WK綜合論壇, WK综合论坛

 找回密碼
 立即注册
樓主: wk007

鄉下的妹子太便宜,一次四個都要了[12P]

[複製鏈接]
發表於 2025-1-4 03:25:35 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
Sexual Precocity in a 16-Month-Old
  m# b0 y3 F) S" U. U4 rBoy Induced by Indirect Topical) B& ~" J; U& f5 `. U+ |
Exposure to Testosterone
8 s; c; G+ t! V" ~0 hSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! F& J: g6 I/ z" ?2 b+ dand Kenneth R. Rettig, MD1& J6 S- \# E1 ^1 k& ]  ~* P2 ]
Clinical Pediatrics
# q4 B+ b* z+ X  LVolume 46 Number 6
& N: b9 {: N7 V5 c4 a5 aJuly 2007 540-543( s8 G, D9 y: H% |/ v( @5 V0 U
© 2007 Sage Publications
0 R, E- J4 V) A, z10.1177/0009922806296651  }6 X) \( Z' d* ~* t' ?
http://clp.sagepub.com
% M/ f3 q: ~* G$ P' V, _hosted at" O5 |& c0 I4 L. j2 w% W
http://online.sagepub.com3 N- Q' i% O: c. L7 f
Precocious puberty in boys, central or peripheral,8 c6 N1 o) V" e7 I$ ~0 s
is a significant concern for physicians. Central/ _5 g3 _! n( f! r& q  z! R
precocious puberty (CPP), which is mediated
, S# F/ s6 N/ i* H( v, Sthrough the hypothalamic pituitary gonadal axis, has+ F$ A7 K5 O( {; e3 b: K
a higher incidence of organic central nervous system
7 v2 F" j, D. j' X3 H4 m  N5 Rlesions in boys.1,2 Virilization in boys, as manifested; s4 m3 K6 F% z! `! G! s% M
by enlargement of the penis, development of pubic( r5 Z# S! K: x# A* g1 D3 z5 s( J
hair, and facial acne without enlargement of testi-
6 c$ W2 x+ M- i9 n  p3 G0 |% lcles, suggests peripheral or pseudopuberty.1-3 We3 ?% Q) D! g. e6 ?. @/ o6 x
report a 16-month-old boy who presented with the
1 o. w/ }! B. _" U! x. Denlargement of the phallus and pubic hair develop-  {- h2 }, G* ?5 v! F
ment without testicular enlargement, which was due* }( n  K. w1 h) k' X: s# h
to the unintentional exposure to androgen gel used by6 E6 d3 h+ v! r
the father. The family initially concealed this infor-
; q/ \) ?% j# {% v: W0 l% D: nmation, resulting in an extensive work-up for this. b- l" i4 j  q. v
child. Given the widespread and easy availability of4 F" R" {9 K; ]+ w5 R* j& L
testosterone gel and cream, we believe this is proba-4 L/ i( Q, S) O! N" ]
bly more common than the rare case report in the% X$ U- u9 o' b
literature.47 d  w8 `/ j3 h# s4 C0 i1 P  K0 L
Patient Report8 m- Y+ v! e& T: e& u# T! C" g  X* W
A 16-month-old white child was referred to the: s+ _1 R# N" K$ p7 I, r+ B
endocrine clinic by his pediatrician with the concern, _/ N5 c9 j( i* y  \8 Q
of early sexual development. His mother noticed
0 f5 M" V6 w. j6 ]light colored pubic hair development when he was
7 a& a  I6 l& g- z% y% yFrom the 1Division of Pediatric Endocrinology, 2University of7 ~) p" q8 F. Z
South Alabama Medical Center, Mobile, Alabama.
  u& Q) ^" i. s# }7 q  W" PAddress correspondence to: Samar K. Bhowmick, MD, FACE,
7 y% I" b( k# t5 a3 FProfessor of Pediatrics, University of South Alabama, College of; k( l2 y0 J5 m
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" U& ]0 {5 J. |) B
e-mail: [email protected].- q" D1 O  _1 F+ x* C
about 6 to 7 months old, which progressively became2 |; h9 B5 w7 M$ S* m" p
darker. She was also concerned about the enlarge-
0 I$ h6 Y& d) P( I$ c- c9 Q! G( a% @7 xment of his penis and frequent erections. The child
0 r6 x" e' L/ Y$ S9 T2 N! z( hwas the product of a full-term normal delivery, with  i5 i: Z% h+ y: ], s& l; X8 z
a birth weight of 7 lb 14 oz, and birth length of* I0 S9 ~) L3 p7 r, _
20 inches. He was breast-fed throughout the first year
% H6 m1 E% w. x; R  r' q) u1 O( C: K* Bof life and was still receiving breast milk along with
0 t! Y8 b! M4 |4 X3 V9 |/ Q5 d, g# W+ Ksolid food. He had no hospitalizations or surgery,
5 T( N% e, @% d, H3 C# J& O* {and his psychosocial and psychomotor development9 ^( S9 z# X, @3 t
was age appropriate.* E' r9 \+ Q) t5 c
The family history was remarkable for the father,0 A4 W  T7 p7 ]
who was diagnosed with hypothyroidism at age 16,' e* M* R; H* K
which was treated with thyroxine. The father’s8 h# X9 ^6 X; r
height was 6 feet, and he went through a somewhat  j: c5 k9 [6 a6 S/ a8 M. W
early puberty and had stopped growing by age 14.! `* I- H3 y6 z
The father denied taking any other medication. The) J7 l( O4 u9 D' R8 h6 c
child’s mother was in good health. Her menarche8 o2 M' v2 b; \/ ?! v2 O2 l
was at 11 years of age, and her height was at 5 feet4 l7 i$ H; O) t2 h6 y& x
5 inches. There was no other family history of pre-
  A4 s/ d# I! r' Vcocious sexual development in the first-degree rela-# f; q. k& ?$ w) l, S
tives. There were no siblings.7 ?& @9 s- G, [) h7 t  _
Physical Examination
$ k, ?$ k! e* i* c5 H. F5 CThe physical examination revealed a very active,4 m6 z. q! ^) w- c& v) Q
playful, and healthy boy. The vital signs documented
, S" W5 z* R" [+ ga blood pressure of 85/50 mm Hg, his length was
, b# l) u( E$ j/ k90 cm (>97th percentile), and his weight was 14.4 kg
9 {! p" w$ C/ V$ l8 J(also >97th percentile). The observed yearly growth
& l9 M/ ]) ]  c( C. L+ Mvelocity was 30 cm (12 inches). The examination of$ {2 }4 f8 v% D8 J* h3 A
the neck revealed no thyroid enlargement., H) e2 v% X8 {/ W$ q
The genitourinary examination was remarkable for
+ d! k0 @, C" y" J3 N* w' yenlargement of the penis, with a stretched length of
9 `" `2 {8 y0 l6 U; Z8 cm and a width of 2 cm. The glans penis was very well  r- c1 Q: `4 z- E  J: K4 w
developed. The pubic hair was Tanner II, mostly around
  m( [$ ]2 v' N/ n" x/ \# V& y540$ u" |: j6 h1 c9 x8 Y7 H1 L
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; r3 t. o, j8 @* C+ Ithe base of the phallus and was dark and curled. The, f/ q3 c. s2 ], A
testicular volume was prepubertal at 2 mL each.8 q  h, y  X# j
The skin was moist and smooth and somewhat0 m* O+ t3 O8 j7 v. X/ m5 c2 b
oily. No axillary hair was noted. There were no8 i) N/ X  a4 \9 b, B! i
abnormal skin pigmentations or café-au-lait spots." c! D& Z( u. l4 t: H# u8 f9 q
Neurologic evaluation showed deep tendon reflex 2+8 p/ |+ C4 z5 \' V+ x  d! h
bilateral and symmetrical. There was no suggestion) }2 i! f7 X4 U% x4 p, p
of papilledema.
