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, h; u" C! I/ y1 e7 t0 f
Boy Induced by Indirect Topical
  ~( \, M' z% p- A. h) s: \Exposure to Testosterone
1 a) s4 O1 c! Y4 NSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
8 ^: H0 w1 p' s. R% `/ o6 O6 A; b: cand Kenneth R. Rettig, MD1) y, U0 w& W0 b& c5 @
Clinical Pediatrics) W) k0 ^+ u6 I+ @* e" K+ U. O* x; D4 d
Volume 46 Number 6
% S0 @0 X( ^2 x' SJuly 2007 540-543
  O& G5 |7 `# h/ A2 z8 X, y! h0 X© 2007 Sage Publications
7 q0 d' R& n' Y* u1 q2 G5 ^% H10.1177/0009922806296651
7 i- J( L3 n) m& ?8 ~8 jhttp://clp.sagepub.com
, e2 l( Q4 p0 }- y, b' ?6 ?$ {hosted at
  r+ x1 P6 Y6 `0 thttp://online.sagepub.com
2 @. V! w! N$ }1 T! C" J- JPrecocious puberty in boys, central or peripheral," s+ w  W& P. a( [
is a significant concern for physicians. Central  d6 _; W/ h# F  [5 M
precocious puberty (CPP), which is mediated  D) d) @  ^6 t3 U$ C0 |$ q
through the hypothalamic pituitary gonadal axis, has% X+ |# M: S$ p: ^/ A. i6 P- b
a higher incidence of organic central nervous system
6 [* w3 ^; C' f( T! q1 Z  ?lesions in boys.1,2 Virilization in boys, as manifested1 ~0 K1 r4 Y% R8 @! Y. K
by enlargement of the penis, development of pubic
0 J: d+ |* [: G1 t1 i9 hhair, and facial acne without enlargement of testi-3 L, |- P3 r6 [3 V
cles, suggests peripheral or pseudopuberty.1-3 We- `# Q; i* ]. k# f( o
report a 16-month-old boy who presented with the
* y; l" f' f3 Yenlargement of the phallus and pubic hair develop-
2 i4 p% m& h- L8 Z+ E: jment without testicular enlargement, which was due: g2 z1 B* ^# D
to the unintentional exposure to androgen gel used by
- p9 L5 i* E) ?the father. The family initially concealed this infor-1 x3 ]- b$ W( p6 L
mation, resulting in an extensive work-up for this
: f9 T( m- E2 S! Gchild. Given the widespread and easy availability of2 w6 a, W4 Y7 R2 Y' O7 `) S5 z
testosterone gel and cream, we believe this is proba-/ F/ y; |- N: @8 H" |* L5 `8 i# F
bly more common than the rare case report in the( e5 t/ t) R1 `
literature.4
. M/ t* d: c. j2 X0 X4 ePatient Report
' N. x2 K( s7 T' pA 16-month-old white child was referred to the
, P( s, p. G1 \7 Nendocrine clinic by his pediatrician with the concern
. t# W3 u& u) Q) W- _# Uof early sexual development. His mother noticed6 ?, Q% n9 O% A& t
light colored pubic hair development when he was) a$ U$ G# p' f- i
From the 1Division of Pediatric Endocrinology, 2University of
0 z' x3 Q' i& ]* P7 pSouth Alabama Medical Center, Mobile, Alabama.& G6 X) J0 Q  V% ?3 R
Address correspondence to: Samar K. Bhowmick, MD, FACE," _; T) K" C# r
Professor of Pediatrics, University of South Alabama, College of
! _& L4 ~( m2 v, j6 WMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 W/ R: W+ ]0 y% f2 L! A9 I
e-mail: [email protected].: M/ r  e+ m1 @7 d* M8 V+ E# A; `
about 6 to 7 months old, which progressively became
2 R& r" o1 c, _6 E% f( v# u& ndarker. She was also concerned about the enlarge-6 ]7 j3 A+ y+ J. W& O) l. P
ment of his penis and frequent erections. The child
3 b7 \6 y* `% A) b( [, P7 ?, cwas the product of a full-term normal delivery, with! c0 m7 I0 ~! t0 |* O9 v
a birth weight of 7 lb 14 oz, and birth length of
; V3 s5 f: Q, u" l) M: `' |20 inches. He was breast-fed throughout the first year' H5 {3 i& N# \. s, A$ p
of life and was still receiving breast milk along with
3 d4 G7 y! {6 Gsolid food. He had no hospitalizations or surgery,
) e- s# j- W. M: F: d; _* Land his psychosocial and psychomotor development8 e2 y/ Z& Q' u& H. q7 b* ~
was age appropriate.
