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, s+ P+ [. `+ R4 [
Boy Induced by Indirect Topical
* Z' x3 a, V, g1 ^6 oExposure to Testosterone
. W7 ]: ~7 r( a" DSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 l1 a; u: s0 a! ]# M9 e- uand Kenneth R. Rettig, MD1
( F: [& o5 Y1 s5 wClinical Pediatrics
1 e& R* q) S* v: qVolume 46 Number 6. ~# o. Q+ o. |
July 2007 540-543
5 Q" o( o+ ^2 b3 [2 s© 2007 Sage Publications
8 y' P2 G7 c' m10.1177/0009922806296651
! @/ m8 Z/ P$ F$ ]0 i& Fhttp://clp.sagepub.com
( }8 U0 |* D4 b2 nhosted at
$ F1 {5 k: f3 i( g( Jhttp://online.sagepub.com* k0 n6 L( P& z7 j% V7 O
Precocious puberty in boys, central or peripheral,% ^3 f3 S8 X# ]1 @0 C: J; O$ S
is a significant concern for physicians. Central
5 T: D, ~& L) Pprecocious puberty (CPP), which is mediated( F) _% R+ A8 a4 {  ~" G
through the hypothalamic pituitary gonadal axis, has3 o7 A' C$ I, d5 x
a higher incidence of organic central nervous system
) }: j1 }* i3 Z0 ylesions in boys.1,2 Virilization in boys, as manifested9 s/ u- K: y6 N3 K+ E% \
by enlargement of the penis, development of pubic
2 q9 ?& m& R( [) |hair, and facial acne without enlargement of testi-
: K$ }) p/ r) Icles, suggests peripheral or pseudopuberty.1-3 We
" @3 f: f9 ~3 ~4 O- k0 @: Greport a 16-month-old boy who presented with the' O: S7 b* {7 \7 R8 c7 p
enlargement of the phallus and pubic hair develop-5 a# i/ m, D  N, Y! u, Y' `
ment without testicular enlargement, which was due
" Q3 E9 H* ?4 p+ g5 f  cto the unintentional exposure to androgen gel used by5 f! H8 U! g% B) @& O$ ]
the father. The family initially concealed this infor-# v1 ^  A4 ?" b. u2 G! \4 f
mation, resulting in an extensive work-up for this. y% s+ u* E3 a4 D. K, A: D
child. Given the widespread and easy availability of* p. x. K& d9 R
testosterone gel and cream, we believe this is proba-
/ J$ J* _8 C4 z- _! z$ v/ i5 Obly more common than the rare case report in the
# F! _! O) _8 B, {3 r- H; lliterature.44 b$ X/ ^, U' N0 F0 H9 E
Patient Report" \* Z; A  W+ X+ Q
A 16-month-old white child was referred to the
! G9 n' O! j5 ~5 T  m1 @endocrine clinic by his pediatrician with the concern& v! u7 c: s) M4 {
of early sexual development. His mother noticed" G0 i' q! y! m3 B- M, [0 Y5 _
light colored pubic hair development when he was
1 E  k9 `# t* w( e- i' T% [# BFrom the 1Division of Pediatric Endocrinology, 2University of# G  @" q' k+ `5 ~
South Alabama Medical Center, Mobile, Alabama., w: w' i- B. ~9 A( D" }
Address correspondence to: Samar K. Bhowmick, MD, FACE,, V$ K. _7 M$ E; Z+ T6 L9 P; `
Professor of Pediatrics, University of South Alabama, College of
  c5 {1 a7 ]+ I9 KMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;  {  u0 q8 \* e* i5 Q1 D# B( u7 P4 X
e-mail: [email protected].. l) I7 B! T5 a* _' [: A# F3 D
about 6 to 7 months old, which progressively became
: z. q* u7 D2 i3 O, mdarker. She was also concerned about the enlarge-& `! r0 @) N5 J  Y
ment of his penis and frequent erections. The child9 f. {  O0 v9 O0 {+ {7 m' Y4 Q7 g
was the product of a full-term normal delivery, with
1 U2 O$ [0 l3 T; ya birth weight of 7 lb 14 oz, and birth length of
! m! r" h' E# Y7 e20 inches. He was breast-fed throughout the first year
, I. H* F' {5 x0 w- Gof life and was still receiving breast milk along with
0 @- @0 u2 [, ]+ n. B6 e  a- Ksolid food. He had no hospitalizations or surgery,  r) M9 F& j" ~) w. F( |0 y
and his psychosocial and psychomotor development8 ^( W6 f9 t% M; a% X. u! s
was age appropriate.
1 E1 T$ B% E4 I( Y( M2 rThe family history was remarkable for the father,: c& \2 |5 ]# l& e: T5 O" G' z
who was diagnosed with hypothyroidism at age 16,6 ~2 v- J! n& X( L0 ~6 q
which was treated with thyroxine. The father’s
, ?  s7 ?" B; n/ [1 {9 vheight was 6 feet, and he went through a somewhat
8 W# z7 W  c5 C. kearly puberty and had stopped growing by age 14.+ |9 j" F/ D0 Z: R6 ?
The father denied taking any other medication. The+ M. H$ @; O$ n5 B  r) s7 Z
child’s mother was in good health. Her menarche) D& j# G+ Z! i  m/ d
was at 11 years of age, and her height was at 5 feet4 @8 V, ~- L  T
5 inches. There was no other family history of pre-
$ T7 P' J+ g3 ccocious sexual development in the first-degree rela-4 U' _  l1 }& |
tives. There were no siblings.
" @) z6 L; v6 ^7 b' }) n! HPhysical Examination
( ]; g9 s1 E  `The physical examination revealed a very active,
. s6 r# h( G5 T1 Qplayful, and healthy boy. The vital signs documented
4 o7 H3 Y" _0 \a blood pressure of 85/50 mm Hg, his length was/ D1 u" {) [' z8 k6 Y# T# W
90 cm (>97th percentile), and his weight was 14.4 kg2 @! q8 P- B' L0 ^
(also >97th percentile). The observed yearly growth# F5 Q7 e# v# _: ~
velocity was 30 cm (12 inches). The examination of
) C7 g7 F0 ~  r* T8 pthe neck revealed no thyroid enlargement.0 U' w3 o$ L0 Z  G& N. A# ]
The genitourinary examination was remarkable for
3 ^: `$ \3 A. t% V. [enlargement of the penis, with a stretched length of4 a6 L8 I; G% O2 X1 Q# O
8 cm and a width of 2 cm. The glans penis was very well4 T# }8 [; M) P, e5 x2 Q0 M
developed. The pubic hair was Tanner II, mostly around* e- s6 i* \0 ?8 x, w/ p. a
540! n6 ?: S" n3 P4 r. P4 Y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& O7 O6 a- p+ k& e/ V
the base of the phallus and was dark and curled. The  j& a1 l: @5 Z6 h) C
testicular volume was prepubertal at 2 mL each.
