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* C9 U' N( Z8 ?
Boy Induced by Indirect Topical
; u, e* g6 \3 y) `, t  ]) J: Y7 J8 fExposure to Testosterone# f) V+ _2 ~2 R& w, g
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: O# w0 b; B0 y2 x! m: r
and Kenneth R. Rettig, MD1
) e. B( `/ j7 L* _5 U; iClinical Pediatrics! r. F. p9 s  K
Volume 46 Number 6( l  R: y* c& X, ^" H% c& n
July 2007 540-5433 x2 `$ T4 G& g5 Z) D) N
© 2007 Sage Publications& L( M" J& z; T4 w3 \5 R1 M% t
10.1177/0009922806296651
/ a/ I, T; z0 x+ |http://clp.sagepub.com$ a: U( Q2 o0 K+ ~% B
hosted at9 i& F* W8 O1 R2 }# s, ]$ r* V: R
http://online.sagepub.com( f1 r2 F2 l" t  [) K
Precocious puberty in boys, central or peripheral,
1 k4 C. b. @% ^5 z7 M, N+ Tis a significant concern for physicians. Central
, {  t) E$ t9 @; z2 `" J( o- Wprecocious puberty (CPP), which is mediated
1 T1 g6 Q( S2 |; G* I8 zthrough the hypothalamic pituitary gonadal axis, has
, M; S( _9 H7 Wa higher incidence of organic central nervous system
4 a# a+ |3 O- z! F, \lesions in boys.1,2 Virilization in boys, as manifested
! [" h9 p+ {6 g) k4 Uby enlargement of the penis, development of pubic# ?: d2 D7 e8 c4 O  c- n! S
hair, and facial acne without enlargement of testi-
2 N4 z' b4 A5 D* scles, suggests peripheral or pseudopuberty.1-3 We+ s: |7 M& h  I$ w
report a 16-month-old boy who presented with the" _* {$ d# P! m+ c3 B+ V, l
enlargement of the phallus and pubic hair develop-
- T3 l) d6 h! c' {7 ?( N& r8 B3 Z" Oment without testicular enlargement, which was due/ q7 L4 V! E, J, B* Z' [% @
to the unintentional exposure to androgen gel used by9 n& w! e+ k6 z4 e6 i% P
the father. The family initially concealed this infor-
1 \8 d& J' u8 H, pmation, resulting in an extensive work-up for this
  g' ~" m* _" K2 r2 X" H2 Bchild. Given the widespread and easy availability of
, i0 b" b$ U5 G0 b0 Btestosterone gel and cream, we believe this is proba-! Z# u1 i; u1 [0 D
bly more common than the rare case report in the
5 D, i- N( @0 Lliterature.4
0 o* ?. {* g8 z- R  s$ M  _Patient Report: d; ?$ V5 b* G
A 16-month-old white child was referred to the
  \! C8 r( E1 O, k% t; L' Cendocrine clinic by his pediatrician with the concern; M* m0 |2 s6 l! }! i; O
of early sexual development. His mother noticed
/ f, K+ s2 G  `light colored pubic hair development when he was& j; d, i/ Q- ^
From the 1Division of Pediatric Endocrinology, 2University of
8 D* i$ G1 ?/ j5 d1 P$ qSouth Alabama Medical Center, Mobile, Alabama.
5 {) w) `/ h  a+ |Address correspondence to: Samar K. Bhowmick, MD, FACE,
: e* |5 \" C$ G/ o) H! `, A9 w- BProfessor of Pediatrics, University of South Alabama, College of; Z9 I( c/ {1 G, A- t, N
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) v. ^( C+ j/ A3 \6 ]5 h* S8 E
e-mail: [email protected].
) e; W' l% S) X1 N  }5 d# L: `# Labout 6 to 7 months old, which progressively became
" a% G7 W0 }* h. O* cdarker. She was also concerned about the enlarge-% ?6 @+ L  l+ t
ment of his penis and frequent erections. The child1 O% N6 F+ V' n
was the product of a full-term normal delivery, with
3 n5 Y8 {( K! k5 W: m  n1 G* L; Va birth weight of 7 lb 14 oz, and birth length of- ]7 x! V) L4 X" L: k" v
20 inches. He was breast-fed throughout the first year
/ a0 c$ r+ @+ {. F+ wof life and was still receiving breast milk along with
/ z4 w. Q7 X7 @+ T5 f4 K7 nsolid food. He had no hospitalizations or surgery,
8 _) o) r) U; W, Iand his psychosocial and psychomotor development
4 \1 e! ~% j( W0 a. G9 r9 M/ Swas age appropriate.  ?. u3 V7 X/ J3 l( \* N: }
The family history was remarkable for the father,, V7 h, P7 C- g) m! {
who was diagnosed with hypothyroidism at age 16,! c! j$ H1 O" _5 n0 z& @
which was treated with thyroxine. The father’s) `$ Y0 a/ o4 V
height was 6 feet, and he went through a somewhat
8 u! ^" ^7 i2 C, f6 j$ hearly puberty and had stopped growing by age 14.
: o$ U" O+ \) k  N# ]The father denied taking any other medication. The$ q. |) l) [1 t2 ^
child’s mother was in good health. Her menarche
* U0 Y+ L  j  t8 }2 vwas at 11 years of age, and her height was at 5 feet+ z8 f( l1 u& P+ q: Q
5 inches. There was no other family history of pre-/ v/ s% S2 T/ q6 x' I
cocious sexual development in the first-degree rela-* d. o2 }; O. ~9 ]
tives. There were no siblings.
: F" W8 U0 i6 qPhysical Examination& _1 H5 G5 g9 S8 B% P+ T
The physical examination revealed a very active,
# r4 g/ Z; b$ ?: O. X( Dplayful, and healthy boy. The vital signs documented
8 ?4 U5 A7 T5 {; J0 @0 m+ va blood pressure of 85/50 mm Hg, his length was8 l- k) C6 H' m  W
90 cm (>97th percentile), and his weight was 14.4 kg2 _' I; Q5 {; N1 D* h6 N
(also >97th percentile). The observed yearly growth$ Z8 V* i7 q! v9 _5 C; F1 b
velocity was 30 cm (12 inches). The examination of/ J4 t8 ~. Z( x
the neck revealed no thyroid enlargement.% X1 J' {+ T! b/ i4 c
The genitourinary examination was remarkable for
  L* O! C! I0 s9 [enlargement of the penis, with a stretched length of
% q5 J6 d) l3 s& C) d$ `! N% U- j8 cm and a width of 2 cm. The glans penis was very well
7 |) {$ Y4 k4 ^" P; Jdeveloped. The pubic hair was Tanner II, mostly around
+ s2 m  H. `( T% h. K; N- a# p/ F% U540
' p* r; g5 y. [& {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ T+ I, X/ E  x  qthe base of the phallus and was dark and curled. The
: V7 C: _, i+ J4 ftesticular volume was prepubertal at 2 mL each.
