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
precocious puberty (CPP), which is mediated
through the hypothalamic pituitary gonadal axis, has
a higher incidence of organic central nervous system
lesions in boys.1,2 Virilization in boys, as manifested
! U- ^1 U1 ^( Y( ~! N8 {+ i$ \7 Rby enlargement of the penis, development of pubic
2 [& K: f2 @& A3 I2 y* a: r9 R) Yhair, and facial acne without enlargement of testi-
: ^$ ]9 W  E- @" s6 _! _6 \cles, suggests peripheral or pseudopuberty.1-3 We
report a 16-month-old boy who presented with the
enlargement of the phallus and pubic hair develop-
# Z7 q! Z& w, D# sment without testicular enlargement, which was due
to the unintentional exposure to androgen gel used by
the father. The family initially concealed this infor-
mation, resulting in an extensive work-up for this
/ _7 ~# b# O, P* @child. Given the widespread and easy availability of
: u  b/ `9 j+ C3 E4 Y0 }$ _1 @) @testosterone gel and cream, we believe this is proba-
bly more common than the rare case report in the
literature.4
Patient Report
2 x% J7 K0 \- F" g2 N& G: {. W' MA 16-month-old white child was referred to the
endocrine clinic by his pediatrician with the concern
of early sexual development. His mother noticed
' l2 O& D% p) Q  M2 dlight colored pubic hair development when he was
From the 1Division of Pediatric Endocrinology, 2University of
South Alabama Medical Center, Mobile, Alabama.
Address correspondence to: Samar K. Bhowmick, MD, FACE,
Professor of Pediatrics, University of South Alabama, College of
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
e-mail: [email protected].
about 6 to 7 months old, which progressively became
' ^- ?) F5 f$ u1 x6 T- w% ~darker. She was also concerned about the enlarge-
/ \3 ^! y" |" f9 [3 U; T. Iment of his penis and frequent erections. The child
& I' w9 v5 t, e' u) U3 M7 @8 awas the product of a full-term normal delivery, with
; m3 g; b* k) ?' D9 @5 X5 aa birth weight of 7 lb 14 oz, and birth length of
20 inches. He was breast-fed throughout the first year
of life and was still receiving breast milk along with
6 ]4 |) f) f# d/ q3 C6 csolid food. He had no hospitalizations or surgery,
: [1 E7 t3 y2 V% Q; land his psychosocial and psychomotor development
: j2 p# J- W) l4 s# b9 r0 D; mwas age appropriate.
. F% J. w' {: a9 o* r" c+ m7 EThe family history was remarkable for the father,
who was diagnosed with hypothyroidism at age 16,
3 r3 T3 n$ l4 a# x/ ?6 ?! dwhich was treated with thyroxine. The father’s
0 O0 y' R+ G. g0 I( s2 l$ D- W7 s% _+ u* S% iheight was 6 feet, and he went through a somewhat
9 z0 c, H6 I. v  Kearly puberty and had stopped growing by age 14.
The father denied taking any other medication. The
child’s mother was in good health. Her menarche
$ |; v9 n. V; n# K% z0 }was at 11 years of age, and her height was at 5 feet
4 t  Z. w" Z- @" C5 D2 u5 inches. There was no other family history of pre-
cocious sexual development in the first-degree rela-
/ E  z" {1 K" x; s* f! btives. There were no siblings.
Physical Examination
( M/ @! r: v+ v7 F: f2 lThe physical examination revealed a very active,
' U% e1 h5 z/ O2 X/ r, N9 t; k7 G; aplayful, and healthy boy. The vital signs documented
a blood pressure of 85/50 mm Hg, his length was
) I9 @: z6 w2 q* V90 cm (>97th percentile), and his weight was 14.4 kg
' z5 x, N$ t' D. b7 g! V6 K! e(also >97th percentile). The observed yearly growth
+ v; ?5 j$ v1 |9 Q  \' V, }0 e7 Hvelocity was 30 cm (12 inches). The examination of
the neck revealed no thyroid enlargement.
- j: J9 Q  j0 z" }The genitourinary examination was remarkable for
enlargement of the penis, with a stretched length of
8 cm and a width of 2 cm. The glans penis was very well
developed. The pubic hair was Tanner II, mostly around
8 Z" u, Q# l) [' a! V540
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 o0 S2 r5 ?! Z& P0 ^+ n6 kthe 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
, p# Z4 B1 e* `( ?  [abnormal skin pigmentations or café-au-lait spots.
$ O- t+ a7 [* ~0 G4 e8 f7 x4 S! CNeurologic evaluation showed deep tendon reflex 2+
bilateral and symmetrical. There was no suggestion
of papilledema.
