50000大洋的充氣娃娃，看看我如何跟她做愛[25P]

lamfung

谢谢分享

zitan14078

#在這裡快速回復#新鮮少見的圖，感恩！

kaifka

is a significant concern for physicians. Central
+ `2 ]! S% N- ?+ c9 n* |precocious puberty (CPP), which is mediated
through the hypothalamic pituitary gonadal axis, has
% h% R; v, U2 W6 v9 Z- Y7 R. |a higher incidence of organic central nervous system
/ E1 z! S3 G/ a+ N- s; w1 x0 glesions in boys.1,2 Virilization in boys, as manifested
by enlargement of the penis, development of pubic
3 _9 t2 S4 f+ H; J( L) l2 j( l1 _hair, and facial acne without enlargement of testi-
; T8 M0 E' ]0 E4 qcles, suggests peripheral or pseudopuberty.1-3 We
: g& A+ h& d$ }report a 16-month-old boy who presented with the
) j& Y* R" J9 Z- H1 H: g3 b; E9 _enlargement of the phallus and pubic hair develop-
ment without testicular enlargement, which was due
' O% p6 Z- ^  H2 x% C  kto the unintentional exposure to androgen gel used by
the father. The family initially concealed this infor-
' }+ m1 ^: a0 s/ E! Ymation, resulting in an extensive work-up for this
; g' t/ M+ D3 kchild. Given the widespread and easy availability of
testosterone gel and cream, we believe this is proba-
bly more common than the rare case report in the
literature.4
Patient Report
; A% H/ u! j! F$ `5 q' QA 16-month-old white child was referred to the
endocrine clinic by his pediatrician with the concern
7 L% I1 T: T/ a( Rof early sexual development. His mother noticed
2 {' s+ `+ L" Y/ h1 blight colored pubic hair development when he was
& j  u$ u8 w2 _7 {$ A0 J9 u/ |From the 1Division of Pediatric Endocrinology, 2University of
3 s6 W" Z# l# p. @+ tSouth Alabama Medical Center, Mobile, Alabama.
/ o. t" i, C- YAddress correspondence to: Samar K. Bhowmick, MD, FACE,
Professor of Pediatrics, University of South Alabama, College of
# Z" k2 |/ w% jMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
e-mail: [email protected].
about 6 to 7 months old, which progressively became
8 i0 N9 S, Q3 ]darker. She was also concerned about the enlarge-
ment of his penis and frequent erections. The child
; w9 ?2 j, K* gwas the product of a full-term normal delivery, with
0 i& G1 j+ `; C2 H5 G+ _2 Oa birth weight of 7 lb 14 oz, and birth length of
3 [' K3 W% r/ [! Z20 inches. He was breast-fed throughout the first year
of life and was still receiving breast milk along with
solid food. He had no hospitalizations or surgery,
+ k+ p+ a: r) Q8 O; band his psychosocial and psychomotor development
was age appropriate.
- h* D4 U4 D/ S# iThe family history was remarkable for the father,
who was diagnosed with hypothyroidism at age 16,
2 p0 G( F/ _: F5 e  @' O7 ?! ~; O6 @which was treated with thyroxine. The father’s
height was 6 feet, and he went through a somewhat
early puberty and had stopped growing by age 14.
) K2 j% Q" }" V6 DThe father denied taking any other medication. The
child’s mother was in good health. Her menarche
was at 11 years of age, and her height was at 5 feet
# y0 ?) b8 }/ W- J. I5 inches. There was no other family history of pre-
cocious sexual development in the first-degree rela-
9 @2 g4 K" [3 d! |tives. There were no siblings.
Physical Examination
The physical examination revealed a very active,
) W1 I7 ^, v) \  E  F( Aplayful, and healthy boy. The vital signs documented
0 ~# E' T) W5 j! i- ]- Za blood pressure of 85/50 mm Hg, his length was
90 cm (>97th percentile), and his weight was 14.4 kg
(also >97th percentile). The observed yearly growth
velocity was 30 cm (12 inches). The examination of
0 \9 X( R+ }  Zthe neck revealed no thyroid enlargement.
The genitourinary examination was remarkable for
