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-Old8 j3 v. r% [: U$ Y0 M
Boy Induced by Indirect Topical
' L) b* P6 {$ j' J# f! @% I: lExposure to Testosterone- h: T* f/ i" g" Q+ e, m
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) Z* c- m1 M" m* T& g& l/ d) i5 a
and Kenneth R. Rettig, MD13 r9 Z% q- N$ i
Clinical Pediatrics4 u/ ]( r/ o: H9 R$ g% F
Volume 46 Number 6
7 |4 k( v- I1 BJuly 2007 540-5435 P/ t" i  \. I% t
© 2007 Sage Publications! }+ Z7 c0 h3 p- v
10.1177/0009922806296651
/ F+ i4 g. {6 Y& x6 l8 H6 Ghttp://clp.sagepub.com1 m: A' V# X: d$ L; G* e9 R3 a
hosted at/ J* h1 M% S/ X3 |% _& K: j5 U/ X
http://online.sagepub.com4 w/ i* z; c! E/ J% r! h
Precocious puberty in boys, central or peripheral,# W2 i9 X: O! f, {+ \* ?! y
is a significant concern for physicians. Central2 W5 h5 H/ w) Y/ X: X8 v- |
precocious puberty (CPP), which is mediated' x$ }% Q! k4 M) M0 w9 c+ Y/ y
through the hypothalamic pituitary gonadal axis, has. y  Z9 H! j# m$ A2 e% j3 }
a higher incidence of organic central nervous system
; h' [$ E3 q1 A" g" Blesions in boys.1,2 Virilization in boys, as manifested
9 f/ f9 l9 ^4 l. U4 R+ Xby enlargement of the penis, development of pubic  O1 C' H3 O5 L3 g3 a
hair, and facial acne without enlargement of testi-
1 v8 i1 |9 D: w2 W3 ocles, suggests peripheral or pseudopuberty.1-3 We
: W* W* q! T' b+ m9 b! L+ zreport a 16-month-old boy who presented with the3 E: J% I; |$ _( P
enlargement of the phallus and pubic hair develop-9 S( F: e3 ^. R1 t9 t4 E
ment without testicular enlargement, which was due
) b% `0 _% q  V; }* ito the unintentional exposure to androgen gel used by) B* t: f8 z/ T4 ]# a
the father. The family initially concealed this infor-
1 u% n4 k% C* W1 Mmation, resulting in an extensive work-up for this' F( R' \0 x; ~& W8 [4 `
child. Given the widespread and easy availability of$ v- m( h0 N/ ~0 Y( U) \) I
testosterone gel and cream, we believe this is proba-, W, O) Q3 Q; I
bly more common than the rare case report in the/ C" J% _7 Y' q' s5 c" h2 N- U
literature.4% c5 u# N$ w3 [( d6 {5 H3 ]/ i4 Q
Patient Report
. G. A+ t4 I" c0 j4 [$ s: c4 nA 16-month-old white child was referred to the( V* M3 a6 `0 b
endocrine clinic by his pediatrician with the concern' i4 F& j- [1 S# y  I  V
of early sexual development. His mother noticed
5 N0 d& B! C5 J% q  Rlight colored pubic hair development when he was
- Q5 p8 j2 ]3 c+ H0 TFrom the 1Division of Pediatric Endocrinology, 2University of
% b  o% Y6 W  _, g, E  v9 o$ sSouth Alabama Medical Center, Mobile, Alabama.# X$ R. z6 e. D) n% q. n
Address correspondence to: Samar K. Bhowmick, MD, FACE,6 @6 z$ F% a6 N2 q! A8 X
Professor of Pediatrics, University of South Alabama, College of. y) b/ a& S1 Y# H2 v
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! s' C8 U3 i1 E! ^8 {5 `8 Ee-mail: [email protected].0 G, ~/ e8 j( G2 E
about 6 to 7 months old, which progressively became
6 p; m+ ]7 @. D+ N# [7 ]# Z; Wdarker. She was also concerned about the enlarge-# ~) ?5 a; z: H0 d$ c, I2 G4 I# i
ment of his penis and frequent erections. The child0 Z# H7 ~) }2 b( E
was the product of a full-term normal delivery, with6 F! G5 ?3 M3 k! \' B
a birth weight of 7 lb 14 oz, and birth length of
3 v1 L" O0 |1 }4 i! S6 Y20 inches. He was breast-fed throughout the first year
' D4 X  v8 `# }- L- oof life and was still receiving breast milk along with/ D% U1 F$ C5 U+ ^" J( j' o3 P4 [. ]
solid food. He had no hospitalizations or surgery,
% ^# t9 d% n+ zand his psychosocial and psychomotor development
4 Y. U- t* m2 D* k; Hwas age appropriate.( \, A6 J" o  B* u3 Q- b
The family history was remarkable for the father,
( Z+ U1 R  G) C! g1 Q# gwho was diagnosed with hypothyroidism at age 16,: W# c9 z% n* U. c5 a
which was treated with thyroxine. The father’s6 s7 d6 C1 m3 C- w6 X
height was 6 feet, and he went through a somewhat2 H9 k5 M6 i/ r3 S# L
early puberty and had stopped growing by age 14.9 a  i% s2 N" m  h9 e0 B( L
The father denied taking any other medication. The
( S6 A! N9 _% U5 X, `child’s mother was in good health. Her menarche
) s; A2 t' S8 C' E. w# q7 _was at 11 years of age, and her height was at 5 feet
  I/ s" y# ^2 V, W: [5 inches. There was no other family history of pre-
- {% m" j* s" }9 g; k' ccocious sexual development in the first-degree rela-3 s) E* v6 n+ j9 T4 M7 N
tives. There were no siblings." S: P- M4 I  i- A% n$ J9 t5 d$ r( w, b
Physical Examination
. x" @: \4 X+ }The physical examination revealed a very active,
; w/ ^  J! g; F3 {playful, and healthy boy. The vital signs documented& u, K* [3 v3 D2 s  `2 P
a blood pressure of 85/50 mm Hg, his length was
( }/ K0 `7 p1 f90 cm (>97th percentile), and his weight was 14.4 kg
; p" e( P& K" T/ X9 F(also >97th percentile). The observed yearly growth  }1 L3 J3 ^# c8 m+ ^
velocity was 30 cm (12 inches). The examination of/ x- }- d8 v7 T7 h9 G
the neck revealed no thyroid enlargement.