, `* q) F( Y+ NThe skin was moist and smooth and somewhat
! |/ K. c' p- ^. ?# M3 _oily. No axillary hair was noted. There were no1 H8 d; z1 X) p
abnormal skin pigmentations or café-au-lait spots./ ~7 u# O0 S, U4 l, x' i/ L
Neurologic evaluation showed deep tendon reflex 2+9 Y9 R  X) ~& W  S
bilateral and symmetrical. There was no suggestion( j+ ^9 p9 n" X
of papilledema.
( {5 w6 N8 N, L) A" m5 fLaboratory Evaluation4 q) _  c- P2 j( ?. n' D
The bone age was consistent with 28 months by
& \! Q; d8 A" ]3 \  |8 \3 nusing the standard of Greulich and Pyle at a chrono-" W& ^, d- r5 [$ L, I4 ]) ?9 U
logic age of 16 months (advanced).5 Chromosomal3 y  S. f0 Y9 l, j' h0 W
karyotype was 46XY. The thyroid function test% }' v. {4 u- {( J0 ]# _+ m* G7 b
showed a free T4 of 1.69 ng/dL, and thyroid stimu-" C1 F' P% r# j
lating hormone level was 1.3 µIU/mL (both normal).- G3 `: p8 c/ S$ E7 d$ z
The concentrations of serum electrolytes, blood
& I6 Q5 Y6 B  p. M6 gurea nitrogen, creatinine, and calcium all were
, f+ D+ ~$ W5 _3 \within normal range for his age. The concentration; w* Y6 p* ]0 X2 k; _- b$ J
of serum 17-hydroxyprogesterone was 16 ng/dL+ X" S% e- X* c/ N- W- C
(normal, 3 to 90 ng/dL), androstenedione was 20
; ]% l% E, u: {; e( nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
+ J, Z3 p$ Y; ~. r0 M% ~terone was 38 ng/dL (normal, 50 to 760 ng/dL),. r* D- l6 P7 k$ Q/ Q$ ^
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ @: Z" J( ?; A. Z& W49ng/dL), 11-desoxycortisol (specific compound S)8 O2 V7 `- n# e
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! v" g; P* N0 T; r! F
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ t( c/ U6 [6 {3 W2 l( M4 F% U2 Q
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),) F* y0 m0 S! |4 t% w& S- t, @
and β-human chorionic gonadotropin was less than
( O0 }( `  W1 |8 e9 L! d- k- ]- H5 mIU/mL (normal <5 mIU/mL). Serum follicular9 i% l6 L& y+ v  X# [
stimulating hormone and leuteinizing hormone
/ X: b; I5 [( o: U; N1 Zconcentrations were less than 0.05 mIU/mL/ t- {& V8 y4 m
(prepubertal)." t- z. R$ D+ O5 O* p* O1 H
The parents were notified about the laboratory
! ]" ]+ _- n& q  ]6 @results and were informed that all of the tests were
8 @# t6 X; r% Y% Z2 S# g2 snormal except the testosterone level was high. The8 G8 k" N' q, z% X
follow-up visit was arranged within a few weeks to; D9 K- c, Y/ K$ E' }/ V1 B
obtain testicular and abdominal sonograms; how-3 L! A4 W$ I9 s3 m$ ^1 D
ever, the family did not return for 4 months.( j" g: u/ ?) Z* i% S2 B3 b
Physical examination at this time revealed that the
0 N5 x3 A) o! E- y) H% p( {; p8 Z; X$ ]child had grown 2.5 cm in 4 months and had gained1 H) D/ W2 N" c
2 kg of weight. Physical examination remained
2 D) u7 o* J( n' f+ T. {unchanged. Surprisingly, the pubic hair almost com-% r1 Q2 m5 k6 H! W
pletely disappeared except for a few vellous hairs at
# s0 @8 F4 Q$ A; {) A7 Tthe base of the phallus. Testicular volume was still 21 S# ]! F8 E$ r, V: \+ x, f
mL, and the size of the penis remained unchanged.
. q# O9 l2 b, n$ d+ ^# iThe mother also said that the boy was no longer hav-
3 C, [6 ~7 P" t2 ping frequent erections.* x- z8 l5 O5 O% I* u7 b! J9 G
Both parents were again questioned about use of
; H1 S/ C+ A( C( tany ointment/creams that they may have applied to8 z' y+ ^) I2 B5 I7 c
the child’s skin. This time the father admitted the7 m! b- M4 x1 r5 C" b7 S
Topical Testosterone Exposure / Bhowmick et al 541
8 {. m4 _9 v: i( {1 ^use of testosterone gel twice daily that he was apply-
4 e4 ^( S$ L5 P0 P$ |, p" e( _* ?ing over his own shoulders, chest, and back area for7 Y( ?6 {1 Y% A+ x. w
a year. The father also revealed he was embarrassed+ o2 L1 n1 U! c# ^& K" }
to disclose that he was using a testosterone gel pre-
: q' n+ ~+ D% Wscribed by his family physician for decreased libido
$ k+ `% w; S- B# s( x9 N$ nsecondary to depression.7 t9 G" a6 l6 A
The child slept in the same bed with parents.! C( R8 U. _6 `' e1 V; Z3 R
The father would hug the baby and hold him on his, M; l) L3 z* O
chest for a considerable period of time, causing sig-, y. X' ]; T4 F
nificant bare skin contact between baby and father.
