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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-Old2 A9 f. X& L( [+ w! }" n
Boy Induced by Indirect Topical0 }5 p/ l2 L: S7 s) J$ F$ f
Exposure to Testosterone' u+ x' T/ a+ u0 O9 f
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' O2 G4 r  v" jand Kenneth R. Rettig, MD1
/ P$ U7 A# x0 K5 AClinical Pediatrics
2 v0 @$ m; J4 cVolume 46 Number 6* k3 `0 {4 n& p" U# y) ^
July 2007 540-543
& c' a7 D) T0 e© 2007 Sage Publications& _; k% p# c" |9 d5 P" P
10.1177/0009922806296651
0 W; Q) R' q6 y/ lhttp://clp.sagepub.com
5 j! |. s+ ~" K; T% t2 J* O& o- H7 f% shosted at
9 A. ?, i( u1 R7 J# mhttp://online.sagepub.com" t9 ?- |5 ^0 W
Precocious puberty in boys, central or peripheral," ^. ~& z7 [: p  g
is a significant concern for physicians. Central) z" n( M- [. k
precocious puberty (CPP), which is mediated
. {4 s) p/ P4 F7 o' I% t  d& pthrough the hypothalamic pituitary gonadal axis, has
/ o( f. M4 ]( e5 h( B+ ^" Za higher incidence of organic central nervous system9 k" y/ H  U1 I( C+ R- V* u8 x
lesions in boys.1,2 Virilization in boys, as manifested+ k' S( s, e# h. J& I3 N8 F6 F: A
by enlargement of the penis, development of pubic6 Y: p, o) A& H) ^6 j: B9 v
hair, and facial acne without enlargement of testi-$ H+ b. B) N5 a4 K$ `; d# O4 \: \
cles, suggests peripheral or pseudopuberty.1-3 We
1 m- v$ I( f' _( s% Dreport a 16-month-old boy who presented with the' o: L4 ?3 ]9 v, d( _9 V+ d) w
enlargement of the phallus and pubic hair develop-9 F2 G4 S6 f* c) c- M8 K
ment without testicular enlargement, which was due6 B: w0 u/ B0 Q& u+ w
to the unintentional exposure to androgen gel used by2 ~+ a3 y6 Z( w. D3 W
the father. The family initially concealed this infor-
: s( F2 U4 o9 j+ t9 h. e1 Cmation, resulting in an extensive work-up for this% ~# w$ p- j! F: l
child. Given the widespread and easy availability of( E7 ~( L7 k2 H! ?$ F9 M. ]8 r
testosterone gel and cream, we believe this is proba-
$ M2 }: r0 ]7 X6 v  c* Sbly more common than the rare case report in the
+ e( P" s7 w8 ]- }/ cliterature.4
% R3 C2 j3 s! \( x  nPatient Report( N: A2 c/ E: j- u2 e  v
A 16-month-old white child was referred to the
3 L1 v/ _$ ~( _, a8 D. z& V2 _: p3 pendocrine clinic by his pediatrician with the concern# j5 V" R# L) @9 a0 G. _
of early sexual development. His mother noticed# u5 F" j& b% v7 B3 K; ^
light colored pubic hair development when he was! Y0 J+ e9 c6 Z6 V, _1 [% w! {
From the 1Division of Pediatric Endocrinology, 2University of; c2 X% c; W0 ?7 c  K0 g
South Alabama Medical Center, Mobile, Alabama.5 @" \1 \, H2 W7 m! e  ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,
- O2 c& }, D0 l; y! g4 wProfessor of Pediatrics, University of South Alabama, College of6 c9 v2 L6 @5 [% J3 e1 r
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 M  l# q& w1 z+ ~" `& ^
e-mail: [email protected].+ E6 i! O$ ~- X: O) P
about 6 to 7 months old, which progressively became, l, G* m# o8 N: \; [
darker. She was also concerned about the enlarge-
/ [2 l7 h+ d  bment of his penis and frequent erections. The child) C! m' S5 N* h8 U) f) N
was the product of a full-term normal delivery, with, }: L4 _6 @2 Q+ i8 t  j) Z
a birth weight of 7 lb 14 oz, and birth length of2 H. R  g9 g  `+ }$ P
20 inches. He was breast-fed throughout the first year
4 I% B$ s+ S6 d" d' Qof life and was still receiving breast milk along with
1 T' V7 W' I, m7 e# q& E* lsolid food. He had no hospitalizations or surgery,
! q* ~; `7 t9 j9 A& `- a  h" j% a6 Wand his psychosocial and psychomotor development, T! ~% e# T9 X8 p( x# g* x  v
was age appropriate.
- j& P+ W) y- n( Z, C8 IThe family history was remarkable for the father," e' ^& v" x6 K
who was diagnosed with hypothyroidism at age 16,1 g7 w0 ~$ ]2 @9 B  v0 J5 r
which was treated with thyroxine. The father’s! V! ^/ o5 R( q- u% j: y' s
height was 6 feet, and he went through a somewhat2 e9 G8 P8 w. ?# |9 z! X1 Z
early puberty and had stopped growing by age 14.
; J- `$ s8 l" d! Z1 N5 e7 fThe father denied taking any other medication. The4 r; ?! K: V! C; l
child’s mother was in good health. Her menarche  G( X2 n$ e$ Q
was at 11 years of age, and her height was at 5 feet  s- V6 e5 y' y+ ?9 K! l! R: s
5 inches. There was no other family history of pre-
/ _% A! @' z# @( l+ a6 l9 f8 acocious sexual development in the first-degree rela-! a: {: F$ r. e
tives. There were no siblings.
$ B3 ]; [8 @( N9 U7 x! @Physical Examination3 D: X& L  X: x6 n
The physical examination revealed a very active,
2 e) b; e0 F+ _) |3 n, nplayful, and healthy boy. The vital signs documented, S0 Q5 d; o# R3 A* m' Y6 R
a blood pressure of 85/50 mm Hg, his length was% |8 B  u% b: O. Z' x, f/ ^
90 cm (>97th percentile), and his weight was 14.4 kg  g3 s, R8 ~7 V  X! s: L* |# z
(also >97th percentile). The observed yearly growth% Z5 ~8 l# {0 z: Y& |) H! o3 ~
velocity was 30 cm (12 inches). The examination of3 |0 d$ w+ I/ S# Q
the neck revealed no thyroid enlargement.: G! v' j! V0 W. q8 @. b
The genitourinary examination was remarkable for& {7 E6 m! n) _+ f! G4 a. l
enlargement of the penis, with a stretched length of
; j( q7 c, x; f8 x! y0 E2 N, A- q8 cm and a width of 2 cm. The glans penis was very well
' b1 q: E$ S4 D/ M3 q5 Ldeveloped. The pubic hair was Tanner II, mostly around+ v" \9 f1 M  D+ C9 Q1 i0 K/ g
540& C5 T* E% Y5 {; s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( C0 G) @- w) K2 L! e0 ^: X! Pthe base of the phallus and was dark and curled. The
) ^: ~# j: M% z# wtesticular volume was prepubertal at 2 mL each.
