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( R  D. Q' X5 l7 K7 _
Boy Induced by Indirect Topical! V  z7 R# V( ~" z2 y( ^
Exposure to Testosterone
( _. ]6 l2 k3 \3 i5 F0 uSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  R, x  S+ L) z* K
and Kenneth R. Rettig, MD10 M0 T+ M$ z. d: U- z. F: F/ Q
Clinical Pediatrics9 |0 ?+ u9 U" ~' l4 `
Volume 46 Number 67 N# T/ H$ b& G4 Q, Q  i9 R/ u
July 2007 540-543
& Y6 W% v2 m& N" R  M© 2007 Sage Publications* |5 Z$ Y4 D+ }1 Y7 b
10.1177/0009922806296651
! A+ I4 L6 b# \; F, n2 s5 Rhttp://clp.sagepub.com
8 O& Z: x+ B; _  Q2 ~, Bhosted at
1 P( u3 B2 L0 C/ A# ], L& a3 ?3 f0 khttp://online.sagepub.com
% M& n; f, T' Q! QPrecocious puberty in boys, central or peripheral,& O0 w- p. l& l
is a significant concern for physicians. Central# K4 i6 p- f0 n2 y( Z
precocious puberty (CPP), which is mediated
5 J( f5 b5 V4 Y) Vthrough the hypothalamic pituitary gonadal axis, has
9 z2 ~# ?9 w- O8 Y  Ka higher incidence of organic central nervous system$ r: ^$ e4 }0 r, L6 q
lesions in boys.1,2 Virilization in boys, as manifested! d# w  O4 w$ N
by enlargement of the penis, development of pubic
2 q2 `7 n- u( Y1 \% n# Z; H0 x; Dhair, and facial acne without enlargement of testi-& w' w1 }; i& o1 I+ V& X
cles, suggests peripheral or pseudopuberty.1-3 We# X5 `6 K8 P" a2 Z  l
report a 16-month-old boy who presented with the0 Y' u) K/ O$ F3 i, w& G! k
enlargement of the phallus and pubic hair develop-
( }! {* x2 G8 \) Y' p3 |2 y& Pment without testicular enlargement, which was due
+ ^( F& y/ C7 @% lto the unintentional exposure to androgen gel used by
" r9 f1 A2 X8 x6 \the father. The family initially concealed this infor-5 v/ |# ^( X  J" j! @
mation, resulting in an extensive work-up for this4 \+ m+ ~# b7 S2 C+ ?1 x
child. Given the widespread and easy availability of0 A6 O5 I; @" Z$ ?
testosterone gel and cream, we believe this is proba-
; U% o* P0 I! j) `7 f8 Vbly more common than the rare case report in the# x8 U$ [$ k1 d# x4 J
literature.4( x+ G, w6 v7 `6 i
Patient Report
+ @7 p7 R/ {$ o& l7 W: O5 @- gA 16-month-old white child was referred to the; a  b* U) C( E8 ]$ y  G
endocrine clinic by his pediatrician with the concern; e& U; d/ Y% i0 \/ Y6 D" E1 F! U
of early sexual development. His mother noticed4 ^% o( J3 r: l* f3 z% l, h5 u3 H$ {
light colored pubic hair development when he was/ P  z: S1 E) X0 _( j
From the 1Division of Pediatric Endocrinology, 2University of
7 h* N( P: @4 Q" C1 p; u* g4 USouth Alabama Medical Center, Mobile, Alabama.8 `8 N" O4 T4 W
Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 N, j5 v- |( m* E# ?6 o( [) QProfessor of Pediatrics, University of South Alabama, College of. y- u4 Z- B3 j% L! U, {# |
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;- V9 m2 u8 ~0 D; [" D2 R
e-mail: [email protected].- U- W$ F( ?, b7 K+ R
about 6 to 7 months old, which progressively became  N) W1 P! p, L0 w+ I9 G% G
darker. She was also concerned about the enlarge-; `$ _) S7 M5 Q! ^4 k3 _
ment of his penis and frequent erections. The child
3 l- C0 m( F# U# twas the product of a full-term normal delivery, with8 t' N' E# j7 J! F; b! z# ~
a birth weight of 7 lb 14 oz, and birth length of
9 k/ a. W" y' t6 F20 inches. He was breast-fed throughout the first year
% M* P2 N- J/ hof life and was still receiving breast milk along with5 A# C0 g- _( f2 c8 o* D) K
solid food. He had no hospitalizations or surgery,* I& ^; ?# E! d: I9 U
and his psychosocial and psychomotor development7 [' J8 i. H0 {- a! k
was age appropriate.2 w# X, L; f8 y' n
The family history was remarkable for the father,- K2 _% Z& V. {& v% g# _/ Y; B  X# z
who was diagnosed with hypothyroidism at age 16,) e6 D: @0 V2 w% C
which was treated with thyroxine. The father’s
1 g2 d- X4 {6 k/ O: v' O: F4 I6 zheight was 6 feet, and he went through a somewhat/ Y9 h/ K' x8 B# S1 ~
early puberty and had stopped growing by age 14.
' ?9 N. s3 K1 J, v0 ~! S6 [9 @The father denied taking any other medication. The7 C) d- G: [2 r& S- s% @
child’s mother was in good health. Her menarche
1 E$ a" \! e( y6 P6 y4 K' T% mwas at 11 years of age, and her height was at 5 feet0 {2 L9 S( ?) ^  m, c
5 inches. There was no other family history of pre-9 B- x& L5 h& J# e8 l) W) \
cocious sexual development in the first-degree rela-+ _) W0 V) H6 C
tives. There were no siblings.! i% n$ X4 Q( {: g; @3 l
Physical Examination
: L; _0 C1 Q6 D  ]( s) ~3 cThe physical examination revealed a very active,
! F! E( Y$ Y- aplayful, and healthy boy. The vital signs documented0 `( y' I& U) A8 H& g. C/ N* n' `
a blood pressure of 85/50 mm Hg, his length was
& W7 h, h- }; U- k# M8 K90 cm (>97th percentile), and his weight was 14.4 kg
  B8 ?6 a: r( k0 j: F( D(also >97th percentile). The observed yearly growth. V* R$ y1 x2 k3 K( }
velocity was 30 cm (12 inches). The examination of- S5 l$ r5 U2 a& o5 @& k" O) J
the neck revealed no thyroid enlargement.- U7 g/ V9 v1 e
The genitourinary examination was remarkable for
+ F# f$ a; C/ v  t$ S' s3 Benlargement of the penis, with a stretched length of' h3 Q: b% Q# n. j/ v
8 cm and a width of 2 cm. The glans penis was very well8 E+ c% q  j+ z9 |
developed. The pubic hair was Tanner II, mostly around
. F3 G4 z7 x$ E# d. H0 g& e2 \# m( j540
$ P9 L4 W8 y" q+ v1 \" I+ e4 \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ S) a0 z. u9 K; \6 O) Z0 Z- Nthe base of the phallus and was dark and curled. The
) G) x" e) m% e: C4 i1 otesticular volume was prepubertal at 2 mL each.