$ z6 i% i% l' q; Z- d8 z: @/ G$ GThe father also admitted that after the phone call,
8 q1 `; A. g0 `9 v% ?  a% N4 lwhen he learned the testosterone level in the baby! \( C* w, Y. y, w# ~; u
was high, he then read the product information9 x, }% R9 h, t3 M( p! M& [
packet and concluded that it was most likely the rea-
+ g2 l' \  G" i8 Json for the child’s virilization. At that time, they
6 u0 h: Q" T1 \, adecided to put the baby in a separate bed, and the
% o2 N, p$ G. S% o- Q1 Jfather was not hugging him with bare skin and had
( M. o4 w4 R" R8 C7 O" _8 kbeen using protective clothing. A repeat testosterone
, Q$ H. M6 S! R8 A$ c9 atest was ordered, but the family did not go to the5 v9 v6 G) U( C# j0 d9 ]/ `* |
laboratory to obtain the test.  N! S0 D5 U: P; {; P
Discussion3 p# Q" O4 P* s6 h: `
Precocious puberty in boys is defined as secondary% X$ e. T% \' e. s0 N8 |: i" D# Y
sexual development before 9 years of age.1,4
7 ~+ D% m  ]2 F3 i! i( W' p3 HPrecocious puberty is termed as central (true) when! P: o4 z& _7 n
it is caused by the premature activation of hypo-
: d) {, O$ G: q1 J" A/ C/ {! cthalamic pituitary gonadal axis. CPP is more com-! M. `( V3 G! F$ D: f. `# e
mon in girls than in boys.1,3 Most boys with CPP9 O6 E. n( x! Y3 E2 P; b9 ]3 l
may have a central nervous system lesion that is2 R( }; J; E$ @0 T1 C/ a
responsible for the early activation of the hypothal-: m( g" Y' i1 g9 L/ K
amic pituitary gonadal axis.1-3 Thus, greater empha-
+ C% h8 o+ E0 Z, S% Hsis has been given to neuroradiologic imaging in  y+ B+ \9 ]8 k" `) i
boys with precocious puberty. In addition to viril-; @1 d5 u5 p, ]9 L" V
ization, the clinical hallmark of CPP is the symmet-! O/ j  `  C4 n3 c$ k3 ~
rical testicular growth secondary to stimulation by
9 f0 m6 w: B+ x3 s- T2 m; f) kgonadotropins.1,3" ]  c8 R3 Y8 `/ a' n
Gonadotropin-independent peripheral preco-
+ M: S( P( ~- Q8 l: p2 Kcious puberty in boys also results from inappropriate
/ _9 T0 ~2 N) Q# ]& fandrogenic stimulation from either endogenous or
$ e  ^- i( A) B$ T1 x! @2 k7 aexogenous sources, nonpituitary gonadotropin stim-) ?& Y3 c1 W; L& y1 M0 G$ Y! S
ulation, and rare activating mutations.3 Virilizing) ^/ z; z5 @4 l/ c) a
congenital adrenal hyperplasia producing excessive
/ D6 q3 j) L) o  Nadrenal androgens is a common cause of precocious9 P0 |' J( s0 J$ y3 L7 G
puberty in boys.3,4" Q+ h, d0 ~: w% I0 k; y; q
The most common form of congenital adrenal
6 J1 n( y9 H5 d) N6 h- I5 b$ T; ghyperplasia is the 21-hydroxylase enzyme deficiency.& h, ]  x) S8 x6 W+ V5 \5 G# W
The 11-β hydroxylase deficiency may also result in; X7 B9 ]) X% W5 j
excessive adrenal androgen production, and rarely,
( ^# N9 E5 t$ Zan adrenal tumor may also cause adrenal androgen
0 O# g0 Y8 Q( d- ~: _: S" eexcess.1,35 i5 l& K$ t# c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; M2 q2 H% R: }8 k( d2 x: }
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 J5 z5 Y" U0 BA unique entity of male-limited gonadotropin-
( K- H: Q0 l8 U7 e; Sindependent precocious puberty, which is also known
1 w) e6 s$ j5 ]as testotoxicosis, may cause precocious puberty at a
6 h% k7 m% B. j) y9 gvery young age. The physical findings in these boys" Z9 p2 F3 _" u. ~
with this disorder are full pubertal development,2 a9 I2 P8 p/ e7 s* ~1 j
including bilateral testicular growth, similar to boys# u! x. m, `5 s" b. d" m
with CPP. The gonadotropin levels in this disorder
9 O, c3 N" b$ R' a% J1 w/ kare suppressed to prepubertal levels and do not show
: s; l1 d9 E( u* Y2 N4 |. apubertal response of gonadotropin after gonadotropin-# g( p- |4 a- j
releasing hormone stimulation. This is a sex-linked
+ j$ R# ^. l/ u) {* Q; i/ A9 Lautosomal dominant disorder that affects only* l, ^5 Z# n7 B4 h4 A4 w, t
males; therefore, other male members of the family1 ^. Z( h4 K7 k8 f2 Q
may have similar precocious puberty.3/ U, o4 F* \$ v+ A& y) g- t8 i
In our patient, physical examination was incon-8 s" {. l* J$ J+ I$ P
sistent with true precocious puberty since his testi-- n) x7 K' z1 K1 ^
cles were prepubertal in size. However, testotoxicosis  R9 O, w; V7 U5 a  L* U
was in the differential diagnosis because his father
! u5 `- h" Y" P! S( i8 @5 j/ Qstarted puberty somewhat early, and occasionally,1 I# k! W+ C0 ^+ T8 h& y  ^* j; ]0 K" w
testicular enlargement is not that evident in the
6 K4 V0 B; I7 \) R/ w/ ibeginning of this process.1 In the absence of a neg-. r4 ]9 e+ i2 T5 L- D1 c
ative initial history of androgen exposure, our
+ I5 Y# _! z( h, qbiggest concern was virilizing adrenal hyperplasia,* H) G+ }! V, ^" l2 I
either 21-hydroxylase deficiency or 11-β hydroxylase* h5 Z2 J, z. n0 E" H( N
deficiency. Those diagnoses were excluded by find-1 ^9 x* P! ?" F; o! B8 O0 k7 ~8 f) ^
ing the normal level of adrenal steroids.0 t1 b3 H& W# E6 r; z- b; f
The diagnosis of exogenous androgens was strongly9 ?  r2 W2 m" ^4 T2 R! i
suspected in a follow-up visit after 4 months because0 P* b1 R5 b4 F9 T7 x
the physical examination revealed the complete disap-7 D5 }1 g: V" w  v8 \; }1 k
pearance of pubic hair, normal growth velocity, and
; h$ ?5 z" T3 I8 |; D- jdecreased erections. The father admitted using a testos-
8 z) u& R* J% P8 L4 w; pterone gel, which he concealed at first visit. He was
7 f" J1 z! g) j: Gusing it rather frequently, twice a day. The Physicians’& m! ]2 G  M0 ?. L
Desk Reference, or package insert of this product, gel or# \4 a4 T" O0 }: _
cream, cautions about dermal testosterone transfer to
* J: o/ }( y8 s0 a* g7 vunprotected females through direct skin exposure.