' l+ Y4 s/ [% K2 u" BThe skin was moist and smooth and somewhat
+ q8 T/ e# e5 Moily. No axillary hair was noted. There were no- u4 l5 A# B3 |7 a# d
abnormal skin pigmentations or café-au-lait spots.1 O8 w3 ~5 G: ]7 {
Neurologic evaluation showed deep tendon reflex 2+( U5 U6 }1 j* l7 i$ H; @
bilateral and symmetrical. There was no suggestion
) f# z' h, o( X$ h9 P3 Aof papilledema.; H1 A" }2 b( l5 N/ F5 u* j! A
Laboratory Evaluation
8 A4 S5 a0 _  v* SThe bone age was consistent with 28 months by$ ?  S/ v! k5 {$ g
using the standard of Greulich and Pyle at a chrono-
: g# [; h% K1 o% j+ X0 r: r9 {# [logic age of 16 months (advanced).5 Chromosomal
% b, T2 h5 A, r5 Jkaryotype was 46XY. The thyroid function test" g, h- H+ g; H( n8 |7 g4 [' p
showed a free T4 of 1.69 ng/dL, and thyroid stimu-% j- ]" X$ r( n6 q- l
lating hormone level was 1.3 µIU/mL (both normal).: u: b+ K/ V- V$ s: F" r
The concentrations of serum electrolytes, blood+ ?' W* D4 N  |% W' y6 w# M9 D/ d
urea nitrogen, creatinine, and calcium all were" f* ^0 l' Y# ^! k
within normal range for his age. The concentration
( s- N6 t  ^& U: z/ {of serum 17-hydroxyprogesterone was 16 ng/dL
* I% f! k, F, P# a# y8 M(normal, 3 to 90 ng/dL), androstenedione was 200 ^3 m: `  ]- B1 z! N& J& u. O2 y
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, N  ]6 f0 n' H0 O
terone was 38 ng/dL (normal, 50 to 760 ng/dL),6 N, F" l- b( @
desoxycorticosterone was 4.3 ng/dL (normal, 7 to/ b8 D# m( e  U9 @
49ng/dL), 11-desoxycortisol (specific compound S)0 x8 _8 W) H) w  [$ |( `
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: f# K& e  _% q( K( @. o; x3 utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( z' B$ L( R/ u# D5 p# f) qtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),: B- }( O$ `9 m4 n
and β-human chorionic gonadotropin was less than
+ F5 {( B& N9 q6 t) |# ^5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 W. B) g3 _3 I/ M; ^% Z0 Ustimulating hormone and leuteinizing hormone
3 x3 Y. T+ _9 L8 J! T, vconcentrations were less than 0.05 mIU/mL
9 n# L; B3 k' w(prepubertal).+ Y  D3 ~) M2 j1 |" ?* {" N8 Y
The parents were notified about the laboratory1 q9 S! N0 m8 T
results and were informed that all of the tests were; d( |: z( D7 r% \4 f1 F/ ^
normal except the testosterone level was high. The
7 @1 [  v; {1 l. C  R8 @! A  m8 rfollow-up visit was arranged within a few weeks to
+ Z$ k" |! f; k' T1 K% i- }obtain testicular and abdominal sonograms; how-
6 e3 V6 Y8 U- Y: D8 Jever, the family did not return for 4 months.
4 N5 s) D3 i; B3 DPhysical examination at this time revealed that the
+ \: x% D1 N  e# H- L5 A4 Dchild had grown 2.5 cm in 4 months and had gained" p" ]$ M3 U9 z; x/ N8 \4 d
2 kg of weight. Physical examination remained
; _9 p  y2 c) V( H, bunchanged. Surprisingly, the pubic hair almost com-
/ \$ L$ d' L* f+ gpletely disappeared except for a few vellous hairs at
/ R9 R% h+ U1 g, }the base of the phallus. Testicular volume was still 26 J. K% c3 N* _- [, H; B5 T) {
mL, and the size of the penis remained unchanged.
+ t9 C. Q+ c6 {: N/ A- W9 eThe mother also said that the boy was no longer hav-' p' E3 v8 c8 B" G/ d# H+ Z
ing frequent erections.
$ q6 B, ]& @8 YBoth parents were again questioned about use of
$ ~, }+ I8 V2 x, b1 pany ointment/creams that they may have applied to
8 P* n1 ?% ]6 _" K6 A+ Othe child’s skin. This time the father admitted the; P9 T/ i0 Q5 T( \8 b" H
Topical Testosterone Exposure / Bhowmick et al 541
: E, l6 W$ e, Z  v1 buse of testosterone gel twice daily that he was apply-$ a% y4 @: Q1 P& C3 X5 G
ing over his own shoulders, chest, and back area for
* x4 _4 P1 W2 }! {6 [+ e& Q+ E* s5 ja year. The father also revealed he was embarrassed% f4 b; P- ~$ v) p6 O! A: c
to disclose that he was using a testosterone gel pre-
) x, o; k6 j: C- \+ i0 n& H1 zscribed by his family physician for decreased libido
+ Q) `# d4 {: _$ [" L. Ssecondary to depression.
