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-Old1 D& p2 z% P. t! y
Boy Induced by Indirect Topical  |  Q) }! ?) @8 {( c" {
Exposure to Testosterone
( y0 l8 Y% D1 S4 [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% n' f6 x: i% M; ]4 m2 u2 W+ r% [and Kenneth R. Rettig, MD1) Y5 {+ O  B' r& e% T* U4 _
Clinical Pediatrics8 q  n( Y. d1 f- S% z4 x
Volume 46 Number 6
' ~+ V! F' K' B6 {July 2007 540-543
$ V# d% H" B' U  Q. y7 Y% W. i© 2007 Sage Publications
+ [$ M2 T6 k3 }; D) S+ P10.1177/0009922806296651
9 ~- i0 b2 A4 b7 L" d: D# o* N& ~3 R# Dhttp://clp.sagepub.com
7 n3 [# h, F0 ^# m2 g/ ~hosted at+ ~) T; g: |3 y3 t; q1 B
http://online.sagepub.com
/ _* U! ^0 w  Z" o* uPrecocious puberty in boys, central or peripheral,& d& A% @! K8 u5 |% u6 B8 k
is a significant concern for physicians. Central
( h1 V# b* A( f/ `- v! D& fprecocious puberty (CPP), which is mediated
5 k: @3 h7 r6 j3 w- F6 e* Dthrough the hypothalamic pituitary gonadal axis, has! h9 l" e& a* C* t% W% W# W& X, B% Q4 Y
a higher incidence of organic central nervous system1 C" R5 l* g' v$ I0 ~7 t* G% W
lesions in boys.1,2 Virilization in boys, as manifested
9 C7 _8 L9 F* R/ _, o# u. x1 zby enlargement of the penis, development of pubic
: ?% j* `( b( h1 x6 nhair, and facial acne without enlargement of testi-
! \& R7 S) J5 S- u0 Mcles, suggests peripheral or pseudopuberty.1-3 We( Y: g  U/ [7 s2 K0 f/ O9 q
report a 16-month-old boy who presented with the& e& G! ^# t- I9 X. A2 Z
enlargement of the phallus and pubic hair develop-
" Y6 I% w  G' b4 lment without testicular enlargement, which was due8 n6 b+ s# B; u  s7 Z+ t' q) N
to the unintentional exposure to androgen gel used by
7 B- `1 x* W8 h. I1 c: X* A2 ]the father. The family initially concealed this infor-. G$ F! _- F2 [4 ~, b, P
mation, resulting in an extensive work-up for this6 \% Y( g0 Y9 w# Q' L8 a/ p
child. Given the widespread and easy availability of
3 Y8 O2 k$ `% ctestosterone gel and cream, we believe this is proba-
" A8 `) E/ d9 vbly more common than the rare case report in the
% l& h0 ~# N: R2 X$ e3 b" [3 Hliterature.4
$ p1 y" {4 b' ]4 vPatient Report: W) i# L% G1 v2 D3 C
A 16-month-old white child was referred to the
" G6 o7 C$ o; ]8 ?! ]endocrine clinic by his pediatrician with the concern
6 O( L; T- r' J; Cof early sexual development. His mother noticed" s" r8 @. h5 p' t) T" N7 t
light colored pubic hair development when he was. q/ P$ ~( T1 z3 @! S
From the 1Division of Pediatric Endocrinology, 2University of) A! j. s' ]3 `
South Alabama Medical Center, Mobile, Alabama.
$ Q; [3 m3 T! RAddress correspondence to: Samar K. Bhowmick, MD, FACE,
1 A2 P2 ]; e& e5 uProfessor of Pediatrics, University of South Alabama, College of2 L2 ]" {/ I( b( G5 \
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;; i5 n: ^! \! ^5 e6 y. s7 `/ V
e-mail: [email protected].: m4 _/ R* H1 d& q5 V6 I: Y
about 6 to 7 months old, which progressively became
5 Z2 d7 h3 `+ q6 E$ odarker. She was also concerned about the enlarge-
9 f: l5 _& |, yment of his penis and frequent erections. The child" P; n# z, k& P$ g% [  j0 g
was the product of a full-term normal delivery, with
# N& {2 c. w5 i# w  ca birth weight of 7 lb 14 oz, and birth length of
" }( x  j0 D# m1 }20 inches. He was breast-fed throughout the first year! M1 z& [- Y, ?7 V- _$ @: E; S* r
of life and was still receiving breast milk along with' S" i! G  D, `6 q( O8 U
solid food. He had no hospitalizations or surgery,
6 D% G+ C: f9 Xand his psychosocial and psychomotor development- G; w$ G( ]+ l' h
was age appropriate.
% T. c& O1 F! A2 AThe family history was remarkable for the father,4 z) s/ }- l9 W. s) E; `* E
who was diagnosed with hypothyroidism at age 16,
. S3 T& H: N/ V3 kwhich was treated with thyroxine. The father’s
4 Y' J5 X' j' T8 W3 \height was 6 feet, and he went through a somewhat
& p5 }; @  V# Y+ B2 f, {" k+ Tearly puberty and had stopped growing by age 14.0 {; P5 W0 n/ G, M: O; A) o
The father denied taking any other medication. The' F& d& ]) W1 o/ e% E! w
child’s mother was in good health. Her menarche! e% i" r$ C; g5 l9 r
was at 11 years of age, and her height was at 5 feet' d: U3 ~5 u* c( d# ~( }1 c* l
5 inches. There was no other family history of pre-# _7 e5 A( N7 X" }8 s8 T7 |
cocious sexual development in the first-degree rela-/ O# n# L$ d  o* K- B
tives. There were no siblings.. u' A' Q2 d& f6 |- ?- d& @5 |
Physical Examination3 Q9 a" B3 G# |+ k6 w. J+ r
The physical examination revealed a very active,! h- S+ _% m9 t) r: I( I4 U6 W: I
playful, and healthy boy. The vital signs documented6 ~% _6 [7 F) u
a blood pressure of 85/50 mm Hg, his length was1 V: r+ D% _6 F# ^
90 cm (>97th percentile), and his weight was 14.4 kg* P9 }" {/ u7 A( o6 R' R! y
(also >97th percentile). The observed yearly growth
* A% A- b* Q7 C# J7 yvelocity was 30 cm (12 inches). The examination of
  o: t( S2 a; ethe neck revealed no thyroid enlargement.# D8 [6 ~0 H5 x* c* g
The genitourinary examination was remarkable for' W: \' d" k0 i- M1 v
enlargement of the penis, with a stretched length of
1 u, x8 S5 P; W0 X9 u: D8 cm and a width of 2 cm. The glans penis was very well6 R& Y7 q: `* z
developed. The pubic hair was Tanner II, mostly around2 l" l. n# Z7 [5 o" }5 z( v2 \
540
; t, k, Y4 |; L* Q5 Wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: I) n, G0 J2 f3 Q7 Ethe base of the phallus and was dark and curled. The  ]; h7 O) W! w+ o8 J# v- y
testicular volume was prepubertal at 2 mL each.