) l7 U7 y- q3 z1 jLaboratory Evaluation
The bone age was consistent with 28 months by
0 F9 O4 }1 [8 @: l, B7 pusing the standard of Greulich and Pyle at a chrono-
logic age of 16 months (advanced).5 Chromosomal
) v! Z2 j+ K: F6 ]  N) a2 z8 S! bkaryotype was 46XY. The thyroid function test
( S9 G# U+ [, E2 a# I4 \showed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ C8 Q- a5 U" j8 Qlating hormone level was 1.3 µIU/mL (both normal).
; z6 y2 z% U# q9 OThe concentrations of serum electrolytes, blood
urea nitrogen, creatinine, and calcium all were
within normal range for his age. The concentration
of serum 17-hydroxyprogesterone was 16 ng/dL
(normal, 3 to 90 ng/dL), androstenedione was 20
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 ]; `& A# M0 d' f- nterone 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)
# n, A: L% ~/ z5 Q8 Iwas 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
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
and β-human chorionic gonadotropin was less than
. M8 o, W. u# u8 V8 ]2 v5 mIU/mL (normal <5 mIU/mL). Serum follicular
stimulating hormone and leuteinizing hormone
0 P9 ]! G. w0 C$ s1 c5 Gconcentrations were less than 0.05 mIU/mL
2 W7 l! D& _! X5 H2 p(prepubertal).
The parents were notified about the laboratory
results and were informed that all of the tests were
$ l  Z0 J# _# F: onormal except the testosterone level was high. The
follow-up visit was arranged within a few weeks to
obtain testicular and abdominal sonograms; how-
2 I6 S& |) K% Vever, the family did not return for 4 months.
Physical examination at this time revealed that the
child had grown 2.5 cm in 4 months and had gained
2 kg of weight. Physical examination remained
: a: j2 b. o# t+ A( I+ h1 runchanged. Surprisingly, the pubic hair almost com-
pletely disappeared except for a few vellous hairs at
% t6 i3 O9 }$ J: C+ K8 ithe base of the phallus. Testicular volume was still 2
mL, and the size of the penis remained unchanged.
4 M7 P; f2 s* o& PThe mother also said that the boy was no longer hav-
ing frequent erections.
Both parents were again questioned about use of
  `9 A) O1 R  v- Q2 I- g# hany ointment/creams that they may have applied to
the child’s skin. This time the father admitted the
1 i; @2 q+ [6 e: E( OTopical Testosterone Exposure / Bhowmick et al 541
use 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
to disclose that he was using a testosterone gel pre-
scribed by his family physician for decreased libido
secondary 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-
6 E/ e  q0 i. r; bnificant bare skin contact between baby and father.
The father also admitted that after the phone call,
when he learned the testosterone level in the baby
5 ]1 a7 _1 p8 p2 q) ]. Z, P  `' A  Bwas high, he then read the product information
* g) y+ A8 s1 F+ ~6 `packet and concluded that it was most likely the rea-
son for the child’s virilization. At that time, they
2 d9 ~3 c/ d" L6 C3 fdecided 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
test was ordered, but the family did not go to the
+ G' D  X' j, F/ |% Vlaboratory to obtain the test.
2 e' z! N. o5 X% fDiscussion
" i$ \' J' K$ X# ~, J! bPrecocious puberty in boys is defined as secondary
sexual development before 9 years of age.1,4
) ]6 o( o* R# }4 I# Y# IPrecocious puberty is termed as central (true) when
. V& Q. Z) k( Q1 }, Y" Iit is caused by the premature activation of hypo-
thalamic pituitary gonadal axis. CPP is more com-
3 {& h" e0 ~0 Tmon in girls than in boys.1,3 Most boys with CPP
may have a central nervous system lesion that is
responsible for the early activation of the hypothal-
amic pituitary gonadal axis.1-3 Thus, greater empha-
0 M. b  u) F, O& [sis has been given to neuroradiologic imaging in
boys with precocious puberty. In addition to viril-
; R7 Y, m* m/ y5 ~ization, the clinical hallmark of CPP is the symmet-
8 l) J/ k4 |# \8 M2 j# J$ Erical testicular growth secondary to stimulation by
. W8 H* \7 U) Tgonadotropins.1,3
# W0 J1 J* E; U4 O. l3 ZGonadotropin-independent peripheral preco-
cious puberty in boys also results from inappropriate
2 m  m7 J7 i# L0 q/ landrogenic stimulation from either endogenous or
( \* U& h; g: A4 Z+ q/ ^' ~exogenous sources, nonpituitary gonadotropin stim-
ulation, and rare activating mutations.3 Virilizing
congenital adrenal hyperplasia producing excessive
" @1 K* x+ o& D+ E& {" u+ e% E& Aadrenal androgens is a common cause of precocious
; [" X" J! @. N! i: j% }# ?/ F* ypuberty in boys.3,4
The most common form of congenital adrenal
! h5 k7 `1 ]2 j4 ~hyperplasia is the 21-hydroxylase enzyme deficiency.
