WK綜合論壇, WK综合论坛

 找回密碼
 立即注册
樓主: wk007

鄉下的妹子太便宜,一次四個都要了[12P]

[複製鏈接]
發表於 2025-1-4 03:25:35 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
Sexual Precocity in a 16-Month-Old
' O  g5 n* r* P' D8 ZBoy Induced by Indirect Topical5 K" C: x  t) I* n7 G
Exposure to Testosterone
6 w9 z6 \( U% \; J6 L# ASamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
6 D0 y  ~  E2 Z5 C; ^and Kenneth R. Rettig, MD1! X# \$ Z  [3 z2 I+ r( G: k
Clinical Pediatrics
: m: k& [! Y. `8 t! A! o+ ^" DVolume 46 Number 63 |* J" s& Q2 ~* e) m& Q9 q0 T
July 2007 540-5434 d& z7 q+ K- \0 X
© 2007 Sage Publications
* Q0 Q+ i# P# |# |( D10.1177/0009922806296651
  Q3 V1 {1 d" y; d# Qhttp://clp.sagepub.com; w5 l4 Y8 l, a$ e* m8 ^; w
hosted at
1 P, N' q( l: k( B9 _$ e* Ghttp://online.sagepub.com
' v7 U9 n, }( m4 b) ]( APrecocious puberty in boys, central or peripheral,+ ]2 A9 W# H) c- ]
is a significant concern for physicians. Central
# P1 f: i6 T& h! o- l4 eprecocious puberty (CPP), which is mediated
+ N/ m/ a9 g; D( {: Ethrough the hypothalamic pituitary gonadal axis, has3 _9 B+ E% b3 i3 M& j5 @
a higher incidence of organic central nervous system7 t$ H0 V/ M* ^7 U) l% q0 y; U
lesions in boys.1,2 Virilization in boys, as manifested
, |' |" g; j4 N" k! K( d% N) jby enlargement of the penis, development of pubic
/ I, L$ ~5 ^' L5 A2 p8 Whair, and facial acne without enlargement of testi-
" D* X& R, q* r5 L5 W! w8 {  H4 q: Qcles, suggests peripheral or pseudopuberty.1-3 We
8 m, n; L! z  Creport a 16-month-old boy who presented with the3 D3 G2 O' Y0 l/ p
enlargement of the phallus and pubic hair develop-7 n$ R3 l# v" N
ment without testicular enlargement, which was due; i/ ~' |, ]( [" y) e
to the unintentional exposure to androgen gel used by8 @5 M; R. a3 c8 I  R  y
the father. The family initially concealed this infor-
  [4 F& \1 R( }0 Xmation, resulting in an extensive work-up for this
$ e4 k5 Q3 {+ P, e, u" mchild. Given the widespread and easy availability of! L1 l* p% ^' x
testosterone gel and cream, we believe this is proba-
" r' x% g+ V. f5 v6 Xbly more common than the rare case report in the
9 [2 ?5 n6 v9 v, B% H2 u+ rliterature.47 x( y0 u2 ^& X  O1 T
Patient Report
4 `6 C) U" t2 B  E3 dA 16-month-old white child was referred to the
/ n) Z8 }6 N8 Z/ oendocrine clinic by his pediatrician with the concern
3 [* i$ N/ E/ ?' k2 q5 s& Yof early sexual development. His mother noticed; h: I, t; q, R3 m. @0 f
light colored pubic hair development when he was
4 `, o/ z- v5 E7 G7 zFrom the 1Division of Pediatric Endocrinology, 2University of
" Z; j4 q6 C! O2 MSouth Alabama Medical Center, Mobile, Alabama.
( l& U/ X+ C! N8 g9 g4 kAddress correspondence to: Samar K. Bhowmick, MD, FACE,+ h. a) _1 P' I
Professor of Pediatrics, University of South Alabama, College of& R9 v. p4 }) C+ E( k. N
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) u4 t9 k8 L  xe-mail: [email protected].( D+ m1 H6 ~- [* S
about 6 to 7 months old, which progressively became' c9 G+ q  x) W; g' c( T; L
darker. She was also concerned about the enlarge-' Q0 X" }2 s( A# D  t1 l
ment of his penis and frequent erections. The child6 R; w# m! `5 j$ R0 W
was the product of a full-term normal delivery, with
, m; }3 S* Q0 w, Pa birth weight of 7 lb 14 oz, and birth length of
0 q  f4 }! w. I4 l0 ?0 _! q6 T20 inches. He was breast-fed throughout the first year
2 F+ I( q' b. @8 u4 t! P: S0 bof life and was still receiving breast milk along with: R' Y& ^: f- m6 I+ F$ i" Q# v
solid food. He had no hospitalizations or surgery,
- t! v$ V! |$ Q$ j  Mand his psychosocial and psychomotor development
5 F9 ?; e+ U5 Twas age appropriate.
* O1 N$ Z: A3 n4 _9 eThe family history was remarkable for the father,
8 r! H8 ^/ Q+ [  p! F  ewho was diagnosed with hypothyroidism at age 16,  O' D( ]( ]8 u' w0 s
which was treated with thyroxine. The father’s0 t9 ^: A9 X# n3 \
height was 6 feet, and he went through a somewhat2 G% g- b+ C4 E0 z$ k: u
early puberty and had stopped growing by age 14.5 ?. p0 X" i9 ]# q
The father denied taking any other medication. The* v8 n2 D: A- }& y0 _
child’s mother was in good health. Her menarche
& I4 N  u4 n( g  nwas at 11 years of age, and her height was at 5 feet
8 k- y/ }8 d; q( o( J: p+ u+ [5 inches. There was no other family history of pre-: p+ [( v5 |. y
cocious sexual development in the first-degree rela-3 Z2 H" m+ |1 Z" ~9 S' A0 C. F- U
tives. There were no siblings.2 A7 ]; l6 u4 @
Physical Examination, f7 e) _, a5 D7 _" k- a# ]8 ~. }
The physical examination revealed a very active,
1 c& e6 y8 F+ m$ V9 Gplayful, and healthy boy. The vital signs documented$ d6 ^! Q) U) }- e, f
a blood pressure of 85/50 mm Hg, his length was  K) E; B, U, c! o
90 cm (>97th percentile), and his weight was 14.4 kg
9 a' w8 Q# _$ H0 ]9 n(also >97th percentile). The observed yearly growth
5 q" E. U' Y" g3 }3 L, Svelocity was 30 cm (12 inches). The examination of
) O0 x9 K3 J9 {. P: p: H; u" ethe neck revealed no thyroid enlargement." e, \  ]# W8 M
The genitourinary examination was remarkable for
0 M2 ^0 B, N! W; nenlargement of the penis, with a stretched length of  [# Q: `) a: V+ A1 o: m$ I5 @
8 cm and a width of 2 cm. The glans penis was very well
- {$ S/ P0 _: w: c- U  G" ~4 M8 gdeveloped. The pubic hair was Tanner II, mostly around
# r6 f" O( N7 K# t3 ]540
$ {0 [4 p9 s% `3 \2 t' }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- }0 c9 M; [* pthe base of the phallus and was dark and curled. The" z2 M% Q( K& l' M2 T- [
testicular volume was prepubertal at 2 mL each.+ P. `. M. x# |0 m0 I* i
The skin was moist and smooth and somewhat
) p" x7 E8 f6 U# Coily. No axillary hair was noted. There were no( ?' C9 h& e8 ~4 I
abnormal skin pigmentations or café-au-lait spots.