# N" `, L: C& ]& Z# MThe skin was moist and smooth and somewhat3 f& y; b( V* w7 z3 U9 \# r7 Y* r
oily. No axillary hair was noted. There were no
2 t+ \' i; p2 ~; B: {/ Kabnormal skin pigmentations or café-au-lait spots.
! ~* S( a, k0 k% S: `$ |) INeurologic evaluation showed deep tendon reflex 2+9 t% v$ P. i+ W& j7 H/ }: u
bilateral and symmetrical. There was no suggestion
2 _7 a% J. `5 E' H  m- d, N( H) hof papilledema.
' z& u( k+ _  C. iLaboratory Evaluation: b% p; b; P7 a2 C; P, N
The bone age was consistent with 28 months by7 ?# C, A. [7 k3 \
using the standard of Greulich and Pyle at a chrono-
6 o. j! p( L/ S- n6 ologic age of 16 months (advanced).5 Chromosomal
  b, L% o) y) P& V9 L6 Qkaryotype was 46XY. The thyroid function test$ L1 U4 q, ]# g% |' _) A2 ~
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
; ^! O( |$ f$ b! [6 R. Dlating hormone level was 1.3 µIU/mL (both normal).+ x: ~0 e1 I! u
The concentrations of serum electrolytes, blood( x  k# `# ^$ q" B4 z
urea nitrogen, creatinine, and calcium all were) a$ f$ r2 [& q) f
within normal range for his age. The concentration; `- m+ U5 U" X. l8 j
of serum 17-hydroxyprogesterone was 16 ng/dL# h% D8 n& Q0 U7 P+ g/ J8 e/ n
(normal, 3 to 90 ng/dL), androstenedione was 20
0 O& `5 b+ z  c3 Gng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. A9 T* Q: e2 e+ l' Zterone was 38 ng/dL (normal, 50 to 760 ng/dL),
. x) [* ^9 B' Mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 m2 r) Q+ ?& Z# n  i3 J49ng/dL), 11-desoxycortisol (specific compound S): G/ u  L4 B) e
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
0 R" i( O& j4 atisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 b. `& E' G$ d" ^+ a
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 o2 O$ r" e6 G4 i# I# N
and β-human chorionic gonadotropin was less than
4 f. M0 c9 X# _. d- H% C0 n5 mIU/mL (normal <5 mIU/mL). Serum follicular- A8 r8 H( d2 a9 W3 O7 G
stimulating hormone and leuteinizing hormone
" ~/ }1 P: Y# [7 s9 S" t  vconcentrations were less than 0.05 mIU/mL
* X6 V+ Q9 F* j# g  d(prepubertal).& E' o3 a7 l" ]9 i' Q: _# w
The parents were notified about the laboratory
3 J  `$ o! P/ e$ n3 \results and were informed that all of the tests were
, u! T3 L+ l/ q  j. w# p2 a0 inormal except the testosterone level was high. The
/ ^# z# [' }& T# mfollow-up visit was arranged within a few weeks to7 E$ V- c' b  m) o: u- Q, u9 F$ A+ R
obtain testicular and abdominal sonograms; how-* _. s# k, N1 i- k
ever, the family did not return for 4 months.2 `5 v2 K# n$ C  d) l
Physical examination at this time revealed that the( E6 Q& i- [5 }6 }
child had grown 2.5 cm in 4 months and had gained
, v! e3 N% [3 Y: i2 kg of weight. Physical examination remained0 |( ~3 {# A& z. z0 a
unchanged. Surprisingly, the pubic hair almost com-
( W* h( T/ u9 N4 _8 Ypletely disappeared except for a few vellous hairs at
/ x& \; Y9 Q: x: Zthe base of the phallus. Testicular volume was still 2* h6 q% c4 s' P3 P3 E  @1 g
mL, and the size of the penis remained unchanged.
5 o, R' l4 i+ }3 ]+ G" D* eThe mother also said that the boy was no longer hav-; I6 l, D9 D9 O, u6 v5 j) n: v( B
ing frequent erections.
! r9 Y) x3 a* d$ L( }Both parents were again questioned about use of+ Z0 j: n9 V: ?8 ^& f, D% j. E! ]
any ointment/creams that they may have applied to1 v) \/ C. D( p1 @
the child’s skin. This time the father admitted the
2 T" l) @7 A) U, ITopical Testosterone Exposure / Bhowmick et al 541
; L: U. k4 q2 Z0 K( Z5 u4 quse of testosterone gel twice daily that he was apply-0 X$ ?( r; ~% Y: L
ing over his own shoulders, chest, and back area for& y7 I7 A+ d% W
a year. The father also revealed he was embarrassed( [' O5 c2 U& D" l) e5 h& |
to disclose that he was using a testosterone gel pre-% A3 F  m8 P7 Q; Z
scribed by his family physician for decreased libido
2 k* l, V$ H0 o  g8 D6 ^/ K& ^( `secondary to depression.4 M' v. `) ^) w( _4 j
The child slept in the same bed with parents.0 X( R, d& s8 J$ V9 t
The father would hug the baby and hold him on his
. b( j- B% s. c1 d  Ichest for a considerable period of time, causing sig-
& g) O4 K2 z  i: s& x* Tnificant bare skin contact between baby and father.. |0 A' M& t' [7 a
The father also admitted that after the phone call,
8 H8 ^( O3 b" h+ y" [8 kwhen he learned the testosterone level in the baby6 f1 R0 c6 U! ~1 I9 V/ ~/ N
was high, he then read the product information) u% V5 i& [' f. ?% c4 d4 Y* ?
packet and concluded that it was most likely the rea-3 ?, k9 }' T' j0 W1 N0 e
son for the child’s virilization. At that time, they9 i& n$ H. r& ~1 z6 _
decided to put the baby in a separate bed, and the
6 ]3 r8 A# M$ ?2 Nfather was not hugging him with bare skin and had, K+ g  c2 ]- T1 N1 l: [/ x
been using protective clothing. A repeat testosterone
3 v- z7 F& I! h- A0 B1 T6 vtest was ordered, but the family did not go to the' E: U. U+ B9 w, @. p% _: _
laboratory to obtain the test.