3 ^5 Z; M  w2 C  kThe skin was moist and smooth and somewhat' ~- Z$ d7 A, }0 S) X" j
oily. No axillary hair was noted. There were no7 ^0 Y0 F" g# Q5 m' c
abnormal skin pigmentations or café-au-lait spots.: _6 ?" C! g, p& h0 [
Neurologic evaluation showed deep tendon reflex 2+
8 r) v% z* C# Cbilateral and symmetrical. There was no suggestion
# u, |$ w! w8 L0 t" |# N' \1 F5 {# iof papilledema.
+ K) z7 {# s4 i# JLaboratory Evaluation! h/ W- _/ K% c% ?: x" D( {( b1 O) R
The bone age was consistent with 28 months by2 X& X2 _0 x4 N- Q8 `8 U' j" n
using the standard of Greulich and Pyle at a chrono-) u1 m2 U$ H' a  K
logic age of 16 months (advanced).5 Chromosomal. Z. k) s+ \2 D5 q* v( z
karyotype was 46XY. The thyroid function test) d5 B" l  K, d: W1 Q7 b$ V6 T$ g# F
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 p" z) K: A8 M1 r+ d6 Tlating hormone level was 1.3 µIU/mL (both normal).( S% v, |: @5 ~+ C- ?$ g
The concentrations of serum electrolytes, blood: [' |, n; o' I) O
urea nitrogen, creatinine, and calcium all were) b! P+ X( m1 D7 i# s6 Z
within normal range for his age. The concentration
3 C  I4 b% R7 x! K2 wof serum 17-hydroxyprogesterone was 16 ng/dL. l) ^5 O+ v( q) c8 ^0 x/ i
(normal, 3 to 90 ng/dL), androstenedione was 20
& X# x/ f& l0 H: V! W$ q7 eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ s$ i- n2 b8 B) v' q* L
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
5 q6 d5 X  [) u; |9 `4 [desoxycorticosterone was 4.3 ng/dL (normal, 7 to
# z# }- k3 O' p2 y/ t% }# u) e! O49ng/dL), 11-desoxycortisol (specific compound S)5 a9 m/ k. u. q  b
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
6 H3 t* U0 ?+ y8 Z6 `5 ~; L: `tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( V+ z$ {# v# otestosterone was 60 ng/dL (normal <3 to 10 ng/dL),# r4 V5 b2 O: r8 a
and β-human chorionic gonadotropin was less than- @% s& f2 q  r3 H. k
5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 f' C. J) l/ ?( h) K! Tstimulating hormone and leuteinizing hormone
5 h# a, h+ n4 X8 w, W! U+ j0 Jconcentrations were less than 0.05 mIU/mL
, [$ M: Q% @2 T5 p$ |7 [(prepubertal).
3 G1 C' S) m; p- _/ K$ n0 AThe parents were notified about the laboratory+ u2 C4 V, a- ^, }
results and were informed that all of the tests were
. m% C8 f6 v  i! Znormal except the testosterone level was high. The9 i% w* O- h0 w
follow-up visit was arranged within a few weeks to
! K' E1 b4 e7 C6 _obtain testicular and abdominal sonograms; how-6 Y& U8 p; c0 c$ N0 t1 L3 [
ever, the family did not return for 4 months.
- n3 W+ u* Q: H. k$ ^5 KPhysical examination at this time revealed that the6 v% P1 z+ K5 u+ }& [( @/ l. T
child had grown 2.5 cm in 4 months and had gained
% l( _& F, i5 f! G* k/ E7 N* E2 kg of weight. Physical examination remained/ X, r( }5 f5 t+ M% C
unchanged. Surprisingly, the pubic hair almost com-9 G  Y" ], [3 ?& N  m6 y
pletely disappeared except for a few vellous hairs at; d3 o0 l1 ?& y4 A9 a
the base of the phallus. Testicular volume was still 2
6 i. x% \6 J, H4 j6 I; v0 ymL, and the size of the penis remained unchanged.! U* x9 r9 B2 V2 m! B1 K& r
The mother also said that the boy was no longer hav-
0 i* Q  G7 R8 Ting frequent erections.7 `7 {" {* ]+ x: \* a/ t
Both parents were again questioned about use of
& M6 b+ Z5 b" W) N0 Lany ointment/creams that they may have applied to
( E6 U" m% |9 e# w7 e& L- k6 b) f3 _7 Hthe child’s skin. This time the father admitted the- R0 f, l; U* g5 r/ l6 s# n
Topical Testosterone Exposure / Bhowmick et al 541
* r- r# U, A9 guse of testosterone gel twice daily that he was apply-
  H  G! e$ u- g2 U9 p7 _ing over his own shoulders, chest, and back area for
+ X" M5 Q+ U! N5 ]( ya year. The father also revealed he was embarrassed0 t  Z8 G9 N3 E. F
