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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$ c; S, ^" F( u9 j. Z6 k
Boy Induced by Indirect Topical
/ ]# q5 u+ z# a. k- I5 V8 eExposure to Testosterone+ S) f1 h2 \) q- Q( K
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  L7 ^; \: O) U% band Kenneth R. Rettig, MD1$ ?$ ~* G5 D6 E& R4 {: r
Clinical Pediatrics
; W; D7 J  P- j$ c/ TVolume 46 Number 6+ t: o$ T$ z9 p. z. O
July 2007 540-543
' G5 s; v2 S& }" x" j© 2007 Sage Publications, b  j/ E: a0 w* z  [) [
10.1177/0009922806296651, o% F' X+ e' t/ U5 @6 E  }, W4 ^
http://clp.sagepub.com
+ h' l" {8 ~. C: R+ u$ lhosted at
5 Q) ?: ~; m  A+ ^' Ghttp://online.sagepub.com
& H6 {' `5 G. X( {) qPrecocious puberty in boys, central or peripheral,
: y% B5 b* B" O4 W* ^  Ois a significant concern for physicians. Central4 v3 ]2 L: l& _
precocious puberty (CPP), which is mediated
2 _5 S0 U. X; N5 X+ W( f3 R* j* pthrough the hypothalamic pituitary gonadal axis, has
1 F% ]6 ~* }: S: k0 e6 ma higher incidence of organic central nervous system6 X2 q/ X4 ?) h& e+ X
lesions in boys.1,2 Virilization in boys, as manifested7 `2 H6 e4 L6 q8 m2 S3 {$ Y6 N
by enlargement of the penis, development of pubic
% d  J* r6 x5 q" r* ?hair, and facial acne without enlargement of testi-
0 o9 N3 I  T( X$ u0 H. D4 jcles, suggests peripheral or pseudopuberty.1-3 We" P: p6 m0 F7 F8 j- O" E# s
report a 16-month-old boy who presented with the/ o& W9 J( \( }1 W  E
enlargement of the phallus and pubic hair develop-
- ~. G# g$ u; i, Xment without testicular enlargement, which was due4 Y1 E& j- a3 l. ~; E5 Q
to the unintentional exposure to androgen gel used by
7 V, [6 b0 j, ^3 T# D$ i5 r0 |+ H8 Cthe father. The family initially concealed this infor-, `( _6 m. ^+ k: g8 ]2 W
mation, resulting in an extensive work-up for this
0 L5 E+ D3 S+ h7 r7 Cchild. Given the widespread and easy availability of* l/ M6 Z+ J+ N; K
testosterone gel and cream, we believe this is proba-
/ x" l7 _% E: R* J9 ~: _3 Y( tbly more common than the rare case report in the
$ ]2 t' a. _/ Y' eliterature.41 _1 d; ^0 x" s% V' F6 h8 d
Patient Report
, ~! T6 X3 K2 X: l/ @A 16-month-old white child was referred to the
* @9 x; L  M5 x* hendocrine clinic by his pediatrician with the concern
% y; I9 b8 @5 e6 ^0 O* W3 jof early sexual development. His mother noticed; \, o' P7 C; V0 ~* l2 t
light colored pubic hair development when he was) M$ Y7 C* o8 {! D7 B8 J
From the 1Division of Pediatric Endocrinology, 2University of
7 a% @. Y( s( s0 N2 H2 E9 NSouth Alabama Medical Center, Mobile, Alabama.
# x$ @5 e2 @  H( b5 q  Q) m! dAddress correspondence to: Samar K. Bhowmick, MD, FACE,
4 O8 H% J( d& f, i' B$ R0 YProfessor of Pediatrics, University of South Alabama, College of
) n( |! Q% h8 g+ |3 gMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;* I1 M. @6 y' {5 _3 h# `; Y
e-mail: [email protected].* @5 c& N% o# q5 G; Y, C
about 6 to 7 months old, which progressively became
: ^% w1 P# |4 |9 H4 K/ k: b6 wdarker. She was also concerned about the enlarge-# q; [" ^) e; ]$ \- d$ l, ]
ment of his penis and frequent erections. The child
0 j. \. _* B; W6 swas the product of a full-term normal delivery, with
9 ~; i& o. J6 c# ~! O8 [9 x1 Na birth weight of 7 lb 14 oz, and birth length of$ N3 @, I2 P% \! {5 P! F2 g! N; G
20 inches. He was breast-fed throughout the first year
9 {+ k% p' P& Q0 _- Y6 xof life and was still receiving breast milk along with! H1 N7 X. B* g; c
solid food. He had no hospitalizations or surgery,7 w- y9 V& t. u
and his psychosocial and psychomotor development& p# X/ d' }4 B4 Y
was age appropriate.2 g4 F3 C0 n4 v  v- `/ a# T
The family history was remarkable for the father,
4 [& C: ^0 D  b- ~  @* G$ o" |% iwho was diagnosed with hypothyroidism at age 16,& ]7 d/ I) [2 z8 r2 M1 O& b' `
which was treated with thyroxine. The father’s6 N+ I+ x, e8 C
height was 6 feet, and he went through a somewhat
% {  M5 ?+ {, x- [( d/ }' ~early puberty and had stopped growing by age 14., F/ r# x* L1 Q/ T; P
The father denied taking any other medication. The
! l) h* }. J& X- pchild’s mother was in good health. Her menarche
/ N0 y9 B' F( t1 u# V* a+ fwas at 11 years of age, and her height was at 5 feet
  A* n( a, V7 _# J5 inches. There was no other family history of pre-3 Y: V) T7 H" k" {2 q1 B) a
cocious sexual development in the first-degree rela-5 L6 U5 {8 E: Q6 ~0 ~) `7 C8 B
tives. There were no siblings.! ]9 f  s0 s; `! U* K/ T
Physical Examination  I, x; m* i' ~9 b
The physical examination revealed a very active,
( g. W4 ]$ B8 e5 L4 Rplayful, and healthy boy. The vital signs documented
. T+ t+ b+ C' ?8 N) C2 I8 e; D; Wa blood pressure of 85/50 mm Hg, his length was& q# j, |3 t; T6 i
90 cm (>97th percentile), and his weight was 14.4 kg
! o9 |6 y. l0 A4 e1 p* _0 O/ l  F1 g% O(also >97th percentile). The observed yearly growth
6 j- f& u7 J: {velocity was 30 cm (12 inches). The examination of
; T$ |/ ^% x' u( h* J$ Othe neck revealed no thyroid enlargement.