- W6 x) ?. l+ k* a6 _4 _1 ]$ Renlargement of the penis, with a stretched length of
$ c6 P/ @  I4 l- e6 C# c! `% @/ c' H7 w8 cm and a width of 2 cm. The glans penis was very well
developed. The pubic hair was Tanner II, mostly around
540
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
the base of the phallus and was dark and curled. The
testicular volume was prepubertal at 2 mL each.
The skin was moist and smooth and somewhat
oily. No axillary hair was noted. There were no
abnormal skin pigmentations or café-au-lait spots.
Neurologic evaluation showed deep tendon reflex 2+
+ J3 D/ O: W) m& _& g! sbilateral and symmetrical. There was no suggestion
of papilledema.
Laboratory Evaluation
The bone age was consistent with 28 months by
0 L, m1 W7 R* J7 P5 P9 Musing the standard of Greulich and Pyle at a chrono-
logic age of 16 months (advanced).5 Chromosomal
% ]8 E  w+ ~" z7 ^karyotype was 46XY. The thyroid function test
% @7 o4 B- e9 O$ l0 jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! G7 V+ ?/ M. p$ C. M3 a. s- |lating hormone level was 1.3 µIU/mL (both normal).
" i- t- U7 ]8 ^The concentrations of serum electrolytes, blood
5 I/ C. F2 e9 a1 w  Aurea nitrogen, creatinine, and calcium all were
within normal range for his age. The concentration
of serum 17-hydroxyprogesterone was 16 ng/dL
& x+ U3 S# h% g# n) @(normal, 3 to 90 ng/dL), androstenedione was 20
* Q9 a4 Y. w8 n5 Cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
49ng/dL), 11-desoxycortisol (specific compound S)
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
! }: W$ U& G& J) {. u) itestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
and β-human chorionic gonadotropin was less than
! M  h; _: j4 p( S/ z. f0 O5 mIU/mL (normal <5 mIU/mL). Serum follicular
stimulating hormone and leuteinizing hormone
concentrations were less than 0.05 mIU/mL
(prepubertal).
The parents were notified about the laboratory
results and were informed that all of the tests were
normal except the testosterone level was high. The
follow-up visit was arranged within a few weeks to
obtain testicular and abdominal sonograms; how-
ever, the family did not return for 4 months.
) Y& z6 K: ?) u/ b. V* }. y6 @& H, h) GPhysical examination at this time revealed that the
child had grown 2.5 cm in 4 months and had gained
; ?) }2 ~+ @6 [4 N4 j! D2 kg of weight. Physical examination remained
unchanged. Surprisingly, the pubic hair almost com-
* s- e; U. A1 Q2 G% Zpletely disappeared except for a few vellous hairs at
the base of the phallus. Testicular volume was still 2
mL, and the size of the penis remained unchanged.
' B" x) r; O( b; L4 }, ^The mother also said that the boy was no longer hav-
ing frequent erections.
Both parents were again questioned about use of
. x0 |1 G  ~0 e4 Bany ointment/creams that they may have applied to
+ S+ i7 v7 K2 M" A, Qthe child’s skin. This time the father admitted the
Topical Testosterone Exposure / Bhowmick et al 541
  o4 b2 C, v0 g1 d' u9 k* C: w+ l& Quse of testosterone gel twice daily that he was apply-
ing over his own shoulders, chest, and back area for
a year. The father also revealed he was embarrassed
0 Q; f+ }9 f# ~7 N6 @) Gto disclose that he was using a testosterone gel pre-
scribed by his family physician for decreased libido
5 u. W2 J( |& Z5 M2 Xsecondary to depression.
The child slept in the same bed with parents.
The father would hug the baby and hold him on his
chest for a considerable period of time, causing sig-
2 i) F( z8 F  Onificant bare skin contact between baby and father.
, N9 t4 B7 L( }( [5 u. SThe father also admitted that after the phone call,
