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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& U0 G$ z) h" `' H) P% k
Boy Induced by Indirect Topical4 p" h7 h+ I. ~8 i
Exposure to Testosterone
7 H3 j+ ~: M9 DSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 I7 T& r+ m: ]and Kenneth R. Rettig, MD1
: X0 u$ X: u5 D: E# C* @Clinical Pediatrics
  d1 C! y9 J, z9 b9 u2 t) IVolume 46 Number 6
3 G' ~4 ?) }( D9 x$ \* t, H2 jJuly 2007 540-543- Q+ S+ U9 v, W; r2 L/ f
© 2007 Sage Publications
3 H2 E4 k. t8 J# I5 s. F+ w10.1177/0009922806296651
, H" `: y. @: [9 D1 Yhttp://clp.sagepub.com
5 n7 z$ F9 W3 Ihosted at
8 M. A4 L9 _, P& C% g$ g1 Ghttp://online.sagepub.com
0 W4 }, b: ~( ?4 ]2 FPrecocious puberty in boys, central or peripheral,# B, L( \" t6 k8 P1 ]8 u# v1 i
is a significant concern for physicians. Central
1 ]  c; s! F! G$ m4 H& E6 E. g% V' ?precocious puberty (CPP), which is mediated0 B) D9 A# }' Z7 v
through the hypothalamic pituitary gonadal axis, has1 m3 L3 c( f! d* @6 a" L
a higher incidence of organic central nervous system
9 _. W1 B, Q# c- nlesions in boys.1,2 Virilization in boys, as manifested
2 W2 l/ U; V  S3 eby enlargement of the penis, development of pubic
. Y! v3 B$ i, a/ V: _8 x- I4 Whair, and facial acne without enlargement of testi-6 u. W- w0 o' G% Z
cles, suggests peripheral or pseudopuberty.1-3 We
( M6 Q6 z" O. z  \# hreport a 16-month-old boy who presented with the
2 W. i) S+ a# \' B) |enlargement of the phallus and pubic hair develop-
' \1 S$ r8 w/ m# L  z: Fment without testicular enlargement, which was due
' ?2 W4 h: Z0 q6 ?# ^% G6 oto the unintentional exposure to androgen gel used by( J, L7 D2 b) [( R2 F* ^. _( P1 v
the father. The family initially concealed this infor-
2 I* r/ k; M  p' V( I& {mation, resulting in an extensive work-up for this
& ?6 P5 ?2 H9 hchild. Given the widespread and easy availability of
1 u/ ^* H+ R+ Y* U- w, Wtestosterone gel and cream, we believe this is proba-! ~% s! H9 x& L$ T
bly more common than the rare case report in the7 [* i# W4 O& z2 W% F
literature.4, `& K8 }! I! K
Patient Report
$ u/ I) A3 X7 ^" a! jA 16-month-old white child was referred to the
* W" [  W9 e! V: T: k5 W5 Uendocrine clinic by his pediatrician with the concern
  J7 J2 P3 D" R: |- \; F1 Zof early sexual development. His mother noticed
( @" M! O2 U  Z, z0 h* z; {light colored pubic hair development when he was
# X6 Z$ v6 F. OFrom the 1Division of Pediatric Endocrinology, 2University of$ N' v8 ]9 ~7 [- s/ e, t- O
South Alabama Medical Center, Mobile, Alabama.0 h2 d; @3 R6 i. z  `4 |
Address correspondence to: Samar K. Bhowmick, MD, FACE,7 y2 k1 i  J2 S( R4 O$ \3 \0 y9 P6 i
Professor of Pediatrics, University of South Alabama, College of
* L! B# E  w6 X+ b  FMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;' w) U! ]  D8 O0 p7 U, P" ~; D
e-mail: [email protected].9 A- \( r. ~7 h
about 6 to 7 months old, which progressively became/ S# o/ `& L, D8 K& J+ f
darker. She was also concerned about the enlarge-' a/ G- H6 D' e
ment of his penis and frequent erections. The child
% g' F8 L2 w' P- g( ^3 qwas the product of a full-term normal delivery, with
, |, J) O1 J; N; b8 }a birth weight of 7 lb 14 oz, and birth length of
; }( b# [; v% ]9 v! k20 inches. He was breast-fed throughout the first year
% t" r: e7 d1 ]/ ?+ Aof life and was still receiving breast milk along with- P$ D1 Y2 U# \5 N" s3 J
solid food. He had no hospitalizations or surgery,0 _8 n9 _4 b/ @7 F
and his psychosocial and psychomotor development- `0 \7 [; s/ `' E' R- J
was age appropriate.# d& }7 H. |, U% @+ I. K
The family history was remarkable for the father,+ t8 c9 v0 h+ r7 ?  x
who was diagnosed with hypothyroidism at age 16,
: w1 [! f4 t# \) }1 ~+ pwhich was treated with thyroxine. The father’s( m$ ^3 y7 e5 h. M2 U* `; T
height was 6 feet, and he went through a somewhat" Y1 a2 i# q/ l: W- {
early puberty and had stopped growing by age 14.* R! N6 t, `0 o) J+ u
The father denied taking any other medication. The. s5 i2 z- L' _8 k! r- X8 d
child’s mother was in good health. Her menarche
% }, V6 l- {  v) Ewas at 11 years of age, and her height was at 5 feet
  J% f2 o6 y+ i9 \5 inches. There was no other family history of pre-
* t2 n) V/ H6 ccocious sexual development in the first-degree rela-* A( J% z+ u) L( y9 {' c9 n; ?3 L
tives. There were no siblings.