) V; d& Y0 c- E+ ]/ V" y+ Q) t, EDiscussion' P' W4 l3 w. R7 `5 a
Precocious puberty in boys is defined as secondary9 k3 K  e* s% s) ~: ]3 d; y8 \1 c
sexual development before 9 years of age.1,45 Y. v, P5 M1 x# M
Precocious puberty is termed as central (true) when$ k5 X+ M; a. N
it is caused by the premature activation of hypo-) f3 R" g3 ]6 @' L- z
thalamic pituitary gonadal axis. CPP is more com-8 O9 r7 |% x# h! u
mon in girls than in boys.1,3 Most boys with CPP4 ]/ ^" O5 b$ u* w, ]" u& z0 _! ]8 w
may have a central nervous system lesion that is, C$ V( j7 ^; T! H0 y$ O
responsible for the early activation of the hypothal-0 v0 F* j! j/ H# ~9 d0 F
amic pituitary gonadal axis.1-3 Thus, greater empha-9 X3 h9 ?4 Q: u4 J, H
sis has been given to neuroradiologic imaging in
6 v' J. G) L: t* p% r) ?5 E' ?& Aboys with precocious puberty. In addition to viril-
, R* w, D# [( {- b3 h1 F: X  pization, the clinical hallmark of CPP is the symmet-
* c) h: _" K  D5 k& _5 xrical testicular growth secondary to stimulation by
6 i: k2 j" ^% I" ~9 r6 hgonadotropins.1,35 L% \9 K* {' _- _5 u
Gonadotropin-independent peripheral preco-
8 V) w6 s6 H4 ?7 L! o3 mcious puberty in boys also results from inappropriate
& k) w* N; h) X$ P' Handrogenic stimulation from either endogenous or+ B% ^( Y1 P- u* T1 Y) z
exogenous sources, nonpituitary gonadotropin stim-
: F* N9 o$ n7 S, F+ pulation, and rare activating mutations.3 Virilizing( X# U/ g5 l& _, C  {, N  Q
congenital adrenal hyperplasia producing excessive
, J& L9 Z: x- u- Nadrenal androgens is a common cause of precocious
' x, n: |& ~% ^. q5 d/ ?" ^puberty in boys.3,4
! j; S* n. L* z4 b2 m0 J0 aThe most common form of congenital adrenal  v; ~& A' j4 E# n1 T0 J5 d8 d& T
hyperplasia is the 21-hydroxylase enzyme deficiency.
. K( R  H' u& ?* j' s; ]( j5 C1 BThe 11-β hydroxylase deficiency may also result in& x7 M+ E( D8 B1 e$ m
excessive adrenal androgen production, and rarely,
+ O, k: y% O: Q% l! B' Tan adrenal tumor may also cause adrenal androgen
: W1 z* q$ e/ E2 I* c2 m( I) j. Bexcess.1,3" ?% C7 X) @, ?- N3 G5 X; b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 x6 U' S5 k  Q9 |  J' b' h
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: M1 ]7 O4 G+ p# f) r+ ~1 R5 |A unique entity of male-limited gonadotropin-
' p8 b+ e# t: m  Yindependent precocious puberty, which is also known
* A" P  u- i+ P$ t, T8 o; W9 ras testotoxicosis, may cause precocious puberty at a- |7 d: T% i5 e6 g1 f. j
very young age. The physical findings in these boys3 F  I- }, L) n0 f* R  ~1 E& l
with this disorder are full pubertal development,
: H# L' A8 y2 o/ P9 fincluding bilateral testicular growth, similar to boys3 |8 x7 p) L3 J' @! t$ I
with CPP. The gonadotropin levels in this disorder
1 R5 b6 @6 G/ [- x) Y4 zare suppressed to prepubertal levels and do not show
4 h$ \; O. i9 ppubertal response of gonadotropin after gonadotropin-
. c" y: R: B. Sreleasing hormone stimulation. This is a sex-linked' z6 E0 l/ o' k1 [3 @0 F
autosomal dominant disorder that affects only
3 n( |/ |% y5 {males; therefore, other male members of the family
: N& }! O4 P: t# zmay have similar precocious puberty.3
% J; o) I3 x  C4 ?- y( IIn our patient, physical examination was incon-5 e: L, k' h' Z5 V5 C/ V
sistent with true precocious puberty since his testi-
# ]+ d! L6 W* K2 ]) O/ T$ kcles were prepubertal in size. However, testotoxicosis- i7 {: i! I2 ~' k6 V0 i
was in the differential diagnosis because his father
& q8 A/ S, G7 q. Z5 ~; a! V0 f! Xstarted puberty somewhat early, and occasionally,
4 N  i* Y, T- J" Ctesticular enlargement is not that evident in the
! Y3 ~  \; I% z( ~+ ubeginning of this process.1 In the absence of a neg-9 B. Y7 s) x( q
ative initial history of androgen exposure, our
) }8 |7 b, F/ A' O+ q  h4 t2 s+ V& @biggest concern was virilizing adrenal hyperplasia," U: i2 y4 d4 p' T% B$ n
either 21-hydroxylase deficiency or 11-β hydroxylase. W& ^) A0 s& C' B
deficiency. Those diagnoses were excluded by find-
& ~: u; h6 w* V" y! n7 p- ting the normal level of adrenal steroids.