; T2 y  P8 l& q5 g8 T* c' tThe family history was remarkable for the father,
, u$ C% C9 s" ~: k0 i3 Gwho was diagnosed with hypothyroidism at age 16,
+ t: B3 Y8 }/ r6 j; P: Bwhich was treated with thyroxine. The father’s7 g8 B! t' n1 _$ `7 G. O% y  [
height was 6 feet, and he went through a somewhat* e$ _! F" N2 W8 @& K" P
early puberty and had stopped growing by age 14.1 p' s. V6 Z  V/ }
The father denied taking any other medication. The
5 c  v7 D/ r7 k/ m( |& l$ Rchild’s mother was in good health. Her menarche
! L9 a0 c; p9 t' M% q- p7 ]7 ^was at 11 years of age, and her height was at 5 feet
' W. }5 m' J' [; z" V5 inches. There was no other family history of pre-4 N8 a6 _$ j$ P! F
cocious sexual development in the first-degree rela-  O& C, F3 W) Z! Q) |
tives. There were no siblings.1 Z1 |8 J% Z# U& b! Z6 L4 J
Physical Examination
  f% A' B; Y( A4 N* U' W* aThe physical examination revealed a very active," q+ y# h1 G. P
playful, and healthy boy. The vital signs documented
  O6 x9 G- `3 x% V' f. j6 V7 qa blood pressure of 85/50 mm Hg, his length was
) z3 t: q: p  {  m* l90 cm (>97th percentile), and his weight was 14.4 kg  M* B3 a' ?$ ?6 l  K; k3 n; o
(also >97th percentile). The observed yearly growth) }+ w) c- Z" K, P& N5 E8 E
velocity was 30 cm (12 inches). The examination of3 j9 ^. Q; l3 K& T5 Y4 L- d
the neck revealed no thyroid enlargement.* ~5 D5 `4 |. @5 P8 a; _0 Z' l7 x
The genitourinary examination was remarkable for
$ l! E( j& m. [( u* Henlargement of the penis, with a stretched length of
2 b0 ^$ D& O( W2 q- C7 R8 cm and a width of 2 cm. The glans penis was very well
: {, Z! D2 ?2 |- F5 H9 Ldeveloped. The pubic hair was Tanner II, mostly around* j8 h3 y' O3 |% Y; n0 H
540
! `' x1 `. q9 p( d" {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 g+ R6 H( W5 P4 ^- N" Xthe base of the phallus and was dark and curled. The
  O0 P; f! p- ~) htesticular volume was prepubertal at 2 mL each.
& Y+ l( _, D4 Q8 X+ u3 w) y  {The skin was moist and smooth and somewhat. C' b6 @9 b' C$ T5 r# e
oily. No axillary hair was noted. There were no
! w% r* e% |1 z* G7 Eabnormal skin pigmentations or café-au-lait spots.
0 q* Q; ^! U9 c6 H/ o) ENeurologic evaluation showed deep tendon reflex 2+
) n" \7 `) H7 f8 k; {bilateral and symmetrical. There was no suggestion( J; g2 I' I0 H, F
of papilledema.
6 o# n( q. _# [Laboratory Evaluation$ s4 _# E% F0 a9 m7 r
The bone age was consistent with 28 months by
8 y. j% x9 [1 n" S6 R# Susing the standard of Greulich and Pyle at a chrono-
! |: s4 l8 B! l6 Zlogic age of 16 months (advanced).5 Chromosomal  i4 J2 w1 H3 o6 H+ B9 K& o
karyotype was 46XY. The thyroid function test
4 r1 [9 ?* ?. O  H, Fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ ^, f$ N; ]6 ~0 r/ i, ilating hormone level was 1.3 µIU/mL (both normal).
8 w) X" A! Z; MThe concentrations of serum electrolytes, blood
( Y/ s8 j- M) ^7 @$ G4 Hurea nitrogen, creatinine, and calcium all were) v! M1 z9 ^) S7 C1 o. e/ ]
within normal range for his age. The concentration
  N4 W: b* {5 I5 F# O0 [$ a6 bof serum 17-hydroxyprogesterone was 16 ng/dL
' }! v3 {! t! N$ K3 Y6 z3 O( V(normal, 3 to 90 ng/dL), androstenedione was 20
$ d9 a4 m) f* z( K7 yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
" g3 m; l/ p8 c7 I% N7 r% a/ dterone was 38 ng/dL (normal, 50 to 760 ng/dL),' m' I) _- g" v4 Z' j+ d) t
desoxycorticosterone was 4.3 ng/dL (normal, 7 to' J: {9 |; C1 U
49ng/dL), 11-desoxycortisol (specific compound S)
& a$ R7 R- ]- Z+ Twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ |( |" l: C6 i, w/ Z  j0 `
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, P9 {- F3 Z, Ftestosterone was 60 ng/dL (normal <3 to 10 ng/dL),; Z- E6 \6 l, W( G
and β-human chorionic gonadotropin was less than: ]6 ]/ C) m" G" s" H" b
5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 o) A- h# J% x6 ^3 K3 f0 ostimulating hormone and leuteinizing hormone
& c+ F  b/ r: Jconcentrations were less than 0.05 mIU/mL' v" B4 r% b9 ~
(prepubertal).
6 H; S$ e1 j7 q" U% p8 }: MThe parents were notified about the laboratory9 N+ Q; l' z* Q8 Y
results and were informed that all of the tests were
- p: q" D: E8 D8 M2 pnormal except the testosterone level was high. The
0 M; m" f0 }; Y2 y3 m* j' Q7 }follow-up visit was arranged within a few weeks to) S; ^9 C& j, c; ?
obtain testicular and abdominal sonograms; how-9 l: @$ C7 `3 J, ~+ V1 {1 M. u
ever, the family did not return for 4 months.