, f$ I1 b' a  |- v4 Q5 [7 [6 J/ uPhysical Examination
9 {! N( v2 Q7 r2 yThe physical examination revealed a very active,
4 H2 {" k. m0 eplayful, and healthy boy. The vital signs documented. m5 p6 W5 H8 P5 A6 g% [/ X
a blood pressure of 85/50 mm Hg, his length was
) B6 q0 e: f/ @4 D" ^90 cm (>97th percentile), and his weight was 14.4 kg+ {- J7 c, k- t* Y2 S; J7 _) |' {9 [6 y
(also >97th percentile). The observed yearly growth& u. h, X5 t4 a5 }7 V& ]
velocity was 30 cm (12 inches). The examination of
* R4 {; [# o2 N  Athe neck revealed no thyroid enlargement.9 q2 `" r* a1 W
The genitourinary examination was remarkable for& J9 T' k5 f5 T4 _
enlargement of the penis, with a stretched length of* T1 ?1 @1 A3 d
8 cm and a width of 2 cm. The glans penis was very well7 Q/ [/ M' q; a* t$ n8 F; `; K" @
developed. The pubic hair was Tanner II, mostly around
) m  K# [5 n8 b540
9 S1 M& P) {' ]0 z/ g& Z" e9 Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; `' B% f  y3 c6 athe base of the phallus and was dark and curled. The& L* }" g# K2 Z& A! b
testicular volume was prepubertal at 2 mL each., ?2 f) e$ v! A4 C
The skin was moist and smooth and somewhat
2 O% v! K% h# O4 v8 o' U3 goily. No axillary hair was noted. There were no- e- J4 r5 K  G1 e
abnormal skin pigmentations or café-au-lait spots.+ {1 Y5 F+ H5 B7 ~
Neurologic evaluation showed deep tendon reflex 2+( A" `7 I8 i2 H
bilateral and symmetrical. There was no suggestion
1 k! b4 [) H8 _% q# T) v0 Wof papilledema.
/ c" V$ I0 G( i- d& l0 X2 e) i( ULaboratory Evaluation
+ p' U  L; G- Y3 j$ lThe bone age was consistent with 28 months by# `* f2 u6 O& h4 K# V
using the standard of Greulich and Pyle at a chrono-
$ Z7 ?0 |: ^; m) O( U) N' s* G' I6 Jlogic age of 16 months (advanced).5 Chromosomal( Z5 n4 @. H- q+ Q2 W; t; _! \- Y
karyotype was 46XY. The thyroid function test
+ G1 h& G$ T( g4 Dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-* T& c2 t) [3 V5 x) P5 v
lating hormone level was 1.3 µIU/mL (both normal).
5 k; Y3 h5 v* ^, D2 f: v4 @The concentrations of serum electrolytes, blood
6 }- ]0 x" `* n) g1 Y% |urea nitrogen, creatinine, and calcium all were! [9 g& @" C6 k& Q% [( X
within normal range for his age. The concentration/ F  ~0 t1 p1 m3 J$ m9 M, u5 f
of serum 17-hydroxyprogesterone was 16 ng/dL$ f6 U. N' W% }
(normal, 3 to 90 ng/dL), androstenedione was 20# F7 r/ A4 s, ~9 S$ r
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 v1 y. C, s& g. a" fterone was 38 ng/dL (normal, 50 to 760 ng/dL),7 M$ N& A. P! g& L7 t4 m
desoxycorticosterone was 4.3 ng/dL (normal, 7 to' o, E2 r8 b' S; l2 C) L1 l
49ng/dL), 11-desoxycortisol (specific compound S)
1 G) A* @% L# W( @was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. C, H' G1 Y" {! D, Dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" V) k$ T. |8 E7 G) {# Mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),, z+ P- f# ]5 h! ?, L8 f4 U& V
and β-human chorionic gonadotropin was less than
9 z8 a/ {" n) j7 x/ ^4 {& i5 mIU/mL (normal <5 mIU/mL). Serum follicular8 B1 t% E8 |8 I8 v3 }
stimulating hormone and leuteinizing hormone
* ?& }- v5 V% T) ~7 o2 Vconcentrations were less than 0.05 mIU/mL8 W' D* T3 k& K9 i0 C% M
(prepubertal)." \) x3 u9 Q: e/ G  A4 n. s# J$ X
The parents were notified about the laboratory
: R  [* {! ]/ D6 t1 u2 J0 Hresults and were informed that all of the tests were% J1 n- g0 h  }3 L. K1 J# L; y
normal except the testosterone level was high. The
) Y# v0 }, R7 \$ O! X( cfollow-up visit was arranged within a few weeks to+ @% W+ u+ a7 [, \2 n% y
obtain testicular and abdominal sonograms; how-( R& \3 T2 C) I8 ^  [6 C9 U# p
ever, the family did not return for 4 months.% m8 f0 P4 H, ]3 Z+ x
Physical examination at this time revealed that the
5 o+ {! z( z' g- ]0 h+ \6 ochild had grown 2.5 cm in 4 months and had gained$ \/ \9 @6 B7 U4 Y6 @
2 kg of weight. Physical examination remained
4 L" ?# m. v+ a, b% q; Runchanged. Surprisingly, the pubic hair almost com-& c6 x  S3 R' z. [9 z: c: r
pletely disappeared except for a few vellous hairs at- c, }( G$ }+ I# F) n
the base of the phallus. Testicular volume was still 25 e! f3 {2 a- S; h4 i
mL, and the size of the penis remained unchanged.
& K2 c, Y& Q% k8 CThe mother also said that the boy was no longer hav-& R% \& l5 X5 T7 D2 E- E4 @* K
ing frequent erections.
  ~$ N( h0 x1 G7 B! G8 xBoth parents were again questioned about use of
, f7 [1 `, @$ b* m! yany ointment/creams that they may have applied to
* a  n5 I! e' P- A$ Q# C+ x+ Bthe child’s skin. This time the father admitted the. I3 L; b# u9 Y/ \# r
Topical Testosterone Exposure / Bhowmick et al 541
+ ~" m/ Y: {# |/ U# N% ^& m9 {8 fuse of testosterone gel twice daily that he was apply-# C4 Y5 `- T7 n
ing over his own shoulders, chest, and back area for' ^1 O; K6 C7 C- z# }
a year. The father also revealed he was embarrassed* @; C. L$ z& J  \1 N
to disclose that he was using a testosterone gel pre-
5 E( O1 l. m/ i$ cscribed by his family physician for decreased libido% G/ B3 w2 q- M$ v' E
secondary to depression.
9 t& m6 U. {: @9 H4 Y" lThe child slept in the same bed with parents.
