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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# N2 M# T, K* N! r( e! O
Boy Induced by Indirect Topical
; r: D6 x7 c0 o% u" I4 S" VExposure to Testosterone
6 ?- z- I- c. y7 L9 G1 WSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 a$ `2 \' }5 land Kenneth R. Rettig, MD1
( S; N; ]1 ]3 ~+ u7 BClinical Pediatrics
1 j' F* Y& s7 k8 WVolume 46 Number 6
% w0 J5 p8 J! _) RJuly 2007 540-543
8 b; q6 L& V( e) n5 E© 2007 Sage Publications" G* X1 c# Y$ w0 @
10.1177/0009922806296651
+ g* p4 ?+ A% l4 D6 Phttp://clp.sagepub.com# d+ ^* k6 \7 o9 X4 x$ v  \
hosted at' a! I& _( p- Y4 m5 X" v
http://online.sagepub.com
( S9 Z* }. z! s- ~, [; d4 GPrecocious puberty in boys, central or peripheral,7 Y- S7 z1 u9 J/ p+ D+ T% T( Z+ z* }
is a significant concern for physicians. Central
* r0 u( R8 M$ V- s7 L, J  w+ `precocious puberty (CPP), which is mediated9 m) u$ X( X# @/ ?$ m0 R: {
through the hypothalamic pituitary gonadal axis, has
. x/ r0 v% B" q3 I( ia higher incidence of organic central nervous system& A& A' `* g$ N  X$ K
lesions in boys.1,2 Virilization in boys, as manifested  x9 z4 N/ x- e
by enlargement of the penis, development of pubic) a+ L" D$ m: [2 w3 }
hair, and facial acne without enlargement of testi-
& i0 u8 G0 ]' Z' c: N* ]cles, suggests peripheral or pseudopuberty.1-3 We& y% \) v0 ^. H. \" S+ S3 Q
report a 16-month-old boy who presented with the
8 T2 {' G  M$ [) o2 I8 R8 C$ z$ renlargement of the phallus and pubic hair develop-# n% L- u# `0 Z' q$ _: O9 j/ W; I
ment without testicular enlargement, which was due) q" M: T7 v) F* K+ x0 z- f
to the unintentional exposure to androgen gel used by
; o3 v0 ^* t( Q# Y' tthe father. The family initially concealed this infor-
. x$ z. ]3 v# F7 g& O4 @mation, resulting in an extensive work-up for this
7 b4 j7 i; ^$ _* a! i" m6 q& Fchild. Given the widespread and easy availability of
- z7 a4 o! v+ ~, {+ btestosterone gel and cream, we believe this is proba-
5 V- X( B3 N! o& ~* ~bly more common than the rare case report in the
* \6 P" C) u/ eliterature.4
' z) c' e5 Q9 d4 DPatient Report
& J2 ^  P; `  ~) T# HA 16-month-old white child was referred to the# a+ L4 A1 W& H9 m4 V" e
endocrine clinic by his pediatrician with the concern1 N0 @( ~- s" W9 @  Y% U
of early sexual development. His mother noticed% G6 p9 H8 Y. V& t% O
light colored pubic hair development when he was, U- f9 P0 B  B# k7 O1 I9 R  H
From the 1Division of Pediatric Endocrinology, 2University of9 L- u- m. [. C# ]# d" t9 Y0 C
South Alabama Medical Center, Mobile, Alabama./ C; P' s& [4 l# s' c3 D
Address correspondence to: Samar K. Bhowmick, MD, FACE,. E$ q. b7 s, w  v; h$ s. e
Professor of Pediatrics, University of South Alabama, College of
: ]3 F; \: A4 f! WMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) k% f+ E& l- @5 W1 Z$ J2 {( x9 G
e-mail: [email protected].0 b( c. p7 e' u
about 6 to 7 months old, which progressively became
. m* j. z% K: k) Xdarker. She was also concerned about the enlarge-. b2 h, o) N& ~; }& E
ment of his penis and frequent erections. The child
$ {/ Q9 N7 K$ @; _8 ~was the product of a full-term normal delivery, with
. K% q- `' J2 ~a birth weight of 7 lb 14 oz, and birth length of
* T, j/ n# L0 c20 inches. He was breast-fed throughout the first year3 {. V0 N' a! F+ A! R9 T, }' [
of life and was still receiving breast milk along with- i+ T- f( n" h- ]* y' H( e
solid food. He had no hospitalizations or surgery,
8 d6 |- f' R; F* b# J2 F: Iand his psychosocial and psychomotor development5 m5 p/ Z  ^, w1 N
was age appropriate.. d' j7 v( b# V! k4 z
The family history was remarkable for the father,! B2 r" f2 v/ {" O$ |, {
who was diagnosed with hypothyroidism at age 16,! o$ {/ B/ A; D7 M4 _. x/ x
which was treated with thyroxine. The father’s. F, _' J/ Q& r; e" U/ F, Y) J6 m
height was 6 feet, and he went through a somewhat
+ d5 H7 E* u' \! x& }7 I' [early puberty and had stopped growing by age 14.
2 @; |5 T; I9 SThe father denied taking any other medication. The  K6 Q$ r5 v( p8 W
child’s mother was in good health. Her menarche7 s9 P$ \0 _& l
was at 11 years of age, and her height was at 5 feet' H0 W' G- t9 P- F/ z
5 inches. There was no other family history of pre-& S5 B0 w5 }+ u7 e" @. O
cocious sexual development in the first-degree rela-/ G' C2 L; ]. ]( Q; E
tives. There were no siblings.
+ G& N6 x/ L6 F8 ~/ a9 e8 PPhysical Examination
+ c1 E- s1 p  r- A( D" K( `/ QThe physical examination revealed a very active,
8 v7 X/ Z4 @" ~$ F7 D8 hplayful, and healthy boy. The vital signs documented
! }* v+ G; V& j; C, ]a blood pressure of 85/50 mm Hg, his length was+ b+ V/ A2 P7 b
90 cm (>97th percentile), and his weight was 14.4 kg( d& F9 t4 L0 C  W$ {
(also >97th percentile). The observed yearly growth
& `! L- o  c: w( D9 Xvelocity was 30 cm (12 inches). The examination of
  b; F" Y) a$ A. [the neck revealed no thyroid enlargement.