/ ?7 G7 v; l$ H# QThe skin was moist and smooth and somewhat) _+ ]" H4 C0 b6 q
oily. No axillary hair was noted. There were no% y, d$ @& [& x: [
abnormal skin pigmentations or café-au-lait spots.4 D( x( u- V" V' g& s( F& X9 v
Neurologic evaluation showed deep tendon reflex 2+
+ c" A# L% Z  K+ Q# F# Wbilateral and symmetrical. There was no suggestion, W; g; m5 z+ h% H/ C' B$ L
of papilledema.
" m- p  k5 F- J1 ILaboratory Evaluation3 z3 S6 @( n( A* V/ m) u
The bone age was consistent with 28 months by. o/ w& l) V6 M# i* n; t1 O6 G
using the standard of Greulich and Pyle at a chrono-
% ?3 y" J& k# D# Blogic age of 16 months (advanced).5 Chromosomal
' F( V" F2 ~: d- nkaryotype was 46XY. The thyroid function test
, U2 t' n- N& h. ~showed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 Q6 m: Z# x! n) H0 Rlating hormone level was 1.3 µIU/mL (both normal).4 x' C8 B; C6 q7 q7 b# u
The concentrations of serum electrolytes, blood* t: q* J  b" {( D: O! }  _
urea nitrogen, creatinine, and calcium all were
$ ]5 c* t0 Q: Q' Awithin normal range for his age. The concentration
" j/ X: q! M& |- ~9 F5 Oof serum 17-hydroxyprogesterone was 16 ng/dL
8 Q9 S$ V* I+ O0 X4 S(normal, 3 to 90 ng/dL), androstenedione was 206 S8 K3 g. |, H8 \  y5 ^$ w1 C
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-' \' Q9 ~5 `/ W& q) ~& C/ R* l
terone was 38 ng/dL (normal, 50 to 760 ng/dL),  B# M% ~7 r3 m( r
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
! S0 W2 w# b  s49ng/dL), 11-desoxycortisol (specific compound S)0 M0 t1 {; M- e4 b% a# a" O$ o
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& U6 j- X- [5 B* `tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 S8 b% a$ S2 s# f6 g* E' {
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ {6 T$ E! r& [$ I/ V2 M8 ?and β-human chorionic gonadotropin was less than6 k1 y; E0 g+ D3 H/ b( \
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 h! T. k: j( ^' G, @# T( ?$ U: z# Ostimulating hormone and leuteinizing hormone% J4 Z' P5 }9 h0 |
concentrations were less than 0.05 mIU/mL
$ |2 h+ ?3 c9 c! Z1 O2 W8 ^- F6 ?(prepubertal).; ]+ K5 V( d) j3 ?( g
The parents were notified about the laboratory
$ J! i- ^& U) L# {# L1 Iresults and were informed that all of the tests were
2 m! g6 D3 z  x% a% L9 Hnormal except the testosterone level was high. The
" W+ E" c  x6 v; k6 o' Vfollow-up visit was arranged within a few weeks to) S; M6 g/ w) X' s1 A
obtain testicular and abdominal sonograms; how-
1 M5 p) T. q( s; z8 f/ i7 A( a. tever, the family did not return for 4 months.
4 v5 t2 i2 D9 _& [, lPhysical examination at this time revealed that the9 l* o5 s( \! u- _) t
child had grown 2.5 cm in 4 months and had gained  r! o" T% e  U0 s$ I, t9 d
2 kg of weight. Physical examination remained% Q6 x9 U2 O5 t! C3 b- U
unchanged. Surprisingly, the pubic hair almost com-& ]# D6 s& h5 c: L! T& B( H, [
pletely disappeared except for a few vellous hairs at
& G1 e" o) Y+ Z" ^1 I- i/ Vthe base of the phallus. Testicular volume was still 23 P* k1 q2 n8 y
mL, and the size of the penis remained unchanged.