& w0 p# Y, E- I9 TPhysical examination at this time revealed that the4 E8 \# ^3 F0 d8 V9 Z
child had grown 2.5 cm in 4 months and had gained+ R: M$ h# u* U' P
2 kg of weight. Physical examination remained2 K5 y& }' L* O/ y/ ]. u# ~: R1 h
unchanged. Surprisingly, the pubic hair almost com-
- h$ i1 k" N# _3 a+ r/ D( {7 Fpletely disappeared except for a few vellous hairs at
# j% Q. R& |+ Fthe base of the phallus. Testicular volume was still 2! n6 z3 g) q" G. @
mL, and the size of the penis remained unchanged.( M# D# d/ [9 @" D
The mother also said that the boy was no longer hav-
" p. P2 G* e1 ling frequent erections.+ w- U( U9 V; p7 u
Both parents were again questioned about use of
- B, m4 ?  b1 K- {, A/ ?/ Zany ointment/creams that they may have applied to
% ^" q- D2 Y6 X$ z: j  kthe child’s skin. This time the father admitted the
7 B; I, `5 o! \' kTopical Testosterone Exposure / Bhowmick et al 541
: G+ Q6 L! d5 Y7 {: g. Luse of testosterone gel twice daily that he was apply-
, |2 [8 C' n5 y2 B4 @, Zing over his own shoulders, chest, and back area for; o( Q" H' M) q+ a9 `
a year. The father also revealed he was embarrassed
) H( q0 P8 d8 Y* Mto disclose that he was using a testosterone gel pre-+ K6 L2 v3 G+ L. |6 z
scribed by his family physician for decreased libido% ~8 O; T" {( Z# i  T
secondary to depression.
5 Q* S" j) g: E3 iThe child slept in the same bed with parents.' l8 x8 j: x, q" P
The father would hug the baby and hold him on his% R- ~, l# L" c1 |# i# O
chest for a considerable period of time, causing sig-
8 ^1 N( Q3 Z. Y% A4 Qnificant bare skin contact between baby and father.
' I& I$ X  ^2 j5 p* N3 u( f4 ?9 YThe father also admitted that after the phone call,- |/ S4 r3 a, h& k& a
when he learned the testosterone level in the baby
  ?% c% i& U  z+ L& Q6 R! ^9 rwas high, he then read the product information2 A  N5 }" j0 n; c( n1 U" ~
packet and concluded that it was most likely the rea-5 M7 T3 d' l4 T7 `( h: y
son for the child’s virilization. At that time, they' g5 |! m. K) o& P! m" ?" ?1 V+ L
decided to put the baby in a separate bed, and the
3 D5 V9 e/ t. k; Q! L; P9 X% N% bfather was not hugging him with bare skin and had& f! x) K6 k* J) j7 Z. R+ r0 E! m
been using protective clothing. A repeat testosterone8 m; @8 w  [) Z  ^. L
test was ordered, but the family did not go to the; Y! N" h* |! b$ Q. l  ?
laboratory to obtain the test.2 _' T* H' C, f# O
Discussion
) O: n6 S& U# j: aPrecocious puberty in boys is defined as secondary
, G, f2 p$ a* r! W% dsexual development before 9 years of age.1,4
0 g9 V$ }8 w  g6 OPrecocious puberty is termed as central (true) when8 m! C8 a8 H2 [" m
it is caused by the premature activation of hypo-3 i; }9 c0 ?3 F
thalamic pituitary gonadal axis. CPP is more com-- r% w$ {+ f3 J. I2 |8 P
mon in girls than in boys.1,3 Most boys with CPP
  _! |# l! u6 W0 smay have a central nervous system lesion that is
0 O0 H. y% y( `7 }  `; W$ Tresponsible for the early activation of the hypothal-
1 P+ Y9 [* A  O, Y/ G: o5 S4 M- Xamic pituitary gonadal axis.1-3 Thus, greater empha-
9 H% T' \9 X% Tsis has been given to neuroradiologic imaging in8 A4 V5 x' U# v6 P" l
boys with precocious puberty. In addition to viril-: \9 W  P0 @+ k/ K. \
ization, the clinical hallmark of CPP is the symmet-0 v6 b6 z4 P( w7 i. a5 d
rical testicular growth secondary to stimulation by6 H( R. n1 }, s9 x0 {$ J5 [# x1 I
gonadotropins.1,38 @' P' H# M* y0 ]) p
Gonadotropin-independent peripheral preco-
+ v2 }4 S# w9 ]  v& l, ~. ]$ }cious puberty in boys also results from inappropriate
) K# A) }7 T) r( k( ?1 C9 _  jandrogenic stimulation from either endogenous or+ i- C' X$ Z* a* D2 i+ p' z  Y4 a
exogenous sources, nonpituitary gonadotropin stim-
( A" @+ @/ I1 d# iulation, and rare activating mutations.3 Virilizing3 T. l+ ]; E+ R# N( Q& i