' S8 u9 |! L( d. eThe genitourinary examination was remarkable for
9 j! ]0 w$ E. P" f( I( v( Senlargement of the penis, with a stretched length of
+ F8 R( _# w8 E$ V1 s; P% n) h! K$ w8 cm and a width of 2 cm. The glans penis was very well
7 G3 s: r$ Q( A3 ~* jdeveloped. The pubic hair was Tanner II, mostly around
& C- @, j+ a1 W& T3 M! @, I540
; D: q  |1 j) n! x1 ]- r2 ~at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) J7 [( m8 j$ C5 w$ C# x
the base of the phallus and was dark and curled. The: d5 ^$ z4 C0 {* \1 i
testicular volume was prepubertal at 2 mL each.9 o. r3 y. ~8 r
The skin was moist and smooth and somewhat2 [" u! h; f3 D) ?
oily. No axillary hair was noted. There were no! {1 l+ z9 A- X7 M
abnormal skin pigmentations or café-au-lait spots.
/ ]7 H) ^4 P) w3 ENeurologic evaluation showed deep tendon reflex 2+
8 a, r5 q1 y. F7 R( [- tbilateral and symmetrical. There was no suggestion1 F: ~5 {  Q5 [# p; H5 I0 |3 b0 r: X
of papilledema." I* h2 T; c$ E
Laboratory Evaluation5 S, R' H# f1 f/ \2 d5 {
The bone age was consistent with 28 months by# A- o% |7 s( }( a- p  o
using the standard of Greulich and Pyle at a chrono-
  {6 a! Q) ?  I+ H% Vlogic age of 16 months (advanced).5 Chromosomal
( V' m/ C7 m% W' R) }( wkaryotype was 46XY. The thyroid function test
; Q' u0 f& v; S, o7 h" Vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 t8 m& K5 {1 k* ylating hormone level was 1.3 µIU/mL (both normal).# B, m0 P3 `+ ]; b
The concentrations of serum electrolytes, blood  ^; e' A% i  f/ P  X8 q
urea nitrogen, creatinine, and calcium all were
5 E7 I4 J# U0 M% I% i) gwithin normal range for his age. The concentration  U$ S2 r) R& J) b1 K1 h
of serum 17-hydroxyprogesterone was 16 ng/dL
+ g. f# M- T  c( a& A8 d/ o(normal, 3 to 90 ng/dL), androstenedione was 206 g5 J9 }1 h/ T) k
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
$ i5 q7 |$ X. W: U* Q: O" ]terone was 38 ng/dL (normal, 50 to 760 ng/dL),
$ c  y- p0 F7 u) t" ~9 Mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 u7 y$ _7 I  \0 J% {49ng/dL), 11-desoxycortisol (specific compound S)5 _8 y* ~  L# Z! j* T
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-6 f5 P: h9 |6 z" Y7 V5 R+ r; R( M
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' v0 c% l& v& H, W; f. l* B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 s1 L! E8 ~; `9 O4 u* yand β-human chorionic gonadotropin was less than1 g5 Y2 L; I3 }* I5 U3 G/ {
5 mIU/mL (normal <5 mIU/mL). Serum follicular2 I# U# p3 \2 f
stimulating hormone and leuteinizing hormone3 i% [. [5 D) K7 R* j5 p8 Q, H
concentrations were less than 0.05 mIU/mL
+ M0 }5 r$ x1 n8 e6 q(prepubertal).
* z8 ]- w4 e2 v/ tThe parents were notified about the laboratory0 Z! \1 O6 c# x5 ~
results and were informed that all of the tests were
! R7 x! @' m' R' j. @$ dnormal except the testosterone level was high. The
4 k8 V. o) X* R( N- Q' ifollow-up visit was arranged within a few weeks to9 ^* v: W4 ^1 f! C$ _, N
obtain testicular and abdominal sonograms; how-
) D6 z  j9 w1 V7 K+ k# T4 Wever, the family did not return for 4 months.. b- g' n0 M& G% L' Q* [
Physical examination at this time revealed that the
, D1 \0 P' O- T* Y/ ochild had grown 2.5 cm in 4 months and had gained
8 z8 D) p+ \1 U' a7 M3 w2 ^2 kg of weight. Physical examination remained
6 G2 v5 N) b# Kunchanged. Surprisingly, the pubic hair almost com-
6 m9 G, _- K- L8 R7 x. a2 Hpletely disappeared except for a few vellous hairs at
  a/ N* j8 c3 j, Dthe base of the phallus. Testicular volume was still 2
4 N& m+ b5 ?7 _  u2 e3 O$ ^mL, and the size of the penis remained unchanged.
: S3 e" |: \: s; U; zThe mother also said that the boy was no longer hav-
* U# t( P* d8 }% ?1 M4 qing frequent erections.
1 E- R1 L  @, t8 P, B& wBoth parents were again questioned about use of
- N7 V, ]* Y# C! fany ointment/creams that they may have applied to
3 e, F* a% ^/ x* Sthe child’s skin. This time the father admitted the1 S( Y5 x5 {2 `: {" m( D. d, |
Topical Testosterone Exposure / Bhowmick et al 541
' q% M" m; T3 I7 tuse of testosterone gel twice daily that he was apply-0 l  o, ^; |2 B0 I- X1 E& V
ing over his own shoulders, chest, and back area for2 V8 M1 U& x- b, P8 v+ W
a year. The father also revealed he was embarrassed
2 C* e0 \7 H6 q$ S0 xto disclose that he was using a testosterone gel pre-9 z8 h6 Z* E  t- g) W. |; `
scribed by his family physician for decreased libido
% s0 r& x* o) {: qsecondary to depression.6 `8 t  K2 D; Z$ y
The child slept in the same bed with parents.. `4 }# ~7 y  Y6 {( Q7 r& d: q
The father would hug the baby and hold him on his
- k; f! S4 L- K  _# Q: w8 N7 ^4 fchest for a considerable period of time, causing sig-' Z2 s7 L8 o6 V0 D
nificant bare skin contact between baby and father.# ?4 H/ N$ Y& D
The father also admitted that after the phone call,& t. L% I, ^0 E% w8 X, s  ~- O
when he learned the testosterone level in the baby- I) Y* R8 E5 G) o
was high, he then read the product information1 l3 Z" H: b4 C/ h
packet and concluded that it was most likely the rea-
8 Y; q" G5 [# f1 Tson for the child’s virilization. At that time, they
# D5 ?0 V% r  u+ {8 m: Ldecided to put the baby in a separate bed, and the
: f; y% w3 @; g- o" c$ R8 k3 X( Mfather was not hugging him with bare skin and had
" \- C$ P0 H3 q& Abeen using protective clothing. A repeat testosterone0 i5 p  E3 |0 {
test was ordered, but the family did not go to the
& L8 U# @& ~0 A" dlaboratory to obtain the test.