" }4 m" H6 |: f5 lThe genitourinary examination was remarkable for
9 R9 N+ `0 S+ D6 ]7 `& lenlargement of the penis, with a stretched length of, O. G9 {0 r4 H. V8 Z
8 cm and a width of 2 cm. The glans penis was very well' k$ ^7 e0 D% h- _, J1 W$ a
developed. The pubic hair was Tanner II, mostly around. X4 m7 H: w, H' \( C
540. O; g& l" b' E% w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 u# Z# z5 g4 n1 ^
the base of the phallus and was dark and curled. The: o. M' \$ h7 [7 N3 {
testicular volume was prepubertal at 2 mL each.6 S& z/ f, r+ J  W4 Z. @
The skin was moist and smooth and somewhat1 a; T! k1 B; M- i
oily. No axillary hair was noted. There were no
# R) j# t, B: Q7 _( a; p0 qabnormal skin pigmentations or café-au-lait spots.( A. t3 j4 [+ j
Neurologic evaluation showed deep tendon reflex 2+1 c/ d! M9 l6 g8 C, O
bilateral and symmetrical. There was no suggestion
! f/ H1 O% i/ ^; Q& Z- H$ J; o+ Jof papilledema.% p3 h/ c: X' A- v
Laboratory Evaluation2 W' N0 g% {+ p( |& ^7 o. R2 }: s
The bone age was consistent with 28 months by5 ^( }- u( A  d: m/ i% ]  X
using the standard of Greulich and Pyle at a chrono-
( ~9 x5 u1 {$ N* Rlogic age of 16 months (advanced).5 Chromosomal5 Y/ S8 U3 x# \5 l
karyotype was 46XY. The thyroid function test
% e# t: @6 C2 S* @  ]; _showed a free T4 of 1.69 ng/dL, and thyroid stimu-4 O3 c. ?5 Q" S1 P
lating hormone level was 1.3 µIU/mL (both normal).
) R+ r; h! q! e- `# O! j+ [1 @" eThe concentrations of serum electrolytes, blood
; Y# d7 @+ u9 L9 v3 murea nitrogen, creatinine, and calcium all were5 a7 O6 p% h) E+ W. W. i2 M/ {
within normal range for his age. The concentration) l5 d8 P) `; S5 b6 X) B7 ]
of serum 17-hydroxyprogesterone was 16 ng/dL
5 T6 W# E* _* w, P9 T! h1 m. `6 {(normal, 3 to 90 ng/dL), androstenedione was 20
& P+ C. T1 L# V! y5 H$ T$ bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( C7 K* l- e, }! F4 l- e
terone was 38 ng/dL (normal, 50 to 760 ng/dL),/ e6 T9 G' [, \/ w2 C
desoxycorticosterone was 4.3 ng/dL (normal, 7 to. s* ?' B+ T7 p; u  t8 O: @0 ^& X
49ng/dL), 11-desoxycortisol (specific compound S)
3 `- Y& a+ T, F6 C0 j7 E% Awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) `6 h& G  g! Q; n0 \
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ C: g& P# i; K. \5 ^& L
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),' A. j7 P+ p4 x
and β-human chorionic gonadotropin was less than$ r9 x2 V* ?- Q+ a2 ?9 |, h
5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 E) [7 s, C; x% M# k" X" I6 Ustimulating hormone and leuteinizing hormone
7 k$ Z% M# Q! N9 A- k+ ~concentrations were less than 0.05 mIU/mL
& n$ Q2 E) Y/ Y9 F9 [  z(prepubertal).
( y: f) `8 K  u  Q. f% `The parents were notified about the laboratory
" T% R5 j' o! }* q2 M# m; [results and were informed that all of the tests were8 w/ @1 f# h( Q7 l6 z) z2 d
normal except the testosterone level was high. The
$ }9 c9 k+ D5 rfollow-up visit was arranged within a few weeks to0 R2 @% z" d5 T, r- o3 _
obtain testicular and abdominal sonograms; how-" b0 W  p: Q. m: q+ [  i
ever, the family did not return for 4 months.
0 ^4 y! S! m  F' E! HPhysical examination at this time revealed that the
+ p9 C! ?! Z) K% {) Ychild had grown 2.5 cm in 4 months and had gained
- m3 k2 F& `$ `2 kg of weight. Physical examination remained2 D- _& R& \( q( U& X7 U! P
unchanged. Surprisingly, the pubic hair almost com-
) \. s7 k' Q4 n9 o( Z! ~/ j# g) Zpletely disappeared except for a few vellous hairs at
9 v! ?- z' r; o3 I& w2 ~# |the base of the phallus. Testicular volume was still 2' U9 U2 d+ j3 i* t/ H
mL, and the size of the penis remained unchanged.
* h7 e* K2 Y, V& N! ~" z! g& J1 v1 `The mother also said that the boy was no longer hav-/ `3 q: B# O( k1 a. H; j7 w
ing frequent erections.
+ M) }& u6 V5 s$ xBoth parents were again questioned about use of& w" {8 A4 |3 w; `% c
any ointment/creams that they may have applied to/ c( x/ `1 J" [  E: H, h  m
the child’s skin. This time the father admitted the
4 B1 U: I8 T& z$ L& Z0 b2 |Topical Testosterone Exposure / Bhowmick et al 541' N' l7 p3 g1 Y/ a  y$ m
use of testosterone gel twice daily that he was apply-$ K1 _  v% D, o# A; K3 L
ing over his own shoulders, chest, and back area for/ H( \/ y. j" _" h! \7 u$ k6 @
a year. The father also revealed he was embarrassed
! {2 \8 @7 [  z! `to disclose that he was using a testosterone gel pre-6 Z5 N4 @) k4 o0 D6 J* S
scribed by his family physician for decreased libido
0 e' Y4 o6 U. P, ^8 f! N# w6 a7 ssecondary to depression.