8 U: Y  f3 Z1 P' H2 v- vThe child slept in the same bed with parents.
7 G5 q: s& T9 u. I6 EThe father would hug the baby and hold him on his
- c$ q. ?$ L: u' |/ Z% r$ o5 b+ ochest for a considerable period of time, causing sig-! d% v6 ~& {9 H$ m* |* Z8 G
nificant bare skin contact between baby and father.- g- V5 j8 M  w
The father also admitted that after the phone call,
9 k" X- |/ G8 \' m8 q6 kwhen he learned the testosterone level in the baby. a6 w0 w* W$ `
was high, he then read the product information
3 f# T& |% p9 fpacket and concluded that it was most likely the rea-% I( R7 U% G# Q/ j+ d
son for the child’s virilization. At that time, they$ V; d: J; W8 b4 R$ H5 y
decided to put the baby in a separate bed, and the8 v& g+ K" W5 s! V
father was not hugging him with bare skin and had
4 i$ _/ `; j1 g  J+ Ubeen using protective clothing. A repeat testosterone
: B; X& m) V9 ftest was ordered, but the family did not go to the9 L" u! U7 i2 _; ~
laboratory to obtain the test.3 U5 A' ^5 k5 z9 Z+ G+ T
Discussion0 M+ v7 D4 @; `) B) ^+ F
Precocious puberty in boys is defined as secondary- P; l4 z* l9 b. Z! K+ O# j& u0 `
sexual development before 9 years of age.1,4
8 C# o1 y2 J+ Q% IPrecocious puberty is termed as central (true) when
& o9 x7 [, o' Fit is caused by the premature activation of hypo-8 S$ O( K: ^) K9 T& I- u* t
thalamic pituitary gonadal axis. CPP is more com-3 d( W# L- a+ h& H( ~
mon in girls than in boys.1,3 Most boys with CPP
4 B! i8 z0 y2 lmay have a central nervous system lesion that is
+ J/ H4 H! W+ m% u* m5 v4 b6 t% p. @responsible for the early activation of the hypothal-
7 j( I& R4 j/ v& samic pituitary gonadal axis.1-3 Thus, greater empha-
9 a" q8 e- c+ l. `! vsis has been given to neuroradiologic imaging in& ]% z3 V) X! _: _* H0 f$ |
boys with precocious puberty. In addition to viril-/ C& Z, k$ c" ~/ Q
ization, the clinical hallmark of CPP is the symmet-$ Y2 H. F5 s3 z2 R
rical testicular growth secondary to stimulation by0 s% D4 o/ W4 D$ i% [. q8 u! r5 d
gonadotropins.1,3' t  J; w$ B# ^; c; _
Gonadotropin-independent peripheral preco-9 F" ]0 M: {" W" r. }
cious puberty in boys also results from inappropriate+ m) M/ f6 t" ?# Y% F3 V
androgenic stimulation from either endogenous or9 p2 p" Y( G3 q6 E, p
exogenous sources, nonpituitary gonadotropin stim-& b! b7 f8 {3 Y- `4 a: d' }( @
ulation, and rare activating mutations.3 Virilizing
- H$ a4 _/ T: Ycongenital adrenal hyperplasia producing excessive" ]$ P- B, z, Z
adrenal androgens is a common cause of precocious
0 G/ A; f" I! q3 p5 T# qpuberty in boys.3,4
& @2 ?1 Q# J9 y. f3 `The most common form of congenital adrenal
  k# f7 ?, S' hhyperplasia is the 21-hydroxylase enzyme deficiency.+ ?& F! o5 T" S7 K! v1 F9 q
The 11-β hydroxylase deficiency may also result in
+ I% y2 K8 c/ P- Z4 Gexcessive adrenal androgen production, and rarely,
3 r) A2 s5 Y+ a2 ~2 Qan adrenal tumor may also cause adrenal androgen) x# A9 |, r3 ~5 H/ o4 K
excess.1,3
5 @; F7 I0 r+ [5 S5 }7 Sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' X9 n  m$ i* t6 m/ V8 r
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 Z2 w8 V) j! l& f; \' }5 \: Q4 iA unique entity of male-limited gonadotropin-3 S: M6 z3 r3 b0 D6 n
independent precocious puberty, which is also known
5 Q7 T- @: s3 \$ q; O8 ~1 las testotoxicosis, may cause precocious puberty at a5 g6 F+ A4 w4 P  L
very young age. The physical findings in these boys
1 W6 z6 v- H. Uwith this disorder are full pubertal development,  t# n1 c4 K: Z- {, b
including bilateral testicular growth, similar to boys
( ?7 E4 [6 s$ [/ z3 _5 ^$ hwith CPP. The gonadotropin levels in this disorder: |) M  y( W* Q2 Q- f
are suppressed to prepubertal levels and do not show
+ I1 [5 n) U1 W6 i0 Y2 Kpubertal response of gonadotropin after gonadotropin-
. p$ V5 h' c8 K4 s: F; l* d. K9 u) b7 creleasing hormone stimulation. This is a sex-linked# y% ~* W+ M0 D  m7 |1 N3 d( q
autosomal dominant disorder that affects only7 Z# S( h$ s% V+ f
males; therefore, other male members of the family7 u- B* I7 p4 S$ e
may have similar precocious puberty.3
4 ~' r% A- M- t$ KIn our patient, physical examination was incon-% B% R( |6 I) _* E" D  Z9 J
sistent with true precocious puberty since his testi-# D( @5 r9 G  \2 O7 x
cles were prepubertal in size. However, testotoxicosis
- j- l/ D. w  pwas in the differential diagnosis because his father! h, _; t3 v  P: ?3 O0 `% c7 k
started puberty somewhat early, and occasionally,/ h+ [: G( W) t$ M, V4 f. g5 g8 E
testicular enlargement is not that evident in the+ L3 w* K+ g3 |
beginning of this process.1 In the absence of a neg-+ p* ^5 Z) n0 ]/ j$ q4 x/ k
ative initial history of androgen exposure, our. A' `8 t; e( j- D. \
biggest concern was virilizing adrenal hyperplasia,2 s% u$ C( q0 S5 ]
either 21-hydroxylase deficiency or 11-β hydroxylase
2 v0 Q4 [. c" T0 t/ s9 f5 K  v' jdeficiency. Those diagnoses were excluded by find-
: B. n, X9 d, D7 B1 n* ?ing the normal level of adrenal steroids.
! y$ Z6 u# e& h# S& iThe diagnosis of exogenous androgens was strongly! T2 v" y, d* R
suspected in a follow-up visit after 4 months because
) N: T, W/ F/ {; ythe physical examination revealed the complete disap-
6 v- a2 b' G7 S7 C0 k0 fpearance of pubic hair, normal growth velocity, and. R5 f( P/ Z% Q# Y5 [; [3 r
decreased erections. The father admitted using a testos-
+ j; u# y2 v- Z7 _; Fterone gel, which he concealed at first visit. He was
5 U4 g+ X6 M* I9 n8 ?using it rather frequently, twice a day. The Physicians’
6 \( N  o2 n9 Z% _) IDesk Reference, or package insert of this product, gel or
  j+ O; t, C$ R$ B% ncream, cautions about dermal testosterone transfer to- h, x+ g" Q4 A$ p" a. N
unprotected females through direct skin exposure.