. ?# y# o" b: B6 g6 xNeurologic evaluation showed deep tendon reflex 2+6 Q! V/ s' {; Q$ @8 m
bilateral and symmetrical. There was no suggestion
: T! o3 D+ _$ tof papilledema.8 b, d9 p* B5 |5 M# z4 N2 B
Laboratory Evaluation
; R9 C! ?3 k( Z$ pThe bone age was consistent with 28 months by
) d- H' E0 F( C+ E' Fusing the standard of Greulich and Pyle at a chrono-% u" d; _) S$ H. A
logic age of 16 months (advanced).5 Chromosomal( d. z- _: _+ a$ j, W) W
karyotype was 46XY. The thyroid function test
" Z+ ?' r1 n2 u+ s# Sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
. w! G$ e! }3 v) f4 j8 slating hormone level was 1.3 µIU/mL (both normal).4 p3 B* b; Q9 k( `
The concentrations of serum electrolytes, blood
6 `4 A3 C3 ^& a( E" B$ V  E- xurea nitrogen, creatinine, and calcium all were% ]; O* ~8 z5 @6 q
within normal range for his age. The concentration
" R9 y& Y; j" q. l3 y" Z6 c6 F5 `/ Mof serum 17-hydroxyprogesterone was 16 ng/dL
: h$ F5 g- X; G(normal, 3 to 90 ng/dL), androstenedione was 20
# p5 I7 C8 @8 tng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-4 ^2 n9 I- S2 S. b7 _" b- O
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 I# `+ z0 w) j, P" [6 O6 [desoxycorticosterone was 4.3 ng/dL (normal, 7 to' a0 D8 S5 w5 ~2 @
49ng/dL), 11-desoxycortisol (specific compound S)
/ K9 ~7 f+ R4 X" G5 |was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, I2 a' |9 P, `1 @tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- }. i9 m  k! Z8 E- R' h( v
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
7 X8 O; l# n( _+ _5 x8 wand β-human chorionic gonadotropin was less than8 Z/ N( s/ F5 n) r& ^/ u& N! @1 h
5 mIU/mL (normal <5 mIU/mL). Serum follicular9 C: _# w% r: Z3 D
stimulating hormone and leuteinizing hormone
$ J6 E& @) d/ ]2 U3 cconcentrations were less than 0.05 mIU/mL
: G) ~4 g4 D; @: f- n9 B(prepubertal).* U0 H; m2 j) K6 X
The parents were notified about the laboratory, N& C7 _0 M/ a2 b  l" V* q: N
results and were informed that all of the tests were* a) b3 l  E) }) v' @* B) I8 L5 i
normal except the testosterone level was high. The
; w+ x+ c, D% z) Ffollow-up visit was arranged within a few weeks to
: m) ^  v. \: o1 O$ aobtain testicular and abdominal sonograms; how-9 a4 i0 w  U1 L6 t, X8 ], B( d/ z
ever, the family did not return for 4 months.
# g, P$ v, U: y9 J, W( Y+ ~* APhysical examination at this time revealed that the
9 o, ?2 c  o" L3 X3 q9 P5 N( h' Q$ zchild had grown 2.5 cm in 4 months and had gained0 U6 X( j& {0 F0 j
2 kg of weight. Physical examination remained
! Q& V" s) p. ~unchanged. Surprisingly, the pubic hair almost com-
3 e7 [: F2 t4 W! L, X# r8 @pletely disappeared except for a few vellous hairs at
) l& i* O4 Q9 Y- T  @# M+ K1 \the base of the phallus. Testicular volume was still 2
( k& Q. Z* j6 y5 amL, and the size of the penis remained unchanged.  [4 A. Q/ n* U& x" _; b
The mother also said that the boy was no longer hav-# q* M2 R' t8 F) _+ Y
ing frequent erections.
6 o) r) L' E" ~. Z+ oBoth parents were again questioned about use of. @0 Q( q0 W  I4 B+ {+ K' m
any ointment/creams that they may have applied to
  V9 M: M" ?. F7 L4 A. cthe child’s skin. This time the father admitted the
) h8 w! w) ]2 l- Z* zTopical Testosterone Exposure / Bhowmick et al 541: G% m3 W- n3 D& w( O0 c) G
use of testosterone gel twice daily that he was apply-
- U, v3 I. P. c/ ~: r' Wing over his own shoulders, chest, and back area for
  H; F  b! k+ [3 u6 _a year. The father also revealed he was embarrassed, N) f' O% {# r- u5 S3 h4 b
to disclose that he was using a testosterone gel pre-# @4 U4 d6 }: k' e' n# w- P, j
scribed by his family physician for decreased libido+ U6 _# B# c# o# A) p; T
secondary to depression.  e9 o  m9 n0 ]/ R! q* W; z
The child slept in the same bed with parents.
6 e( N$ P2 s2 G9 B2 ^6 I: }4 M7 |The father would hug the baby and hold him on his( C; e" A' L# [0 l8 U& S- z' S, d
chest for a considerable period of time, causing sig-
+ b4 ]6 k+ G2 q4 {) \* bnificant bare skin contact between baby and father.