& `9 e0 c8 J. W; z# q! gThe mother also said that the boy was no longer hav-  `# E1 v4 @# @8 H3 V  G" [* {
ing frequent erections.. u3 Z) ^2 ]' p: [; g6 a
Both parents were again questioned about use of
1 o) D/ W! Z& t. X' I+ Yany ointment/creams that they may have applied to( D+ m( G  q) _( u& E
the child’s skin. This time the father admitted the4 ?- W2 Y2 r3 w# T" d6 q
Topical Testosterone Exposure / Bhowmick et al 541; \2 v. f  c9 `& }6 `
use of testosterone gel twice daily that he was apply-
% C4 Z8 f3 z; `* a+ W7 u6 ting over his own shoulders, chest, and back area for+ r" C; {3 p- o* @% F! X
a year. The father also revealed he was embarrassed: _4 ^5 u! u9 @( t
to disclose that he was using a testosterone gel pre-
. E' w$ ]3 t' ]2 K: Tscribed by his family physician for decreased libido
7 q; X2 ^6 [7 b+ h7 _secondary to depression.( R) Z6 d/ j) k
The child slept in the same bed with parents.; ?- e  Q  |( K) m5 ^7 K. ^8 @1 p" L% X
The father would hug the baby and hold him on his
% J2 s4 u' ^* f' x7 v* h7 ochest for a considerable period of time, causing sig-
* w8 O5 d+ I2 Q# l# Y4 B* \) lnificant bare skin contact between baby and father.( b( ]& p1 J! K  p
The father also admitted that after the phone call,
! U% m$ Y) Y3 O  t9 Z! Mwhen he learned the testosterone level in the baby
, |) v5 i8 p' p: N7 n' }was high, he then read the product information
+ z, T( s  D2 e) k- I7 T& Qpacket and concluded that it was most likely the rea-8 R8 F+ R3 D+ l1 R
son for the child’s virilization. At that time, they+ e4 P8 S( [- B5 |& y
decided to put the baby in a separate bed, and the6 j" s4 o: Z. L  Z
father was not hugging him with bare skin and had, J1 I& G7 J, }
been using protective clothing. A repeat testosterone
$ T1 k  E# v9 Btest was ordered, but the family did not go to the
' M5 C+ v4 s, t4 S1 @' U# S: f  slaboratory to obtain the test.- J5 j( F" f: N$ |) l. P  t
Discussion1 V- y! b& p  k' o
Precocious puberty in boys is defined as secondary
1 I8 y& k# Q$ Qsexual development before 9 years of age.1,4
. O4 N7 }' ~; N* o, T0 A: }Precocious puberty is termed as central (true) when" g! a* O$ E3 P) \  c6 n! G
it is caused by the premature activation of hypo-
6 K; w- M1 u4 K% z# ]1 R) S: Othalamic pituitary gonadal axis. CPP is more com-% {# j* ~5 p( e. [
mon in girls than in boys.1,3 Most boys with CPP
" r: x: ~. D' x5 e0 D, j% G5 g5 R: omay have a central nervous system lesion that is4 p: x3 ~$ D0 u
responsible for the early activation of the hypothal-. o8 Z6 s6 ]  [
amic pituitary gonadal axis.1-3 Thus, greater empha-
3 ?9 q% c: B5 R( Z3 A% {sis has been given to neuroradiologic imaging in
6 ]& v$ K2 c$ i" N6 tboys with precocious puberty. In addition to viril-1 H6 ]/ L' s) z% M
ization, the clinical hallmark of CPP is the symmet-
( e2 I6 V* V9 \, j' t0 ?; Brical testicular growth secondary to stimulation by$ {2 x$ |" }9 t
gonadotropins.1,34 v+ d6 z. i2 w, o0 N
Gonadotropin-independent peripheral preco-
* \% O! h$ F% `3 H. m6 \3 w$ ecious puberty in boys also results from inappropriate
$ i8 W: L: v) oandrogenic stimulation from either endogenous or( ~$ u3 X" h" Y* V3 H
exogenous sources, nonpituitary gonadotropin stim-
0 h9 u, x, N; R) p5 t* z' vulation, and rare activating mutations.3 Virilizing/ R3 l! ~3 @4 v
congenital adrenal hyperplasia producing excessive$ X# K+ g  u( ?2 L
adrenal androgens is a common cause of precocious6 F0 E: y, m+ n) d
puberty in boys.3,4
- i* C0 x9 d6 s/ K  mThe most common form of congenital adrenal7 N3 }7 B$ ~* g
hyperplasia is the 21-hydroxylase enzyme deficiency.0 {/ O" \+ P6 r  Q% q  X
The 11-β hydroxylase deficiency may also result in, S  @4 S% j) t6 H* v7 N
excessive adrenal androgen production, and rarely,
" W0 F% {+ t8 a& ~) \6 Can adrenal tumor may also cause adrenal androgen+ _0 E6 d; i7 h/ j$ D
excess.1,3
0 @3 U# {# w7 u2 }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  T( N: U6 o3 L5 K542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! @, \# ]2 n: `) k: F1 ?. g: ?A unique entity of male-limited gonadotropin-
- P" e6 a+ y7 k$ Y7 b3 Findependent precocious puberty, which is also known
. b5 ]# r5 V& {- kas testotoxicosis, may cause precocious puberty at a8 q# I% q  O6 T. b
very young age. The physical findings in these boys
1 O3 \0 p0 g0 u; owith this disorder are full pubertal development,
+ H; O9 q" d$ S/ e1 H6 c) cincluding bilateral testicular growth, similar to boys
' A- d9 O# {6 |* o! c% Nwith CPP. The gonadotropin levels in this disorder
: A0 ~( N1 x  R1 z4 Z" ]2 U. @are suppressed to prepubertal levels and do not show! M/ m5 B3 q. C) D7 d5 Y
pubertal response of gonadotropin after gonadotropin-
( A9 o2 D/ x4 j1 ]releasing hormone stimulation. This is a sex-linked
8 ?: q2 a& c" l2 @) H: ~autosomal dominant disorder that affects only% u$ B1 T) I. n* c9 i9 M% p
males; therefore, other male members of the family! G7 K. h* _' Y0 n
may have similar precocious puberty.3
+ m; ~  [  U1 m4 t/ W/ {In our patient, physical examination was incon-
. x. i$ P. d7 G! \sistent with true precocious puberty since his testi-# h# R% {1 K$ h% p0 h
cles were prepubertal in size. However, testotoxicosis9 q8 x9 U; n6 i8 T
was in the differential diagnosis because his father
4 `- ~6 Y3 n) f  M! x1 \+ @started puberty somewhat early, and occasionally,
- p5 k' p: v& s$ O! ptesticular enlargement is not that evident in the
6 N7 W8 l- K3 M3 b1 w3 @6 g; A# Rbeginning of this process.1 In the absence of a neg-4 X$ w- I$ c+ v( R
ative initial history of androgen exposure, our2 m8 i- Q0 I* z% \4 Y5 H& S
biggest concern was virilizing adrenal hyperplasia,
6 R: p/ F5 l3 b  Y, Neither 21-hydroxylase deficiency or 11-β hydroxylase/ W. R/ r- d2 f, X' B
deficiency. Those diagnoses were excluded by find-
" ?$ X7 ?9 x% _8 u4 a1 t( D7 [7 h4 `ing the normal level of adrenal steroids.