& \2 D0 \. c0 M$ rDiscussion
1 W. y! R4 l* D2 G, k- A  Z2 lPrecocious puberty in boys is defined as secondary
# S. N; ^0 {4 o$ {7 \sexual development before 9 years of age.1,4
9 v* ^4 {" M  |% B/ W* Q2 NPrecocious puberty is termed as central (true) when
& t. \& f" ?! G5 z+ git is caused by the premature activation of hypo-5 p; ]" g, c+ ]1 j+ Q
thalamic pituitary gonadal axis. CPP is more com-3 |  f3 x( c" c4 c( s
mon in girls than in boys.1,3 Most boys with CPP1 E4 o. u  z) U, D' Z
may have a central nervous system lesion that is/ t8 @: U, g6 _6 O
responsible for the early activation of the hypothal-
7 t9 e& D& G: m* O5 E( r, {# Zamic pituitary gonadal axis.1-3 Thus, greater empha-
' ]3 ^! f# X& V6 s. Q# h0 k) E7 Y6 @sis has been given to neuroradiologic imaging in
$ \6 ]/ F# d5 T2 y0 g" _5 [boys with precocious puberty. In addition to viril-6 M0 ]  c8 e7 M+ o/ e5 ]/ |
ization, the clinical hallmark of CPP is the symmet-+ [0 r4 k" v0 E
rical testicular growth secondary to stimulation by: @7 Q" y  A1 u# W& i0 V1 ]( H3 R
gonadotropins.1,3' H* Y1 [" _, ~# s/ {! J! D6 J
Gonadotropin-independent peripheral preco-2 Z  b% o8 S# U- t' `5 F
cious puberty in boys also results from inappropriate$ S: d- I) V0 F8 ]
androgenic stimulation from either endogenous or
2 S/ X8 ]9 p7 Oexogenous sources, nonpituitary gonadotropin stim-, ^% I  h) k: ?( F" `4 |
ulation, and rare activating mutations.3 Virilizing
% i, E/ f$ n5 J& z" o( kcongenital adrenal hyperplasia producing excessive2 b! j. E0 k5 k3 s' ~
adrenal androgens is a common cause of precocious+ I2 {* X, x( P, d
puberty in boys.3,48 Q% E) t( [% H& N, u$ ]! W
The most common form of congenital adrenal9 y+ O/ z2 ^4 \
hyperplasia is the 21-hydroxylase enzyme deficiency.
' o& Q6 @# g1 _6 K: [8 V! m, B# gThe 11-β hydroxylase deficiency may also result in
* F& a( C* y- X6 Lexcessive adrenal androgen production, and rarely,
0 P  ]# ^5 A5 `% h+ Van adrenal tumor may also cause adrenal androgen
, A8 R; [" S' \: lexcess.1,3
. Q6 x. q6 o) V6 e8 \1 Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. l% {; Q$ T( c+ `: k3 p  }! T542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 m+ ]7 f0 Z' ?1 z3 S
A unique entity of male-limited gonadotropin-4 t  B$ D- c4 P$ f
independent precocious puberty, which is also known
  G/ |* O  i/ Xas testotoxicosis, may cause precocious puberty at a  L. @9 G- X! S, x* l
very young age. The physical findings in these boys
; p1 e& T; f2 z5 Zwith this disorder are full pubertal development,' K+ z2 w/ H9 D8 H; c4 s
including bilateral testicular growth, similar to boys. L& }+ Q% C5 p: q
with CPP. The gonadotropin levels in this disorder5 d* T1 S# _* f% ^
are suppressed to prepubertal levels and do not show
2 p2 S% O$ g3 x  u) X' @4 k7 a1 @" Upubertal response of gonadotropin after gonadotropin-0 Q. p, \6 R# Z; F8 O
releasing hormone stimulation. This is a sex-linked
/ r( }; I$ C! Z4 Yautosomal dominant disorder that affects only) r( r- ]7 k1 T' e+ ^5 o% F3 A; E1 x
males; therefore, other male members of the family
3 k, y5 |, t: Q+ u0 i+ mmay have similar precocious puberty.3
+ a% [! H9 F' M5 F$ o6 U- i$ F- dIn our patient, physical examination was incon-
6 T' T; I" U2 {sistent with true precocious puberty since his testi-
. i) \# s0 x% Gcles were prepubertal in size. However, testotoxicosis
7 ~' U  g  M! x6 ~" owas in the differential diagnosis because his father) N6 u2 B" N4 t) a" {( r
started puberty somewhat early, and occasionally,
( |2 \( z7 I" @  T% |( G0 N5 L- Btesticular enlargement is not that evident in the" ?6 ~2 n/ N) Q
beginning of this process.1 In the absence of a neg-% W: K: A! C' o# O6 m* a
ative initial history of androgen exposure, our
* ^) |4 l: e. M* ubiggest concern was virilizing adrenal hyperplasia,
6 b& q+ G4 i2 m. Seither 21-hydroxylase deficiency or 11-β hydroxylase
* F3 l* x$ o7 S( Vdeficiency. Those diagnoses were excluded by find-
4 Q1 ?. ^( P  F) King the normal level of adrenal steroids.; ?2 S) U0 m! X$ S7 p- ?0 Z2 _
The diagnosis of exogenous androgens was strongly
: O5 L2 ?% {6 b# d4 l5 i: ?suspected in a follow-up visit after 4 months because
0 H9 V. v' X( r& dthe physical examination revealed the complete disap-9 G2 m/ D7 m' X5 _$ J
pearance of pubic hair, normal growth velocity, and
+ b9 J, i. {8 O! @/ y1 gdecreased erections. The father admitted using a testos-, v$ b' a% U+ g( C7 p
terone gel, which he concealed at first visit. He was, M, E' \# ~5 ^2 u& U$ L
using it rather frequently, twice a day. The Physicians’
( P5 B* E8 F0 b. E  L* a4 kDesk Reference, or package insert of this product, gel or& j2 R7 J$ o/ }- r7 z
cream, cautions about dermal testosterone transfer to2 P# W3 h, N+ d& ]$ m- b