- @/ w. e+ u9 k$ f. ^0 JThe father also admitted that after the phone call,7 h9 U0 Y& [1 E4 |, [: m3 _
when he learned the testosterone level in the baby5 d. b# \5 s6 O5 l/ H
was high, he then read the product information
) I2 q& L  [# U% _packet and concluded that it was most likely the rea-$ `" e! {' _9 s. Z  J
son for the child’s virilization. At that time, they7 ^$ ?7 c' b7 N+ ]* a
decided to put the baby in a separate bed, and the& E* W& X+ j& n
father was not hugging him with bare skin and had
: r& D) j( w$ b: abeen using protective clothing. A repeat testosterone
0 d, z7 o* [7 Utest was ordered, but the family did not go to the. t: B( {4 D( f% {8 p
laboratory to obtain the test.' r, n9 `6 U; W
Discussion7 U8 `) `9 l' ?% L6 [6 `- S6 m
Precocious puberty in boys is defined as secondary
; z) r8 j4 ]3 a- C6 ^sexual development before 9 years of age.1,46 P# b) O5 \% b9 X0 ^! U
Precocious puberty is termed as central (true) when  W0 q! B7 w) T2 Z
it is caused by the premature activation of hypo-
+ p1 \8 o8 H+ Y7 J1 A6 f; sthalamic pituitary gonadal axis. CPP is more com-' \. k4 @" e7 B# t3 m" [
mon in girls than in boys.1,3 Most boys with CPP5 H/ }  ]  e! v
may have a central nervous system lesion that is( t+ h$ M  S7 E2 Q9 `
responsible for the early activation of the hypothal-
+ L- e; O, }! |: Iamic pituitary gonadal axis.1-3 Thus, greater empha-
. K, R( Z) u( w) z/ Isis has been given to neuroradiologic imaging in/ Q7 x$ ]7 [1 g! t6 O; T0 }2 ~, D
boys with precocious puberty. In addition to viril-" |& g3 E& k: w% K" V0 |# ], Y0 z
ization, the clinical hallmark of CPP is the symmet-
+ d" K  j5 C2 P' p) irical testicular growth secondary to stimulation by, W( w. a$ ^0 _- a# h& O7 x7 ~  s& s
gonadotropins.1,32 D% W# a; P9 X* O* ?2 W) S5 O0 }" S
Gonadotropin-independent peripheral preco-
# I8 s0 W9 T! ~# d8 f) ~2 ycious puberty in boys also results from inappropriate. x4 A2 `( r* R& |$ D2 m
androgenic stimulation from either endogenous or
9 d  i* e- a8 M! H) {exogenous sources, nonpituitary gonadotropin stim-$ g( R5 F& w2 Z# z, a1 f, _. K& o: ?
ulation, and rare activating mutations.3 Virilizing& b' @" ]1 L4 W- j7 c3 N5 x2 _4 B+ Q
congenital adrenal hyperplasia producing excessive
9 H& P3 q& d1 `" f2 tadrenal androgens is a common cause of precocious
3 D, |( a2 @3 F: a1 }/ _: Z' P' ?4 apuberty in boys.3,4& u. n4 l; W7 K
The most common form of congenital adrenal' C# }- r7 L3 }, A
hyperplasia is the 21-hydroxylase enzyme deficiency.
0 `7 n$ f7 _- }5 e9 MThe 11-β hydroxylase deficiency may also result in& D) F1 c3 W6 x
excessive adrenal androgen production, and rarely,  W7 Y1 E# b  |
an adrenal tumor may also cause adrenal androgen! X' P  A. A5 c1 }# J
excess.1,35 Z4 ?9 |3 l4 l. y3 E7 T  Y! x0 c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 S# K) H6 i3 R3 ^$ C
542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 u" I4 `" s7 x! Y4 f
A unique entity of male-limited gonadotropin-: p/ h1 b& _* f. a' U/ N9 m
independent precocious puberty, which is also known4 x. D6 S$ F& K7 F7 M! f* `8 z
as testotoxicosis, may cause precocious puberty at a
* s5 m# b, ]3 _, Zvery young age. The physical findings in these boys; g1 O5 F0 [  W
with this disorder are full pubertal development,2 a2 n% m' C5 w' T9 x5 q1 B
including bilateral testicular growth, similar to boys
" z: I5 w2 G) T+ Jwith CPP. The gonadotropin levels in this disorder
  [" y) M/ p( vare suppressed to prepubertal levels and do not show
! v8 x0 Y. R& e' U# }1 opubertal response of gonadotropin after gonadotropin-
9 K9 y. \! J" M: ~# Treleasing hormone stimulation. This is a sex-linked$ h9 A6 q' I5 u' o
autosomal dominant disorder that affects only5 K2 [, M& U/ I8 ]& I
males; therefore, other male members of the family
5 i% ]/ f5 }- B- y2 c% bmay have similar precocious puberty.3
: J; [$ `8 s4 l% y' M2 bIn our patient, physical examination was incon-$ j( Y/ I3 b2 Y  g1 z( V, P
sistent with true precocious puberty since his testi-" C" N# X0 e/ d! i; W  Z8 A7 m) a- g4 V
cles were prepubertal in size. However, testotoxicosis
3 d/ D6 ]) ^; p, ?was in the differential diagnosis because his father+ a7 N* k& a6 U0 A. ^" E0 @
started puberty somewhat early, and occasionally,& r# r- J7 H9 U& w0 o& x
testicular enlargement is not that evident in the
1 \  G$ l) Q2 V+ A' M2 {# zbeginning of this process.1 In the absence of a neg-
% \3 C2 e+ V' _4 q0 }# _& M! _ative initial history of androgen exposure, our' X5 l' C% s% y9 l+ i
biggest concern was virilizing adrenal hyperplasia,
, A! z! B' V/ k% G  }- heither 21-hydroxylase deficiency or 11-β hydroxylase
: }6 ~- n8 u, X* T0 Wdeficiency. Those diagnoses were excluded by find-( ]0 p9 _$ c3 W
ing the normal level of adrenal steroids.
