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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
2 W) @: U2 X  g% j: b) d6 ^Boy Induced by Indirect Topical
7 A" _" j  [, [0 R5 O% dExposure to Testosterone
! R) W, z' ~+ P( K6 fSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2, M2 g: B- @' @" v7 u+ G- t
and Kenneth R. Rettig, MD19 L; J& ~! S/ g0 F
Clinical Pediatrics% o) M# ?" @: {
Volume 46 Number 6
, |% B( R" S) ^7 {* D! D* BJuly 2007 540-543
" {5 |2 u( k: v! l" y5 z7 x© 2007 Sage Publications' E+ T  b+ a+ j
10.1177/0009922806296651; p+ T# ?$ _9 d4 Y6 e1 d
http://clp.sagepub.com% f% J$ m9 p7 }( z& `$ L7 T
hosted at4 M. c  E1 Q1 Z
http://online.sagepub.com
0 C4 e8 b3 o; i+ b* h6 G6 d3 K0 QPrecocious puberty in boys, central or peripheral,( d' @0 z4 x( o0 b
is a significant concern for physicians. Central8 n) N3 u7 u# l, s; e
precocious puberty (CPP), which is mediated' S% J1 w! p6 f
through the hypothalamic pituitary gonadal axis, has
$ J+ h: |4 U2 d4 Ea higher incidence of organic central nervous system
: m8 F! c- B. ~) R1 U9 {lesions in boys.1,2 Virilization in boys, as manifested+ U" h0 l  e% p! x  V' O7 e' X
by enlargement of the penis, development of pubic) C: l# K  J9 Q5 w, d$ p/ @' c
hair, and facial acne without enlargement of testi-
. p7 N5 n" x8 p* p; zcles, suggests peripheral or pseudopuberty.1-3 We9 f8 Z/ u7 q& X
report a 16-month-old boy who presented with the
+ m. K' w0 r, P4 j! Menlargement of the phallus and pubic hair develop-
: Y$ s2 u! l& u# Ement without testicular enlargement, which was due
: u' i. U4 t6 C$ Dto the unintentional exposure to androgen gel used by2 _& \7 z; T3 C* N
the father. The family initially concealed this infor-; h8 p' e# s+ L2 |2 p. U8 U
mation, resulting in an extensive work-up for this6 J0 z" Q, K+ H0 w; p4 J2 w8 r
child. Given the widespread and easy availability of2 M" t" m8 Y1 A! G6 ?# v
testosterone gel and cream, we believe this is proba-
( Y! F4 \9 Y- j9 D$ mbly more common than the rare case report in the0 F* K3 s( }; ~7 ^# j0 Y4 ^# l
literature.4
" y+ ?: y7 E5 O3 a6 j$ ]; @Patient Report. G1 K% l5 N8 W, G) g. y5 J
A 16-month-old white child was referred to the: I% b$ d6 r  [% Y* K6 r' M5 @
endocrine clinic by his pediatrician with the concern6 n2 e& V1 @, j+ D2 N  _) v
of early sexual development. His mother noticed
# R, b; h! ^" T$ ulight colored pubic hair development when he was
; }+ v; e, T- @& Q: `: iFrom the 1Division of Pediatric Endocrinology, 2University of  }+ ^9 C5 A) F0 X
South Alabama Medical Center, Mobile, Alabama.6 p6 \- s" D& v) ^8 i* q
Address correspondence to: Samar K. Bhowmick, MD, FACE,7 Q: r$ N% E( j3 [2 Q! }
Professor of Pediatrics, University of South Alabama, College of9 k, i- x$ r& a) ~8 b
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ F. a3 Y' R+ |. P8 we-mail: [email protected].* d+ b0 N5 q! J; h$ [" J4 W
about 6 to 7 months old, which progressively became
* e# c! L  y7 D1 ndarker. She was also concerned about the enlarge-& b# t( B9 z5 w& r2 r
ment of his penis and frequent erections. The child
0 f) Z0 G( U  b& L7 K" C# zwas the product of a full-term normal delivery, with
/ n2 u! S/ Z* s) ~# ?1 u4 \2 sa birth weight of 7 lb 14 oz, and birth length of
3 a' U0 |2 K3 o- T20 inches. He was breast-fed throughout the first year. s  ?4 N' ~0 m4 p
of life and was still receiving breast milk along with3 J4 g8 e4 U9 a/ _' w4 a) y
solid food. He had no hospitalizations or surgery,
  B: {% m0 Z4 t) n* R3 w2 land his psychosocial and psychomotor development
7 l& @0 Z4 S: x! O# [) ]was age appropriate.1 @$ A! v) ^, a+ X. Q# L
The family history was remarkable for the father,
9 f* P: `/ d) w6 t" v2 O) Twho was diagnosed with hypothyroidism at age 16,
5 a; G, F6 z- J4 Ewhich was treated with thyroxine. The father’s
' R3 L; m! _0 d3 Yheight was 6 feet, and he went through a somewhat
0 m6 M8 M2 w1 d/ Zearly puberty and had stopped growing by age 14.+ G* l" l' I4 u4 N4 @7 W+ @4 ]
The father denied taking any other medication. The
2 t( L3 s9 w9 T* {% B2 z6 gchild’s mother was in good health. Her menarche
  I9 w) a4 j& ?was at 11 years of age, and her height was at 5 feet3 _% \. z6 R0 v& w
5 inches. There was no other family history of pre-
7 u* Q7 ^+ k# \! Ucocious sexual development in the first-degree rela-& {3 q1 L1 O, a* {' j5 U
tives. There were no siblings.