unprotected females through direct skin exposure./ V! @: R. c4 _& b
Serum testosterone level was found to be 2 times the
; h) G$ k2 a: y( {baseline value in those females who were exposed to$ L  L. K) z/ t7 W& G" Y
even 15 minutes of direct skin contact with their male! ?8 `( D! ?. }9 @3 c- o, X
partners.6 However, when a shirt covered the applica-
  A9 V, w2 f# f1 @5 vtion site, this testosterone transfer was prevented.' v) A- ~8 ~) R2 t* X# `
Our patient’s testosterone level was 60 ng/mL,
5 g/ C) {: f6 W) |" r( @3 hwhich was clearly high. Some studies suggest that
$ s$ W( C$ S' W1 h! bdermal conversion of testosterone to dihydrotestos-
- J4 x0 s  C" Gterone, which is a more potent metabolite, is more( x. h* F2 p( F$ z$ r5 |
active in young children exposed to testosterone
) w3 ]/ T; _3 Y4 H& H1 lexogenously7; however, we did not measure a dihy-' g/ q3 a0 s9 ^; f# e
drotestosterone level in our patient. In addition to
: R9 D( P$ [  ^0 q% h; D4 G5 Dvirilization, exposure to exogenous testosterone in
8 [2 c* @5 A5 v# Y0 c" [& xchildren results in an increase in growth velocity and
' v& G, ?3 P8 m7 J5 eadvanced bone age, as seen in our patient.2 L3 {7 u1 H! X9 \  X  I) @8 O& Q
The long-term effect of androgen exposure during  P! }8 ~. o6 V9 ]/ V. J: T
early childhood on pubertal development and final$ O5 E( p  c& N3 [
adult height are not fully known and always remain% Q6 e% t+ g' b  Y5 N1 D
a concern. Children treated with short-term testos-
' x( g. H. V3 q# K* m2 Eterone injection or topical androgen may exhibit some$ a8 ^# ?2 A7 m/ r$ ?" M6 d$ t
acceleration of the skeletal maturation; however, after
  I$ Q; @. I) |9 j$ Ecessation of treatment, the rate of bone maturation8 V+ O, ?" E' t  p
decelerates and gradually returns to normal.8,92 M6 n! n/ G3 T1 p6 n
There are conflicting reports and controversy8 d7 G/ b) w) e6 ~# {- w) R& m! j$ Q
over the effect of early androgen exposure on adult
: y% @& x) ~: q! G5 o+ tpenile length.10,11 Some reports suggest subnormal
) n% F/ `& A3 H+ Padult penile length, apparently because of downreg-
: r9 @, P: E( f4 o! S2 b/ qulation of androgen receptor number.10,12 However,* S4 i+ P4 l1 F7 E$ ?
Sutherland et al13 did not find a correlation between8 A& F/ v1 y- y8 q# |6 E
childhood testosterone exposure and reduced adult
8 b4 Z7 h% w, J* {( |! g3 }penile length in clinical studies.
4 a& J, ^2 u( @# }* V& xNonetheless, we do not believe our patient is
9 M% X% h) s8 e" L, E& }% @" W' jgoing to experience any of the untoward effects from# {! _- R6 U  o; q
testosterone exposure as mentioned earlier because$ i; h) y9 y& R3 ]  `0 n0 Y$ a
the exposure was not for a prolonged period of time.( U( X0 G' G8 E) V0 ]* w. r* h
Although the bone age was advanced at the time of3 M1 A; U: ]# I9 s" ?
diagnosis, the child had a normal growth velocity at
5 n( q# n$ l2 u8 ~  Tthe follow-up visit. It is hoped that his final adult
; X$ V9 {: G8 W; G% o4 hheight will not be affected.
1 W4 l" z+ A2 f4 A  YAlthough rarely reported, the widespread avail-
4 ]4 e( u# h% }& y2 U( x" r- t( Uability of androgen products in our society may
1 g8 r: l0 ?$ \& K, W7 P. \' Pindeed cause more virilization in male or female
8 c( t' Z* D2 \: O. Fchildren than one would realize. Exposure to andro-
9 k; e% N6 E2 M% v6 egen products must be considered and specific ques-
2 P/ D- B6 ]0 o3 u8 Ttioning about the use of a testosterone product or/ ~- t) v( |5 m: a) L. s
gel should be asked of the family members during2 t9 d0 j! g, p' j9 [5 }
the evaluation of any children who present with vir-
/ {% B3 x  `: x- m( e3 Rilization or peripheral precocious puberty. The diag-
* Z8 d( `0 `  {nosis can be established by just a few tests and by+ X' L; ^+ {$ y2 ?$ ?5 A
appropriate history. The inability to obtain such a
: D) s* y  _& q4 p) |history, or failure to ask the specific questions, may2 Z9 K3 T6 w  V  U) J" G' _
result in extensive, unnecessary, and expensive
' G" }6 w$ S8 s* Qinvestigation. The primary care physician should be+ ^- T9 G1 }1 W5 a6 j+ i) C; p
aware of this fact, because most of these children' n% D+ b, a! ~3 m. Y/ H. L8 h
may initially present in their practice. The Physicians’
& Y+ h' j9 U8 Q& P* tDesk Reference and package insert should also put a
- x% g. M  Y/ G' Y, z# Kwarning about the virilizing effect on a male or; }/ A* g2 A" H0 p
female child who might come in contact with some-
  y/ K% D3 ?( Fone using any of these products.
5 m* v  A3 }2 f/ tReferences2 m3 p, K- ^+ ~- T5 f
1. Styne DM. The testes: disorder of sexual differentiation
. o8 @: L- R8 A% qand puberty in the male. In: Sperling MA, ed. Pediatric! s6 b) _6 y) _+ R7 F+ |
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 O/ f* a& I6 A. U2 b3 x2002: 565-628.