# R9 f- ^& N. Y0 bLaboratory Evaluation$ A" ^0 ]$ W; t! _3 O3 D
The bone age was consistent with 28 months by
, ^) {7 r5 d/ g( n' H9 ~# Ausing the standard of Greulich and Pyle at a chrono-
8 a8 g- g+ h; h# P# v2 {logic age of 16 months (advanced).5 Chromosomal
. q7 X. I) j# Y" Y- {- r9 Ukaryotype was 46XY. The thyroid function test
2 D3 ~6 X6 ?" q+ B$ _6 fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
% G; z4 x3 }4 g1 H) llating hormone level was 1.3 µIU/mL (both normal).
3 Z( x3 @$ ~, H( M5 \" Q$ l. G5 FThe concentrations of serum electrolytes, blood
" u8 t) w1 O6 J% o5 k4 i$ \, _urea nitrogen, creatinine, and calcium all were* @* e' m8 o$ W6 A) B5 j
within normal range for his age. The concentration
& K- A8 }8 C7 X9 `' r* D8 mof serum 17-hydroxyprogesterone was 16 ng/dL
5 D5 I: J8 ~, Q/ j8 P( M: J. y% m3 f(normal, 3 to 90 ng/dL), androstenedione was 20
* {$ o8 w; Z0 k8 ?' F2 m- y% H  tng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, [1 u2 ~9 ]5 b0 r3 _
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
# c, P) B) n9 ^# Udesoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 v% y% o/ {( T/ v/ U% v49ng/dL), 11-desoxycortisol (specific compound S)
; J1 z8 N+ C" \$ f- l8 |4 [was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-$ p7 q) u0 I6 k& F
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 g8 D( ^: e( \" Qtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# K9 b( _- m2 ~  Aand β-human chorionic gonadotropin was less than
1 ]! r8 ?3 Z$ V6 o5 mIU/mL (normal <5 mIU/mL). Serum follicular
% A# m9 l6 F. ]  M1 c# q0 Rstimulating hormone and leuteinizing hormone, K! y0 ~  W9 T# ?2 g
concentrations were less than 0.05 mIU/mL
3 J% c" Q4 |" a/ B: X(prepubertal).8 o/ H9 H; P* ]2 c9 ~- B+ o! z, w: v
The parents were notified about the laboratory
: k8 T; R2 F" A; Vresults and were informed that all of the tests were
9 G9 a2 `) V8 @0 `normal except the testosterone level was high. The
% l, [# c+ D) o' ~0 l; ~follow-up visit was arranged within a few weeks to1 O& j5 c* }- V4 k$ L% ^) S
obtain testicular and abdominal sonograms; how-( z  P( r7 R& e/ w4 [
ever, the family did not return for 4 months.5 p) G/ i- W1 m* |- ]. Y8 O# b! |
Physical examination at this time revealed that the4 L+ s: v* W6 o) C9 L
child had grown 2.5 cm in 4 months and had gained3 I, Y9 D$ t  Y
2 kg of weight. Physical examination remained& X7 t" a- z4 W* n. G7 X
unchanged. Surprisingly, the pubic hair almost com-
" U4 g7 R, g& c/ R5 apletely disappeared except for a few vellous hairs at! n" f% G) p; L& m1 F/ B
the base of the phallus. Testicular volume was still 2
, }  Z+ w: t6 gmL, and the size of the penis remained unchanged.
' G! b+ K+ v* z6 G7 N* k" dThe mother also said that the boy was no longer hav-
$ q4 \2 s! L3 }5 A+ fing frequent erections.! o5 ?! n' v8 X) x1 S0 F8 Q
Both parents were again questioned about use of
; f/ p3 }: `/ O7 o9 O6 v, sany ointment/creams that they may have applied to
; ?9 Z" z; @# j  S  @8 r1 ?the child’s skin. This time the father admitted the
, o  h% P% n8 pTopical Testosterone Exposure / Bhowmick et al 541) V9 ^8 I0 {- W3 k4 y  @
use of testosterone gel twice daily that he was apply-& d$ H% @% Z4 f9 x' ^. M# s
ing over his own shoulders, chest, and back area for
7 |9 M6 z0 i% E- G  x* Da year. The father also revealed he was embarrassed8 [) j9 C# h& O7 W# S0 ^  F
to disclose that he was using a testosterone gel pre-
3 g+ E# U1 \5 ascribed by his family physician for decreased libido
5 X  z0 }  g; n( e/ d! |' W/ h4 B, ?secondary to depression.. e1 n4 e$ H% U) u! g$ G
The child slept in the same bed with parents.; Z9 V. q+ v6 K5 k" m% n" P: w
The father would hug the baby and hold him on his
% x* r# A9 s) s8 L1 X1 echest for a considerable period of time, causing sig-/ A" A$ b# |5 x
nificant bare skin contact between baby and father.+ g4 c6 b) |4 A# f+ v- R
The father also admitted that after the phone call,
5 c: a* |# Q0 o1 v+ Xwhen he learned the testosterone level in the baby+ D  ~( T( \: B7 f1 x' T- N
was high, he then read the product information
6 y# _+ P% e5 G. L: k1 \9 Ipacket and concluded that it was most likely the rea-7 ?1 f* ]4 m0 M; x4 l  i# Q
son for the child’s virilization. At that time, they: u8 p& [2 Z9 M) k5 `
decided to put the baby in a separate bed, and the
, Q1 _* p; e7 R. t, efather was not hugging him with bare skin and had
  E/ I' c1 X; qbeen using protective clothing. A repeat testosterone" E0 c, f6 V" s$ v
test was ordered, but the family did not go to the
) L! G3 K/ W0 A7 ^laboratory to obtain the test.