3 v% Q7 t% G9 v$ l( kThe genitourinary examination was remarkable for; Y. j* ~: l# B4 c" O+ ]2 R+ s
enlargement of the penis, with a stretched length of$ X& h, J# {% w8 [$ U8 Q+ P
8 cm and a width of 2 cm. The glans penis was very well
0 g8 g8 U8 W# I7 X) X- cdeveloped. The pubic hair was Tanner II, mostly around
- `9 `( q& G4 T1 I1 Z& ^540$ L5 y1 r* k- O7 H# U! f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& M6 @' s  i# ethe base of the phallus and was dark and curled. The
4 _1 P& e8 j. x' K: I9 u( t- Otesticular volume was prepubertal at 2 mL each.
; b1 a" I% j' x$ X3 `! [2 K+ QThe skin was moist and smooth and somewhat
" y4 d7 P- v) b$ H% S" K# J. foily. No axillary hair was noted. There were no
4 I# S$ _/ ^' Y) S! V8 q6 z; _abnormal skin pigmentations or café-au-lait spots.' [) @2 o9 H' p! h' a+ n
Neurologic evaluation showed deep tendon reflex 2+
* N1 a. P& ]$ m6 E0 _" ?& abilateral and symmetrical. There was no suggestion+ R/ r2 E3 c) ^" c# J8 t8 g
of papilledema.: F& H) [9 i; b7 ~* y$ Z
Laboratory Evaluation+ a5 H5 M1 J2 E+ H, g( y+ \% @
The bone age was consistent with 28 months by0 {1 K3 J7 |# q3 d
using the standard of Greulich and Pyle at a chrono-7 F* Y- z+ h' G% X
logic age of 16 months (advanced).5 Chromosomal$ n: l' P' ]) }5 D) Y, j. Q, U
karyotype was 46XY. The thyroid function test
3 c3 m# }! G  \; y" {8 ~showed a free T4 of 1.69 ng/dL, and thyroid stimu-  F1 @4 G8 I; K3 o& g9 ~: D
lating hormone level was 1.3 µIU/mL (both normal).+ m, E' }) w2 a# n9 W4 p
The concentrations of serum electrolytes, blood
; A. C. \- a5 O/ kurea nitrogen, creatinine, and calcium all were% m5 R7 k. R, {1 {4 j
within normal range for his age. The concentration& p1 X8 k" \. N$ [
of serum 17-hydroxyprogesterone was 16 ng/dL4 a+ P6 L4 B6 U9 u
(normal, 3 to 90 ng/dL), androstenedione was 20
7 A6 j5 c; l6 V6 H- i- `  ?; s8 A! Ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) N& I' i% m$ o" A+ J3 K
terone was 38 ng/dL (normal, 50 to 760 ng/dL),0 ]* R8 L% C2 U2 u/ }+ I+ _
desoxycorticosterone was 4.3 ng/dL (normal, 7 to; |/ s$ J+ V2 s9 l! f. Z+ R
49ng/dL), 11-desoxycortisol (specific compound S)3 j6 I0 x9 w- w
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" D0 }, s5 J4 o0 S
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 h, j* G- t. Z) ?- }/ Ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 o; w+ I- J' H- pand β-human chorionic gonadotropin was less than
3 m1 Z. m  V& N5 mIU/mL (normal <5 mIU/mL). Serum follicular6 o) t) K3 }1 z9 v0 {
stimulating hormone and leuteinizing hormone
* h6 q( q2 p- W7 i. Sconcentrations were less than 0.05 mIU/mL0 ], N/ r$ `0 t2 {2 T4 H9 h6 c5 ~
(prepubertal).
6 Y# }. B' h% j( BThe parents were notified about the laboratory+ ?( J! w7 w/ V
results and were informed that all of the tests were
2 _% [& j; J# i4 D4 C: M4 Enormal except the testosterone level was high. The
8 D2 a( \1 ?3 q" @8 Hfollow-up visit was arranged within a few weeks to
* Y) r) R% d  U( dobtain testicular and abdominal sonograms; how-
7 C6 J8 f8 c3 j1 T% l8 b$ [8 Tever, the family did not return for 4 months.4 j$ o5 L5 s6 |! u) o4 f( w  ?4 w' ?% q0 t/ a
Physical examination at this time revealed that the
0 C/ d1 E3 `+ B5 Ichild had grown 2.5 cm in 4 months and had gained' K2 z3 X  Z5 l# `) h' x4 j: {
2 kg of weight. Physical examination remained
7 I# l1 F8 q+ u  ?unchanged. Surprisingly, the pubic hair almost com-
" A3 @, L$ D1 m7 N( B  D+ ^! h3 ^pletely disappeared except for a few vellous hairs at
0 ?7 R2 [/ f7 F" r  X8 d. Ythe base of the phallus. Testicular volume was still 2
# F" Z7 c) e/ n0 P5 c9 ~2 kmL, and the size of the penis remained unchanged.* q* z# R. x) T7 v
The mother also said that the boy was no longer hav-$ L4 B3 F6 T- ]3 w1 e0 ~  k$ M1 W
ing frequent erections.
( h! L, J. ]5 R- a) h! z7 tBoth parents were again questioned about use of
6 H4 f6 q0 _2 ~- e1 m6 X, r1 {any ointment/creams that they may have applied to, k3 L+ r9 y4 z  h# c
the child’s skin. This time the father admitted the
' k3 u- `. f' V2 g, K( Y4 {Topical Testosterone Exposure / Bhowmick et al 541
1 j' a+ m1 u# a  q- t; q, buse of testosterone gel twice daily that he was apply-
% X3 K. J4 h7 G- a" `$ T7 {ing over his own shoulders, chest, and back area for, |% D2 o( a# S7 g1 D3 I  |  o
a year. The father also revealed he was embarrassed4 w/ g- j) J9 V2 B
to disclose that he was using a testosterone gel pre-
$ c! [5 {/ ^: P" Zscribed by his family physician for decreased libido
, h! j: S4 q* ?" F4 t2 ^secondary to depression.0 ^: O7 Z  ~2 x
The child slept in the same bed with parents.
