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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old
2 w9 e! e7 H+ RBoy Induced by Indirect Topical  N  Y  ^5 v; D+ e1 l
Exposure to Testosterone
" U# N% E6 k  h) {Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  h$ x- {, W6 N1 Q& h
and Kenneth R. Rettig, MD1
3 P0 c- i, D) i5 P4 X& U, O4 |- ~Clinical Pediatrics; }6 n, n4 X$ L& A4 K! P
Volume 46 Number 6) A: N" D' g1 M* @
July 2007 540-543) K1 W# r4 f- n& x( \: q1 b" V
© 2007 Sage Publications9 {$ b+ I) l$ O1 Y' U
10.1177/0009922806296651% n' b% |3 g- {5 {3 w( o
http://clp.sagepub.com
" W9 b8 s: v( l5 `hosted at
7 f! z1 t: a" W+ W4 Y; \http://online.sagepub.com
; S) F5 I3 [0 J7 JPrecocious puberty in boys, central or peripheral," b9 E8 m7 j# D, k, ^$ ~+ j# P
is a significant concern for physicians. Central  |6 {6 q0 u3 L) M, s, e
precocious puberty (CPP), which is mediated/ p/ i$ ?8 Z$ N/ A. n; S  i
through the hypothalamic pituitary gonadal axis, has& c! F/ g8 |6 H9 p3 o3 P" b8 l, D
a higher incidence of organic central nervous system; t- n$ Y! K/ M. a; ^
lesions in boys.1,2 Virilization in boys, as manifested' I$ ]' W- j. J3 c
by enlargement of the penis, development of pubic# z8 L* a' s6 Y8 c: s+ N: n* t
hair, and facial acne without enlargement of testi-+ y. `8 }  O0 |& {
cles, suggests peripheral or pseudopuberty.1-3 We
3 ^. L" Z, w  f4 b0 p, X- Ureport a 16-month-old boy who presented with the
2 {2 z- l7 ^0 x' Senlargement of the phallus and pubic hair develop-4 A8 r( F9 g5 t( e
ment without testicular enlargement, which was due; f% W" k5 I+ d/ I
to the unintentional exposure to androgen gel used by5 p: E% \8 ~1 w1 w
the father. The family initially concealed this infor-
# Y$ Q' a) g, B4 q. Bmation, resulting in an extensive work-up for this
; Z$ R) m# n0 _child. Given the widespread and easy availability of
8 @1 ~4 j6 h& J# q% Dtestosterone gel and cream, we believe this is proba-
  a0 I! |' r5 Ubly more common than the rare case report in the  ~" e: [1 D$ e/ \5 a" u
literature.4" R5 G& e  R: y  B5 I/ _
Patient Report' f% u% X6 Z  r* z( e* t$ a( V
A 16-month-old white child was referred to the
; ]7 @. c! m" j* `( k6 \' J0 j0 Zendocrine clinic by his pediatrician with the concern2 \* e3 D4 b; d$ m9 d
of early sexual development. His mother noticed
2 P8 A1 L7 P2 Jlight colored pubic hair development when he was! J9 \0 t: X& M
From the 1Division of Pediatric Endocrinology, 2University of
' i8 G. p* J6 [3 Y6 g% W( R2 SSouth Alabama Medical Center, Mobile, Alabama.
0 j/ J+ w- ^3 \; ]  r0 b/ eAddress correspondence to: Samar K. Bhowmick, MD, FACE,; X* W( o2 w% r/ C* p. u4 ?7 z
Professor of Pediatrics, University of South Alabama, College of' t, C" w: g9 \' V/ T- h% S) Y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" H* F* A' V- }( V$ O9 @& L2 K
e-mail: [email protected].: p  N* g6 X8 \; V* L
about 6 to 7 months old, which progressively became2 z) f8 e2 A, n" c- e- S
darker. She was also concerned about the enlarge-6 d% z' ]- p5 \7 E
ment of his penis and frequent erections. The child
) e! h/ @0 H2 M) i. [was the product of a full-term normal delivery, with
  u2 u' x; j& R" l3 q; [! N, |a birth weight of 7 lb 14 oz, and birth length of
4 I' ?: k' ?* g+ w8 ^20 inches. He was breast-fed throughout the first year
# q3 W/ ]. N6 y2 Fof life and was still receiving breast milk along with
, S* |- v4 u5 b& F5 o% V; zsolid food. He had no hospitalizations or surgery,
4 H1 z; |2 [( dand his psychosocial and psychomotor development
8 x9 M! Q$ E5 Y! Vwas age appropriate.* ~2 y5 H( L$ E1 N# J
The family history was remarkable for the father,0 ~, L3 i9 `4 ~% i. B6 ?6 r8 O3 n  U
who was diagnosed with hypothyroidism at age 16,
$ Y5 F2 \" ^/ Q/ S3 Q0 Owhich was treated with thyroxine. The father’s
  o  w+ G1 n! M0 oheight was 6 feet, and he went through a somewhat
% a: @% ?: W7 Iearly puberty and had stopped growing by age 14.
. F$ N3 {  R; q5 @$ PThe father denied taking any other medication. The3 Q; T/ z* N; @5 s7 ~
child’s mother was in good health. Her menarche- a" X. J1 W8 o# j
was at 11 years of age, and her height was at 5 feet
$ ?, D' ?2 b' N$ u5 inches. There was no other family history of pre-4 O& A, h& R: C' b
cocious sexual development in the first-degree rela-& b7 L! ?' `5 [7 [+ j
tives. There were no siblings.
1 x- t' S5 Y! WPhysical Examination: o! v  Z( b+ ~- A
The physical examination revealed a very active,! _# X; A  {$ F' c8 J: X" V. R
playful, and healthy boy. The vital signs documented
. E7 n& h# x/ la blood pressure of 85/50 mm Hg, his length was' g& j, j' U* s5 z$ X, H
90 cm (>97th percentile), and his weight was 14.4 kg
) r- ~: Q3 E) y; F( m9 R(also >97th percentile). The observed yearly growth1 c) }+ Q) C. X, [$ _- c
velocity was 30 cm (12 inches). The examination of
1 X, K6 Y1 \/ X* p) v. s  c* }- O2 kthe neck revealed no thyroid enlargement.
& v+ C! R7 _7 YThe genitourinary examination was remarkable for$ z/ |' m: Q1 ~6 w5 U/ M
enlargement of the penis, with a stretched length of' L4 x9 K3 c- h1 P! s2 L) {) x# L6 ^
8 cm and a width of 2 cm. The glans penis was very well
0 A2 V9 A& ]2 k# T3 K5 h9 Q) d! bdeveloped. The pubic hair was Tanner II, mostly around
& n2 W1 E. v' E, ?0 m540
1 i5 _% ]2 B: Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( q+ T' s8 X' I8 ]0 H5 N) m7 E( I. fthe base of the phallus and was dark and curled. The4 h1 d5 w; ]3 Z! \2 v
testicular volume was prepubertal at 2 mL each.