* w5 R1 }+ e  T$ H1 S. M2 uDiscussion
% q) t& f. j, _Precocious puberty in boys is defined as secondary7 u$ }, P" z/ w! Q/ J
sexual development before 9 years of age.1,4( c4 Q% G8 d# g4 z% U1 H: M
Precocious puberty is termed as central (true) when
  Y$ A  H, C4 t# @it is caused by the premature activation of hypo-
% U$ S. G) L, O8 [) W$ ythalamic pituitary gonadal axis. CPP is more com-, Q/ ]# a: F  I2 Y$ g
mon in girls than in boys.1,3 Most boys with CPP
2 H9 g. U1 m- H  |" A9 V/ Imay have a central nervous system lesion that is1 V  {. i4 E1 i+ @7 L
responsible for the early activation of the hypothal-4 H, Q+ |  m9 Y0 C
amic pituitary gonadal axis.1-3 Thus, greater empha-
% C. H- O" T6 B7 Y: G! \0 Tsis has been given to neuroradiologic imaging in! v6 S, |; e! m: X3 `
boys with precocious puberty. In addition to viril-
4 ^' _/ l/ @  p4 k# L! a; Xization, the clinical hallmark of CPP is the symmet-( o* {; M7 Z& M6 l9 G
rical testicular growth secondary to stimulation by
- K# c5 w; _4 x, W4 Tgonadotropins.1,35 X( f' c# X! h! q8 ?4 v
Gonadotropin-independent peripheral preco-; l  m" J! h8 K% N  I. t) i/ B$ W
cious puberty in boys also results from inappropriate9 w( ]" J- l" }2 |- p/ L* T
androgenic stimulation from either endogenous or, u2 Z( U" E) P# J, _9 }5 X- }0 }
exogenous sources, nonpituitary gonadotropin stim-
' `% |1 k. Q4 x; Oulation, and rare activating mutations.3 Virilizing1 K# J: C" y2 M0 |" f) U$ ~2 G
congenital adrenal hyperplasia producing excessive
3 e3 M& l, E7 [2 p- Sadrenal androgens is a common cause of precocious: F  [3 U9 [, `  s
puberty in boys.3,40 v! Y9 W, J2 |! y0 e% h1 i$ B: ~
The most common form of congenital adrenal
% K. \3 q/ q& q/ Y' Phyperplasia is the 21-hydroxylase enzyme deficiency.
$ v7 Z; F1 g) \: QThe 11-β hydroxylase deficiency may also result in
# ^$ J% q0 Q- H" Iexcessive adrenal androgen production, and rarely,) s/ c. c% a% b' x$ ^! H
an adrenal tumor may also cause adrenal androgen  g7 y. D9 {* \9 S8 m
excess.1,3
! W& g) M/ n& }8 C$ N0 l! pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 s5 a& C; ?3 T# v4 y542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 |! ]+ B) B( H0 bA unique entity of male-limited gonadotropin-
/ U3 @% N  F9 q7 ]' `* iindependent precocious puberty, which is also known/ I* m0 S4 n  W2 {8 X+ [; k, h) {
as testotoxicosis, may cause precocious puberty at a. n( W  N2 J3 E) z$ T9 }) G* H! w
very young age. The physical findings in these boys1 }/ F. e; |5 B( |1 S7 d; i
with this disorder are full pubertal development,9 ]) N% ^7 H3 N) @7 w# e
including bilateral testicular growth, similar to boys
, Y( r9 Z; o% U, iwith CPP. The gonadotropin levels in this disorder
: R" T% i; G" U. kare suppressed to prepubertal levels and do not show% a6 B7 A3 d# T! l' f
pubertal response of gonadotropin after gonadotropin-
6 {6 ^5 p* W& D% m6 A. preleasing hormone stimulation. This is a sex-linked: }. M! C! @! S( ^
autosomal dominant disorder that affects only+ P6 }1 [5 \" ^! w
males; therefore, other male members of the family) S3 n4 ]; b/ b! t
may have similar precocious puberty.3( f: ?' v: |& y: R& C
In our patient, physical examination was incon-+ h& @4 |- k* W' S: r
sistent with true precocious puberty since his testi-
) K5 w) m' x7 Lcles were prepubertal in size. However, testotoxicosis
6 `  s/ F  M; z7 Mwas in the differential diagnosis because his father4 J6 j" ~0 c! L; F4 z2 I
started puberty somewhat early, and occasionally,; J4 e+ ~- j; P8 o3 ^; O3 F- E
testicular enlargement is not that evident in the
; w# m& G9 m" jbeginning of this process.1 In the absence of a neg-4 _2 Y9 s) D; @- z
ative initial history of androgen exposure, our
, r6 Z) v  K# c9 B% Vbiggest concern was virilizing adrenal hyperplasia,& h: t: X# }+ G& t! ]9 P% V* g# \
either 21-hydroxylase deficiency or 11-β hydroxylase
& V, S8 q+ \: `* o- @! gdeficiency. Those diagnoses were excluded by find-" E% \$ r+ C. j, e+ \0 t
ing the normal level of adrenal steroids.