6 h; S# _* X. \4 ]2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ ]+ y" f/ F( G% i! Jpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old4 b( O; `( j" n4 _  V7 }
Boy Induced by Indirect Topical
1 A3 F9 z1 O8 R9 z" ~4 C; }8 hExposure to Testosterone# Y* W- C* p& R5 {& P4 [
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# {7 q$ O7 v/ \+ f% vand Kenneth R. Rettig, MD12 d+ @+ s4 w8 ~; o7 Q( {* L5 n) T
Clinical Pediatrics6 s7 j# @& a# d5 _4 Y
Volume 46 Number 65 Y& o  o" c+ g! G2 l, f
July 2007 540-543
5 o: i& V' h- B© 2007 Sage Publications
- k# N+ G6 u0 e9 k7 K10.1177/0009922806296651
+ w, W5 r1 @& \& Ahttp://clp.sagepub.com; U0 b" H! k" F% ^$ b, I- b
hosted at0 k: F9 D& ~; ^) R/ W; _/ v& o
http://online.sagepub.com
/ v* `+ T& H6 v& U" @5 f/ ZPrecocious puberty in boys, central or peripheral,
1 }, ^" K6 m: E  [is a significant concern for physicians. Central
. z5 ]- V' u/ l3 v# vprecocious puberty (CPP), which is mediated
8 d0 t' Q) y$ X" Z0 U- K2 m0 T9 zthrough the hypothalamic pituitary gonadal axis, has5 L; g! Z, C) K9 e4 a
a higher incidence of organic central nervous system4 ]  E/ w) [0 v: E) f) K3 d
lesions in boys.1,2 Virilization in boys, as manifested
1 N2 B7 w% ?$ H6 c7 S3 U" Hby enlargement of the penis, development of pubic: h5 D4 G& O* i" u% X5 k
hair, and facial acne without enlargement of testi-8 \2 g1 ~4 q/ e: b) C
cles, suggests peripheral or pseudopuberty.1-3 We
- W2 R: d& x" z' {0 J6 `) \report a 16-month-old boy who presented with the/ ^& A& \) R, K( |- h* E3 X
enlargement of the phallus and pubic hair develop-8 t" i+ o0 U2 n! Q# @$ D
ment without testicular enlargement, which was due( b8 y: @  a. ?; o7 s
to the unintentional exposure to androgen gel used by, q7 r& @# K! j2 k% ^+ r; k6 S, U
the father. The family initially concealed this infor-: Z8 C% U# F. r. d( L
mation, resulting in an extensive work-up for this
) D5 [' K/ i, b3 U4 S/ Jchild. Given the widespread and easy availability of
4 Y  v# q2 W# I/ T. J% Y* Btestosterone gel and cream, we believe this is proba-
$ p3 C# j3 k. N6 [bly more common than the rare case report in the
+ s4 S# y0 _8 ?8 j( H$ Lliterature.4- I- W& S) z; s: @5 ]
Patient Report/ @* G* B. p* v- g/ S+ H
A 16-month-old white child was referred to the1 \6 W0 h5 v3 _! g
endocrine clinic by his pediatrician with the concern
% E6 g/ Q4 Y% c: y/ q' s1 ^of early sexual development. His mother noticed! Q. J) I2 u3 k& U2 J" a
light colored pubic hair development when he was
# ]/ s' K" |9 n" k, V$ \+ xFrom the 1Division of Pediatric Endocrinology, 2University of% q' B- ~: X6 B' o
South Alabama Medical Center, Mobile, Alabama.6 l. Q, T* ]# F6 x( U2 q4 [: V
Address correspondence to: Samar K. Bhowmick, MD, FACE,
. E2 v2 w! C" Z$ UProfessor of Pediatrics, University of South Alabama, College of
1 `8 r/ S6 R4 E6 K4 O: E; [" pMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 f) |3 m% {( r4 z, q0 A) l+ B
e-mail: [email protected].; v$ E; ?1 @; M( d) B
about 6 to 7 months old, which progressively became1 S0 E* _4 ]5 |# c' U# x- n1 J- z# r
darker. She was also concerned about the enlarge-5 W( i+ g* j! G% Y7 Z3 r
ment of his penis and frequent erections. The child
: h+ P+ y) e/ v6 [7 m  jwas the product of a full-term normal delivery, with
$ f, ]1 t+ |! \6 y. Ja birth weight of 7 lb 14 oz, and birth length of8 N* M, P) b7 \' q" U; ?
20 inches. He was breast-fed throughout the first year
! \* s6 Q- g( N% t8 n: Rof life and was still receiving breast milk along with
& @% T2 o3 b; {: H' ^- W& _) msolid food. He had no hospitalizations or surgery,$ I  ^, L$ Q6 p0 m
and his psychosocial and psychomotor development
' V1 B% Y7 B# p( gwas age appropriate.% P3 W: [" A1 T9 i4 w
The family history was remarkable for the father,% y: q% d5 a+ X: k4 W
who was diagnosed with hypothyroidism at age 16,
1 Z' m( j+ y) w5 }. _. I) Iwhich was treated with thyroxine. The father’s! {$ m. F! t, Y$ a
height was 6 feet, and he went through a somewhat
7 x. ^) c  a- Jearly puberty and had stopped growing by age 14.
3 C  u0 R1 a7 t( A9 V# pThe father denied taking any other medication. The
/ g4 Q+ Y0 A$ ?/ m9 echild’s mother was in good health. Her menarche
. [! Y) Z! D  g: j# T* Bwas at 11 years of age, and her height was at 5 feet
" p/ u4 [, l: x  z* e7 d/ k5 inches. There was no other family history of pre-% y- r1 u; f9 r  H% j) F
cocious sexual development in the first-degree rela-. \/ [& X0 T7 r& _. K0 |
tives. There were no siblings.+ u- n" b1 f& w3 @* b! O
Physical Examination" X; m! J7 I5 U" Y1 Y
The physical examination revealed a very active,1 Q" h% G" h" {& V" [' I
playful, and healthy boy. The vital signs documented7 i, u  v: d5 I, }: j8 ^
a blood pressure of 85/50 mm Hg, his length was
% @6 V: o+ p- r, Z, D6 z90 cm (>97th percentile), and his weight was 14.4 kg
5 \% R3 V4 g- R& ](also >97th percentile). The observed yearly growth( `. R3 \2 J8 F. U1 M/ S" U6 k
velocity was 30 cm (12 inches). The examination of9 |; h5 N. }; F' u3 E# D9 B- S
the neck revealed no thyroid enlargement.