! n1 N9 T0 y9 ^The skin was moist and smooth and somewhat
, V& R3 L5 S+ soily. No axillary hair was noted. There were no4 L* |+ G" n+ t$ M& E$ ]) Q
abnormal skin pigmentations or café-au-lait spots." q- S! G+ R3 @
Neurologic evaluation showed deep tendon reflex 2+5 T, d$ f! z, e( B( L2 Z; x
bilateral and symmetrical. There was no suggestion8 L0 B4 v- ?. R: w$ y# a5 ~3 g
of papilledema.
% t+ O' S$ C5 l( _4 _  q2 VLaboratory Evaluation
5 g4 n; T0 w! q8 t) x& ]. C1 b$ g6 NThe bone age was consistent with 28 months by
4 `# R6 O: P5 X6 b3 o0 Yusing the standard of Greulich and Pyle at a chrono-
4 e' p2 ^: Y1 z7 nlogic age of 16 months (advanced).5 Chromosomal
" J1 U+ D* ]5 Y# t+ y8 f. n- {6 vkaryotype was 46XY. The thyroid function test
9 C  e. k5 ~  Q5 F7 Jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-; R4 @! `( U9 X3 N/ ~: ^
lating hormone level was 1.3 µIU/mL (both normal).
' @* N& M8 G6 U# c; iThe concentrations of serum electrolytes, blood8 j$ k) I, u9 R! x
urea nitrogen, creatinine, and calcium all were
2 ~. Y- D( [' p4 t7 y, I% _( ^# ywithin normal range for his age. The concentration
8 ?7 V9 S5 ]6 r& Mof serum 17-hydroxyprogesterone was 16 ng/dL
, W$ V9 H0 U) @: J, Y% V(normal, 3 to 90 ng/dL), androstenedione was 20/ q2 z" |8 f0 D7 d! |
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( O  }! K# L& g4 n/ _terone was 38 ng/dL (normal, 50 to 760 ng/dL),# q/ K& A) X  r; T
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
: x1 E3 [& X4 X6 g49ng/dL), 11-desoxycortisol (specific compound S)9 D8 g- e' ~0 w, H
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 g+ s: s3 `) a4 O
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 B7 v' H& t& o$ C0 l# Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 X1 q( A% ]3 J, ?* land β-human chorionic gonadotropin was less than
/ I4 m6 [* u. A; w! k5 mIU/mL (normal <5 mIU/mL). Serum follicular
+ c5 B5 {4 ]5 astimulating hormone and leuteinizing hormone
0 @; F! k4 q3 Wconcentrations were less than 0.05 mIU/mL, R, O# R; Z/ h
(prepubertal)./ ]4 R% ~2 o/ T4 T1 q. P
The parents were notified about the laboratory
0 T6 Z: N; t) s4 E' presults and were informed that all of the tests were
; ?& c7 W, u* E% Enormal except the testosterone level was high. The
8 W7 x! a5 @4 v8 o  p9 S4 {- Yfollow-up visit was arranged within a few weeks to2 O/ ]1 b# C7 n; G- V+ y6 \  T! F
obtain testicular and abdominal sonograms; how-
" v  |. n0 F0 k! \ever, the family did not return for 4 months.
# X, W6 ?7 v# e- d- L4 z5 pPhysical examination at this time revealed that the5 e1 [( e6 d7 m
child had grown 2.5 cm in 4 months and had gained: ?# _  e4 n2 W8 ?/ a3 n" [# a
2 kg of weight. Physical examination remained
" X" S3 Y' }& u+ z9 B- {unchanged. Surprisingly, the pubic hair almost com-
2 @3 e! `# y8 H9 S3 @5 k: Cpletely disappeared except for a few vellous hairs at
* g9 V$ S& \0 p1 F: Nthe base of the phallus. Testicular volume was still 2) @2 N- \3 J+ ]/ ^
mL, and the size of the penis remained unchanged.. b3 A/ W% M' Y9 w9 [5 k) K/ Y) a
The mother also said that the boy was no longer hav-
3 [9 k7 p% W* t  x9 r  aing frequent erections.# g+ j) r4 x4 s' }6 T
Both parents were again questioned about use of
% Y" h" F- f6 U9 X7 P7 qany ointment/creams that they may have applied to6 P0 M+ U, j% \) W* j
the child’s skin. This time the father admitted the
% X6 N. q+ O9 s2 H, h) @: VTopical Testosterone Exposure / Bhowmick et al 541
$ F) f+ w+ N* T2 juse of testosterone gel twice daily that he was apply-
5 N) s1 z$ [3 V$ Eing over his own shoulders, chest, and back area for; G0 P: |9 ~/ Y6 L9 {3 i8 i
a year. The father also revealed he was embarrassed, [# ~; u& g; L! O' n' ]$ F& E0 A
to disclose that he was using a testosterone gel pre-
3 }! V( {$ A- h: V7 ~- F& Kscribed by his family physician for decreased libido
/ y2 J- V& \0 o: Hsecondary to depression.
1 f3 [7 H  L$ v0 \The child slept in the same bed with parents.$ Q6 Q# @' [9 I
The father would hug the baby and hold him on his
  k# H& F0 e3 k' h8 ~) Q5 B; {8 H4 M' p+ Rchest for a considerable period of time, causing sig-. d6 o# d* t( b/ k6 S$ S
nificant bare skin contact between baby and father.