; r3 o9 w! D4 q  m5 uThe father would hug the baby and hold him on his. f2 d2 o5 B$ Z$ j
chest for a considerable period of time, causing sig-
0 ?6 l1 n' H& o* ~$ h7 X5 F% ~" Tnificant bare skin contact between baby and father.. C/ Q' h. r  l5 X6 o
The father also admitted that after the phone call,
1 L  o4 H! Y! m8 J6 k9 H' Hwhen he learned the testosterone level in the baby! F8 a! l- [* e* L3 K) b
was high, he then read the product information
( d9 ^6 ?) S8 Cpacket and concluded that it was most likely the rea-7 L! @( g: n) ?, T  }
son for the child’s virilization. At that time, they* m* [. e; m9 Z9 W( `) j
decided to put the baby in a separate bed, and the
0 @1 E) M. `2 p2 c4 nfather was not hugging him with bare skin and had1 c4 x7 ^3 P5 E, J7 J/ Q# C* g
been using protective clothing. A repeat testosterone
( Q& J% x9 s! s* ^1 V8 y. Jtest was ordered, but the family did not go to the
( Z3 |' I7 U4 d4 \laboratory to obtain the test.
8 d/ Q" U9 u6 R, E+ k3 M1 bDiscussion, @  U6 I, g; S7 B  N7 ]
Precocious puberty in boys is defined as secondary5 i, V( S, m& G6 \. y& \- r
sexual development before 9 years of age.1,4# w8 Y: S3 }+ X0 r4 p* y. b
Precocious puberty is termed as central (true) when# R8 c+ R" k4 `7 S3 ^/ C
it is caused by the premature activation of hypo-/ i4 P  @$ z! t7 ]
thalamic pituitary gonadal axis. CPP is more com-! i' v: ?9 C# [1 A5 \0 _
mon in girls than in boys.1,3 Most boys with CPP
( V& b8 ~8 U& ~3 u" k$ Ymay have a central nervous system lesion that is
6 b$ B2 W; Q) s$ sresponsible for the early activation of the hypothal-
- y# e* b0 L# `amic pituitary gonadal axis.1-3 Thus, greater empha-2 w' X' R  [. [# R
sis has been given to neuroradiologic imaging in
/ D1 j0 Z, h8 E8 k' b0 ~boys with precocious puberty. In addition to viril-
( V) f4 D. j! u6 e, {, O3 Jization, the clinical hallmark of CPP is the symmet-
! x0 `6 T- }. e8 v' Z/ v; Wrical testicular growth secondary to stimulation by+ p  p9 B# u) R* N; L( x
gonadotropins.1,3
7 O  D. |/ |% c3 U' L3 ]Gonadotropin-independent peripheral preco-6 p. K6 {6 D3 m3 h9 g( x
cious puberty in boys also results from inappropriate2 f. }2 l( x- z: h" h
androgenic stimulation from either endogenous or
, f* y9 y$ F% S. V8 Qexogenous sources, nonpituitary gonadotropin stim-
% W& s4 Z7 K  `( ]( oulation, and rare activating mutations.3 Virilizing0 r. ^: J; X) v+ Z. w6 e7 `" U, l4 v5 H
congenital adrenal hyperplasia producing excessive
5 z* o& K0 G' ^9 f* k/ I8 dadrenal androgens is a common cause of precocious
5 {/ g5 R5 x6 R) D% x" D, Y1 f7 ^puberty in boys.3,4
4 J' W7 ?( Z6 sThe most common form of congenital adrenal
3 U3 b: t8 v- p( L. l8 R8 n& D: vhyperplasia is the 21-hydroxylase enzyme deficiency.3 M- ~( p. Y$ t9 F( w
The 11-β hydroxylase deficiency may also result in
$ a  E! n" A/ v, l; H! Zexcessive adrenal androgen production, and rarely,/ }& u. |+ E  v% a8 R' \* K& [
an adrenal tumor may also cause adrenal androgen
8 U" {! o& }3 q! kexcess.1,3
  y" k' \' O& t) N( Kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  T9 N. ~3 Q9 N& A* Z2 S2 q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007  x. r/ |; C5 s
A unique entity of male-limited gonadotropin-; Q! F4 E! e, `5 q5 M0 n, D
independent precocious puberty, which is also known+ g- o" B) o' I. K8 b3 ^( P( s
as testotoxicosis, may cause precocious puberty at a
7 S% y6 j+ t- y/ b, j6 ~very young age. The physical findings in these boys
7 c! T+ _) v* H2 y( w/ L6 l/ w! Ewith this disorder are full pubertal development,
% A' ]8 z  Z2 d! j, ^including bilateral testicular growth, similar to boys/ G6 r* p! v8 U2 M9 D' k5 ?$ ^5 L
with CPP. The gonadotropin levels in this disorder
: c/ a& s3 x/ Aare suppressed to prepubertal levels and do not show5 \# Z# ~9 @/ o1 ^* x! w
pubertal response of gonadotropin after gonadotropin-
0 \: C9 B' G5 N* Z' H" Greleasing hormone stimulation. This is a sex-linked9 v) I8 e  u; d+ A; _
autosomal dominant disorder that affects only% j' d' Z8 O+ F7 k
males; therefore, other male members of the family
: D  _5 N" A' i! E6 Tmay have similar precocious puberty.3- [0 _+ ^& ?7 {& t. j+ L( S/ K) Q2 e
In our patient, physical examination was incon-
6 x$ o7 \6 W: ]sistent with true precocious puberty since his testi-
/ c# P7 u4 c5 e6 ]. U4 l- }: M" ccles were prepubertal in size. However, testotoxicosis1 f6 e6 e, P( d4 a* h
was in the differential diagnosis because his father
* P; a) j( H$ E8 ^. |started puberty somewhat early, and occasionally,
; m  A7 W. S# ]) r7 Mtesticular enlargement is not that evident in the
8 n! E+ P6 o1 X8 |) j' |beginning of this process.1 In the absence of a neg-1 e1 I+ j- B0 u+ {$ Y
ative initial history of androgen exposure, our$ y" y& Q5 \- B# o
biggest concern was virilizing adrenal hyperplasia,
0 u5 _* a. r% q1 _either 21-hydroxylase deficiency or 11-β hydroxylase6 j- v; g3 l, E; o2 s. l# y/ m( s
deficiency. Those diagnoses were excluded by find-: F2 n  D( w- b& r
ing the normal level of adrenal steroids.
