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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
# T; H  ^& v- i& `+ nBoy Induced by Indirect Topical
5 g2 p; R3 `: o$ ~6 w1 kExposure to Testosterone/ ~5 P1 \! N9 Z7 n  c4 Q
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. O3 i& k( d/ q3 T, d7 _8 Q1 j
and Kenneth R. Rettig, MD1
; W/ L* M+ C" @2 I' s/ c9 vClinical Pediatrics
8 R: ?6 Y* J5 J3 OVolume 46 Number 67 H: s2 M1 P9 U" L" a
July 2007 540-5437 K' ^+ A3 {2 T% K
© 2007 Sage Publications: u; F6 z* y# s. Y/ @8 U" U: B. m
10.1177/0009922806296651
6 c0 ?  @: }3 \9 vhttp://clp.sagepub.com
' U9 c) O4 H& Y, [' c) Ehosted at
. n" p/ M( q5 H1 z& ]& }+ r  ^, @http://online.sagepub.com
, |9 _% g. c: {& L1 Y- @2 EPrecocious puberty in boys, central or peripheral,
9 I3 T. Y3 Z# v; Y8 t( r0 }  h# iis a significant concern for physicians. Central/ \' T2 y9 T$ i2 p" a& f
precocious puberty (CPP), which is mediated
! C0 `, C  O# Dthrough the hypothalamic pituitary gonadal axis, has
" y, E& o# d7 y8 \# V6 ia higher incidence of organic central nervous system
! b7 h) ^6 F5 o3 xlesions in boys.1,2 Virilization in boys, as manifested
1 \! Z& B, M) ]4 G% t3 aby enlargement of the penis, development of pubic
; T. X- z' }- U: i6 Q& ^hair, and facial acne without enlargement of testi-; p, Q/ m8 F4 h) j% I
cles, suggests peripheral or pseudopuberty.1-3 We- T' y/ Z3 ^7 a% F. Q
report a 16-month-old boy who presented with the
% P3 h  g  b6 g  j4 D" b7 Q3 @: aenlargement of the phallus and pubic hair develop-
) a7 R; M4 z( jment without testicular enlargement, which was due
/ {; u* k+ f( ~: W: Z2 y4 {to the unintentional exposure to androgen gel used by0 k! _" L  |$ G8 }/ m) O
the father. The family initially concealed this infor-$ }* u% \  q" h8 d  B5 c, p
mation, resulting in an extensive work-up for this
: y  E6 F% i4 lchild. Given the widespread and easy availability of4 S; I4 H2 |( [# E3 X% K
testosterone gel and cream, we believe this is proba-
. V  S% W, _, x5 o. z1 R# Kbly more common than the rare case report in the
' y: p. t5 n% X. j7 N, d2 ^, ?, eliterature.4
3 P1 R9 ~- h6 [% r( MPatient Report9 `/ u6 H+ ]- J) }* ^
A 16-month-old white child was referred to the2 g* J' Y: f9 d6 i  G* X" N$ c+ w
endocrine clinic by his pediatrician with the concern
4 J8 }/ ~. |# U4 r7 D2 p/ wof early sexual development. His mother noticed5 i1 S% L/ a2 P) J) v2 r2 y( p: g$ y
light colored pubic hair development when he was
& z  x2 g6 K( q7 v# c; Y6 hFrom the 1Division of Pediatric Endocrinology, 2University of
0 [, h( D! }+ PSouth Alabama Medical Center, Mobile, Alabama.
1 T, y; ?! H7 k6 D" H! IAddress correspondence to: Samar K. Bhowmick, MD, FACE," Z" ^8 _9 w& P5 Z; ^: a0 V- m
Professor of Pediatrics, University of South Alabama, College of
, Z* n3 T3 f- _7 C9 i  C: G$ NMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 ]& d, \! b/ y2 V% p! ~
e-mail: [email protected].