& F$ W1 [. g0 u  BThe father also admitted that after the phone call,, n1 F* N" F5 T: ~2 o
when he learned the testosterone level in the baby
5 m5 J+ C7 z, Hwas high, he then read the product information
) a7 z) Z/ a8 Y" Qpacket and concluded that it was most likely the rea-
+ u* V5 n& Y3 q6 dson for the child’s virilization. At that time, they) m0 n- E9 E+ f; _
decided to put the baby in a separate bed, and the# ]7 }+ U. r1 [  u! ]' a
father was not hugging him with bare skin and had
# K' C- f4 m: @4 L* b2 w! sbeen using protective clothing. A repeat testosterone
  W% v/ h$ D, t$ l7 P* s* mtest was ordered, but the family did not go to the
/ b! i1 N$ w: x3 J8 c- V2 |laboratory to obtain the test.2 x! D4 ]# c5 K& Z" \
Discussion- @4 z6 ^! n6 u9 T/ n& B
Precocious puberty in boys is defined as secondary
' R) M# ~5 h9 ~; M8 N2 Hsexual development before 9 years of age.1,4
" O- k9 E0 `3 q' ?1 ?Precocious puberty is termed as central (true) when) {% C$ R% M7 V( d* b
it is caused by the premature activation of hypo-2 H$ d  F% }0 O! x
thalamic pituitary gonadal axis. CPP is more com-
5 R- W2 O9 d0 bmon in girls than in boys.1,3 Most boys with CPP
9 V* I! S. w. p& [* N$ qmay have a central nervous system lesion that is
  Q) M( }. j$ A. f8 rresponsible for the early activation of the hypothal-
: D$ C6 D( F  B: [% vamic pituitary gonadal axis.1-3 Thus, greater empha-% h2 v" C/ n9 }( q
sis has been given to neuroradiologic imaging in$ I5 W% h9 D2 ]& J
boys with precocious puberty. In addition to viril-
9 y. `$ \( J( p" r  Nization, the clinical hallmark of CPP is the symmet-5 p, |; {" J4 R2 v+ e
rical testicular growth secondary to stimulation by
3 w. D# B0 q1 N" ?' @8 v) J; agonadotropins.1,3
1 F' W  \0 y! H: R. l( c2 HGonadotropin-independent peripheral preco-
- x# H- S* A5 S% ^cious puberty in boys also results from inappropriate
) F$ d. y: d; E6 E) D% {androgenic stimulation from either endogenous or, e* q! r- K* q; H5 I
exogenous sources, nonpituitary gonadotropin stim-" w) \2 b; k$ P. R+ V
ulation, and rare activating mutations.3 Virilizing+ f% o2 X0 f$ R
congenital adrenal hyperplasia producing excessive
+ D5 s, L% U4 }/ `+ t2 K' D6 Uadrenal androgens is a common cause of precocious  T. B! O6 r' ?: ?6 ]1 |
puberty in boys.3,4+ i* }. w6 z- O. ^2 R
The most common form of congenital adrenal7 c% K5 M: s+ C% t% ?
hyperplasia is the 21-hydroxylase enzyme deficiency.
3 w8 i; ?* m7 z5 Z: x; ?' HThe 11-β hydroxylase deficiency may also result in
0 f' i2 Z* f# ^+ uexcessive adrenal androgen production, and rarely,# d( z/ }: d9 X1 P5 v. C
an adrenal tumor may also cause adrenal androgen- r- O2 S6 z8 x" n: e
excess.1,35 _/ ^2 {2 k* G" g) _3 H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 V7 B$ G1 E7 E3 j3 X5 E, U3 ^542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ {$ }0 _6 \7 D$ w3 ^: D5 G
A unique entity of male-limited gonadotropin-. |; b- E' N0 o: b9 M& h% F
independent precocious puberty, which is also known
2 G  o2 ]0 }! ^as testotoxicosis, may cause precocious puberty at a
: P' {' s% ?2 ]. i' E7 Svery young age. The physical findings in these boys5 o. J0 }& \' ^
with this disorder are full pubertal development,; m( \0 E) A- g& ~
including bilateral testicular growth, similar to boys/ ^0 H7 {9 I) Q7 l  T( X
with CPP. The gonadotropin levels in this disorder4 j# v9 m2 `' f* n8 ]( h
are suppressed to prepubertal levels and do not show! @) O# M6 n# c/ E
pubertal response of gonadotropin after gonadotropin-1 _7 p6 m4 m6 j
releasing hormone stimulation. This is a sex-linked; y0 |! l7 z7 i7 F
autosomal dominant disorder that affects only
+ t+ V6 i% C  a# X9 M6 m8 B/ jmales; therefore, other male members of the family# S1 Q$ j6 K' P, `4 m( S) s/ O
may have similar precocious puberty.3# a6 g. A( `# G# y* A2 B% o5 P" T
In our patient, physical examination was incon-
5 X, k2 c9 ~% f6 xsistent with true precocious puberty since his testi-3 \( K, j0 O; Z: l: j: ~1 Q
cles were prepubertal in size. However, testotoxicosis
$ g+ l* _- f; O& Hwas in the differential diagnosis because his father. l8 s2 b* [$ h- v
started puberty somewhat early, and occasionally,$ O4 b8 Q0 |" G( E; J/ I4 o3 M$ k1 s7 S4 ~
testicular enlargement is not that evident in the
4 \9 R1 @# b: nbeginning of this process.1 In the absence of a neg-
+ V4 w0 ?3 a4 v" }! |- o& Rative initial history of androgen exposure, our
! T- _3 F/ P# o3 r, P$ n" ~biggest concern was virilizing adrenal hyperplasia,
; M" E, h" n' a3 l4 q& `either 21-hydroxylase deficiency or 11-β hydroxylase
# s( l" j' ?, P0 p# Zdeficiency. Those diagnoses were excluded by find-% J& l7 ]+ }0 [2 ~/ X- {* L* X
ing the normal level of adrenal steroids.! Q# D; d, l+ B' V/ J" a7 K. D
The diagnosis of exogenous androgens was strongly/ Y/ v1 B/ ~. ^7 H! [% ^* E
suspected in a follow-up visit after 4 months because2 ]+ y8 |- O8 `9 @  Q
the physical examination revealed the complete disap-" a$ d2 u, E7 c6 i7 P
pearance of pubic hair, normal growth velocity, and
: S& u) \! _+ i4 r- [$ p5 qdecreased erections. The father admitted using a testos-
6 R- B- `; e+ B" j$ Wterone gel, which he concealed at first visit. He was% d: w' o* K: {5 L6 A: r( [0 C
using it rather frequently, twice a day. The Physicians’$ W' }) X  B$ s5 b" H! }& U  m, Y
Desk Reference, or package insert of this product, gel or
$ R# }( E! z- S8 _cream, cautions about dermal testosterone transfer to0 R( o7 V) N' M, z5 a5 b
unprotected females through direct skin exposure.