1 x* l: ]3 u. ]The child slept in the same bed with parents.% t: M9 w* l9 |/ j6 \2 i. q
The father would hug the baby and hold him on his! T" `& v8 K5 K2 W
chest for a considerable period of time, causing sig-$ Q) F* p( f; u3 T; D! O9 h  m
nificant bare skin contact between baby and father.. s8 V1 r4 j0 J+ ^) U; W, x% q
The father also admitted that after the phone call,
+ |5 q3 ?) k* {) N7 L4 H& C, y4 Kwhen he learned the testosterone level in the baby
* |, [+ P2 R( Cwas high, he then read the product information) F2 U: y) Q& H" P! ~1 |( Y
packet and concluded that it was most likely the rea-
9 U' ~+ k- N% C# t0 cson for the child’s virilization. At that time, they1 p0 b0 {. i4 d; U9 E9 _1 G" ~
decided to put the baby in a separate bed, and the
4 E' C+ H( I/ n% I% X8 jfather was not hugging him with bare skin and had3 M8 D5 r" G( v
been using protective clothing. A repeat testosterone' I2 a) ~& P/ U
test was ordered, but the family did not go to the- i  U: b! a  V* x" W/ X
laboratory to obtain the test.
8 T) g! I! T" FDiscussion' N2 I" l, U; G3 J& {
Precocious puberty in boys is defined as secondary, W8 Y) K0 J0 p0 X
sexual development before 9 years of age.1,4( L' r( E2 {6 }' Q
Precocious puberty is termed as central (true) when, z1 ^9 v( [2 d6 u$ D
it is caused by the premature activation of hypo-( [% ~/ l" Z! }  M, G
thalamic pituitary gonadal axis. CPP is more com-" J% [; A; y4 t7 p" j- r
mon in girls than in boys.1,3 Most boys with CPP
, g. A" j, ~6 G7 ?may have a central nervous system lesion that is
8 r) d. w7 |# @; Sresponsible for the early activation of the hypothal-
; b' u8 T, z4 v8 j1 ~amic pituitary gonadal axis.1-3 Thus, greater empha-) |! w* ^0 E/ z4 N  n
sis has been given to neuroradiologic imaging in
* h5 ?8 n0 a" L2 ^. h8 n  Qboys with precocious puberty. In addition to viril-
( Q; U2 p5 l% l% l/ o- e6 L+ H/ Jization, the clinical hallmark of CPP is the symmet-
  ?0 `- W. B- F8 n9 ~' Grical testicular growth secondary to stimulation by" V2 u( j+ j3 ]8 e$ s. M8 A
gonadotropins.1,3
: q* G6 h0 W9 h7 q. [; vGonadotropin-independent peripheral preco-# W$ w/ D% P  G
cious puberty in boys also results from inappropriate  H9 W, ]2 P# J2 C1 r! Q( T
androgenic stimulation from either endogenous or
* l+ ]" W: i- b4 E$ f1 M% Mexogenous sources, nonpituitary gonadotropin stim-4 `; _! s% I" C7 t# A% I+ S
ulation, and rare activating mutations.3 Virilizing
5 S- l6 c# \2 L; ]* \! h, y* W+ hcongenital adrenal hyperplasia producing excessive
1 l) h3 X' c% L% `8 nadrenal androgens is a common cause of precocious
; z6 w: Q0 {! `% ipuberty in boys.3,4  X5 n* p; U* f# t! R% [0 Y  G
The most common form of congenital adrenal
% [5 O1 F- U; {hyperplasia is the 21-hydroxylase enzyme deficiency.
8 W, w8 ^* y" V3 ~The 11-β hydroxylase deficiency may also result in% R0 s* \& F2 z& l, i
excessive adrenal androgen production, and rarely,& Q! @: f  }3 q( _) [
an adrenal tumor may also cause adrenal androgen3 a& S, C9 O5 g: F8 R* Z3 |' `
excess.1,3
. n- y* @) B1 L/ ]1 qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. w7 H+ o" @2 Z, G/ D
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
( \( i0 H% r& a8 F% TA unique entity of male-limited gonadotropin-" O7 Z) l4 I* Z. n
independent precocious puberty, which is also known
' f, L$ N- i( a  {. q/ w+ das testotoxicosis, may cause precocious puberty at a
$ Z% J6 g! z0 ]- T! D0 ]very young age. The physical findings in these boys, [9 ^  Q) Y8 Q( C* b2 x
with this disorder are full pubertal development,& u6 z( C( Z- x6 r
including bilateral testicular growth, similar to boys$ Y- P% V# {3 x. A( |, D
with CPP. The gonadotropin levels in this disorder
/ `: |+ A1 f) z) m* k, v% rare suppressed to prepubertal levels and do not show
7 g% V4 s+ P% E4 Q* gpubertal response of gonadotropin after gonadotropin-
$ q# P9 n: b3 q: \7 k5 Oreleasing hormone stimulation. This is a sex-linked# h5 O$ k, O: B* Y
autosomal dominant disorder that affects only# _$ T6 S. x( y9 U% e! |
males; therefore, other male members of the family
" }" a$ w0 o) j  \" ^7 Mmay have similar precocious puberty.34 Q( P' b9 V; J# Y5 e+ T
In our patient, physical examination was incon-
4 M/ J7 m+ M/ g2 ~. @8 jsistent with true precocious puberty since his testi-
' x4 B4 X8 j( Y4 \$ X) e% B- `cles were prepubertal in size. However, testotoxicosis: {& V" O1 s) H5 s0 K  I
was in the differential diagnosis because his father
8 |: i/ b0 E5 ~6 k% h" y0 gstarted puberty somewhat early, and occasionally,
' D! e2 h' v; \testicular enlargement is not that evident in the: K# k/ b3 C- x6 g. b" \
beginning of this process.1 In the absence of a neg-
: K- F9 N9 R  P! Hative initial history of androgen exposure, our, ^& ]6 T- t& P& X- }
biggest concern was virilizing adrenal hyperplasia,
6 t6 r' b; S4 Qeither 21-hydroxylase deficiency or 11-β hydroxylase
: ?4 [/ |2 }& u, t" ldeficiency. Those diagnoses were excluded by find-$ R0 [; I# c2 q+ \  g+ j: G
ing the normal level of adrenal steroids.4 O7 k. J6 e& f! C1 B
The diagnosis of exogenous androgens was strongly
: [' ]1 c4 g  t) H: wsuspected in a follow-up visit after 4 months because+ D4 p& \. R/ S5 T2 \) d
the physical examination revealed the complete disap-
* _6 M3 z# F. o6 ]+ |2 Fpearance of pubic hair, normal growth velocity, and
+ K/ y8 O$ F7 @& [+ M& Edecreased erections. The father admitted using a testos-
  a' L7 [# e6 u4 U' m! V" j' vterone gel, which he concealed at first visit. He was
1 E! e/ j4 F7 h* d6 l2 Vusing it rather frequently, twice a day. The Physicians’
0 C3 n7 n3 j' SDesk Reference, or package insert of this product, gel or0 a" W% Q) B' S5 ^% l
cream, cautions about dermal testosterone transfer to6 |/ w, h! R1 D* M& h
unprotected females through direct skin exposure.