, K+ f8 z$ A0 X" w2 A# sThe diagnosis of exogenous androgens was strongly* ]9 e2 G: r$ v/ |
suspected in a follow-up visit after 4 months because
" ]2 Y5 h- N: K/ f) i( r" f: hthe physical examination revealed the complete disap-
0 ]; }: h/ K, n3 u, Wpearance of pubic hair, normal growth velocity, and
8 V. V& C; e9 O+ b2 ^* Fdecreased erections. The father admitted using a testos-, g* n+ n3 d; x
terone gel, which he concealed at first visit. He was
: j* i, q8 B! I& r. l% E( e- b1 susing it rather frequently, twice a day. The Physicians’5 v; S2 _$ w: c3 X( e% [% |& u; {
Desk Reference, or package insert of this product, gel or6 b0 o1 Z/ A8 `9 z' `
cream, cautions about dermal testosterone transfer to
  \: g! @4 N, W- y# xunprotected females through direct skin exposure.
  w# p2 K4 ?9 H  i, nSerum testosterone level was found to be 2 times the
( a/ o* Z: c& v$ K. u, {8 }: M/ _baseline value in those females who were exposed to
3 t7 R& x3 U2 G8 a" {1 `even 15 minutes of direct skin contact with their male
3 h7 j% h# _: cpartners.6 However, when a shirt covered the applica-3 G$ R5 b& M, N5 v, y, M$ n
tion site, this testosterone transfer was prevented.
- {- Q8 v, k& W1 o; c( Q4 V' N4 |Our patient’s testosterone level was 60 ng/mL,# `7 A5 g7 h2 K9 I% u9 N2 w
which was clearly high. Some studies suggest that+ ^4 ^1 _+ q8 v* Z! H# X9 T
dermal conversion of testosterone to dihydrotestos-
9 r; K) L6 `9 ?0 @7 {( aterone, which is a more potent metabolite, is more9 n3 K  ?4 C$ k- ~# B5 J0 J+ |
active in young children exposed to testosterone
: D$ u2 {9 z$ V4 T8 f* sexogenously7; however, we did not measure a dihy-! G$ M. B+ F' H) g" W4 I
drotestosterone level in our patient. In addition to
0 {3 w0 _9 e' Q4 |0 s9 [/ s! cvirilization, exposure to exogenous testosterone in
1 m8 o3 N# E2 m% }  ^children results in an increase in growth velocity and9 F7 S! B% ^$ e. F
advanced bone age, as seen in our patient.
$ l' H5 ]# Q( a7 dThe long-term effect of androgen exposure during
9 |) n; ?% S- R& Y- R# K/ x) nearly childhood on pubertal development and final
& c1 T" r/ \; s" B$ h8 ?( }6 `; \adult height are not fully known and always remain
3 I& @! a7 S& P3 q+ La concern. Children treated with short-term testos-1 v' ]' l! ~' s7 N
terone injection or topical androgen may exhibit some
& u9 q% i$ L7 Macceleration of the skeletal maturation; however, after
& s5 l9 ^0 o; @cessation of treatment, the rate of bone maturation
+ \1 m) l/ z) W6 Rdecelerates and gradually returns to normal.8,9
8 D$ G( a: g3 J* U) E: R5 I$ jThere are conflicting reports and controversy
$ R7 O2 A1 y# L/ Aover the effect of early androgen exposure on adult/ O, C6 d/ F% M- l: O2 u
penile length.10,11 Some reports suggest subnormal
8 S4 h& J& {1 u! }7 dadult penile length, apparently because of downreg-& q1 U. l+ b( `/ v* O; B
ulation of androgen receptor number.10,12 However,
3 x8 L6 F2 K, a+ M  gSutherland et al13 did not find a correlation between
( a2 \8 }' C+ c% W' Uchildhood testosterone exposure and reduced adult2 c9 w) f  @$ m* ]2 b" Q" |) Y
penile length in clinical studies.
  Z! y$ k% A' O3 P  N+ ONonetheless, we do not believe our patient is4 |% H* O7 O. Z9 S. j  ^9 ^9 l% l
going to experience any of the untoward effects from+ y( V+ t& m4 W! |
testosterone exposure as mentioned earlier because3 P" O( \( E% O2 i$ y
the exposure was not for a prolonged period of time.) m7 R& M9 o  o
Although the bone age was advanced at the time of
& ^; b. M& ]& w" {0 U- Ediagnosis, the child had a normal growth velocity at
5 [2 [' K' j& Athe follow-up visit. It is hoped that his final adult. x! J1 h0 [; I, G( _  r: p
height will not be affected.
9 C  `3 i# M  ^* a( a2 j8 WAlthough rarely reported, the widespread avail-
3 R) p* u7 r# M0 o( L( X/ Y1 r4 Tability of androgen products in our society may
' ~. F- J: `8 L4 [indeed cause more virilization in male or female' l- [! f' m7 @( h5 ]: {, S3 Q
children than one would realize. Exposure to andro-( G7 E+ C, A8 C( |) }: Q
gen products must be considered and specific ques-4 K3 x0 V: F' Q6 T- ?4 u
tioning about the use of a testosterone product or
8 |$ p  D; x+ W5 @gel should be asked of the family members during. ~* |5 y5 Y7 |+ ^" |: ?4 N! l3 O# r
the evaluation of any children who present with vir-; u1 R* }% Y6 v% b$ w) B1 X; g& ?
ilization or peripheral precocious puberty. The diag-3 h- z/ O) u8 X2 Z2 R+ v$ w
nosis can be established by just a few tests and by4 p9 x, m2 S8 H3 }* {. I
appropriate history. The inability to obtain such a+ Z  J3 i5 D9 r, [6 f/ B
history, or failure to ask the specific questions, may9 O7 _5 G& }' f1 h- R) w
result in extensive, unnecessary, and expensive9 n+ f; O1 p9 X$ _' `
investigation. The primary care physician should be
* V  v3 N3 w+ H" _/ E; |. A4 Y7 Q( Faware of this fact, because most of these children6 j9 O8 }5 h. f2 U& k% j3 M
may initially present in their practice. The Physicians’
8 Z! K0 _. w- Y7 d/ D/ QDesk Reference and package insert should also put a$ Q* B8 m8 h6 }! B( P  H
warning about the virilizing effect on a male or
1 b3 h2 v6 h6 x' Q% M( N  H: j6 o$ Gfemale child who might come in contact with some-
! s+ y! c. o3 p& Gone using any of these products.! R2 G" P1 ^% X2 l9 O
References* l1 ~( c8 k2 d4 K$ O; u; D- ^
1. Styne DM. The testes: disorder of sexual differentiation
0 y  l- ]! O: u2 P2 b* i2 j( a6 W" aand puberty in the male. In: Sperling MA, ed. Pediatric
3 T( ~0 A7 p; v4 dEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;9 n; W8 }2 ^% x8 `% q6 |: q
2002: 565-628.2 V4 q3 O& }+ q: @
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious5 Y* L- {  f2 |  H1 g5 a; r
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-4 03:27:02 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
Sexual Precocity in a 16-Month-Old5 [; E8 Q/ F! _5 u
Boy Induced by Indirect Topical9 y! t! ^; ]0 ?, _
Exposure to Testosterone0 D- s/ I/ X" Q2 ?