: I! v2 ~6 o; X% f5 s) C" Mabout 6 to 7 months old, which progressively became  m4 D5 W! o; E0 [% m
darker. She was also concerned about the enlarge-* n: Y+ N& c; N$ _" n) V* j  Q
ment of his penis and frequent erections. The child) h% g* v* m2 I1 L# L- L/ e
was the product of a full-term normal delivery, with
6 R1 u, O) t( y+ M, _a birth weight of 7 lb 14 oz, and birth length of: c! h# N# F- G' T/ K- p) m+ R, t
20 inches. He was breast-fed throughout the first year: ?8 X9 K! B  i9 [. T
of life and was still receiving breast milk along with
. [$ |7 j6 o7 s( |+ r* V+ w5 Hsolid food. He had no hospitalizations or surgery,
& V- z6 B( `5 |8 C6 T# F% r& Fand his psychosocial and psychomotor development' [" g& D2 b1 x$ p9 ^
was age appropriate.( |( v! O( Z& ^7 L1 `. K8 R. y  _
The family history was remarkable for the father,7 T3 [% s1 ^: ?
who was diagnosed with hypothyroidism at age 16,
4 @% W$ \7 X! ~% L0 [4 k0 ?which was treated with thyroxine. The father’s
$ V: M7 N/ }$ E" P* F3 Iheight was 6 feet, and he went through a somewhat
: B4 _" r7 |7 d/ }. \" r1 }1 Fearly puberty and had stopped growing by age 14.' L! `! |5 j* L" ~+ _
The father denied taking any other medication. The0 X( i- q$ _. \
child’s mother was in good health. Her menarche* F' n+ {$ p, C) k+ _4 R& X
was at 11 years of age, and her height was at 5 feet; ?% w4 D8 n' `8 V+ e2 G
5 inches. There was no other family history of pre-7 Q% @1 G$ P5 y% _& Y
cocious sexual development in the first-degree rela-
1 C) E9 Q7 O* r. d1 _tives. There were no siblings.6 i& f2 P7 w% V0 I7 h9 `5 b
Physical Examination
4 R9 c$ d; [9 s9 m" MThe physical examination revealed a very active,
* n" m* b$ s8 P" C# t# bplayful, and healthy boy. The vital signs documented
* X# U& n5 Q" c0 ^5 F* ?a blood pressure of 85/50 mm Hg, his length was( A4 E& C5 X; j
90 cm (>97th percentile), and his weight was 14.4 kg
0 B6 J: P1 v3 n2 `, w* L# T# N2 k(also >97th percentile). The observed yearly growth8 W8 i) ~7 a1 W9 \- q
velocity was 30 cm (12 inches). The examination of& \( v5 i4 G  k
the neck revealed no thyroid enlargement.' W+ m2 d0 W% R5 K( D
The genitourinary examination was remarkable for
+ h2 J$ i9 b7 Q  ]' \( }. {7 Venlargement of the penis, with a stretched length of
7 b! G, W3 X7 V8 cm and a width of 2 cm. The glans penis was very well
$ E6 ^6 o7 y9 r7 X( k/ _6 K; J3 \developed. The pubic hair was Tanner II, mostly around
% C- f: P  {9 q540
- ?0 S  Z- l+ K" H. {0 kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; Q% V) q* G2 X' I' E4 f: V( {/ b
the base of the phallus and was dark and curled. The
) O# f$ z0 |; l; ?# w+ }testicular volume was prepubertal at 2 mL each.
4 D/ U# B( z( G+ B0 zThe skin was moist and smooth and somewhat2 d' s* z! L- C1 D/ b' k
oily. No axillary hair was noted. There were no
& _) h0 D& y( O; W& T' yabnormal skin pigmentations or café-au-lait spots.6 ~9 Y2 T0 ^) {6 ]$ X
Neurologic evaluation showed deep tendon reflex 2+
( X2 T2 o6 B: {* rbilateral and symmetrical. There was no suggestion$ y- I  @2 b/ r
of papilledema.
( e' ~* }' ]5 V) `2 [% ^4 F1 B5 P5 fLaboratory Evaluation
. c% C( ~2 e" u; mThe bone age was consistent with 28 months by
6 O' C. N  {3 s/ l# J4 |  Busing the standard of Greulich and Pyle at a chrono-
' Z* Q& C6 I) y6 C( f/ s2 plogic age of 16 months (advanced).5 Chromosomal
5 ?+ X6 V+ I/ ?( ^! Jkaryotype was 46XY. The thyroid function test7 }! A0 R- Q1 O8 [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-4 U- t! C$ X5 P( h1 G7 V
lating hormone level was 1.3 µIU/mL (both normal).