congenital adrenal hyperplasia producing excessive+ w4 V+ V3 Q- H' `8 U! j
adrenal androgens is a common cause of precocious
- H# ~5 x0 q4 H2 P; @8 w4 U1 w) p3 h. gpuberty in boys.3,4
# D) T( ~. ?0 m; J. GThe most common form of congenital adrenal0 Y7 P1 A' e, s  x- |- u
hyperplasia is the 21-hydroxylase enzyme deficiency.* O/ Y: `/ O- E) q
The 11-β hydroxylase deficiency may also result in
0 C' K( O0 R% q9 Y" L2 w8 vexcessive adrenal androgen production, and rarely,) R: d( L9 N) P: H1 Z3 }
an adrenal tumor may also cause adrenal androgen) m/ N  N8 n1 X; I' ]
excess.1,3
. t7 V( q2 s4 Y) nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 c$ S4 `3 m* K! O: Q4 M$ a542 Clinical Pediatrics / Vol. 46, No. 6, July 2007$ j7 t# |4 v# ]# M0 h$ G; i
A unique entity of male-limited gonadotropin-
* v, P; `: }% M; j/ M" o) zindependent precocious puberty, which is also known
% T% P+ h& V7 P* g# A6 mas testotoxicosis, may cause precocious puberty at a
2 r7 }' m+ V- a8 A) h1 Avery young age. The physical findings in these boys1 R! K3 w/ e: b* {- |4 x8 ~
with this disorder are full pubertal development,8 f/ x# t! [4 E4 X% ~0 y4 L
including bilateral testicular growth, similar to boys
% J8 t9 H# \8 M, I; M4 ~- ]with CPP. The gonadotropin levels in this disorder& u1 `  V3 W) w6 ]! m! t
are suppressed to prepubertal levels and do not show
- v8 X1 r: M5 ]pubertal response of gonadotropin after gonadotropin-
- P, F0 K" R% c8 greleasing hormone stimulation. This is a sex-linked
; Z& ~; i) d, K! H" fautosomal dominant disorder that affects only4 _4 v- H+ i% n
males; therefore, other male members of the family
* a! z, M8 e# ~) ^4 O/ P4 vmay have similar precocious puberty.3
. P; [3 w+ A# U& Z$ T0 V) fIn our patient, physical examination was incon-  x  H+ Q: D$ N( {1 y+ d
sistent with true precocious puberty since his testi-) I+ x# P1 f+ c+ T" G0 L# E6 U
cles were prepubertal in size. However, testotoxicosis
* ?' L; g) J" v6 t! Q, C9 Bwas in the differential diagnosis because his father  q5 \9 j' X" F2 g. {9 Q+ r. Z$ _
started puberty somewhat early, and occasionally,/ j- R! }3 Z" X1 D# u0 [' r9 v4 V
testicular enlargement is not that evident in the7 R3 W% O4 q% Z9 o6 V) N  V! E& n
beginning of this process.1 In the absence of a neg-% C6 w1 l  i1 u* ~8 I
ative initial history of androgen exposure, our2 @1 x: d7 ^+ M- X/ e% p
biggest concern was virilizing adrenal hyperplasia,
. U5 k4 O* u5 Feither 21-hydroxylase deficiency or 11-β hydroxylase
, F/ Y! N7 m0 k0 L% ]: e) Qdeficiency. Those diagnoses were excluded by find-
2 L! m. M/ y4 ?2 A' O9 Cing the normal level of adrenal steroids.
; M" @* Q7 _" wThe diagnosis of exogenous androgens was strongly
) V" `4 p+ w0 L  ~suspected in a follow-up visit after 4 months because
' V; r7 [/ s+ ^% Z% p; t. g9 ^, \the physical examination revealed the complete disap-
5 F% z1 r! v4 A( j. t0 _pearance of pubic hair, normal growth velocity, and
  B5 ~; O, m4 ]7 P2 xdecreased erections. The father admitted using a testos-
! x$ [/ ]+ K: \0 p1 F- ^; n  L  ~terone gel, which he concealed at first visit. He was& x' Y& `7 F( c' q0 P2 Y$ a- d
using it rather frequently, twice a day. The Physicians’- P" G& N: g+ s  O2 \* U" T
Desk Reference, or package insert of this product, gel or& S( H9 l% Y* h; M
cream, cautions about dermal testosterone transfer to* P4 f; l( f) c: Z2 m
unprotected females through direct skin exposure.
9 x; h4 k: I8 R1 ?Serum testosterone level was found to be 2 times the3 f7 M6 l1 z2 X( A) a
baseline value in those females who were exposed to" b( C2 X0 Z8 ~3 B8 d
even 15 minutes of direct skin contact with their male; F6 H4 Q4 |1 M: R  ~
partners.6 However, when a shirt covered the applica-
$ x% f/ B. c' F* y1 O# Etion site, this testosterone transfer was prevented.