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 a$ {6 B6 P& D, hand Kenneth R. Rettig, MD1
3 s' V' E5 i/ n7 `3 k/ eClinical Pediatrics. K+ f* H$ t- r; Q* z: U- x+ n
Volume 46 Number 6! N# ^' _2 B0 [6 O% `" Q0 d8 ]. p2 M) [
July 2007 540-543! |- O7 ?# y* v( z% r8 h3 u
© 2007 Sage Publications
7 [6 m# E6 b( P% f/ y1 W$ E10.1177/0009922806296651, L* n- A+ d$ p
http://clp.sagepub.com
* c* h6 b1 |2 z4 H- Rhosted at
( g! R0 ~1 {& R5 J) ~; G, ~http://online.sagepub.com9 ]/ e, F( o+ Q- W8 Z6 I+ I: T
Precocious puberty in boys, central or peripheral,
. l# P% Z* o  K4 O3 f; Y* [is a significant concern for physicians. Central
0 q4 G+ F$ E$ }3 }8 `' {0 }$ `precocious puberty (CPP), which is mediated
. p9 d, z8 G0 s! a0 f8 y5 I  Cthrough the hypothalamic pituitary gonadal axis, has0 f( o" Z9 \' W2 f, T0 Z, ]: P
a higher incidence of organic central nervous system7 E( ~& u$ E8 s& Q- b
lesions in boys.1,2 Virilization in boys, as manifested/ _; V3 O7 v9 `6 L& y
by enlargement of the penis, development of pubic
+ y0 t) d8 D5 P7 vhair, and facial acne without enlargement of testi-# C1 J' `0 Z1 x6 ^# t
cles, suggests peripheral or pseudopuberty.1-3 We" G% u0 M8 U. V" A' S# c. A
report a 16-month-old boy who presented with the" k: p( n3 b$ ~/ @% w' |* a* [
enlargement of the phallus and pubic hair develop-2 P7 u7 a6 h* G
ment without testicular enlargement, which was due" [5 r5 d8 L+ W0 {$ L" O  v" O
to the unintentional exposure to androgen gel used by
  X0 _9 H$ v& }the father. The family initially concealed this infor-/ j% [( b% R& z3 M  y
mation, resulting in an extensive work-up for this
. E3 b! a3 m% ~% ]6 Tchild. Given the widespread and easy availability of
0 {8 |5 T0 I1 ttestosterone gel and cream, we believe this is proba-: m1 A4 F( {' o5 J1 C; Q; b
bly more common than the rare case report in the
: p: B, {! w3 a) O+ x" ?  d. I) [literature.4* o0 o8 d6 A- ~
Patient Report8 e/ Y5 W1 B0 w8 t! y- W
A 16-month-old white child was referred to the
2 B* D( v( K4 ^! Nendocrine clinic by his pediatrician with the concern
% A4 \3 L+ X8 @. ^: k% b1 o% u9 Bof early sexual development. His mother noticed
' C1 K" d6 I9 B9 G& E  w& x2 Plight colored pubic hair development when he was
- K2 l# i) h, k7 SFrom the 1Division of Pediatric Endocrinology, 2University of
" j/ g7 c5 X& O9 mSouth Alabama Medical Center, Mobile, Alabama.
5 O; G  l; e- p# pAddress correspondence to: Samar K. Bhowmick, MD, FACE,' ?& r* t! j0 ]2 {' T
Professor of Pediatrics, University of South Alabama, College of7 F5 [) H1 d8 B, x
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 L  Y/ A! j% Q8 Y
e-mail: [email protected].
# h. M. c' u9 a& X8 z9 }3 O2 W9 O- wabout 6 to 7 months old, which progressively became5 ?: N+ V  E5 `9 S! ~' R
darker. She was also concerned about the enlarge-5 L; H$ b5 G+ `
ment of his penis and frequent erections. The child6 v) z6 j4 V: D- W% d: f
was the product of a full-term normal delivery, with9 V1 G2 S2 l# [1 a5 F: @
a birth weight of 7 lb 14 oz, and birth length of0 W( Q+ t) r1 {! a: q  `
20 inches. He was breast-fed throughout the first year, p6 x4 G8 V6 P" M$ i
of life and was still receiving breast milk along with% q. P; V& ]. x! C
solid food. He had no hospitalizations or surgery,4 f6 n9 A8 ]" I# j8 ^
and his psychosocial and psychomotor development* S+ ?( y2 T! P$ n+ Z4 ?* z
was age appropriate.
4 P) F! f) q; j5 q1 |The family history was remarkable for the father,- ~8 Y% X. w0 A9 _7 A
who was diagnosed with hypothyroidism at age 16,5 S. c4 ?: Y# [4 Z+ S0 \9 O
which was treated with thyroxine. The father’s# x7 D: {. t5 @1 B0 V- @% C
height was 6 feet, and he went through a somewhat2 Z  B5 H6 ]" H/ d! C/ f- u
early puberty and had stopped growing by age 14.
2 z+ n- O2 j/ D) ~* \The father denied taking any other medication. The- m& ]2 A2 c* ?+ z  m
child’s mother was in good health. Her menarche, `1 X$ \3 k, a8 W$ G
was at 11 years of age, and her height was at 5 feet
. a# S! o0 E4 t; o7 \5 |' @5 inches. There was no other family history of pre-
0 N& i, O- b2 e# Ycocious sexual development in the first-degree rela-" Q) o) Y. e. h
tives. There were no siblings.