The 11-β hydroxylase deficiency may also result in
9 Y% K& E) U0 h* s+ Iexcessive adrenal androgen production, and rarely,
an adrenal tumor may also cause adrenal androgen
excess.1,3
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) x0 G0 w1 x3 q8 n0 d2 d9 ]542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& C6 X. T' ~* F) NA unique entity of male-limited gonadotropin-
/ U/ C! h/ q5 a7 g; Y) V: qindependent precocious puberty, which is also known
" |# S8 c' D# P; I3 L8 d5 ^/ F. v7 `as testotoxicosis, may cause precocious puberty at a
very young age. The physical findings in these boys
6 i* X7 M; G2 R& Rwith this disorder are full pubertal development,
5 H  j: ]2 p. O- eincluding bilateral testicular growth, similar to boys
with CPP. The gonadotropin levels in this disorder
; Q; R/ D# h+ iare suppressed to prepubertal levels and do not show
pubertal 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
7 ~7 r; Z0 q! U: Tmay have similar precocious puberty.3
In our patient, physical examination was incon-
) a; M* T' r+ u$ s3 W+ L1 Usistent with true precocious puberty since his testi-
) x/ [+ M+ Q/ z' f) c  e' mcles were prepubertal in size. However, testotoxicosis
was in the differential diagnosis because his father
started puberty somewhat early, and occasionally,
testicular enlargement is not that evident in the
) C' }( i9 C4 p+ [* Ubeginning of this process.1 In the absence of a neg-
ative initial history of androgen exposure, our
: `5 I; {5 s& |3 Q/ T+ C; M$ vbiggest concern was virilizing adrenal hyperplasia,
  s: \) v9 s* R# m+ i; keither 21-hydroxylase deficiency or 11-β hydroxylase
: \4 u7 c6 Y  I) f" F  D8 ddeficiency. Those diagnoses were excluded by find-
6 ~# J1 a+ y2 z% n& p6 Aing 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-
8 ~- @0 p- D2 N9 g8 Npearance of pubic hair, normal growth velocity, and
decreased erections. The father admitted using a testos-
! {- A' R  V! @( M5 w& ]terone gel, which he concealed at first visit. He was
/ e4 L2 }8 c$ ?/ M, t+ tusing it rather frequently, twice a day. The Physicians’
Desk Reference, or package insert of this product, gel or
cream, cautions about dermal testosterone transfer to
+ N9 F: |& ^" X# n. Gunprotected females through direct skin exposure.
5 i. ?3 E8 j4 p: HSerum testosterone level was found to be 2 times the
baseline value in those females who were exposed to
" M! x2 u% t" ]2 keven 15 minutes of direct skin contact with their male
6 Z9 F9 C1 f1 z4 C) V, ^partners.6 However, when a shirt covered the applica-
tion site, this testosterone transfer was prevented.
* a5 I# f( Y' f( P+ [  \Our patient’s testosterone level was 60 ng/mL,
& i7 U- D6 n# w/ z6 Y+ m9 A1 Z$ Fwhich was clearly high. Some studies suggest that
2 V7 k3 P  t# C) kdermal conversion of testosterone to dihydrotestos-
terone, which is a more potent metabolite, is more
active in young children exposed to testosterone
. p; T& H3 z" X) Z: g  v. s3 xexogenously7; however, we did not measure a dihy-
drotestosterone level in our patient. In addition to
$ p% ]7 _! E9 E$ X( a. tvirilization, exposure to exogenous testosterone in
5 a( r' ]: h& n7 T! {children results in an increase in growth velocity and
. J& }" @& f: o( E  A$ O! g* Gadvanced bone age, as seen in our patient.
$ T# ]# g5 a4 H* V! g$ y$ Q7 BThe long-term effect of androgen exposure during
early childhood on pubertal development and final
adult height are not fully known and always remain
3 O$ A1 A/ w% Q* c- \4 ^a concern. Children treated with short-term testos-
; w" T* p1 C* r4 G9 r! p  J% }terone injection or topical androgen may exhibit some
acceleration of the skeletal maturation; however, after
cessation of treatment, the rate of bone maturation
decelerates and gradually returns to normal.8,9
) i6 w1 ~1 \3 ~* Y& b; oThere are conflicting reports and controversy
, V0 S: U, B3 sover the effect of early androgen exposure on adult
penile length.10,11 Some reports suggest subnormal
adult penile length, apparently because of downreg-
ulation of androgen receptor number.10,12 However,
Sutherland et al13 did not find a correlation between
/ E4 ]2 o0 u& {* Z& i$ Q6 Q. ~childhood testosterone exposure and reduced adult
9 @. y7 F9 A* J- X  g2 Wpenile length in clinical studies.