7 b* |/ o& A' P+ A5 v4 wSerum testosterone level was found to be 2 times the6 A4 _# Z6 C! \3 i: y
baseline value in those females who were exposed to; l6 ]$ Z5 [' L* d& t' M
even 15 minutes of direct skin contact with their male
. u. }* v- z$ lpartners.6 However, when a shirt covered the applica-& Y$ {* g" E  F$ H( A
tion site, this testosterone transfer was prevented.; c/ ^7 ^; K* \* @- H8 f; P
Our patient’s testosterone level was 60 ng/mL,
# y8 J! L3 n7 E! J- I/ H% Ewhich was clearly high. Some studies suggest that# x+ x8 _- C/ T9 U0 X1 p4 E; @6 C# @
dermal conversion of testosterone to dihydrotestos-  \& o9 H8 W: [- K
terone, which is a more potent metabolite, is more* h0 i% k! q: @
active in young children exposed to testosterone
( M6 V5 U8 b/ v% qexogenously7; however, we did not measure a dihy-/ v' J" _# {& Y; O, r
drotestosterone level in our patient. In addition to. K! |4 Y& `7 {8 j1 _
virilization, exposure to exogenous testosterone in
/ A2 U" M4 z! Z, b7 A5 v/ Tchildren results in an increase in growth velocity and6 I) L3 N, U1 \% @
advanced bone age, as seen in our patient.1 H/ ]3 c9 x7 Z# D: ]1 V) K3 V( C
The long-term effect of androgen exposure during
- Q" [: D6 H4 f9 ~" Z: C2 hearly childhood on pubertal development and final8 T; h' B* I. D' d) ^; T0 j% }
adult height are not fully known and always remain4 q& w5 C2 b2 e2 \- d$ T1 A
a concern. Children treated with short-term testos-7 N5 t) L% B& v3 }0 f1 H
terone injection or topical androgen may exhibit some
( A( `2 K! s. G( gacceleration of the skeletal maturation; however, after  [' X- t2 W( t
cessation of treatment, the rate of bone maturation
4 Y8 X- f. Y) [; N+ hdecelerates and gradually returns to normal.8,9) Y0 X# @: Y2 _* K7 S) F' K0 E3 w
There are conflicting reports and controversy& {! a/ l) ^' h2 v
over the effect of early androgen exposure on adult2 h3 e" ?) x  g, u: o, @
penile length.10,11 Some reports suggest subnormal& t% b3 b4 ^  R% h0 J
adult penile length, apparently because of downreg-2 w$ s7 |, B0 R
ulation of androgen receptor number.10,12 However,
! a% _) c( o0 |' a7 E! USutherland et al13 did not find a correlation between- s/ R# k9 p9 f% ~( b8 Y
childhood testosterone exposure and reduced adult4 S. L; N6 k4 q
penile length in clinical studies.+ w3 f6 v" L0 {4 P' `4 b; Y+ K
Nonetheless, we do not believe our patient is7 d/ G3 y8 e3 \& m) E
going to experience any of the untoward effects from8 Q! R2 B' C8 \
testosterone exposure as mentioned earlier because% ^9 T7 H' t" d) C5 i9 R, C# m
the exposure was not for a prolonged period of time.7 ^( O1 T) _- z( B/ p* H$ U- J
Although the bone age was advanced at the time of
, j; `. W& C  J/ t# C. c3 idiagnosis, the child had a normal growth velocity at
3 f& H2 e+ r% C. Z+ _% rthe follow-up visit. It is hoped that his final adult
; G) [! Y) t3 g$ ~% A/ Theight will not be affected.  x/ b0 u+ p2 J- i, s9 X2 `
Although rarely reported, the widespread avail-- W, o; V# _9 d  V$ Y
ability of androgen products in our society may# D7 j% R. B9 C  y: L; S
indeed cause more virilization in male or female5 c; K* {. E4 M8 p& I* g
children than one would realize. Exposure to andro-, p6 X5 G- E' _8 }  q% v
gen products must be considered and specific ques-
! Y/ \5 r* I; X; J, }tioning about the use of a testosterone product or7 b, H8 j8 \9 J5 e5 {  S9 Q/ r
gel should be asked of the family members during
# G- k" }0 W  D8 J: N4 Tthe evaluation of any children who present with vir-4 l# V) F8 H7 c  M1 O: M, X
ilization or peripheral precocious puberty. The diag-
; P0 t  o" ]( n, Y0 {1 Qnosis can be established by just a few tests and by
& N* J6 A6 E9 P) {appropriate history. The inability to obtain such a
. i& D* s4 G: l( K0 C1 ~history, or failure to ask the specific questions, may
4 e: }0 z/ Q+ K7 ~% J1 m3 aresult in extensive, unnecessary, and expensive4 w6 {3 {2 d# E; w
investigation. The primary care physician should be
$ L  i  W4 F% @, G+ Maware of this fact, because most of these children
; g* z2 @; o3 d# [: Rmay initially present in their practice. The Physicians’
' {, \: U& f  h* k3 Z* y# [2 qDesk Reference and package insert should also put a
) {8 S( g9 y% ~! {warning about the virilizing effect on a male or0 ]" J) l$ E: [
female child who might come in contact with some-
6 T' C" F6 Z% d( C( wone using any of these products./ Q( D, V9 ~  G  x4 d7 A
References1 w* I! t: F7 F9 @$ f6 B, }4 Y. G
1. Styne DM. The testes: disorder of sexual differentiation; s' Q9 M9 S9 ~
and puberty in the male. In: Sperling MA, ed. Pediatric; y0 T6 z1 d/ G* q, d: F
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;+ O3 v! t/ L1 f1 [
2002: 565-628.