9 o7 Q$ f' r6 S8 x# TSerum testosterone level was found to be 2 times the6 Y" H7 ?: O: t& d9 F
baseline value in those females who were exposed to# y. {: Q1 N# \  S
even 15 minutes of direct skin contact with their male
* P8 a, r+ X2 o8 d! h& a2 spartners.6 However, when a shirt covered the applica-& N9 a  D! I. }' A
tion site, this testosterone transfer was prevented.3 b9 o& n2 _$ w, P2 \6 A
Our patient’s testosterone level was 60 ng/mL,* H( F! Q$ j2 E5 y% }
which was clearly high. Some studies suggest that; q: w9 c) w. E
dermal conversion of testosterone to dihydrotestos-0 Z, c' a- y6 G" X" x+ I
terone, which is a more potent metabolite, is more
- c! M3 ~/ L; r5 D; Xactive in young children exposed to testosterone
; Q+ p# D5 \* g  `exogenously7; however, we did not measure a dihy-
! O! m: \: Q% i3 C0 R. L7 M& Pdrotestosterone level in our patient. In addition to* u* T. H7 [  \, Y. ^0 f* _) Z
virilization, exposure to exogenous testosterone in
! @: }9 m+ y) j: Kchildren results in an increase in growth velocity and* A% {- Y- K2 ?; N  v/ @
advanced bone age, as seen in our patient.2 {# S; h5 P" O, D9 X- o
The long-term effect of androgen exposure during9 q4 w9 D: C' s0 E2 Z. v
early childhood on pubertal development and final7 Z* R; e3 }0 b- G
adult height are not fully known and always remain$ s* h1 p, U- e# w$ K" B0 n4 @
a concern. Children treated with short-term testos-
" D$ z; J9 Y' g* v# Q7 W" Wterone injection or topical androgen may exhibit some" P3 Z) _; g+ @3 i4 n; i
acceleration of the skeletal maturation; however, after
# k9 w. H, K* u' O- Scessation of treatment, the rate of bone maturation* H$ g8 k: j8 S" v
decelerates and gradually returns to normal.8,9$ z# @5 H0 C+ h' ~/ X, E
There are conflicting reports and controversy
! Y$ t6 L$ S/ ]over the effect of early androgen exposure on adult3 G8 |! t( \, S4 A7 ]9 F8 c
penile length.10,11 Some reports suggest subnormal
1 N! a* r9 Z/ L. B% kadult penile length, apparently because of downreg-& s8 v7 y  s, i! \7 ~* U# L
ulation of androgen receptor number.10,12 However,1 @' c; G9 g$ k. u) R
Sutherland et al13 did not find a correlation between
& p( G; A9 ]/ w5 \. o2 W3 F4 u6 ychildhood testosterone exposure and reduced adult1 E/ Y7 q$ ]( X: |
penile length in clinical studies.
: ^! `' t& }6 n7 QNonetheless, we do not believe our patient is3 K  p# T! P, `  ], D5 s# i6 O  z
going to experience any of the untoward effects from
% }: p1 S) ?; N3 M' K. B! r9 D$ R3 f' dtestosterone exposure as mentioned earlier because  {2 P9 [! F# F! e
the exposure was not for a prolonged period of time.: u! _  F' c. E, U1 |& d' h) w8 n
Although the bone age was advanced at the time of
- I! J. B, E6 ^9 ?2 U6 D, V' Udiagnosis, the child had a normal growth velocity at& ^/ r9 O/ e! j/ P  C* d( C
the follow-up visit. It is hoped that his final adult
1 E- f2 x3 x3 t& m( g$ Qheight will not be affected.
% m( u0 R) O7 [+ J$ s5 W" e* tAlthough rarely reported, the widespread avail-
* ]+ a: A4 U1 E( F4 uability of androgen products in our society may
, f/ [( b* v4 y, m7 }' Aindeed cause more virilization in male or female
: t8 [" ?& B$ U/ z' s) ychildren than one would realize. Exposure to andro-
3 v/ A) u* I% Ygen products must be considered and specific ques-
' B! `* u1 C* r" I8 H# jtioning about the use of a testosterone product or
+ ^& \& e9 w! P5 d+ q6 v6 L$ U  I4 z/ |gel should be asked of the family members during. |+ s# M) }- h0 v
the evaluation of any children who present with vir-
0 a$ ?$ f( L2 E* u. A( Bilization or peripheral precocious puberty. The diag-
. O, R2 E6 L% x. _- p# Knosis can be established by just a few tests and by
1 e3 Y& j: O+ D/ x( H# N: `' dappropriate history. The inability to obtain such a4 c5 ?) h* q( q6 ?
history, or failure to ask the specific questions, may  s- t7 c5 P  ^" s
result in extensive, unnecessary, and expensive3 H$ M- q/ N/ X4 B# q
investigation. The primary care physician should be
# S' ?; W& R0 e" saware of this fact, because most of these children5 X( ~6 Q" u, s1 w. S; C. ~( a
may initially present in their practice. The Physicians’
8 f) |6 j" Z3 ]Desk Reference and package insert should also put a
- u( `; L' g! n  m4 O  xwarning about the virilizing effect on a male or) y7 |4 f4 I& ?2 ]4 Q5 e
female child who might come in contact with some-
6 }% ]# g; p) O! c+ k( V0 Gone using any of these products.
6 }0 O) I! V3 I# W. p: k$ }References. y, }, y4 X- Z$ b/ w4 n/ Z
1. Styne DM. The testes: disorder of sexual differentiation" X, x' }% B6 @: j; T
and puberty in the male. In: Sperling MA, ed. Pediatric
+ ?8 y  _: Y3 _1 }1 v1 pEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 F4 D) K3 s0 _6 l2002: 565-628.