to disclose that he was using a testosterone gel pre-$ {7 b" C) {" g& D: H
scribed by his family physician for decreased libido
9 U+ D8 r- Q5 w; B/ asecondary to depression.
3 _3 s  _! J' P5 i1 j+ H7 AThe child slept in the same bed with parents./ f/ V2 `, F& j8 |
The father would hug the baby and hold him on his
$ C! T- @: y$ D! B) G% F) x5 }chest for a considerable period of time, causing sig-
- w2 u5 ^3 k! n' e% @. Hnificant bare skin contact between baby and father.2 Z; k: k' o  S! Z% }8 X
The father also admitted that after the phone call,9 N& a1 j5 g2 Q( T& M  m
when he learned the testosterone level in the baby
, |( k0 A  h  |( Y" P* g, Iwas high, he then read the product information' p( b! Y$ j3 v/ k5 _
packet and concluded that it was most likely the rea-
. b  d! i8 d- @( R: ~* sson for the child’s virilization. At that time, they- d& d  i+ \) f6 C
decided to put the baby in a separate bed, and the5 y1 y( g3 ?6 O% o
father was not hugging him with bare skin and had
, D8 D" m* {% D' w9 H5 [4 ]been using protective clothing. A repeat testosterone  Y; l) f  A/ i) ]$ B+ f. b
test was ordered, but the family did not go to the1 X. E# F3 o& }/ t/ T, D9 |4 F1 G6 G
laboratory to obtain the test./ |5 X. i/ E: W9 y! v# v
Discussion
* w7 p7 J6 T$ O% l- z! kPrecocious puberty in boys is defined as secondary2 L7 T  y1 d' A% K. Q7 T: Y
sexual development before 9 years of age.1,4
; e# Y$ A5 \- [' x* O  S- q+ ^* W/ xPrecocious puberty is termed as central (true) when' {/ N1 c$ f4 }! d: p4 l; \
it is caused by the premature activation of hypo-5 Q; S# o9 d8 A& z" y2 J
thalamic pituitary gonadal axis. CPP is more com-$ q$ }# m% ^# A1 l7 P
mon in girls than in boys.1,3 Most boys with CPP
: e4 O0 V) ~8 m2 F# |9 Gmay have a central nervous system lesion that is( }6 E+ n3 C+ c. n
responsible for the early activation of the hypothal-
0 k3 A/ v+ F1 }; Z& Samic pituitary gonadal axis.1-3 Thus, greater empha-( v$ m' _! J& S: K
sis has been given to neuroradiologic imaging in
( q" n3 e' z9 `; a, N! d. {8 q2 uboys with precocious puberty. In addition to viril-+ }: n3 V& l8 `3 K( h/ g
ization, the clinical hallmark of CPP is the symmet-
# A7 B9 p% g" lrical testicular growth secondary to stimulation by) T. S* E  t# N& `
gonadotropins.1,31 G+ m' k0 B5 E# e  p7 Q6 N
Gonadotropin-independent peripheral preco-# o1 U3 a  E' s6 T4 W2 W
cious puberty in boys also results from inappropriate: L* z6 }8 b( t+ ~* }$ E
androgenic stimulation from either endogenous or
. |7 e- X% h0 g0 w5 y. Y) l5 z& }exogenous sources, nonpituitary gonadotropin stim-- @5 b3 [, u8 Z# W2 t4 E, j: K
ulation, and rare activating mutations.3 Virilizing8 h* w# R: e( }
congenital adrenal hyperplasia producing excessive
( }0 I" R( x" ?5 d4 A2 badrenal androgens is a common cause of precocious; x# J8 }/ V3 O
puberty in boys.3,4
& w3 l. o0 x- |$ F% T4 PThe most common form of congenital adrenal0 Q" y, [  h" K# ?$ g; G7 ]
hyperplasia is the 21-hydroxylase enzyme deficiency.
- b+ X0 q4 g1 s9 I2 UThe 11-β hydroxylase deficiency may also result in
0 l( j7 _/ t" x" `: K- _excessive adrenal androgen production, and rarely,
( L4 W$ X: I: a1 x% z4 n/ xan adrenal tumor may also cause adrenal androgen4 I+ O6 C1 I8 S+ l6 R4 O
excess.1,37 C4 h! R- T% M" X
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 L) ?' d( A. \# s) b4 N& \542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ w$ u8 C& N) S5 qA unique entity of male-limited gonadotropin-/ }3 S  e% P! n7 R  j4 @
independent precocious puberty, which is also known; d  @8 E4 o' |- x  f7 Y
as testotoxicosis, may cause precocious puberty at a' V6 t0 u# {0 u& w
very young age. The physical findings in these boys1 f! `- f) m; r1 g- e
with this disorder are full pubertal development,* n) C. @. q& v* M: o
including bilateral testicular growth, similar to boys4 e* r, j+ p( x2 \
with CPP. The gonadotropin levels in this disorder
/ d: s7 q) e/ Q* t; v# aare suppressed to prepubertal levels and do not show* O) T. ^3 ^1 I! `) E  l
pubertal response of gonadotropin after gonadotropin-
. b2 e5 O0 K# k0 g8 d% D( zreleasing hormone stimulation. This is a sex-linked# {) N! F) ?; N6 E3 G8 U' C
autosomal dominant disorder that affects only
5 y' v; A( T4 x5 B& b; {6 ~males; therefore, other male members of the family0 j. b' I% |5 F+ _% L4 J+ k, }9 m+ P
may have similar precocious puberty.34 J/ K  u! c1 l9 a5 {
In our patient, physical examination was incon-
3 W: P1 F2 K  C% W$ [; C0 ysistent with true precocious puberty since his testi-& P- b9 T% D3 z/ }; _$ R
cles were prepubertal in size. However, testotoxicosis
# q3 s$ m6 u& Xwas in the differential diagnosis because his father- x( Q+ ^# k0 V2 z6 E$ l# _
started puberty somewhat early, and occasionally,' t8 r/ A) }% K: W& p
testicular enlargement is not that evident in the2 A! w6 O! C# b5 u# _$ g3 v5 Z
beginning of this process.1 In the absence of a neg-
6 D0 g, c# c2 G) Y. b+ I7 Fative initial history of androgen exposure, our- ?  X5 n2 z% T2 Y
biggest concern was virilizing adrenal hyperplasia,$ h/ H. S( Q8 j: r# f
either 21-hydroxylase deficiency or 11-β hydroxylase
. O) m1 H/ K! ldeficiency. Those diagnoses were excluded by find-( e8 T2 d* ~7 G" T% h3 n
ing the normal level of adrenal steroids.. B! N* \3 G! F4 S' u' {
The diagnosis of exogenous androgens was strongly
  J0 q: g" S" _" j; J$ y/ @suspected in a follow-up visit after 4 months because2 |; K+ E% e( x! w& v! S& O, F' _
the physical examination revealed the complete disap-
: H% n! v( a$ ^6 o9 Rpearance of pubic hair, normal growth velocity, and
' @' ^" o* w9 n& T7 [decreased erections. The father admitted using a testos-! B9 H& s) b8 ~3 Z2 `
terone gel, which he concealed at first visit. He was
; o8 S1 i$ ~+ _) Y2 W% i3 Susing it rather frequently, twice a day. The Physicians’
& L9 _- O9 @! ~9 GDesk Reference, or package insert of this product, gel or# u( G) C6 m5 w/ }) z1 j. U9 r' ~. A; I: n
cream, cautions about dermal testosterone transfer to. W# s4 |/ `4 _, v
unprotected females through direct skin exposure., a1 y2 C+ p; M2 b1 f
Serum testosterone level was found to be 2 times the
. W9 P; O# I+ q1 S( xbaseline value in those females who were exposed to" P( f) S$ q3 i5 _' x
even 15 minutes of direct skin contact with their male9 I, H' W" P( ~
partners.6 However, when a shirt covered the applica-
' L% j$ l$ M  X/ ation site, this testosterone transfer was prevented.