# |  V8 m$ Q  l2 {, m- R1 b; h2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 u1 }- P8 [, ^7 z
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
2 o. u" R+ H3 u. S# P; kBoy Induced by Indirect Topical
( ?% m5 e# S( \7 k" c" S5 @Exposure to Testosterone
" L& v/ M1 b) I' o& e' P, jSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! }7 Z3 x' j1 X! F7 ^% T' _
and Kenneth R. Rettig, MD1
$ D3 {9 L( C# u  g# M8 q6 aClinical Pediatrics
7 ?0 J& T* w6 }1 D$ VVolume 46 Number 6. w! N' [/ b/ U/ q% ^. Y
July 2007 540-543
4 Y/ }+ \! t& N© 2007 Sage Publications4 i. Z6 ~. Q& \& O$ u1 y3 G
10.1177/0009922806296651% H5 y$ J5 p: s+ e
http://clp.sagepub.com
& u+ E' w% T4 u% Qhosted at3 w$ T3 y- F; v5 d4 u( A
http://online.sagepub.com- S. g1 c# Q2 E( }
Precocious puberty in boys, central or peripheral,
- s7 t1 B, R9 i9 H! iis a significant concern for physicians. Central
% Z% G7 B. e% g1 I! V; L0 Lprecocious puberty (CPP), which is mediated
( G6 s# C2 M. athrough the hypothalamic pituitary gonadal axis, has
0 |- {/ b' U' D+ D9 M# b$ P1 da higher incidence of organic central nervous system
- i7 {) u- ~: n* V7 Ulesions in boys.1,2 Virilization in boys, as manifested
9 q( ~% }" s! B" p( C$ D* _1 Uby enlargement of the penis, development of pubic
3 u8 t* q/ b  Ohair, and facial acne without enlargement of testi-: h  T) C6 T( z7 W& P/ \
cles, suggests peripheral or pseudopuberty.1-3 We1 }2 _" w" @) R9 g$ G
report a 16-month-old boy who presented with the
8 U3 V' H6 o  [, n7 \! cenlargement of the phallus and pubic hair develop-1 t1 A0 D7 [3 r7 _) M
ment without testicular enlargement, which was due% m- F7 ]2 j# \/ q. |; Z* u& T  ^3 Y- o
to the unintentional exposure to androgen gel used by2 K/ C+ ^+ k1 U$ y$ \
the father. The family initially concealed this infor-# V% \- r2 P1 r& o) S) W
mation, resulting in an extensive work-up for this
1 L. ^9 O+ ^8 M8 r/ H0 achild. Given the widespread and easy availability of, j/ _1 t, y7 e  X. ^
testosterone gel and cream, we believe this is proba-
$ |# n! O0 R  J( f4 C+ U! x8 Kbly more common than the rare case report in the
6 t9 m  Q/ B, k6 C, K; J9 T. Cliterature.4& a7 j4 w% p+ @; T, b
Patient Report
& o9 o( g' L% s3 d4 Z. qA 16-month-old white child was referred to the& ^1 O4 N" f) k5 V- G$ ?) A2 B3 @
endocrine clinic by his pediatrician with the concern; O: X# F+ V/ r& P1 m+ Z! R* Q4 Q
of early sexual development. His mother noticed
1 k# z5 _1 q' j$ N  D9 Clight colored pubic hair development when he was, @5 y& ]) V" [# X! k, ~2 M' b
From the 1Division of Pediatric Endocrinology, 2University of$ e6 ~7 F# w& Z' O8 M  I1 i
South Alabama Medical Center, Mobile, Alabama.6 x2 _9 u0 b/ u1 y3 v: @
Address correspondence to: Samar K. Bhowmick, MD, FACE,  T! n- E' `9 d
Professor of Pediatrics, University of South Alabama, College of, d: r5 U/ I, C8 z# Z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
0 E6 P1 g' y8 C1 I& _2 Le-mail: [email protected].
: P- M: J( [4 K* b+ b: f3 T( v; }about 6 to 7 months old, which progressively became
+ q2 I. [5 A3 |0 ]9 Odarker. She was also concerned about the enlarge-: R1 p+ m' \" K: D( @
ment of his penis and frequent erections. The child
: q3 M7 H1 R" X+ {6 w+ W+ s1 S; O1 cwas the product of a full-term normal delivery, with
  _: M9 l9 r. p8 o$ m0 x9 sa birth weight of 7 lb 14 oz, and birth length of
' A2 s1 X% \; v4 T20 inches. He was breast-fed throughout the first year" I* T$ [" X- b! H  v2 T
of life and was still receiving breast milk along with
( y) X1 R4 B# l1 ]: h8 Fsolid food. He had no hospitalizations or surgery,
7 Y* z: q# }3 I3 |- I9 w* B; Nand his psychosocial and psychomotor development
4 [) z: ~( h+ P( s& {% E# O* Iwas age appropriate.2 i. _: `- h) M$ C
The family history was remarkable for the father,7 G  r0 K( E' r  j1 Z! v
who was diagnosed with hypothyroidism at age 16," S3 e( S; ]  f
which was treated with thyroxine. The father’s/ I5 K/ ]8 C$ X! ~. [
height was 6 feet, and he went through a somewhat
9 h2 X* c) Q! ]& aearly puberty and had stopped growing by age 14.