; s1 y& z$ h3 U( F6 G3 C2 UPhysical Examination) L3 W! i/ {( i' s
The physical examination revealed a very active,
5 z$ l! x3 B2 q: Z& F) _playful, and healthy boy. The vital signs documented
7 _/ X; [; K/ B; D0 I7 o& A: Ia blood pressure of 85/50 mm Hg, his length was* B8 a$ ^+ g5 W! _, [# a
90 cm (>97th percentile), and his weight was 14.4 kg' r0 c. z' i2 T' E
(also >97th percentile). The observed yearly growth
! H# f- P) t, G! @3 G1 m  S; {& ~' Pvelocity was 30 cm (12 inches). The examination of+ b0 i2 i& q. c
the neck revealed no thyroid enlargement.! o2 R; H3 {7 y
The genitourinary examination was remarkable for1 p8 b- I4 A5 |4 X5 d& J2 n) j& f
enlargement of the penis, with a stretched length of
. R- s' f9 G* b( n3 ]( ^8 cm and a width of 2 cm. The glans penis was very well
2 t! x' c2 ~+ a0 ?" ~( Qdeveloped. The pubic hair was Tanner II, mostly around
. h# U! z( ^, z# H7 Y2 j, G- |5400 C7 Z  O: B  O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; c% X& {# j" ]  K( w4 A8 y
the base of the phallus and was dark and curled. The$ k+ j- W7 R5 o  s$ y
testicular volume was prepubertal at 2 mL each.$ f% C* r9 f# k. G8 J* Q
The skin was moist and smooth and somewhat( {2 S- |6 y4 g) g
oily. No axillary hair was noted. There were no' {6 t3 |9 Z, K; Q8 m- o' M
abnormal skin pigmentations or café-au-lait spots.! G3 l1 l3 [2 _5 g2 g) |1 f
Neurologic evaluation showed deep tendon reflex 2+% X  p+ |1 {+ N, L7 w$ E
bilateral and symmetrical. There was no suggestion( ?+ D1 E9 i+ O$ j% W* S$ d
of papilledema.* I( u) W$ @! P8 @7 E8 `- q/ F
Laboratory Evaluation# B2 b1 h$ R0 o1 z
The bone age was consistent with 28 months by( d7 _# C% K. s" k  y1 |4 q9 A
using the standard of Greulich and Pyle at a chrono-
. d7 s$ W3 `5 i! k# _6 U4 s/ Ylogic age of 16 months (advanced).5 Chromosomal" G# x7 k7 Q. I' C# K* m
karyotype was 46XY. The thyroid function test
; m8 b- y7 a" A! [showed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ o! v( S/ C7 t9 slating hormone level was 1.3 µIU/mL (both normal).4 C. K* J* ]/ B
The concentrations of serum electrolytes, blood
3 X* G; H$ h( b( L# b2 Vurea nitrogen, creatinine, and calcium all were
" V1 M' S3 H8 A- q5 ?! jwithin normal range for his age. The concentration
, ~4 V6 |7 H4 B% X* `of serum 17-hydroxyprogesterone was 16 ng/dL! m6 O3 A# C- e
(normal, 3 to 90 ng/dL), androstenedione was 20$ m5 B' i: a& p  K% o9 g  R+ z% y
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
# l* d$ q( s& ^4 N% z% _terone was 38 ng/dL (normal, 50 to 760 ng/dL),
; f1 q4 ^1 W2 \& h# C; Mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 A9 W( e; f4 P49ng/dL), 11-desoxycortisol (specific compound S)
- |  ]; i  `' z$ }) @3 Nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! G9 J5 S8 F9 |( G6 b5 A/ f0 ]
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* g+ F- L8 b2 E. h  g
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),# \' D. t* |: a8 |, ?
and β-human chorionic gonadotropin was less than5 h2 _' p3 z" x0 @7 }, i# T3 g
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  c3 l* ^+ B, D# i3 C: jstimulating hormone and leuteinizing hormone4 g+ w7 Z) ^* P; A5 o
concentrations were less than 0.05 mIU/mL
8 s; ~3 J# [1 c6 J& v( D. E2 m(prepubertal).7 L% s% L" j+ o5 y- d$ u+ t# e0 K
The parents were notified about the laboratory
6 d5 e9 t3 P& c4 f; R8 @results and were informed that all of the tests were
+ x1 ^- v' [% t! }9 D4 l, d2 o1 ynormal except the testosterone level was high. The
8 b+ I3 U( c  _- `follow-up visit was arranged within a few weeks to& f& f) C: d; W( O' x1 e
obtain testicular and abdominal sonograms; how-0 h- v( ~" t2 c: P6 u' y6 l
ever, the family did not return for 4 months.7 G1 v6 u2 Z" w; p1 S4 v, S
Physical examination at this time revealed that the: X7 h. S* i1 F
child had grown 2.5 cm in 4 months and had gained
5 Y; L# i4 J  I3 l  D# F2 kg of weight. Physical examination remained
8 e5 j( Y4 z; e: S" j4 funchanged. Surprisingly, the pubic hair almost com-
' [% p2 e4 s: @: @8 w& Z9 f- kpletely disappeared except for a few vellous hairs at
" A' N. t. [+ i7 Vthe base of the phallus. Testicular volume was still 2
2 {6 p. p0 r% }0 P6 O/ rmL, and the size of the penis remained unchanged.
( u* o( U, r7 vThe mother also said that the boy was no longer hav-8 w0 `3 G( T9 X9 w
ing frequent erections.
/ g2 M/ Z+ [- G' r5 Z7 iBoth parents were again questioned about use of
+ v# z1 a( L8 \& v( m  hany ointment/creams that they may have applied to- H" |! Q0 H. ]. k" M0 i1 E
the child’s skin. This time the father admitted the; U6 }* \, }! I5 w1 w
Topical Testosterone Exposure / Bhowmick et al 541
. y+ d8 `/ z. ~. u( _1 M9 @use of testosterone gel twice daily that he was apply-
) N: `1 ^% ^* n% _1 Ting over his own shoulders, chest, and back area for# Y1 A0 m+ E6 F; b5 ^
a year. The father also revealed he was embarrassed
, I3 I, B, T, s6 I- y2 E' Yto disclose that he was using a testosterone gel pre-; z: {8 b2 b$ Y( r
scribed by his family physician for decreased libido0 {5 l, b1 @7 z  _
secondary to depression.
+ I9 |' g1 `: W3 S/ k# r, e! E$ \The child slept in the same bed with parents.  @! h$ o  x- Q5 q( m3 Z
The father would hug the baby and hold him on his
9 n$ q$ f  D6 A$ Fchest for a considerable period of time, causing sig-& a& G7 a2 b2 z- l' Z
nificant bare skin contact between baby and father.0 c& m( c1 |2 u" w" c! c9 X$ u
The father also admitted that after the phone call,% W+ R) Z+ q$ S% N% G
when he learned the testosterone level in the baby
0 A( I) e- E* f  F6 cwas high, he then read the product information/ J: s- D$ N8 p0 @; X6 E
packet and concluded that it was most likely the rea-
. @. s8 r7 R% _" I$ |  Y4 c5 h+ Eson for the child’s virilization. At that time, they6 j/ y. e: g/ q3 J0 v8 T, p
decided to put the baby in a separate bed, and the; T# O7 V  a, b/ o% M
father was not hugging him with bare skin and had* }$ s5 g; L7 A8 L# D
been using protective clothing. A repeat testosterone6 F7 x% `% f" y" y8 H
test was ordered, but the family did not go to the
; K1 e+ T0 y4 P; m, P- Y9 rlaboratory to obtain the test.