' ^3 r! K7 B5 p  G- y/ NThe concentrations of serum electrolytes, blood! m% w' v+ R' U3 x2 y, z& D* d
urea nitrogen, creatinine, and calcium all were
6 H9 r1 H5 @6 K/ O) n8 @1 x& E4 k6 Dwithin normal range for his age. The concentration
! w/ l# x. }' C; Iof serum 17-hydroxyprogesterone was 16 ng/dL  c8 x! C0 w9 H
(normal, 3 to 90 ng/dL), androstenedione was 20
5 F$ i. K. [( E0 |ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, O( O! ]" d! K) lterone was 38 ng/dL (normal, 50 to 760 ng/dL),' x9 T. e4 U, m! M, E% s
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 `9 s. E4 q1 ?' E+ N, J
49ng/dL), 11-desoxycortisol (specific compound S)+ y3 G6 U5 c6 j5 z4 f" e
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( _2 O2 D- @, I1 j5 d
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: `% [& T- @( @8 [4 s% |7 A1 M
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# P0 A, s, v# I  land β-human chorionic gonadotropin was less than
8 L: R- m* P. ~" O+ G& @7 R- f4 g! F5 mIU/mL (normal <5 mIU/mL). Serum follicular! D; k" S2 r3 w& C1 y8 ]! `5 K2 A0 j
stimulating hormone and leuteinizing hormone
( S& f6 C. x2 h4 }* R* _! d, hconcentrations were less than 0.05 mIU/mL; h+ J. x. N) o/ C* c. I$ a
(prepubertal).3 _, e: `  ]; v4 _7 s# U* b
The parents were notified about the laboratory# e+ Y) U7 {( D) P4 H+ Z* o& X
results and were informed that all of the tests were( _( |$ b& i% G' k9 [) Y/ d  E6 O% t( ?
normal except the testosterone level was high. The9 j7 ^8 Q( a3 d; T
follow-up visit was arranged within a few weeks to
: v" k& s" s0 n' s$ V; }$ ]1 @3 qobtain testicular and abdominal sonograms; how-
, X$ S6 e& P2 {4 K5 e% V! _6 [ever, the family did not return for 4 months.
. G0 C: R: t/ I( y! g$ w$ F( WPhysical examination at this time revealed that the, }3 R. y- B* }4 ?4 P" ?
child had grown 2.5 cm in 4 months and had gained
) L6 a! U7 i0 v! y9 W; W( h2 kg of weight. Physical examination remained
& t% C9 g  n; F3 Q& b6 [unchanged. Surprisingly, the pubic hair almost com-0 ?- h" N  Z% c( U6 B: O* i% j: R
pletely disappeared except for a few vellous hairs at
0 J( ]( S! |9 fthe base of the phallus. Testicular volume was still 2. P# j' [* R) H) D
mL, and the size of the penis remained unchanged.% j1 T% |# p8 P1 N" D, }: d
The mother also said that the boy was no longer hav-. v  x! h( L" k
ing frequent erections.. l3 @5 Q9 N6 H4 i" v6 H
Both parents were again questioned about use of
  L( n: M' \5 }# t1 @any ointment/creams that they may have applied to
3 \! D, l& ?, h' u. ?4 ?7 v0 Fthe child’s skin. This time the father admitted the$ a5 R0 Q- Z4 [: ~. Q( ]
Topical Testosterone Exposure / Bhowmick et al 541, P6 E3 {  N, y1 j' L8 T
use of testosterone gel twice daily that he was apply-% j) s, s0 O. J( n1 C3 Z
ing over his own shoulders, chest, and back area for
+ z* b$ Y8 i7 N4 ^a year. The father also revealed he was embarrassed9 [* s1 V1 H8 I6 _4 G0 J) _
to disclose that he was using a testosterone gel pre-1 h5 X7 K6 y) ~4 q; q  r7 ?
scribed by his family physician for decreased libido9 |) Y" b5 X# \+ l5 P
secondary to depression.
0 M7 Q6 }- b2 d6 t; QThe child slept in the same bed with parents.5 Z6 ]2 k- s$ q
The father would hug the baby and hold him on his7 j4 H  s. y( s9 J3 r5 g
chest for a considerable period of time, causing sig-- Z1 U8 ?$ `" S% h1 ~
nificant bare skin contact between baby and father.