" c+ \; m# z- O, y+ LThe diagnosis of exogenous androgens was strongly
" ]  Y5 c/ \4 J) G/ jsuspected in a follow-up visit after 4 months because( A2 @3 q/ o) U3 y9 k& f2 p; q9 ~, e  T
the physical examination revealed the complete disap-- O& P  q- U2 H& V$ g3 J8 @
pearance of pubic hair, normal growth velocity, and
2 ~! Z9 I% D1 Z1 U& Kdecreased erections. The father admitted using a testos-9 r. B. }  M9 Q- K" J
terone gel, which he concealed at first visit. He was* r( }3 M: Q$ H! u! ?
using it rather frequently, twice a day. The Physicians’
9 r6 [& |: t6 u3 Q9 t' N* G5 KDesk Reference, or package insert of this product, gel or0 J' w5 [/ w0 ]- z! _
cream, cautions about dermal testosterone transfer to# q' l( m$ S( r1 f
unprotected females through direct skin exposure.; K+ I  `# @: Y6 |% g! ~8 c2 R
Serum testosterone level was found to be 2 times the
8 L: z* [( W% _/ Z: ]# J& L; Ibaseline value in those females who were exposed to1 R1 w. M7 u. o( |' ?! I+ k1 ]
even 15 minutes of direct skin contact with their male9 H" W! w. _& r1 D# K% q) J
partners.6 However, when a shirt covered the applica-8 D' |' M/ _9 V% h
tion site, this testosterone transfer was prevented.* L/ ?* `* ]/ c; R; C9 E
Our patient’s testosterone level was 60 ng/mL,
9 E+ B4 ~! t2 R7 p7 m6 Nwhich was clearly high. Some studies suggest that
/ o- z# ~: `! g! q; gdermal conversion of testosterone to dihydrotestos-$ ]. P! O( C) M6 S' n5 v
terone, which is a more potent metabolite, is more. K6 n" ?* i2 R, k
active in young children exposed to testosterone. {- P! W' n6 G7 c# c$ f4 ^
exogenously7; however, we did not measure a dihy-
/ }1 ~+ r, i0 x8 rdrotestosterone level in our patient. In addition to0 ^/ H  _% l3 Z/ `' q" D
virilization, exposure to exogenous testosterone in
% k  {/ l$ g: `* }1 f) m* [) ]children results in an increase in growth velocity and
# l2 S, Z0 Q2 c% W& padvanced bone age, as seen in our patient.1 R  L) B! E$ S6 Q8 z. u, r5 ~
The long-term effect of androgen exposure during
) `1 J5 |- x) _- \7 I/ g: D5 _early childhood on pubertal development and final4 H& N& z: u: I4 {4 C. m
adult height are not fully known and always remain
6 j8 k  J$ {0 ia concern. Children treated with short-term testos-: S2 G4 ^) ]- A: I. o
terone injection or topical androgen may exhibit some
  L( G8 q+ q: Y$ Tacceleration of the skeletal maturation; however, after; |6 }. _) f" I5 p* t
cessation of treatment, the rate of bone maturation
; ~# I* U* b4 C! E4 E# C. mdecelerates and gradually returns to normal.8,9
+ U/ F* ^. _/ I7 t2 U' _! {8 NThere are conflicting reports and controversy
# \. A) t! b4 p$ ?over the effect of early androgen exposure on adult/ z  S4 w' i* D. ]- D% c+ C+ p8 e
penile length.10,11 Some reports suggest subnormal
, v" M8 \1 x+ \) [  h1 radult penile length, apparently because of downreg-$ k+ V- Z/ F# q# W1 J
ulation of androgen receptor number.10,12 However,0 [# S) O  G7 N) U
Sutherland et al13 did not find a correlation between& i$ V' b1 T# Z- Z3 _$ V4 z8 R
childhood testosterone exposure and reduced adult/ Z. ]2 ~5 f9 Z! }/ O1 r, C0 D- w
penile length in clinical studies.1 b0 T: U; p& E; e
Nonetheless, we do not believe our patient is
. `* u. C3 h) bgoing to experience any of the untoward effects from4 G" T% C( i8 n  p
testosterone exposure as mentioned earlier because
7 w% G/ Q9 ^( v9 z0 _" B, athe exposure was not for a prolonged period of time.) y" f( W1 F7 {
Although the bone age was advanced at the time of
5 e5 ^4 k0 m$ B4 a: T, w2 Xdiagnosis, the child had a normal growth velocity at" r/ W6 {" j# J7 N8 b! D: L
the follow-up visit. It is hoped that his final adult
( A- z2 l& Q5 O# N' x3 H# a- cheight will not be affected.2 G$ E3 w4 k$ t9 T* [: [, P
Although rarely reported, the widespread avail-) ?& F, L7 x! d+ ?+ M/ L2 Q( J% I, l- a
ability of androgen products in our society may
0 b1 x2 ]- D6 Gindeed cause more virilization in male or female$ t. G" W6 y* M  u) j# A: L, Y% ]
children than one would realize. Exposure to andro-
' S0 l3 {: p* G% c! ]* E  Ngen products must be considered and specific ques-. n" u, q! J, i# q  T  g
tioning about the use of a testosterone product or
+ T* O+ E6 I" M7 j6 wgel should be asked of the family members during
( {$ I+ j7 i5 C6 N5 G' k2 Lthe evaluation of any children who present with vir-
8 C" Y) h# w- E4 F9 \ilization or peripheral precocious puberty. The diag-! ], E5 v9 v8 X+ E! g- V8 o- Y
nosis can be established by just a few tests and by
! v- B: |! h$ \/ p7 ^" o# e' s2 }appropriate history. The inability to obtain such a
6 j6 t6 f, v9 shistory, or failure to ask the specific questions, may
/ A& x% }/ C* m" z' @* D2 i* ]% Iresult in extensive, unnecessary, and expensive! `: C- A0 t# G  c) t
investigation. The primary care physician should be
" G3 c! p8 W! \! d/ Maware of this fact, because most of these children% f- \- o/ {- j! H
may initially present in their practice. The Physicians’- Z6 k# m- S: b0 r5 z- q7 d8 T
Desk Reference and package insert should also put a, `) V' e" W- g2 ]+ u* d8 b! h
warning about the virilizing effect on a male or' ]$ p% Q" K9 a. }1 p# f
female child who might come in contact with some-
% U# N0 Z: w6 cone using any of these products.
4 D+ q) o3 M5 D0 b$ KReferences
$ T/ h; M! B5 \. k; N8 {/ p" c2 |1. Styne DM. The testes: disorder of sexual differentiation
& K5 K3 q& m! mand puberty in the male. In: Sperling MA, ed. Pediatric1 c: J! j5 g) r# \
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- e2 w( {, d) Y2 S2002: 565-628.