3 o' X  z3 v- r0 G# c% JDiscussion
3 [- p+ I/ d0 Y/ n( t& fPrecocious puberty in boys is defined as secondary! @6 n( Z) ]5 b1 y+ v
sexual development before 9 years of age.1,4( ~3 v. @- O& X. f- v0 @+ X
Precocious puberty is termed as central (true) when
" r6 H* F& o! oit is caused by the premature activation of hypo-6 [( I" i) K- _
thalamic pituitary gonadal axis. CPP is more com-
0 c: D! D5 |0 Y- rmon in girls than in boys.1,3 Most boys with CPP/ W( a& {5 _# `* k" M2 f/ m/ Z- K
may have a central nervous system lesion that is
1 S6 {% y: V  {# h6 c  F* Rresponsible for the early activation of the hypothal-* F/ G9 ]7 j6 B/ U
amic pituitary gonadal axis.1-3 Thus, greater empha-# n* `; o/ x$ {' N& i* H, u" l
sis has been given to neuroradiologic imaging in+ ?& t2 }7 ]. ?' ]
boys with precocious puberty. In addition to viril-
0 ]8 R9 p% F! L6 q$ T$ aization, the clinical hallmark of CPP is the symmet-" w, B- X7 t# e* ^2 Z5 O: o: D
rical testicular growth secondary to stimulation by2 _7 {( f: x$ P7 {& x
gonadotropins.1,38 V) U+ T% o. l( p5 [
Gonadotropin-independent peripheral preco-, T& ?0 J4 I$ k  U8 F9 q5 `6 a
cious puberty in boys also results from inappropriate
# Y2 b3 w% I6 x7 Tandrogenic stimulation from either endogenous or
' g# g$ B9 g& P) ~4 I6 _/ Z0 @exogenous sources, nonpituitary gonadotropin stim-
5 I. h! M! A: e- l7 d. _4 ?ulation, and rare activating mutations.3 Virilizing
5 X# i( Z' ^0 P# i" O  I/ Kcongenital adrenal hyperplasia producing excessive6 K1 W# I4 q) r9 ^$ J
adrenal androgens is a common cause of precocious
. Y0 c4 ?: Y8 B' C2 Dpuberty in boys.3,42 A0 w  _; @8 S* c6 k
The most common form of congenital adrenal
8 t# ], c) x$ Chyperplasia is the 21-hydroxylase enzyme deficiency.
& s0 _3 J7 p& g& }* ~( T) i( t8 iThe 11-β hydroxylase deficiency may also result in6 X# X! i! j, _2 b5 W& u. ]; N+ X
excessive adrenal androgen production, and rarely,! {" L# F7 B  {" a
an adrenal tumor may also cause adrenal androgen* g* s, S! ]. J! X" c( s
excess.1,3; A2 L+ _+ ~0 F& M. Q: V
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ W: N: W$ M! _  l! q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( x$ B! n0 g$ e$ b
A unique entity of male-limited gonadotropin-
) U$ `6 H# m& N. t1 P, Kindependent precocious puberty, which is also known
& `& |& s" x0 R& |as testotoxicosis, may cause precocious puberty at a8 }6 m2 l" W: e, J2 T
very young age. The physical findings in these boys
- ?$ Q! y8 ?+ ~1 V6 Y9 Lwith this disorder are full pubertal development,
2 R" W1 n; ~8 wincluding bilateral testicular growth, similar to boys: i9 x, F  O( T3 W4 ^
with CPP. The gonadotropin levels in this disorder
" u2 d8 F/ k4 x! o- J1 D. q  T& ^are suppressed to prepubertal levels and do not show
$ v' y5 a8 b" A) G" spubertal response of gonadotropin after gonadotropin-' X+ o2 |; P* M) r! w) |; t
releasing hormone stimulation. This is a sex-linked9 ^! S# Z1 q7 v) u) [
autosomal dominant disorder that affects only
) M( S  Z$ @+ ]9 o3 S2 s& u3 @/ amales; therefore, other male members of the family( Q0 v1 H# H1 w9 J* H8 U
may have similar precocious puberty.33 c& k8 b, G+ h* k
In our patient, physical examination was incon-
. L2 D5 e. `2 h" o0 u5 asistent with true precocious puberty since his testi-
% H& t" I  N1 }5 m0 p* [cles were prepubertal in size. However, testotoxicosis
. M3 i3 a; t4 Qwas in the differential diagnosis because his father
2 v8 |* a! K9 K6 cstarted puberty somewhat early, and occasionally,; M& H0 Y" w/ V
testicular enlargement is not that evident in the, ~, M# B  t4 ^8 l! W  V4 C
beginning of this process.1 In the absence of a neg-
9 z& ^3 c3 j+ t# E# o7 m" |ative initial history of androgen exposure, our
3 ]; P8 m) L+ ?7 t5 \& `biggest concern was virilizing adrenal hyperplasia,
3 S- F8 d/ ]6 n; A# D, P' {either 21-hydroxylase deficiency or 11-β hydroxylase9 l6 E7 @( @5 Z9 c8 u3 v! }
deficiency. Those diagnoses were excluded by find-
) I7 u: N7 K" A: cing the normal level of adrenal steroids.# d& G) l" S( A% \, v6 P6 t
The diagnosis of exogenous androgens was strongly
6 a$ [! e' c( C. _8 fsuspected in a follow-up visit after 4 months because! w" S7 c9 Z" x% ?, |4 }
the physical examination revealed the complete disap-4 v$ y7 G9 `9 m1 i2 k2 W1 r
pearance of pubic hair, normal growth velocity, and
+ f. `  o" v" s5 J* M3 Bdecreased erections. The father admitted using a testos-
6 N' k" V) T; jterone gel, which he concealed at first visit. He was
: K7 j/ @! ]% x, O+ g, Dusing it rather frequently, twice a day. The Physicians’
3 G1 @+ [( L7 \, Z$ P& M* |Desk Reference, or package insert of this product, gel or
# x  |; _4 t# D; X3 L  x/ @cream, cautions about dermal testosterone transfer to
6 d6 Y0 R% }# |/ S9 E+ F; @0 j% Wunprotected females through direct skin exposure.- O, j: o. F2 i0 X: ?. M
Serum testosterone level was found to be 2 times the
: Q+ }9 B& S+ A$ `0 b! i* d$ Dbaseline value in those females who were exposed to
( Q$ T! A1 k" o% d8 h/ keven 15 minutes of direct skin contact with their male
  m7 |( C% {0 b( m$ _partners.6 However, when a shirt covered the applica-0 F5 O, y7 K" b" ~2 a$ A, h
tion site, this testosterone transfer was prevented.