5 p9 \+ S. `" f! U3 GThe father denied taking any other medication. The
% A1 f5 z0 p( c# C2 c- r% ^child’s mother was in good health. Her menarche/ \* X6 o; W7 ]. U
was at 11 years of age, and her height was at 5 feet3 Y( b0 @; ]3 U2 [5 |
5 inches. There was no other family history of pre-
  m0 R' z( l* ]7 j/ P/ ucocious sexual development in the first-degree rela-# e! g2 {% C! ?' l+ L* x
tives. There were no siblings.' Z5 D1 N% N2 v# q
Physical Examination0 T! k; s9 [0 m) W9 l3 G
The physical examination revealed a very active,% j3 T0 q$ |* d) Z& }+ X! c$ H
playful, and healthy boy. The vital signs documented) H+ O8 t( P4 s1 g
a blood pressure of 85/50 mm Hg, his length was
7 S/ _; |4 W* l* v90 cm (>97th percentile), and his weight was 14.4 kg
: V: j; Q) v5 `% |, [  K8 k3 p(also >97th percentile). The observed yearly growth
, t) s1 z( a) e; B7 @velocity was 30 cm (12 inches). The examination of, ]: x3 v' n* K) c1 r
the neck revealed no thyroid enlargement.+ e. g. Z6 P1 ?6 z3 r$ a7 L' }
The genitourinary examination was remarkable for8 G3 Z7 w+ S/ ^; j7 [: B
enlargement of the penis, with a stretched length of" R7 y% `# t* m9 h( D: ^
8 cm and a width of 2 cm. The glans penis was very well
7 L# W7 W7 H4 _$ s: z' ldeveloped. The pubic hair was Tanner II, mostly around
8 B" Q2 W4 o, k* H8 @540. K$ Q) {5 r3 F, m9 s# W* o! m
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, Z; Z0 P4 N4 o9 }* M, C
the base of the phallus and was dark and curled. The
" N/ n% d! P$ k+ ~7 u5 u$ ]testicular volume was prepubertal at 2 mL each.) l" K4 g- y% V0 J6 W2 F
The skin was moist and smooth and somewhat
; m6 D: e: y# z  o# I; J9 ioily. No axillary hair was noted. There were no5 y: u5 u1 _3 Q' R1 }
abnormal skin pigmentations or café-au-lait spots.7 C! ~9 y2 k5 A, g
Neurologic evaluation showed deep tendon reflex 2+$ T; a+ Q+ v! q* R( Q- `7 K  d, ~, F
bilateral and symmetrical. There was no suggestion( M9 o7 @4 N  m* e& S
of papilledema.6 n2 f1 y1 p5 G8 L1 f
Laboratory Evaluation& n0 u# s: r1 ~# W
The bone age was consistent with 28 months by, w2 f: w/ `) l1 M, ~( M
using the standard of Greulich and Pyle at a chrono-
, d$ \$ ]5 n8 L6 r7 p! ?! ?logic age of 16 months (advanced).5 Chromosomal6 H; X' L6 `, t' @7 O) X0 D
karyotype was 46XY. The thyroid function test3 J5 _' |; S* P; G& {
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
) a; a4 W/ c. b0 [5 slating hormone level was 1.3 µIU/mL (both normal).. A% M3 n$ p5 e, p& w
The concentrations of serum electrolytes, blood1 {" ~* B$ @& Z7 L$ M
urea nitrogen, creatinine, and calcium all were$ f) d; P. l& `) M1 }' H) s7 _
within normal range for his age. The concentration/ Q4 a% M, v4 i9 T3 z; E& E
of serum 17-hydroxyprogesterone was 16 ng/dL
" I7 Q- i  p6 B(normal, 3 to 90 ng/dL), androstenedione was 20; G& C+ M. I' h5 z( E8 {8 ]0 i
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. k. n4 H7 a2 ^0 B7 L% Qterone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 \6 ^+ Y, O. T  n# l) ?6 u& adesoxycorticosterone was 4.3 ng/dL (normal, 7 to' [/ u" V- q! V. G8 v
49ng/dL), 11-desoxycortisol (specific compound S)
; ?2 d5 r5 f. p6 u; P, Z# Jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! F7 r5 [$ R% A) `; ~- b
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total( o: {+ F1 P, t+ R
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  R, {4 q% G3 I1 i  Y2 Pand β-human chorionic gonadotropin was less than  W' G; S, Q- ~* M  e$ N
5 mIU/mL (normal <5 mIU/mL). Serum follicular7 J0 G$ Z# w9 e) h1 s0 O
stimulating hormone and leuteinizing hormone
, Q0 r7 E0 N% J7 k$ ^( X$ vconcentrations were less than 0.05 mIU/mL
$ K* K. O- i8 V+ k: V$ Q$ L% T(prepubertal).& ?/ U; `4 D9 v2 W* V/ x! e
The parents were notified about the laboratory1 c5 v+ o; @5 l. {3 N
results and were informed that all of the tests were
, f' R, V- ?3 w0 i  Fnormal except the testosterone level was high. The
: B0 L5 O; [7 N3 j' Ofollow-up visit was arranged within a few weeks to4 y% r  I" N4 ]9 s: Z$ Z5 I
obtain testicular and abdominal sonograms; how-
) a8 U7 [8 M( m/ E, Kever, the family did not return for 4 months.
3 S, _% k, ]$ V1 O) sPhysical examination at this time revealed that the
" S/ N& `9 ?. p, G+ [' u6 H5 F% dchild had grown 2.5 cm in 4 months and had gained& ?0 _: f; S5 V- x5 [8 E- G
2 kg of weight. Physical examination remained/ r. H' o6 |/ j1 g
unchanged. Surprisingly, the pubic hair almost com-2 D6 j( v' F; C% A1 A2 `
pletely disappeared except for a few vellous hairs at
/ G- _& B2 ]4 T7 I& ~the base of the phallus. Testicular volume was still 2
- A/ z& }; L$ K2 VmL, and the size of the penis remained unchanged.
& O, i% \* }2 s  AThe mother also said that the boy was no longer hav-
1 @/ {- }$ y) ?9 `& M; Iing frequent erections.
8 z! d+ j$ y9 q! ~2 i0 \Both parents were again questioned about use of
) P9 w2 l: S5 Y# K" Sany ointment/creams that they may have applied to4 K  W& N% S( U0 n( ]
the child’s skin. This time the father admitted the
3 r8 Y! X% \# `3 u" k3 u  M6 a0 l0 gTopical Testosterone Exposure / Bhowmick et al 541
- U0 o, G! I5 w7 z! Huse of testosterone gel twice daily that he was apply-
5 }5 d% n' F; Z) U4 jing over his own shoulders, chest, and back area for( ^% s9 e$ n; Q4 X
a year. The father also revealed he was embarrassed
) a- j9 P7 [( I4 ^/ E5 P$ ?( k5 }to disclose that he was using a testosterone gel pre-' u) y. f& x. P2 H# ~
scribed by his family physician for decreased libido; Z8 t& H9 h4 c* Y! ^0 h
secondary to depression.9 V0 g: j. q2 F& C1 I3 S4 m
The child slept in the same bed with parents.