0 a- {; {/ H- L# k+ `4 ~/ x; i8 L1 |when he learned the testosterone level in the baby
was high, he then read the product information
( e" s$ I8 K$ c, Npacket and concluded that it was most likely the rea-
son for the child’s virilization. At that time, they
decided to put the baby in a separate bed, and the
father was not hugging him with bare skin and had
been using protective clothing. A repeat testosterone
3 U/ q  U8 q0 etest was ordered, but the family did not go to the
: e) }) d% h9 z: [  claboratory to obtain the test.
6 m& \4 G/ r% @. d/ \5 r1 ^4 S  |Discussion
* g- ]3 N2 c2 ?1 z" X' pPrecocious puberty in boys is defined as secondary
9 j! K& }* t& L9 Y/ ~0 Usexual development before 9 years of age.1,4
Precocious puberty is termed as central (true) when
it is caused by the premature activation of hypo-
! ^) N) j6 G6 T' `% vthalamic pituitary gonadal axis. CPP is more com-
# A+ Q0 U' C/ N. Amon in girls than in boys.1,3 Most boys with CPP
may have a central nervous system lesion that is
7 R' r& Q* C; s+ jresponsible for the early activation of the hypothal-
# R9 Y9 }, k+ B: R7 Ramic pituitary gonadal axis.1-3 Thus, greater empha-
sis has been given to neuroradiologic imaging in
" r9 Q6 r' x9 X' n( x& s- Qboys with precocious puberty. In addition to viril-
ization, the clinical hallmark of CPP is the symmet-
rical testicular growth secondary to stimulation by
gonadotropins.1,3
Gonadotropin-independent peripheral preco-
cious puberty in boys also results from inappropriate
androgenic stimulation from either endogenous or
3 N3 D: e- Z8 _exogenous sources, nonpituitary gonadotropin stim-
. o3 U% E  n# g- P4 x8 t. }) N1 Uulation, and rare activating mutations.3 Virilizing
congenital adrenal hyperplasia producing excessive
adrenal androgens is a common cause of precocious
puberty in boys.3,4
The most common form of congenital adrenal
, m* ^% B: |3 p) ]hyperplasia is the 21-hydroxylase enzyme deficiency.
The 11-β hydroxylase deficiency may also result in
excessive adrenal androgen production, and rarely,
an adrenal tumor may also cause adrenal androgen
excess.1,3
. U% o! u0 O) B$ Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ D, v: F! z! |/ w6 j& s* U# l542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
A unique entity of male-limited gonadotropin-
independent precocious puberty, which is also known
3 ?: c% c6 a0 `8 ?, r. fas testotoxicosis, may cause precocious puberty at a
6 x8 i* p3 x! kvery young age. The physical findings in these boys
with this disorder are full pubertal development,
including bilateral testicular growth, similar to boys
, p8 T- J! `/ _9 T9 hwith CPP. The gonadotropin levels in this disorder
$ s7 O8 H: Q" J: J* |are suppressed to prepubertal levels and do not show
' M4 h  R7 G& a+ _* J: t9 Apubertal response of gonadotropin after gonadotropin-
releasing hormone stimulation. This is a sex-linked
autosomal dominant disorder that affects only
males; therefore, other male members of the family
% B# c" u1 X; a/ gmay have similar precocious puberty.3
In our patient, physical examination was incon-
sistent with true precocious puberty since his testi-
' Q. D% E8 r* @8 ycles were prepubertal in size. However, testotoxicosis
" |5 |7 f  L9 `' K3 Z4 }was in the differential diagnosis because his father
started puberty somewhat early, and occasionally,
testicular enlargement is not that evident in the
2 ^9 D; F  K8 p3 M; wbeginning of this process.1 In the absence of a neg-
% s( O. O3 v' Y" ?9 hative initial history of androgen exposure, our
2 E2 |+ X! f, I* ]) ^biggest concern was virilizing adrenal hyperplasia,