. e1 |+ h5 Z! v5 @Serum testosterone level was found to be 2 times the3 L; f4 h' z$ q. y; u4 J
baseline value in those females who were exposed to! {" @# e8 N% U9 F4 J% c
even 15 minutes of direct skin contact with their male
8 A, P8 Q3 Y5 h: T" x9 M$ apartners.6 However, when a shirt covered the applica-3 n- J/ f( b& J/ s4 |
tion site, this testosterone transfer was prevented.
4 w( I3 j# x+ bOur patient’s testosterone level was 60 ng/mL,
. G  b9 k" a' v% Ewhich was clearly high. Some studies suggest that
2 P0 d1 s( A$ P' u4 ]' Y' ]dermal conversion of testosterone to dihydrotestos-
$ F2 J8 i5 P: oterone, which is a more potent metabolite, is more
* G' v; Y3 O/ ~" @active in young children exposed to testosterone6 M  a) a& }2 j! ^- G
exogenously7; however, we did not measure a dihy-
) G% z- T) g7 t2 r" X/ x3 vdrotestosterone level in our patient. In addition to
2 l' y/ _1 j( P+ ~3 lvirilization, exposure to exogenous testosterone in
- L+ F" e# _" n4 |/ I0 h1 D  K- Y: i$ pchildren results in an increase in growth velocity and( q# d6 H9 @* g% J. B0 \( {$ {( g9 @% I
advanced bone age, as seen in our patient.4 y, C0 X* u0 Y$ B, d! n" O
The long-term effect of androgen exposure during; x; d' [+ g( a
early childhood on pubertal development and final3 J7 F6 ?3 P7 {) a) r7 T3 l
adult height are not fully known and always remain
9 D% R: q8 T. k7 l. fa concern. Children treated with short-term testos-$ O' m  |- d8 w% l
terone injection or topical androgen may exhibit some0 [! E" T: t7 s8 B+ }
acceleration of the skeletal maturation; however, after0 w& ]- \2 g; Z# |- r3 i2 a$ r
cessation of treatment, the rate of bone maturation
/ @7 s5 \5 O8 ?7 O3 \/ Hdecelerates and gradually returns to normal.8,9/ ?* O4 ?% g9 s
There are conflicting reports and controversy6 e! S( S/ y* r! ]
over the effect of early androgen exposure on adult7 ?  W+ v3 |& N2 x, [: L  r, {9 s
penile length.10,11 Some reports suggest subnormal) W* L3 `0 T( Y" r7 S( I$ T' a
adult penile length, apparently because of downreg-* @+ u+ T- P" x$ S' W
ulation of androgen receptor number.10,12 However,
$ \- o) `  |9 `; _5 {Sutherland et al13 did not find a correlation between2 u% M# D+ p4 b0 |: I
childhood testosterone exposure and reduced adult; j7 V5 Y6 m: l' q# Y
penile length in clinical studies.! s4 }% |' T$ t8 ?. x
Nonetheless, we do not believe our patient is/ O. W! i0 z3 J) H  k0 I9 w
going to experience any of the untoward effects from' \6 G7 j+ `* o" X
testosterone exposure as mentioned earlier because
6 a2 a( Y) u) C" B  Nthe exposure was not for a prolonged period of time.) ~6 \. V  ?8 E: z2 K% {
Although the bone age was advanced at the time of- n, e, n, G: `/ k. @8 J
diagnosis, the child had a normal growth velocity at
' X) B, x3 f- X* tthe follow-up visit. It is hoped that his final adult
0 w/ A* ^' s$ H" ]. Iheight will not be affected.
- D% S1 _4 z+ b; K7 ~Although rarely reported, the widespread avail-  P' W! G8 H- H8 n
ability of androgen products in our society may
, e5 z$ M  Z3 F4 T, [5 a$ t0 Zindeed cause more virilization in male or female
. R9 H2 f. U+ c4 ^( L% K1 bchildren than one would realize. Exposure to andro-
4 U# C. b0 `7 R# ?; Zgen products must be considered and specific ques-* `! S- o9 I0 V& m/ x  `
tioning about the use of a testosterone product or
9 v& [- `% f( ]3 q. |1 Cgel should be asked of the family members during
$ N. E: ]8 H, [* B1 |+ `the evaluation of any children who present with vir-
$ D' L2 z4 E# Y: E4 Kilization or peripheral precocious puberty. The diag-- A# E3 ]( a/ c# w" ]! d7 H
nosis can be established by just a few tests and by' f  G  R8 G3 z! D1 }+ |9 D& m% t
appropriate history. The inability to obtain such a1 n# q8 B9 v- @3 ^/ k7 Z1 m
history, or failure to ask the specific questions, may
$ b$ v: \! _' x9 T9 U2 ]- Z% I- Kresult in extensive, unnecessary, and expensive% b1 R5 O% g* N5 }/ K
investigation. The primary care physician should be
( b& K  x" f* q' E( o) x6 ]aware of this fact, because most of these children
& C  M4 F3 x" jmay initially present in their practice. The Physicians’
1 @1 b9 j1 D5 |4 v! Y" a3 X6 [Desk Reference and package insert should also put a, i1 C/ V/ @, [0 z0 r
warning about the virilizing effect on a male or/ ~+ O" G+ `- V
female child who might come in contact with some-- A/ O% i7 [, _& D: Y+ [
one using any of these products.
; v7 W, O, ~" h  y5 ^( |References2 a1 W) `! M  @- A. [% C6 ^, y
1. Styne DM. The testes: disorder of sexual differentiation# W& n2 I$ ?" y8 [: k
and puberty in the male. In: Sperling MA, ed. Pediatric/ o" I6 F' M8 N9 M
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 [+ ~  m) h* j+ S3 W2002: 565-628.