" {  ?( @$ c. {8 V8 `; Y7 a% S# G$ G+ i! vSerum testosterone level was found to be 2 times the
5 F- M4 Y8 t7 O5 z7 k' Mbaseline value in those females who were exposed to
' G& F  i0 G0 M  }( _even 15 minutes of direct skin contact with their male
& z7 b5 a7 @. ppartners.6 However, when a shirt covered the applica-
) k# h8 K: M8 V, Q3 v3 Ition site, this testosterone transfer was prevented.
+ L1 ]( n9 U1 I0 j5 }, ~0 sOur patient’s testosterone level was 60 ng/mL,
; m/ r5 U9 i: L) o! l9 Bwhich was clearly high. Some studies suggest that* ~; y9 u- |$ d  G
dermal conversion of testosterone to dihydrotestos-
( m; U1 p7 F) D! z& ?: s& yterone, which is a more potent metabolite, is more
2 T' i! k! S. Zactive in young children exposed to testosterone
9 E8 s3 t; a' b# C' ^" E$ ]exogenously7; however, we did not measure a dihy-
6 x/ T; M; m! U: x6 ]7 H+ Ndrotestosterone level in our patient. In addition to
, c, @6 R. p( a) Pvirilization, exposure to exogenous testosterone in
" o* n( \' t$ f6 ~, ~9 u8 L* }children results in an increase in growth velocity and# ?9 a$ H% \* L, k
advanced bone age, as seen in our patient.
5 m9 m9 r# t4 q( E+ R- `The long-term effect of androgen exposure during' E8 i3 }0 d3 I2 @) m
early childhood on pubertal development and final: D3 T9 P, w. u7 W
adult height are not fully known and always remain
) L  K$ d+ |$ }7 U9 Z- n( {) za concern. Children treated with short-term testos-
8 Z% {# w$ X4 [; Tterone injection or topical androgen may exhibit some
! c' z4 \# D0 Z6 \3 hacceleration of the skeletal maturation; however, after
0 s: U' a8 ?% v. T( B0 F; ncessation of treatment, the rate of bone maturation+ V' ]% u3 L+ s! P
decelerates and gradually returns to normal.8,9
! A: I) P  u6 }1 |; GThere are conflicting reports and controversy
  J7 y% @- h' h0 mover the effect of early androgen exposure on adult
# W. ^* E+ i4 v% ipenile length.10,11 Some reports suggest subnormal5 g* p' R! D! v# L$ i' I
adult penile length, apparently because of downreg-
/ b$ E- f6 d" L/ Fulation of androgen receptor number.10,12 However,
' _) C7 F( z* g4 r! m& vSutherland et al13 did not find a correlation between
; S; Q- r/ x/ x  o/ W! r  Ychildhood testosterone exposure and reduced adult
' t: j& c' P- Zpenile length in clinical studies.
9 W4 R' t" @4 X7 ANonetheless, we do not believe our patient is
: z5 @% P) E1 I: L# ~going to experience any of the untoward effects from
& O( F4 e, ?3 v* M6 [! X/ w. ptestosterone exposure as mentioned earlier because2 I0 P2 @) o) F: c9 Z
the exposure was not for a prolonged period of time.
1 _% t7 W) U& ~( I5 X& eAlthough the bone age was advanced at the time of
1 S# Y% ?0 R# J  H/ {/ o  ~diagnosis, the child had a normal growth velocity at
2 {( N" D+ a8 t6 Rthe follow-up visit. It is hoped that his final adult
6 W, ~4 ^$ a5 o8 F2 J) Q+ b- R9 kheight will not be affected.
3 v4 |! f) e+ Y& v& t) wAlthough rarely reported, the widespread avail-
- v! d, P( k0 v, ^& m0 @- s4 ^ability of androgen products in our society may
# X2 [2 i- H$ q2 J8 _. ~8 Zindeed cause more virilization in male or female" V( C! w7 B2 k5 B3 m- W0 Z* h
children than one would realize. Exposure to andro-
! f+ I5 Q$ Y; X0 ]. wgen products must be considered and specific ques-
3 D% I# x0 {6 i) E7 }- P% Utioning about the use of a testosterone product or
1 R/ ^* }% e% g0 P8 ^gel should be asked of the family members during
$ a# k& ]  i# N( \the evaluation of any children who present with vir-
, |  `$ R; v% F" b' c+ ?. G. r) }! Pilization or peripheral precocious puberty. The diag-
, Q9 A; v8 O. X% l& p* N; ~nosis can be established by just a few tests and by
4 a8 y  g  N- ]9 m: Zappropriate history. The inability to obtain such a1 l% X2 H) Q4 M" M
history, or failure to ask the specific questions, may
2 q3 J$ I, Q% h: Presult in extensive, unnecessary, and expensive
: P8 N6 V1 v/ A+ R; |investigation. The primary care physician should be
2 `4 @2 n$ D6 Y# C' `3 xaware of this fact, because most of these children
  n+ G0 Q% F" q' U5 kmay initially present in their practice. The Physicians’
1 B1 N8 X6 F3 z+ A; VDesk Reference and package insert should also put a4 e: R3 ^& K5 Q, k
warning about the virilizing effect on a male or
8 U; D4 B1 L8 ]# h) Y3 f0 {; m7 tfemale child who might come in contact with some-
4 s& F, l* r* A( B; W9 x1 O- j: n6 @, uone using any of these products.( q$ Q9 F! j( N, }6 p8 U% k
References
/ Z5 @  ~3 N' `3 z1. Styne DM. The testes: disorder of sexual differentiation
# ~2 A" ?- J1 U! q2 I0 Gand puberty in the male. In: Sperling MA, ed. Pediatric4 R4 j7 P4 O( x) l
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) O+ A; Y" B% g" i
2002: 565-628.) B3 f* G7 H& f
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, a- ]: A4 f4 b9 f0 J- ?