! s# K$ X( @3 r# ]! e$ X2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& V* g0 J1 B- ?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-Old+ A) G8 g3 X  i! X, p' r8 z
Boy Induced by Indirect Topical
2 a1 L7 E$ {3 L' K8 KExposure to Testosterone
( R0 f! ~- J3 n# P* ISamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2+ |' L  v% @& W& B( j
and Kenneth R. Rettig, MD1
6 O, I8 K/ u/ E) g! o3 gClinical Pediatrics
! G0 u2 N3 ]; B9 qVolume 46 Number 6; W5 S/ I9 M  U  a
July 2007 540-5434 |, A0 l" [' c% h/ w1 ?
© 2007 Sage Publications) @" o- Y* K& X% T
10.1177/0009922806296651/ ]0 c; t. I( A. K6 D
http://clp.sagepub.com
# B; K0 j' ?( j7 o0 N' Lhosted at
/ c* V( e* ~) ]2 |( vhttp://online.sagepub.com
- e, l; n& h) ^* Y1 c1 v, @* VPrecocious puberty in boys, central or peripheral,, K! h$ H' \3 a4 Z6 S
is a significant concern for physicians. Central/ p: D5 m( K/ Q0 Y# Z
precocious puberty (CPP), which is mediated& x% Q+ ], r4 [+ q: Q
through the hypothalamic pituitary gonadal axis, has2 q3 U& S% |* X" G4 ?; j' ?+ e3 _
a higher incidence of organic central nervous system
- d, b* u3 w1 ]: blesions in boys.1,2 Virilization in boys, as manifested6 V, Y0 L( f' N( E0 v
by enlargement of the penis, development of pubic
4 o( B8 q8 ^: Nhair, and facial acne without enlargement of testi-
2 t/ x4 }: \0 o% ?' m. ?. Wcles, suggests peripheral or pseudopuberty.1-3 We
6 ?" p. m3 k; z! Jreport a 16-month-old boy who presented with the
7 R* U2 k; _2 ~2 X9 C  Q! Denlargement of the phallus and pubic hair develop-
3 K8 h) i9 ?# B. x% w" H* @ment without testicular enlargement, which was due+ P4 D+ y# J9 X
to the unintentional exposure to androgen gel used by, q& {& N7 M8 M7 R2 H- N2 W
the father. The family initially concealed this infor-
- W! g$ ~: Y/ [, ^8 @/ V3 F5 Jmation, resulting in an extensive work-up for this1 c9 d) @) ?# U; o2 l/ |. G: X3 U
child. Given the widespread and easy availability of
6 d( T9 e  r' [testosterone gel and cream, we believe this is proba-' @5 D" b* o* q: T( D; H" W& _7 ~
bly more common than the rare case report in the; _2 e8 N+ \  e; y: D: f
literature.4; J/ G5 O5 {/ a8 @# z- |; [
Patient Report# E' T5 k" }0 z1 [- J- @$ W/ ?* |4 q: e
A 16-month-old white child was referred to the) P; a) U% {) a1 @0 q
endocrine clinic by his pediatrician with the concern
% y! z. D: x' @6 k* P6 r0 D" ]) fof early sexual development. His mother noticed# M& b/ p6 |' h; I3 p7 e3 S$ {
light colored pubic hair development when he was
! ]9 I9 k, h$ D; D6 IFrom the 1Division of Pediatric Endocrinology, 2University of
, I+ a2 s/ _$ z3 {2 E6 Q' fSouth Alabama Medical Center, Mobile, Alabama., e, w; b) E" R$ {- O
Address correspondence to: Samar K. Bhowmick, MD, FACE,
& E8 T, ?8 o9 F( \3 qProfessor of Pediatrics, University of South Alabama, College of
. ]& \1 ^1 O8 b8 n) D3 e9 _) TMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 {% F0 B8 m0 n& e0 b4 X1 R
e-mail: [email protected].: M9 \  M- z+ x" y' ~1 T) [
about 6 to 7 months old, which progressively became
1 k1 {) B! ~/ G1 L4 wdarker. She was also concerned about the enlarge-
/ i8 k$ U2 X, c5 L8 Nment of his penis and frequent erections. The child) Y4 S9 p5 X; A; v  n6 ?
was the product of a full-term normal delivery, with7 m) H  P, e3 u  F) ~
a birth weight of 7 lb 14 oz, and birth length of
% N1 j* L; u. r0 A: {20 inches. He was breast-fed throughout the first year) O9 u# h9 M+ K$ O
of life and was still receiving breast milk along with+ D4 m0 P' S; |  Q
solid food. He had no hospitalizations or surgery,
: k; ~; S5 x9 aand his psychosocial and psychomotor development
6 G' s+ J; v) X! T+ b* v1 T' ]was age appropriate.
7 S( l4 m4 Z8 c# o' a+ G2 J6 i$ nThe family history was remarkable for the father,  y% d- ]# N! o$ G4 D
who was diagnosed with hypothyroidism at age 16,/ [/ W, l  n5 B% R! Y
which was treated with thyroxine. The father’s. }- Q/ y# F& t2 L
height was 6 feet, and he went through a somewhat
2 B, @; ~2 E0 d0 ?! n, J* ?' Zearly puberty and had stopped growing by age 14.
  M6 B3 w) K* A# UThe father denied taking any other medication. The4 H8 V6 E# i, ?& H
child’s mother was in good health. Her menarche
) x/ j; }3 F2 e# O# o" x: ^was at 11 years of age, and her height was at 5 feet- ^& n. L% H3 c+ H
5 inches. There was no other family history of pre-
& E2 e8 q/ d, mcocious sexual development in the first-degree rela-3 b5 S7 H7 N. ^7 D5 y: l/ L( ^
tives. There were no siblings.
- d6 r  L0 @8 GPhysical Examination4 R% N7 u: V# l* Q+ E  E
The physical examination revealed a very active,
3 k; l5 c* s" _% J0 x6 wplayful, and healthy boy. The vital signs documented
+ `- w' I4 I+ F' E8 b6 P9 sa blood pressure of 85/50 mm Hg, his length was7 _; N# Q$ n2 Z
90 cm (>97th percentile), and his weight was 14.4 kg% P7 X) q" H/ I# a
(also >97th percentile). The observed yearly growth
* a3 o& y+ i/ X/ h, yvelocity was 30 cm (12 inches). The examination of
7 v; Q0 s4 A9 N' sthe neck revealed no thyroid enlargement.: `% W! v! S$ Y& X- p
The genitourinary examination was remarkable for
3 t$ N/ A8 a- p0 H3 B7 Penlargement of the penis, with a stretched length of! d/ G6 X& T6 t8 N) I
8 cm and a width of 2 cm. The glans penis was very well2 l4 E. y) J5 G
developed. The pubic hair was Tanner II, mostly around9 C- _$ i& O( b+ {2 f
540
2 c1 |; c$ l: P; @7 e: E" b- X$ Jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 q' q; N  P# |: P  Z  B
the base of the phallus and was dark and curled. The9 p. f; T- r  K3 @. ?: H6 E- m
testicular volume was prepubertal at 2 mL each.