) s9 C8 ]4 E, \/ e6 _6 QPhysical Examination5 D8 e- D. j7 P9 C. J
The physical examination revealed a very active,
8 Z9 e; Z% n0 a$ p* C/ Splayful, and healthy boy. The vital signs documented
) v8 b  W; S6 n) F  ~a blood pressure of 85/50 mm Hg, his length was
) S- [3 J: H% D3 ?90 cm (>97th percentile), and his weight was 14.4 kg
# k  j' ^( h( t- C* X( i(also >97th percentile). The observed yearly growth: h5 R6 J- {# k4 z0 T1 R
velocity was 30 cm (12 inches). The examination of
$ J+ z7 `, A1 E. b5 ~; Bthe neck revealed no thyroid enlargement.+ J4 P9 u/ h& i2 [
The genitourinary examination was remarkable for
6 D. f8 U# x3 t: wenlargement of the penis, with a stretched length of3 d& i; Z* y) `3 X- r
8 cm and a width of 2 cm. The glans penis was very well! w6 U7 W$ s$ ?2 _& u4 Y0 e' w
developed. The pubic hair was Tanner II, mostly around
! U: p3 t3 J6 X8 e5 z' U% m& _; G, Z540
7 m2 e% _8 s0 Q" `2 A( P+ |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 E1 A9 p1 s0 c) E. }9 k
the base of the phallus and was dark and curled. The2 `6 t) z- [( j1 Y, A. w6 x- K
testicular volume was prepubertal at 2 mL each.0 f' o9 G* l/ m) w9 v
The skin was moist and smooth and somewhat1 _: \; }) s) i, C" t" @
oily. No axillary hair was noted. There were no
% N4 w8 `! o( G- L& ^1 F5 g+ d% Nabnormal skin pigmentations or café-au-lait spots.
1 @3 [( w* u4 M: _Neurologic evaluation showed deep tendon reflex 2+
& A% l, M( i- _2 W' [9 ~bilateral and symmetrical. There was no suggestion7 ^6 f: S" K% R
of papilledema.
. ^  i0 ?: T0 T6 J. h% a/ rLaboratory Evaluation$ S& d, q2 p: y1 g
The bone age was consistent with 28 months by* Y' f9 [$ d1 @! t9 w( ^. a
using the standard of Greulich and Pyle at a chrono-
6 y0 z& Q6 c3 ]* X& l% {9 `logic age of 16 months (advanced).5 Chromosomal
% j9 M3 `5 |5 D& @( q6 s' Akaryotype was 46XY. The thyroid function test
9 S* u- ~0 }3 x) Z- h) C8 }/ N* Bshowed a free T4 of 1.69 ng/dL, and thyroid stimu-! j- c! R, n9 J3 m* g4 N
lating hormone level was 1.3 µIU/mL (both normal).
% C; p+ w" t1 @7 b5 W0 dThe concentrations of serum electrolytes, blood6 Y9 E9 y' x% c5 t$ ?
urea nitrogen, creatinine, and calcium all were1 f) y6 k* y1 s1 L
within normal range for his age. The concentration
2 F- A' F. P* J  u5 y9 wof serum 17-hydroxyprogesterone was 16 ng/dL+ u* U4 S1 |- k
(normal, 3 to 90 ng/dL), androstenedione was 20
/ q: J" J4 w! }0 }* e' c" o7 X- J; Dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# B) W- N# F) ?" \1 G- J, e
terone was 38 ng/dL (normal, 50 to 760 ng/dL),1 `: ~" G+ E5 e
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 P, b/ J. G7 @6 L: e, }* L6 Y! `  |49ng/dL), 11-desoxycortisol (specific compound S)
" z$ ~/ Q4 P( l$ }+ R* owas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
6 g* l" ~/ v3 w; I+ J6 k; J) w8 Itisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* _( \$ C9 w. ^3 p0 ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ k3 P5 ~$ v: [7 W2 {and β-human chorionic gonadotropin was less than/ s% B2 M  ^4 Y. A1 [
5 mIU/mL (normal <5 mIU/mL). Serum follicular* \7 ^- Y. z' ]! y, J
stimulating hormone and leuteinizing hormone, }5 W. Z5 T  ^# z/ |
concentrations were less than 0.05 mIU/mL
1 ^+ N) T  {- r2 w/ y" Y8 ?$ a(prepubertal).
7 f2 A9 Y0 L+ m2 y) ~" jThe parents were notified about the laboratory
$ S6 }) M' L' \" C3 hresults and were informed that all of the tests were
( S  H( }( q0 L( onormal except the testosterone level was high. The
8 X; L* Q' v7 R! Cfollow-up visit was arranged within a few weeks to( y; q% E0 b% j) T9 Q) n$ R( B2 g9 i. ^, z
obtain testicular and abdominal sonograms; how-
; ]2 E8 U/ A6 [$ }ever, the family did not return for 4 months.5 _, N5 N7 k( J. u' h! H' I
Physical examination at this time revealed that the* T, g5 @* S. s; c9 D
child had grown 2.5 cm in 4 months and had gained, D  G' _, x: j
2 kg of weight. Physical examination remained" o  X3 ], l& y" g: R) U
unchanged. Surprisingly, the pubic hair almost com-% P; a% B7 y$ w3 \
pletely disappeared except for a few vellous hairs at
" k# W/ @1 W+ ]3 T7 _4 Qthe base of the phallus. Testicular volume was still 2, ~$ n2 J) m1 X7 Y
mL, and the size of the penis remained unchanged.7 T4 A: g4 ~% w: P" c: E
The mother also said that the boy was no longer hav-
: e: e7 z' |+ H) V3 a+ B9 t* `ing frequent erections.
+ H; F: c( Q3 ]( U- s  hBoth parents were again questioned about use of0 r- Q) H/ F& Y- n8 s
any ointment/creams that they may have applied to
! ]& D( v% b* o8 r2 rthe child’s skin. This time the father admitted the* [. D2 ]; I8 ^' p! }- ~
Topical Testosterone Exposure / Bhowmick et al 5419 S' c) b% E% Q8 Y" l* z+ D
use of testosterone gel twice daily that he was apply-, m. y: j' n" k3 [
ing over his own shoulders, chest, and back area for
1 T- j; Q# T) X: v" p3 W& Ca year. The father also revealed he was embarrassed
+ ^" ^% a* H. `* sto disclose that he was using a testosterone gel pre-9 K/ P1 H5 O8 X" s& z
scribed by his family physician for decreased libido8 J4 J, O& \+ k# o! w' D9 ?" K
secondary to depression.
, N5 t; p) f( W$ A* {The child slept in the same bed with parents.
* [2 d0 A: a9 P7 cThe father would hug the baby and hold him on his; T8 L) P# H4 R$ ~) U
chest for a considerable period of time, causing sig-7 s! D3 H  {. f) S
nificant bare skin contact between baby and father.