, ?- r9 o, Q% h6 L+ g8 g# [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  q0 A6 F& E+ ^. U/ N5 |3 jpuberty 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
- ?9 g" R* \2 {/ u# O0 UBoy Induced by Indirect Topical% ~( `8 b3 U  ~0 Z" T, {
Exposure to Testosterone
* C; X2 u1 k2 nSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( a) D4 M5 I6 G8 }# F! K/ ^- Y2 M& u7 U& w
and Kenneth R. Rettig, MD1
7 `" \7 T; }1 w: a0 Q! S0 RClinical Pediatrics4 K( j7 [- `9 |" d$ i' Q" c
Volume 46 Number 6; ?8 q6 `* o) k$ c
July 2007 540-543
+ @1 e/ L: O0 P$ j/ K- K© 2007 Sage Publications
2 f; V  _, I6 n  i) T+ ]% m; k, w4 @10.1177/0009922806296651
# ?& o; j4 j1 G5 u" g$ H& j- e$ N& rhttp://clp.sagepub.com. D: x" {, Z! H: D) K, {
hosted at
7 v; U3 l* V  W6 d% L' Y% W) uhttp://online.sagepub.com- \  v  K) E. D3 W0 m
Precocious puberty in boys, central or peripheral,
) ]9 @" a8 E8 |. q+ m+ G4 D+ [is a significant concern for physicians. Central7 G4 a# H7 H8 D, H
precocious puberty (CPP), which is mediated
; E3 ~7 e  q3 q. M3 F" o5 g6 A$ athrough the hypothalamic pituitary gonadal axis, has
) N3 z5 A& {$ d' u: v4 Qa higher incidence of organic central nervous system
& N3 o4 U  c8 X1 {- f. ^! C5 Glesions in boys.1,2 Virilization in boys, as manifested
1 V' t* j; g0 d4 X# x+ _8 q6 {by enlargement of the penis, development of pubic, f/ H& N7 z% [" x; x
hair, and facial acne without enlargement of testi-
! m1 Y) `9 i2 U6 ~. F8 [  \cles, suggests peripheral or pseudopuberty.1-3 We' L  L' Z' q) p! C5 a/ H+ Z
report a 16-month-old boy who presented with the
- @" T- _& P) i) E: Jenlargement of the phallus and pubic hair develop-
/ u$ X2 Y* z; F8 P  s5 dment without testicular enlargement, which was due
9 M2 {6 g; K  h( yto the unintentional exposure to androgen gel used by
) Y/ D) L' L. E/ }" A. i* Ethe father. The family initially concealed this infor-9 f- K. \" H4 `, `! u6 G
mation, resulting in an extensive work-up for this* I1 ^; I2 c7 x$ |' ^. H
child. Given the widespread and easy availability of: G+ [/ y4 v- z" z' H) t
testosterone gel and cream, we believe this is proba-7 b8 ?: S, e0 l2 S5 ?6 l3 _, D
bly more common than the rare case report in the$ s$ Y7 `# U; E. g9 ?
literature.4
8 I8 @3 u- d; A8 {% k) Y2 MPatient Report
2 K. G2 T) H2 h( J0 YA 16-month-old white child was referred to the
; i: N+ X1 K( b6 J  B  H5 P  r3 v; x9 Iendocrine clinic by his pediatrician with the concern$ a0 Q* d; R' G$ z
of early sexual development. His mother noticed
& g) D( K8 p! o! A. W3 m+ `2 e! R/ mlight colored pubic hair development when he was( B( f5 b2 V, j$ D& o
From the 1Division of Pediatric Endocrinology, 2University of
3 E) J3 W! X* n% b7 ZSouth Alabama Medical Center, Mobile, Alabama.% Z- ~# y! ]2 _8 p
Address correspondence to: Samar K. Bhowmick, MD, FACE,
9 c3 C' ]4 J: g2 w; m; T. L7 |Professor of Pediatrics, University of South Alabama, College of
1 z0 c# W8 R$ n  M* A  OMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) r. C  U/ T$ le-mail: [email protected].
' G' M! f! Z! c/ j5 z, cabout 6 to 7 months old, which progressively became- P- \" ]( _0 D+ ]# R; m" \( w( Q! d: N
darker. She was also concerned about the enlarge-
) H# P0 v3 y5 j/ x; a3 ement of his penis and frequent erections. The child
% C5 M. C/ w' y) xwas the product of a full-term normal delivery, with
' t( S7 m6 m/ T7 A  u' Ea birth weight of 7 lb 14 oz, and birth length of
2 `6 M) C; T0 q8 x) ~- K* B* o! n8 k- k20 inches. He was breast-fed throughout the first year+ H# c0 k$ {: j" Q/ u
of life and was still receiving breast milk along with
0 K+ K/ J* m" [: }! t, bsolid food. He had no hospitalizations or surgery,
4 b! @2 {8 x6 b& hand his psychosocial and psychomotor development
3 ?4 G. o6 A9 I# w6 ?/ Owas age appropriate.1 i( S* g# U; o( a0 c( Z
The family history was remarkable for the father,  g1 D3 F8 r% z  M9 e- a9 W
who was diagnosed with hypothyroidism at age 16,& i- ]0 p% n7 E
which was treated with thyroxine. The father’s# o4 Q0 ^9 C6 p
height was 6 feet, and he went through a somewhat+ [' F) [6 |" Q
early puberty and had stopped growing by age 14." u5 n6 ~; G8 p0 E
The father denied taking any other medication. The. `/ B  t- r, D) s
child’s mother was in good health. Her menarche" K$ N3 F( E) W  ~, W
was at 11 years of age, and her height was at 5 feet
% w0 m" F6 u8 k6 v& ]5 K2 G5 inches. There was no other family history of pre-
* a1 M! k  w8 d6 G! I3 K2 ucocious sexual development in the first-degree rela-
2 G# `% L7 W  S+ P6 ftives. There were no siblings.
& W' |, l+ ]6 BPhysical Examination
$ [  @6 `4 d& ~The physical examination revealed a very active,
5 A8 B0 c# A, Y2 ~4 E3 v3 _7 yplayful, and healthy boy. The vital signs documented( Y8 k( c5 Y' P: Q; c2 K
a blood pressure of 85/50 mm Hg, his length was4 o4 ?7 d3 D3 P. U& q
90 cm (>97th percentile), and his weight was 14.4 kg
6 O  Y5 ^2 @  A7 l! [/ ^( {(also >97th percentile). The observed yearly growth
" }% h- C. @. Gvelocity was 30 cm (12 inches). The examination of
8 L% n/ y( q% X& Fthe neck revealed no thyroid enlargement.
& d3 x4 E( X0 E  a3 sThe genitourinary examination was remarkable for& Z% b' B# l2 T& i2 U( {; T: u" V
enlargement of the penis, with a stretched length of
2 H% O& S' N2 [3 Y6 @. |& u' e8 cm and a width of 2 cm. The glans penis was very well9 t9 B1 k% u3 h3 x: A  s  J( M
developed. The pubic hair was Tanner II, mostly around
6 U9 V" I1 N8 X540
7 A$ D' M) Y3 i( y/ R. e0 C+ gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 W& P. X1 n; d; {5 A4 P! i! kthe base of the phallus and was dark and curled. The  D; z9 ?5 C- {: {7 L7 n$ P
testicular volume was prepubertal at 2 mL each.