1 h( V  Y6 H9 z  Y' Q/ k3 NThe father also admitted that after the phone call,
/ g  ^5 t) F: {9 K$ H/ L* d$ o, E6 wwhen he learned the testosterone level in the baby
" i: E6 ^; [8 u& iwas high, he then read the product information; \) g1 h" i( u- @
packet and concluded that it was most likely the rea-2 d8 d  \' K* o9 G6 }2 ?* Y% e5 y0 }% Y
son for the child’s virilization. At that time, they
; i0 o3 A) ~" N* B7 t) _decided to put the baby in a separate bed, and the
2 ]( U5 y" [% N( ofather was not hugging him with bare skin and had% n; o- `- o1 p
been using protective clothing. A repeat testosterone% E9 C4 T, ?5 s) q2 s
test was ordered, but the family did not go to the
1 u2 ^- V) v( q# u0 P5 N! ~6 E$ qlaboratory to obtain the test.& ~8 e9 d0 c: y% U4 R# f( m
Discussion6 Z4 q+ _5 B' o7 m0 m4 N
Precocious puberty in boys is defined as secondary
+ C  b* h( f5 e2 {% Isexual development before 9 years of age.1,4
& r& C9 a' Y) l9 m3 BPrecocious puberty is termed as central (true) when8 t, d" }5 K1 w4 \
it is caused by the premature activation of hypo-1 i( W0 X& X$ N, J
thalamic pituitary gonadal axis. CPP is more com-
+ J8 k8 i9 p% W2 Pmon in girls than in boys.1,3 Most boys with CPP0 ?2 W+ S9 d6 G
may have a central nervous system lesion that is% M3 T5 N  e5 E3 i- ]
responsible for the early activation of the hypothal-
6 H" \2 t& o5 r; A5 _/ Z% r  G% S7 V1 zamic pituitary gonadal axis.1-3 Thus, greater empha-
8 s. t) r$ {) j# }sis has been given to neuroradiologic imaging in1 {! {% F# w; S! O
boys with precocious puberty. In addition to viril-
! s" @0 i* m1 K9 U# V4 M! Rization, the clinical hallmark of CPP is the symmet-& @+ f! V( c- f* U3 A  @
rical testicular growth secondary to stimulation by
0 l. y; H  Y& c) y. X* ]0 T9 ugonadotropins.1,3
1 V& g- ^: [: FGonadotropin-independent peripheral preco-$ `7 X# m+ r0 q: s
cious puberty in boys also results from inappropriate1 t% P( o; F7 Z  ?. }" J
androgenic stimulation from either endogenous or4 _, v+ i: J7 B. R# @7 q
exogenous sources, nonpituitary gonadotropin stim-
+ D( P- e- j; w% p" X5 w& O. eulation, and rare activating mutations.3 Virilizing
8 z  ]2 y$ O5 Q3 Y7 Fcongenital adrenal hyperplasia producing excessive
) N0 `  }7 U! a# Nadrenal androgens is a common cause of precocious
; }5 @1 ?% M: E( X  ^+ H! f- C- gpuberty in boys.3,4
- M+ N% u0 ^$ O1 ^# S+ h+ qThe most common form of congenital adrenal- b4 [4 C  U+ p- w6 ~: T: c
hyperplasia is the 21-hydroxylase enzyme deficiency." S: K+ ~, A* |& |" \
The 11-β hydroxylase deficiency may also result in
7 H; S5 X+ l" c; ^" `excessive adrenal androgen production, and rarely,; W7 k0 l! \% O/ i9 {. Y& m
an adrenal tumor may also cause adrenal androgen
) Z- j6 X) h4 G7 |* mexcess.1,3/ L* ^& a" v# I" @7 [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# E) R) u3 Q- {542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 z% y7 P% _( @3 [8 n: ]& nA unique entity of male-limited gonadotropin-* `; q2 H" F- F0 [: ]$ [
independent precocious puberty, which is also known0 c. W7 L; l* J* \& g% t7 q# B
as testotoxicosis, may cause precocious puberty at a
8 ~. M. c7 c  r% _very young age. The physical findings in these boys- a& D+ a% ~# N  b; U2 [
with this disorder are full pubertal development,4 [2 d, P2 J; M