8 e" C5 ]% v$ x. OThe diagnosis of exogenous androgens was strongly
; o9 A: U2 b% a# o9 @suspected in a follow-up visit after 4 months because$ Z" ?- e5 a1 e9 `3 X: B# W% ?
the physical examination revealed the complete disap-/ ?/ J6 \- m3 \& S0 C9 D, C
pearance of pubic hair, normal growth velocity, and; T8 R# I1 D5 B$ M0 R
decreased erections. The father admitted using a testos-' D; \( J4 C' U$ ]7 J* H+ g3 |
terone gel, which he concealed at first visit. He was
- X, h& L; N! ^! H# Y2 jusing it rather frequently, twice a day. The Physicians’: j, O. H% L' L0 S1 k1 s' L2 G
Desk Reference, or package insert of this product, gel or
% ?1 }/ o2 _7 ?2 {8 y/ rcream, cautions about dermal testosterone transfer to7 V- `" n" F  ]7 {
unprotected females through direct skin exposure.$ v  d, ]: B2 j8 M, d: X4 g: o
Serum testosterone level was found to be 2 times the% F: v, ^3 Y' W/ A+ q& f; G
baseline value in those females who were exposed to& R) v+ }! r" }$ U
even 15 minutes of direct skin contact with their male, z$ Q+ B  b$ v, t2 F
partners.6 However, when a shirt covered the applica-- W9 j" T4 E# A: x" J0 V' \
tion site, this testosterone transfer was prevented.
1 U2 H$ t7 O% M9 W% y& [& JOur patient’s testosterone level was 60 ng/mL,
% p3 c1 I- }* X" c# uwhich was clearly high. Some studies suggest that/ Q7 V+ v9 J! j: w
dermal conversion of testosterone to dihydrotestos-# y' n- D/ m9 L7 x) ~9 Q5 w: \
terone, which is a more potent metabolite, is more/ V7 _+ H: |* {/ [
active in young children exposed to testosterone
% s0 T% @5 _; r- F- qexogenously7; however, we did not measure a dihy-3 O& S( l, w2 [  H! f- r, ?
drotestosterone level in our patient. In addition to, ]  Y7 @7 }3 X
virilization, exposure to exogenous testosterone in" c) Y* Y; A. o1 h
children results in an increase in growth velocity and+ O, v: S4 F' v3 z7 j: {$ D+ u
advanced bone age, as seen in our patient., M8 _/ \" O  j  {  R# J/ J, T5 r
The long-term effect of androgen exposure during. l, M! f, ?6 p. d% e. w
early childhood on pubertal development and final
- s* s3 B1 B% S; X9 Padult height are not fully known and always remain0 K" y5 h( Y2 m. p3 {
a concern. Children treated with short-term testos-; |, J- T6 m  m1 l1 }4 B
terone injection or topical androgen may exhibit some% b% F% h$ G4 w$ N
acceleration of the skeletal maturation; however, after9 y* ?8 v: S" t/ b6 Z/ u/ c
cessation of treatment, the rate of bone maturation6 z$ @0 @0 R. l1 v
decelerates and gradually returns to normal.8,9
) K+ A  D& @5 k6 G1 o' `( ~: AThere are conflicting reports and controversy
8 E0 J4 \% g6 W1 w* [over the effect of early androgen exposure on adult. Y" |0 L8 Y) h; {
penile length.10,11 Some reports suggest subnormal
: s% i- G7 C- T( U! w, ladult penile length, apparently because of downreg-) @7 }  b$ l9 Y: \5 u7 u
ulation of androgen receptor number.10,12 However,
' |1 h  z/ i" ~3 aSutherland et al13 did not find a correlation between4 ~4 ?' B$ P6 ?+ h9 u# Q  Q. c
childhood testosterone exposure and reduced adult
: r  P/ w* c$ @: Tpenile length in clinical studies.
) P5 _/ V1 H5 V, N3 L9 B: YNonetheless, we do not believe our patient is$ X9 A- r5 F9 c2 @, R) |
going to experience any of the untoward effects from6 c9 y+ e/ n4 ~0 \
testosterone exposure as mentioned earlier because5 k3 t3 r! R& D1 h  n4 }
the exposure was not for a prolonged period of time.
5 x$ t% I' Y, d, M7 P2 ]1 AAlthough the bone age was advanced at the time of) S1 K3 W$ `+ A- C
diagnosis, the child had a normal growth velocity at0 V$ u, X$ k, }% z* V4 x
the follow-up visit. It is hoped that his final adult
8 Z% m) a# w5 h; i" Z7 Bheight will not be affected.
6 \2 `* _2 I7 B' BAlthough rarely reported, the widespread avail-
7 W- }. |8 D1 i" r3 N3 iability of androgen products in our society may" |  U0 y7 E/ D" w% q
indeed cause more virilization in male or female6 P0 F- X4 [' }
children than one would realize. Exposure to andro-2 f: R, r0 O5 N$ {: {3 M' y
gen products must be considered and specific ques-
7 M- \: J8 m, \# o1 Otioning about the use of a testosterone product or
0 r: }* w& c0 Z8 g* Lgel should be asked of the family members during
% t, G+ i7 z9 r4 Y$ lthe evaluation of any children who present with vir-5 R) p% A2 q0 F0 o
ilization or peripheral precocious puberty. The diag-
: D: N0 w+ t, J) C- enosis can be established by just a few tests and by. g& y7 Z0 N9 u4 N& q1 c3 D
appropriate history. The inability to obtain such a
2 a/ y+ I5 I, w( U$ Dhistory, or failure to ask the specific questions, may0 q  y1 ^, I+ o: U
result in extensive, unnecessary, and expensive4 Q9 {5 |" E9 M
investigation. The primary care physician should be; n1 w# {7 |3 j3 f0 y3 C
aware of this fact, because most of these children
5 H. u3 S/ N2 _! xmay initially present in their practice. The Physicians’
( S0 [9 _, q1 D( A4 k  z8 ~% QDesk Reference and package insert should also put a
  t  \1 H9 x/ {$ _8 iwarning about the virilizing effect on a male or
$ R: @% j! F3 N4 h9 g8 X. rfemale child who might come in contact with some-; Z% {* m$ [$ ^5 |; Y( x1 r
one using any of these products.) S, i3 T( J7 p* q( q
References6 @& @0 ]8 N! r  q7 S' {
1. Styne DM. The testes: disorder of sexual differentiation; A: y- Y, ^, s; U) X
and puberty in the male. In: Sperling MA, ed. Pediatric- h! v0 P$ D1 w; [3 G
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& n" ^/ n; B( S* C2002: 565-628.