0 o# w* Q+ l! s; m5 e  P  CThe father would hug the baby and hold him on his
; B+ p5 w& a) wchest for a considerable period of time, causing sig-
* C1 s" ~5 q1 s# N* D! n  @nificant bare skin contact between baby and father.' E9 V9 f- a  z, F4 [  d. }
The father also admitted that after the phone call,- n4 b; G. h! L- m: S- s! V8 \
when he learned the testosterone level in the baby
6 v( [2 O" n* n4 D! ?/ Xwas high, he then read the product information
* ^# P) c+ }  Y1 dpacket and concluded that it was most likely the rea-
1 M9 t/ `& k5 l) X. }; q7 nson for the child’s virilization. At that time, they, k' s- w- ~# I( x) j5 ^# B
decided to put the baby in a separate bed, and the3 W3 c8 W2 r2 x% P' \
father was not hugging him with bare skin and had& Y, J( ?% L3 }2 M2 U
been using protective clothing. A repeat testosterone, T4 S# S' J, b7 @0 s
test was ordered, but the family did not go to the
* y0 P: b0 L0 z# F( m0 I: Xlaboratory to obtain the test.. ~: Z2 `; x  \
Discussion7 g! U, S2 V( V) \8 {; U
Precocious puberty in boys is defined as secondary
: f% T) q+ U, L- {/ J9 M7 msexual development before 9 years of age.1,4
0 ]! n9 u: S# w5 J% Q+ u: j' \Precocious puberty is termed as central (true) when6 [* H% q8 `+ e1 x3 E8 H1 e8 \7 X% n  v
it is caused by the premature activation of hypo-
$ J" a6 M9 E; o  x) k1 L+ T8 F3 Sthalamic pituitary gonadal axis. CPP is more com-
8 K1 G  ?3 o% w1 T+ Rmon in girls than in boys.1,3 Most boys with CPP: A* x! F4 W0 N
may have a central nervous system lesion that is' m/ b  _+ c$ c* c* M# q
responsible for the early activation of the hypothal-
* f) ^, I4 T1 d1 N. Tamic pituitary gonadal axis.1-3 Thus, greater empha-% Y* G# G) f0 V6 q: a6 |9 x
sis has been given to neuroradiologic imaging in
! d$ |+ F! E+ `& q7 R0 V% Dboys with precocious puberty. In addition to viril-( x, c5 t5 U- j8 M# W* e" U
ization, the clinical hallmark of CPP is the symmet-
( q- U" k4 |9 q$ d; R  l: mrical testicular growth secondary to stimulation by
9 H; e! Q% W' ]& r9 k+ Zgonadotropins.1,3
/ M. I: ?3 c" H# XGonadotropin-independent peripheral preco-" o) I3 H. `  d4 n; R
cious puberty in boys also results from inappropriate; ^: G% u1 t/ ?- M$ ^
androgenic stimulation from either endogenous or) b, g6 x3 ], J. i
exogenous sources, nonpituitary gonadotropin stim-
0 i" ~: f8 @* |9 y- |- b/ O' X$ fulation, and rare activating mutations.3 Virilizing
( u4 P; S4 a9 K8 G1 o2 J2 wcongenital adrenal hyperplasia producing excessive
  y0 C9 C4 t( s+ X' `adrenal androgens is a common cause of precocious
, R& Q7 g" s! j8 p- j: xpuberty in boys.3,4
& ^& A. U) l8 _The most common form of congenital adrenal' v$ P) t5 ~# N' a4 e! @( [# l
hyperplasia is the 21-hydroxylase enzyme deficiency.3 z5 @2 M! d2 e# [, w
The 11-β hydroxylase deficiency may also result in6 `9 x  J6 }( r0 i! K
excessive adrenal androgen production, and rarely,3 H; T3 ?+ {  b' b
an adrenal tumor may also cause adrenal androgen
3 e7 k" B% ^( D6 Aexcess.1,3
! Q7 D3 u' W; h9 [/ Kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& _, c, p3 p1 C9 Y542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& Q  s, w% @4 k4 R5 ?3 uA unique entity of male-limited gonadotropin-) @. L8 p8 o$ M  |) L' Z
independent precocious puberty, which is also known
# l* J( h. T; M7 Zas testotoxicosis, may cause precocious puberty at a
% F. s5 C, W8 Z/ v" E9 a! x1 Q$ o  s0 [very young age. The physical findings in these boys
3 \. H& {7 @9 k/ R6 _& u- mwith this disorder are full pubertal development,0 b8 f; j; W9 E1 M2 I
including bilateral testicular growth, similar to boys
1 N$ u1 J- f% N* h% ~, ]# bwith CPP. The gonadotropin levels in this disorder
) D. |! `6 k' fare suppressed to prepubertal levels and do not show; W3 e; g  j" e: I* g. O
pubertal response of gonadotropin after gonadotropin-9 ?+ v. h- u  O+ k6 S3 @
releasing hormone stimulation. This is a sex-linked! ^3 C4 J3 ^- h5 E5 _( a: l
autosomal dominant disorder that affects only3 C' V( C8 Q, f6 I- V" P! B7 Y
males; therefore, other male members of the family
6 ?; h& g6 H: J( T' ^may have similar precocious puberty.3) d6 Q3 F6 s+ J2 d: R2 y
In our patient, physical examination was incon-
* {, d* D2 |6 h5 ^/ b+ Ksistent with true precocious puberty since his testi-
" u! A2 d" {/ Y8 `1 F; n6 ^cles were prepubertal in size. However, testotoxicosis
& U2 C0 g+ `: K4 R7 m6 [7 bwas in the differential diagnosis because his father8 G5 l% J# s# I: [* d2 ?