, q0 _; O: z6 C2 v. N1 F7 FThe genitourinary examination was remarkable for
/ m) l+ E1 e, w/ \/ c; T% Qenlargement of the penis, with a stretched length of
7 u- e& D7 `6 z* @( {; }8 cm and a width of 2 cm. The glans penis was very well
# b+ n0 i* m* R" B6 V- tdeveloped. The pubic hair was Tanner II, mostly around2 M* ]" z  {3 T1 ~
540
4 P  P% w' l, Jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& R3 m4 @' T5 m' m$ g; ?# {7 M2 l# m
the base of the phallus and was dark and curled. The
6 D4 B- z  j2 \0 Ltesticular volume was prepubertal at 2 mL each., A  |  {0 ^  o# T; p% F. s0 U
The skin was moist and smooth and somewhat
5 T) w+ G, E9 p3 m, roily. No axillary hair was noted. There were no. Q% F+ A$ Z3 K' |( M9 \& e
abnormal skin pigmentations or café-au-lait spots.
9 b9 j, i" y$ ]9 o2 yNeurologic evaluation showed deep tendon reflex 2+
3 T+ H: q) t% Lbilateral and symmetrical. There was no suggestion4 e3 ^0 Y9 x- |" N
of papilledema.7 ~8 E3 T0 q$ E) v" ~- Y
Laboratory Evaluation! l( {5 F7 z+ h* N! q
The bone age was consistent with 28 months by$ V  i8 g' R; ?9 t: N$ L( {
using the standard of Greulich and Pyle at a chrono-2 n% p5 I! S) A6 a& q7 u
logic age of 16 months (advanced).5 Chromosomal* ]5 f$ g8 s9 ?; E* [4 m
karyotype was 46XY. The thyroid function test! }% w$ C' ^3 h
showed a free T4 of 1.69 ng/dL, and thyroid stimu-: v3 K0 J8 U! D7 [$ v% n
lating hormone level was 1.3 µIU/mL (both normal).
5 }& T0 D# {' k  s; h' l' KThe concentrations of serum electrolytes, blood
, D' T  L  W7 u+ p- }urea nitrogen, creatinine, and calcium all were7 t/ o0 C: h5 F- s- U. z6 i1 i
within normal range for his age. The concentration# n' M- }& j+ M, n9 P
of serum 17-hydroxyprogesterone was 16 ng/dL: \. A, v& ]* f7 s
(normal, 3 to 90 ng/dL), androstenedione was 20
( F1 \: ?( ~4 Dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 s7 c' F; R  g7 d+ Z2 D8 wterone was 38 ng/dL (normal, 50 to 760 ng/dL),
! W  I# @3 I5 j: ?# a3 T) ndesoxycorticosterone was 4.3 ng/dL (normal, 7 to- a7 Y+ A  G# }; T9 Q3 X
49ng/dL), 11-desoxycortisol (specific compound S)* O+ C& e5 |$ n2 X
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ Y% B% ?. h6 R. D0 rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total( V4 e! `# y  y5 u4 X
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
% r  r3 @% v* B. r" h  U! Wand β-human chorionic gonadotropin was less than
2 B5 e# `1 G  N3 i; i5 mIU/mL (normal <5 mIU/mL). Serum follicular$ |& _: _( `; G. J0 F( M: d3 K
stimulating hormone and leuteinizing hormone7 s& Z# s8 C& ]& `  q
concentrations were less than 0.05 mIU/mL3 [# d' ^, c' A! G8 I7 `! k- F1 M
(prepubertal).. a# `) l4 ~3 G8 I, E
The parents were notified about the laboratory( B8 z. T7 C! Y1 o2 M
results and were informed that all of the tests were( C, s5 |/ v) c4 u
normal except the testosterone level was high. The
$ p! ^' {2 Q# [: J) K" |: Ufollow-up visit was arranged within a few weeks to* R% Z, T' r/ x5 d: C
obtain testicular and abdominal sonograms; how-9 p* g. I$ K7 s8 J, \' S; l
ever, the family did not return for 4 months.& Z/ k2 t2 N5 Z
Physical examination at this time revealed that the; I1 g( A  F8 Q- m9 |7 r' ~& @4 _/ L
child had grown 2.5 cm in 4 months and had gained
% j' y* d  O0 N" T  `1 i4 a2 kg of weight. Physical examination remained, K" `" l/ c. H/ \, @+ {
unchanged. Surprisingly, the pubic hair almost com-
0 `6 f* {7 f$ m* s6 Lpletely disappeared except for a few vellous hairs at: y8 ]2 e9 d! A+ m  u
the base of the phallus. Testicular volume was still 26 t2 M. n2 m* X
mL, and the size of the penis remained unchanged.5 i2 ]; d$ ~1 S: J4 h+ u
The mother also said that the boy was no longer hav-
9 |* L. F: M' }. Zing frequent erections.
: ?# N2 I/ N# i; v" ABoth parents were again questioned about use of
6 l; j5 h6 s: p; a0 G6 f& Cany ointment/creams that they may have applied to
. v( q  T2 J) ^' z1 N& b6 ]the child’s skin. This time the father admitted the
3 C& E9 B0 B$ ~3 o! R" `Topical Testosterone Exposure / Bhowmick et al 541
* m3 l' O. O: v$ B4 Ruse of testosterone gel twice daily that he was apply-! z9 K; ]( n' p0 b$ j/ l# m# C
ing over his own shoulders, chest, and back area for
2 p& b; x/ n! _7 |a year. The father also revealed he was embarrassed+ y$ A4 I# e6 m1 P8 @% b. N  D
to disclose that he was using a testosterone gel pre-
5 x5 O4 x+ u" U0 Oscribed by his family physician for decreased libido
. P! x7 \" U6 P$ I& dsecondary to depression.2 F& r$ j+ E$ u! o
The child slept in the same bed with parents.
7 f- L1 Q* U0 L! E7 p5 AThe father would hug the baby and hold him on his' }. a- s2 S: I8 j2 c* {
chest for a considerable period of time, causing sig-/ K; O; h% w, {9 C% F! N' S
nificant bare skin contact between baby and father., w3 t# b6 |4 [" y, n7 A" \* W
The father also admitted that after the phone call,, x6 C0 ?& p0 d
when he learned the testosterone level in the baby
( k: L+ G& v) Q6 rwas high, he then read the product information. y5 a! C9 Q7 }, r& g6 d, a% T7 e! z
packet and concluded that it was most likely the rea-
7 `2 k( `! b3 w: e2 e* a- vson for the child’s virilization. At that time, they
7 Q& Q. A( `& |6 r% d. P/ }decided to put the baby in a separate bed, and the
- T0 v- U& n! d; R; [# |father was not hugging him with bare skin and had
7 a6 _2 }1 m. }3 v* T, `been using protective clothing. A repeat testosterone" `0 O4 T9 O) w8 s4 q6 R: p
test was ordered, but the family did not go to the& `7 N6 l( @/ P  t& L7 m) j' l- q
laboratory to obtain the test.