$ l  X4 s  I2 L& }0 |0 }) A. p* ROur patient’s testosterone level was 60 ng/mL,- s- D  {+ L! o6 X" e1 G8 [
which was clearly high. Some studies suggest that' ~7 F! m3 I) u" g; P, U
dermal conversion of testosterone to dihydrotestos-
0 T, C; g% {$ ?7 [& X* U. ~0 a* Mterone, which is a more potent metabolite, is more, }  H" ]1 K1 ?7 @2 Z
active in young children exposed to testosterone3 \0 q" w: t- m* P
exogenously7; however, we did not measure a dihy-: H0 O; \7 j* a% k6 E, V
drotestosterone level in our patient. In addition to
: k) c/ a: m( B7 f$ q: d% S+ R1 Evirilization, exposure to exogenous testosterone in
; t0 l0 W( P  b6 F& Wchildren results in an increase in growth velocity and
' i8 l. E5 d/ Zadvanced bone age, as seen in our patient.
, A6 U: j8 X' z0 m4 HThe long-term effect of androgen exposure during& A0 y4 l7 J" q0 X& I5 n
early childhood on pubertal development and final7 O( G! k: A( X6 ^
adult height are not fully known and always remain" z+ N1 E9 N2 V# a3 X9 u
a concern. Children treated with short-term testos-# Z* B3 B' |7 |. S% e, \" x& K
terone injection or topical androgen may exhibit some
* q( A4 i: Y( m8 x8 Y- z2 @acceleration of the skeletal maturation; however, after* {. ^$ a1 p$ r( L, |
cessation of treatment, the rate of bone maturation
, U* O: n1 t& d6 O; K) k7 ^decelerates and gradually returns to normal.8,9* g' U/ h. y' w, E
There are conflicting reports and controversy/ [. Z/ [1 B! R: X& _' X
over the effect of early androgen exposure on adult
# W+ N" U9 U7 Q$ a2 m( S8 |penile length.10,11 Some reports suggest subnormal
/ [6 D# R( `1 t4 H! U  ^3 P7 Eadult penile length, apparently because of downreg-0 @# p1 X5 t( N$ n
ulation of androgen receptor number.10,12 However,5 S0 R( j' P8 U; z% j' D
Sutherland et al13 did not find a correlation between, p5 c6 \% r# e1 i1 C: w
childhood testosterone exposure and reduced adult
1 X: V8 S  y: y5 x# vpenile length in clinical studies.0 o' @! {1 ^: J
Nonetheless, we do not believe our patient is, \3 n' n& ]8 `: T
going to experience any of the untoward effects from4 F3 N2 H, p4 U0 C+ _/ Q) o% q3 q
testosterone exposure as mentioned earlier because
/ T/ g5 j; |! a8 ^: dthe exposure was not for a prolonged period of time.) R  f; ^( H. ]: D' X: f1 l
Although the bone age was advanced at the time of- {# o# q) @( h+ x0 F& J5 D2 o5 ]6 h
diagnosis, the child had a normal growth velocity at: A7 W3 ^) |& ^! S) l2 V% P
the follow-up visit. It is hoped that his final adult
% j1 K+ M0 w" t5 {6 r3 U* {/ h) iheight will not be affected.  E2 d3 A, w8 I- S- d& z  W0 {) m
Although rarely reported, the widespread avail-3 H3 c9 ?; b' Z, I& u
ability of androgen products in our society may
6 e. D' U1 S- O: X5 C/ Eindeed cause more virilization in male or female
) e2 ^/ G. y" y8 \7 z' nchildren than one would realize. Exposure to andro-: k" O! b+ K5 p0 ?  @" i$ R
gen products must be considered and specific ques-
( \$ z; U# n7 o0 Stioning about the use of a testosterone product or
  r2 l  K! _" hgel should be asked of the family members during- m# f2 D6 l8 w6 v& y% S/ v* T, s
the evaluation of any children who present with vir-7 v6 E7 W  d: @5 z! n4 K% \( S
ilization or peripheral precocious puberty. The diag-
. ?% {1 b! V( t. Z9 r8 k8 X6 K% vnosis can be established by just a few tests and by% s) w" ?8 m/ l
appropriate history. The inability to obtain such a7 N9 g0 ^, @: }1 ?) G$ j2 R- D
history, or failure to ask the specific questions, may/ `/ {& n$ L9 I$ X" J- U9 c. F( f
result in extensive, unnecessary, and expensive
0 b, q! y& Q( I& c1 D: _' |# binvestigation. The primary care physician should be
5 M. ]/ I  N5 z  i) `aware of this fact, because most of these children
, T) J0 k4 }0 i0 q. O) z. Z3 a, Jmay initially present in their practice. The Physicians’
# Q: O. Z% _4 R) k0 wDesk Reference and package insert should also put a
2 A5 h& Y0 L' twarning about the virilizing effect on a male or
9 u- n# {) T( P' U8 Z2 n2 Wfemale child who might come in contact with some-8 I2 f$ L& ]" a% `. p
one using any of these products." F8 B7 h; m% I
References5 U" n8 \9 P9 e7 d. {; [& i" u( O
1. Styne DM. The testes: disorder of sexual differentiation4 i1 E2 P5 `' x7 B! w/ p6 ^! F
and puberty in the male. In: Sperling MA, ed. Pediatric/ n% O7 O( `+ X
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
$ v# K" S2 m$ `9 Q2002: 565-628.