4 S" B- z! v8 T+ @% `" O' ]The diagnosis of exogenous androgens was strongly
  _- z  i5 V" w, tsuspected in a follow-up visit after 4 months because0 V& Y# _- N* {. k' L8 Q' ~
the physical examination revealed the complete disap-! }+ [) P0 G7 |5 |1 J: E5 \1 ?, y
pearance of pubic hair, normal growth velocity, and6 l1 K8 r! k8 H* H3 E
decreased erections. The father admitted using a testos-' a( }: ~2 `: u! C6 u
terone gel, which he concealed at first visit. He was
& P& Y" l. o5 K: h; J3 Wusing it rather frequently, twice a day. The Physicians’
% Z( L; s* ~. u( w% [6 u) i( w  Q. oDesk Reference, or package insert of this product, gel or
* O1 g" I+ ?) l( ^: xcream, cautions about dermal testosterone transfer to! e  o7 r! L4 I7 ]
unprotected females through direct skin exposure.2 v% T3 _3 e2 K5 f/ v3 G
Serum testosterone level was found to be 2 times the# n7 K6 d' e/ t, |; P1 q) A/ {* U
baseline value in those females who were exposed to
. V4 w8 Q  ~7 @6 Qeven 15 minutes of direct skin contact with their male3 D, d+ t0 L0 u& Y/ D9 T
partners.6 However, when a shirt covered the applica-
- T3 s; L% p5 H* Gtion site, this testosterone transfer was prevented.& @, _9 ?' M2 v" j* D! }
Our patient’s testosterone level was 60 ng/mL,
, k: T' o" r; p' }7 `$ ]& n7 Lwhich was clearly high. Some studies suggest that! Q% n: P7 @! H1 m  S- ^! F
dermal conversion of testosterone to dihydrotestos-
' N( ?4 B* c8 D# P  a) [terone, which is a more potent metabolite, is more
# f2 g* G7 ?4 F2 {& j2 p8 Lactive in young children exposed to testosterone
  {5 y8 U( A/ d/ @  B$ W0 a+ Iexogenously7; however, we did not measure a dihy-
! M! Y, w: c8 |- z% Udrotestosterone level in our patient. In addition to: v; F+ N+ l3 E
virilization, exposure to exogenous testosterone in8 Z* g5 y1 Y+ f7 p3 K/ v5 h
children results in an increase in growth velocity and& R! ?7 F% }& Z- h' n2 W
advanced bone age, as seen in our patient.9 X8 K; b+ o8 y- Q, S# w/ t
The long-term effect of androgen exposure during0 q( Z" M1 A7 @7 U* V" ?
early childhood on pubertal development and final
' [. r& k6 z- C( y+ f3 |adult height are not fully known and always remain
8 |8 P2 @( W1 {" j: Qa concern. Children treated with short-term testos-
% ]3 r  o. B& uterone injection or topical androgen may exhibit some
, L& E2 q5 {; ^; {; |; Racceleration of the skeletal maturation; however, after
. w6 C8 D, _& f! W. U5 e+ Ycessation of treatment, the rate of bone maturation
+ a# G, o2 L% k" adecelerates and gradually returns to normal.8,9$ j1 O6 y* ]+ T! K+ c
There are conflicting reports and controversy  P) y7 m; G: B4 x9 W- _3 V* u% A  ~
over the effect of early androgen exposure on adult) I/ j2 Y  R4 D: u
penile length.10,11 Some reports suggest subnormal* S' X2 S* e! H& [/ k" k, d
adult penile length, apparently because of downreg-0 S! q. I7 M- `/ N! I: u
ulation of androgen receptor number.10,12 However," [+ y  C& c% l+ a: |+ u
Sutherland et al13 did not find a correlation between
2 r8 L- ^8 Z7 q- f, tchildhood testosterone exposure and reduced adult  F' Y( X7 j+ |6 n9 H
penile length in clinical studies.# r" |; l* S' [1 F# L+ Q
Nonetheless, we do not believe our patient is
0 ^" o! @7 G2 V& U! Z9 z2 ogoing to experience any of the untoward effects from/ B& V% P& k7 S* N$ L, Y8 I* d& L
testosterone exposure as mentioned earlier because
! M; B8 X$ H% [4 k/ X, P4 Gthe exposure was not for a prolonged period of time.  d% M, T  e4 r$ O( W+ g
Although the bone age was advanced at the time of
& x& }  l2 @( M' B' H" Ndiagnosis, the child had a normal growth velocity at
9 B% D6 g9 a  L  O; C  {the follow-up visit. It is hoped that his final adult
8 ?: X4 [! D5 z8 w* t; @8 }& Uheight will not be affected.
" N0 h0 ~" q, v+ oAlthough rarely reported, the widespread avail-. t4 Z% ]! Y, v, p
ability of androgen products in our society may
. E  O2 Z0 }5 M, d* oindeed cause more virilization in male or female
( t$ `3 j9 O2 k1 f! K4 ~- R" M% kchildren than one would realize. Exposure to andro-" V7 E; b- A+ U) _8 O, m
gen products must be considered and specific ques-
& r" F! v0 E8 ~% Z' a' o5 k, Itioning about the use of a testosterone product or7 s* _' Y) T* M
gel should be asked of the family members during
6 c9 n/ D8 m: S# q. \. b, Ythe evaluation of any children who present with vir-0 r& z: B5 B# }6 {. A! c) d% ^
ilization or peripheral precocious puberty. The diag-
& Z( k2 _: q* u' c" a& K2 Y8 pnosis can be established by just a few tests and by6 i0 c/ x8 s  c) [
appropriate history. The inability to obtain such a1 ]' y( i( b( t( F9 x5 F
history, or failure to ask the specific questions, may3 N* p4 k7 i4 S: D; K" p
result in extensive, unnecessary, and expensive8 l5 _; J) ?2 B! A. B  T
investigation. The primary care physician should be
( T- B5 ^/ |& f. Q% |aware of this fact, because most of these children& B7 Q3 @/ ~( S
may initially present in their practice. The Physicians’5 _' z- ]: _2 N2 m
Desk Reference and package insert should also put a
- A, G4 x9 X4 o. V* y& ]warning about the virilizing effect on a male or
- r% i0 k8 h3 E* Zfemale child who might come in contact with some-
- A7 p) o! `: o& done using any of these products.# m3 N* n7 X' [: B7 i' C
References$ Z$ L0 @5 |' }) t# V. P
1. Styne DM. The testes: disorder of sexual differentiation
0 d, c* p$ U7 f/ tand puberty in the male. In: Sperling MA, ed. Pediatric0 P; C. @! e  V; e4 r$ s
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 ?" h( F; |, L. Z% z7 z+ X2002: 565-628.