( D, H4 @8 k3 e7 L3 b+ tThe diagnosis of exogenous androgens was strongly
7 P4 K4 s& X, \/ t& V  H: I3 x+ Ysuspected in a follow-up visit after 4 months because
9 Z/ |2 u0 P1 T, w) Kthe physical examination revealed the complete disap-
# u9 m5 B' A8 _* b+ }pearance of pubic hair, normal growth velocity, and" |+ q/ O* J% U$ M- B
decreased erections. The father admitted using a testos-
$ {9 D4 ~1 e( h4 uterone gel, which he concealed at first visit. He was1 d1 H# U% M: k' B0 n  m9 x  ]( Q
using it rather frequently, twice a day. The Physicians’
$ y# V0 p# ]( J( l" wDesk Reference, or package insert of this product, gel or* M4 l, d: T1 Q3 z6 g$ m% Z
cream, cautions about dermal testosterone transfer to
1 d" E! F) e6 m' funprotected females through direct skin exposure.
( n8 J6 S. B- d6 }Serum testosterone level was found to be 2 times the" u4 K+ n7 H% N( ?  `
baseline value in those females who were exposed to4 Z) [; Z4 m, T  ~+ Q
even 15 minutes of direct skin contact with their male
. a7 ?  o1 D3 {4 [, jpartners.6 However, when a shirt covered the applica-# |: n! x+ C1 [# H
tion site, this testosterone transfer was prevented.
! {' F% j7 s7 W7 s0 k5 COur patient’s testosterone level was 60 ng/mL," D/ P) Y- K* y9 t9 k$ ^+ ]' [
which was clearly high. Some studies suggest that$ C6 H6 I3 l0 o% K! M) B! u/ |
dermal conversion of testosterone to dihydrotestos-
5 B6 X  X4 O9 Dterone, which is a more potent metabolite, is more7 F% y' l9 @6 i& A! N# y& {3 L
active in young children exposed to testosterone+ j( I3 t! y: R8 Z9 S' q' N8 i) F
exogenously7; however, we did not measure a dihy-
! s: }6 G; E3 b" t& f$ |$ bdrotestosterone level in our patient. In addition to" e7 }" h4 m% g" M* [6 `9 {4 Y! _4 m
virilization, exposure to exogenous testosterone in
( E& c3 k# D! K* ?( echildren results in an increase in growth velocity and
, J! p4 [% C% v4 A  ~5 sadvanced bone age, as seen in our patient.
0 h$ G' G& Q( A% `1 K2 fThe long-term effect of androgen exposure during
7 s) |1 i% Q. Z  A4 d, _  jearly childhood on pubertal development and final
7 v( o3 ^2 n: r+ ladult height are not fully known and always remain
! c# h; ?" ^/ {% g3 f, ga concern. Children treated with short-term testos-
! X1 i/ @5 ?% ]! u+ B* x5 gterone injection or topical androgen may exhibit some
* D9 A0 [; L- p5 R& y0 V) Qacceleration of the skeletal maturation; however, after" @1 x( b' y3 ~0 ^! r" }
cessation of treatment, the rate of bone maturation" t0 `! d" Q( L- _
decelerates and gradually returns to normal.8,9
9 _+ i* `1 c2 O. s5 Z& T; P& A! G1 B- |There are conflicting reports and controversy* p3 e" }. K- k! [
over the effect of early androgen exposure on adult. b( m% M* `: _1 n( ]* \+ n
penile length.10,11 Some reports suggest subnormal
% H' N' e! u. x3 {# D! Ladult penile length, apparently because of downreg-
% P/ Y3 Y7 j/ l/ Nulation of androgen receptor number.10,12 However,6 M+ a! r  c8 m; X. x
Sutherland et al13 did not find a correlation between
' P' ?4 u. @  \( Ochildhood testosterone exposure and reduced adult
$ i9 F: Q2 h" J+ t) H9 Ipenile length in clinical studies.- S8 ^1 L' B$ \
Nonetheless, we do not believe our patient is. V! y* o6 R9 |& D9 c; p
going to experience any of the untoward effects from* `+ h. q( ~7 k) _. V8 d
testosterone exposure as mentioned earlier because
- h6 Y1 R, X4 J, v0 U" p  uthe exposure was not for a prolonged period of time.( K/ `6 U0 Z) k# F$ t5 Y
Although the bone age was advanced at the time of8 I/ ~7 ?  ]+ k! [* Y1 l0 Z
diagnosis, the child had a normal growth velocity at
% a$ o, ?. K% Cthe follow-up visit. It is hoped that his final adult( }6 U# J. B% m; f5 s' i
height will not be affected.( }9 |& O) t  q5 b
Although rarely reported, the widespread avail-
1 B) z3 S8 Z3 H, S/ B& mability of androgen products in our society may
. w# Q: G, {' Y' `indeed cause more virilization in male or female2 O, T4 ^0 q: B: S+ z2 B
children than one would realize. Exposure to andro-
' m2 p4 F/ ~6 Z" M; y2 S1 S8 Ngen products must be considered and specific ques-6 W  m  A2 [7 Y# {
tioning about the use of a testosterone product or% {. |6 T) a# I2 g9 A. J
gel should be asked of the family members during2 R, {6 F5 |5 ?0 u- ?! J1 A
the evaluation of any children who present with vir-% t( d$ Y0 g6 x7 `, [2 Z7 K
ilization or peripheral precocious puberty. The diag-
7 a8 S+ W, v9 O+ s. l& g! Onosis can be established by just a few tests and by
6 D' f! c/ D9 |2 i8 O, J. Oappropriate history. The inability to obtain such a
1 ]% T$ l  @8 q' Z) S* F! Shistory, or failure to ask the specific questions, may5 d5 b3 y9 r7 k$ V$ S- N
result in extensive, unnecessary, and expensive
% n2 ]+ r3 i# D$ E( Jinvestigation. The primary care physician should be
; a& ~5 a* n$ s5 oaware of this fact, because most of these children- u7 x& \5 d$ @% F9 d, u5 w
may initially present in their practice. The Physicians’
' m$ S6 j: ]. d3 RDesk Reference and package insert should also put a
8 Y6 L+ S* C0 dwarning about the virilizing effect on a male or
) p* T% h* z7 R; @female child who might come in contact with some-
( ~5 r$ ~' U' z8 @, P8 o& M. Rone using any of these products.