5 [# D0 v4 ?8 Y; T$ g2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) A( O9 [* r3 t1 ^
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old. q, v" n) w9 h5 `
Boy Induced by Indirect Topical; v, s0 k/ g* @  }9 w
Exposure to Testosterone  n8 n' L* Y/ X9 G: Q3 n
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2, j, w. @& J* |3 I2 g% E  z& I
and Kenneth R. Rettig, MD1) B/ i! p' q6 y2 q. }
Clinical Pediatrics
8 f9 z* w; N% A, k6 vVolume 46 Number 6+ }; p1 o, w1 h* W: @- O1 `
July 2007 540-543
/ o5 T# B3 [7 M: t© 2007 Sage Publications+ Z0 c" g% f( X2 t2 S' [
10.1177/00099228062966513 f- G# M$ g+ w: H! p, c
http://clp.sagepub.com
4 l( U, J( N7 L+ N2 x  Rhosted at
4 u- W8 C% ?0 e6 ^( ahttp://online.sagepub.com+ _7 N& K% O' O( Q( I* O! z& ]
Precocious puberty in boys, central or peripheral,
6 q  z% B, h  v3 B4 K1 q5 Z( @) Ois a significant concern for physicians. Central
! E" g- j) m8 Hprecocious puberty (CPP), which is mediated
7 w- u) E$ n1 K: |2 f; T( Rthrough the hypothalamic pituitary gonadal axis, has
. e8 [: Q1 G& m) ]/ ?1 ^4 L: [a higher incidence of organic central nervous system
7 N4 E) o% z- H- `4 ~8 V+ ]lesions in boys.1,2 Virilization in boys, as manifested
7 o2 U; }( N* ?by enlargement of the penis, development of pubic
7 D0 T5 @# d. ~( s! Rhair, and facial acne without enlargement of testi-
" C- V# S% a4 M; S6 m5 j' @cles, suggests peripheral or pseudopuberty.1-3 We
, B, [4 _/ V- wreport a 16-month-old boy who presented with the) w1 L# t# s3 L0 U* u
enlargement of the phallus and pubic hair develop-, I8 s7 j1 I# G
ment without testicular enlargement, which was due+ }2 R& O! x& l2 `- q* x
to the unintentional exposure to androgen gel used by
. s5 L! q% ^( E2 e0 l# pthe father. The family initially concealed this infor-; }0 r& H4 {" k& E) [7 c* ?
mation, resulting in an extensive work-up for this2 a& {9 {8 [' Z, ?8 o  s9 g- C* S
child. Given the widespread and easy availability of
$ r! U8 Z9 P' E* D- {6 ntestosterone gel and cream, we believe this is proba-  m# u9 d; W9 |9 Q* W
bly more common than the rare case report in the& B0 B/ g3 \) e; |1 {; x
literature.45 T2 F& G, D6 f# i( Y% M
Patient Report
# F- b5 m8 O! N" S2 n) `  X2 ZA 16-month-old white child was referred to the
* [. Z  f1 f8 G3 P, wendocrine clinic by his pediatrician with the concern3 }  W# l& q$ d
of early sexual development. His mother noticed
% J2 ?6 |( `. slight colored pubic hair development when he was) A# ?9 Q0 S3 ~7 v+ c
From the 1Division of Pediatric Endocrinology, 2University of
6 z8 e* j4 N. gSouth Alabama Medical Center, Mobile, Alabama.
6 L/ @. H' v) TAddress correspondence to: Samar K. Bhowmick, MD, FACE,! a. H& a. N0 x* \/ C% V5 B) R' w) F
Professor of Pediatrics, University of South Alabama, College of" W' Q- u- u* h7 U/ b& \; Y( E0 z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 ]- A& T: y/ w9 |; A
e-mail: [email protected].
' J! U3 A4 q! L( j0 Rabout 6 to 7 months old, which progressively became
7 p' Z/ D( o# e8 Z! l/ Adarker. She was also concerned about the enlarge-6 a2 m" f+ h$ v" C
ment of his penis and frequent erections. The child1 S) {1 t5 d( C* Q
was the product of a full-term normal delivery, with5 G& o3 z, m- F4 f5 s# ?" b
a birth weight of 7 lb 14 oz, and birth length of
5 s/ H& z5 w, d/ ~20 inches. He was breast-fed throughout the first year
; r' g" L  Z4 G2 s3 L) eof life and was still receiving breast milk along with$ O9 k1 c& I% @; s* V9 b+ ~
solid food. He had no hospitalizations or surgery,+ B9 l: `  R& C* s2 x/ B
and his psychosocial and psychomotor development
( J# @+ ]# h+ M" c7 Gwas age appropriate.
/ p: O2 F2 k6 e5 X- v* H: aThe family history was remarkable for the father,
( e. f: C3 E* T) p( j9 M% Q' Rwho was diagnosed with hypothyroidism at age 16,1 W  T& G1 b! u: _
which was treated with thyroxine. The father’s
9 m& }. k4 u8 |height was 6 feet, and he went through a somewhat
  R6 c7 s6 v& U& Q; \0 Yearly puberty and had stopped growing by age 14.
4 {( z1 r4 v' X2 K* z, p6 RThe father denied taking any other medication. The
3 t( f2 N% L& x7 B, @) v' ~child’s mother was in good health. Her menarche( |- W% E1 D$ D& @5 M; m4 _
was at 11 years of age, and her height was at 5 feet
$ X- r1 B& g; y! o  u7 o5 |5 inches. There was no other family history of pre-
$ q& ~8 O# z1 g* n' r, Vcocious sexual development in the first-degree rela-
, p+ P  }4 |1 H/ Stives. There were no siblings.
/ p8 Q6 ~- \7 F3 U5 xPhysical Examination# J' R2 q6 d/ A. @. t
The physical examination revealed a very active,
9 B/ i% b5 w3 V" o& zplayful, and healthy boy. The vital signs documented6 S4 L5 Z5 ?+ b+ [0 N2 k  J
a blood pressure of 85/50 mm Hg, his length was
; D# o, m' r" \* W. P90 cm (>97th percentile), and his weight was 14.4 kg
% D" ~& G/ y0 G: B, f5 e6 S(also >97th percentile). The observed yearly growth
4 |5 s5 c, p) |& u) cvelocity was 30 cm (12 inches). The examination of) P8 s6 j- d/ f' j4 D- f" C# G
the neck revealed no thyroid enlargement.