% G: r+ V/ j8 B/ ?6 i5 l7 MThe skin was moist and smooth and somewhat
+ o/ C) @5 [, M  _7 v4 l) Moily. No axillary hair was noted. There were no. V6 {: R% I4 i8 u
abnormal skin pigmentations or café-au-lait spots.
; Y9 i6 F/ @, w! |0 H% Q; X5 INeurologic evaluation showed deep tendon reflex 2+# N7 F" ?) T4 ~5 S+ m$ ~( b
bilateral and symmetrical. There was no suggestion
1 H- s6 i6 P( h. _$ K7 ?, wof papilledema.
5 I+ r0 Q# O5 M( b! R# `Laboratory Evaluation0 Z  d4 x9 |0 M# k) \0 s! D$ B) A
The bone age was consistent with 28 months by% ]& [# k; d: y( z4 t/ W7 e  T- D
using the standard of Greulich and Pyle at a chrono-  g! ^+ ?4 D' d3 _
logic age of 16 months (advanced).5 Chromosomal
9 c/ M) K% y! J! C& S2 s7 `karyotype was 46XY. The thyroid function test. k" k" e7 k$ j, D: ?2 c6 `7 H
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
/ p, ~8 N/ f  wlating hormone level was 1.3 µIU/mL (both normal).
5 u% H4 Y9 [* D  AThe concentrations of serum electrolytes, blood; m+ _/ J, g" {0 \/ z' p. r! J7 s
urea nitrogen, creatinine, and calcium all were
, T" P8 S8 t' B9 L$ Bwithin normal range for his age. The concentration; ^  b! P4 ^6 v4 O
of serum 17-hydroxyprogesterone was 16 ng/dL' t- v5 @6 \1 N" z! I7 |$ B
(normal, 3 to 90 ng/dL), androstenedione was 20
. _$ w: K7 D) j0 @) c/ H4 M: G& tng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-! c1 w7 g9 I; r  z* `+ m
terone was 38 ng/dL (normal, 50 to 760 ng/dL),9 n8 t/ o  G* z- P
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
  x' Z* h4 C3 D, s: ~49ng/dL), 11-desoxycortisol (specific compound S)
, a* p% a5 s4 O0 r. ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 ?# k6 q6 l1 t6 v
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total6 [% ?" p9 {+ Y: I/ E7 R
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 j9 \: N: Y2 X$ o6 p& M
and β-human chorionic gonadotropin was less than$ x# d8 d8 O( k1 \& v
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 A# n/ C3 i' O* mstimulating hormone and leuteinizing hormone
* y1 W( k1 H: y. C% Wconcentrations were less than 0.05 mIU/mL, T/ a, Y1 v/ P- A  U8 b# w9 }
(prepubertal).( h* _  {+ r1 t' p7 X
The parents were notified about the laboratory
# P( S( K, A3 F3 i! ]6 hresults and were informed that all of the tests were
% i9 I% N9 r  F9 Y: p7 tnormal except the testosterone level was high. The$ S+ x& V! q7 j6 s  b8 H3 e4 f! l
follow-up visit was arranged within a few weeks to. z& e0 Y* {7 d
obtain testicular and abdominal sonograms; how-; u& _9 U' ^4 N7 u
ever, the family did not return for 4 months.
" M* C) c4 O$ n% U. |. y2 @Physical examination at this time revealed that the; B3 y# r( ^$ U' z$ a* p* d2 ?
child had grown 2.5 cm in 4 months and had gained
8 ?; ]1 A% U/ [9 O  N: {2 kg of weight. Physical examination remained- B& f3 d4 P. O2 Y! N" @' l* [' U
unchanged. Surprisingly, the pubic hair almost com-' ^3 [3 w2 a: \7 Z4 V9 ~5 f$ U! a% R  W
pletely disappeared except for a few vellous hairs at( _+ X$ S0 ?( J* W
the base of the phallus. Testicular volume was still 2
/ Z2 S9 J4 g& A+ A  F; r, |! a- CmL, and the size of the penis remained unchanged., a5 F/ s: z" N
The mother also said that the boy was no longer hav-. N2 |7 s4 q& n3 a
ing frequent erections.9 B5 C% ?( ?3 E0 `. F
Both parents were again questioned about use of
1 `+ Y& p4 K1 m" Iany ointment/creams that they may have applied to; c' Z# e5 t9 O
the child’s skin. This time the father admitted the2 E! T# j% C. G  s/ J6 p8 f; r2 d
Topical Testosterone Exposure / Bhowmick et al 5419 n3 E3 P/ h2 s6 P( @# H' U+ W
use of testosterone gel twice daily that he was apply-5 {8 ?) E% K% {
ing over his own shoulders, chest, and back area for
2 n5 ~( b, X. ^. F' z+ Ha year. The father also revealed he was embarrassed" w1 A5 g. c# s# X3 B
to disclose that he was using a testosterone gel pre-
2 E5 E3 N; H( v3 e" ascribed by his family physician for decreased libido
, {4 n) i* S+ l9 U6 c9 e( asecondary to depression.
0 x" w3 `$ `  nThe child slept in the same bed with parents.% M1 }/ P! a- Z) h& {9 r
The father would hug the baby and hold him on his* K2 U2 Q" B1 }
chest for a considerable period of time, causing sig-$ C) @4 n) w$ d0 Z: E' v, K
nificant bare skin contact between baby and father.3 B7 O7 L4 s; v$ J( Z9 a
The father also admitted that after the phone call,! S. v* F( O) y
when he learned the testosterone level in the baby
. b% Z+ {1 L0 Q( ]! F- i) J' |1 k) m* xwas high, he then read the product information6 k: I. J4 P6 J2 A5 k# J* N
packet and concluded that it was most likely the rea-, i  |! J& d7 n
son for the child’s virilization. At that time, they4 L* G+ T7 A" b
decided to put the baby in a separate bed, and the* Z- A9 f* p- J# l. ^, O8 W
father was not hugging him with bare skin and had
- F8 n, p$ R0 G* xbeen using protective clothing. A repeat testosterone
. G  l' m2 Z9 z3 C* Mtest was ordered, but the family did not go to the
" i$ Q/ R: \8 f4 alaboratory to obtain the test.