' D+ U# s5 K4 s+ ]1 R. U4 M3 {7 B' pOur patient’s testosterone level was 60 ng/mL,
0 D2 t6 ?3 c; R+ uwhich was clearly high. Some studies suggest that
* F! ], c) x9 L4 ~, w+ C9 ldermal conversion of testosterone to dihydrotestos-
% r6 P. r8 I& l; U( xterone, which is a more potent metabolite, is more
8 S+ L% S1 c, I3 l# N9 h+ Factive in young children exposed to testosterone! `7 j4 F2 V7 A4 Y4 h+ r
exogenously7; however, we did not measure a dihy-% k' c  i- m( r
drotestosterone level in our patient. In addition to
8 ~9 ?! W2 l' j4 C# Ovirilization, exposure to exogenous testosterone in( t1 x5 j) {+ S
children results in an increase in growth velocity and
& r$ {0 W* @" ]" `6 T: Qadvanced bone age, as seen in our patient.% P& Z2 P" k5 {4 K; D. ]
The long-term effect of androgen exposure during
9 A; x8 Y) K; @8 Oearly childhood on pubertal development and final1 [' `# D" F9 W: R* b
adult height are not fully known and always remain
7 q* D' p$ h% ga concern. Children treated with short-term testos-
: q/ v6 m6 l8 Y2 a* Y$ Aterone injection or topical androgen may exhibit some2 ]. {" h; s. N6 V% v, R* T
acceleration of the skeletal maturation; however, after$ `4 v7 U+ W+ J% ?& {2 y
cessation of treatment, the rate of bone maturation7 Q: ~, R7 w$ ]2 K! q# B# y
decelerates and gradually returns to normal.8,9
0 P; R7 W2 y, l4 S+ JThere are conflicting reports and controversy4 q: u# B0 ^7 n
over the effect of early androgen exposure on adult8 l- n3 ]  |& j- K
penile length.10,11 Some reports suggest subnormal' K4 R$ z  ~4 a( U4 Q9 Y
adult penile length, apparently because of downreg-
) O( K2 Y) G9 \; \- w( yulation of androgen receptor number.10,12 However,+ x" E# ?* _- M1 T- I- A
Sutherland et al13 did not find a correlation between
% N% a8 S" \& n3 N7 Lchildhood testosterone exposure and reduced adult( G7 X2 [8 r7 J. i+ V" Y
penile length in clinical studies.
' z. t1 h, c) I/ MNonetheless, we do not believe our patient is
/ K# `9 C7 P- s9 U& F* }  w$ Z; F; g1 Lgoing to experience any of the untoward effects from9 u) ^7 p- s/ s6 |0 W6 y5 Y( y
testosterone exposure as mentioned earlier because1 ?8 g0 T9 J8 U* f3 L* U
the exposure was not for a prolonged period of time.
9 {! a- Q0 u0 K/ |7 aAlthough the bone age was advanced at the time of
4 [; ?8 Z' U4 m% w: \diagnosis, the child had a normal growth velocity at
2 B3 u- W. r6 }0 p4 _# wthe follow-up visit. It is hoped that his final adult: q% i' Q1 V. ]5 H, t' ]
height will not be affected.  ^3 J/ x6 q$ v, A: w8 ~3 W
Although rarely reported, the widespread avail-
: D: o* |3 r/ i2 r9 \ability of androgen products in our society may
* ~; i: Y9 @- r. e- \. _indeed cause more virilization in male or female
  t# {6 T, L! j+ J+ Z3 _+ |0 Fchildren than one would realize. Exposure to andro-
% c3 L$ r) T! ngen products must be considered and specific ques-
, u0 x( {. D/ O5 U- U" l  Htioning about the use of a testosterone product or
& }/ x7 x8 N  ]: z5 d% [gel should be asked of the family members during$ N6 q; N( \4 O* c+ f2 o9 H
the evaluation of any children who present with vir-9 R% _+ v* p! ~, q9 o- k
ilization or peripheral precocious puberty. The diag-; s6 O: ]1 o9 H- L% B! y
nosis can be established by just a few tests and by0 v/ N4 i3 n) O6 K
appropriate history. The inability to obtain such a
) b4 A: e5 Q" B" ^: Phistory, or failure to ask the specific questions, may
4 ]% ?2 n7 \0 v5 ]% Gresult in extensive, unnecessary, and expensive9 u. x* [5 \0 r4 }
investigation. The primary care physician should be. k* ]5 J3 k- h. k
aware of this fact, because most of these children
3 S0 q2 }0 D3 E5 C" B# }may initially present in their practice. The Physicians’' f5 ~. r. ^, l0 s: U8 o
Desk Reference and package insert should also put a6 c9 B5 I+ c# i1 t3 G) ]
warning about the virilizing effect on a male or
  [3 h! Q. z" @' i' pfemale child who might come in contact with some-' y+ ^- B7 j! `8 G7 C9 ]' b
one using any of these products.
7 t9 B: i/ c/ P3 t' A( X  V' Z: }References
' V/ q. r8 m. }# ]6 u: T1. Styne DM. The testes: disorder of sexual differentiation, S7 ]* Q/ ]& e! L
and puberty in the male. In: Sperling MA, ed. Pediatric! [( z% T% U2 K, n
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" t( @3 H  V( V' R1 W4 P7 C2002: 565-628.7 [: G) E7 |) F# n' Y
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. o& @+ Z- a4 u+ I' ipuberty 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
: z  T, ]  h5 h0 Q$ N- g  Q4 U' ]Boy Induced by Indirect Topical
, j/ A* \% K7 W3 `$ ]# u9 _. M7 cExposure to Testosterone
0 o, i4 U+ P* T7 H9 T6 n) [1 j/ @( XSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: N! |5 {% M/ [and Kenneth R. Rettig, MD1$ f- @; ~. C! @. f% |. Y: {4 v9 b
Clinical Pediatrics+ R4 _# c! o, U+ O
Volume 46 Number 6
& ^2 w( C% Y: D' X" lJuly 2007 540-543
# b9 R1 K' P- V© 2007 Sage Publications
- G" `1 g- }7 Y+ D" e6 \7 `2 e: A10.1177/00099228062966510 [3 h8 s7 |' _8 k" @
http://clp.sagepub.com6 m: H0 ~' O1 {9 G% ]3 ]2 R
hosted at
: }# T! Q; x* F8 Ahttp://online.sagepub.com" l! ^6 C, U( w
Precocious puberty in boys, central or peripheral,0 O& B6 M+ B; _0 q; ^% f
is a significant concern for physicians. Central3 Z; |. N0 R8 Y
precocious puberty (CPP), which is mediated
* {3 K, m) r0 B, k, z9 a* `1 x- l7 xthrough the hypothalamic pituitary gonadal axis, has
  d1 [2 H8 Q+ b) R' d4 }! Y- H; Va higher incidence of organic central nervous system8 L2 q; I2 n3 i$ {# s1 V
lesions in boys.1,2 Virilization in boys, as manifested' d) g' K' ~) z. H% S' f
by enlargement of the penis, development of pubic3 B1 b* I  [. ?