4 P5 L9 k7 C% _  o7 b+ JThe father would hug the baby and hold him on his8 x7 Q! [' W9 y% g1 R
chest for a considerable period of time, causing sig-
3 z* m) G# D3 J; a8 _nificant bare skin contact between baby and father.8 {; ], E3 }5 P% [
The father also admitted that after the phone call,
& `4 X; Y( }( C, @) h! w# Cwhen he learned the testosterone level in the baby
& V8 i3 `! I7 Q- H; E1 y, y! }was high, he then read the product information
4 ?$ w; }  U0 I# ~packet and concluded that it was most likely the rea-% H' q; d; h6 ~8 o
son for the child’s virilization. At that time, they; X5 {+ {. S. l0 _! P5 ], a
decided to put the baby in a separate bed, and the
5 `" g2 i$ B* xfather was not hugging him with bare skin and had
2 C0 g* R1 a% M. vbeen using protective clothing. A repeat testosterone
! l& ?& X- p7 Q& F! L& v( ]test was ordered, but the family did not go to the. e3 G# k: X$ B
laboratory to obtain the test., q4 \8 W! Q, i7 Q& l( w
Discussion! u' e& R# y/ A; t5 z
Precocious puberty in boys is defined as secondary
' n& f- @1 p1 h7 A) Isexual development before 9 years of age.1,4; V0 i6 o5 u7 H, U& Y1 d
Precocious puberty is termed as central (true) when
0 r( C9 H9 \! Z! V* v* bit is caused by the premature activation of hypo-$ M: t5 g$ m0 e& \3 d, }! g1 q
thalamic pituitary gonadal axis. CPP is more com-1 w+ z& `/ b8 A0 w9 e; F4 S
mon in girls than in boys.1,3 Most boys with CPP
: V( W9 c( t$ ]3 T6 W. Hmay have a central nervous system lesion that is0 C- [7 x( Z  d3 s4 B1 z
responsible for the early activation of the hypothal-; ]4 i; o- x; ?$ d; c+ {% H' i
amic pituitary gonadal axis.1-3 Thus, greater empha-% n- u$ P8 p" V$ z
sis has been given to neuroradiologic imaging in
1 p, c0 D! K. n' F* q2 s0 yboys with precocious puberty. In addition to viril-
* D& t1 N+ s2 Xization, the clinical hallmark of CPP is the symmet-( I4 [7 m: B7 I% e& b, l  y0 a
rical testicular growth secondary to stimulation by
: ^" a, z% A& F* ]gonadotropins.1,3( ~3 w2 J2 S  q, r' v
Gonadotropin-independent peripheral preco-7 f. K, ?# O" H" Y5 v' Z
cious puberty in boys also results from inappropriate9 I# z; B2 [# x4 L
androgenic stimulation from either endogenous or8 c9 A' c, g1 w
exogenous sources, nonpituitary gonadotropin stim-) z* d+ K. P$ m5 X5 y0 J
ulation, and rare activating mutations.3 Virilizing
) z4 F) r0 l6 ~; l2 Xcongenital adrenal hyperplasia producing excessive7 U5 P: p+ {+ O3 A
adrenal androgens is a common cause of precocious% i- }. G& F1 Q5 e
puberty in boys.3,4
9 S+ U, x! W% ]7 [  ZThe most common form of congenital adrenal
7 g& V/ |  m, s4 nhyperplasia is the 21-hydroxylase enzyme deficiency." h7 J- t/ W4 v- y- z' J
The 11-β hydroxylase deficiency may also result in
' L# m" [0 b2 pexcessive adrenal androgen production, and rarely,
$ [% }1 O8 [  }% Y& ^  ean adrenal tumor may also cause adrenal androgen7 g. V: x2 I4 T" H+ a3 Y" x/ S
excess.1,3
+ a3 t/ x, i3 j2 V# \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 y4 Q3 ?) c5 c( x542 Clinical Pediatrics / Vol. 46, No. 6, July 2007% u7 f3 a4 g2 a! Q) ?. Z& P$ A
A unique entity of male-limited gonadotropin-( b; n, k4 L3 C6 ?, w6 e
independent precocious puberty, which is also known
% U- z; A5 u# r  X$ das testotoxicosis, may cause precocious puberty at a0 Y. U- B( x( l+ H
very young age. The physical findings in these boys; H: n8 K$ A# C& x: e6 h5 k4 s0 ]
with this disorder are full pubertal development,* E- C* l8 z% `3 Q
including bilateral testicular growth, similar to boys
2 F) O' q  \# b$ s! ^+ c5 {, Ywith CPP. The gonadotropin levels in this disorder
, p2 Q( ?" N, o$ |; q" vare suppressed to prepubertal levels and do not show
" u( i2 D$ A; xpubertal response of gonadotropin after gonadotropin-
( P' k! H( K1 c) [4 Vreleasing hormone stimulation. This is a sex-linked
6 \. Q7 j' R7 G: [! M$ {8 @autosomal dominant disorder that affects only3 K/ U7 G  s9 y; \  c: R
males; therefore, other male members of the family
$ O; b' {5 |1 {0 B+ l( Omay have similar precocious puberty.3
  k9 E! t5 R* B, O0 d3 g5 U) e9 _In our patient, physical examination was incon-4 }4 y' H! y- A
sistent with true precocious puberty since his testi-
8 y# E- k: b( {$ ~$ J: l: Fcles were prepubertal in size. However, testotoxicosis; `5 B, b% I/ ]
was in the differential diagnosis because his father
7 ?9 z* F/ |! L7 C  l5 f. Gstarted puberty somewhat early, and occasionally,
: e& f! _" j/ `* J) Ztesticular enlargement is not that evident in the3 C, S: _2 c/ d
beginning of this process.1 In the absence of a neg-8 K6 ?& Y! N; L3 T- Y
ative initial history of androgen exposure, our- H; L, U( x' @! y# |
biggest concern was virilizing adrenal hyperplasia,
0 h" E1 F. F3 v2 h, \2 @% h0 Weither 21-hydroxylase deficiency or 11-β hydroxylase) I- `# R1 o1 F" v
deficiency. Those diagnoses were excluded by find-
! h! B6 C) o4 c6 D2 ying the normal level of adrenal steroids.+ B2 N' p. ]) `& Q# X: `
The diagnosis of exogenous androgens was strongly$ ~+ v6 S; z( i  u
suspected in a follow-up visit after 4 months because7 j4 R5 b; U- [3 q( }
the physical examination revealed the complete disap-1 s& m! o; |( h/ B+ ]5 P4 @- `
pearance of pubic hair, normal growth velocity, and" N  v2 k( X+ ]+ Y
decreased erections. The father admitted using a testos-* ^9 h. A! ]0 n8 }
terone gel, which he concealed at first visit. He was5 \" v& J, L) S& U
using it rather frequently, twice a day. The Physicians’1 R* ~% I4 U7 i% b; K# k
Desk Reference, or package insert of this product, gel or
+ ?  d- I3 a# O* m: y  w/ Icream, cautions about dermal testosterone transfer to- `+ m' O1 \% G/ ?; F
unprotected females through direct skin exposure.  [( r# H, r6 l
Serum testosterone level was found to be 2 times the
" V4 s+ Q( w7 ebaseline value in those females who were exposed to% |  T9 R: ]( G% r' h, v( U
even 15 minutes of direct skin contact with their male. C& b( o( H' E7 n3 s9 ]
partners.6 However, when a shirt covered the applica-
; I% A/ S' f3 x1 W% T" k& Ktion site, this testosterone transfer was prevented.