! i3 P* i- N" Y. J) Q8 {7 wReferences+ S& Q% I# I  Q
1. Styne DM. The testes: disorder of sexual differentiation7 ~8 a: M6 P/ {" s, \7 G
and puberty in the male. In: Sperling MA, ed. Pediatric
( M6 `  N" a: y; f0 QEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 }) c, x7 Y8 u+ p0 Z# K3 Y$ S2002: 565-628.' y3 U5 U0 \. V* ~3 A
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& H  S& G! ~: U3 O" y, C
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
. F$ p' x. H5 v4 wBoy Induced by Indirect Topical# O# }  B4 c, X) U( F5 |
Exposure to Testosterone
# t) T7 r$ P/ c6 q! o  I% {& USamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# ^* [, K3 a0 ^1 rand Kenneth R. Rettig, MD1( r5 K) {# `! y9 @/ ]; R0 u
Clinical Pediatrics, d- Q- w& _3 j: T- s! h
Volume 46 Number 65 R- z  l: {, l! M& m
July 2007 540-543
% m+ I7 i5 r: j3 U  i( s© 2007 Sage Publications, Z& L7 x2 R' [, W' M4 I
10.1177/0009922806296651% ?( [  R, X9 F9 z2 N
http://clp.sagepub.com
* h& K, D2 C: b' ihosted at- G% ?3 ?# E8 B9 [2 Y
http://online.sagepub.com
, O, f1 q' h/ e' f6 f* o, DPrecocious puberty in boys, central or peripheral,
+ Y( u* r6 c. h" ^is a significant concern for physicians. Central
) t+ M; [: L  M" Dprecocious puberty (CPP), which is mediated
; h9 J( X5 x) ?+ x- Zthrough the hypothalamic pituitary gonadal axis, has
2 S% s" k7 k4 I- h8 fa higher incidence of organic central nervous system
. S9 O$ p: h# zlesions in boys.1,2 Virilization in boys, as manifested
# }& O5 U, o% sby enlargement of the penis, development of pubic
) C2 F# q" f2 _" n- Q5 m% t" Fhair, and facial acne without enlargement of testi-7 ^2 A- S. M  N3 h" J
cles, suggests peripheral or pseudopuberty.1-3 We4 M  V6 @/ o. ^( W
report a 16-month-old boy who presented with the
7 Q. J4 Q$ i+ y; q" oenlargement of the phallus and pubic hair develop-
* M4 |1 j! B3 ?5 Cment without testicular enlargement, which was due' C  n* _$ U. o+ [
to the unintentional exposure to androgen gel used by, q2 H4 Z; i' I  l" z' [7 b* d' i' j
the father. The family initially concealed this infor-3 I: l8 G+ K. K+ z5 J, v
mation, resulting in an extensive work-up for this
: n# B) u$ g- F3 ~+ `child. Given the widespread and easy availability of
9 d2 i5 r- C0 q7 |) Z& F# [; ?& _7 stestosterone gel and cream, we believe this is proba-) C' c1 E( r7 t2 C8 |7 @9 E
bly more common than the rare case report in the, v8 f& m; n# X
literature.4$ P1 \5 g# n1 W* {
Patient Report' M- V, K+ z$ N; Q
A 16-month-old white child was referred to the
3 K" J$ ~7 O2 v. Z. S& X' a$ W  tendocrine clinic by his pediatrician with the concern
- z9 G( U# |) {% Z0 v# B: A) O& i- Pof early sexual development. His mother noticed+ V" g7 K% b  a+ u+ A; ~! |% [
light colored pubic hair development when he was
8 a0 ]& T! E6 o/ ^3 W$ RFrom the 1Division of Pediatric Endocrinology, 2University of% I/ c3 w& e( z: W5 V, ~
South Alabama Medical Center, Mobile, Alabama.
& q, D8 p0 S6 C% |5 X. d3 f. HAddress correspondence to: Samar K. Bhowmick, MD, FACE,
* e8 y6 P5 G7 u0 O% P' I7 R3 bProfessor of Pediatrics, University of South Alabama, College of1 }' Q% Q) I0 p6 m' D" M( }
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 _1 Y9 O# E- M* S' X
e-mail: [email protected].
2 O6 Z: t) e- o$ a' @# i; [1 M' xabout 6 to 7 months old, which progressively became5 h5 e7 S7 m( K2 U* }
darker. She was also concerned about the enlarge-9 l# z6 [! j3 O% o/ g* Q2 `: f' ]
ment of his penis and frequent erections. The child
& I- G' ]8 C/ f7 L% \* a0 w! q/ v: }; xwas the product of a full-term normal delivery, with; s: ]; T! {1 O4 C  X3 l
a birth weight of 7 lb 14 oz, and birth length of8 b* R# `9 r" {, s! p
20 inches. He was breast-fed throughout the first year  R7 H* }2 h4 v" B7 J; T
of life and was still receiving breast milk along with6 e8 M- a7 @1 u# t& y  b- a
solid food. He had no hospitalizations or surgery,3 ~) [& }, d$ @* i
and his psychosocial and psychomotor development1 `- I  U4 A6 B9 Q+ C$ y& L
was age appropriate.9 ]6 g5 _" [) r( G$ Z% \
The family history was remarkable for the father,) s8 g* t2 ]; i7 A  l
who was diagnosed with hypothyroidism at age 16,5 W& t4 f- p" M) M+ A
which was treated with thyroxine. The father’s8 F& k9 ?1 F$ k! A6 d. `' h1 Y
height was 6 feet, and he went through a somewhat
' P8 K6 P* Y" B% r+ L5 s1 l/ n# W( learly puberty and had stopped growing by age 14.
( \  f- V) J8 {! rThe father denied taking any other medication. The
3 u# [3 D5 n+ Q9 echild’s mother was in good health. Her menarche
1 E+ N7 m7 D4 O' q- B; [& Ewas at 11 years of age, and her height was at 5 feet8 a# p4 _4 G2 D
5 inches. There was no other family history of pre-
5 j/ ?5 `. x1 K1 I; ?7 ccocious sexual development in the first-degree rela-+ f$ U3 x7 O  G8 G
tives. There were no siblings.
  \0 n! e* t* J# o- n: m  dPhysical Examination
& q' A1 S" m9 y5 N- `8 Q1 a- hThe physical examination revealed a very active,
. G5 ~' Y/ E2 ?( ^& f- ]- Oplayful, and healthy boy. The vital signs documented3 j2 P% m, \! ]+ l3 e
a blood pressure of 85/50 mm Hg, his length was
  p* U" B  {- O1 {90 cm (>97th percentile), and his weight was 14.4 kg5 k+ G4 B: g: D3 K# q1 `6 e" e' |: S9 `
(also >97th percentile). The observed yearly growth
; A; E. v5 S; w; L! g! ivelocity was 30 cm (12 inches). The examination of
/ `$ x: p5 V: Z' W! p# zthe neck revealed no thyroid enlargement.