hair, and facial acne without enlargement of testi-
) u$ ^: S6 H; @: X5 r% icles, suggests peripheral or pseudopuberty.1-3 We# V9 R7 Q' u# h! u% `
report a 16-month-old boy who presented with the) S( `3 O6 Y3 z5 f
enlargement of the phallus and pubic hair develop-3 Z7 ?. P* l" A6 p' |
ment without testicular enlargement, which was due5 k4 l3 z1 i$ c* `
to the unintentional exposure to androgen gel used by
( w% }7 T- p7 F0 qthe father. The family initially concealed this infor-+ b1 i' ^- C/ y; x& m
mation, resulting in an extensive work-up for this2 {% j5 [1 t7 i  y- Q: ^- d$ k
child. Given the widespread and easy availability of
: T4 E  A, @7 w/ p: {& s1 t2 k) `testosterone gel and cream, we believe this is proba-5 O- Y5 n$ r  L0 t8 F
bly more common than the rare case report in the+ e0 ^" e5 }5 m, \" \
literature.4
* J* i3 ~1 z) g  cPatient Report9 E4 x6 u4 Q+ P  s& }$ A
A 16-month-old white child was referred to the5 o$ C4 }$ w2 g
endocrine clinic by his pediatrician with the concern
0 \# J4 Y. k' _of early sexual development. His mother noticed
3 z9 r- u, P) `& klight colored pubic hair development when he was
3 |+ @- f/ J" A8 J! q4 Z3 cFrom the 1Division of Pediatric Endocrinology, 2University of
7 I& Z& U# K0 W# hSouth Alabama Medical Center, Mobile, Alabama.
6 Y9 g+ ^' w' O. v! A0 xAddress correspondence to: Samar K. Bhowmick, MD, FACE,
% w9 Z) z0 h. Q7 o7 N' k" ^$ MProfessor of Pediatrics, University of South Alabama, College of! q! \: p' S9 x# n- @
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 N2 ^  ?5 X2 g
e-mail: [email protected].
* M# f5 r. I9 @! R+ \about 6 to 7 months old, which progressively became, ]% T9 Z# k+ Q% [4 s& [6 W
darker. She was also concerned about the enlarge-# f2 A3 m9 Q' H
ment of his penis and frequent erections. The child4 {; R& Q- S3 Y; \1 G  @
was the product of a full-term normal delivery, with
) ?9 e  A8 i4 n. A: |* u) Ya birth weight of 7 lb 14 oz, and birth length of: {: \% h) ?5 T% Q8 D: y* n
20 inches. He was breast-fed throughout the first year
: _3 k% E" {: x0 I5 i9 T1 Cof life and was still receiving breast milk along with
6 j% D8 b2 r- x2 p( k; lsolid food. He had no hospitalizations or surgery,( Q( Y% K2 T4 T
and his psychosocial and psychomotor development5 T* Q% \& w% ]( C1 q$ [$ w9 Y
was age appropriate.
9 O- f. d& A: n3 I3 QThe family history was remarkable for the father,
. X, }2 T3 X+ \/ M0 A/ y, x3 i. gwho was diagnosed with hypothyroidism at age 16,
. r- x/ E- c, l6 m& ~9 ]4 Jwhich was treated with thyroxine. The father’s
) q2 I3 X) r. Sheight was 6 feet, and he went through a somewhat8 A/ N* j, p: e0 F  F
early puberty and had stopped growing by age 14.; ^- _0 l2 r' m) O  X6 K- R/ d
The father denied taking any other medication. The  Y# [  G5 Y& [, s6 ]  d
child’s mother was in good health. Her menarche0 }) G$ h+ P/ Z
was at 11 years of age, and her height was at 5 feet! w! b6 L$ y8 g
5 inches. There was no other family history of pre-% N1 i8 X' ?) h7 a8 g+ ~  Q
cocious sexual development in the first-degree rela-7 u# \+ o4 {% T7 X7 O6 m+ h) h5 M
tives. There were no siblings.