4 _2 m8 p5 I( G$ B) ~Discussion5 _" W8 ?  F, U4 }. c0 Y; E1 ?
Precocious puberty in boys is defined as secondary
) t3 T: G; M* G$ `3 }( s/ p; usexual development before 9 years of age.1,4. T; E- C6 n) ?3 W  s- Z# t; _
Precocious puberty is termed as central (true) when
1 c' Q  Q1 e, |it is caused by the premature activation of hypo-
$ |% k7 |+ |, n& p2 i. hthalamic pituitary gonadal axis. CPP is more com-
  w1 W- J) z9 |+ K2 _' O' K0 C# B( ]mon in girls than in boys.1,3 Most boys with CPP
' `  n. D8 o/ t* p6 ~4 ymay have a central nervous system lesion that is/ Z# E3 L! s9 Z
responsible for the early activation of the hypothal-
4 B. ^9 q" Q( U. i( {% ^) {amic pituitary gonadal axis.1-3 Thus, greater empha-
3 t% C$ b) H! u: J$ ?sis has been given to neuroradiologic imaging in5 O/ y/ s3 i2 b5 o8 M
boys with precocious puberty. In addition to viril-
# o; P6 C6 t/ v& p' q0 sization, the clinical hallmark of CPP is the symmet-3 r- r, z( X) A+ U  L* _
rical testicular growth secondary to stimulation by' o6 l# K% ~$ P* v2 P( E+ [8 T
gonadotropins.1,3: ]; m( P  G: L) h( v# ?5 t7 U1 u5 L& U
Gonadotropin-independent peripheral preco-
. U& _# @7 \! ^: E6 j! e' M! }  }cious puberty in boys also results from inappropriate
. c2 H+ h( t6 K# ?androgenic stimulation from either endogenous or& |  k  |( Z& `. }8 \9 x& n
exogenous sources, nonpituitary gonadotropin stim-
8 I: J* t% H( p2 H! Aulation, and rare activating mutations.3 Virilizing
/ t/ `% m7 ~( v  e; @: ?5 c- ncongenital adrenal hyperplasia producing excessive
8 _4 v1 u0 Y" m+ U" l/ i6 n+ Jadrenal androgens is a common cause of precocious
, J; y" X( C5 i$ b5 A5 vpuberty in boys.3,4
1 v% P% \7 ~3 _" C4 V  v" XThe most common form of congenital adrenal" p+ j+ [  r; d3 O
hyperplasia is the 21-hydroxylase enzyme deficiency.- d  a: j6 [: v' `0 ^) F( Q5 \
The 11-β hydroxylase deficiency may also result in) O2 Q8 ~, V/ b- }) `% J4 R0 K' P
excessive adrenal androgen production, and rarely,$ e) S) P7 y) l* w. ^
an adrenal tumor may also cause adrenal androgen3 I* R& ]- R6 c* }& m- m
excess.1,3
: W: o& I5 D' R& vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 ^; a: Y8 o3 {- G, W; P
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
/ l: V; W$ L- gA unique entity of male-limited gonadotropin-2 [0 z2 K: H6 h, C6 S9 G8 D6 L
independent precocious puberty, which is also known+ h% u- R0 y+ z( q3 J
as testotoxicosis, may cause precocious puberty at a- @; C* p$ e3 l8 ~8 W  a
very young age. The physical findings in these boys
$ ?5 W+ B3 V: y% Lwith this disorder are full pubertal development,
8 j% P  P8 d. P+ L$ e6 U; }' zincluding bilateral testicular growth, similar to boys
" V7 u3 [" D8 b9 t/ S' Owith CPP. The gonadotropin levels in this disorder0 }) j' i6 I( Z: R" x& |" f
are suppressed to prepubertal levels and do not show/ t  w; D! o* h7 V. ^) |  O0 I
pubertal response of gonadotropin after gonadotropin-
' o% R* ~- F' G$ V, g  Yreleasing hormone stimulation. This is a sex-linked
! {( V. F6 Y) b, J/ Zautosomal dominant disorder that affects only8 K/ K/ V( D4 u, _+ M
males; therefore, other male members of the family& {# a/ P( }$ T4 B8 v7 k
may have similar precocious puberty.3' k* u" N8 l! K
In our patient, physical examination was incon-
4 \2 k& y5 R& Z9 ~9 M8 {sistent with true precocious puberty since his testi-: q( e# M8 N  {
cles were prepubertal in size. However, testotoxicosis" f$ {' |9 C% U) l# K$ a# Z! d9 ]
was in the differential diagnosis because his father9 i/ ^  R- [0 ~# c4 g5 ~
started puberty somewhat early, and occasionally,& f% Z( f8 `3 k+ o: q) }
testicular enlargement is not that evident in the
8 g1 _$ z: `- zbeginning of this process.1 In the absence of a neg-" f9 h2 Z# g; J+ g) d! _7 E
ative initial history of androgen exposure, our4 m7 C6 c) j% d  }# V* t" }& g) K
biggest concern was virilizing adrenal hyperplasia,
' V! a4 S! j% \either 21-hydroxylase deficiency or 11-β hydroxylase8 p4 L( w+ Q/ Y! V1 e3 ^3 v
deficiency. Those diagnoses were excluded by find-% o; i5 Y& `: d, Z( _9 c
ing the normal level of adrenal steroids.+ w) {, n7 F9 S. ?' P
The diagnosis of exogenous androgens was strongly) g- \- s- e* I) Y( d! H
suspected in a follow-up visit after 4 months because
9 h% l  e' ]9 L! K3 g! |/ [the physical examination revealed the complete disap-
) f. y3 T8 K3 r5 Upearance of pubic hair, normal growth velocity, and  Q1 Z8 C$ J/ O+ a" w6 A5 w
decreased erections. The father admitted using a testos-
' K8 R8 F4 A: f  u& e! W& sterone gel, which he concealed at first visit. He was
  O1 {) _/ H& O/ H. c, Q( fusing it rather frequently, twice a day. The Physicians’& L) ^, z  G; m! g9 r$ T
Desk Reference, or package insert of this product, gel or- f5 z9 ^* n! o$ U, V5 R7 }% m, d
cream, cautions about dermal testosterone transfer to
" C3 }9 _# }! M, j: s( f2 ]unprotected females through direct skin exposure.! y' H1 H" a5 ~7 s9 }; E# M# F
Serum testosterone level was found to be 2 times the
+ V- `5 O9 f1 V" i. B& q! ibaseline value in those females who were exposed to
6 ?) J, y  f! s6 seven 15 minutes of direct skin contact with their male
3 b1 t* w8 U. j( cpartners.6 However, when a shirt covered the applica-, b& q4 u& R* c
tion site, this testosterone transfer was prevented.