% Q' ?+ s' }  }2 iThe skin was moist and smooth and somewhat" R! p# [: I; F, {% v1 s4 R* y
oily. No axillary hair was noted. There were no
- V: V" c; m9 G9 q/ D8 Pabnormal skin pigmentations or café-au-lait spots./ U  W% s$ N; X9 f, _5 B' J% T
Neurologic evaluation showed deep tendon reflex 2+6 u  d# }2 G7 y& V9 Q& T4 I8 c
bilateral and symmetrical. There was no suggestion, f7 ?" Y% x/ V
of papilledema.
" Y9 B& {6 j/ p6 pLaboratory Evaluation# C: }- c6 b- [/ v5 y% w
The bone age was consistent with 28 months by
5 w5 `% }7 r' Jusing the standard of Greulich and Pyle at a chrono-
; _* @5 z- s9 J& X% x9 T. Z1 glogic age of 16 months (advanced).5 Chromosomal! T' r. C' @; X3 C0 z" c
karyotype was 46XY. The thyroid function test$ @* c7 o3 i8 R: x( g. E+ q
showed a free T4 of 1.69 ng/dL, and thyroid stimu-& \% t, L2 W9 M) W$ m4 m
lating hormone level was 1.3 µIU/mL (both normal).- D6 d  B9 `" A; r
The concentrations of serum electrolytes, blood9 p, \& q' \* W8 P  ~4 p
urea nitrogen, creatinine, and calcium all were! l0 B4 _  b8 l9 l* M" A
within normal range for his age. The concentration+ Z4 g  T2 e  Y0 q! J: c; J  e  ^
of serum 17-hydroxyprogesterone was 16 ng/dL
: `2 Y0 M4 P# S: }6 l  T% L(normal, 3 to 90 ng/dL), androstenedione was 206 `( `/ [3 V* U. ~
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 r9 L6 |1 ~/ F: c7 Zterone was 38 ng/dL (normal, 50 to 760 ng/dL),5 O1 P( Q, r# M! K4 n4 G+ \/ J* o
desoxycorticosterone was 4.3 ng/dL (normal, 7 to5 W/ _* ?/ ?: k+ }5 H3 t
49ng/dL), 11-desoxycortisol (specific compound S)9 M2 r' M6 {7 d! ]% W$ ^
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 b+ v9 O9 o/ L; [1 ~1 B& ^7 p
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
2 G- k$ }; Z: {. w  `; i0 gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) G: L. Q0 [( J: [and β-human chorionic gonadotropin was less than
% G+ K  J' ~7 j5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 f3 u! t( S& n  cstimulating hormone and leuteinizing hormone
! _. _0 A; V" j2 fconcentrations were less than 0.05 mIU/mL* x! {8 a2 o' S% v' m, j) U
(prepubertal).
" @! T  A  Q, V+ O/ k/ q$ Y! rThe parents were notified about the laboratory
1 S5 I& S: X- sresults and were informed that all of the tests were
7 H' x% a8 t1 W* D0 Z" Znormal except the testosterone level was high. The$ F" }4 L  y7 Y# E
follow-up visit was arranged within a few weeks to
  ^9 n& m/ r& [- e$ D/ G( uobtain testicular and abdominal sonograms; how-
6 E) _+ E0 [( Iever, the family did not return for 4 months." [+ w7 [! l  f+ `  N
Physical examination at this time revealed that the  p( S+ Y" d$ I0 k2 p
child had grown 2.5 cm in 4 months and had gained
: Q0 h  P+ {! Z. U' `" a& ]4 J2 kg of weight. Physical examination remained2 A# }- O! e! Z7 E/ g$ X% g
unchanged. Surprisingly, the pubic hair almost com-
- @$ u0 B9 ~% ~) l, k  P& ~pletely disappeared except for a few vellous hairs at0 X5 L! w9 H: Q/ d6 M
the base of the phallus. Testicular volume was still 27 s* V3 ~$ ^9 j/ f$ `2 {
mL, and the size of the penis remained unchanged.
0 I5 ?0 Z! M2 ^  X. H( OThe mother also said that the boy was no longer hav-( \$ c) }; G' n! k! u
ing frequent erections.6 @# D2 g  W, M9 O, }! ~. @
Both parents were again questioned about use of
3 H3 m8 K$ H( W8 Zany ointment/creams that they may have applied to3 w( F5 g5 E+ d8 d3 q( y
the child’s skin. This time the father admitted the3 z: W1 f6 X; O( e3 F
Topical Testosterone Exposure / Bhowmick et al 541
* l' `$ D; }' R, p1 @use of testosterone gel twice daily that he was apply-9 s4 V7 d9 G7 A7 u: h& n) U& g
ing over his own shoulders, chest, and back area for
8 j7 R8 }& F5 y3 Va year. The father also revealed he was embarrassed3 x$ d# j& m6 M, W( P! @
to disclose that he was using a testosterone gel pre-2 Q  P* V5 T; N' R, t- d# m/ Z% H
scribed by his family physician for decreased libido
# |0 v! ?" X1 ^7 X7 p8 y+ ]$ Esecondary to depression.' t5 `! a4 c5 b1 e: V( j* i! e8 e  [& Y
The child slept in the same bed with parents.' i" j, m8 C+ h8 s! l
The father would hug the baby and hold him on his
0 \& J3 Z) ~0 S6 ?& Y; Kchest for a considerable period of time, causing sig-
( ~7 z( \5 d* k( B4 q9 O1 R, knificant bare skin contact between baby and father.. u( Q% Y) o. ^  H- J9 y# o
The father also admitted that after the phone call,0 C) b# L0 h+ a# O$ q
when he learned the testosterone level in the baby
6 Y' w& i6 Z3 N# Bwas high, he then read the product information
7 [+ R8 s+ B2 opacket and concluded that it was most likely the rea-
4 v9 U, n( Z0 K# ]) L& Wson for the child’s virilization. At that time, they
! O* h5 I* l; @8 b* Ddecided to put the baby in a separate bed, and the
  @4 A5 y( d" H, w$ hfather was not hugging him with bare skin and had( S0 @! ]- Q) y( p
been using protective clothing. A repeat testosterone
1 T2 |2 z, l: z# j+ Mtest was ordered, but the family did not go to the
' G" ]0 ^+ m8 n2 _. [! ^laboratory to obtain the test.