- ^- k1 i* {" c; q+ |0 `The genitourinary examination was remarkable for* [4 i+ k, `) r' {6 n: B: B
enlargement of the penis, with a stretched length of
' S# O& R: ^5 P) e8 cm and a width of 2 cm. The glans penis was very well- t8 {# W' Q3 a, u# I6 X
developed. The pubic hair was Tanner II, mostly around
+ g% B3 G4 [% g3 e: k540
" w7 l0 c8 `* Z1 S9 Xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. k; ]# P3 g( T1 g
the base of the phallus and was dark and curled. The% N1 R" _$ I% |5 x+ e0 g
testicular volume was prepubertal at 2 mL each.
4 Z' X$ T4 d7 n3 J, u) {8 Z. ~The skin was moist and smooth and somewhat7 Q$ G1 R6 v6 C
oily. No axillary hair was noted. There were no% k1 }" L9 t1 ]3 y- i
abnormal skin pigmentations or café-au-lait spots.' Z5 _+ ?& @2 {: l3 M( b& M* E% q
Neurologic evaluation showed deep tendon reflex 2+4 X4 d3 O/ X1 o0 A1 c% o) x
bilateral and symmetrical. There was no suggestion
& Y, e# s4 Q6 _7 yof papilledema.$ ^2 U  _$ t( D6 _. k& ^+ q/ y& j6 U1 N
Laboratory Evaluation, L1 i( k( \+ ]( M0 Z% q" ~
The bone age was consistent with 28 months by" v' Y6 |2 h) ]
using the standard of Greulich and Pyle at a chrono-
0 h3 p6 L/ Y2 ~; T6 B1 [9 h$ Xlogic age of 16 months (advanced).5 Chromosomal
& v1 D, r' j! Ekaryotype was 46XY. The thyroid function test
* G# R3 I9 s$ l- g3 T7 G7 Gshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
/ m8 T. i1 ?0 m! wlating hormone level was 1.3 µIU/mL (both normal).
8 u" g$ z# Y/ U2 ^9 r* ]The concentrations of serum electrolytes, blood5 V4 h& X4 H' O4 F1 Y+ c
urea nitrogen, creatinine, and calcium all were
7 J8 ?2 z) T) o* m- A# h  uwithin normal range for his age. The concentration
. \+ q  g7 R1 dof serum 17-hydroxyprogesterone was 16 ng/dL2 K- b2 b! h% S) L6 D1 _
(normal, 3 to 90 ng/dL), androstenedione was 20
, N) w  z% V. O7 `( S! }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 a/ u  L0 d( J4 r6 p7 O! Q. nterone was 38 ng/dL (normal, 50 to 760 ng/dL),
* s' r, l" F& J9 F- ddesoxycorticosterone was 4.3 ng/dL (normal, 7 to: H- w$ {5 h% P: E  ^/ g) n. _: E0 ^
49ng/dL), 11-desoxycortisol (specific compound S)
0 p( K8 D: p* G- X8 v& S  S: rwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: ~  J6 a* d3 w* `- k2 `8 j' otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 z$ Q" }6 Q2 R1 e. @' etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ N% s2 f' `# @; h# U- K+ F! u' [and β-human chorionic gonadotropin was less than3 ~% y' n7 i/ Y; X5 H% Y6 Z
5 mIU/mL (normal <5 mIU/mL). Serum follicular% |) c5 h& n/ \0 O$ L) b3 ?
stimulating hormone and leuteinizing hormone
, o7 o" @2 c8 Q* v6 ]6 L3 c  M( dconcentrations were less than 0.05 mIU/mL* F- \6 F; {' Y+ l% B1 t3 ^
(prepubertal).
% L" m; T8 e* K+ j* SThe parents were notified about the laboratory
8 ~! m7 Z1 i. E/ V2 @" F, F7 j# s. @results and were informed that all of the tests were2 Z& P# M9 u: z0 H: e( d
normal except the testosterone level was high. The3 T: e  x& \9 n7 I) _
follow-up visit was arranged within a few weeks to
4 n: j4 o7 h/ J: C3 jobtain testicular and abdominal sonograms; how-& h% x9 S% r% X0 A9 t7 Q  P: e
ever, the family did not return for 4 months.6 D; f$ M! E. v, G8 C/ L" f
Physical examination at this time revealed that the& S. F8 t5 N' Q% N) T, e2 [7 B5 \
child had grown 2.5 cm in 4 months and had gained; a0 ^' I# W! I# T$ D. b4 {( ?3 l
2 kg of weight. Physical examination remained9 n) l: R9 c6 _  \& W4 P) l( R8 w5 q
unchanged. Surprisingly, the pubic hair almost com-
, [8 D7 k' Y0 z+ Y) fpletely disappeared except for a few vellous hairs at
, V+ R3 V9 `7 o  Z1 B& ?; kthe base of the phallus. Testicular volume was still 21 i; P, N- G* o8 [
mL, and the size of the penis remained unchanged.' q9 ]4 U+ H: \3 S  c- U; E9 n) S
The mother also said that the boy was no longer hav-
2 Z* S* D  I+ ~; P/ @ing frequent erections.* l! y9 k' _/ i3 d
Both parents were again questioned about use of# X- J9 f. B9 @9 D& y! t. c4 h2 m- q
any ointment/creams that they may have applied to0 s# ~, h- g5 Z& u
the child’s skin. This time the father admitted the/ W- z7 s8 S. Q- g; D  Q* [
Topical Testosterone Exposure / Bhowmick et al 5413 g7 U0 r7 R$ Q0 N+ V
use of testosterone gel twice daily that he was apply-, k" ^, z7 G& l% I4 B3 H
ing over his own shoulders, chest, and back area for* q+ y, J+ G! |: ]. S, M; l0 a
a year. The father also revealed he was embarrassed
3 J$ b, }) j' N( vto disclose that he was using a testosterone gel pre-
% G9 K7 v0 J0 y) L  H0 B+ gscribed by his family physician for decreased libido
$ i6 s$ j! {% R6 y8 A! nsecondary to depression.