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
8 A7 S: k9 p, a* K( ]3 e2 l5 V) pBoy Induced by Indirect Topical4 A3 e  H8 s$ J, |
Exposure to Testosterone
0 Z% g. a8 z2 n3 a% [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  t7 P( v# q8 b6 h  Nand Kenneth R. Rettig, MD1
- n5 d; @' f3 r0 m- L* i3 o1 x- DClinical Pediatrics
0 ~$ [0 ^6 x6 E% `Volume 46 Number 6; D6 v& a+ W8 N) _
July 2007 540-543
" L; d$ j  `: A" x3 X# `7 T7 s© 2007 Sage Publications
, f( u2 L% ?& R# `+ v& n10.1177/00099228062966517 V8 \- |4 J3 v4 b' Y+ X
http://clp.sagepub.com
9 E% z7 E) ^* a+ m, O5 f4 z6 F1 }/ jhosted at( |  K- ~$ N0 G' Z9 g2 Y
http://online.sagepub.com
0 {) N! }7 O' Y7 PPrecocious puberty in boys, central or peripheral,
8 l) F6 t1 H' xis a significant concern for physicians. Central  U  f, ~' T+ @: \& p$ Y* w
precocious puberty (CPP), which is mediated
  U7 Q8 |$ F& ~0 }: uthrough the hypothalamic pituitary gonadal axis, has
) ?$ w# B, G. R$ da higher incidence of organic central nervous system
+ W4 H7 p& P9 U) I# M( Flesions in boys.1,2 Virilization in boys, as manifested" p$ _( m  ]0 q$ b/ W7 A
by enlargement of the penis, development of pubic
9 l8 V+ x. U# h- N+ rhair, and facial acne without enlargement of testi-
1 w4 }5 L. p! z9 tcles, suggests peripheral or pseudopuberty.1-3 We9 O$ S* y0 z$ Z" V1 W2 a( C8 X
report a 16-month-old boy who presented with the
! k5 i% O# y* v) q, \enlargement of the phallus and pubic hair develop-0 |# W! Y% V  q5 J- t
ment without testicular enlargement, which was due
5 k8 t# F, b; n' q" Lto the unintentional exposure to androgen gel used by
4 b8 P! i: T/ i+ ~) hthe father. The family initially concealed this infor-
/ Z6 G: W' ~0 K) K" P3 n* n. cmation, resulting in an extensive work-up for this* D4 s. \/ h0 y# R! B5 }& w
child. Given the widespread and easy availability of
  p. ~; X5 S" htestosterone gel and cream, we believe this is proba-
. l) O% z3 E; q& a# a/ j2 X; ]) P3 _& Ably more common than the rare case report in the' a/ l$ S' z$ C8 e( k: I" o; Z
literature.4
0 ~' J/ W& s1 o/ d% N) @3 ?3 aPatient Report
: y5 H) D$ l; d5 UA 16-month-old white child was referred to the
9 r$ Q* Y% T! o4 a1 z" A3 \) Tendocrine clinic by his pediatrician with the concern" v& e: Q4 _. t7 m1 T" w2 q
of early sexual development. His mother noticed
# X/ S5 C1 Y/ r8 I. n* d1 Plight colored pubic hair development when he was4 T0 c& g5 A- s/ t* g( \
From the 1Division of Pediatric Endocrinology, 2University of
3 @: Q! ?0 x  M: K9 V$ TSouth Alabama Medical Center, Mobile, Alabama.
, ^; x  y2 b# t9 RAddress correspondence to: Samar K. Bhowmick, MD, FACE,
0 s" N, {. x7 D8 a% h) aProfessor of Pediatrics, University of South Alabama, College of
. w1 W( R( F% @Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, q) u# a9 M! N3 P& I
e-mail: [email protected].
& e  p- x" P- C- P& ~. ^about 6 to 7 months old, which progressively became
! |' c8 z, X! F, b6 o6 Qdarker. She was also concerned about the enlarge-- E, H! e8 U5 A& }3 x: m$ e
ment of his penis and frequent erections. The child
! d0 e7 b6 A5 P) iwas the product of a full-term normal delivery, with  p3 m4 C- X5 @) h$ j) [& B
a birth weight of 7 lb 14 oz, and birth length of6 z  o  l6 {6 ?( k2 s1 d: K
20 inches. He was breast-fed throughout the first year, j! {( k7 d/ w% F! {$ V
of life and was still receiving breast milk along with# g; u. y; s( L  J
solid food. He had no hospitalizations or surgery,
* h, ^1 U+ T1 m' f$ m8 D2 Vand his psychosocial and psychomotor development  I, g+ E, r0 p
was age appropriate.
- N- P2 |# n" |! ^' ?2 cThe family history was remarkable for the father,
+ F( L( ]' O. @% w1 W8 Mwho was diagnosed with hypothyroidism at age 16,# ^( n5 I! {# g+ J5 B: \* t
which was treated with thyroxine. The father’s
; I, _7 V' h+ |+ N  D# d3 @2 K& m9 R' Aheight was 6 feet, and he went through a somewhat
5 z' W/ O. O3 k. ^7 cearly puberty and had stopped growing by age 14.
- b8 d/ [/ }1 r1 O0 x8 Y) gThe father denied taking any other medication. The8 Q+ E8 x5 f  D( H9 k" q% ?  L& `
child’s mother was in good health. Her menarche
) M: `% u5 L& x/ `" C7 {; a6 h1 ]4 xwas at 11 years of age, and her height was at 5 feet& `% a  v0 o8 g! x2 ^. u6 w& E
5 inches. There was no other family history of pre-
6 Q6 L6 `( ^+ V1 G5 B! r2 ncocious sexual development in the first-degree rela-9 b2 b4 q: E  S& B) G% T
tives. There were no siblings.7 R) g7 Q/ R7 C! u; x. u0 l5 R' v
Physical Examination
( m' y5 c! V- _9 q8 s5 r- D1 vThe physical examination revealed a very active,
6 E/ k+ [7 j2 x7 `  Pplayful, and healthy boy. The vital signs documented
/ {9 V) u/ W$ O7 W3 Ia blood pressure of 85/50 mm Hg, his length was: w) m0 O* V0 j2 u8 V) b
90 cm (>97th percentile), and his weight was 14.4 kg. I- R# a* P5 u+ P
(also >97th percentile). The observed yearly growth
! V' J8 N9 U! N& H5 lvelocity was 30 cm (12 inches). The examination of
( i' s: }+ _4 Ythe neck revealed no thyroid enlargement.5 @8 z; W# }* ^: {# l! t
The genitourinary examination was remarkable for  _. e0 N0 [  H. d
enlargement of the penis, with a stretched length of) J2 S3 w$ n" u1 j
8 cm and a width of 2 cm. The glans penis was very well! T$ t, Y" [6 s* b; B6 r1 `6 V/ E
developed. The pubic hair was Tanner II, mostly around
; t4 \' [4 D- `' S4 j, u! N0 P540  U4 t9 R7 e7 p. c# N0 i
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% ~# S1 e7 a% r' C/ w4 ?& M- b7 X2 y
the base of the phallus and was dark and curled. The" o) q4 a: q6 |. t: U; I+ z
testicular volume was prepubertal at 2 mL each.6 S3 S+ \$ _' l* g+ }7 ?# B
The skin was moist and smooth and somewhat
1 y6 {: K! E; }: f9 boily. No axillary hair was noted. There were no* O: \4 ~: ?1 l
abnormal skin pigmentations or café-au-lait spots.: I# ^* l7 A* w* d* z5 C3 a5 G
Neurologic evaluation showed deep tendon reflex 2+# X- n3 ~" ~7 x+ w6 n- _7 ~1 M' [5 X
bilateral and symmetrical. There was no suggestion: t5 s/ f$ R) S
of papilledema.