! m2 }8 v  \; x( f' \7 |Our patient’s testosterone level was 60 ng/mL,
0 B# K2 M7 M. t+ D7 Iwhich was clearly high. Some studies suggest that
/ M# V/ E. s" L$ M6 Y: K! Q' `dermal conversion of testosterone to dihydrotestos-
6 h- V- \& v4 y7 s- K1 q% Rterone, which is a more potent metabolite, is more& N  D! f# u+ q8 O1 p5 q5 C+ j
active in young children exposed to testosterone) {* V' N% A# D- t  a* [
exogenously7; however, we did not measure a dihy-+ ]& S& W& _4 e6 x8 Z  o( [
drotestosterone level in our patient. In addition to3 W# c: J9 ]5 M/ {
virilization, exposure to exogenous testosterone in. T% G# f! d% X1 ?( m& B3 ~/ ]
children results in an increase in growth velocity and. G# V$ e* v* z# c7 Y6 i
advanced bone age, as seen in our patient.
' }/ O6 q% \  s" O4 i: G6 Y8 AThe long-term effect of androgen exposure during& ?$ ]4 f, K- _" y5 y6 p
early childhood on pubertal development and final
+ ~4 K& y) |. T1 U5 Q# ]adult height are not fully known and always remain
" H0 W7 r' Q8 Ga concern. Children treated with short-term testos-! o* n- x5 y; y# y
terone injection or topical androgen may exhibit some* E- r' ^6 H7 t5 w
acceleration of the skeletal maturation; however, after
& E  M/ X7 ^6 S0 E2 u, R+ k) wcessation of treatment, the rate of bone maturation1 e2 B& e( d* W$ i/ Y
decelerates and gradually returns to normal.8,96 X' ^2 p0 t$ |2 O( n
There are conflicting reports and controversy
) v/ R4 W  C  A/ Nover the effect of early androgen exposure on adult# D; @/ F' x5 e$ H7 N; c" Y1 B
penile length.10,11 Some reports suggest subnormal
2 [  H! S( h' ?# A% \! }; P& r9 p7 Xadult penile length, apparently because of downreg-
0 _4 T' ?* v" a* J$ h- Z- ]" S$ qulation of androgen receptor number.10,12 However,# O0 E5 L  N1 B
Sutherland et al13 did not find a correlation between
) `' T0 B" K( |1 wchildhood testosterone exposure and reduced adult3 p& a" V1 Z3 Z" W8 H' x2 A! ^
penile length in clinical studies.5 ^/ o+ u; r" E- h2 R7 c( s
Nonetheless, we do not believe our patient is
5 E' Q0 J" N4 \( O0 d2 ?6 kgoing to experience any of the untoward effects from/ n: [( d4 d( m9 Z& z- g; K
testosterone exposure as mentioned earlier because
& O7 q8 h# L' [  ?% ^7 Fthe exposure was not for a prolonged period of time.4 y: ]" x- F4 ?  n
Although the bone age was advanced at the time of
+ Q$ t7 \. `5 Q8 `* k' b! Hdiagnosis, the child had a normal growth velocity at+ r; ?' g* f! \) n, b; B/ `
the follow-up visit. It is hoped that his final adult
( H6 ~. _/ J) d  q9 W) e5 _height will not be affected.; [. R5 P. S0 }( w- M1 {4 V( P/ h( ]
Although rarely reported, the widespread avail-' ]: K) {  G- D- o, [: {
ability of androgen products in our society may8 i% v! @$ [' @3 g  g
indeed cause more virilization in male or female7 E8 S  x2 n' r2 l& \
children than one would realize. Exposure to andro-8 f1 {' O- [4 t4 g& v' E7 _
gen products must be considered and specific ques-+ F! p1 j  p" \$ B8 x/ L8 T5 _4 [- d
tioning about the use of a testosterone product or, c( z5 A5 [8 K1 ]5 x" t- _
gel should be asked of the family members during8 W! @5 U( b$ f& g8 v
the evaluation of any children who present with vir-: e9 d1 z; f  M0 `, H* C; S$ v
ilization or peripheral precocious puberty. The diag-
2 h& A( M" h" Enosis can be established by just a few tests and by7 x6 X, h: M$ `: F6 j3 V% A
appropriate history. The inability to obtain such a; `; G3 D$ T  M
history, or failure to ask the specific questions, may) e- C" E& {) Z" L
result in extensive, unnecessary, and expensive
7 ^1 Y  d( U+ y# p  e; Qinvestigation. The primary care physician should be
( R/ m+ ^) B) x. {& I: Iaware of this fact, because most of these children
% h4 ]+ a& P4 Umay initially present in their practice. The Physicians’6 S) C* F+ e3 m' M) ~
Desk Reference and package insert should also put a
# x, o  S* N8 i" fwarning about the virilizing effect on a male or
# F5 |6 D6 r0 q0 l* j! Ufemale child who might come in contact with some-  D$ A* _3 B' Y" B1 _. z
one using any of these products.