  S5 ^$ q9 r% U! S1 rOur patient’s testosterone level was 60 ng/mL,8 @1 x& ]7 j3 U  D- Z* U
which was clearly high. Some studies suggest that% ]. {& D. M4 E- Q4 }' b9 ]
dermal conversion of testosterone to dihydrotestos-
3 Q& i+ @  x( iterone, which is a more potent metabolite, is more
5 ?2 \: i6 Z1 N& N  wactive in young children exposed to testosterone, H1 i, _: D) P( A3 S9 ^, V" M
exogenously7; however, we did not measure a dihy-# K: R1 i, q# o* v) M
drotestosterone level in our patient. In addition to
& S* m1 b& }  a" J3 g; S; x0 Yvirilization, exposure to exogenous testosterone in, |7 Q; L& C1 U
children results in an increase in growth velocity and! d- e7 ]/ g3 ^8 a
advanced bone age, as seen in our patient.6 z$ R# ^' [% x3 k7 y4 P
The long-term effect of androgen exposure during
6 v- Q( d* `7 a0 d) o9 S8 Xearly childhood on pubertal development and final; r# d! W1 x/ |: _7 Z
adult height are not fully known and always remain
+ x, N& ^. b# j$ b( za concern. Children treated with short-term testos-- e4 v7 T& l$ Y6 E& |  ?
terone injection or topical androgen may exhibit some7 O8 g# U* a  u  m6 ~$ c9 W' V
acceleration of the skeletal maturation; however, after
8 E- B) B) q! {/ Kcessation of treatment, the rate of bone maturation
. S: a. R. J& `7 M# d  @decelerates and gradually returns to normal.8,9
0 \4 X: m8 V/ N9 }7 jThere are conflicting reports and controversy: R- K! t: O& l" q  F
over the effect of early androgen exposure on adult0 X% \, A& h1 I+ Q# X
penile length.10,11 Some reports suggest subnormal* i0 q) f8 @: `/ P
adult penile length, apparently because of downreg-) O  V# T6 ]. v+ a! X
ulation of androgen receptor number.10,12 However,
; ~( i' j& {  \0 R6 s9 W3 rSutherland et al13 did not find a correlation between
' |- x$ c3 A9 J6 ochildhood testosterone exposure and reduced adult$ C+ S4 I6 G  S( w; }
penile length in clinical studies.
- y2 Z% I( q4 _2 c9 RNonetheless, we do not believe our patient is
0 B9 P4 h* I+ \; {5 u; Xgoing to experience any of the untoward effects from1 f9 w+ A8 x& s  m; `
testosterone exposure as mentioned earlier because
1 r9 {5 z2 }! T1 l( xthe exposure was not for a prolonged period of time.
" V: g% C! {' rAlthough the bone age was advanced at the time of
) r8 W( [5 |4 Zdiagnosis, the child had a normal growth velocity at7 a, R( @, p. v, F# h' S
the follow-up visit. It is hoped that his final adult- y4 Y# H' C4 W' a: U
height will not be affected.. U; a- m% i) Y: }/ d: e% P
Although rarely reported, the widespread avail-: K, n- ]& x9 `, X( ]6 ]" K7 D
ability of androgen products in our society may0 b1 o0 h) d% T* I! T
indeed cause more virilization in male or female. R0 V/ ?1 k- k: u1 z4 G* N+ q2 s
children than one would realize. Exposure to andro-
, v/ S. Y" u8 Fgen products must be considered and specific ques-! H. Q  \2 u, G5 h( b6 h
tioning about the use of a testosterone product or
6 T2 O7 W( @$ R7 U/ `% J- S  ?1 Zgel should be asked of the family members during
+ k5 [2 N5 p; {/ E% @the evaluation of any children who present with vir-' V5 W0 h; y$ K1 d+ N
ilization or peripheral precocious puberty. The diag-
/ X$ y# p1 f5 a9 j+ E4 }nosis can be established by just a few tests and by
7 I$ C0 |! m: e7 p" [8 W' j+ w- Q2 Lappropriate history. The inability to obtain such a
' C, Z9 U9 L1 l4 Ghistory, or failure to ask the specific questions, may
' ?6 M7 [7 ~) B* G7 q, w, G  dresult in extensive, unnecessary, and expensive
. j3 k: D. u$ w" Finvestigation. The primary care physician should be6 F2 r: }2 R4 I
aware of this fact, because most of these children
! @2 Y# y. ^/ J9 g1 e, y. I  ?. pmay initially present in their practice. The Physicians’% a0 n  I6 g$ y+ i% H  p; k$ S0 s: P
Desk Reference and package insert should also put a
  C  D& e& _: ~$ xwarning about the virilizing effect on a male or
5 b6 }' X( ?: g2 Efemale child who might come in contact with some-
! g% u) A5 N) h" ]one using any of these products.
0 `8 x% C$ K7 TReferences; G- a4 b& T" t/ @* x" |8 {; B
1. Styne DM. The testes: disorder of sexual differentiation2 C& A# U3 o3 s5 d8 a# `, q$ U! J
and puberty in the male. In: Sperling MA, ed. Pediatric. X/ k8 V2 g( @. g! T7 p
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 ^! u* E! A) L1 _' @
2002: 565-628.