4 @3 P# l5 N4 t1 d' vDiscussion
' X3 Y: T, I+ m6 ]0 S" k. o0 LPrecocious puberty in boys is defined as secondary
7 Q! B' b1 \) V$ q6 ]: r9 k" Jsexual development before 9 years of age.1,4
% f0 r' O  C8 l3 M* g- @Precocious puberty is termed as central (true) when3 R# Z  Y5 ]: U) R" I0 w* _8 V& i0 h
it is caused by the premature activation of hypo-( Z* {9 f" }9 c0 X* j: u9 p! }
thalamic pituitary gonadal axis. CPP is more com-0 _( {# J0 r. n7 Q
mon in girls than in boys.1,3 Most boys with CPP6 ~" B5 A% _5 L- M* |' J" B! @# p% [
may have a central nervous system lesion that is
" ?8 g; \" E$ n: `responsible for the early activation of the hypothal-
& p: V/ q; t, namic pituitary gonadal axis.1-3 Thus, greater empha-
! n6 R8 J+ c. G- b+ X; Z; c, gsis has been given to neuroradiologic imaging in
3 J# R, \, _/ W& kboys with precocious puberty. In addition to viril-, N4 }8 @7 i+ C* N- q) g) f
ization, the clinical hallmark of CPP is the symmet-, b) J# q9 i: \* x% I0 }1 N+ a
rical testicular growth secondary to stimulation by; V6 T: v* a7 @
gonadotropins.1,3
3 P0 p) Q1 V3 x' }0 BGonadotropin-independent peripheral preco-7 W* T1 G$ T7 D# S, z8 D
cious puberty in boys also results from inappropriate; z6 ]2 D: {! E3 V: O. V! s6 _! F, t
androgenic stimulation from either endogenous or
) C- N+ _: z" r( G! L" Q6 n, Bexogenous sources, nonpituitary gonadotropin stim-% f9 W+ ]9 t* N5 _, U
ulation, and rare activating mutations.3 Virilizing  _5 x; D) U0 @* j% w  E
congenital adrenal hyperplasia producing excessive. B/ Z' f' h6 b: q. M# T
adrenal androgens is a common cause of precocious: W: @( c' _( V& u
puberty in boys.3,4) ^  n. ^/ C$ ~0 Z% c7 H
The most common form of congenital adrenal2 |1 E7 Y8 ~2 {2 n) H5 S$ l
hyperplasia is the 21-hydroxylase enzyme deficiency.
; Y9 v6 Q7 h8 e+ i2 l' T4 q) CThe 11-β hydroxylase deficiency may also result in; W$ K( Q6 Q; n4 R+ [
excessive adrenal androgen production, and rarely,
: S3 S5 Q2 _5 `/ A" Pan adrenal tumor may also cause adrenal androgen% G' x6 X3 ~. x
excess.1,3
* B! S* j) \5 cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* @/ ]" @" C9 n" l% _- Z7 `8 @542 Clinical Pediatrics / Vol. 46, No. 6, July 20077 d# E4 _( [0 E
A unique entity of male-limited gonadotropin-) B: `; M* M5 T) K/ x
independent precocious puberty, which is also known8 c" k3 j. _- \" X& C
as testotoxicosis, may cause precocious puberty at a
& o8 g% w" U% t- b! w/ Svery young age. The physical findings in these boys4 G. g1 ^- x" k" L- n1 d0 n
with this disorder are full pubertal development,/ P  U$ `3 Z6 L; G
including bilateral testicular growth, similar to boys/ S3 J  e( a5 w5 q' k
with CPP. The gonadotropin levels in this disorder
8 x- ^  M, f) W6 k+ Qare suppressed to prepubertal levels and do not show: [5 C" u0 V+ D$ k0 F0 U+ `' @7 ]
pubertal response of gonadotropin after gonadotropin-
0 u, X, F" i/ L, `% Rreleasing hormone stimulation. This is a sex-linked+ W: h; Q$ Z6 }% e
autosomal dominant disorder that affects only- S& i$ H% V5 B* j9 E
males; therefore, other male members of the family: d- D, n, L4 C7 t6 |- x
may have similar precocious puberty.34 n7 P% a9 ~2 \* i9 T) `
In our patient, physical examination was incon-
4 Z+ g/ @: U4 @" Y9 fsistent with true precocious puberty since his testi-
4 w% W0 }; x  @$ ?cles were prepubertal in size. However, testotoxicosis
# v8 M8 Q9 |/ w* kwas in the differential diagnosis because his father
" P9 @: [9 U1 q3 ?started puberty somewhat early, and occasionally,$ e: w8 H/ ^, u* @9 L1 M; c) k
testicular enlargement is not that evident in the7 [- f5 U# ~. {- J+ N7 [
beginning of this process.1 In the absence of a neg-: |6 U7 ?3 `, I- C( `
ative initial history of androgen exposure, our7 y9 U, M5 A" I( Q1 v* r8 `6 H
biggest concern was virilizing adrenal hyperplasia,) S5 G# N5 v: J& l/ Z
either 21-hydroxylase deficiency or 11-β hydroxylase* J' x2 r- K0 P/ W& M
deficiency. Those diagnoses were excluded by find-3 V) h- c$ G' L/ l! i4 c
ing the normal level of adrenal steroids.