0 B1 g1 S! a$ I8 A* N7 W9 i3 I0 s- ^Laboratory Evaluation
4 r6 }# j+ l& {. }5 H% T9 fThe bone age was consistent with 28 months by
; A/ a+ d, \) Z# J2 j& H6 pusing the standard of Greulich and Pyle at a chrono-9 S- s7 ~( H3 o( D7 D
logic age of 16 months (advanced).5 Chromosomal
- u+ C- K. L1 `2 @5 I$ `karyotype was 46XY. The thyroid function test
/ _4 i/ Z2 S% h0 Wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-6 G6 ~* Q) [# V/ k0 x! o
lating hormone level was 1.3 µIU/mL (both normal).) Q- Q& Y$ T- v% K' @" t
The concentrations of serum electrolytes, blood
5 T# X& g6 X( H8 p& M" rurea nitrogen, creatinine, and calcium all were
( W" h7 s2 R4 u7 m$ C  Qwithin normal range for his age. The concentration
7 n" V4 \* N, h+ _of serum 17-hydroxyprogesterone was 16 ng/dL
3 j- q8 b$ ]% \( M9 O(normal, 3 to 90 ng/dL), androstenedione was 20
7 v/ s. [$ l) mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( q& h  {- X& g! D9 `5 {: Hterone was 38 ng/dL (normal, 50 to 760 ng/dL),
- {2 a! J0 O  {2 U$ c$ i; Mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
3 _5 Q$ F' [1 L% F) B49ng/dL), 11-desoxycortisol (specific compound S)
; [, S0 ^9 K! |7 R" w  B2 Lwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 q# f9 I+ N& R9 u7 j3 otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
6 Q" X) ?! ~/ Y/ c- \! Ptestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 |( ^) T7 S3 A/ Y7 c# f8 xand β-human chorionic gonadotropin was less than/ y9 |. A4 p% E$ f/ N5 [  n/ O
5 mIU/mL (normal <5 mIU/mL). Serum follicular
+ K9 b  i* z6 T8 Lstimulating hormone and leuteinizing hormone! [3 W# E  g+ Y( D
concentrations were less than 0.05 mIU/mL
: U  u3 @: q! X0 y5 U6 `" U- f- }2 e(prepubertal).) N. A: J% f  B" [; h% l
The parents were notified about the laboratory
% \5 l9 p- C& g1 b5 `( j7 uresults and were informed that all of the tests were7 u( D9 d- j" o* U
normal except the testosterone level was high. The, |  J7 y2 E$ a9 d4 g3 \( _# w
follow-up visit was arranged within a few weeks to" A' l2 e' G8 f, R& Q
obtain testicular and abdominal sonograms; how-6 x9 Y) \% n/ @6 `6 Z8 i: n6 Y6 f! t% D
ever, the family did not return for 4 months.5 G+ x& b8 p) |
Physical examination at this time revealed that the
; H" a& j; K; @: Y% R7 jchild had grown 2.5 cm in 4 months and had gained4 B. v7 Z, `! ?/ {/ u& Z
2 kg of weight. Physical examination remained) P' l9 B. n# l1 F
unchanged. Surprisingly, the pubic hair almost com-
3 t% i) p' P2 d0 X! n6 N9 Npletely disappeared except for a few vellous hairs at( H' |9 M6 O- v9 G
the base of the phallus. Testicular volume was still 2/ w& M! y( {8 [( u1 ~
mL, and the size of the penis remained unchanged.
8 r+ P! Z! q1 \9 r$ VThe mother also said that the boy was no longer hav-
+ Q0 }5 N4 A8 z+ F! zing frequent erections./ m& N, ^5 c- U
Both parents were again questioned about use of% l4 _3 J# T6 M
any ointment/creams that they may have applied to9 |& i% ^- ?: V8 ~6 g- ?( e- f, N
the child’s skin. This time the father admitted the, g+ @. Y3 N% I6 A& g, S3 a
Topical Testosterone Exposure / Bhowmick et al 5414 ]3 h) [: Q" |7 M$ ~6 A8 Y
use of testosterone gel twice daily that he was apply-
4 C/ p5 {* j9 Y- O5 d. [ing over his own shoulders, chest, and back area for  ~2 h0 q$ X3 X. |: m4 P( O* W
a year. The father also revealed he was embarrassed
: r2 S5 u; }/ Fto disclose that he was using a testosterone gel pre-. I7 i: S$ @9 `7 ?2 J: o
scribed by his family physician for decreased libido
' u) z$ Y0 ?6 T. \secondary to depression.1 y! g9 k) g* g* w" [  \
The child slept in the same bed with parents.
& m; S" t* ^6 Y/ iThe father would hug the baby and hold him on his$ m, T0 X$ o, ^; L9 B2 |
chest for a considerable period of time, causing sig-
3 j1 V- O1 a# r9 b& v! g' R2 Y0 rnificant bare skin contact between baby and father.