; o3 {. ]: b6 v6 w4 U2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% N9 Q: I, K* |6 S
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old( C( @  P% o9 j8 C. W& N
Boy Induced by Indirect Topical( a5 e+ T& l# F4 {" d- Z  t
Exposure to Testosterone, [$ ?, ?1 H% k  x/ z, K. }" c
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 p4 [7 u+ s2 L6 N) Kand Kenneth R. Rettig, MD1
4 s  B" E% P, q) L2 B9 CClinical Pediatrics2 k$ e' y* s5 I- R, d
Volume 46 Number 6
& ^2 P; I8 w5 r, L4 xJuly 2007 540-543
0 n& a0 r, s  v1 [© 2007 Sage Publications7 ]& V6 W+ C1 t/ C4 w, E( n
10.1177/00099228062966513 M' F, Y4 i2 y/ C- i
http://clp.sagepub.com* ?( m4 d3 \( r0 Z" Q5 r  k( ^2 q
hosted at  j8 h* N9 L3 m1 b% L7 U+ X" f
http://online.sagepub.com
& u; b* ?$ ]. Q) o, L6 \- rPrecocious puberty in boys, central or peripheral,
" p5 u/ N4 }& v  S+ b% iis a significant concern for physicians. Central
; b9 |+ w% g! n1 n. E; j3 n: E6 Y+ bprecocious puberty (CPP), which is mediated2 j1 w: n! J/ A. O$ E
through the hypothalamic pituitary gonadal axis, has
+ w3 D& k' _1 Y/ u/ o7 Z$ ta higher incidence of organic central nervous system
( v2 u7 S+ V$ G" Slesions in boys.1,2 Virilization in boys, as manifested& A) A& L% _* t* K  K  I
by enlargement of the penis, development of pubic! h3 u; |4 C6 P$ n- V3 H5 _
hair, and facial acne without enlargement of testi-
/ z/ K/ `. J$ a3 Fcles, suggests peripheral or pseudopuberty.1-3 We
% l( @  P! x* U. Xreport a 16-month-old boy who presented with the, O, I1 _& |" }5 L; N
enlargement of the phallus and pubic hair develop-, E  w5 ]5 r, m' {; i5 W/ s
ment without testicular enlargement, which was due+ D" |. h  J% A9 ?3 E
to the unintentional exposure to androgen gel used by
, M$ S: g: I' E; ^9 t0 A2 P2 cthe father. The family initially concealed this infor-- _2 E% Q/ s1 P3 g( R: v
mation, resulting in an extensive work-up for this
1 @- U/ F% W; x3 G% `  o5 o1 T4 Gchild. Given the widespread and easy availability of
; h4 Z  s% G& A5 B0 p5 V9 Atestosterone gel and cream, we believe this is proba-
$ V1 W9 c/ d  P- E  S8 m  Ybly more common than the rare case report in the
; y; `9 a# h2 i# D- s; zliterature.4
, k, [( k# Z4 x7 y/ VPatient Report. |. q! K& J9 f4 b
A 16-month-old white child was referred to the( u$ A( P% [& M1 c4 t3 g# p9 _
endocrine clinic by his pediatrician with the concern
$ |& _/ d* s+ ^( K9 [of early sexual development. His mother noticed
1 y% l9 U& i; s, u0 V5 z3 j1 jlight colored pubic hair development when he was# S3 P  d. }* p  |
From the 1Division of Pediatric Endocrinology, 2University of
0 `  z' a. Q9 c1 S4 PSouth Alabama Medical Center, Mobile, Alabama.* |  f, ~, J1 g) i% k
Address correspondence to: Samar K. Bhowmick, MD, FACE,* c$ ^8 J; y& {  s+ `- m
Professor of Pediatrics, University of South Alabama, College of
6 [: I2 j/ R4 I( q' V& oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" B: I2 Y6 l4 M0 ?
e-mail: [email protected].
/ H& x7 B% t! b- j# Iabout 6 to 7 months old, which progressively became
6 Q" k3 G4 e7 o0 f4 W/ _darker. She was also concerned about the enlarge-
, G" H5 y/ s6 e6 e7 n6 l7 Vment of his penis and frequent erections. The child
7 q9 l/ v0 ]" {% y. G+ F5 dwas the product of a full-term normal delivery, with* }8 {. W3 p/ t6 P
a birth weight of 7 lb 14 oz, and birth length of
4 d. V1 D' p; N* ^( f1 N20 inches. He was breast-fed throughout the first year
8 n0 B- l  P, fof life and was still receiving breast milk along with
4 }2 u: H3 H3 {( P: Q& s: w, G' z% t8 Jsolid food. He had no hospitalizations or surgery,3 T6 y! c. U. F- ?! m$ r
and his psychosocial and psychomotor development
1 O% U$ I) R9 R1 pwas age appropriate.9 j5 k/ Q3 W0 w7 @& J' A* e( O
The family history was remarkable for the father,7 a( I/ U5 T% Q! f
who was diagnosed with hypothyroidism at age 16,8 M1 e# Z9 x7 Q. l* ~/ A, n- y
which was treated with thyroxine. The father’s
3 [; E2 U  B1 D  k9 Xheight was 6 feet, and he went through a somewhat
8 M! m' E  Y: L% x4 g4 |3 j+ U% R7 Q; qearly puberty and had stopped growing by age 14.: E( X* s! Z! x3 Q
The father denied taking any other medication. The2 Y& c( e9 c! y6 d5 X3 t
child’s mother was in good health. Her menarche
% [3 O- k) |0 ~4 ], Z4 r! A1 e8 hwas at 11 years of age, and her height was at 5 feet; y6 ]2 n6 U; S0 x
5 inches. There was no other family history of pre-
% I7 S$ d; C2 p% y, lcocious sexual development in the first-degree rela-) ~/ Q5 c9 w+ j6 y/ Q/ L( D
tives. There were no siblings.. L- c% R$ Y1 a% R7 u
Physical Examination
( k% @! e  [6 K3 H0 ?0 mThe physical examination revealed a very active,
* b9 ~" L8 k* H2 _+ o$ qplayful, and healthy boy. The vital signs documented6 [, @: X6 K: U9 |8 H1 F
a blood pressure of 85/50 mm Hg, his length was
- {) z" r) B. z0 H90 cm (>97th percentile), and his weight was 14.4 kg
7 n! V  I* }" H8 {: y* |(also >97th percentile). The observed yearly growth
' w2 F' P" z2 v" X4 |velocity was 30 cm (12 inches). The examination of7 {, b0 L; ?: H3 ~! L) V
the neck revealed no thyroid enlargement.