) X4 s( q( W7 [) }9 t2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( B) Z$ b- M$ N; K6 e0 Q
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+ {1 H) F/ ~0 k. d
Boy Induced by Indirect Topical
8 }+ Q( A$ m; n- O% g  c. x' e( \Exposure to Testosterone( s+ x! d3 `6 [, L+ N
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: {& w% M: v, q5 r
and Kenneth R. Rettig, MD1
- C. R+ I- a  m2 s9 ?- A% ~* I' fClinical Pediatrics
. t0 l  {5 j# a6 @; G) XVolume 46 Number 6
# [  G$ K  O1 v( ]# T6 gJuly 2007 540-543
8 I  f) y7 m7 b; N2 F$ w# }" ]© 2007 Sage Publications
% i; ^" C6 k6 P$ L5 m10.1177/00099228062966513 Y9 x4 [' I, n+ S0 j* l+ b  B
http://clp.sagepub.com
) N. D, h+ e5 Lhosted at$ n8 s9 I3 l' E+ R# m0 S
http://online.sagepub.com
, ^# {  }: m" r7 K* X& g0 fPrecocious puberty in boys, central or peripheral,
4 u* ]" F8 p8 m, ^is a significant concern for physicians. Central
. U( Z& u! D8 vprecocious puberty (CPP), which is mediated  W8 V/ [/ Z/ d" p. `& N
through the hypothalamic pituitary gonadal axis, has
$ V1 }3 @* N+ P. z% k/ v+ Ka higher incidence of organic central nervous system
- S7 O0 F& C4 z) Ilesions in boys.1,2 Virilization in boys, as manifested
$ I; ^+ ]# H0 l' D0 U* aby enlargement of the penis, development of pubic, X2 X! l1 D0 ^# m( o
hair, and facial acne without enlargement of testi-& ?$ ^( m* q$ m3 j& ]. b" @
cles, suggests peripheral or pseudopuberty.1-3 We" l* y+ f3 h5 S/ |$ f* ~9 r0 n3 q
report a 16-month-old boy who presented with the
4 [0 |! w1 }$ m5 J$ renlargement of the phallus and pubic hair develop-
  r9 q2 o& a; |6 c; w6 Yment without testicular enlargement, which was due
, a3 X1 y  @& K; a- ?( pto the unintentional exposure to androgen gel used by
5 q+ y2 p6 v; W% r/ Z  x8 p, _  Sthe father. The family initially concealed this infor-
% _/ O4 _9 x" I6 [) J) [, N" Qmation, resulting in an extensive work-up for this; F& h$ A2 t- `5 d' k
child. Given the widespread and easy availability of6 `2 C8 v$ l( l0 r& {8 k- [! n6 P/ m
testosterone gel and cream, we believe this is proba-- e! j+ E/ y7 F- q( D
bly more common than the rare case report in the4 j. q$ A4 a" G/ B
literature.4
# \# O2 P8 [' O. [! c$ vPatient Report% z3 z! v* h8 D4 K: A+ A6 c
A 16-month-old white child was referred to the" T3 O, x) C. A4 `  r5 M
endocrine clinic by his pediatrician with the concern8 E+ i8 w% F9 N1 N4 e: G6 f5 o* U
of early sexual development. His mother noticed
) v2 L4 l$ Y3 Z/ t. y2 mlight colored pubic hair development when he was
" H. W% R' t+ R; rFrom the 1Division of Pediatric Endocrinology, 2University of
. [* P/ H& V6 ^% M9 jSouth Alabama Medical Center, Mobile, Alabama.
. ~) R  h0 H8 ZAddress correspondence to: Samar K. Bhowmick, MD, FACE,( M" I) ?8 G! T! T; h; {" w* J' T
Professor of Pediatrics, University of South Alabama, College of
2 e( b- f. R& ?( i% QMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. |* W2 j+ J4 G6 p2 Ne-mail: [email protected].  ?6 r1 M( O: n: U
about 6 to 7 months old, which progressively became- a$ r3 B$ K( N6 t4 }; }7 z' m
darker. She was also concerned about the enlarge-/ b( Q: q+ [$ v9 M
ment of his penis and frequent erections. The child
- x$ Z3 U: o8 s0 D$ gwas the product of a full-term normal delivery, with% k7 k. j$ J! _  o
a birth weight of 7 lb 14 oz, and birth length of
2 j) R+ ~5 ~# g& R* g20 inches. He was breast-fed throughout the first year$ T( m3 m; D8 j5 z5 M
of life and was still receiving breast milk along with
' R. ]% Z: v  y3 Dsolid food. He had no hospitalizations or surgery,
6 X' q- y( J. m, eand his psychosocial and psychomotor development
+ L. [4 p/ d5 V- v, j/ T( Y# nwas age appropriate.7 s/ p6 f5 [% ]5 C
The family history was remarkable for the father,
. W7 C, }5 O2 n+ ywho was diagnosed with hypothyroidism at age 16,* q9 J. w, D. q/ t* v5 M1 q: k; Q
which was treated with thyroxine. The father’s
! W5 n" I1 C! H3 q, @# E/ t1 `7 eheight was 6 feet, and he went through a somewhat
2 r% m$ k. V! s, y! h5 }early puberty and had stopped growing by age 14.' C# Z* B0 k. R& l1 }" S2 M
The father denied taking any other medication. The6 s+ |; ?4 [9 o# a4 t5 R) `
child’s mother was in good health. Her menarche! X# N& q* _. w+ I/ q3 F: p; X
was at 11 years of age, and her height was at 5 feet) N; O# d# m! K( M& Q% V, I
5 inches. There was no other family history of pre-
! {4 ]/ h* i9 N3 c, e5 zcocious sexual development in the first-degree rela-9 L8 R' b! N* n6 u8 O
tives. There were no siblings.4 G7 G7 A+ Z3 |" A( _
Physical Examination
! @. w$ g+ r4 H( R' b5 U0 m: OThe physical examination revealed a very active,! O8 v% E* s3 Y, u
playful, and healthy boy. The vital signs documented5 s! Y- y9 j; Q/ u3 v
a blood pressure of 85/50 mm Hg, his length was+ k; j7 S4 M, L  j( b
90 cm (>97th percentile), and his weight was 14.4 kg
  H4 W3 ~5 M" p) G- B3 \(also >97th percentile). The observed yearly growth
0 z, Y4 l7 E3 ?7 _velocity was 30 cm (12 inches). The examination of( T- w9 c5 {4 U8 k+ T6 J
the neck revealed no thyroid enlargement.