" s5 o7 T+ m& G/ x) iReferences( b) P9 n6 f  B# i0 {$ N" g
1. Styne DM. The testes: disorder of sexual differentiation
9 d; ~  O9 U+ P% Q7 @# p  Vand puberty in the male. In: Sperling MA, ed. Pediatric
) k% V& W7 l; [! qEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, p) {6 a! J) c
2002: 565-628.5 v. t5 b5 A' @; @$ S) M
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, [+ ?3 \& a9 n' opuberty 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-Old1 b8 A$ p- k) k' |2 [; ~% u
Boy Induced by Indirect Topical
: k: y0 J. `9 ^* F+ [% m3 t; OExposure to Testosterone
- @7 K8 p- Z; s- h, `+ sSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 d7 a! e$ _0 s! [
and Kenneth R. Rettig, MD1
! Q9 ~0 X1 @! y$ l' w0 k( OClinical Pediatrics& B+ w1 k1 r: ~
Volume 46 Number 6
3 a& X" F" D+ j, C" i& r; IJuly 2007 540-5431 F  p6 h2 a; n0 z1 Y" e
© 2007 Sage Publications
' V; m6 R8 s7 S8 `# H( b# _10.1177/0009922806296651
7 q0 M- Z& ?9 ]http://clp.sagepub.com
' G' B) y% ^8 t4 T# yhosted at) M  ?1 N: E6 G$ w) Y1 T" }. [4 R& E
http://online.sagepub.com, _0 p5 S7 W: ?) M( [; s- p: `/ ^# I  |( X
Precocious puberty in boys, central or peripheral,
% @. S9 G; d& A6 Ois a significant concern for physicians. Central
$ [; u3 `+ P+ N5 {precocious puberty (CPP), which is mediated
- q. l: d# |$ m. E9 D4 E/ Rthrough the hypothalamic pituitary gonadal axis, has
  F" b" K5 ^  l/ f" N5 a% Qa higher incidence of organic central nervous system& S% @# I3 T3 u7 \% p8 M" F4 P
lesions in boys.1,2 Virilization in boys, as manifested
8 }5 H8 u' U, X. dby enlargement of the penis, development of pubic
. r5 r5 I) k( H. A+ h5 u# a) Shair, and facial acne without enlargement of testi-
% v. {4 O4 S) G# X# }cles, suggests peripheral or pseudopuberty.1-3 We5 y; \, i2 E1 V, r4 e) w
report a 16-month-old boy who presented with the& M: w8 {9 q' M
enlargement of the phallus and pubic hair develop-  {' F1 {9 [' k
ment without testicular enlargement, which was due
1 W8 L5 Q$ R9 Ito the unintentional exposure to androgen gel used by
* j7 ^3 ~% o$ m/ z( w+ w  Cthe father. The family initially concealed this infor-/ X. U; N* O3 W, V" a- g! R
mation, resulting in an extensive work-up for this# R$ G# }0 B8 ?$ Q% Y7 Y
child. Given the widespread and easy availability of8 e- ]6 S6 _  k! K0 J; B3 V
testosterone gel and cream, we believe this is proba-# p- R$ q3 g5 E6 o6 _/ _/ D+ V7 s
bly more common than the rare case report in the
* E$ Y  c, h+ [  q/ Kliterature.4, x' i+ t1 f# [; ?* W, `8 B' l4 ~
Patient Report9 t+ s, I9 f# r, e) ]8 l
A 16-month-old white child was referred to the
3 \/ z/ Y! v3 k5 d/ o+ Pendocrine clinic by his pediatrician with the concern
9 s" o' k: h% I7 X( |of early sexual development. His mother noticed- a3 l4 B* k4 h+ @# i
light colored pubic hair development when he was
4 n9 A7 K* z) _; R0 bFrom the 1Division of Pediatric Endocrinology, 2University of
  C; i9 U4 o8 N; y  xSouth Alabama Medical Center, Mobile, Alabama.
+ u( ?! `, n7 K) S2 {0 v+ iAddress correspondence to: Samar K. Bhowmick, MD, FACE,. b! E2 V) W5 G$ r
Professor of Pediatrics, University of South Alabama, College of
- Z0 h( E' G' N/ U# n* NMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ q: W+ i( G5 He-mail: [email protected].: C1 i. u6 A. v: k* B- g4 {
about 6 to 7 months old, which progressively became& l, e5 |6 J+ l/ ^. w
darker. She was also concerned about the enlarge-6 X/ Y! d: o4 k! l0 t9 S, o! }
ment of his penis and frequent erections. The child
- C4 r+ J- e" _$ B% _3 r8 Q# Gwas the product of a full-term normal delivery, with0 `) I2 r0 i' O4 \+ b1 L* `  t
a birth weight of 7 lb 14 oz, and birth length of. Y  @: a0 ]6 K$ f& j
20 inches. He was breast-fed throughout the first year
4 y, Q8 G8 ^: }4 `# Dof life and was still receiving breast milk along with: b- g3 J, z, N8 K$ I- h5 l2 K
solid food. He had no hospitalizations or surgery,
3 C" Z8 k8 Z2 q1 y2 e" a- X; Land his psychosocial and psychomotor development
/ ]; d8 D8 i1 f% c& L4 \9 vwas age appropriate.2 C5 R5 F9 F- a- a$ Q
The family history was remarkable for the father,
8 Q0 ^1 M1 Q3 H, z, A7 ]& |' Lwho was diagnosed with hypothyroidism at age 16,1 ~0 I$ P2 @0 i% x2 o
which was treated with thyroxine. The father’s
; q" `9 b5 l9 q  c% Fheight was 6 feet, and he went through a somewhat
9 F2 ]0 m$ j# Z2 ~early puberty and had stopped growing by age 14.
1 e, [7 X. ^1 X6 Y: {! [+ H- O2 L1 TThe father denied taking any other medication. The) I9 d) i$ @( k( [
child’s mother was in good health. Her menarche
. G! M: ~0 Y& p- G# uwas at 11 years of age, and her height was at 5 feet
6 I. g* H" r9 u4 i0 j0 \. `5 inches. There was no other family history of pre-1 c( w* d& E( ~: X4 i  _6 C5 H
cocious sexual development in the first-degree rela-
3 |, L0 f$ p, e. Wtives. There were no siblings.
; N# B' C% V+ }- bPhysical Examination
8 g; u! S2 n. |/ UThe physical examination revealed a very active,
- l9 A* H1 p5 d' @4 Q$ Vplayful, and healthy boy. The vital signs documented
6 P. l% O+ q; D/ D# ^/ \. R' ~a blood pressure of 85/50 mm Hg, his length was
1 X; q$ k; O1 F1 ^9 D90 cm (>97th percentile), and his weight was 14.4 kg" ^! z. l+ p+ h% F% ]3 d. W9 e
(also >97th percentile). The observed yearly growth
; x2 N7 z2 D# |7 {+ `- Z' zvelocity was 30 cm (12 inches). The examination of; z. W, A& e9 m; O5 @. S4 C
the neck revealed no thyroid enlargement.