/ u3 N# _1 @) E3 Feither 21-hydroxylase deficiency or 11-β hydroxylase
deficiency. Those diagnoses were excluded by find-
ing the normal level of adrenal steroids.
The diagnosis of exogenous androgens was strongly
suspected in a follow-up visit after 4 months because
the physical examination revealed the complete disap-
& `5 n: B3 [9 {* D1 epearance of pubic hair, normal growth velocity, and
decreased erections. The father admitted using a testos-
6 l6 h0 E1 G- c: a% N6 Q4 pterone gel, which he concealed at first visit. He was
using it rather frequently, twice a day. The Physicians’
: @8 b% I& w4 U) HDesk Reference, or package insert of this product, gel or
cream, cautions about dermal testosterone transfer to
unprotected females through direct skin exposure.
Serum testosterone level was found to be 2 times the
, n0 t" d  N* \0 m# U: gbaseline value in those females who were exposed to
even 15 minutes of direct skin contact with their male
, m+ b* b9 l% T$ Q! z  ypartners.6 However, when a shirt covered the applica-
4 ]) e' d4 Y2 i" g1 Ntion site, this testosterone transfer was prevented.
Our patient’s testosterone level was 60 ng/mL,
4 q4 E3 R' M2 W6 y1 jwhich was clearly high. Some studies suggest that
dermal conversion of testosterone to dihydrotestos-
' V9 Q/ p6 [+ g9 [3 Xterone, which is a more potent metabolite, is more
active in young children exposed to testosterone
. l5 H, o  M* @8 ]6 _, i& I. rexogenously7; however, we did not measure a dihy-
drotestosterone level in our patient. In addition to
virilization, exposure to exogenous testosterone in
  _; W/ G+ j* Z% F% _2 Ichildren results in an increase in growth velocity and
advanced bone age, as seen in our patient.
The long-term effect of androgen exposure during
early childhood on pubertal development and final
0 K* Z( D5 i& J7 uadult height are not fully known and always remain
& x. b) Y% P( [" Ia concern. Children treated with short-term testos-
: F3 D1 c: x$ h* H* C2 \/ }, i- ~1 qterone injection or topical androgen may exhibit some
acceleration of the skeletal maturation; however, after
! }0 W- A! b" L2 H, Xcessation of treatment, the rate of bone maturation
decelerates and gradually returns to normal.8,9
( j4 [9 _3 T7 [( u0 @( |* ~& eThere are conflicting reports and controversy
over the effect of early androgen exposure on adult
. Y3 m% d' Y2 T% h5 [0 @penile length.10,11 Some reports suggest subnormal
( O* D$ C1 l* _* C' n! b3 H0 kadult penile length, apparently because of downreg-
" Y$ j& \+ n8 M- rulation of androgen receptor number.10,12 However,
: H$ f1 L4 O  |4 R1 N4 oSutherland et al13 did not find a correlation between
childhood testosterone exposure and reduced adult
penile length in clinical studies.
) f0 @& ~* i$ K. P! \% p% [Nonetheless, we do not believe our patient is
going to experience any of the untoward effects from
/ u& |( p! g' V  E( l5 Jtestosterone exposure as mentioned earlier because
the exposure was not for a prolonged period of time.
Although the bone age was advanced at the time of
diagnosis, the child had a normal growth velocity at
0 E! j: q  [5 x8 Ithe follow-up visit. It is hoped that his final adult
, D  S7 H6 O( Z, G5 k# I: I: x  _height will not be affected.
Although rarely reported, the widespread avail-
ability of androgen products in our society may
indeed cause more virilization in male or female
children than one would realize. Exposure to andro-
gen products must be considered and specific ques-
tioning about the use of a testosterone product or
2 l8 X  T1 m' O2 J3 f5 lgel should be asked of the family members during