! B  M/ W. _& D% qThe genitourinary examination was remarkable for$ S" F' z6 x: D' \( ?. ~
enlargement of the penis, with a stretched length of
1 E, Z0 b; h: i- P2 c4 l3 X8 cm and a width of 2 cm. The glans penis was very well
9 d  {; \4 x7 z2 ^+ w2 _developed. The pubic hair was Tanner II, mostly around
. M  r) @  k) T' @" o5406 R; g5 H5 I! Z6 G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 ?5 ^" }8 m" A8 ~) e, b0 Zthe base of the phallus and was dark and curled. The
' ~) S) [+ x4 n7 A& l5 Vtesticular volume was prepubertal at 2 mL each.8 D! R) v7 M( R' `
The skin was moist and smooth and somewhat
  Q/ u, `/ f" Voily. No axillary hair was noted. There were no/ G! V& E& I3 D0 P; W
abnormal skin pigmentations or café-au-lait spots.
- @" R' S; q0 e1 Z- C9 `9 w" P) uNeurologic evaluation showed deep tendon reflex 2+7 d. O6 p5 E4 @  k
bilateral and symmetrical. There was no suggestion# `4 n5 N- v' h$ H
of papilledema.6 I! {6 R  i' k9 K4 a8 f" b
Laboratory Evaluation
4 v; Z5 }+ f0 u: O- b" L5 ZThe bone age was consistent with 28 months by' i3 U3 G  z+ c1 I' T% \
using the standard of Greulich and Pyle at a chrono-
, l; f4 Q  j) Qlogic age of 16 months (advanced).5 Chromosomal3 G8 E; S+ n1 l7 c
karyotype was 46XY. The thyroid function test
9 G/ d4 I# f5 Fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 n% c5 E2 d& o9 W" K1 H; d
lating hormone level was 1.3 µIU/mL (both normal).
1 }- _( u7 `5 L/ O2 zThe concentrations of serum electrolytes, blood* ]2 V. G& D& U4 n
urea nitrogen, creatinine, and calcium all were
$ S: n5 _3 ]7 N! l7 \5 v( `within normal range for his age. The concentration2 |! J9 G$ y# z8 A$ ]- f. v8 y
of serum 17-hydroxyprogesterone was 16 ng/dL4 m4 L5 {3 ^4 _* h7 `
(normal, 3 to 90 ng/dL), androstenedione was 20' ~' A$ s0 ^5 C" J( y0 l8 Y
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 O( W( G; _' C3 l+ b* Q' {4 [- M+ m1 fterone was 38 ng/dL (normal, 50 to 760 ng/dL),( @% G1 Y7 m9 I2 p4 H% W; h
desoxycorticosterone was 4.3 ng/dL (normal, 7 to% I+ \9 ^4 u; @
49ng/dL), 11-desoxycortisol (specific compound S)
1 {! Y. E+ K6 L7 |+ Wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 j( g- k; I9 v$ C$ a5 r
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% ?1 B* O6 R( f' w, ?
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ P" V9 Z1 W2 T: Q5 j" Jand β-human chorionic gonadotropin was less than9 j% [" o: X3 W' Q+ w
5 mIU/mL (normal <5 mIU/mL). Serum follicular" E+ m) P0 y8 ?2 c1 C
stimulating hormone and leuteinizing hormone
5 ~5 J; |4 m! h  bconcentrations were less than 0.05 mIU/mL
  R5 k: K/ O/ f$ P(prepubertal).
' i% T) B/ O9 e$ H2 I$ gThe parents were notified about the laboratory2 f) l$ M) ?9 t1 E& g
results and were informed that all of the tests were
5 E( ]1 `+ e/ u: T0 knormal except the testosterone level was high. The
0 x  M" T8 A* Jfollow-up visit was arranged within a few weeks to
' u/ L' B7 y  H7 ?5 [7 m; E* @6 D8 B$ Xobtain testicular and abdominal sonograms; how-
/ c! q  m$ S4 r% I% m# W# Cever, the family did not return for 4 months.1 \' \; K/ ^! B- H' i( G
Physical examination at this time revealed that the$ F1 r$ m6 I6 J  g& |) N
child had grown 2.5 cm in 4 months and had gained9 J$ x" N9 k3 ^0 \8 ^; N+ u* R1 U
2 kg of weight. Physical examination remained
! m  y" _0 g- `0 L: F6 g- nunchanged. Surprisingly, the pubic hair almost com-. K4 k+ H+ j  d; ^; i7 D  D0 s
pletely disappeared except for a few vellous hairs at
8 l4 n( h, }" T$ `) e8 S; K6 R2 w( q% Mthe base of the phallus. Testicular volume was still 2- ~6 C8 _& {/ b! i& n8 y
mL, and the size of the penis remained unchanged.