+ N# K7 p/ \1 B6 |' FThe genitourinary examination was remarkable for, h5 F  [& x- M; p- l
enlargement of the penis, with a stretched length of1 P. W9 L" _3 M$ g6 ?4 H
8 cm and a width of 2 cm. The glans penis was very well
$ C9 J9 T1 r' j$ E, D  ~$ Ydeveloped. The pubic hair was Tanner II, mostly around; u; _% T' T' Z6 i# d( e
540
/ X) q! |* g7 r- M* {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 p- t8 h% Y* K! _1 \6 e
the base of the phallus and was dark and curled. The/ }3 ?0 m0 Q2 P" r" g9 E0 q# D" l
testicular volume was prepubertal at 2 mL each.
3 Y+ R' l  _0 c3 K7 I" Z5 zThe skin was moist and smooth and somewhat, W. H- g: P3 f- D# D& h! Y1 r
oily. No axillary hair was noted. There were no
" z8 j- t% G3 D2 Vabnormal skin pigmentations or café-au-lait spots.! ?+ F' ~9 t. t& R# R
Neurologic evaluation showed deep tendon reflex 2+
. w' K! [) X2 \) @bilateral and symmetrical. There was no suggestion
2 l7 A' q. c" o5 m# b" x7 A6 A& t; zof papilledema.7 J7 _' T& x* a. `, Y! ]
Laboratory Evaluation; m6 W% g- m/ l! p- n! N
The bone age was consistent with 28 months by/ V, s! v% m0 I! k) q
using the standard of Greulich and Pyle at a chrono-
& I  C& _+ f0 b7 Hlogic age of 16 months (advanced).5 Chromosomal( C% P, p. C% }8 Y4 M, ^7 b
karyotype was 46XY. The thyroid function test
+ w5 h9 s  U* fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 S7 c- Q& Y  |" hlating hormone level was 1.3 µIU/mL (both normal).
* p7 ?& }/ ]4 b% IThe concentrations of serum electrolytes, blood
* q( ?) l( l& S! R$ Q! i  F* m8 curea nitrogen, creatinine, and calcium all were5 ]; f. v/ [- Q/ H; N- @
within normal range for his age. The concentration
6 h6 x- d5 v; g. |1 K7 Xof serum 17-hydroxyprogesterone was 16 ng/dL1 v6 U% B1 V7 i( P' o% c' x9 V* \
(normal, 3 to 90 ng/dL), androstenedione was 202 _! Q. C( w. U5 A
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& w# H- C5 v4 c. T
terone was 38 ng/dL (normal, 50 to 760 ng/dL),  z3 e' V$ g. ]* F& Q3 p
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
* w1 _7 @3 L# S3 \3 c, W9 T49ng/dL), 11-desoxycortisol (specific compound S)5 K( u' r  t* Y& D* h  i
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
- k6 |3 s6 ?7 Z! B( ttisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, p2 Y/ P7 K7 s  e$ Y* G4 Jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 `0 u! T! a5 N9 g) l. P( iand β-human chorionic gonadotropin was less than
% Y7 x; Q$ P* r* \8 N9 c' J& t5 mIU/mL (normal <5 mIU/mL). Serum follicular' S4 J5 X+ L, ^+ ~
stimulating hormone and leuteinizing hormone( e' ~0 W8 O# e3 w
concentrations were less than 0.05 mIU/mL
6 \5 i0 u* R# d(prepubertal)., S+ Y4 U/ S( m8 \7 o& n
The parents were notified about the laboratory
0 _" F6 H  ], |8 i, ~0 C! }results and were informed that all of the tests were1 [4 z9 I) e5 S# p5 w2 ^$ g" W
normal except the testosterone level was high. The
. ?( u1 ~8 ~2 V# q& e( K3 Kfollow-up visit was arranged within a few weeks to
& w0 f1 l9 V8 xobtain testicular and abdominal sonograms; how-5 \& J9 ?7 c9 `& k3 A
ever, the family did not return for 4 months.9 K5 g. s! |, h* s' K2 s
Physical examination at this time revealed that the
, |( z/ s/ t9 y# |child had grown 2.5 cm in 4 months and had gained
+ w1 M3 @+ p5 t% ^0 K1 `0 ]: H+ O2 kg of weight. Physical examination remained7 ~- o- l& Y- |3 M
unchanged. Surprisingly, the pubic hair almost com-: |) C9 |% J( |
pletely disappeared except for a few vellous hairs at
) J6 b4 P* K* T% W- Fthe base of the phallus. Testicular volume was still 2
! \5 h. ~- V6 SmL, and the size of the penis remained unchanged.+ h2 O" s! H" s, V. R) `! S; o
The mother also said that the boy was no longer hav-
4 X9 x, x7 ?* @. F" ging frequent erections.6 R$ h* ~, Q2 \( J
Both parents were again questioned about use of# D, E& N- b# x1 x" n) b/ Z/ i
any ointment/creams that they may have applied to" A2 M- L" W  {
the child’s skin. This time the father admitted the* x( z- m- c7 \' D7 B1 U4 Y! T$ O# ?
Topical Testosterone Exposure / Bhowmick et al 5419 K6 W/ S" E! ]$ a. z
use of testosterone gel twice daily that he was apply-
' O2 G- d' B2 w, s! q# G$ ]' Eing over his own shoulders, chest, and back area for
1 ?* i) J. q" c& `% I2 e1 t: wa year. The father also revealed he was embarrassed
% e$ O% M& C- w" z2 J0 xto disclose that he was using a testosterone gel pre-
7 w3 p% @. f+ E5 n) Zscribed by his family physician for decreased libido: d3 N, f- S  O1 p2 k
secondary to depression.2 Y6 I; q+ N& @7 q
The child slept in the same bed with parents.
# J; ?3 l( l5 Z& W/ Q0 q; TThe father would hug the baby and hold him on his- r/ S; }9 q7 u% C
chest for a considerable period of time, causing sig-
0 c/ t5 B6 v6 z0 znificant bare skin contact between baby and father.