: ], F+ ]) J9 l, ?3 J2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 @. j! I3 R. ~7 O7 ppuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old2 Z4 ]0 V1 }  A
Boy Induced by Indirect Topical! K7 v1 X/ G- G' l. b
Exposure to Testosterone/ {+ h( c2 R8 J, [
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
3 C1 S: [0 Z' ^" p1 w2 Oand Kenneth R. Rettig, MD10 E/ }6 S  a2 @  J$ Q5 {8 V
Clinical Pediatrics
8 S/ [( p$ z" r+ k0 T1 v) jVolume 46 Number 6
& g4 T9 X: x0 l) P7 Q  u, g: c, bJuly 2007 540-543( \; e; S$ J5 l; O7 I+ f- h
© 2007 Sage Publications
8 U2 {* R. [! d0 ]( S) j9 b" \" m! R2 m10.1177/00099228062966512 _; h$ F* {; w4 n# K# o  G+ f
http://clp.sagepub.com# P3 H/ i1 }6 m. G( g+ z
hosted at+ M6 g" t2 R# k! `
http://online.sagepub.com
9 S* A# r+ |6 m8 x' GPrecocious puberty in boys, central or peripheral,
3 c9 o( i; a) d/ m7 P. z/ tis a significant concern for physicians. Central
! }4 X& ?# Z) f: E+ Hprecocious puberty (CPP), which is mediated2 f& L/ H0 J2 T# j9 i& A9 c
through the hypothalamic pituitary gonadal axis, has! \# F  {& [$ ^" [" `) ?
a higher incidence of organic central nervous system
4 d( C) m  e# c9 Ylesions in boys.1,2 Virilization in boys, as manifested7 p3 M2 h, `! P% u' {
by enlargement of the penis, development of pubic% k1 J; y! m0 K8 u. G3 U
hair, and facial acne without enlargement of testi-  T$ T8 C9 `; N1 }$ ^7 n; M
cles, suggests peripheral or pseudopuberty.1-3 We8 D" U: Q2 C/ N  P$ R3 _! u) L
report a 16-month-old boy who presented with the
: i0 e  H4 }! p2 y2 D' ~/ c% _$ tenlargement of the phallus and pubic hair develop-
4 n' `3 A( X, `ment without testicular enlargement, which was due  {) S% f6 b: K# ^% s
to the unintentional exposure to androgen gel used by# q7 s3 J: n1 W% F) @
the father. The family initially concealed this infor-
! T! g5 i  A/ {8 ]- m" h: o: hmation, resulting in an extensive work-up for this
5 e, B3 C% e  @* P2 Uchild. Given the widespread and easy availability of; B# f, z. ]* e4 ~; p% l: M
testosterone gel and cream, we believe this is proba-7 u4 _4 _; B2 a' Y! O/ D0 u  Y
bly more common than the rare case report in the! h4 _) f9 `5 I0 X5 E
literature.4, f, `1 c; X1 b: x% e% t
Patient Report* O" G- Z6 u5 Y2 z$ E
A 16-month-old white child was referred to the# L; o2 ^7 L  F2 O6 z2 z5 V* O
endocrine clinic by his pediatrician with the concern
0 M! w& q1 ^1 vof early sexual development. His mother noticed
3 _3 }  E7 n3 vlight colored pubic hair development when he was
+ m& B: ]  h% yFrom the 1Division of Pediatric Endocrinology, 2University of* ~4 x& X3 m: S/ v
South Alabama Medical Center, Mobile, Alabama.
. c# \5 [1 u( i2 D& Z$ e7 GAddress correspondence to: Samar K. Bhowmick, MD, FACE,1 [4 h9 ?8 m* Y
Professor of Pediatrics, University of South Alabama, College of
% n  B; |# u( ]+ B9 W6 xMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
' t% Y; J: J, ~% W* te-mail: [email protected].
' g1 L# Q6 \; iabout 6 to 7 months old, which progressively became$ o! W, z& w, S0 f2 S
darker. She was also concerned about the enlarge-8 Q2 {$ n' s5 ]. O5 [" f- q
ment of his penis and frequent erections. The child
9 u+ Z* S! I% l5 uwas the product of a full-term normal delivery, with+ U" h" ^9 @; b' b* h
a birth weight of 7 lb 14 oz, and birth length of, b2 }+ c4 n  ]2 c# m
20 inches. He was breast-fed throughout the first year
2 q! z$ ~4 J' _/ P1 E3 f; Wof life and was still receiving breast milk along with8 j2 p! `7 U! T) O3 r
solid food. He had no hospitalizations or surgery,
0 F" F  A- K7 m% A0 mand his psychosocial and psychomotor development& p1 ~  j8 G5 ^# J& f
was age appropriate.
" `% n% v7 L- W1 lThe family history was remarkable for the father,: Z5 f5 {* }5 W
who was diagnosed with hypothyroidism at age 16,
6 v8 D7 R. L5 @+ o  uwhich was treated with thyroxine. The father’s
% B8 w9 T( p! j, `9 q& \  bheight was 6 feet, and he went through a somewhat; X& \9 P! ~/ L1 \& }$ R) s. |
early puberty and had stopped growing by age 14.4 l- c. U2 f2 A5 u. L
The father denied taking any other medication. The
4 }& G, \( V3 U. j3 j: o$ n7 echild’s mother was in good health. Her menarche
0 P" `1 z% q: q% Q, a& nwas at 11 years of age, and her height was at 5 feet
" b. y  }8 P9 C' z3 I$ k# j5 inches. There was no other family history of pre-
, l2 l. a1 H% O: z; i5 l) k% {. Ucocious sexual development in the first-degree rela-
' P; n: n& _3 E  z) Ctives. There were no siblings.6 y8 d0 P9 r8 D- \4 l' k* r* E
Physical Examination1 W! h+ ~- O$ x5 e
The physical examination revealed a very active,
4 a1 N, g/ L' Y+ F3 ]playful, and healthy boy. The vital signs documented0 g2 ?  H' W! f' j+ u4 A( X6 [! k
a blood pressure of 85/50 mm Hg, his length was8 \9 I" v$ s* o( N; Y
90 cm (>97th percentile), and his weight was 14.4 kg. J" T6 s, Y! e! ~
(also >97th percentile). The observed yearly growth& [- r3 B2 p/ I* Y' [: @  n$ K
velocity was 30 cm (12 inches). The examination of
  E, r% H- n# F: @$ ~% G( r2 \the neck revealed no thyroid enlargement.( _  P4 Z" y$ N8 N; J
The genitourinary examination was remarkable for6 y% {/ m4 p4 S5 I" F' A
enlargement of the penis, with a stretched length of0 R. ?5 ]1 a2 Q& G  P
8 cm and a width of 2 cm. The glans penis was very well7 y) G9 B% r* A
developed. The pubic hair was Tanner II, mostly around. M' J+ Q( u/ {
540
  x" J) [9 z' r  Yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- q* U% w2 E0 S7 \$ Fthe base of the phallus and was dark and curled. The
$ E2 a! u4 \! ~( m* l( Ctesticular volume was prepubertal at 2 mL each.