4 E( _8 }/ V7 w% S: A/ m" ?The mother also said that the boy was no longer hav-
5 k: v0 B) z$ t" ?ing frequent erections.5 X2 M8 @9 A# b+ f: u% t+ U% l
Both parents were again questioned about use of" j9 ~' @: P8 X: O5 O$ b9 a; y/ D
any ointment/creams that they may have applied to, Q6 J! ^3 t7 V- Q
the child’s skin. This time the father admitted the
7 P- c2 c; Q/ s) D6 vTopical Testosterone Exposure / Bhowmick et al 541
$ t* Z3 ]3 @1 t. H  xuse of testosterone gel twice daily that he was apply-
. s! M5 a0 Z/ X: H: n& Y& y7 _ing over his own shoulders, chest, and back area for4 r* E% _7 R& s) O6 [' u- n5 M. r: l
a year. The father also revealed he was embarrassed1 B  k4 H4 F( b) L
to disclose that he was using a testosterone gel pre-
" G7 e* k6 t6 Mscribed by his family physician for decreased libido
# v' @, T( O: w" Esecondary to depression.' e, ?& W. y5 ^  b" h$ d
The child slept in the same bed with parents.* j# t: I9 k6 A% ]8 M/ k: f
The father would hug the baby and hold him on his
( f/ n6 M; t; ?chest for a considerable period of time, causing sig-  g2 R6 Z% r6 V
nificant bare skin contact between baby and father.0 j4 I9 W" C+ D5 v$ _
The father also admitted that after the phone call,
5 t5 T8 o7 O) ~# D; w+ ^* U8 bwhen he learned the testosterone level in the baby
$ A4 z% [7 B. Q0 {* U) d4 C8 bwas high, he then read the product information% B8 W4 A5 Z! p$ _) u6 H7 A5 m
packet and concluded that it was most likely the rea-  d" S* v0 B3 d+ L
son for the child’s virilization. At that time, they2 }9 k2 t# Y" L, u, r9 r
decided to put the baby in a separate bed, and the
/ I+ V9 E$ d4 M% {( W  Kfather was not hugging him with bare skin and had+ c) v) |1 q5 n5 y) y
been using protective clothing. A repeat testosterone2 Y/ d% w+ c+ }. V, X) w
test was ordered, but the family did not go to the4 p  A% `4 f, c1 ~0 `; N: m3 ~6 `
laboratory to obtain the test.# a1 b% H" L1 m$ z9 v
Discussion: _+ l6 e. n& I7 i# `4 r+ A- V) K. e
Precocious puberty in boys is defined as secondary
/ h- s! Y5 C, _" J" s8 X7 psexual development before 9 years of age.1,4* d( g$ q- C, i
Precocious puberty is termed as central (true) when* t, U6 x, Z1 S2 ~$ w- w2 Q
it is caused by the premature activation of hypo-
+ C* S1 _: R& [+ rthalamic pituitary gonadal axis. CPP is more com-  C* T" F; k! f
mon in girls than in boys.1,3 Most boys with CPP
( x* |6 m3 {# D/ ^may have a central nervous system lesion that is
, q# ?& P3 `* oresponsible for the early activation of the hypothal-: b% g; K' |- o2 U6 \, g
amic pituitary gonadal axis.1-3 Thus, greater empha-
# J# \) p# Y0 d, T. s6 Bsis has been given to neuroradiologic imaging in
5 }# W& Q: g  vboys with precocious puberty. In addition to viril-
- a! q3 O, A* I8 Sization, the clinical hallmark of CPP is the symmet-
! `. t- k( \9 N1 O3 {9 F4 Jrical testicular growth secondary to stimulation by: H* w$ r* V7 n
gonadotropins.1,3; Q3 }! b/ @& \
Gonadotropin-independent peripheral preco-8 ^8 z  X' t+ I3 D+ _  T3 D
cious puberty in boys also results from inappropriate! w2 G3 N& P, F( p! I" n. S
androgenic stimulation from either endogenous or0 R3 L, l% w. C) ^. s+ ~
exogenous sources, nonpituitary gonadotropin stim-( b1 }3 g; H( R7 B, \  A
ulation, and rare activating mutations.3 Virilizing. `% [8 k0 a& J/ u  N* D; S# L0 {
congenital adrenal hyperplasia producing excessive
% i& W6 @8 `8 I8 }adrenal androgens is a common cause of precocious
( P' f- H/ c2 Y2 c& N2 @puberty in boys.3,4
# o4 D! ~' L  X4 T5 m1 ^! WThe most common form of congenital adrenal0 [% H' I5 A" L: j( N: i
hyperplasia is the 21-hydroxylase enzyme deficiency.
, {6 T/ R( N' [( `: \  _$ bThe 11-β hydroxylase deficiency may also result in
# d0 r* ]' M9 xexcessive adrenal androgen production, and rarely,: e7 N0 `) |5 V: x8 @2 |6 h
an adrenal tumor may also cause adrenal androgen3 v; T5 z. h9 `4 d; w
excess.1,3
. F4 @! j& @8 C  s( ~# Yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 A% j; M) {, _6 B542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ s6 O5 J2 x! ?# t( G) _8 UA unique entity of male-limited gonadotropin-
6 F9 b( X% N& O, Q1 L' {& V" hindependent precocious puberty, which is also known
, ~5 ~! ?# o* |. }# vas testotoxicosis, may cause precocious puberty at a1 }% C+ \1 l4 U1 V- u9 }9 M
very young age. The physical findings in these boys
# U  z; U  ^7 x6 m& V% Q8 xwith this disorder are full pubertal development,
4 W' r/ Q2 Y9 ]$ E5 ^including bilateral testicular growth, similar to boys& q! h4 d3 c4 c- v! K9 `% G  b
with CPP. The gonadotropin levels in this disorder
) }, f" o8 c) m# W! pare suppressed to prepubertal levels and do not show
$ [/ ]  C% k& M; J# W9 h. Y2 Epubertal response of gonadotropin after gonadotropin-; k: R: s( A7 R" H+ b$ I4 J
releasing hormone stimulation. This is a sex-linked/ q/ E( ^# h/ W* _3 m- B7 R) {
autosomal dominant disorder that affects only
2 x3 Q2 W3 g7 j) i0 l* l9 e: Ymales; therefore, other male members of the family
8 `0 [$ D0 h: a" D' t/ emay have similar precocious puberty.3% F' ?- B  B$ r
In our patient, physical examination was incon-: C4 b8 g2 y% }
sistent with true precocious puberty since his testi-; n1 F8 _, Z9 s' l
cles were prepubertal in size. However, testotoxicosis) ?5 V( f' k4 Y6 F& [5 y7 V
was in the differential diagnosis because his father
) [% N4 J& v/ m5 E0 |& f. j- _& wstarted puberty somewhat early, and occasionally,# E6 Y# c: d3 [
testicular enlargement is not that evident in the
) K  {. p' u! Z. {1 dbeginning of this process.1 In the absence of a neg-
, }$ g) X  K% b# t) Hative initial history of androgen exposure, our
2 p$ g, ?7 m& h* q+ p, m: Hbiggest concern was virilizing adrenal hyperplasia,
+ V" c  y' B6 z1 |either 21-hydroxylase deficiency or 11-β hydroxylase: X7 M: t1 g  ~$ r; f
deficiency. Those diagnoses were excluded by find-
) t# ^- X# ?9 k/ L9 g! p/ u3 w6 ping the normal level of adrenal steroids.1 B- T  ]1 Z/ H' p. u3 S+ c" v$ v
The diagnosis of exogenous androgens was strongly- {7 L" g" x  b
suspected in a follow-up visit after 4 months because% t. C! [: Z. i) h7 K" z' A. W
the physical examination revealed the complete disap-
2 S3 |( H: @9 W& u9 C" r# Xpearance of pubic hair, normal growth velocity, and4 H$ I- c$ c/ z. K
decreased erections. The father admitted using a testos-3 ?& D5 ?2 b. \% Z" e% G
terone gel, which he concealed at first visit. He was7 |" T1 _( _) p5 ^: [( w
using it rather frequently, twice a day. The Physicians’# Y! j  v9 w4 s% b: S2 ?