# ^/ {6 v' J9 t2 D+ X) {) R2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 y, H5 @. K& n% _# J8 \$ ~6 m2 Cpuberty 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-Old5 H! X* d' m0 X. v' [7 p1 Z
Boy Induced by Indirect Topical) ^% I$ _, i+ Z; a5 v  C( I6 q
Exposure to Testosterone& Q* ~3 I8 p6 a& I5 _& R
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 o( \* G: c4 [1 W! M" v) y
and Kenneth R. Rettig, MD19 h# {+ c5 s  ~' @
Clinical Pediatrics' P: A7 }' h/ O4 P4 n
Volume 46 Number 6& d. ^/ H+ o# M5 _
July 2007 540-543
7 X" o1 v( w' C6 W! t" D% U© 2007 Sage Publications
4 _& e1 j) U, h10.1177/0009922806296651  p4 A! R9 E+ M) z! P
http://clp.sagepub.com
/ c9 x9 i8 m" mhosted at+ e" V  ]# i; `/ c& P3 L
http://online.sagepub.com% x7 z1 b8 I+ R& f" L( y" E
Precocious puberty in boys, central or peripheral,
' P5 a2 Z2 C6 sis a significant concern for physicians. Central3 T- N- j) v0 X2 D3 H' ^7 w
precocious puberty (CPP), which is mediated2 r2 F* {& |& u4 |" t  y
through the hypothalamic pituitary gonadal axis, has- q! G$ O" u0 `/ Z4 t& \1 K
a higher incidence of organic central nervous system; M! q  P1 @, ?  E
lesions in boys.1,2 Virilization in boys, as manifested
( b0 u) T$ l( l5 x( h1 K2 v4 Lby enlargement of the penis, development of pubic
: Q- W0 d6 o+ b7 r; s/ ihair, and facial acne without enlargement of testi-
3 u3 m, `* r& w1 @! h* M% P+ Dcles, suggests peripheral or pseudopuberty.1-3 We
3 A7 @, d" J5 k5 b5 A+ S0 Yreport a 16-month-old boy who presented with the% E. r* j+ P6 N& v) ^
enlargement of the phallus and pubic hair develop-4 f$ ]5 h# ^6 u+ w; I& c
ment without testicular enlargement, which was due' z& o# ^; A2 V
to the unintentional exposure to androgen gel used by0 h( l3 x8 R3 z" K+ B( v
the father. The family initially concealed this infor-
* ~+ f3 F: c2 o/ I' s0 c( h  kmation, resulting in an extensive work-up for this
0 B+ a5 T7 U/ C0 O* R# lchild. Given the widespread and easy availability of
5 W3 a# Z# K2 f$ s, atestosterone gel and cream, we believe this is proba-8 s/ j  J& q3 G7 w+ L3 V0 _
bly more common than the rare case report in the
7 L; o! O, y3 d$ @+ lliterature.4
9 s! E3 u% X- s% q4 w4 }3 CPatient Report) u/ q6 T- c1 B7 @5 R
A 16-month-old white child was referred to the" R, ?$ ^) I+ w; Y& O
endocrine clinic by his pediatrician with the concern
  w/ M. f: A( v9 p/ \+ l$ }! Jof early sexual development. His mother noticed
+ I% ?( f5 p3 }% B% rlight colored pubic hair development when he was2 d) L! O, i$ _5 ~6 \7 j
From the 1Division of Pediatric Endocrinology, 2University of
# T2 F3 E! `+ E. Z# M3 QSouth Alabama Medical Center, Mobile, Alabama.
0 X/ K+ H6 D3 F* w8 NAddress correspondence to: Samar K. Bhowmick, MD, FACE,
7 I0 p8 g) u8 V  v1 [; HProfessor of Pediatrics, University of South Alabama, College of
7 q1 {( v  S7 \, m) a0 s' dMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
% ~8 U; i/ s/ w+ L8 Y. ye-mail: [email protected].6 a0 e# H+ A8 N' J: e
about 6 to 7 months old, which progressively became5 C6 W+ B1 v) V, Y1 [
darker. She was also concerned about the enlarge-
  k: P. k/ l8 T! j, h  qment of his penis and frequent erections. The child
2 {. y) V5 ~1 ?4 P. Qwas the product of a full-term normal delivery, with4 ?; k) Z9 H1 {( |2 Z
a birth weight of 7 lb 14 oz, and birth length of& Z1 j" C. R6 Y" u
20 inches. He was breast-fed throughout the first year
" V/ t; D. m. `  ?. wof life and was still receiving breast milk along with
% ]; p1 N6 s* S8 Msolid food. He had no hospitalizations or surgery,
! m3 ]1 }; I( S( j% a8 u, v1 x* ]and his psychosocial and psychomotor development
9 }$ u5 K, }* A6 ~! ywas age appropriate.4 q5 T4 c/ b% [7 w
The family history was remarkable for the father,
3 D3 B( e9 `2 O$ N" ywho was diagnosed with hypothyroidism at age 16,2 [2 F) ^; {2 a' P3 s  a$ q, L( z" o
which was treated with thyroxine. The father’s
% m, E1 N, I8 U( [* z4 yheight was 6 feet, and he went through a somewhat+ @# p  \) Q; ^* W7 h
early puberty and had stopped growing by age 14.1 L8 F1 o; A4 P0 T# Z
The father denied taking any other medication. The
# h6 _) k! D* F' c' C9 T! dchild’s mother was in good health. Her menarche
1 t7 t6 G* l9 W) @' E1 Twas at 11 years of age, and her height was at 5 feet  w4 |: `1 n/ T
5 inches. There was no other family history of pre-5 o, F3 j% c( C+ W: F+ ?# G# h
cocious sexual development in the first-degree rela-1 \5 H- t. f% k6 p8 A" W) |
tives. There were no siblings.5 x! m) N4 ~* T$ d3 f7 k
Physical Examination4 m, i) V' y: Y0 K* J; J
The physical examination revealed a very active,
5 A6 b5 D) P8 U& o+ K3 S2 v$ Dplayful, and healthy boy. The vital signs documented
. q+ P# x# J3 U% t& za blood pressure of 85/50 mm Hg, his length was/ I' D3 @; g4 h
