10,12 However,
. i& \& `& {+ f; u7 o0 U- bSutherland et al13 did not find a correlation between
& h* u8 B: Q0 `! schildhood testosterone exposure and reduced adult
/ L" Z$ `+ X, \1 _/ L3 t6 apenile length in clinical studies.$ @2 N  W+ v/ f( X
Nonetheless, we do not believe our patient is8 m0 z% _$ Q( ~! t6 h
going to experience any of the untoward effects from4 w; w* C* B2 S1 p3 N
testosterone exposure as mentioned earlier because5 X' M+ ^# s$ e1 V. P
the exposure was not for a prolonged period of time.
1 ?( Y" q3 }, Y' r/ JAlthough the bone age was advanced at the time of4 M4 `. k; P" X( n  k
diagnosis, the child had a normal growth velocity at
# F" a- C3 [; }. P% Tthe follow-up visit. It is hoped that his final adult' p; g0 }9 ?7 v, w* f  L9 R# x5 V
height will not be affected.
1 k: ?3 i3 `" j+ r: F: u% i9 o' OAlthough rarely reported, the widespread avail-
9 ?7 {$ I0 i7 [/ ^ability of androgen products in our society may
9 ^; B5 V4 A# J! Qindeed cause more virilization in male or female( `7 [+ k  f6 H$ }2 E
children than one would realize. Exposure to andro-
( L6 ?* B4 b6 F* B) \% c9 x! jgen products must be considered and specific ques-# E" K6 ^9 {# @# {
tioning about the use of a testosterone product or; B/ M, p. X9 A5 |# u7 h
gel should be asked of the family members during
% m/ U* |% T: I( \) H1 D  m4 M/ Nthe evaluation of any children who present with vir-
3 O  l) J+ `; x8 S" p# P) qilization or peripheral precocious puberty. The diag-' z3 M' m7 F! \5 p3 j
nosis can be established by just a few tests and by
/ z0 H& `  H6 V3 m5 Happropriate history. The inability to obtain such a
: J* {/ f% r5 Y3 }7 chistory, or failure to ask the specific questions, may- Z0 p* _) Y: K1 ]
result in extensive, unnecessary, and expensive
; [, o+ |$ Q5 M& F9 G/ D, Tinvestigation. The primary care physician should be9 c0 d+ K& \& H4 \! [% a
aware of this fact, because most of these children, P0 T( e! M" v; e6 k
may initially present in their practice. The Physicians’" i5 g) Z+ a1 K% y% _- h; P
Desk Reference and package insert should also put a
3 Q9 U* r" d" Y, Dwarning about the virilizing effect on a male or
) n& ]- d: X* b3 X( wfemale child who might come in contact with some-+ n& a4 ~, l* b$ X
one using any of these products.
5 p$ x0 u4 d3 n/ G1 s, vReferences* n5 O$ r" }0 N# i5 f: i" r  L
1. Styne DM. The testes: disorder of sexual differentiation% K7 f7 ]9 s2 ~4 d
and puberty in the male. In: Sperling MA, ed. Pediatric7 V5 D, P3 F( f' M. {
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, a0 c' H% p' O- }$ g
2002: 565-628." @2 _' o4 k* X7 S5 \& X4 H9 L
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% \1 Q6 {; @* r' s6 Z( O( i
puberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
2 S# M* g' F# _) G9 u
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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