1 m+ x9 ~  i5 j5 t6 OThe father also admitted that after the phone call,
  y. ?4 O( u" Rwhen he learned the testosterone level in the baby9 q6 q% n1 C9 f' [5 |4 ^4 I
was high, he then read the product information
+ j/ Y, A/ @* ]7 hpacket and concluded that it was most likely the rea-: w: p- C5 j4 t) P
son for the child’s virilization. At that time, they
. z" C* t( k$ D0 G: Qdecided to put the baby in a separate bed, and the
3 H/ U3 N) n6 c0 Q: |: cfather was not hugging him with bare skin and had/ G6 M2 I% W5 N4 P
been using protective clothing. A repeat testosterone' h8 [- G" h8 O4 I; X" I1 j
test was ordered, but the family did not go to the# j. o; D# D8 L2 ?
laboratory to obtain the test.0 U, R) Z( ]) c  w& w; v
Discussion  o1 D) r' {/ O. ~  B; j+ e* ?/ o2 a
Precocious puberty in boys is defined as secondary% k7 D/ F2 E2 V( a4 p
sexual development before 9 years of age.1,44 `* M+ a8 H" d/ U
Precocious puberty is termed as central (true) when
0 E" a2 V9 d5 P3 h# l0 w3 _; [it is caused by the premature activation of hypo-7 n; P1 s- l. I9 ?
thalamic pituitary gonadal axis. CPP is more com-) F2 i4 z6 q8 P/ s
mon in girls than in boys.1,3 Most boys with CPP: M7 Q' J4 P$ _$ i4 G
may have a central nervous system lesion that is4 ?3 x3 D4 u. i7 ^
responsible for the early activation of the hypothal-$ K: i  {1 z* ~& N/ P3 t
amic pituitary gonadal axis.1-3 Thus, greater empha-
; |2 U% p) U2 Z" t* Ksis has been given to neuroradiologic imaging in$ [5 {6 w5 @$ t/ @; c
boys with precocious puberty. In addition to viril-
; z/ x/ M( Q* e$ V$ ]2 yization, the clinical hallmark of CPP is the symmet-
6 C4 K+ f/ g4 p' g7 k9 W- \, Lrical testicular growth secondary to stimulation by
& n. C9 z6 e. e+ D1 E  Rgonadotropins.1,3
4 S% S8 G5 ?( I8 k7 {4 _Gonadotropin-independent peripheral preco-
7 R3 A! A* }& K: ocious puberty in boys also results from inappropriate
0 J! w4 z! G; Y; z0 }" V4 Oandrogenic stimulation from either endogenous or* x4 H. X  p) l  b
exogenous sources, nonpituitary gonadotropin stim-( _6 H) |- O# |. f3 T3 D3 I
ulation, and rare activating mutations.3 Virilizing
9 N1 n5 b5 |  Q4 J; s- U" U2 Ccongenital adrenal hyperplasia producing excessive
  V) ~, Z+ D8 X1 Z. Fadrenal androgens is a common cause of precocious" ]) J& b! i; q$ V6 r
puberty in boys.3,4
0 x) b6 c; ^" i. X; }The most common form of congenital adrenal. E* l( j7 o, ^% N9 ^2 t* H& o
hyperplasia is the 21-hydroxylase enzyme deficiency.
7 G8 }3 v) Z& ]- X8 JThe 11-β hydroxylase deficiency may also result in
2 f  `* E8 N- y) V% p, Uexcessive adrenal androgen production, and rarely,/ Q% h0 J$ z' S) `5 O+ ~- }; V
an adrenal tumor may also cause adrenal androgen
* m4 D, A" @2 C3 X- Uexcess.1,35 E4 Y+ Z6 c6 ?; U) Q6 o0 b' b7 J
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, }7 _' t+ t8 h# X+ S! e542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# D9 |" L3 p- Q3 E* Q
A unique entity of male-limited gonadotropin-
9 J! g2 J8 x" u( C2 f  |# `independent precocious puberty, which is also known
- H! l1 a3 q" j9 X; zas testotoxicosis, may cause precocious puberty at a
7 o- |+ A, O3 a, @, Every young age. The physical findings in these boys4 A5 h8 s1 |5 ^7 C; O+ n
with this disorder are full pubertal development,/ D! ^9 v; I3 f
including bilateral testicular growth, similar to boys
7 z4 |& T4 E7 Nwith CPP. The gonadotropin levels in this disorder) i" \; s. v, K6 t2 d- C
are suppressed to prepubertal levels and do not show- `6 V2 A: P; Y* C. v8 ^* @
pubertal response of gonadotropin after gonadotropin-
% w6 N$ D! s+ e2 b& @& g* b3 c2 Xreleasing hormone stimulation. This is a sex-linked
1 w; ~7 F  T; Y* Q. Tautosomal dominant disorder that affects only# [. e3 \/ m8 e% V' F
males; therefore, other male members of the family
4 u+ p- K  i+ f' r6 @1 p5 B$ pmay have similar precocious puberty.34 @. ?- X; |" c
In our patient, physical examination was incon-
! s- R  |8 k6 ^1 r3 r3 @9 [" X$ [6 vsistent with true precocious puberty since his testi-
! Y- b. [: `. o" C% f: a& {) Icles were prepubertal in size. However, testotoxicosis5 A/ Y, ?+ j. {0 S
was in the differential diagnosis because his father- ^: t1 r$ U; l
started puberty somewhat early, and occasionally,
* y; l6 d. j! w+ M. Ztesticular enlargement is not that evident in the! ?# U. Y" d3 N9 Q' R
beginning of this process.1 In the absence of a neg-8 v9 l: }5 ^  L  Q4 h/ x
ative initial history of androgen exposure, our
1 Y. `* Q% I# wbiggest concern was virilizing adrenal hyperplasia,0 m( p7 e" f. T8 ~6 W- I# {" J
either 21-hydroxylase deficiency or 11-β hydroxylase8 R! t; k  c  g- N2 i2 E- Y3 V. P% ~
deficiency. Those diagnoses were excluded by find-; n- t/ u7 Y8 g% j. ?  R% b
ing the normal level of adrenal steroids.% k* _6 N% t; l; D
The diagnosis of exogenous androgens was strongly( {3 [8 ~! b8 j, m  t- m
suspected in a follow-up visit after 4 months because
0 d. d0 \7 i/ a$ V) x3 n+ N7 lthe physical examination revealed the complete disap-
% v1 Y( s9 u) X! q- I- \& Tpearance of pubic hair, normal growth velocity, and
- [' B9 Q3 [+ z; |) G4 S+ Wdecreased erections. The father admitted using a testos-9 T( c" j1 ]- v2 e& g" g
terone gel, which he concealed at first visit. He was
3 @1 J, U7 {) r  ^7 z+ k& ^5 Qusing it rather frequently, twice a day. The Physicians’, |" U+ ?, w+ D) `2 K
Desk Reference, or package insert of this product, gel or7 J; f/ A) n5 u
cream, cautions about dermal testosterone transfer to( m1 H" n" V( W
unprotected females through direct skin exposure.1 Q3 F$ o4 D2 A! `
Serum testosterone level was found to be 2 times the0 M% \" N4 d" {' i. |
baseline value in those females who were exposed to& D" e+ ~" p8 }
even 15 minutes of direct skin contact with their male
3 W; }( r( u' b+ wpartners.6 However, when a shirt covered the applica-
/ Q  d% g& }0 `: b5 m- _6 ]/ Ition site, this testosterone transfer was prevented.