90 cm (>97th percentile), and his weight was 14.4 kg2 e) g' J$ A, [# q7 C
(also >97th percentile). The observed yearly growth
% R! w, D8 k1 m# I4 Jvelocity was 30 cm (12 inches). The examination of
. ]( v/ N8 k3 Z% |, Jthe neck revealed no thyroid enlargement./ f' z: K4 q3 _* x, t: x5 \& g
The genitourinary examination was remarkable for
! [5 C0 z( T* L: _! k( aenlargement of the penis, with a stretched length of
: x  O7 A  k. s* {% ]/ v$ ?8 cm and a width of 2 cm. The glans penis was very well* h) R/ D5 X  e5 v$ s
developed. The pubic hair was Tanner II, mostly around4 G+ z" S1 @4 k8 A, l6 K, d* q
540
: @) j- k' L. ?; vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- u$ l% s* z6 Q: n8 v( gthe base of the phallus and was dark and curled. The
% p5 J* s8 }( ?& utesticular volume was prepubertal at 2 mL each.  q3 b8 U' S/ ^
The skin was moist and smooth and somewhat
0 W/ P- u  R( m. Eoily. No axillary hair was noted. There were no
& Q( F( k2 p9 N! eabnormal skin pigmentations or café-au-lait spots.4 o1 V4 C* |" R4 g6 [/ ^
Neurologic evaluation showed deep tendon reflex 2+5 Y* S* V8 V2 E6 q& J
bilateral and symmetrical. There was no suggestion
' K+ D& C. m% o0 X/ v5 p- zof papilledema.9 u! A1 i* q% y/ L
Laboratory Evaluation
, q( x& W( L. _The bone age was consistent with 28 months by
% P) S% E) f5 U1 v, pusing the standard of Greulich and Pyle at a chrono-: W0 Z. s6 j$ }# Q! P6 I, C4 H
logic age of 16 months (advanced).5 Chromosomal
: F' C6 Z, s5 @karyotype was 46XY. The thyroid function test
; Y) K- o" S7 S$ `& G8 Qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-" G7 M* I6 K  H* r+ I. ]: R% Z$ |9 m
lating hormone level was 1.3 µIU/mL (both normal).! f' v! w; Q! O/ H' k7 K
The concentrations of serum electrolytes, blood
6 S0 }+ S- D9 H7 Curea nitrogen, creatinine, and calcium all were# |6 h+ a. H# E' ~6 K/ K1 f
within normal range for his age. The concentration# \4 C# i8 o) ^" _( ^
of serum 17-hydroxyprogesterone was 16 ng/dL
5 c. p1 n# V( r4 y2 Y: y(normal, 3 to 90 ng/dL), androstenedione was 20
3 h  H, j' ^$ u  q5 ], n2 w9 [ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 b) I! v3 ]9 {. _
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 ^4 H2 f# s2 |- y4 i# y. M7 h* zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
& M: C+ _7 U# O+ g. d+ l2 K, N! O49ng/dL), 11-desoxycortisol (specific compound S)) g# q5 T% X2 o
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
3 ]! e/ L4 y, Y7 K8 @# N) ttisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. h/ c8 y% |8 i2 Z0 l
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
6 ?: o+ |  q1 k5 R0 c1 cand β-human chorionic gonadotropin was less than; ~6 J: P& j5 K- W% |
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 [( _. |1 v! `1 Pstimulating hormone and leuteinizing hormone
; p1 o2 i5 B+ W; M/ yconcentrations were less than 0.05 mIU/mL
  e4 m$ q' {/ ]) {(prepubertal).
5 \; T9 N& T  TThe parents were notified about the laboratory' D5 J/ Y1 X4 R5 Y, {
results and were informed that all of the tests were
5 P0 m* E& I0 f7 ]1 X% T/ Cnormal except the testosterone level was high. The
: ]5 A  V* j! M# e; Nfollow-up visit was arranged within a few weeks to- W( o  w" s! P6 Y3 H3 D- o, y
obtain testicular and abdominal sonograms; how-
: [3 g1 [4 S6 a5 ~6 S) O+ \ever, the family did not return for 4 months.' V% |0 U% p, ^6 e3 i3 D1 S3 s
Physical examination at this time revealed that the
% M$ }0 `/ t$ L+ P' j! M6 u* @child had grown 2.5 cm in 4 months and had gained2 ]9 }% h; c2 }# c" n; ^: Q7 G, Q
2 kg of weight. Physical examination remained
" H2 S$ L7 w8 Lunchanged. Surprisingly, the pubic hair almost com-( q. Z, K5 |3 y& g+ p' O: {
pletely disappeared except for a few vellous hairs at
" D8 P( G7 e  {" `the base of the phallus. Testicular volume was still 23 ~% Q! b6 y, u! A) ?. ~% i7 U& Y
mL, and the size of the penis remained unchanged.4 g6 y; Z9 Y! `
The mother also said that the boy was no longer hav-
& L7 W, n1 |/ o2 P+ d; D6 w# l5 ling frequent erections.
2 [4 \, R0 R$ N4 o0 bBoth parents were again questioned about use of0 l! @/ o5 x& ~# ?) X2 |: \5 ^
any ointment/creams that they may have applied to7 n- _2 n3 I, f
the child’s skin. This time the father admitted the
% S6 U1 ?( T% l4 x" ]Topical Testosterone Exposure / Bhowmick et al 5410 ~/ D( x+ m7 Q2 S2 N9 E1 W
use of testosterone gel twice daily that he was apply-
- W/ c. [& r9 s3 k, m, f. h4 Ging over his own shoulders, chest, and back area for
: j9 [7 j* v8 r% k$ Aa year. The father also revealed he was embarrassed
# {6 Z5 {, Z% f8 B" F) {- hto disclose that he was using a testosterone gel pre-
2 S2 r, O' ^: z9 c7 E# ascribed by his family physician for decreased libido
  V2 [: s0 G: P# P2 ~# u3 ssecondary to depression.