Desk Reference, or package insert of this product, gel or2 U0 E* X' v8 g6 y
cream, cautions about dermal testosterone transfer to8 t2 |# c/ T( x) w
unprotected females through direct skin exposure.
  U, b% Y+ K; |, {0 O5 [Serum testosterone level was found to be 2 times the
4 O# l) f% I1 J+ L. J2 Ebaseline value in those females who were exposed to
( \- t: W3 p# y8 Q1 I# Oeven 15 minutes of direct skin contact with their male
, U8 I! q/ w6 N; u; _5 ?0 P- o& ypartners.6 However, when a shirt covered the applica-9 A0 ]8 v! i+ l6 j" J& K
tion site, this testosterone transfer was prevented.
) q+ I! y7 c' y4 h' J0 G8 i* FOur patient’s testosterone level was 60 ng/mL,
. @! [7 h+ G; [& s% i  vwhich was clearly high. Some studies suggest that
* B: ?* F- K7 _1 Ydermal conversion of testosterone to dihydrotestos-4 N, h: O( g: r$ [- S7 ?
terone, which is a more potent metabolite, is more, W- Z( i! p2 \( U7 T8 u
active in young children exposed to testosterone
, ?6 V) c, C7 S+ pexogenously7; however, we did not measure a dihy-2 Y4 O$ R0 m- d9 Y. G
drotestosterone level in our patient. In addition to# w1 H8 x; I: s  n
virilization, exposure to exogenous testosterone in
+ {6 m7 h6 K" P3 G" ochildren results in an increase in growth velocity and
( I/ c- h0 U% r2 s* T( hadvanced bone age, as seen in our patient.
! I9 p+ N8 L2 |. ?5 A# }% q7 R6 ZThe long-term effect of androgen exposure during# ~3 w- }1 E5 U
early childhood on pubertal development and final* g" }2 h7 M3 _# M9 ?" y6 s. @
adult height are not fully known and always remain
: o/ W$ N- I1 s6 [+ S# E) J8 Va concern. Children treated with short-term testos-
+ Q( C  \1 t1 z- f& dterone injection or topical androgen may exhibit some, b% c/ |" K& o$ N) x; b
acceleration of the skeletal maturation; however, after
2 T  V9 K5 J/ u/ S- K* k# U( i+ Qcessation of treatment, the rate of bone maturation0 E! P1 _, ^1 [! }' z. e/ g8 f/ [
decelerates and gradually returns to normal.8,9: |1 O1 A$ ~2 O/ g# \8 z4 i  b
There are conflicting reports and controversy
1 @) [/ f& [! Lover the effect of early androgen exposure on adult
; J2 N3 B7 N; h5 j, Ypenile length.10,11 Some reports suggest subnormal  z' R3 |' l$ i
adult penile length, apparently because of downreg-* y& l% _- v. S5 m5 o* D
ulation of androgen receptor number.10,12 However,* ^- z( Z0 o* g* V$ l
Sutherland et al13 did not find a correlation between
" @' r% ?' R5 A$ Rchildhood testosterone exposure and reduced adult
6 T& ^7 M% p/ P( Q: O" Ipenile length in clinical studies.
" b7 f% u; h3 L& L9 KNonetheless, we do not believe our patient is2 ]; D! }; B6 J0 e3 A
going to experience any of the untoward effects from
/ i% m* \1 P4 ftestosterone exposure as mentioned earlier because' R1 ?  R  `8 Q1 S
the exposure was not for a prolonged period of time.
; N' w4 W* \( C! U& L7 EAlthough the bone age was advanced at the time of& K6 r/ F# B1 x* T% w& G* H
diagnosis, the child had a normal growth velocity at$ ]% u4 Q9 @3 {$ u
the follow-up visit. It is hoped that his final adult
" ^8 S0 K* U% R" w( p! n$ {height will not be affected.
, x- J3 p* N8 ]. _Although rarely reported, the widespread avail-$ d5 L0 M% {; E
ability of androgen products in our society may4 q3 f& w& g& z
indeed cause more virilization in male or female- k6 B1 ~1 ?! b! x: V7 `
children than one would realize. Exposure to andro-2 p5 k6 m& r6 n4 W# l2 l
gen products must be considered and specific ques-% k' d8 w- l  |! W- k
tioning about the use of a testosterone product or
: B1 \9 r3 D4 @$ c7 ugel should be asked of the family members during1 l' v: S2 W& _- M2 j! R# U
the evaluation of any children who present with vir-& K6 z, L3 a7 p. A$ Z
ilization or peripheral precocious puberty. The diag-- H" z1 A, }; a" p% f" b
nosis can be established by just a few tests and by
' }' h& P9 F5 M$ k$ ^$ iappropriate history. The inability to obtain such a
6 ~8 s- J  h* x  x' ahistory, or failure to ask the specific questions, may
$ E1 C4 i. K6 g" Y3 {$ r, cresult in extensive, unnecessary, and expensive
2 `5 W0 Q& s% r* H$ y3 linvestigation. The primary care physician should be
; W: y7 U6 M/ b. J% Caware of this fact, because most of these children1 w+ |- M# y* v1 l; C8 O4 t! a5 U
may initially present in their practice. The Physicians’9 e% H5 B7 N* I  `- {
Desk Reference and package insert should also put a
/ X) h" v+ Q7 w; p4 T/ y3 kwarning about the virilizing effect on a male or
1 \. k6 D$ l) Q2 V& xfemale child who might come in contact with some-
3 ~- B$ K% g) y7 u6 }one using any of these products.5 ^4 f5 z& o/ ~2 W; Y4 c1 I
References
; R) S9 p' d; m2 Q1. Styne DM. The testes: disorder of sexual differentiation7 `5 c% v0 O  Y
and puberty in the male. In: Sperling MA, ed. Pediatric
* Y7 I# k: \9 e' X) K+ [/ P, lEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 P7 @- [' b) t1 Z; V. S6 t
2002: 565-628.
+ L# \2 O! U8 b: c. F2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% M  p' V$ g4 T) k8 Ipuberty 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
7 U/ j* s7 A6 s) d
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