8 N- W& E8 N8 J1 [* n2 Q9 L9 d, ZPhysical Examination
" X- ]5 c$ C9 ?( f3 ^  e  BThe physical examination revealed a very active,
5 n# {$ E1 e+ T, B0 y" ~8 bplayful, and healthy boy. The vital signs documented8 p" l2 B& H8 v: K" S
a blood pressure of 85/50 mm Hg, his length was
; n2 Y* H" |; i90 cm (>97th percentile), and his weight was 14.4 kg" X2 `5 M; B: `4 g# x! w2 j: _5 F$ H- @
(also >97th percentile). The observed yearly growth
4 O/ X' N" e- |4 ivelocity was 30 cm (12 inches). The examination of" M/ c- L/ a$ ^8 d9 k
the neck revealed no thyroid enlargement./ c; A) I2 m( D4 L! T
The genitourinary examination was remarkable for* x7 A, P: l% u) p
enlargement of the penis, with a stretched length of
' h; a( Y  ~: b6 Y8 cm and a width of 2 cm. The glans penis was very well" E8 I1 X% E1 k- o# \  K* R
developed. The pubic hair was Tanner II, mostly around- z; w2 {; }9 w" G
540
# v1 g. ?! m7 G, j6 o* Q! x. O. lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( H5 O" X5 ?& `$ u
the base of the phallus and was dark and curled. The6 H" G4 k1 `/ A
testicular volume was prepubertal at 2 mL each.
( s. E, x" T( C4 ]; i9 OThe skin was moist and smooth and somewhat
5 S* ], n) k5 P) n6 E& ^* noily. No axillary hair was noted. There were no' z$ Q5 g9 V: y4 V. X  j
abnormal skin pigmentations or café-au-lait spots./ m- `8 t4 }# X: O+ r8 z
Neurologic evaluation showed deep tendon reflex 2+* |; y& K3 c3 h
bilateral and symmetrical. There was no suggestion% {1 f1 v- ^  v# f7 p4 |: x
of papilledema.  T9 K# O+ w; z4 U3 G; g- g1 y
Laboratory Evaluation0 @3 J) p; c$ U4 f
The bone age was consistent with 28 months by
  i" C+ N9 u/ x) h( _using the standard of Greulich and Pyle at a chrono-! `: I7 K% T& g  r8 C; J9 i3 J
logic age of 16 months (advanced).5 Chromosomal- e/ m/ V4 O$ Q- K  ]- Z
karyotype was 46XY. The thyroid function test
# U. O  X8 x+ {6 C5 r5 g' ]showed a free T4 of 1.69 ng/dL, and thyroid stimu-' U3 t8 v2 F3 L- b/ g
lating hormone level was 1.3 µIU/mL (both normal).
. u7 T: l2 O* D2 K5 y' iThe concentrations of serum electrolytes, blood8 f$ t5 q$ f6 A8 O
urea nitrogen, creatinine, and calcium all were
" E, `7 B+ z2 @$ k, Rwithin normal range for his age. The concentration; `2 w/ _: S" `2 H* b. [
of serum 17-hydroxyprogesterone was 16 ng/dL
3 @8 S0 G3 J4 J% s' U. l8 c(normal, 3 to 90 ng/dL), androstenedione was 20
  B# k' d! n4 F, E4 R8 f2 R- M0 Nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ h6 N4 \& l0 D/ `
terone was 38 ng/dL (normal, 50 to 760 ng/dL),; I. l1 e, Q1 p( j7 D/ u
desoxycorticosterone was 4.3 ng/dL (normal, 7 to/ ?3 \2 K1 |& ~& i
49ng/dL), 11-desoxycortisol (specific compound S)) I1 r% B$ I  I. \. t' z% O' V
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- j- B' \' s2 o$ F* ]' X, y3 ]8 {
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 T$ h  F' p# h6 Q6 R. P* Y& ^# Ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
- N2 C; a! U& u9 tand β-human chorionic gonadotropin was less than
: r2 P% g) b5 P5 mIU/mL (normal <5 mIU/mL). Serum follicular( w9 T  G% n% F% ?2 k$ \
stimulating hormone and leuteinizing hormone$ |% C# f$ M+ X& E
concentrations were less than 0.05 mIU/mL' B1 Y% P1 T) u7 O+ f
(prepubertal).
6 N1 ~4 X' h6 ]- L( h1 BThe parents were notified about the laboratory8 C9 p5 m; t5 j& C
results and were informed that all of the tests were
2 ]- O/ h7 J& A& t# z/ Znormal except the testosterone level was high. The" s" N6 E" l3 O
follow-up visit was arranged within a few weeks to
" H( d2 C0 H: x" qobtain testicular and abdominal sonograms; how-, O- c. l% ^- h! R# H: v2 C! f
ever, the family did not return for 4 months.
) q1 }8 h* E. `Physical examination at this time revealed that the
) ?$ T3 Y9 |2 j* C+ nchild had grown 2.5 cm in 4 months and had gained
. G7 S' ]( }% J( o2 kg of weight. Physical examination remained
2 ~+ P6 L" E1 M4 d  J  Xunchanged. Surprisingly, the pubic hair almost com-- H) O4 j% ?! P; \$ V* K
pletely disappeared except for a few vellous hairs at: c' h& w2 S* Q" B3 U2 g
the base of the phallus. Testicular volume was still 2
. P6 W  g7 ^+ t; [3 r' I: hmL, and the size of the penis remained unchanged.$ Y3 E4 A, V# `' Y( ^+ s3 ?