. Z, w! }  z0 d& ]# C1 ]& QThe skin was moist and smooth and somewhat
5 A- p- L) s3 Foily. No axillary hair was noted. There were no
0 x5 V) o# o' }+ p% x. X1 @abnormal skin pigmentations or café-au-lait spots.
- N9 p; U$ |+ U* |, _7 c: w3 @% uNeurologic evaluation showed deep tendon reflex 2+7 f4 l- g4 r1 W( }; ~9 k$ U- C
bilateral and symmetrical. There was no suggestion$ R  m6 l( v6 Z3 V$ y) Y
of papilledema.
( ^4 q6 {* I; V1 HLaboratory Evaluation" k: T/ g- Z1 P- g
The bone age was consistent with 28 months by7 x) w+ k( R  d( |$ g4 Z
using the standard of Greulich and Pyle at a chrono-8 [$ `+ M" R" A5 ^( p- T$ e7 L9 R
logic age of 16 months (advanced).5 Chromosomal
) w8 F6 v  t* l6 g/ C) Mkaryotype was 46XY. The thyroid function test0 k" r' R- Z: i3 z. B8 C6 P; F
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
$ W$ t* y- {3 @& A/ ?lating hormone level was 1.3 µIU/mL (both normal).3 q- x+ E; v& m  A; r
The concentrations of serum electrolytes, blood
8 L4 i) F8 K& ~0 x9 _/ }urea nitrogen, creatinine, and calcium all were
( _+ M3 K, K! e" owithin normal range for his age. The concentration
, C% O3 \. n0 |5 j; Cof serum 17-hydroxyprogesterone was 16 ng/dL. ]# O3 K8 P6 W) [  u
(normal, 3 to 90 ng/dL), androstenedione was 20
4 |! H% N" o: }8 p7 E+ Bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, j  ~/ h* H9 y2 s; B2 L- X' aterone was 38 ng/dL (normal, 50 to 760 ng/dL),
! T% ~* y* w& e/ W9 x% f  o+ a0 ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to0 S; E; P) g) `% N5 p
49ng/dL), 11-desoxycortisol (specific compound S)# \4 F: |6 b6 f$ F/ ?& o
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) }, F  \: I, k0 Otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: a  p& d1 Z6 h( i, ]  B0 J! i
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
3 I( S8 V+ i5 u. J' Y" E' Q# P$ r+ mand β-human chorionic gonadotropin was less than0 r. G/ s2 V+ a4 b/ D7 ^1 j
5 mIU/mL (normal <5 mIU/mL). Serum follicular
( ?) `! d- `: Y+ J) ~stimulating hormone and leuteinizing hormone) ^  I6 C( e. s: \+ R- W! l
concentrations were less than 0.05 mIU/mL
4 m% W6 J5 h5 J$ s(prepubertal).
/ l0 V" j1 m9 Q3 `The parents were notified about the laboratory7 L/ ~( J2 v) R8 H6 M- U1 H
results and were informed that all of the tests were
& z5 D5 s7 {& Vnormal except the testosterone level was high. The
& f  ]: [2 b% z+ \  @6 Ifollow-up visit was arranged within a few weeks to
; [0 W  D/ b7 D3 \3 f$ b9 J1 z- oobtain testicular and abdominal sonograms; how-6 J  ]7 s' W. `1 k0 J
ever, the family did not return for 4 months.
. t; x, p8 f8 F0 b$ P& g9 ]  CPhysical examination at this time revealed that the& z5 p5 A( C4 M) Q9 t! r( b( {1 l, H8 N
child had grown 2.5 cm in 4 months and had gained
: n5 v2 U( w5 w8 S2 kg of weight. Physical examination remained8 n$ T/ ?7 [; N1 B
unchanged. Surprisingly, the pubic hair almost com-
. [' S; O3 v& i1 X) V1 R& D% \pletely disappeared except for a few vellous hairs at3 f# t2 W, e  B
the base of the phallus. Testicular volume was still 2* _* G$ r$ y! f* G& `
mL, and the size of the penis remained unchanged.
  t5 M" V0 T1 d+ E  A( j9 EThe mother also said that the boy was no longer hav-: I! E& A' c1 L" P/ j( B) p
ing frequent erections./ D: H% D6 _0 N/ v8 R: O1 P
Both parents were again questioned about use of* L$ ]$ P( V( X$ d8 U7 O8 l" T2 T/ E
any ointment/creams that they may have applied to8 a" n: w4 R( m+ s( J/ r
the child’s skin. This time the father admitted the+ c2 f* V/ M& T( s
Topical Testosterone Exposure / Bhowmick et al 541, J- q: a' ]5 N- ]# w2 i( g
use of testosterone gel twice daily that he was apply-
* N/ }4 c2 x7 z& l$ Bing over his own shoulders, chest, and back area for: D+ N: r0 g: q. F! M, D5 d, N5 w6 H; b9 v. T
a year. The father also revealed he was embarrassed
8 m, p* o) J3 K/ G- {9 ]: d' p/ oto disclose that he was using a testosterone gel pre-1 Y1 M4 Q7 k: p
scribed by his family physician for decreased libido
% m/ c8 D( j: ?5 r$ O: `secondary to depression., `3 O: V8 X' f9 P( R
The child slept in the same bed with parents.