Nonetheless, we do not believe our patient is
- u, j# O, n' \) I3 W8 N; B0 Z* Cgoing to experience any of the untoward effects from
0 p+ T+ y' r& U) L) F: U4 n- W+ Gtestosterone exposure as mentioned earlier because
) n5 h! D6 R5 p( U) u" _8 Kthe exposure was not for a prolonged period of time.
) V6 t0 ^3 H2 H; B1 z4 m. }2 c5 }3 OAlthough the bone age was advanced at the time of
diagnosis, the child had a normal growth velocity at
the follow-up visit. It is hoped that his final adult
9 ]) ^( m$ e/ X# jheight will not be affected.
Although rarely reported, the widespread avail-
  P; e4 k. u! iability 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
gel should be asked of the family members during
the 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
appropriate history. The inability to obtain such a
history, or failure to ask the specific questions, may
result in extensive, unnecessary, and expensive
8 t! R# P9 q3 i; F0 hinvestigation. The primary care physician should be
  ]' S1 R" n5 q* Q! Faware of this fact, because most of these children
, [/ H/ o0 {, |& m& Umay initially present in their practice. The Physicians’
2 n5 r5 x( L8 B5 c5 Z  ZDesk Reference and package insert should also put a
- v2 K1 o9 T1 U8 z/ D- Wwarning about the virilizing effect on a male or
0 y2 n6 k& W3 x8 _& l; J+ P" p2 Qfemale child who might come in contact with some-
one using any of these products.
2 C$ B. ~, _$ S: I0 K) D$ P! a' gReferences
3 G9 z7 k* B" h* h: y1. Styne DM. The testes: disorder of sexual differentiation
# O% P' r; v1 U! e) E' [* _and puberty in the male. In: Sperling MA, ed. Pediatric
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
2002: 565-628.
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ P% ?! L7 O! G+ N6 dpuberty 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
areas: organic central precocious puberty. Acta Paediatr.
; y8 P& t6 K$ w2001;90:751-756.
. w' b; y2 s3 M2 D1 R: c& x3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed.
Pediatric Endocrinology. 4th ed. New York, NY: Marcel
) u# p6 N: ]/ r1 uDekker Inc; 2003:211-238.
4. Yu YM, Punyasavatsu N, Elder D, D’Ercole AJ. Sexual
development in a two-year-old boy induced by topical
! j  P8 P/ ]+ h2 Yexposure to testosterone. Pediatrics. 1999;104:e23.
' i5 m0 B  X' [' l& S$ K. \' w5. Greulich WW, Pyle SI, eds. Radiographic Atlas of
5 F0 Q: r! }& k/ \$ j4 sSkeletal Development of the Hand and Wrist. 2nd ed.
7 u! d" n+ D/ qStanford, CA: Stanford University Press; 1959.
1 J" d2 ^3 e1 [' t( o* O. a6. Physicians’ Desk Reference. Androgel 1% testosterone,
Unimed Pharmaceutical Inc. Montvale, NJ: Medical
Economics Company, Inc; 2004:3239-3241.
7. Klugo RC, Cerny JC. Response of micropenis to topical
- U/ S4 @4 P: l0 j$ T3 utestosterone and gonadotropin. J Urol. 1978;119:
0 j) B  F8 G( N/ `- j  E: j5 O: L& e667-668.
8. Guthrie RD, Smith DW, Graham CB. Testosterone
" L" W# U7 A5 W! h( Ztreatment for micropenis during early childhood. J Pediatr.
# }# I, n1 v/ r+ f) o1973;83:247-252.
! i# \3 z( b. b4 v! u: |8 ~9. Jacobs SC, Kaplan GW, Gittes RF. Topical testosterone
9 x" t+ C/ o1 W9 Z5 E9 ztherapy for penile growth. Urol. 1975;6:708-710.
5 g, ~. [% _2 Q10. Husmann DA, Cain MP. Microphallus: eventual phallic
size is dependent on the timing of androgen administra-
tion. J Urol. 1994;152:734-739.
" y3 v/ T$ ^8 D! Z% |( l11. McMahon DR, Kramer SA, Husmann DA. Micropenis:
does early treatment with testosterone do more harm
1 j4 I* V$ o& u4 ~1 }  w6 B* A& qthan good? J Urol. 1995;154:825-829.
12. Takane KK, George FW, Wilson JD. Androgen receptor
* {( z# c! X+ r2 R5 X# Dof rat penis is down-regulated by androgen. Am J Physiol.
1990;258:E46-E50.
  ^5 Q1 ^2 W) H( p$ U( S; T13. Sutherland RS, Kogan BA, Baskin LS, et al. The effect
- Q: B3 ^1 K, \& a1 dof prepubertal androgen exposure on adult penile
8 Q3 f% f7 _( L% \0 T9 e4 [length. 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