7 {$ {+ D2 ]4 ~The child slept in the same bed with parents.9 b  g3 M2 L0 z5 n
The father would hug the baby and hold him on his
3 ?) ~( O) a$ I% N( hchest for a considerable period of time, causing sig-
# p; D& p0 z% \5 ~+ \: inificant bare skin contact between baby and father.
3 r( f0 E1 Q2 B8 e( HThe father also admitted that after the phone call,. x4 e) L! r% }: `/ W* w
when he learned the testosterone level in the baby
  u! ?% [2 ^. N+ d  o! @7 f, bwas high, he then read the product information9 K# n& X( v0 z7 [( f$ X8 A
packet and concluded that it was most likely the rea-$ Y' W% O9 T' @
son for the child’s virilization. At that time, they8 k/ @3 E) s4 c7 S
decided to put the baby in a separate bed, and the
+ A6 I3 J& u5 Qfather was not hugging him with bare skin and had% W* o& X5 \- r6 _8 d/ C+ D# R' O
been using protective clothing. A repeat testosterone' P8 `; Z3 m! O6 O
test was ordered, but the family did not go to the8 x8 m( T0 j$ H+ h8 o3 i
laboratory to obtain the test.! o- r  d( W- p, y# u
Discussion. I8 v, \% j2 v1 d
Precocious puberty in boys is defined as secondary
1 I3 E6 L, _* M0 h: E! y" |& D+ @) wsexual development before 9 years of age.1,4
7 U! P0 u9 {1 ~% ]- lPrecocious puberty is termed as central (true) when
3 x; @( H* r# Y! ^! {/ n! l- H  uit is caused by the premature activation of hypo-
6 D( `: i$ j/ G" B, ?: |! _thalamic pituitary gonadal axis. CPP is more com-
9 j' D/ R' ?( Dmon in girls than in boys.1,3 Most boys with CPP  q* x7 l9 D1 I* z# C& T( _
may have a central nervous system lesion that is
0 n2 P" X" Z) ^# E9 Nresponsible for the early activation of the hypothal-
3 H4 V* i6 d& J% B& ], t7 Pamic pituitary gonadal axis.1-3 Thus, greater empha-6 b7 J# J& C" e! Z
sis has been given to neuroradiologic imaging in0 W5 F8 X2 o) M0 y0 o
boys with precocious puberty. In addition to viril-: J! ]- n* R% E+ ]* e
ization, the clinical hallmark of CPP is the symmet-
' s" C8 M+ Q% O$ qrical testicular growth secondary to stimulation by
$ [( E. \. C" U8 D! r; m( U) jgonadotropins.1,37 Q& q5 H0 V# o: M( I% Y
Gonadotropin-independent peripheral preco-
& M/ D# @2 P' m: g) c* B$ Y9 xcious puberty in boys also results from inappropriate
  G8 R% {0 T0 e* H9 Kandrogenic stimulation from either endogenous or) R( D% v1 {& N. S& D4 @
exogenous sources, nonpituitary gonadotropin stim-% ?- W' H: X1 K0 d  N( g
ulation, and rare activating mutations.3 Virilizing; T2 ]3 o7 C; P, K$ H
congenital adrenal hyperplasia producing excessive
4 ~. i5 @, F+ ]- k, X7 h" \adrenal androgens is a common cause of precocious
+ z: L0 E" n$ i( Hpuberty in boys.3,4
. O9 c7 k1 Y" {$ Y3 Z0 z9 XThe most common form of congenital adrenal
, C, v2 n: Q4 G2 c# S. yhyperplasia is the 21-hydroxylase enzyme deficiency.
. b7 V$ L, g/ e2 e0 V2 _/ zThe 11-β hydroxylase deficiency may also result in
! J% A' k. l% d8 Oexcessive adrenal androgen production, and rarely,
) p" I9 [% p' U. k* V1 Xan adrenal tumor may also cause adrenal androgen
$ E/ Z/ i6 t/ d  Z6 L" s' @excess.1,3
( i9 o; }! u# n, Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( _. n# Q& l! M! E542 Clinical Pediatrics / Vol. 46, No. 6, July 2007  k3 n0 ?4 ?. M
A unique entity of male-limited gonadotropin-: ?- }, u% G6 {- e
independent precocious puberty, which is also known
5 N2 w! u# G' v/ a7 Kas testotoxicosis, may cause precocious puberty at a
9 S  D. P: k/ E9 hvery young age. The physical findings in these boys
, N& {8 |: r7 J3 `. ?- F' Owith this disorder are full pubertal development,
5 b* C9 W3 e7 fincluding bilateral testicular growth, similar to boys: j% n0 h" E, ]4 Z7 i
with CPP. The gonadotropin levels in this disorder% _% f8 c1 V& z
are suppressed to prepubertal levels and do not show! g9 F( S2 m4 t: H
pubertal response of gonadotropin after gonadotropin-
' c) I$ j! I: D1 ~8 j+ Areleasing hormone stimulation. This is a sex-linked
; I, ]" L! A4 Pautosomal dominant disorder that affects only
  b$ g) E3 ]- p$ ?- ymales; therefore, other male members of the family+ c3 }% `% F7 D
may have similar precocious puberty.3
3 {' W! }- t1 p2 i; VIn our patient, physical examination was incon-: d8 K, N# v, T9 {  e
sistent with true precocious puberty since his testi-
( j# x- }5 t) xcles were prepubertal in size. However, testotoxicosis
2 I$ K6 b# q1 g7 Z4 Pwas in the differential diagnosis because his father
% A2 q7 y3 a5 y' x; G7 Q* istarted puberty somewhat early, and occasionally,
4 h7 y, P! Z# |/ J8 Qtesticular enlargement is not that evident in the. X  k, Q6 s$ E4 U- D  p
beginning of this process.1 In the absence of a neg-# K/ u$ k# l' \: G9 o
ative initial history of androgen exposure, our
7 z2 u" s, O6 v/ f$ h( c( }0 abiggest concern was virilizing adrenal hyperplasia,
. o+ e$ y' {" _3 w) Ieither 21-hydroxylase deficiency or 11-β hydroxylase
) O* R% `+ a$ v7 p, ddeficiency. Those diagnoses were excluded by find-# e1 m' S4 o2 w( `/ i
ing the normal level of adrenal steroids.