! x# @1 `- @9 R) j% E: \The father also admitted that after the phone call,
4 |) E/ A& K- {) L+ {when he learned the testosterone level in the baby
9 h! [* U" W2 x( nwas high, he then read the product information- I" O' J+ @; z7 `% e
packet and concluded that it was most likely the rea-, k+ @2 `, h5 c3 |! p
son for the child’s virilization. At that time, they! P$ J  w  Y( g7 W
decided to put the baby in a separate bed, and the
' F+ y4 v/ \( Bfather was not hugging him with bare skin and had
0 |) F8 \# V3 u/ |9 P! Cbeen using protective clothing. A repeat testosterone
- T. @- Q4 |  O+ f; S; Qtest was ordered, but the family did not go to the+ y4 O& d3 ~* ^+ y  K" p: R
laboratory to obtain the test.
! ]; C( S/ {9 o1 Y  O- JDiscussion
4 U0 _/ Z" E1 I$ p: {) DPrecocious puberty in boys is defined as secondary& y& p& M1 a5 L3 D
sexual development before 9 years of age.1,4
) Q5 m! Q) r" U. P9 x. K8 PPrecocious puberty is termed as central (true) when, o$ a  e, T4 G+ D* c* a6 Q
it is caused by the premature activation of hypo-
9 Y$ u4 z( B9 c+ C5 j  T% {1 jthalamic pituitary gonadal axis. CPP is more com-
* q# I- N4 }2 O, l% z% Nmon in girls than in boys.1,3 Most boys with CPP
% V0 q7 N0 R1 I- `may have a central nervous system lesion that is) B% p! Y! l. _  D9 j( a7 p# \4 K
responsible for the early activation of the hypothal-
& \- f' ]5 b# R- I$ Namic pituitary gonadal axis.1-3 Thus, greater empha-
4 L- r7 e2 F/ _sis has been given to neuroradiologic imaging in1 u+ F" c+ G6 J2 f8 a/ M
boys with precocious puberty. In addition to viril-- }& i; N2 g0 a8 n/ c& x& Z/ U
ization, the clinical hallmark of CPP is the symmet-
, ^1 M( I8 G2 D8 drical testicular growth secondary to stimulation by) G: i; a0 p8 M
gonadotropins.1,3+ `% g4 Q  E) d4 ?+ ?% }
Gonadotropin-independent peripheral preco-
0 h/ l+ t6 T3 R9 d' S6 l0 c! n- q* ]cious puberty in boys also results from inappropriate- Y! z* i) \' w) n0 G
androgenic stimulation from either endogenous or
* \; y7 m0 W: Lexogenous sources, nonpituitary gonadotropin stim-/ g7 m0 K+ @9 Q! C$ ~
ulation, and rare activating mutations.3 Virilizing
. m% l5 W: \4 w# @; B0 }5 m1 k6 k; Lcongenital adrenal hyperplasia producing excessive" h2 I7 A/ t% n9 j  T3 W9 P
adrenal androgens is a common cause of precocious% J' G) R/ s7 s; i0 v! j+ Z
puberty in boys.3,4
7 \, a4 I8 G4 ~* ~" i6 J1 sThe most common form of congenital adrenal
% n- I- C* b$ {& Jhyperplasia is the 21-hydroxylase enzyme deficiency.
/ `$ v8 u5 p# fThe 11-β hydroxylase deficiency may also result in
0 a) p5 E: X. E2 P) {& z% }" jexcessive adrenal androgen production, and rarely,
1 w8 F( v& P9 Han adrenal tumor may also cause adrenal androgen7 p$ G: z1 K$ O3 [( F: u$ `$ y
excess.1,38 _" Z/ x! E# s/ x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& Y6 U9 p, a$ U0 x$ W
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- ~, D) }, |3 t" b; hA unique entity of male-limited gonadotropin-
8 W% Y4 M9 h2 e/ }$ o4 P6 Uindependent precocious puberty, which is also known
2 b4 O# E; v+ ras testotoxicosis, may cause precocious puberty at a
+ f$ W+ S4 u$ o# Nvery young age. The physical findings in these boys0 ~" J& H9 Z, z( n, f3 K
with this disorder are full pubertal development,
) ?' P* q5 \( ^/ ~% C: m/ V% C5 ^including bilateral testicular growth, similar to boys( N, r" c+ I0 s" B# v1 m
with CPP. The gonadotropin levels in this disorder
8 e- C; }# t8 {+ B4 Uare suppressed to prepubertal levels and do not show( Q6 B' R, g, R' z8 B. d" {
pubertal response of gonadotropin after gonadotropin-; A. Z2 ^; H" L$ f7 d4 @
releasing hormone stimulation. This is a sex-linked) Q2 B3 V; o% ]
autosomal dominant disorder that affects only2 }- |9 W% E4 `2 d" i" x& J
males; therefore, other male members of the family
- e9 t5 E8 i% n  ^; G( ?4 c3 l) Bmay have similar precocious puberty.3" @$ f. |# u# o% s
In our patient, physical examination was incon-
3 h% ^8 K) R$ K  e- w* vsistent with true precocious puberty since his testi-
; y9 d) f' Q- Fcles were prepubertal in size. However, testotoxicosis
- D0 A3 `: h+ k4 c1 s: @" b- twas in the differential diagnosis because his father! V' z0 Y' \, T( u* n
started puberty somewhat early, and occasionally,5 t% M# f. s) ?5 Y3 b0 b
testicular enlargement is not that evident in the
! d: U( T! y6 d$ r& sbeginning of this process.1 In the absence of a neg-! f0 {, ~4 \# Y
ative initial history of androgen exposure, our$ a" h9 \. I: X6 m  M& T" n" v* _
biggest concern was virilizing adrenal hyperplasia,
* n3 d( y5 C: \9 n' s7 beither 21-hydroxylase deficiency or 11-β hydroxylase* A  M7 l* I. R% X& k
deficiency. Those diagnoses were excluded by find-8 g! ^+ |2 r" ?, n8 q$ m
ing the normal level of adrenal steroids.$ W! X1 B/ d+ G6 N( n1 l
The diagnosis of exogenous androgens was strongly- W7 o) `8 u  n+ u
suspected in a follow-up visit after 4 months because3 a, o1 ~# }/ t1 \: |7 I
the physical examination revealed the complete disap-
/ v0 O2 J1 i3 n! `# Y' n) F5 u* hpearance of pubic hair, normal growth velocity, and
0 x% X& ]& e# [/ H, V# |decreased erections. The father admitted using a testos-
* }) r0 Y) y+ Y' ~; t. Rterone gel, which he concealed at first visit. He was
2 {9 O7 g# _" z& Q6 x8 `! W) Qusing it rather frequently, twice a day. The Physicians’
3 v0 Z9 g4 y5 ]1 }9 Z" h" YDesk Reference, or package insert of this product, gel or
! b, a3 u0 ^: e+ d; x: Ecream, cautions about dermal testosterone transfer to, H" o( c* \' i0 I/ H. ^
unprotected females through direct skin exposure./ b. P) e3 O- m( ^) P
Serum testosterone level was found to be 2 times the( k* C/ \( }$ h% b0 Q
baseline value in those females who were exposed to5 Q, Q8 C: g7 H) C( t1 b
even 15 minutes of direct skin contact with their male# j  |" ]! t( J% n4 z
partners.6 However, when a shirt covered the applica-5 J, A! O- O  w; X: b
tion site, this testosterone transfer was prevented.