; f2 X" k$ \/ |2 s7 f6 E1 G. VThe child slept in the same bed with parents.% `5 u8 p) R; U7 g
The father would hug the baby and hold him on his
+ ^* G" p/ k/ C0 V# C; E, Kchest for a considerable period of time, causing sig-
/ W6 ?$ T! {4 b1 c$ P# n! u) p+ Onificant bare skin contact between baby and father.6 N, H. L* y, t1 F
The father also admitted that after the phone call,
7 \( G. M7 v* C: {when he learned the testosterone level in the baby
$ j0 c2 s9 D: J% s/ h1 }$ Q  {( awas high, he then read the product information
1 B% u5 n  u9 }; @6 A* upacket and concluded that it was most likely the rea-* C3 d% e/ K4 z* b+ s  t
son for the child’s virilization. At that time, they
# B8 C) T3 j6 |' x4 Idecided to put the baby in a separate bed, and the  A; {% T$ p; n$ b3 D, M  m
father was not hugging him with bare skin and had
- i7 T! N5 p) l2 I, c5 p) Xbeen using protective clothing. A repeat testosterone/ s% e! x, H6 K2 @& V& G
test was ordered, but the family did not go to the
* X% h# h  W1 ~) z7 y7 |- ulaboratory to obtain the test.0 u" [: X4 r3 M0 U3 ?, h* C; h$ w
Discussion" g0 m  R6 I, Q/ s# N: k2 R
Precocious puberty in boys is defined as secondary
7 R  X5 o& b- Q; `sexual development before 9 years of age.1,4  k! Y6 D% j2 O
Precocious puberty is termed as central (true) when
- x5 ^7 ?+ A7 T2 L3 ]* @8 {; Y6 ~it is caused by the premature activation of hypo-
/ \8 j2 ?& X( S; u* X' u, s0 Vthalamic pituitary gonadal axis. CPP is more com-, @( Y0 ?% {6 S. x- ^5 I% H* F+ ?
mon in girls than in boys.1,3 Most boys with CPP4 [6 w# Y& v3 Q! f
may have a central nervous system lesion that is
0 A4 x5 ~1 t: m0 b# ~  _$ C  P# {* Presponsible for the early activation of the hypothal-7 Q7 n9 N! d/ x5 B
amic pituitary gonadal axis.1-3 Thus, greater empha-
9 N/ L- r% w3 |7 _3 zsis has been given to neuroradiologic imaging in3 x4 u+ D; I3 g1 }# y9 h. ~
boys with precocious puberty. In addition to viril-& [3 c* j$ Z8 O% Q3 b9 f
ization, the clinical hallmark of CPP is the symmet-) m2 H! C8 L8 K4 u9 u
rical testicular growth secondary to stimulation by% \4 w) Y: W6 A* W5 Q
gonadotropins.1,3( O/ R# m% @8 A/ O; o; i( w9 F
Gonadotropin-independent peripheral preco-
5 w9 m0 k, L7 Y/ Ncious puberty in boys also results from inappropriate" }# }  ?) X( y. Q7 u* l7 N: S5 W
androgenic stimulation from either endogenous or
) y. i. P* W3 h# `exogenous sources, nonpituitary gonadotropin stim-
/ c: R: F& @  {9 c9 Y- M, Y  l0 o# Xulation, and rare activating mutations.3 Virilizing2 Z/ t5 _2 F1 [3 a# H7 {! V
congenital adrenal hyperplasia producing excessive
# @" }% `& z" V- K/ _. Nadrenal androgens is a common cause of precocious# M' p+ ]6 U4 U: {  T' y
puberty in boys.3,4
7 Q0 [% l- `$ G; a( j3 d* F' EThe most common form of congenital adrenal
7 m' N2 P  d& S: Dhyperplasia is the 21-hydroxylase enzyme deficiency.. N. k' o& S3 O- b0 u: a
The 11-β hydroxylase deficiency may also result in0 q* R6 D/ M) z8 t6 U7 a5 D# [. o
excessive adrenal androgen production, and rarely,3 Z; h6 T8 b2 D+ m0 h5 ], r+ {! T
an adrenal tumor may also cause adrenal androgen
% ]% i" [- _3 ~8 u; _0 ~; a. pexcess.1,3
  \0 g7 ^# d. e" ~% eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 C: A. u8 D& c, x1 h8 q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 _8 Z3 e6 p! ]9 w# v0 hA unique entity of male-limited gonadotropin-
& J3 Y. q9 l3 ~2 x3 Xindependent precocious puberty, which is also known
3 e% W: ^; q) _% ^$ `* H; g* _as testotoxicosis, may cause precocious puberty at a
+ m* p1 a5 a1 O+ Xvery young age. The physical findings in these boys
- y+ |- V: ]* Vwith this disorder are full pubertal development,8 A; c/ P1 W: o' |/ I" u0 C
including bilateral testicular growth, similar to boys0 t! ?2 J0 r- \& P" S, H
with CPP. The gonadotropin levels in this disorder
/ i. H* e' |! C, @4 B; _are suppressed to prepubertal levels and do not show
2 O' N( b. @. _# bpubertal response of gonadotropin after gonadotropin-7 g. b) Y4 C0 }7 Y% ?) }
releasing hormone stimulation. This is a sex-linked
+ f, G% ~2 f! q( A! z$ I* sautosomal dominant disorder that affects only0 G% d2 l' M5 w- r% k
males; therefore, other male members of the family
; |9 \& ?0 a, W4 Emay have similar precocious puberty.3
3 e! k2 i; X+ x( Z  U, VIn our patient, physical examination was incon-- {% i! v7 G, k# z- r
sistent with true precocious puberty since his testi-6 ?* Y9 L6 Z6 m1 f7 e8 \/ W
cles were prepubertal in size. However, testotoxicosis
/ M  }( m) C- Q# ]* i2 ~$ Iwas in the differential diagnosis because his father
' P% {+ }7 P( E+ Xstarted puberty somewhat early, and occasionally,$ O$ T. M- K3 [1 p
testicular enlargement is not that evident in the3 Q- [$ J% D1 S, b
beginning of this process.1 In the absence of a neg-
! `5 ^2 U0 I& Y" kative initial history of androgen exposure, our0 y1 q' R) L5 H& `/ c0 f! e% u  ]8 ~
biggest concern was virilizing adrenal hyperplasia,  @& C! N: {9 c" \9 p
either 21-hydroxylase deficiency or 11-β hydroxylase- H3 Z1 B& V( s* K7 D% _( O
deficiency. Those diagnoses were excluded by find-
* N- F+ M* Z3 k. W- xing the normal level of adrenal steroids.& X: N. Q% ~( d+ _
The diagnosis of exogenous androgens was strongly
5 R* J! B" y2 @. `4 C4 |! d, esuspected in a follow-up visit after 4 months because9 K3 G* c# q. S8 t0 w
the physical examination revealed the complete disap-$ |# K0 k+ P) K4 d6 X- _
pearance of pubic hair, normal growth velocity, and
6 O  q/ m4 k1 u3 |& ?9 M1 h3 t* Z5 wdecreased erections. The father admitted using a testos-
. y7 }! Y4 J6 D. @1 tterone gel, which he concealed at first visit. He was) _* w% P. i1 K
using it rather frequently, twice a day. The Physicians’
* i; v9 x/ l# q0 F% X! \  SDesk Reference, or package insert of this product, gel or2 d. g: ?/ Z- B6 t
cream, cautions about dermal testosterone transfer to
9 S- o( k, z1 qunprotected females through direct skin exposure.# L5 F; w/ g7 Q/ ~5 x$ `  l
Serum testosterone level was found to be 2 times the/ f7 ]- j3 n3 W1 T
baseline value in those females who were exposed to
4 a9 U% U0 |; C, Q, t+ Ueven 15 minutes of direct skin contact with their male
) [2 G% [. V% [; Fpartners.6 However, when a shirt covered the applica-
6 }: U$ X9 X' v7 Z2 b- L2 S+ X7 etion site, this testosterone transfer was prevented.