including bilateral testicular growth, similar to boys
5 J! r( I! p5 G6 v  ^! `with CPP. The gonadotropin levels in this disorder1 M+ H) J6 i- W" h
are suppressed to prepubertal levels and do not show
# @# n  o( Q$ Zpubertal response of gonadotropin after gonadotropin-
: z# |& K2 d$ o' Preleasing hormone stimulation. This is a sex-linked  }# b" }7 r" ^2 k6 |2 u: y
autosomal dominant disorder that affects only
6 X4 ]( _- q' }; Omales; therefore, other male members of the family* N2 ?5 O& l8 Y1 d2 V6 g
may have similar precocious puberty.3# F! _3 Q) b; s7 p
In our patient, physical examination was incon-
8 D+ L) z$ K: N9 ^sistent with true precocious puberty since his testi-
8 d6 U. ]+ y, Q, U8 m6 gcles were prepubertal in size. However, testotoxicosis
, {" T9 [$ @0 D5 twas in the differential diagnosis because his father
$ K4 y. v) q7 dstarted puberty somewhat early, and occasionally,
0 h9 ]) d) }( E# k  \  W4 Ztesticular enlargement is not that evident in the2 j$ g) J* _5 U% m1 D. @
beginning of this process.1 In the absence of a neg-
5 z) J9 d( M/ x" n- o: T  @! K; _ative initial history of androgen exposure, our: w2 Z4 P9 t* V0 N+ g
biggest concern was virilizing adrenal hyperplasia,2 V2 u. E# |6 N% c0 L1 H
either 21-hydroxylase deficiency or 11-β hydroxylase# f! _  c; [5 }
deficiency. Those diagnoses were excluded by find-, U$ k5 ]0 I5 n  P
ing the normal level of adrenal steroids.
6 \' h- @1 ]3 S8 x6 P: w  \8 XThe diagnosis of exogenous androgens was strongly/ Y; F. P1 q, C$ Y2 L# m, [
suspected in a follow-up visit after 4 months because
8 z7 L0 S0 e& r  e( L* l$ qthe physical examination revealed the complete disap-' X7 `4 V9 t) C
pearance of pubic hair, normal growth velocity, and
, t6 F1 G: ~, X9 q( R8 W# Hdecreased erections. The father admitted using a testos-: u9 V8 f9 a9 v$ u8 k
terone gel, which he concealed at first visit. He was
& S% C; W% B4 ], I0 h5 C+ \- zusing it rather frequently, twice a day. The Physicians’
$ i* u3 W/ ?5 k4 aDesk Reference, or package insert of this product, gel or
" J& K3 V& p% N& e6 l6 G% r+ k- o! Ycream, cautions about dermal testosterone transfer to
5 A2 m1 T+ v, runprotected females through direct skin exposure., i0 _" U9 y8 _' F/ j
Serum testosterone level was found to be 2 times the( E3 }8 w/ x% F* }& B) K! P0 N) x
baseline value in those females who were exposed to
4 R  U  h. t. veven 15 minutes of direct skin contact with their male
* D+ Z5 L7 f1 E) Lpartners.6 However, when a shirt covered the applica-9 ]8 |7 O! q5 c" a% _
tion site, this testosterone transfer was prevented.7 s' `9 T3 p; s0 V5 F
Our patient’s testosterone level was 60 ng/mL,5 Z0 h1 P8 W2 ~# \3 g+ }
which was clearly high. Some studies suggest that1 j1 ~. r& _0 ]# r1 J2 o& U% ?
dermal conversion of testosterone to dihydrotestos-, f. K9 I1 Q; a7 Y9 {
terone, which is a more potent metabolite, is more( N1 x7 N7 J2 \: ~; y
active in young children exposed to testosterone
  ]6 Y7 u4 g5 H, vexogenously7; however, we did not measure a dihy-
- Z3 @0 ~& r' P2 n/ c& ]drotestosterone level in our patient. In addition to  W2 K/ I: `% g  r2 F' y
virilization, exposure to exogenous testosterone in  h9 R7 `" g5 J' a, f4 K
children results in an increase in growth velocity and) p& h  G' A8 e/ d: c
advanced bone age, as seen in our patient.