- A% J' s5 ?! A9 cOur patient’s testosterone level was 60 ng/mL,
# S% _7 _) j8 q; P$ }3 ywhich was clearly high. Some studies suggest that, P% q% ^. y% k* [. |7 s  x) y
dermal conversion of testosterone to dihydrotestos-/ {& e; I6 X1 I+ U6 b
terone, which is a more potent metabolite, is more7 C9 u1 L3 S5 s2 W5 U
active in young children exposed to testosterone2 ^" g* P$ q7 j6 a6 b
exogenously7; however, we did not measure a dihy-% o$ [! m1 ^. j0 A" Y3 D* E
drotestosterone level in our patient. In addition to; c  @+ r) x( P+ l
virilization, exposure to exogenous testosterone in
, u+ q3 b( D2 u% f! \% wchildren results in an increase in growth velocity and8 X+ P7 R3 {) R4 M9 i
advanced bone age, as seen in our patient.
3 j5 V/ |% f1 C% C1 QThe long-term effect of androgen exposure during
5 q# W! k8 U' B/ t2 d* x: m. bearly childhood on pubertal development and final
: W) W( E4 r# g1 H: R; Yadult height are not fully known and always remain
8 ~: t) Y+ U3 A8 Z1 t8 I+ fa concern. Children treated with short-term testos-$ W7 m- I9 T4 |( o
terone injection or topical androgen may exhibit some
+ V$ c6 B5 @$ k# L, Tacceleration of the skeletal maturation; however, after
. T" y! P7 n0 c" Ycessation of treatment, the rate of bone maturation/ ~2 e$ u/ J$ O  b# S6 `1 @, y
decelerates and gradually returns to normal.8,9  B) O& a8 A7 ]5 v* W2 H* j
There are conflicting reports and controversy2 M$ B6 Y4 v5 M+ R8 S. k
over the effect of early androgen exposure on adult
7 b  Z- D0 p8 b; ypenile length.10,11 Some reports suggest subnormal
5 ?6 j$ ?( S4 i. h! t$ N$ badult penile length, apparently because of downreg-- \; E& i$ [+ ]* c3 E* \
ulation of androgen receptor number.10,12 However,
  z! P8 [8 Q; bSutherland et al13 did not find a correlation between
, l; E  H2 Z2 r9 `3 i6 w# qchildhood testosterone exposure and reduced adult- r3 g$ a- c& m" L) z
penile length in clinical studies.. \0 C4 x0 D$ r* ~9 [
Nonetheless, we do not believe our patient is
1 B5 K2 U# l# O: A6 Xgoing to experience any of the untoward effects from
  E; f! q) i2 E3 r# \2 ktestosterone exposure as mentioned earlier because
# Z7 i; o5 q* X: @0 |the exposure was not for a prolonged period of time.  p; p7 A& |5 r* E* G# n
Although the bone age was advanced at the time of
" X2 j4 _( u9 R. ^/ rdiagnosis, the child had a normal growth velocity at9 C& W( y% G5 g3 B# H0 z* s* }
the follow-up visit. It is hoped that his final adult1 e* B9 b! P) Z7 K$ G! z( M) I; n
height will not be affected.3 ?4 X0 f+ O  D
Although rarely reported, the widespread avail-
! O8 r2 N1 t! N2 N" ]* Hability of androgen products in our society may: T: k$ D, w( ~. G' Z2 b* _2 r
indeed cause more virilization in male or female9 m7 m6 y0 Q3 s/ S/ K! P
children than one would realize. Exposure to andro-$ G; C% f1 a4 V% B. a9 S4 X
gen products must be considered and specific ques-% m$ e2 h: x' Q
tioning about the use of a testosterone product or
! A' [( g+ l1 g8 u( `% Ngel should be asked of the family members during! I9 l( L! Y4 W; c( E. x  g
the evaluation of any children who present with vir-/ X" b5 n) U/ B' A& R- R, G
ilization or peripheral precocious puberty. The diag-) @$ ?+ C4 ]& o2 e2 t/ V1 d
nosis can be established by just a few tests and by0 |! V3 `, c. z& T2 a% [' {8 z
appropriate history. The inability to obtain such a
' s# g6 }# c4 z# K2 s& Khistory, or failure to ask the specific questions, may: n9 u% h1 t! d0 m6 b+ s
result in extensive, unnecessary, and expensive  ^  {0 x6 G& t2 T. y6 v
investigation. The primary care physician should be- |; `7 l4 r6 _; D# K+ X+ C$ w3 S
aware of this fact, because most of these children6 S* I% x. i& F2 y
may initially present in their practice. The Physicians’7 [5 B, j$ }4 C  L: k; u) p: |
Desk Reference and package insert should also put a
% `: y/ k/ Z! U. h4 J6 `warning about the virilizing effect on a male or" R7 h6 k9 A$ j5 J
female child who might come in contact with some-. g! E# e& j, v3 A+ M
one using any of these products.
/ ]$ D8 y( F' w; V2 C2 v8 |References7 m) D' T: \3 R
1. Styne DM. The testes: disorder of sexual differentiation; T) _3 W; B* G% p/ ]! \( D. j
and puberty in the male. In: Sperling MA, ed. Pediatric' w3 W# V3 W- A# K
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 c' t0 v, u, x; }9 L$ ?6 B+ n
2002: 565-628.
& h- ?6 Z& b9 \" T2 B7 f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% s. n* n% s+ R" g; ?; Mpuberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
! Q$ C+ |# W2 c9 f% d, d6 W
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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