' f! i8 S3 z. ]/ _% ?Our patient’s testosterone level was 60 ng/mL,
& Q. p# D' [0 a# O, R9 a; m$ Twhich was clearly high. Some studies suggest that
: l4 l+ _& S/ e- Idermal conversion of testosterone to dihydrotestos-
3 R9 n5 V& P2 p9 I& }terone, which is a more potent metabolite, is more& [, M- C1 C* |: k- C: d5 q& q
active in young children exposed to testosterone: b0 M6 j. Y9 |: ^. ?
exogenously7; however, we did not measure a dihy-: \+ ^; ~. o) G( B
drotestosterone level in our patient. In addition to
2 Z# O( `% ]% S$ Zvirilization, exposure to exogenous testosterone in$ f/ g. a' N% i# i# [
children results in an increase in growth velocity and
! l+ R5 b8 x" o" I: }advanced bone age, as seen in our patient.
/ a$ p0 _" X3 Z" E8 f. }5 |$ ]The long-term effect of androgen exposure during
# l3 L. ^2 `/ ]  |' S7 hearly childhood on pubertal development and final7 W- g! b& y: G* L& x( I8 o  F
adult height are not fully known and always remain
/ b" F. n1 `5 c) Y( ma concern. Children treated with short-term testos-2 w3 e, v( l' T, p" u
terone injection or topical androgen may exhibit some8 w8 O$ b/ h8 x0 @. s1 Y+ X
acceleration of the skeletal maturation; however, after: b; _  P  ?5 c8 A" n* w) J
cessation of treatment, the rate of bone maturation
2 e2 f# {7 m7 Tdecelerates and gradually returns to normal.8,9; ~4 Q& [2 f5 W2 h
There are conflicting reports and controversy7 J. X4 A6 p7 s! H6 Z0 J8 [
over the effect of early androgen exposure on adult
; d& M- K  Q% W! s9 X9 o; {penile length.10,11 Some reports suggest subnormal
0 Y5 y) d! v% c1 wadult penile length, apparently because of downreg-
$ M2 {( R2 J" c( ]8 y; K0 }ulation of androgen receptor number.10,12 However,
7 p6 O5 V2 b4 a8 k( a4 {3 L$ JSutherland et al13 did not find a correlation between6 F3 g# W3 R6 y+ m
childhood testosterone exposure and reduced adult0 n1 [. v; x. x) M! |% d
penile length in clinical studies.
: ?$ s  w8 P0 c/ z7 PNonetheless, we do not believe our patient is
% D' Y2 V& _2 ]& N5 `: qgoing to experience any of the untoward effects from
, O. P; E2 A) W0 {, htestosterone exposure as mentioned earlier because
; E7 x3 ^( t5 [9 Ithe exposure was not for a prolonged period of time.* S% T; D" \6 {
Although the bone age was advanced at the time of
9 }; z' r) D1 B. w/ v$ _7 p( H* g  A/ Mdiagnosis, the child had a normal growth velocity at8 H- m$ N+ N6 k! A: @
the follow-up visit. It is hoped that his final adult3 `, k3 w1 d  [$ O( Y
height will not be affected.8 `* p( Z9 O% n: x$ F
Although rarely reported, the widespread avail-
4 F6 y4 u2 X' D7 k3 j! [ability of androgen products in our society may8 d% E, d1 @  m% [
indeed cause more virilization in male or female
2 Q8 @& W' E/ J2 I& u. w" F, bchildren than one would realize. Exposure to andro-1 O: X) e0 b" O$ q& s+ A7 c
gen products must be considered and specific ques-# E. K* u/ N2 t" ]- f# l: l
tioning about the use of a testosterone product or' N& V' S) N; L% }# v  k
gel should be asked of the family members during4 U+ D) e0 n2 Q' C4 C
the evaluation of any children who present with vir-; U/ E! N+ @1 g5 L: Y$ G( d$ V
ilization or peripheral precocious puberty. The diag-
5 [/ |* v* R3 J9 p7 t. ~" inosis can be established by just a few tests and by
- R4 N+ D, G0 w$ H* Iappropriate history. The inability to obtain such a% K3 P% t: v7 v* Q
history, or failure to ask the specific questions, may
; w0 @5 |7 M4 ]result in extensive, unnecessary, and expensive
  M* e! d' N; r# qinvestigation. The primary care physician should be
$ T/ \. z, T6 F7 uaware of this fact, because most of these children$ d! ~! d7 i) g4 m% x0 g7 Y
may initially present in their practice. The Physicians’5 y( G/ L/ ]! t  {
Desk Reference and package insert should also put a
, k, H3 _9 n, ~( T- j3 T# i6 Zwarning about the virilizing effect on a male or
. Y7 t3 N3 }  Zfemale child who might come in contact with some-
3 @$ _" K" _+ F9 t3 s% C' mone using any of these products.
- U0 ^9 D8 o! ^! d& J( MReferences
4 s: c  ^9 r2 |; X" v* }& m1. Styne DM. The testes: disorder of sexual differentiation  }' r0 N! `1 B/ d4 q, Z- U5 h: H
and puberty in the male. In: Sperling MA, ed. Pediatric# C7 X% I' O5 a' S1 K. h  s3 a
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 i8 I6 t# R. \3 l3 K6 n* G" h2002: 565-628.' _, n9 f% |- F. {& T3 f% z
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 R, i. `) L# i7 T' O: Kpuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

; ~, |6 _3 I7 ?# s6 U- E! T) \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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