# ?' `5 S% H0 `" R( |The genitourinary examination was remarkable for8 f2 T2 [5 v+ A
enlargement of the penis, with a stretched length of
8 c4 a1 o7 ]5 u- z4 i1 k7 e8 @8 cm and a width of 2 cm. The glans penis was very well
4 ^8 d9 |2 f0 D2 c6 Udeveloped. The pubic hair was Tanner II, mostly around
$ y2 x) f# m5 V& {+ K540
' |& J) N' z: O, I5 f3 o9 rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& A  ~, S9 @" i1 R( w
the base of the phallus and was dark and curled. The
6 I) `8 w# C* @# S9 F3 C3 S& ?testicular volume was prepubertal at 2 mL each.
6 }) g3 F$ _1 D. c- Q! q8 O  tThe skin was moist and smooth and somewhat
% B; [7 F5 x: k; V2 I2 B) w. B  qoily. No axillary hair was noted. There were no
& `2 _* i9 y( P' b) Rabnormal skin pigmentations or café-au-lait spots.
. L' R' X, d# x3 P/ r% e0 B/ fNeurologic evaluation showed deep tendon reflex 2+( c! S% i3 t, S3 T9 X$ B) G
bilateral and symmetrical. There was no suggestion- n0 b$ O* Z* Z1 r, |9 Z, w. B
of papilledema.' U8 `; O6 K6 W5 }/ @+ u
Laboratory Evaluation5 b8 K, u4 C; {4 i3 A# F
The bone age was consistent with 28 months by
0 Z4 T- A6 R8 ~& ~* J+ Dusing the standard of Greulich and Pyle at a chrono-3 ]2 O' n7 J# R5 M" V, S& n) {" L6 b
logic age of 16 months (advanced).5 Chromosomal/ r& L3 F  l- |# P! M4 x
karyotype was 46XY. The thyroid function test* F0 X! \* F3 M1 P; F8 u% b
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
  j2 K0 }4 t3 f' l$ w2 S1 d; A" j0 [lating hormone level was 1.3 µIU/mL (both normal)., T# G7 q- \7 c: Q! ?, L
The concentrations of serum electrolytes, blood( O0 B& {1 Q3 o. ]0 v: M# X
urea nitrogen, creatinine, and calcium all were- p5 W# x: Y& d. J  f4 e& G# T7 B+ U
within normal range for his age. The concentration
) i+ `3 o# @6 N: C1 W/ C6 Yof serum 17-hydroxyprogesterone was 16 ng/dL6 p. S) s+ J" e* M
(normal, 3 to 90 ng/dL), androstenedione was 200 i5 o7 e) E. p
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* h0 v1 {& ^  H
terone was 38 ng/dL (normal, 50 to 760 ng/dL),9 a: q2 y1 |0 T! ]8 l# |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 G( ~. H! W; D: @( y
49ng/dL), 11-desoxycortisol (specific compound S)
  y) B) |" R( l3 ]- H# l. `was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 B& i7 i# p2 p' r* ?tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ n; D: o9 ^2 u. F7 j  H9 `
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 m( O& M# T, j0 \" k7 |( g
and β-human chorionic gonadotropin was less than( X! o. y4 S* h
5 mIU/mL (normal <5 mIU/mL). Serum follicular8 Z) H2 X9 H" \
stimulating hormone and leuteinizing hormone' X/ [8 E, v; Y. K
concentrations were less than 0.05 mIU/mL  k6 [1 b, @7 D* a) e  H
(prepubertal).& k- n5 @& k) Q2 E  Z7 Q
The parents were notified about the laboratory, U% Z- g8 J( d3 T5 k
results and were informed that all of the tests were
* t$ D& f5 ?# ?) X. q7 Qnormal except the testosterone level was high. The
1 \. c6 j8 j8 C! tfollow-up visit was arranged within a few weeks to
: x" w1 v5 S5 c  dobtain testicular and abdominal sonograms; how-
( o1 s4 N* c% U& Uever, the family did not return for 4 months.4 F) J& k, M2 u# b( A
Physical examination at this time revealed that the
# [5 ~# S3 G6 L7 M$ A* H8 schild had grown 2.5 cm in 4 months and had gained$ Y/ ^' D+ I1 Z5 d
2 kg of weight. Physical examination remained* [9 f. p; w- f9 v
unchanged. Surprisingly, the pubic hair almost com-
8 M3 t: a# |. v" J4 gpletely disappeared except for a few vellous hairs at4 B7 L. t- p3 Y% B6 W' z
the base of the phallus. Testicular volume was still 26 u: p$ t4 e+ Q
mL, and the size of the penis remained unchanged.
3 Y0 Y6 O7 J3 x' ^, i8 o& TThe mother also said that the boy was no longer hav-7 F0 v: |) W  S* t
ing frequent erections.* i8 j  t& o' R/ |
Both parents were again questioned about use of6 z! e8 y* _; i$ J/ {3 [
any ointment/creams that they may have applied to" H+ Q/ `3 b( ]' Q( z; F; U2 N
the child’s skin. This time the father admitted the, [3 U* r5 k' p- Q+ Y
Topical Testosterone Exposure / Bhowmick et al 5415 f4 r( i7 @$ A- F
use of testosterone gel twice daily that he was apply-! \8 E4 e$ U; d7 r: K! q
ing over his own shoulders, chest, and back area for- r/ m) z( v# ^! M4 u- Y- G; g
a year. The father also revealed he was embarrassed/ H; G# ^1 F8 s% ?% V
to disclose that he was using a testosterone gel pre-
5 ]$ l5 ~! `$ oscribed by his family physician for decreased libido3 a6 q" o* p( R5 B. j! {
secondary to depression.
5 o" `' d- [7 p# B4 W$ d0 r# LThe child slept in the same bed with parents., ^; b4 C( a  }8 W- _
The father would hug the baby and hold him on his5 X5 F2 j' _' W' g
chest for a considerable period of time, causing sig-1 Y/ P, \- ^% h4 W& O- d% K( G
nificant bare skin contact between baby and father.