* h" K7 }* k5 b7 FThe genitourinary examination was remarkable for
) |3 Q  d: q& O2 Yenlargement of the penis, with a stretched length of, s, D9 ^! y# J, \- q" R8 M
8 cm and a width of 2 cm. The glans penis was very well
9 T. E! L6 g3 q% V- y: g" m( J/ gdeveloped. The pubic hair was Tanner II, mostly around1 X- y$ U; @' N2 n- T/ P
540
- y) N; [# @. jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 b/ E: U0 e; Q2 N0 I/ O' F
the base of the phallus and was dark and curled. The1 b" E: a+ F* A: Z
testicular volume was prepubertal at 2 mL each." g7 F$ u9 C0 t0 U( i
The skin was moist and smooth and somewhat
+ o1 d2 `5 D. `7 f4 m& Roily. No axillary hair was noted. There were no/ z5 S4 y) D7 Y& L
abnormal skin pigmentations or café-au-lait spots.: i: K: d9 M  {- f
Neurologic evaluation showed deep tendon reflex 2+
" J3 U1 s- [3 a- N# h: f; U) w- ibilateral and symmetrical. There was no suggestion
2 x) e* `8 `" t+ g! O5 ~of papilledema.1 w! l0 e7 p! Q+ Q, P: a
Laboratory Evaluation/ o. M+ R+ R2 I" H
The bone age was consistent with 28 months by
1 U, i0 [; d5 Z2 _. f% Ausing the standard of Greulich and Pyle at a chrono-
3 C$ S& z: @1 Ulogic age of 16 months (advanced).5 Chromosomal3 l: V5 Z$ C( G! e, d1 ]/ i
karyotype was 46XY. The thyroid function test' e7 q6 M- G5 S- t+ K2 X
showed a free T4 of 1.69 ng/dL, and thyroid stimu-6 f0 Y$ }1 W; p1 `- S4 A. T- K
lating hormone level was 1.3 µIU/mL (both normal).
/ g: w; J, x& ?  q. d5 g# e+ LThe concentrations of serum electrolytes, blood; C0 j7 Y$ M$ ^
urea nitrogen, creatinine, and calcium all were
' e2 U6 c- x. F" E1 bwithin normal range for his age. The concentration
( H# S% }: {4 M! q4 A( o" _" _: O3 ?of serum 17-hydroxyprogesterone was 16 ng/dL
5 X% X8 X$ _4 [6 y% T- M5 _(normal, 3 to 90 ng/dL), androstenedione was 20
) U1 T& u$ s" a) png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! z3 ~- B: x$ S: o' V+ Y, ~) I. L. _terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 M. V3 V7 O$ l% w$ ^9 C' B6 _; b$ ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to9 f% j* b4 i) j! T+ s+ q# h
49ng/dL), 11-desoxycortisol (specific compound S)
1 x6 T$ O& X2 }. N+ l+ S7 Mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-$ M. `4 D0 ~2 I2 Q! A0 e
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 q- t7 _9 F4 S1 a- F' U, l
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, d3 b/ r* {- C* Y; pand β-human chorionic gonadotropin was less than
" `2 k1 k: Y8 u, B  c( J) f( x- Y5 mIU/mL (normal <5 mIU/mL). Serum follicular3 T  o0 d8 @! x  E1 O
stimulating hormone and leuteinizing hormone, Q5 _5 j" B" C# ?: c: l' j9 a
concentrations were less than 0.05 mIU/mL
/ ]% O) z8 K8 K5 |' k, a(prepubertal).7 `% b( u4 h' Z$ T
The parents were notified about the laboratory
9 U9 _; c1 [$ s+ dresults and were informed that all of the tests were
$ ^3 S3 b) L/ u+ ~  rnormal except the testosterone level was high. The
; G8 {1 K7 b. i; V% Q& afollow-up visit was arranged within a few weeks to7 t  G" I1 V( S7 F
obtain testicular and abdominal sonograms; how-
( ?, }9 l$ J, p+ O  n5 Yever, the family did not return for 4 months.! @' `) i; I2 ?& `* Z5 W1 T
Physical examination at this time revealed that the
- X' t+ D1 c& t9 p1 [, `' Mchild had grown 2.5 cm in 4 months and had gained0 W) I, O% l- C- w7 O& d: p6 E. A' }
2 kg of weight. Physical examination remained
- }- J4 `9 [7 b, xunchanged. Surprisingly, the pubic hair almost com-
5 p- n% J$ x! ^0 M7 ypletely disappeared except for a few vellous hairs at
# |+ B; T0 k0 ?2 m8 z/ s6 y. lthe base of the phallus. Testicular volume was still 2% H: V, A. n* _, B0 ?
mL, and the size of the penis remained unchanged.
5 }, w6 G5 X; n8 aThe mother also said that the boy was no longer hav-
: o5 S: o" e( @) `$ e4 ?ing frequent erections.  o0 ]' L% A5 ]' f/ _, c8 V# z9 o
Both parents were again questioned about use of  |3 E/ w" d' N6 f8 ?
any ointment/creams that they may have applied to% x5 r; q7 }( a( ?5 k
the child’s skin. This time the father admitted the
/ U. W/ P4 O3 q; P% rTopical Testosterone Exposure / Bhowmick et al 5417 m: O, Z( I# T7 C5 l) G
use of testosterone gel twice daily that he was apply-) q9 z: |. R& L; a7 m7 y7 x
ing over his own shoulders, chest, and back area for' u) o' T+ V4 d3 Z! I- L4 @
a year. The father also revealed he was embarrassed8 |3 m! \+ Z6 d4 U
to disclose that he was using a testosterone gel pre-
% {: ?! F) p6 s! qscribed by his family physician for decreased libido
3 }/ H( u( Y5 ?$ ]4 A* asecondary to depression.
' Z( N4 C8 Y8 J' FThe child slept in the same bed with parents.
9 m' L7 e' |  H& Z; t$ |7 d0 @The father would hug the baby and hold him on his& y$ G0 E( I+ o) V: ]
chest for a considerable period of time, causing sig-
  x# G; g( O8 V( U* Onificant bare skin contact between baby and father.1 F) v) U0 Z4 e, a! w0 C
The father also admitted that after the phone call,
7 [2 N! y: A2 s0 Rwhen he learned the testosterone level in the baby
) R$ y3 V9 n5 a1 vwas high, he then read the product information+ Q$ Q! ?, V7 |! `; v( K' M0 R
packet and concluded that it was most likely the rea-# F' Z4 @0 q7 a0 `2 t
son for the child’s virilization. At that time, they2 O: ~9 v+ [$ l+ E- B* E
decided to put the baby in a separate bed, and the
8 H7 N# C' u1 \6 U8 v, {! ]father was not hugging him with bare skin and had6 ?) c& U8 {/ r: q; ^" L5 b8 ?3 L
been using protective clothing. A repeat testosterone& j. A' N% z3 _8 _
test was ordered, but the family did not go to the8 W) j$ }6 t3 r& h" n- K
laboratory to obtain the test.