/ [) T: L( O8 n6 |7 n; D8 W" TDiscussion
: u' ^1 y7 V. ePrecocious puberty in boys is defined as secondary
, F3 l( E( }8 r4 }8 y: s& V$ lsexual development before 9 years of age.1,4
" I; |) i' p0 J0 vPrecocious puberty is termed as central (true) when
) ]; N6 H+ C0 X9 wit is caused by the premature activation of hypo-
$ h: C) o6 F5 W0 u4 sthalamic pituitary gonadal axis. CPP is more com-* f' R3 e3 u* {; L6 F& g4 r1 p
mon in girls than in boys.1,3 Most boys with CPP
" [6 \" }9 f/ N3 C9 n" t8 |+ T: Amay have a central nervous system lesion that is% f' L7 l: b1 ?" W& Q
responsible for the early activation of the hypothal-
  z3 B' S# s1 s; k  p# ?amic pituitary gonadal axis.1-3 Thus, greater empha-$ U7 O* n  f/ m3 j7 u0 g
sis has been given to neuroradiologic imaging in
. ^5 ?: ]$ \/ O2 I4 `boys with precocious puberty. In addition to viril-# F1 e) e0 N  r3 Y
ization, the clinical hallmark of CPP is the symmet-/ U' q8 ~( I* I& G  ]4 F
rical testicular growth secondary to stimulation by
" m! O. w# M" Q# O" ngonadotropins.1,3( V, T. ?+ F8 m) ]; Q
Gonadotropin-independent peripheral preco-
; J7 ^4 r2 b' P+ ?3 \( Ccious puberty in boys also results from inappropriate
% {1 u. @( w7 V. A: e8 I/ X$ Landrogenic stimulation from either endogenous or
& k* L. x8 k2 q# y9 Nexogenous sources, nonpituitary gonadotropin stim-. d: N$ U( U5 M7 Z- \% P
ulation, and rare activating mutations.3 Virilizing
; s& K2 i& Z4 [' c8 ^) Z6 o# g1 w8 xcongenital adrenal hyperplasia producing excessive
3 R2 a1 j/ s. Q/ K9 O/ fadrenal androgens is a common cause of precocious
/ D: q% |& n5 W& C2 r/ M4 Y9 Epuberty in boys.3,4
2 Z4 a- v- @* W5 O; E3 {8 kThe most common form of congenital adrenal7 J3 v8 f1 t6 D( Y+ S3 f; b" k+ b: X
hyperplasia is the 21-hydroxylase enzyme deficiency.7 a- G7 [9 s# B- e. d2 K' t8 c5 S
The 11-β hydroxylase deficiency may also result in5 M) v; _3 |% |4 S
excessive adrenal androgen production, and rarely,* u4 ^% O7 M1 _2 |6 Y
an adrenal tumor may also cause adrenal androgen7 \1 }! Q2 |* C5 |( {( o- @
excess.1,3: S2 t3 g, @1 Q+ {
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" L. w3 Y1 u6 D+ I
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& s9 V. ~7 @/ Q4 b$ ]- u8 a/ L
A unique entity of male-limited gonadotropin-
3 h/ B) h0 Q) l8 e6 vindependent precocious puberty, which is also known% b: O- F6 @5 [
as testotoxicosis, may cause precocious puberty at a
, O( T3 Q' h- p* h* n3 cvery young age. The physical findings in these boys6 y' a6 I, w4 O. H
with this disorder are full pubertal development,
' q% |9 i7 e  u2 n* P) T9 Z  N6 eincluding bilateral testicular growth, similar to boys
3 T- R. y& r( Q- J. e1 X2 w+ ~2 ~with CPP. The gonadotropin levels in this disorder
+ N: S- I" k/ D; Q& K1 r0 |% gare suppressed to prepubertal levels and do not show
6 Y3 d( `" o. ~) E) V' O* Ypubertal response of gonadotropin after gonadotropin-
1 o2 t, w' D$ Z0 R5 U" E7 wreleasing hormone stimulation. This is a sex-linked
8 c( k( j% W3 B; Q  F5 a/ U' W( ~% Qautosomal dominant disorder that affects only
+ b3 Z+ ]; c5 }) Omales; therefore, other male members of the family& K$ s3 e0 o  B: u# I2 k- B
may have similar precocious puberty.3( \- x6 t' C6 m- E7 z
In our patient, physical examination was incon-* e; B( M2 h3 l, _
sistent with true precocious puberty since his testi-) {1 s, b$ T0 f% Z8 D
cles were prepubertal in size. However, testotoxicosis
* @- N, A3 [% G- I: ewas in the differential diagnosis because his father2 A8 _, w1 B# A% |
started puberty somewhat early, and occasionally,4 B% z7 h7 Z4 h% l3 f" K9 e2 ^
testicular enlargement is not that evident in the
6 j- f) U. N  j4 h- ]beginning of this process.1 In the absence of a neg-5 b4 ?9 `9 G4 m/ O( k: g' e
ative initial history of androgen exposure, our! h7 v9 A1 c5 a  ~# `
biggest concern was virilizing adrenal hyperplasia,/ `9 z2 z8 K0 Y# D6 z4 v- W
either 21-hydroxylase deficiency or 11-β hydroxylase
  _; l2 i) ]3 V/ C# [& edeficiency. Those diagnoses were excluded by find-9 B% I+ X$ s) I2 m* h
ing the normal level of adrenal steroids.