8 a; v8 @; M8 u( t0 VThe diagnosis of exogenous androgens was strongly
! ^# S9 `: M2 j$ Z( `, Csuspected in a follow-up visit after 4 months because
; N4 Q$ L1 y) t# qthe physical examination revealed the complete disap-! k0 z3 r( u+ V+ ]( ?% I+ h% ^
pearance of pubic hair, normal growth velocity, and% G8 P4 y4 a6 a! s
decreased erections. The father admitted using a testos-" k( q9 q7 k" A7 ]7 P
terone gel, which he concealed at first visit. He was
! p1 i+ f% Y3 W* Q/ B! a  Gusing it rather frequently, twice a day. The Physicians’
; q6 _, d/ h6 G2 f3 G+ WDesk Reference, or package insert of this product, gel or
. Z5 r( M# W8 d6 E$ scream, cautions about dermal testosterone transfer to
" S; h3 L0 Y& ?  r+ A4 q& N# Junprotected females through direct skin exposure.6 J% ?+ f/ Y% D# U+ _$ a, M
Serum testosterone level was found to be 2 times the
' [* _* g# w3 P, M& I" H3 Cbaseline value in those females who were exposed to
3 H" R1 r1 ^9 R, Seven 15 minutes of direct skin contact with their male
' ^# M5 f( w* O  `5 c3 opartners.6 However, when a shirt covered the applica-
$ g6 D% L: s) w: k) K2 ]+ P: wtion site, this testosterone transfer was prevented.
" Z5 @1 o. z( e2 H) U+ {' iOur patient’s testosterone level was 60 ng/mL,
' l2 h6 ?0 H) ~6 lwhich was clearly high. Some studies suggest that
4 y! G% D* E* s0 q9 Qdermal conversion of testosterone to dihydrotestos-
9 a/ U% ~( z/ U6 Wterone, which is a more potent metabolite, is more$ [! o' h2 q6 c
active in young children exposed to testosterone
4 F8 f7 H5 `, g, b4 ~exogenously7; however, we did not measure a dihy-
) X6 u/ ?0 \+ j- tdrotestosterone level in our patient. In addition to
6 M/ w& v/ B3 `  S  Qvirilization, exposure to exogenous testosterone in/ q' ^# P; q& H1 f7 Y) S
children results in an increase in growth velocity and
- S* g) f! l% H" Yadvanced bone age, as seen in our patient.6 u) d: P% p4 ^4 W
The long-term effect of androgen exposure during
+ I# v% s0 C* Oearly childhood on pubertal development and final
% j: x9 }5 \# M2 M7 c1 ]# I3 radult height are not fully known and always remain9 E% H8 W/ _0 S* {: O3 C4 h! N
a concern. Children treated with short-term testos-
3 v1 E' y. ~( r+ U; y- @terone injection or topical androgen may exhibit some: s6 x3 E6 n  P6 W5 t
acceleration of the skeletal maturation; however, after2 l& _# T0 _( W; P4 e# V) O+ L2 E3 E
cessation of treatment, the rate of bone maturation9 w* Y% g; f+ z& W& Z/ h* v
decelerates and gradually returns to normal.8,9
% X2 [0 m. I4 N+ c- p& qThere are conflicting reports and controversy
5 [3 s% b/ i9 J! {5 mover the effect of early androgen exposure on adult' c& a6 t1 M; L7 P% ^; C
penile length.10,11 Some reports suggest subnormal
( Q* m. g) l  V6 q! e, H6 ~3 n  s, jadult penile length, apparently because of downreg-
- a1 r* o1 R: O8 Lulation of androgen receptor number.10,12 However,
3 O2 L0 P* g8 r6 ~5 R4 jSutherland et al13 did not find a correlation between
$ z2 ^5 m- |; B7 J9 }childhood testosterone exposure and reduced adult0 X+ ~  |7 R. K- O5 _6 }( c# i
penile length in clinical studies.
' t( T) n% I+ }) z$ B% B% ]! LNonetheless, we do not believe our patient is! K1 S- V+ P0 \& \: P
going to experience any of the untoward effects from0 r) I. _9 T' s5 E! O. x
testosterone exposure as mentioned earlier because, }. }( T# K. X4 Y! M
the exposure was not for a prolonged period of time.0 ?, v; w7 M3 z+ v- l
Although the bone age was advanced at the time of
% \" Q. O+ s6 F: _8 B2 {# j# L& bdiagnosis, the child had a normal growth velocity at
! N3 b7 Z% F3 L8 }' vthe follow-up visit. It is hoped that his final adult
$ g% S; B; E& f1 R! l, U* \height will not be affected.* K6 V& F: X% E5 l% f* {
Although rarely reported, the widespread avail-6 l5 c; M6 N) f9 ^3 a4 i
ability of androgen products in our society may
* f& _  X/ F: {' o; i- Sindeed cause more virilization in male or female+ A, j; b) N+ a- Q/ a, y
children than one would realize. Exposure to andro-" Z  L# `( ?: t, W8 U3 h8 p5 b
gen products must be considered and specific ques-4 {- ~0 t7 _, ^% ~1 ]  s  ^( y
tioning about the use of a testosterone product or
, N$ e& Z- A2 p) o- Rgel should be asked of the family members during
; |1 G6 \2 e. @  y6 e3 m( t# Y. Gthe evaluation of any children who present with vir-, U) y2 Q0 E1 l  X' s
ilization or peripheral precocious puberty. The diag-
0 P6 }- ]2 c+ B# q$ I7 z+ ?; ~nosis can be established by just a few tests and by0 E$ z# L/ `, x0 o( ~1 u; V0 Q
appropriate history. The inability to obtain such a
6 B+ g* q9 I$ V- T8 O+ d, }history, or failure to ask the specific questions, may, e  Q! l& \% F: o+ X5 y8 l; B
result in extensive, unnecessary, and expensive
) j+ j5 m! A" G0 W( D9 n; Xinvestigation. The primary care physician should be
9 b! B4 H) c2 Oaware of this fact, because most of these children# N( Q7 c% Q7 U. f. F
may initially present in their practice. The Physicians’
# Q% m' t$ ]; m; ~& H# L+ n% qDesk Reference and package insert should also put a) O7 k, l  ]# x* N0 q
warning about the virilizing effect on a male or
% u% e  N& v* Sfemale child who might come in contact with some-
( l( F# [8 v# e* tone using any of these products.
6 t! N. K2 ~6 Z  g( Y& x  L4 t  ^References9 J9 w4 ]9 O  F+ V0 Z/ h' C) X
1. Styne DM. The testes: disorder of sexual differentiation0 T$ w- J( v1 W2 U5 }1 s  P
and puberty in the male. In: Sperling MA, ed. Pediatric. Y% U, t$ b. d
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 T  s; A- h9 V9 y* B* C- ?
2002: 565-628.; F* n' i5 O+ F- r  q' R8 ]
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! q/ F$ a, G+ q( F; Hpuberty 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

& R: D, Z' M0 K' P3 p1 w3 Q* ]# ^5 w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