started puberty somewhat early, and occasionally,# X3 e8 R! A. i0 i. F& x4 `8 N
testicular enlargement is not that evident in the
+ J% f' F' J1 {4 m+ [- rbeginning of this process.1 In the absence of a neg-  v) ]# H9 s8 n$ Y
ative initial history of androgen exposure, our
8 t9 L, V0 z! cbiggest concern was virilizing adrenal hyperplasia,
7 G5 {" ], f  P2 [3 Ieither 21-hydroxylase deficiency or 11-β hydroxylase
/ {9 B- w7 c* j; r+ edeficiency. Those diagnoses were excluded by find-
- W/ r* s  m+ d0 ]$ g: d, v  v1 Y7 l' Ging the normal level of adrenal steroids., \; B+ ?; _! W4 h( m4 F' w, L; W
The diagnosis of exogenous androgens was strongly' G! b( _0 F3 [. G; {; w* R
suspected in a follow-up visit after 4 months because; [" e2 Y& P5 }9 l& \$ T
the physical examination revealed the complete disap-* j( K7 [0 r  J; {
pearance of pubic hair, normal growth velocity, and8 O. q% K7 m1 \
decreased erections. The father admitted using a testos-8 @' o4 L# d- K# D
terone gel, which he concealed at first visit. He was' P  b% f3 x1 Q* r) f
using it rather frequently, twice a day. The Physicians’
6 T7 T; J, j! E5 [" i: o0 FDesk Reference, or package insert of this product, gel or- r. s: `2 o3 |' f
cream, cautions about dermal testosterone transfer to4 s* ^8 [7 a! \, }3 m
unprotected females through direct skin exposure.- n( I+ L9 z. \: z
Serum testosterone level was found to be 2 times the% W8 m1 I/ E* s6 R" b6 t
baseline value in those females who were exposed to) M  l0 Z' F) m, X& @
even 15 minutes of direct skin contact with their male3 i. F* f% `3 K
partners.6 However, when a shirt covered the applica-# w; \/ J" N/ o' M" Y+ Z
tion site, this testosterone transfer was prevented.5 |3 n/ x4 u& D+ a8 N6 y/ u6 h+ U
Our patient’s testosterone level was 60 ng/mL,
2 M0 a! L* ?5 m) l( \# @which was clearly high. Some studies suggest that" z6 q* ]9 J# s) Y8 q0 U
dermal conversion of testosterone to dihydrotestos-1 Z+ J, L: R) \
terone, which is a more potent metabolite, is more# |$ D5 b) H( p/ V$ U  S0 V
active in young children exposed to testosterone0 A& `3 s+ n; o. Y  C+ b* g
exogenously7; however, we did not measure a dihy-/ K) `1 n2 ]8 q) y% X8 b
drotestosterone level in our patient. In addition to7 `4 B2 T  ~5 N. |) c. L5 f0 e) A
virilization, exposure to exogenous testosterone in
1 ]- ~( C4 v8 s! n0 v: xchildren results in an increase in growth velocity and' _* T* g3 K7 Z( u, N
advanced bone age, as seen in our patient.
! ?& v" q' B4 `! Q' o! I. vThe long-term effect of androgen exposure during
0 Y6 U3 O: E* r+ |& I5 u0 t. Searly childhood on pubertal development and final1 h$ y# i" `; ?  N/ n
adult height are not fully known and always remain2 m% p; `6 N: H& [! [4 y: t5 ?
a concern. Children treated with short-term testos-2 k4 _& W' E2 y6 f" Q
terone injection or topical androgen may exhibit some
4 g- H0 t3 ]& d) H3 s4 J0 Cacceleration of the skeletal maturation; however, after
# k1 k: }9 e  o- l: xcessation of treatment, the rate of bone maturation% x- B! J% r! c$ @7 e) j# r5 Z
decelerates and gradually returns to normal.8,9
9 H7 G$ B5 D4 H% T5 tThere are conflicting reports and controversy
' m8 Q" @3 x  c' S  B" m) Cover the effect of early androgen exposure on adult7 b: e! ^+ \' D9 b  t9 \3 j' h
penile length.10,11 Some reports suggest subnormal9 z: c. [4 J& m8 t
adult penile length, apparently because of downreg-( c' I6 d& \: y. \
ulation of androgen receptor number.10,12 However,6 W5 d+ V9 k, B$ b
Sutherland et al13 did not find a correlation between
  M8 J% a6 \& v4 S8 Vchildhood testosterone exposure and reduced adult
, i2 H' G- `: n7 zpenile length in clinical studies.5 p5 f. Q' U2 J
Nonetheless, we do not believe our patient is
- H+ ?' O) `* Kgoing to experience any of the untoward effects from
7 v! ~1 O8 A  l8 T& `# Ntestosterone exposure as mentioned earlier because9 [- l8 S9 b: T! I3 f
the exposure was not for a prolonged period of time.% d+ ?2 v+ K9 G4 y( t4 V7 ]
Although the bone age was advanced at the time of
1 t( O3 ~: ]( e9 R3 i. Pdiagnosis, the child had a normal growth velocity at/ r+ M$ D9 o# l0 f
the follow-up visit. It is hoped that his final adult
' F0 a/ j& u/ B0 A: j, p" yheight will not be affected.2 y' g0 H/ E7 j9 ?2 z
Although rarely reported, the widespread avail-. m6 `; y: W7 k: R
ability of androgen products in our society may
) k+ b; w2 H# o8 _2 x3 Windeed cause more virilization in male or female
+ ]7 w& b/ g9 k8 d! @children than one would realize. Exposure to andro-
8 G8 ~9 L/ X, \  @% _! xgen products must be considered and specific ques-
* M4 G+ |$ o2 i' J( Rtioning about the use of a testosterone product or8 o* O+ [) N/ S8 @6 v1 t
gel should be asked of the family members during* Y* @6 v: m3 S( y1 _3 s9 ]9 x
the evaluation of any children who present with vir-
( A( [8 G% t9 _. M! ^& E- Rilization or peripheral precocious puberty. The diag-0 j" `- Q3 q8 J1 ]
nosis can be established by just a few tests and by' @0 @" Q/ T, P( g, ?4 M
appropriate history. The inability to obtain such a
$ {9 ~  b% X3 }' dhistory, or failure to ask the specific questions, may# p+ X+ l! P  D+ f
result in extensive, unnecessary, and expensive* A# e9 }6 c% ?# F( Z
investigation. The primary care physician should be
) r5 y& R! S8 f& r0 A8 ~, K: jaware of this fact, because most of these children
8 C' C! l4 `  b# M' vmay initially present in their practice. The Physicians’3 e. K, a9 U/ P4 f
Desk Reference and package insert should also put a
. S- {3 d  @" R# A- n4 y2 i3 Swarning about the virilizing effect on a male or9 W! D  e+ k% y. o4 M9 [$ ?8 I2 ~% h
female child who might come in contact with some-: o" q$ g- E- s  J
one using any of these products.
8 v6 t" X3 l/ Y7 r) x% m: f) E$ R3 vReferences
+ j8 _& b- G# Z1. Styne DM. The testes: disorder of sexual differentiation
( _2 d7 L! a, `$ k! xand puberty in the male. In: Sperling MA, ed. Pediatric
2 h0 @  |* n, O' q& _0 i7 L- i  K; KEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 A- D$ t' z' X3 \
2002: 565-628.
/ C( q4 l6 f% J6 K4 Z2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ O0 O( G: o, e( e/ X( J4 Lpuberty in children with tumours of the suprasellar pineal
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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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
) {0 x2 _& r) D) s8 F. D
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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