8 ?4 f% U/ e+ C/ g0 RThe father also admitted that after the phone call,
* y3 [; ^4 I' ]when he learned the testosterone level in the baby5 F, v" M4 r% N2 c1 N, A
was high, he then read the product information. B  G, H+ ~( \7 M( E
packet and concluded that it was most likely the rea-
) W  ~5 @1 Y4 W5 f! cson for the child’s virilization. At that time, they
, J# N: V8 B  [) tdecided to put the baby in a separate bed, and the* T, \' Z: q0 A! O2 f0 m& ?
father was not hugging him with bare skin and had1 t3 O  i* K  m9 }  k
been using protective clothing. A repeat testosterone1 d* m6 J& s: r$ Q% j
test was ordered, but the family did not go to the
8 v8 Z: a8 F3 S% Z8 t, }' ?% C0 Plaboratory to obtain the test.
' S4 z/ P$ N- u2 h- Y4 YDiscussion3 k, _" Q. v4 f8 P
Precocious puberty in boys is defined as secondary) t( s& ]$ `2 O+ N" V5 K
sexual development before 9 years of age.1,4
  G; M: b# I" A2 m5 t4 B" iPrecocious puberty is termed as central (true) when" r& ]5 R/ @9 Y8 M
it is caused by the premature activation of hypo-& C3 W2 d  T) {
thalamic pituitary gonadal axis. CPP is more com-3 `% w$ f7 i2 x& N4 L" p0 n
mon in girls than in boys.1,3 Most boys with CPP
" _3 {* w+ F5 kmay have a central nervous system lesion that is
) f3 h. v, A! Z  W/ h+ n' }responsible for the early activation of the hypothal-
" i9 O/ B9 h2 g; E& K2 A5 Zamic pituitary gonadal axis.1-3 Thus, greater empha-
% N* l. z9 B2 d* e/ Esis has been given to neuroradiologic imaging in+ V* |9 d: e3 T
boys with precocious puberty. In addition to viril-
* s5 x9 s" l1 q* q, {ization, the clinical hallmark of CPP is the symmet-
5 u( F; L, e0 [& Trical testicular growth secondary to stimulation by+ G- O& g. f  b  h) K/ j; k5 Y
gonadotropins.1,35 S* _2 m/ r8 Y9 J$ w5 a% @4 `
Gonadotropin-independent peripheral preco-
. d+ `7 u) p& S* g/ }cious puberty in boys also results from inappropriate0 C, e, W$ k$ F5 T; g: \% [
androgenic stimulation from either endogenous or+ c9 t& E* R) c% s! e- T2 R$ A
exogenous sources, nonpituitary gonadotropin stim-
5 m6 v  L) i' l1 M7 O, |/ ^ulation, and rare activating mutations.3 Virilizing
8 Y6 e0 G( O  X% o2 U5 G8 s' e9 }congenital adrenal hyperplasia producing excessive
; N' K3 J- U) t* t7 F% Jadrenal androgens is a common cause of precocious% K1 E4 K' e9 l4 V
puberty in boys.3,4
. m1 o9 l( w! @8 F$ v0 |3 TThe most common form of congenital adrenal0 t4 X9 R: U- L* g3 u$ A
hyperplasia is the 21-hydroxylase enzyme deficiency.6 b/ _8 H" H; j0 y) [- y; I2 _
The 11-β hydroxylase deficiency may also result in- t; t+ j1 y3 u9 Y, [& B5 I
excessive adrenal androgen production, and rarely,1 z1 f7 t: O' z( ]+ X" e9 a1 A3 d
an adrenal tumor may also cause adrenal androgen1 ^, l+ J+ P3 k- \- T" ?
excess.1,3
/ S! R& n3 ]/ j/ k% r- j( a; }% O" Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 \! K3 G) v# T- j# _% s7 t# c6 A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 M7 E6 e4 j1 ]! z: p8 Y' W* zA unique entity of male-limited gonadotropin-( Y$ {3 I- A' O/ K  U4 _" M
independent precocious puberty, which is also known
& q  V" ?5 h( Y# C8 p. X2 Y8 ~as testotoxicosis, may cause precocious puberty at a. s2 u4 k) L, T+ H, x( b# B' e; {
very young age. The physical findings in these boys
, ^: ~' q& v2 h2 ~1 h) y. x& F( Swith this disorder are full pubertal development,% ~4 y9 |2 S$ q' B
including bilateral testicular growth, similar to boys
* s5 t( [( y5 ?5 c3 x1 U" Qwith CPP. The gonadotropin levels in this disorder5 d6 Z! J! r7 \/ t6 k* {
are suppressed to prepubertal levels and do not show
( _2 [0 ?4 L3 ^. J2 Wpubertal response of gonadotropin after gonadotropin-. j; q, N) ^4 p6 l& G5 d5 Q
releasing hormone stimulation. This is a sex-linked1 V  J- L+ D8 q9 T$ Y
autosomal dominant disorder that affects only! G$ ?7 C2 _" U, x* \
males; therefore, other male members of the family
2 j; p( R) ]" H! L. y1 l4 ymay have similar precocious puberty.3
* M7 x. w) Z$ G8 x0 ^; @In our patient, physical examination was incon-/ z% [: R; I& \
sistent with true precocious puberty since his testi-: M( L9 C: `! g) F
cles were prepubertal in size. However, testotoxicosis
* X, B. w( `# w  Uwas in the differential diagnosis because his father
# Z0 c5 A; G* l1 L7 }started puberty somewhat early, and occasionally,6 `( p* Q# ?2 l8 |, M9 X
testicular enlargement is not that evident in the: E" O  A! A0 Q& T( |# W# k1 ]
beginning of this process.1 In the absence of a neg-
0 n6 f5 G  g7 S/ n% }ative initial history of androgen exposure, our1 c2 }7 q3 i, H
biggest concern was virilizing adrenal hyperplasia,% W1 s* Z$ V% v& i' f9 ^
either 21-hydroxylase deficiency or 11-β hydroxylase$ s9 U( s% D2 F( Q
deficiency. Those diagnoses were excluded by find-0 e5 L0 ~' Y' |0 R
ing the normal level of adrenal steroids.* b7 t( f, k1 M$ P; Z/ e+ w/ w
The diagnosis of exogenous androgens was strongly
& j+ F6 e9 O" ^( ]5 M5 vsuspected in a follow-up visit after 4 months because: F  x+ W2 i9 y/ d/ `! v" h
the physical examination revealed the complete disap-
7 i& z/ ?6 m8 {+ \3 Q: v7 gpearance of pubic hair, normal growth velocity, and2 X+ d2 y" y  H" K4 `2 q! [
decreased erections. The father admitted using a testos-
% |1 S7 g  t! \0 h* }terone gel, which he concealed at first visit. He was
9 d) q1 g) C8 T  T" dusing it rather frequently, twice a day. The Physicians’% {3 p! A0 ~& _3 |: S. e
Desk Reference, or package insert of this product, gel or: ?+ s7 W5 b% e5 T! \4 j( x
cream, cautions about dermal testosterone transfer to6 R6 N3 }* i7 E0 F2 v1 Q
unprotected females through direct skin exposure.