  [/ s/ S$ b- tDiscussion3 o* d% A: L9 Q/ A1 u
Precocious puberty in boys is defined as secondary! r0 Q: {( V3 W. t
sexual development before 9 years of age.1,4
6 ^5 @- V3 q4 E/ wPrecocious puberty is termed as central (true) when0 v6 I$ @! f9 K  c. x- }/ u. K
it is caused by the premature activation of hypo-
+ u. O% x) w  ]thalamic pituitary gonadal axis. CPP is more com-
8 n, b, Z: X. cmon in girls than in boys.1,3 Most boys with CPP0 P- @* e1 b$ x0 X0 a8 @0 m  f
may have a central nervous system lesion that is
/ ^' n& g) T& s: ]responsible for the early activation of the hypothal-
' Y/ m  A" n$ H1 J: q0 ^2 m9 _& Eamic pituitary gonadal axis.1-3 Thus, greater empha-: I* b; E' z* D2 t6 y# y
sis has been given to neuroradiologic imaging in
5 [: M9 ]7 ?$ Z8 S8 }boys with precocious puberty. In addition to viril-
# n9 [. u7 @- L4 J$ R# Nization, the clinical hallmark of CPP is the symmet-
1 z1 q1 }: K0 _% D6 ^rical testicular growth secondary to stimulation by
/ W0 X! p7 v. g+ R+ {/ @* Z4 @gonadotropins.1,39 @3 I8 S& x+ T- W( G' N9 f
Gonadotropin-independent peripheral preco-! e2 E$ D2 q. r$ G
cious puberty in boys also results from inappropriate1 D8 b! ^+ Y- @$ o6 G" B
androgenic stimulation from either endogenous or
- q( k+ P5 x- Cexogenous sources, nonpituitary gonadotropin stim-
& [2 `, _$ K0 P: ]( o' b, `ulation, and rare activating mutations.3 Virilizing
2 ~! q3 t- P# V( Acongenital adrenal hyperplasia producing excessive
  J, u4 f5 P- H, \6 gadrenal androgens is a common cause of precocious  l% a2 R; ^* E4 B7 }
puberty in boys.3,4% d0 S6 N' n9 r9 s
The most common form of congenital adrenal
+ S( M/ c4 E2 [) T1 x, B: khyperplasia is the 21-hydroxylase enzyme deficiency.
' K1 t+ S  z# w, DThe 11-β hydroxylase deficiency may also result in- T4 z" n+ ~8 s, h* {+ m
excessive adrenal androgen production, and rarely,7 U( m$ g" k! p
an adrenal tumor may also cause adrenal androgen
, S: V/ @" [2 g( H4 ~excess.1,3
& d3 y8 Z3 h1 o3 n9 @) j. Wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& V# {( g& h# j, n& i. [+ G
542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 p5 f' [. m% P0 e$ Y3 c- F
A unique entity of male-limited gonadotropin-- D1 ]5 q2 q: y3 @5 O! k6 G! y
independent precocious puberty, which is also known
  O4 A! d: s& O; |as testotoxicosis, may cause precocious puberty at a" K! l4 N$ F+ B) _2 K
very young age. The physical findings in these boys
. v( R* Q* F: R' `& |with this disorder are full pubertal development,+ Q' j# v0 X3 L  L
including bilateral testicular growth, similar to boys5 j2 I9 Y1 b5 U5 K0 u, I7 w
with CPP. The gonadotropin levels in this disorder
1 W  M& Y  \3 y2 J+ a* V" eare suppressed to prepubertal levels and do not show  c# \) K# {( `8 ^
pubertal response of gonadotropin after gonadotropin-
8 N# e, p/ W" k) Nreleasing hormone stimulation. This is a sex-linked
1 |  i- h7 n* H, Y2 X2 P. ~autosomal dominant disorder that affects only
8 T& |0 g$ G$ M: ^, tmales; therefore, other male members of the family# t- j$ V0 R0 |9 U4 `0 g* e5 H
may have similar precocious puberty.3
6 x" n% b2 n0 I/ \2 I  iIn our patient, physical examination was incon-/ l/ z9 t5 `) E% c8 ]" j3 [
sistent with true precocious puberty since his testi-( R" X# ?+ Z8 l- p" V7 D
cles were prepubertal in size. However, testotoxicosis
! S4 `, F6 j3 t8 \5 A0 swas in the differential diagnosis because his father
  z6 x# k9 p* G% L$ `- Wstarted puberty somewhat early, and occasionally,
1 C6 Y- r9 }$ ?: X2 R5 }9 ?( @testicular enlargement is not that evident in the
! C" q' [9 E& c  d" w3 Jbeginning of this process.1 In the absence of a neg-
* ?. g5 ^+ F) r6 V/ ^1 S+ p( kative initial history of androgen exposure, our
9 k  E0 b7 c+ n" ?% Cbiggest concern was virilizing adrenal hyperplasia,
% H! h4 o; |  Neither 21-hydroxylase deficiency or 11-β hydroxylase
' D- [% }. j0 n! ddeficiency. Those diagnoses were excluded by find-# s! d, a( x$ f
ing the normal level of adrenal steroids.. F$ I6 u" h5 x! ^3 Q) z  m
The diagnosis of exogenous androgens was strongly$ b* h1 ?6 J* P* W. e
suspected in a follow-up visit after 4 months because8 i; N9 }$ `5 f' i' ^- S* t
the physical examination revealed the complete disap-5 Q+ f% Y6 v4 Q) q! M
pearance of pubic hair, normal growth velocity, and7 q4 H2 B: ]8 S0 H/ o
decreased erections. The father admitted using a testos-: z: l1 k) N+ ~& P4 N2 J
terone gel, which he concealed at first visit. He was7 T+ E1 t# |0 x$ o* }
using it rather frequently, twice a day. The Physicians’
- j1 Y5 m- H& m* Q8 gDesk Reference, or package insert of this product, gel or9 n. `0 n8 Z3 r! I/ c6 F
cream, cautions about dermal testosterone transfer to# J3 r6 g! j; [. Z5 F6 M5 R+ ]- y) I
unprotected females through direct skin exposure.