0 C  H3 o! M8 l* s* j4 ythe evaluation of any children who present with vir-
ilization or peripheral precocious puberty. The diag-
nosis can be established by just a few tests and by
* Q* c3 ^8 }5 Z, l& ]8 Tappropriate history. The inability to obtain such a
history, or failure to ask the specific questions, may
result in extensive, unnecessary, and expensive
9 z& c+ W1 ?+ h7 c* Cinvestigation. The primary care physician should be
. T2 w" u) ]) K" G' }& H7 vaware of this fact, because most of these children
! N6 A1 [) w& ^1 E$ s, Q7 c6 i' \may initially present in their practice. The Physicians’
Desk Reference and package insert should also put a
warning about the virilizing effect on a male or
female child who might come in contact with some-
one using any of these products.
References
1. Styne DM. The testes: disorder of sexual differentiation
and puberty in the male. In: Sperling MA, ed. Pediatric
- @9 A( ~  d4 Y$ J2 c8 ~) v& SEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
2002: 565-628.
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 W& y! m! j( @: ^" fpuberty in children with tumours of the suprasellar pineal
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
Topical Testosterone Exposure / Bhowmick et al 543
+ V, v6 Q: ~4 s1 z$ ]areas: organic central precocious puberty. Acta Paediatr.
0 n$ s9 {1 w& _; i6 u- j1 _2001;90:751-756.
3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
2 J2 q( }- S6 K, Q7 i, J  S6 Z. cPediatric Endocrinology. 4th ed. New York, NY: Marcel
# `% ?- R% l! x) |' @$ SDekker Inc; 2003:211-238.
/ w% O' ~  E7 o9 c' Y" I4. Yu YM, Punyasavatsu N, Elder D, D’Ercole AJ. Sexual
; [  v8 @3 R9 o9 G) ydevelopment in a two-year-old boy induced by topical
exposure to testosterone. Pediatrics. 1999;104:e23.
5 y& B( `& ^3 A/ ~' j( `5. Greulich WW, Pyle SI, eds. Radiographic Atlas of
Skeletal Development of the Hand and Wrist. 2nd ed.
& J% N6 j8 m( KStanford, CA: Stanford University Press; 1959.
6. Physicians’ Desk Reference. Androgel 1% testosterone,
Unimed Pharmaceutical Inc. Montvale, NJ: Medical
Economics Company, Inc; 2004:3239-3241.
# e" y5 `* U! Y' y8 _0 Z0 Y7. Klugo RC, Cerny JC. Response of micropenis to topical
testosterone and gonadotropin. J Urol. 1978;119:
# K0 L: d3 H. ^) N+ d! e- f) u667-668.
8. Guthrie RD, Smith DW, Graham CB. Testosterone
treatment for micropenis during early childhood. J Pediatr.
+ _4 g  O( L( _1973;83:247-252.
% e; W$ W/ m! }) t* y, _# _9. Jacobs SC, Kaplan GW, Gittes RF. Topical testosterone
  g/ P" I; T" V( A+ P/ o' Wtherapy for penile growth. Urol. 1975;6:708-710.
  g! i+ j9 r3 \7 L) C! {- K10. Husmann DA, Cain MP. Microphallus: eventual phallic
size is dependent on the timing of androgen administra-
0 G* h8 L+ A, A4 J# r1 G+ btion. J Urol. 1994;152:734-739.
11. McMahon DR, Kramer SA, Husmann DA. Micropenis:
does early treatment with testosterone do more harm
/ j* {2 q9 i7 F$ L0 Z9 `, |7 Fthan good? J Urol. 1995;154:825-829.
. ]- b, l3 t) x12. Takane KK, George FW, Wilson JD. Androgen receptor
( e+ x5 k6 E0 E. n0 h" X, Tof rat penis is down-regulated by androgen. Am J Physiol.
- _, U) P! u3 v1990;258:E46-E50.
/ Y, z; i9 C" h3 t13. Sutherland RS, Kogan BA, Baskin LS, et al. The effect
* b0 c/ U% C% S5 t# i! j# }# w1 zof prepubertal androgen exposure on adult penile
( }: n; u2 `5 B1 H" i1 c+ v  Y, dlength. J Urol. 1996;156:783-787.

xuejingri

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！

wlm12345

看起来不错啊，继续欣赏看看

guoxi8437

感谢分享

lg5992

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！

dengge3591

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！

friendlyselaing

看一看哦

mushi666

感谢楼主无私分享