5 E; d: }* f; i$ f9 [. fThe father also admitted that after the phone call,
3 h4 u: T4 h6 m- P; Zwhen he learned the testosterone level in the baby8 S" K1 }- N; b! q3 w; ?
was high, he then read the product information
: i9 X- w: @' P1 L5 `packet and concluded that it was most likely the rea-
/ Q5 a) m8 C% Q- D! \$ l' e+ {son for the child’s virilization. At that time, they3 M8 i) A3 |# `& `( N+ t3 p1 P/ t
decided to put the baby in a separate bed, and the. A1 C3 R  n; W; ^6 e
father was not hugging him with bare skin and had
- }- e2 `- F, M% Z+ i) p! C8 K1 Abeen using protective clothing. A repeat testosterone
3 }6 _* ?4 ^, x3 w/ Vtest was ordered, but the family did not go to the
- c1 h2 H0 h* Qlaboratory to obtain the test.2 v8 T# f- e& O$ X
Discussion
  d  D2 v( V3 g! M0 @" \( \2 gPrecocious puberty in boys is defined as secondary0 A- F$ V5 Z$ l
sexual development before 9 years of age.1,4
+ k7 l$ a7 b8 v- F4 ]3 PPrecocious puberty is termed as central (true) when
5 N4 D8 N+ H  \% q/ J" eit is caused by the premature activation of hypo-
; m" Z2 A) |1 O0 e# [8 s; N, Xthalamic pituitary gonadal axis. CPP is more com-
9 Y' B" @9 g4 z. H# c# rmon in girls than in boys.1,3 Most boys with CPP* G( N- Z, K' G
may have a central nervous system lesion that is
9 U! `) i# S) b) gresponsible for the early activation of the hypothal-8 w' B/ K2 n7 n5 W5 X
amic pituitary gonadal axis.1-3 Thus, greater empha-
/ v7 s% L- }. ~5 f3 B1 F& o  Nsis has been given to neuroradiologic imaging in
4 n$ ]8 M' M+ ]boys with precocious puberty. In addition to viril-6 e; {# i) t6 C7 B" C1 m5 Y) G
ization, the clinical hallmark of CPP is the symmet-9 M: H/ c" F( n: p
rical testicular growth secondary to stimulation by3 i$ n3 }! h0 d0 T0 F$ ?
gonadotropins.1,3
: f5 K; [8 {: l1 y% u. k! CGonadotropin-independent peripheral preco-: n' v1 ~: z0 B: W9 d
cious puberty in boys also results from inappropriate
* D, m7 d$ m/ z! yandrogenic stimulation from either endogenous or
- R8 T; {! p, l' _9 }exogenous sources, nonpituitary gonadotropin stim-
1 X1 @. C0 [; bulation, and rare activating mutations.3 Virilizing9 h& D/ ~( V' J- z
congenital adrenal hyperplasia producing excessive
- q1 `" k) o' V' m* p6 Cadrenal androgens is a common cause of precocious* [" P, q' i8 }# [& m3 `
puberty in boys.3,4( T, c3 \# a5 Z
The most common form of congenital adrenal+ j: A; V* G! l% `7 B/ H
hyperplasia is the 21-hydroxylase enzyme deficiency.! X, @( i1 k* l5 }, _  l
The 11-β hydroxylase deficiency may also result in
# v2 m4 u9 o( _$ q  F" o8 U: fexcessive adrenal androgen production, and rarely,; x) W' s3 a9 b) \! |/ P' J
an adrenal tumor may also cause adrenal androgen
4 x0 ~! S+ k( V: X6 _4 Xexcess.1,33 H3 k" J' s, M' h* o
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 A3 [. _2 D* }* J1 w
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 E1 \' f( D2 ]" [9 w4 i: L2 c" v# ?A unique entity of male-limited gonadotropin-
9 e5 T( p, p. |" D- y. K* n& nindependent precocious puberty, which is also known
7 d* A' s0 L. Gas testotoxicosis, may cause precocious puberty at a
) k& H2 n0 H- r1 n9 C$ @# u; overy young age. The physical findings in these boys
( B7 A$ h# W5 w& Lwith this disorder are full pubertal development,
! O/ S; N2 l( K) H4 _' D$ t# mincluding bilateral testicular growth, similar to boys
$ _) D0 N* `8 x7 X! C& ewith CPP. The gonadotropin levels in this disorder
$ {* H3 v5 R# r) fare suppressed to prepubertal levels and do not show5 H. f5 n1 C% V2 D+ W" y, o
pubertal response of gonadotropin after gonadotropin-
$ R+ ~/ U6 ~- ^2 }" M" B- Mreleasing hormone stimulation. This is a sex-linked
  A3 d2 R" Z; ?/ iautosomal dominant disorder that affects only- I. j6 M- d0 z. \
males; therefore, other male members of the family
+ m: M2 N! n4 z" p& Wmay have similar precocious puberty.35 @8 |  O  y, h) e
In our patient, physical examination was incon-  x8 D9 M: ]7 ~- |+ S$ @/ q
sistent with true precocious puberty since his testi-9 l' Q$ y) a3 }8 l& E, g. `
cles were prepubertal in size. However, testotoxicosis
5 z3 r; C; d& |was in the differential diagnosis because his father
% v8 {: j" A" S+ P2 h. Istarted puberty somewhat early, and occasionally,( u. k  d( u7 r
testicular enlargement is not that evident in the
9 p/ w9 X9 X0 Qbeginning of this process.1 In the absence of a neg-
- w9 z- j0 b8 L5 a% J* i2 Eative initial history of androgen exposure, our/ R$ W# A0 {" G7 g
biggest concern was virilizing adrenal hyperplasia,
3 w* Z& z) L* b2 N/ H$ _0 E4 xeither 21-hydroxylase deficiency or 11-β hydroxylase" J1 `9 f2 ^) K3 K
deficiency. Those diagnoses were excluded by find-
6 y- ~# [' c7 u8 u3 @, ~) K: sing the normal level of adrenal steroids.