7 W" q3 j0 W/ F, HSerum testosterone level was found to be 2 times the
& F( ^  y& Q4 J) X4 N" r2 x" t% jbaseline value in those females who were exposed to) J/ w0 N: {& m
even 15 minutes of direct skin contact with their male8 Z$ J+ z$ i8 `; g8 x) C
partners.6 However, when a shirt covered the applica-
  F* C! V% ~% T: X' A% K6 }tion site, this testosterone transfer was prevented.* {2 l* B. u4 c& a
Our patient’s testosterone level was 60 ng/mL,! _2 `7 F6 }2 w
which was clearly high. Some studies suggest that
, h- s% x% g2 W% Cdermal conversion of testosterone to dihydrotestos-
) X) N3 E0 h' Z6 ~' G2 `! dterone, which is a more potent metabolite, is more
& A: g8 P( i# E0 |0 I) cactive in young children exposed to testosterone
% {. R8 W2 F8 e5 m0 Z: bexogenously7; however, we did not measure a dihy-
6 T) G& c  n2 v+ @4 R+ }3 q. j5 W' ldrotestosterone level in our patient. In addition to. P/ v" |5 n# [( ~
virilization, exposure to exogenous testosterone in
1 p+ r- u) o8 m! [9 dchildren results in an increase in growth velocity and
" x' I6 D) T; {5 a* uadvanced bone age, as seen in our patient.$ P( e( @5 \! R- g! ?4 l- g. Z
The long-term effect of androgen exposure during% F! {- h8 t3 Z5 G
early childhood on pubertal development and final9 O* }% ]' T: K' \
adult height are not fully known and always remain3 L* H/ k! W; G4 l3 e" a
a concern. Children treated with short-term testos-# j8 I, T  F+ L. n: e. f& Z
terone injection or topical androgen may exhibit some, y5 [  U6 v, \/ N, r8 b6 v
acceleration of the skeletal maturation; however, after, [2 K! w# E# v
cessation of treatment, the rate of bone maturation& s" L& g5 D, X8 M3 b' A/ P4 F
decelerates and gradually returns to normal.8,9
$ J6 a6 m  S5 b9 R  A. eThere are conflicting reports and controversy
* a# \$ d0 F( m) q) |over the effect of early androgen exposure on adult
% O% J8 z/ U; [5 u! lpenile length.10,11 Some reports suggest subnormal
$ E2 {6 C* }0 y8 xadult penile length, apparently because of downreg-$ Z% q/ X! l" i; p; b5 U
ulation of androgen receptor number.10,12 However,- t/ R+ Y$ m5 R* G/ o, @
Sutherland et al13 did not find a correlation between# o* R  i: E! ^3 ]3 u
childhood testosterone exposure and reduced adult
7 t! m0 v. w4 }# |penile length in clinical studies., s; g8 B0 o9 J: ]: X7 N3 t
Nonetheless, we do not believe our patient is
+ H0 J* u& f" ?) j3 n5 e- R% ugoing to experience any of the untoward effects from
" G. ~! Z3 _) N! U3 L9 Itestosterone exposure as mentioned earlier because
8 d! \: p; H' Othe exposure was not for a prolonged period of time.
! B2 J$ k2 g; B: J! xAlthough the bone age was advanced at the time of
" r* V6 g6 M6 sdiagnosis, the child had a normal growth velocity at5 J( Q. y, k$ B# P' v
the follow-up visit. It is hoped that his final adult: B6 p# r, V3 W! @. h8 W" m
height will not be affected.
4 ~; p" {, \0 Y4 i, H" LAlthough rarely reported, the widespread avail-9 h' r* I. M$ Z  D# P8 h2 G
ability of androgen products in our society may# a  B' i) o4 D8 ]* N; F* H
indeed cause more virilization in male or female' o, O7 v; {  {  x1 M# z$ q2 `
children than one would realize. Exposure to andro-" t; H1 Y5 G# b
gen products must be considered and specific ques-
, x/ ^; b; x% Ytioning about the use of a testosterone product or; l$ B0 V5 P" z
gel should be asked of the family members during( [( m0 m  l% c4 i9 D* X9 e
the evaluation of any children who present with vir-% m$ v; G& r+ v: H+ B2 Z
ilization or peripheral precocious puberty. The diag-
  ?, l1 P3 a; Q8 Pnosis can be established by just a few tests and by
+ f9 A6 M" W# Tappropriate history. The inability to obtain such a7 c5 r, @5 n. F4 ?' f% W! a
history, or failure to ask the specific questions, may3 x# b! C$ t7 j% a7 E
result in extensive, unnecessary, and expensive$ h3 ^0 o0 N$ s( N
investigation. The primary care physician should be5 p' N) n" E9 W, j# n9 C- C
aware of this fact, because most of these children& U' R( s( Z- U2 ^0 T
may initially present in their practice. The Physicians’
+ P4 ?  `0 Q  `8 C- L) ], yDesk Reference and package insert should also put a! y) T# K7 |& O( [
warning about the virilizing effect on a male or
* j2 @$ z7 n/ ~/ Q/ Xfemale child who might come in contact with some-8 y4 v$ y4 s# F" ?, f
one using any of these products.
! j' G- i0 m  u2 K) B. |/ TReferences" J4 @  L) f' p
1. Styne DM. The testes: disorder of sexual differentiation
1 d; s* m9 N+ G) y% q- ^: ]and puberty in the male. In: Sperling MA, ed. Pediatric
  s+ t# \+ a5 R; \# j7 ]Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. d& A$ e( z! ~& U' S5 Q2002: 565-628.
7 A' |0 [$ p6 F2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious1 D  W2 k$ m1 L) d( A2 q0 Z& S  t
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
1 F: T0 _# ~% S+ ]+ W! @8 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