& N: k$ A% `% Y' _0 a( K2 {$ WThe father would hug the baby and hold him on his9 w$ d2 {! s  X* z; }" J$ K* b
chest for a considerable period of time, causing sig-
% |) N0 O" ], p% O4 S& Z: o" {nificant bare skin contact between baby and father.% {& t6 d) D; z+ k3 s& V* z* @. P4 Y
The father also admitted that after the phone call,+ ?) Z: ~) R# X3 d9 ]; T/ I
when he learned the testosterone level in the baby
9 m: }; h: U% n: ?- kwas high, he then read the product information
, U6 \. |9 M$ c1 {packet and concluded that it was most likely the rea-
  b5 N" E' Q; R5 g+ [; U) ]$ Xson for the child’s virilization. At that time, they
& ^3 |9 M: Q) A0 r$ R. c( ^decided to put the baby in a separate bed, and the% E0 U8 B! g9 T, X
father was not hugging him with bare skin and had
# F8 r2 T2 ~6 g) _  v5 [; Ubeen using protective clothing. A repeat testosterone; ^- W" p7 S, A" }" N9 [
test was ordered, but the family did not go to the, L7 _! R' d9 y: l- D/ }/ v
laboratory to obtain the test.
  |* H# n) p  }+ x+ vDiscussion
, N6 Q; K6 R$ U9 Q" qPrecocious puberty in boys is defined as secondary
  Y, M* _/ w1 _sexual development before 9 years of age.1,4' p6 ^( {5 S: F
Precocious puberty is termed as central (true) when
7 {! e, F0 i' d  b' _it is caused by the premature activation of hypo-
1 z3 p9 O: v, c% ^4 f+ w& G; nthalamic pituitary gonadal axis. CPP is more com-- E: Z& \5 h! Y* \/ \( o: v7 z3 i
mon in girls than in boys.1,3 Most boys with CPP# `' d2 F, ^; c' A" l) h
may have a central nervous system lesion that is2 W7 C8 F7 ^) F5 q$ v* M
responsible for the early activation of the hypothal-2 b. a4 {* T' n
amic pituitary gonadal axis.1-3 Thus, greater empha-
& R4 C, j  h6 Nsis has been given to neuroradiologic imaging in, l- u: \. y; o; J# h* v
boys with precocious puberty. In addition to viril-
: {' `) V! Z, jization, the clinical hallmark of CPP is the symmet-
1 ?2 G) L& Q) t/ }# p) {8 R3 K, urical testicular growth secondary to stimulation by. G2 c  h1 }8 X% a* Z, m* V
gonadotropins.1,3
9 a# c& l3 h( p6 H* LGonadotropin-independent peripheral preco-7 S/ V- F2 d& q' r4 v3 d- Z
cious puberty in boys also results from inappropriate# V6 y4 X9 S- q8 T! W& P/ x- f. @
androgenic stimulation from either endogenous or# B# A7 t, ~% y" M5 m
exogenous sources, nonpituitary gonadotropin stim-5 u  t0 ?; ^* E" l, }; b
ulation, and rare activating mutations.3 Virilizing
1 w$ b' X+ h; p/ f/ k# f! `$ `" X$ Zcongenital adrenal hyperplasia producing excessive
7 i2 ^, A2 ~" o% o( j& Vadrenal androgens is a common cause of precocious- o8 O, v2 T9 r6 s8 N( H2 N4 y
puberty in boys.3,4
6 ^3 ?8 Q% J' e4 BThe most common form of congenital adrenal
. F  O, Z2 e/ K! m# Uhyperplasia is the 21-hydroxylase enzyme deficiency.6 Q6 A  |1 J: z7 L, h4 s* U
The 11-β hydroxylase deficiency may also result in
6 w' v; n/ L( Q2 }0 c) [! [excessive adrenal androgen production, and rarely,
7 J* n: b7 z4 X( {* zan adrenal tumor may also cause adrenal androgen
0 g( Q; K: q" Q& n8 Gexcess.1,3
, h3 q: j8 M  a& a6 J- @at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. K  O) c! w, n' e6 k6 l) K
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ j, n# S6 [  I6 l
A unique entity of male-limited gonadotropin-9 a' I# v( \% w1 x* T* q% i
independent precocious puberty, which is also known
4 X  f; L' D1 r6 bas testotoxicosis, may cause precocious puberty at a
. n) ^; s8 v4 O( Y- tvery young age. The physical findings in these boys
! G7 F$ x7 U8 Swith this disorder are full pubertal development,
, K; b! I8 N* _4 dincluding bilateral testicular growth, similar to boys
/ K1 ^) Y5 {) D5 gwith CPP. The gonadotropin levels in this disorder
7 X) A9 A, ?5 rare suppressed to prepubertal levels and do not show
9 L" l1 p  o7 hpubertal response of gonadotropin after gonadotropin-% i- X! w! B! m. ~
releasing hormone stimulation. This is a sex-linked1 U1 Z. M7 L; s5 w2 r
autosomal dominant disorder that affects only% d- Q& U4 h. ?/ X% Y
males; therefore, other male members of the family# G7 s4 l6 g/ i" V
may have similar precocious puberty.3
  h0 N" ?1 ?. V$ Y% X! UIn our patient, physical examination was incon-' S- N' m4 H, S0 t  V
sistent with true precocious puberty since his testi-% j  E' m7 N% t- N3 r1 r0 [
cles were prepubertal in size. However, testotoxicosis
$ f5 q$ }" w2 v8 Vwas in the differential diagnosis because his father% B, ?: c8 C; ~9 s
started puberty somewhat early, and occasionally,' D" [3 C6 n$ f# [1 }3 t; l! U
testicular enlargement is not that evident in the
$ D* O$ V* p  r+ P$ X" @beginning of this process.1 In the absence of a neg-& w; g- W' H6 d; h+ A) p9 O
ative initial history of androgen exposure, our
; u* L; K* }/ f1 v$ Fbiggest concern was virilizing adrenal hyperplasia,
6 j, C& W" _( I9 Y, T% q& j' X; t3 n6 y; `either 21-hydroxylase deficiency or 11-β hydroxylase" d6 Y( Z" X3 k7 l8 j; l% ]
deficiency. Those diagnoses were excluded by find-
; t9 n: \% ?$ U, A1 {. s- Oing the normal level of adrenal steroids." a( W& l- s) G5 ]
The diagnosis of exogenous androgens was strongly
5 m5 _# L& H/ `suspected in a follow-up visit after 4 months because" j5 ?3 U% e5 d  T- m* F
the physical examination revealed the complete disap-
% }! N" r. i# c4 Fpearance of pubic hair, normal growth velocity, and9 _0 `- Y+ F4 d' P, ^2 A
decreased erections. The father admitted using a testos-4 o1 B, ~9 Q2 u# S0 X
terone gel, which he concealed at first visit. He was0 A& G* y+ K% k$ s2 L2 ^) m
using it rather frequently, twice a day. The Physicians’
9 u$ S' e$ ?% B" v* J3 k: wDesk Reference, or package insert of this product, gel or4 ~% C+ W$ M7 F" f  Q
cream, cautions about dermal testosterone transfer to  @1 p2 J7 P+ K' n" T
unprotected females through direct skin exposure.0 Y" f9 A# n0 V1 [, L4 p5 J* H& o
Serum testosterone level was found to be 2 times the! P  T1 p- q) j" m2 A+ m
baseline value in those females who were exposed to, A6 j) v/ _6 ^  U. J
even 15 minutes of direct skin contact with their male; ^' i  a, T9 d
partners.6 However, when a shirt covered the applica-
0 ~2 M1 _8 v/ g+ s- U( w( j2 y2 ~tion site, this testosterone transfer was prevented.