7 n- z$ h  e7 t4 ~6 w+ Z0 jOur patient’s testosterone level was 60 ng/mL,
3 Z& V4 ~5 x& [4 I% g" a, Wwhich was clearly high. Some studies suggest that
0 L1 y- [4 H% m0 f! i; ^dermal conversion of testosterone to dihydrotestos-* ^, ]) I& e& _8 m5 h
terone, which is a more potent metabolite, is more2 A6 g: k% c4 j6 K. [
active in young children exposed to testosterone
/ y) `  `& i( ?/ Xexogenously7; however, we did not measure a dihy-
% t& X" P6 G# x0 Odrotestosterone level in our patient. In addition to0 u0 w% X# w& X: }2 L/ |
virilization, exposure to exogenous testosterone in# L5 C7 @/ U7 C. l% K" E7 p
children results in an increase in growth velocity and% t. m- j( ~1 o/ [# n- r/ k3 T1 n/ \
advanced bone age, as seen in our patient.
" X/ _9 F- q3 DThe long-term effect of androgen exposure during
0 V4 a2 y" q$ o& I: Vearly childhood on pubertal development and final2 Z) d0 p+ s0 H3 z9 l" \
adult height are not fully known and always remain- R7 u+ m4 a6 h
a concern. Children treated with short-term testos-
  q+ z6 d: m% r* N- Oterone injection or topical androgen may exhibit some# v5 X* C- ?4 E9 {1 ^/ v
acceleration of the skeletal maturation; however, after1 R$ w, }8 b* b3 W/ d- T0 k- j
cessation of treatment, the rate of bone maturation
$ v( V, S8 n3 S) N7 u# H& ?7 ?decelerates and gradually returns to normal.8,9/ S8 c* G* R+ \) F9 x
There are conflicting reports and controversy
# m4 {6 P- u& K3 \1 M, E; Xover the effect of early androgen exposure on adult
& [$ [; s6 F4 K6 G) x* B8 ppenile length.10,11 Some reports suggest subnormal
8 g4 g, j" C+ R/ ^5 _! Padult penile length, apparently because of downreg-
; y# i; v* M+ H7 tulation of androgen receptor number.10,12 However,5 d8 ?& r! @" j1 w  r1 h" e
Sutherland et al13 did not find a correlation between
, S- X: M& s  v' Dchildhood testosterone exposure and reduced adult
. C3 \- G( L& @- S) u' Lpenile length in clinical studies.
5 Z1 W0 R. [2 G# m6 D, M- yNonetheless, we do not believe our patient is
2 b: S+ {( Z4 J  ]/ tgoing to experience any of the untoward effects from; U  A: S9 c, o# c
testosterone exposure as mentioned earlier because
/ v) c6 p% w: s0 h0 Sthe exposure was not for a prolonged period of time.
  Z* l4 P# K; \7 ]+ eAlthough the bone age was advanced at the time of+ {" D% b: y0 B5 ?# _) `2 L& V
diagnosis, the child had a normal growth velocity at
" S4 r8 W5 s* d" b/ Cthe follow-up visit. It is hoped that his final adult, [# k2 m& P. Q0 h; K9 u  z
height will not be affected.  u2 D7 T' r& S( ?: q: k* J, [
Although rarely reported, the widespread avail-
8 w! ?& u+ F0 v5 `" eability of androgen products in our society may5 _  g* B- n% @: h- J
indeed cause more virilization in male or female6 B# R) @% c4 v( k$ s' R! k/ [
children than one would realize. Exposure to andro-! {$ E; i1 V6 Y# ^- }0 H
gen products must be considered and specific ques-
2 |3 z$ J9 q+ C: Htioning about the use of a testosterone product or
2 I4 U- O$ i2 W2 Pgel should be asked of the family members during7 Z# d  e$ {9 q$ Y- r' r( H2 u; z
the evaluation of any children who present with vir-
( b# m% }% t1 h, wilization or peripheral precocious puberty. The diag-
+ A. A- r: }5 `9 M, q7 H9 pnosis can be established by just a few tests and by) y6 e% [/ y2 [. u4 B' J$ j/ E8 ^& B
appropriate history. The inability to obtain such a
, y" v6 Y) s  X! z* ihistory, or failure to ask the specific questions, may; q7 {. n! n5 z. K4 q) O8 I( Y
result in extensive, unnecessary, and expensive- h' }# |6 B% F7 O# @
investigation. The primary care physician should be
0 M  j4 l" P& j! j' V% J5 \+ Gaware of this fact, because most of these children0 h) L% y3 D" q! [  `7 A& f( g# v' E
may initially present in their practice. The Physicians’
: b, u0 v# C! V) }Desk Reference and package insert should also put a; U$ g; S. E$ V/ ~
warning about the virilizing effect on a male or
5 I: X- B2 L7 ~  kfemale child who might come in contact with some-' [; E4 C; y6 y- D/ ~: b
one using any of these products.: R7 |; v: C7 E2 i9 _! x
References
% ]! M' d7 f; d' R( v1. Styne DM. The testes: disorder of sexual differentiation
0 E7 }! M+ _2 ]and puberty in the male. In: Sperling MA, ed. Pediatric9 O; _. R8 K" D/ O& N* F" h
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ h3 G1 e+ j2 y+ q" _: M
2002: 565-628.
: [$ s, m1 j  k. {% T' r2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious8 n2 u& |/ `+ x& D, V3 A* h: U
puberty 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
3 B9 m+ k% ]  D3 Q
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