* E  P2 d" Z7 t: KThe long-term effect of androgen exposure during
; e) c; C* A, m2 gearly childhood on pubertal development and final* n* v7 v) N+ E6 f! c% o) L7 p
adult height are not fully known and always remain0 n$ p  u* v2 |/ R2 V/ {# D
a concern. Children treated with short-term testos-
& e; W( z) F! A5 c  m2 jterone injection or topical androgen may exhibit some3 m/ [/ x, A& Z. \
acceleration of the skeletal maturation; however, after
: ~7 f  ?  m; j8 Q" k$ N7 J7 v# X  }cessation of treatment, the rate of bone maturation
; E) I5 ~' t: _# o  K& P9 q, ndecelerates and gradually returns to normal.8,9* {. R) ]% X7 i3 q% I6 E
There are conflicting reports and controversy5 G6 o% s, i2 @" H5 y
over the effect of early androgen exposure on adult
) x: m2 }$ |5 N$ j1 h" i: npenile length.10,11 Some reports suggest subnormal
9 m9 y2 e$ o5 Jadult penile length, apparently because of downreg-
' w. H( n% J' b* F3 z! _ulation of androgen receptor number.10,12 However,
) Q1 f/ h. K( e. {Sutherland et al13 did not find a correlation between2 q5 ^% `3 E5 s$ s, a" c
childhood testosterone exposure and reduced adult& ^$ N0 c1 W/ b6 S' r
penile length in clinical studies.* _2 m' X7 L* u0 F, F
Nonetheless, we do not believe our patient is% R$ z4 x4 ]! c  H7 L! Z
going to experience any of the untoward effects from
9 F' r) H% X& d8 }% [' D  G9 stestosterone exposure as mentioned earlier because
0 B( I, ^8 x+ {6 Cthe exposure was not for a prolonged period of time.7 j' P; l/ ]% o) _: ], S: ?
Although the bone age was advanced at the time of
2 ^: F' ?5 L, M. x0 d7 cdiagnosis, the child had a normal growth velocity at
+ Q( s( d" \2 z! e/ C/ }# Sthe follow-up visit. It is hoped that his final adult
* ^4 H9 s( e' f& y7 Z. pheight will not be affected.
( m5 K& N8 C1 \3 ~* O, ^. hAlthough rarely reported, the widespread avail-
7 r6 d7 h3 _; C' y: q; |; k) Nability of androgen products in our society may
8 {( P) D3 u  l" t+ S$ \7 nindeed cause more virilization in male or female
* g( ]6 _+ C: A! m# s6 ^children than one would realize. Exposure to andro-7 r5 `  ]; p. d" t3 J! K* L
gen products must be considered and specific ques-
) E) A5 p, c( ftioning about the use of a testosterone product or
/ H. F9 D- @" @9 @  l2 Hgel should be asked of the family members during. R6 S% [+ H1 ^1 E- r
the evaluation of any children who present with vir-
3 v* R5 P/ C- U- vilization or peripheral precocious puberty. The diag-5 D7 V3 ~6 i3 _( b7 j
nosis can be established by just a few tests and by
" t$ ?( Z" _& Wappropriate history. The inability to obtain such a- k$ n5 g  M! m& J% ^+ q
history, or failure to ask the specific questions, may
: ?: H6 b* P: [; n- Kresult in extensive, unnecessary, and expensive# h! ?8 m' U" j3 x
investigation. The primary care physician should be
7 T* {7 e' N2 paware of this fact, because most of these children! ~) Y2 o; K- ~" o$ j. w
may initially present in their practice. The Physicians’
$ l6 S0 G; y% s( m; FDesk Reference and package insert should also put a
1 X0 k4 n, P. z/ D1 _3 Uwarning about the virilizing effect on a male or. _1 L0 a2 v! t- o7 Y% [9 a
female child who might come in contact with some-' M( r: M" P1 G' S% p
one using any of these products.; h8 c$ D3 Y2 S
References$ q# v% b  R+ N7 u! A
1. Styne DM. The testes: disorder of sexual differentiation
: Y- w0 O" p0 Rand puberty in the male. In: Sperling MA, ed. Pediatric, m0 Q) }1 c) E' H, c
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 a& C6 n# u( i6 p& H
2002: 565-628.
2 Z8 T3 H+ a3 A, H; E2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 L/ Q' t" P, {) [  Z* C5 k, Dpuberty in children with tumours of the suprasellar pineal
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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
發表於 2025-1-7 21:59:43 | 顯示全部樓層
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
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
' d# j/ c: d/ E0 A. T& R
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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