- j3 O0 E  d/ {6 P7 }+ l  X3 Z7 z! ~% [The diagnosis of exogenous androgens was strongly' d& c! v% a% _7 L" I- Z
suspected in a follow-up visit after 4 months because
+ e# W- u. c" Q. w9 _& Sthe physical examination revealed the complete disap-
5 p* z# ]5 |4 G% q  ~) l7 S! ]pearance of pubic hair, normal growth velocity, and$ o* A/ R# }3 h$ j/ Y- ]# h& L
decreased erections. The father admitted using a testos-# [( O5 \  p6 i* E" b
terone gel, which he concealed at first visit. He was
  Z: Q/ h3 ]* x- y8 _9 Kusing it rather frequently, twice a day. The Physicians’3 Q# e2 E! Y' z- f
Desk Reference, or package insert of this product, gel or/ P0 B: k: ?+ C& ^4 v1 @
cream, cautions about dermal testosterone transfer to
9 c5 X! f7 @1 _- dunprotected females through direct skin exposure.4 E- M# X" _) d3 x* u$ y0 p( l- h
Serum testosterone level was found to be 2 times the
6 k$ N/ o% p1 X: abaseline value in those females who were exposed to* A% ^# P2 m6 b' U7 r- q, |
even 15 minutes of direct skin contact with their male9 s+ i8 e, y% h7 z, Q) G+ m' v( R2 P
partners.6 However, when a shirt covered the applica-4 D: Z4 U& R% e+ j( o6 m) n
tion site, this testosterone transfer was prevented.  a3 x5 g& X7 V1 E$ `' b
Our patient’s testosterone level was 60 ng/mL,5 U# I0 H$ Z1 t
which was clearly high. Some studies suggest that
- ^' F6 H8 }2 i" q. zdermal conversion of testosterone to dihydrotestos-7 l2 I6 Y/ A* z# L0 \1 s
terone, which is a more potent metabolite, is more! {- D, v. T3 x; \; ^0 z( K; e8 t
active in young children exposed to testosterone* U9 V9 A6 E3 c5 o
exogenously7; however, we did not measure a dihy-
& F; A4 T& F' Y7 J! S$ `3 [- C6 c6 Edrotestosterone level in our patient. In addition to; k' n3 z- d; T6 q
virilization, exposure to exogenous testosterone in- V; L9 d2 J( o) g. n
children results in an increase in growth velocity and
3 u( e3 d9 i! A% g, n, Fadvanced bone age, as seen in our patient.2 y4 T; }. u+ X# J
The long-term effect of androgen exposure during
1 [7 @+ V3 p0 v2 I! Yearly childhood on pubertal development and final4 E& v$ f" G9 C" L# ^8 M
adult height are not fully known and always remain( @! ~9 C3 b: o# Z. @& _
a concern. Children treated with short-term testos-
$ y" j5 l' q* Z* \terone injection or topical androgen may exhibit some' i( y3 G. R; F) I' q
acceleration of the skeletal maturation; however, after7 A2 S' Y* `5 d( O
cessation of treatment, the rate of bone maturation, E7 Y* L0 q7 }4 f" J$ R
decelerates and gradually returns to normal.8,9
5 E9 [4 W) g- R' u, Z  u$ i: kThere are conflicting reports and controversy" E( z2 [; l5 B) P
over the effect of early androgen exposure on adult
+ O! y$ Z- z+ D" spenile length.10,11 Some reports suggest subnormal
  t" g. l; T! d2 Y) a& ^adult penile length, apparently because of downreg-/ G) m' ]) M9 |9 L5 m
ulation of androgen receptor number.10,12 However,0 G6 Q1 Y( A, b6 ]
Sutherland et al13 did not find a correlation between2 w% \/ s( P% B; x- t
childhood testosterone exposure and reduced adult
! l. B: k) M0 I# ^* G) L) Q4 r' dpenile length in clinical studies.
* t3 A, A" v& oNonetheless, we do not believe our patient is
8 U7 U. C% ~2 Kgoing to experience any of the untoward effects from
# Q/ a. c- g7 y- L' f" z! d* ]testosterone exposure as mentioned earlier because/ d, ~7 P( u& {1 k. l
the exposure was not for a prolonged period of time.
1 ?! G* R0 y( o- e4 wAlthough the bone age was advanced at the time of
' K, ?! M: q8 x8 Idiagnosis, the child had a normal growth velocity at
3 S, k4 R1 {! r" pthe follow-up visit. It is hoped that his final adult
' Y4 s9 s2 D  _) x6 o% mheight will not be affected.
2 Q- }0 H" M$ T" D9 o2 mAlthough rarely reported, the widespread avail-
" v* ~% Z4 J& A* Yability of androgen products in our society may( e3 R& V  S/ r/ y6 R; o
indeed cause more virilization in male or female+ V' I  L" {3 j# C5 S% |
children than one would realize. Exposure to andro-
+ H) Q3 o- ^( l6 h4 Hgen products must be considered and specific ques-
9 {* c% ~9 G) \$ Ftioning about the use of a testosterone product or0 ^$ n1 I7 s  J5 M. I0 [
gel should be asked of the family members during
' U! A* p' v% m2 n0 k) _) \3 T) pthe evaluation of any children who present with vir-3 `, j, L7 \( u+ }, l$ {$ \
ilization or peripheral precocious puberty. The diag-
9 ]2 S, N% l! y+ ?. ?' r8 m5 `nosis can be established by just a few tests and by
0 F' H: d3 [+ {7 |* X# V4 c1 Xappropriate history. The inability to obtain such a
, w! t9 i+ A2 Z$ R" phistory, or failure to ask the specific questions, may" S+ G% _6 N. r
result in extensive, unnecessary, and expensive
* ?- L* [9 W1 `' binvestigation. The primary care physician should be' t7 F/ E- z2 t" c, Q
aware of this fact, because most of these children
0 S7 A8 I/ @! D- O9 G8 f* `* [" {may initially present in their practice. The Physicians’
( k& I2 k& A+ W- PDesk Reference and package insert should also put a
6 V" ~* k, K$ ~" Fwarning about the virilizing effect on a male or$ G5 a' T. b# H- V
female child who might come in contact with some-+ U* [/ v7 f7 P9 n  S/ R
one using any of these products.
+ F/ x# t. f% \* P3 yReferences& k( G/ f: ?1 N- Y  y! p3 f
1. Styne DM. The testes: disorder of sexual differentiation) s8 @% {# O+ @
and puberty in the male. In: Sperling MA, ed. Pediatric
3 [3 |7 @4 g7 F$ N! n7 WEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( [3 I5 P+ A/ J; K0 R5 C: u! }$ U
2002: 565-628.  ]* |* a1 D  e4 [7 s
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
4 ~4 [* O/ D4 K; H" @5 q) H8 mpuberty 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
! k8 ?5 C! }, T8 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