3 ~- h+ ]6 v: D$ eThe diagnosis of exogenous androgens was strongly1 m4 |- s$ G: |
suspected in a follow-up visit after 4 months because( w# j) H, H2 z' W8 ^
the physical examination revealed the complete disap-
. R9 P9 b8 v- ^0 J6 h9 Ppearance of pubic hair, normal growth velocity, and0 R: u/ C$ C5 C) d( }8 }* O# c
decreased erections. The father admitted using a testos-
8 i! z. l! P: G2 E7 @terone gel, which he concealed at first visit. He was7 ^+ _0 s3 W( M, f- @
using it rather frequently, twice a day. The Physicians’
6 M6 E, k2 f/ P, u* I7 ~, `Desk Reference, or package insert of this product, gel or/ ]9 o0 k/ S( R3 W9 Y
cream, cautions about dermal testosterone transfer to
; H- H( K( R8 \* W- A& ]. Z. lunprotected females through direct skin exposure.
) W' [+ b, f( _6 k  ?, l$ MSerum testosterone level was found to be 2 times the
+ Y* A. W4 c1 ]) ?baseline value in those females who were exposed to
4 T; |( }% s# S9 L% Leven 15 minutes of direct skin contact with their male
) P. v  D0 Q5 s, [partners.6 However, when a shirt covered the applica-
& R$ |* b, S. X# Q3 |tion site, this testosterone transfer was prevented.
  Q: u; [# h2 XOur patient’s testosterone level was 60 ng/mL,6 W+ c3 Q# N/ Q# o
which was clearly high. Some studies suggest that  c9 E- J% @6 G3 }% Y
dermal conversion of testosterone to dihydrotestos-; ^9 r0 N  e  b: f( d( r2 O# ]
terone, which is a more potent metabolite, is more
, ~4 K1 x, o, @5 ]active in young children exposed to testosterone9 ]7 k2 E( g8 M
exogenously7; however, we did not measure a dihy-+ h/ ]& v, l1 D4 \
drotestosterone level in our patient. In addition to
1 O, O9 a( _, c3 a% tvirilization, exposure to exogenous testosterone in4 w. m2 Y: S5 Q+ C. x; Y
children results in an increase in growth velocity and
* ~8 K! k- o0 radvanced bone age, as seen in our patient.$ q+ t; N* a$ k. b9 u
The long-term effect of androgen exposure during# u" _/ }% u3 T& D  M3 o6 u
early childhood on pubertal development and final; R. I+ l) X, q. [
adult height are not fully known and always remain) O! L2 }7 i4 V  x2 S; U
a concern. Children treated with short-term testos-
6 a# f& O0 n: A4 I, lterone injection or topical androgen may exhibit some3 d, }4 j2 B* g' a" @7 O
acceleration of the skeletal maturation; however, after
+ l. G: y0 F) V( @cessation of treatment, the rate of bone maturation
8 b8 v5 B2 j0 B$ P- z& ^decelerates and gradually returns to normal.8,9
) f. J9 l) O5 G3 oThere are conflicting reports and controversy. ]: z% D! Z! ?6 x+ M# \2 B8 q' w1 b7 L
over the effect of early androgen exposure on adult. w' b7 B$ k; s; E. E: U& e
penile length.10,11 Some reports suggest subnormal
; G# w8 i$ x* Uadult penile length, apparently because of downreg-
6 `5 f- B$ M  ^, G2 L9 sulation of androgen receptor number.10,12 However,
* H% N. l' {+ @9 bSutherland et al13 did not find a correlation between
" l, g7 h; v! X5 mchildhood testosterone exposure and reduced adult" D. {  H( Q$ W. @. S! R# _0 }
penile length in clinical studies.
# S/ t$ Q) r! R$ p8 ]% hNonetheless, we do not believe our patient is
5 Y, o% Z7 K+ k9 X9 Ogoing to experience any of the untoward effects from
$ {1 i0 f- j5 {# m; p* atestosterone exposure as mentioned earlier because% u- ^$ f8 I' O5 R+ L
the exposure was not for a prolonged period of time.
. `8 f# P  a( Z8 B2 |6 p/ PAlthough the bone age was advanced at the time of, B" J6 ^1 T( i$ i2 e" t/ ^
diagnosis, the child had a normal growth velocity at
/ w9 D/ |3 e8 @' |. j: Athe follow-up visit. It is hoped that his final adult& ^7 K! w8 v3 |7 P4 n, n
height will not be affected.
" o0 m; I3 s9 B& \6 J9 C  E3 w, bAlthough rarely reported, the widespread avail-; {+ [5 \( K+ O! S, x! E
ability of androgen products in our society may
6 j" r9 E7 G& s8 i( O" |indeed cause more virilization in male or female
& C8 K- F: i: |3 Achildren than one would realize. Exposure to andro-
! l3 a7 C: W; P( e! Ygen products must be considered and specific ques-2 D  {8 F, V: q, o) \
tioning about the use of a testosterone product or7 i; m; g* U$ K& u% g
gel should be asked of the family members during
; ]$ H' L# c" Y, E" cthe evaluation of any children who present with vir-% e  U' v+ l: {0 _. ~
ilization or peripheral precocious puberty. The diag-8 [8 _+ s7 h$ c2 e
nosis can be established by just a few tests and by1 J+ H' k$ ~6 ^4 [
appropriate history. The inability to obtain such a) j+ w$ `4 V+ X: u' p
history, or failure to ask the specific questions, may8 t& o/ i$ T1 N. u1 t% r! }- o
result in extensive, unnecessary, and expensive/ @7 B4 G* \% I+ x/ L8 ~
investigation. The primary care physician should be
! y7 q4 v4 s5 M) B* Taware of this fact, because most of these children
9 ^3 e" Q2 H( l$ Zmay initially present in their practice. The Physicians’" q. H; D: x0 n( M% W
Desk Reference and package insert should also put a4 f7 l; W% _7 p4 k! I0 R7 H
warning about the virilizing effect on a male or- A, L; y: N' t1 }% v! z, @
female child who might come in contact with some-
; N- @. y7 H( \3 d' i4 H1 _one using any of these products.
, ~6 ^4 w* ^6 Q) Y+ {4 W* E3 iReferences
2 {8 p& h  n' `3 z1. Styne DM. The testes: disorder of sexual differentiation
4 y  E& |& \: W8 E7 Z7 M7 _7 R, xand puberty in the male. In: Sperling MA, ed. Pediatric
& L/ L. s  M( B( sEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 ?$ m+ |- Z, f; n9 |6 q2002: 565-628.2 L- e+ n' X. k# k4 u
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; q2 r; j/ d# \( E$ n6 `
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
- B' w/ ^( p. Q3 @& |2 t
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