4 r+ _3 _) A" qOur patient’s testosterone level was 60 ng/mL,
3 E: M: l6 c  y$ }$ u8 t7 Ywhich was clearly high. Some studies suggest that
6 A! X4 d$ l* {( [2 H1 Jdermal conversion of testosterone to dihydrotestos-0 ]) I9 M5 Q1 ^# L! `9 ^' p8 T
terone, which is a more potent metabolite, is more
) ?! d; [; c$ ?" f( S7 Q. ~active in young children exposed to testosterone
# x0 U+ P. B& d7 qexogenously7; however, we did not measure a dihy-
7 U8 a9 \+ n; Q( t3 x/ ?drotestosterone level in our patient. In addition to
& w0 T5 R  I' T5 F& ^5 g7 t; Wvirilization, exposure to exogenous testosterone in
5 g1 d  [  S6 Q. E8 S: Lchildren results in an increase in growth velocity and
$ f; d: Y/ {+ e; t' o  g6 ~advanced bone age, as seen in our patient.  y9 r+ k3 \: r2 c% q
The long-term effect of androgen exposure during; K3 H7 N3 p6 J! @2 @' C, N, {
early childhood on pubertal development and final
. J  E5 V0 H2 E: y/ d+ b  J, uadult height are not fully known and always remain1 {# _- E; s4 m1 A
a concern. Children treated with short-term testos-" v* B8 m/ m2 H3 b% J
terone injection or topical androgen may exhibit some5 s+ l! w1 o: j5 j+ r
acceleration of the skeletal maturation; however, after
0 k" [: l! Z/ F( v5 Wcessation of treatment, the rate of bone maturation9 B$ g2 Q8 [6 `* E
decelerates and gradually returns to normal.8,90 _- C$ `; }8 T
There are conflicting reports and controversy
  E* e: h- Y1 Q4 ?! g% _" wover the effect of early androgen exposure on adult
. @  U: ^0 ]* h/ R) M; {0 Kpenile length.10,11 Some reports suggest subnormal
. C! D' Q* D9 f+ c6 c# xadult penile length, apparently because of downreg-; K, Z7 O- ~/ H0 r( O! S% y+ {
ulation of androgen receptor number.10,12 However,7 v8 i: F& B8 \6 A0 |  a- F
Sutherland et al13 did not find a correlation between
1 G# o! Q) ^5 D, W. F3 U1 D) gchildhood testosterone exposure and reduced adult+ w. o% |/ U0 m' B! U7 I
penile length in clinical studies.
3 p: A9 o& r7 l1 X% i1 sNonetheless, we do not believe our patient is
2 G2 n, ^# t& J5 ~6 I, egoing to experience any of the untoward effects from
. ]+ _+ c4 v: N3 E% P0 A$ gtestosterone exposure as mentioned earlier because
2 F6 L7 \' \. k5 u4 T* _the exposure was not for a prolonged period of time.7 y8 D( U; s% ^5 c0 o& q) Y6 F. [
Although the bone age was advanced at the time of4 X! l; M7 b) I0 r* N
diagnosis, the child had a normal growth velocity at" W& p8 A2 y3 r9 v# {
the follow-up visit. It is hoped that his final adult
+ D$ `9 K4 h- z7 @& \  O3 fheight will not be affected.
" i! B, ]& w# X. h5 h/ TAlthough rarely reported, the widespread avail-0 Q/ Z6 S2 Z# A, ]
ability of androgen products in our society may. w; V' e% ?5 l" h+ t2 }5 {
indeed cause more virilization in male or female: w* k, T1 {9 P! W/ R  L4 ~
children than one would realize. Exposure to andro-
. q8 i0 f# \) Igen products must be considered and specific ques-4 O# e/ s) S0 ]* h1 x6 [
tioning about the use of a testosterone product or
" l+ P2 t# }6 ~" ygel should be asked of the family members during
: ~, ]( O7 r! K& Z- _the evaluation of any children who present with vir-# y& W0 }  Q: v/ P3 q4 n
ilization or peripheral precocious puberty. The diag-
* H* x# E6 C# y0 O. A  p; e6 \nosis can be established by just a few tests and by( l4 _7 x$ L/ R8 Z' z2 B% S
appropriate history. The inability to obtain such a+ t* K8 Y- h8 X. e/ N* B
history, or failure to ask the specific questions, may/ s+ {8 T. G. C& g' M7 Q1 a
result in extensive, unnecessary, and expensive
; n6 [3 U' f! d  E) [! t& Uinvestigation. The primary care physician should be- i( \# H' j8 e$ s
aware of this fact, because most of these children
# {% ]# D) Q6 u5 [" Z' |may initially present in their practice. The Physicians’
9 `  L, m5 w! l- ~! gDesk Reference and package insert should also put a: V" f) m9 |5 x( [
warning about the virilizing effect on a male or% U, ?8 J, }5 z8 {
female child who might come in contact with some-
# d& `  J2 ?3 n, C! Y2 I& `one using any of these products.1 J3 X% Y: j) f
References, E* @" q  a. t" `) \; R1 c4 v
1. Styne DM. The testes: disorder of sexual differentiation+ o" m1 e6 P9 z( ]
and puberty in the male. In: Sperling MA, ed. Pediatric
0 e) @8 s3 w. ?- G4 t4 d9 e; YEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. e9 J+ J4 b  [- N0 u+ n
2002: 565-628.4 b$ c9 _% \# a3 b+ u3 w
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 K. K6 r6 l& cpuberty 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
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

6 ?+ D. U  ?- `2 J- m# K! H# `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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