$ t+ z) ?$ L+ k& U0 ]Our patient’s testosterone level was 60 ng/mL,; a1 ?; ]; n! [; m1 T% n# @/ w
which was clearly high. Some studies suggest that5 {4 e( `. O! K6 S$ }0 w
dermal conversion of testosterone to dihydrotestos-
3 p. ~3 r4 Z! S1 g; n, aterone, which is a more potent metabolite, is more
7 D' N; B! e) n/ }" t) h' K8 Xactive in young children exposed to testosterone
" l- H$ Q$ N- F) eexogenously7; however, we did not measure a dihy-2 F" k! }5 R# B; o$ u/ d, e; N
drotestosterone level in our patient. In addition to
: L# O, i4 T9 u- dvirilization, exposure to exogenous testosterone in
2 q1 _7 \) J& }  Y8 mchildren results in an increase in growth velocity and
: l- u" q# |  M" Iadvanced bone age, as seen in our patient.
# r9 i* U) n: ?- Q1 IThe long-term effect of androgen exposure during
1 W! b$ q3 L3 A5 u2 M. Y. aearly childhood on pubertal development and final7 O; q& c: `) d9 c5 [
adult height are not fully known and always remain: C' ^) n' F- K2 v, a( @- N. K
a concern. Children treated with short-term testos-
* n( Q) K' Q/ vterone injection or topical androgen may exhibit some
' a6 }" b, Q: q1 Z# E+ Iacceleration of the skeletal maturation; however, after
& y6 q, I5 F( W1 Icessation of treatment, the rate of bone maturation
. j- o0 h. ]- R9 K2 Qdecelerates and gradually returns to normal.8,9
3 k4 H- |6 a5 IThere are conflicting reports and controversy4 ^+ H+ g- h9 ]* ^! Q! H
over the effect of early androgen exposure on adult
5 r. _# x4 g' p0 Hpenile length.10,11 Some reports suggest subnormal
3 x1 v( B) ~8 w% g9 }  J+ l7 Padult penile length, apparently because of downreg-! `  |6 e! D2 U# {" w, r
ulation of androgen receptor number.10,12 However,
( ~6 R( q  v+ x7 x6 fSutherland et al13 did not find a correlation between
8 ~! g2 s+ s( C+ O) X* k# ~childhood testosterone exposure and reduced adult& W' _& |! F9 W% S6 I( t! J- z
penile length in clinical studies.3 p; C* |$ Q+ k
Nonetheless, we do not believe our patient is
7 n' |% J+ v$ `4 h' \% tgoing to experience any of the untoward effects from
" ^0 o. T' \" n0 N3 e  Ttestosterone exposure as mentioned earlier because
; @. c* e* M' r! A/ ~1 j) e" ithe exposure was not for a prolonged period of time.1 Y+ M+ |& V! a7 m3 J# M  n
Although the bone age was advanced at the time of
8 W  `* ]$ Y9 k; `; R1 Ediagnosis, the child had a normal growth velocity at1 x" k( b6 V' k: B! u
the follow-up visit. It is hoped that his final adult. Y  w2 {3 q$ E5 `) ?) I& P
height will not be affected.
, r' f" k7 ?' _, E( N( O0 rAlthough rarely reported, the widespread avail-/ V" ~- b1 H2 [4 L4 P1 P# Y
ability of androgen products in our society may8 ?; c4 l) P7 \* T& H
indeed cause more virilization in male or female
1 M& Z% i: e: ]; |: achildren than one would realize. Exposure to andro-
( r# ?' P$ k' E" o4 |" Fgen products must be considered and specific ques-) O9 Q0 l! P: Q( |4 d% |1 J) L" I
tioning about the use of a testosterone product or
7 `/ D( H) i' L' y0 [gel should be asked of the family members during
/ C6 V+ i' M) O  n4 zthe evaluation of any children who present with vir-
- Q$ Z0 U' s! s8 @+ [ilization or peripheral precocious puberty. The diag-
5 H0 c8 N( L& D- J) T/ Dnosis can be established by just a few tests and by! l( n6 I, |1 r- `( f2 v  R2 O% B2 ?' I
appropriate history. The inability to obtain such a
2 U% `6 c" _5 B& }history, or failure to ask the specific questions, may
& ]+ u9 U: q% z6 _- c$ iresult in extensive, unnecessary, and expensive7 Z; H" Q8 a5 Y6 C+ [3 ^6 i
investigation. The primary care physician should be  a$ M2 P& N  a9 _2 b/ Z; A( K
aware of this fact, because most of these children
6 _6 `0 z& M  Ymay initially present in their practice. The Physicians’
( p) N9 F' ~4 u1 f+ V2 v4 V3 ~# m/ @Desk Reference and package insert should also put a: U& n2 |' r# s2 P
warning about the virilizing effect on a male or( Z5 z, Q2 \, u' r! ~
female child who might come in contact with some-
- p% X; k1 h# I( i, [( qone using any of these products.
) ^  [2 Q  [: K) `8 \# r4 uReferences  m) x! j& T. K0 ~& l
1. Styne DM. The testes: disorder of sexual differentiation* Y5 W$ E5 k- g
and puberty in the male. In: Sperling MA, ed. Pediatric
/ T& X: z4 t% n, gEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* ?: s* P/ C/ k* B
2002: 565-628.
* l  U" B- l8 d8 ~( Z* f3 H: ~2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 Z/ i: W* ~2 [3 U+ e! 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
* e5 y( p+ m" {0 ^% w9 h+ c
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!
您需要登錄後才可以回帖 登錄 | 立即注册

本版積分規則


快速回復 返回頂部 返回列表