# p0 u, X8 k, t5 c6 xSerum testosterone level was found to be 2 times the
! v9 I6 c* q+ ]9 \" r7 J9 Qbaseline value in those females who were exposed to
& h0 n, a( X; X, b, i# T& [even 15 minutes of direct skin contact with their male
& B2 a& L% |# \( t5 Opartners.6 However, when a shirt covered the applica-
- D+ h, Z# ?. |( }* y4 z" jtion site, this testosterone transfer was prevented.3 J  b3 a6 \0 K8 j# Z) B
Our patient’s testosterone level was 60 ng/mL,( r% S9 A; J, t' r, G, [( x" l
which was clearly high. Some studies suggest that4 i5 G; k6 b+ `# Q2 n
dermal conversion of testosterone to dihydrotestos-
5 s" ~  U$ B! [1 s; |+ ]( o* _terone, which is a more potent metabolite, is more
7 }  J  F5 Y: ~. W0 D& {active in young children exposed to testosterone: c" g* o0 f9 {- [( p9 R
exogenously7; however, we did not measure a dihy-& [- d. ?* @1 Z5 q- k0 [0 z
drotestosterone level in our patient. In addition to/ u' T, d" f$ X2 j+ [5 Y
virilization, exposure to exogenous testosterone in
$ v/ t9 E/ J% n) E: xchildren results in an increase in growth velocity and
+ v4 {; g# q& l- G% k. Iadvanced bone age, as seen in our patient.
( w7 M, {5 Z/ B) N! t' p6 Y* Q6 cThe long-term effect of androgen exposure during
% B+ C* {2 s7 `' O- X: dearly childhood on pubertal development and final
7 g7 F6 H6 R' J# q7 G; C/ d( \! ~# Cadult height are not fully known and always remain
" ~, K2 {. t" u. l- j# j" Y$ [a concern. Children treated with short-term testos-& y* {- N8 H) c# H7 X, G& a1 E
terone injection or topical androgen may exhibit some
$ L9 y& O( n! D) C/ g; c, |acceleration of the skeletal maturation; however, after6 z3 e5 X. O6 r
cessation of treatment, the rate of bone maturation
7 X, v( H7 K+ J( f* _decelerates and gradually returns to normal.8,9, Q: X4 o( Q3 D% S3 G/ v
There are conflicting reports and controversy
% S( C+ {3 e+ J+ I9 P  ^over the effect of early androgen exposure on adult1 c2 Z0 I* T" s6 d" `
penile length.10,11 Some reports suggest subnormal' [, [# Z3 d+ A
adult penile length, apparently because of downreg-
: N9 a- D( ]  Q" l2 X9 julation of androgen receptor number.10,12 However,
1 Y8 g, o; a- Q" f' J" g- FSutherland et al13 did not find a correlation between
( M% e7 f4 `. e' z& P2 [0 J+ ochildhood testosterone exposure and reduced adult% C3 g# R+ H4 I
penile length in clinical studies." U- a3 G& h& v3 O* g+ g- L
Nonetheless, we do not believe our patient is
3 `- J4 i5 j, ?9 N7 Ogoing to experience any of the untoward effects from
8 X" X% S2 k+ R6 Btestosterone exposure as mentioned earlier because
! y  @. V( `6 \% Rthe exposure was not for a prolonged period of time.
6 D3 @2 N9 q! {! R$ xAlthough the bone age was advanced at the time of
4 Y9 x! A& @# t$ udiagnosis, the child had a normal growth velocity at
  I% a' H& M$ K+ ~% n, ?$ ]1 Ythe follow-up visit. It is hoped that his final adult
; m6 Q( |! g( B* w! l1 H. r' J4 Oheight will not be affected.
$ F/ A7 Q( ?" V+ B, ~5 g5 Y3 A7 JAlthough rarely reported, the widespread avail-- z% q/ _$ ?' S/ F$ {( W" n
ability of androgen products in our society may9 r* M' H/ b1 l/ H" e: q# K, n
indeed cause more virilization in male or female- _& K: z, X9 {! M$ Y( x
children than one would realize. Exposure to andro-- A% z( N6 f3 E5 b$ s: @" T
gen products must be considered and specific ques-
: P" z1 L! v" J5 I; ?$ ftioning about the use of a testosterone product or2 ~- o1 r3 A; Q8 o$ y
gel should be asked of the family members during' y) x9 c, Y5 _6 A, Q
the evaluation of any children who present with vir-
) F: a5 t1 l: ~2 A& b+ Nilization or peripheral precocious puberty. The diag-7 M$ B/ {0 `) G" i# v
nosis can be established by just a few tests and by. H; Y6 p1 ?5 O1 n* ?
appropriate history. The inability to obtain such a5 @& w4 w+ @$ X" ^. v
history, or failure to ask the specific questions, may/ L9 J0 q8 ^# I+ f  v& x
result in extensive, unnecessary, and expensive6 e; ~$ @, N+ z8 Z
investigation. The primary care physician should be
1 k8 V( Y! I' s1 v9 ]aware of this fact, because most of these children* R/ L: P( Y; Q' w
may initially present in their practice. The Physicians’
' P) }. @2 }1 e: U) m* T7 ^Desk Reference and package insert should also put a
3 J" v: C: A% U/ Ewarning about the virilizing effect on a male or6 G1 _2 [1 r0 }, h; i
female child who might come in contact with some-
( c" E- b. @& s0 N; ^one using any of these products.
  L6 G6 S$ u7 G6 @0 vReferences0 O& f  y$ t1 u1 E0 }. ?$ G5 X
1. Styne DM. The testes: disorder of sexual differentiation; M5 g; P. f# |. D) v0 ^, E
and puberty in the male. In: Sperling MA, ed. Pediatric$ s) N& u/ k; ^. S2 S/ ~
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" H; a& z# Q- ]5 e* k9 }- k8 u
2002: 565-628.
" y% K7 c" ?) f- A2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& C6 _% f, s. _# L( a4 J' T
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

5 Z$ C, @  [  T. s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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