) p9 o  d) `! _* u9 k- j/ pThe diagnosis of exogenous androgens was strongly* f( m- l" c) Q" V# f
suspected in a follow-up visit after 4 months because
, p; b5 g# N$ ~% \7 ]" Kthe physical examination revealed the complete disap-
) m/ H6 ~  e' D3 Y/ Y& `5 y, ipearance of pubic hair, normal growth velocity, and5 I$ t9 H, r, R; \/ V2 z( G1 \9 m* @
decreased erections. The father admitted using a testos-) K2 Q% X6 y; q2 ^! S8 m/ M4 D
terone gel, which he concealed at first visit. He was
# H5 s' V2 |2 `) @using it rather frequently, twice a day. The Physicians’! J2 ?* p' z7 w- D* E  k. L
Desk Reference, or package insert of this product, gel or
+ ~# [/ n& `' m8 X' T7 V5 ?cream, cautions about dermal testosterone transfer to0 l; r9 e1 v  B5 P" ]0 G
unprotected females through direct skin exposure.9 I5 `  E' ^: s) K3 b5 R" q% K/ [
Serum testosterone level was found to be 2 times the" D/ v# w8 a/ ?  `& M. B; Z
baseline value in those females who were exposed to/ l9 v5 T9 r1 H2 M+ o  T4 j
even 15 minutes of direct skin contact with their male' h& U0 Q5 J' m/ j" |4 M) a1 p9 F) X
partners.6 However, when a shirt covered the applica-
: K, T" U6 \5 S9 d+ F0 V) M3 s9 q; _tion site, this testosterone transfer was prevented.& e% Z/ D" \4 p. r
Our patient’s testosterone level was 60 ng/mL,: Z7 x6 w% h0 ^) u, {
which was clearly high. Some studies suggest that- I- x' f/ ?" I- A# u2 c; ]
dermal conversion of testosterone to dihydrotestos-/ S' _% |- {1 Q, i: ~
terone, which is a more potent metabolite, is more' H" B) K! k8 Z" y) l  W
active in young children exposed to testosterone
1 D* H4 r# t; T* {  Xexogenously7; however, we did not measure a dihy-/ i9 z7 h- B$ s0 i
drotestosterone level in our patient. In addition to
& I# k& E7 c( e' \. h  Fvirilization, exposure to exogenous testosterone in9 ^$ K" s$ j2 m
children results in an increase in growth velocity and5 {! J: J* a: J4 l* I
advanced bone age, as seen in our patient.
6 j6 _% g4 `  @5 h" C. ^6 J6 |: r$ jThe long-term effect of androgen exposure during
- P% w6 _4 H' r- o: Rearly childhood on pubertal development and final+ |5 X4 \4 |* A* f# Y' Y4 t+ ^
adult height are not fully known and always remain
( N1 }+ ]% P: S0 w8 F! na concern. Children treated with short-term testos-
5 z5 X+ \, ?" z& P" C: M/ dterone injection or topical androgen may exhibit some
* I  i/ e6 @: I3 P- Aacceleration of the skeletal maturation; however, after" l- F* [1 `4 }& P, X+ M
cessation of treatment, the rate of bone maturation
( f" S% }5 e* b& q1 Y5 hdecelerates and gradually returns to normal.8,9
$ y: M- r9 k" X6 i5 O# f- }There are conflicting reports and controversy
1 Q3 q: I7 P6 N* o, H. F2 lover the effect of early androgen exposure on adult& ^1 I( `3 ~  Q7 z
penile length.10,11 Some reports suggest subnormal
0 N; |  Y% r! i) Nadult penile length, apparently because of downreg-
2 i: K) H6 m: f) T3 Nulation of androgen receptor number.10,12 However,6 ?2 M" _6 Q0 s! z. B
Sutherland et al13 did not find a correlation between2 j) G0 p/ n+ G7 o  X
childhood testosterone exposure and reduced adult+ B/ \+ c# C6 m9 t, G3 Q% ], ]! v
penile length in clinical studies.1 z/ q8 w' c9 z5 o
Nonetheless, we do not believe our patient is
7 \4 _' f% f9 P. O: vgoing to experience any of the untoward effects from" ~* s/ ^' v, x4 U
testosterone exposure as mentioned earlier because
, U, G% _: W7 |6 x7 u' qthe exposure was not for a prolonged period of time.
; C" H' U9 W5 s6 L/ hAlthough the bone age was advanced at the time of: B7 {( ]! |( r: k% U  T1 F/ l
diagnosis, the child had a normal growth velocity at
2 K& q* ?7 ^$ K$ g  |7 \the follow-up visit. It is hoped that his final adult( j4 C% _0 a- F2 g; C/ s( G8 s. J! Z
height will not be affected.
: }3 n7 a9 J: W$ T  T% o, eAlthough rarely reported, the widespread avail-
% n  \3 H7 ]$ Uability of androgen products in our society may
7 H; _* T3 t8 U0 A  Lindeed cause more virilization in male or female( a4 o% I/ |/ M) v$ o
children than one would realize. Exposure to andro-* A) f+ x9 |  V5 J: T( I) s
gen products must be considered and specific ques-) E3 D- x0 C; |$ B, p. s) h
tioning about the use of a testosterone product or9 O8 ^" u/ u3 n6 J+ x& o
gel should be asked of the family members during
! @/ X( ]2 f* j) Y" D, F3 g8 ^the evaluation of any children who present with vir-
( L6 ?7 G) C* l$ n$ D, Silization or peripheral precocious puberty. The diag-) D* N7 E) ~5 U
nosis can be established by just a few tests and by2 F& C, K! B+ B( b
appropriate history. The inability to obtain such a
3 I/ B" n1 _* rhistory, or failure to ask the specific questions, may- |# C0 G9 @8 q$ p+ K% y% p& H
result in extensive, unnecessary, and expensive% W2 `4 I" n4 v
investigation. The primary care physician should be2 R  q: G+ f* P& T
aware of this fact, because most of these children  F/ i* E1 C8 m! }* m1 Z9 z; l. F. M
may initially present in their practice. The Physicians’! g. m) ^, c5 i
Desk Reference and package insert should also put a3 D& n  A7 a2 X2 t; ?# {1 C
warning about the virilizing effect on a male or
. w2 |% E/ g) g( T) u& Pfemale child who might come in contact with some-
8 r8 i8 Z+ B0 n1 A/ C: U/ I" @+ Lone using any of these products.
5 b, m) \- X3 K# Y( X% a" mReferences# ^2 R% X6 h- C5 o
1. Styne DM. The testes: disorder of sexual differentiation
. R  {! k5 V! a2 u5 band puberty in the male. In: Sperling MA, ed. Pediatric
. F  b8 i6 n' v/ o. n& K8 |+ ]* B" t. ?Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; a% V! j' q  r5 w0 a2002: 565-628.* m' e% f$ V% U6 g3 U" k8 r
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 B( j, ?8 C/ {
puberty 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
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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
  X* K3 E) }4 q* f
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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