The mother also said that the boy was no longer hav-
8 U6 H  K/ O! ~- t/ Ving frequent erections.
# w4 t5 J6 M% r8 D2 K. f+ h$ `Both parents were again questioned about use of6 R% u7 v- U5 F& q# e
any ointment/creams that they may have applied to* `0 w9 e" v2 x; G3 [$ F
the child’s skin. This time the father admitted the
9 `! s3 J: u) {2 Z% X9 N7 lTopical Testosterone Exposure / Bhowmick et al 541
$ r* V+ t! P" c. y0 [7 Muse of testosterone gel twice daily that he was apply-) s. j6 T1 d: i7 R5 g
ing over his own shoulders, chest, and back area for. q7 r/ p% h' n* ^1 ?
a year. The father also revealed he was embarrassed
) z, U3 f7 P0 R- h9 uto disclose that he was using a testosterone gel pre-
9 h1 T3 C( y: H8 R& h2 B* sscribed by his family physician for decreased libido
3 i/ |9 A: ?5 z. L0 t) q6 ?secondary to depression.
- H) `- L) m" U1 ~# D* u6 GThe child slept in the same bed with parents./ f6 P3 F! [2 @: ?6 r- [) _6 f
The father would hug the baby and hold him on his
- `0 j5 @1 y0 w! i; H7 }# rchest for a considerable period of time, causing sig-0 N3 t2 k" ~- A. @
nificant bare skin contact between baby and father.
- `. J0 K) b; d0 G  UThe father also admitted that after the phone call,9 B9 ^7 s$ r# e9 j. l; l
when he learned the testosterone level in the baby
" q7 D: t1 ^3 Z# }; Y  Awas high, he then read the product information; |6 k9 O9 M7 L# M. l9 L% l$ g# W
packet and concluded that it was most likely the rea-
' E5 w* Z* K/ P! W$ tson for the child’s virilization. At that time, they5 ~5 A3 w' n/ ?: _5 {
decided to put the baby in a separate bed, and the: L/ V$ B2 R2 K; D3 z6 d2 B
father was not hugging him with bare skin and had
, k6 U9 F$ C' ^1 A# O; ^% N5 Q! Z2 hbeen using protective clothing. A repeat testosterone3 r* @1 n5 K6 _$ S% `; `1 D
test was ordered, but the family did not go to the
! o7 Y: A: Q  |9 q1 Llaboratory to obtain the test.  W7 k. M( `( R( J, ^
Discussion
9 k# E/ G+ K3 X% w4 RPrecocious puberty in boys is defined as secondary7 `9 }& v. c# ]6 R! B5 X% [8 u
sexual development before 9 years of age.1,4
" ?; q, {9 X( IPrecocious puberty is termed as central (true) when: d) U! B, G, E0 o
it is caused by the premature activation of hypo-& g7 E5 b. D9 U! @  T: T
thalamic pituitary gonadal axis. CPP is more com-
/ H- [% h/ G, }( }mon in girls than in boys.1,3 Most boys with CPP! o3 Q1 w1 R" T, k. X
may have a central nervous system lesion that is
% u* u9 [" N) Q& F# ^responsible for the early activation of the hypothal-
( S) h, l8 i: f, ?1 a5 n& ?amic pituitary gonadal axis.1-3 Thus, greater empha-
5 @% R) e* M" c& H& D/ t/ Esis has been given to neuroradiologic imaging in: p/ v4 R) h: c! g' D8 \
boys with precocious puberty. In addition to viril-
1 C# ]  _7 u$ I7 N- Sization, the clinical hallmark of CPP is the symmet-
7 d- y" k/ A8 R1 y$ c& hrical testicular growth secondary to stimulation by: ~% O7 v2 Q# X/ j
gonadotropins.1,33 J& c8 y+ T2 T7 M3 v
Gonadotropin-independent peripheral preco-
. b2 Y$ A2 g, `- M0 S# v0 `cious puberty in boys also results from inappropriate
' ]4 g# _2 _/ b8 p1 C% I6 X( Y7 Q% aandrogenic stimulation from either endogenous or0 G0 N. o3 h" o# R) G+ f  u$ R
exogenous sources, nonpituitary gonadotropin stim-
4 G4 T" a6 w: t% _$ S" h7 j3 uulation, and rare activating mutations.3 Virilizing
3 E6 ~) m# x: j; ~5 m6 kcongenital adrenal hyperplasia producing excessive
$ p3 F: e1 b- q9 s8 N0 vadrenal androgens is a common cause of precocious+ d% t9 _, ~+ C/ B) F9 n5 J2 }
puberty in boys.3,4
8 _! g7 K( N- f& r1 `, k$ P0 QThe most common form of congenital adrenal6 i$ E; \: m/ d5 ?9 p) x
hyperplasia is the 21-hydroxylase enzyme deficiency.: l4 h2 k" t7 o  r
The 11-β hydroxylase deficiency may also result in& v7 G( _0 c9 N& Q1 y
excessive adrenal androgen production, and rarely,
5 f4 B* z7 Y% uan adrenal tumor may also cause adrenal androgen
  H7 C& D3 H3 M5 K" b* Gexcess.1,3
, D5 x: o( M5 Z. x" U3 Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ {% J) `7 v" H; `/ i
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% R) f# N3 ^, |A unique entity of male-limited gonadotropin-
. l' `: v1 v/ X2 o- [8 P9 C. M) ]independent precocious puberty, which is also known
4 l5 K' W+ {: ~& C# Gas testotoxicosis, may cause precocious puberty at a
/ U% q4 t: Z( c! `! `* Tvery young age. The physical findings in these boys& z$ U  F9 H- g) N; Y& j) @# O
with this disorder are full pubertal development,
, X( w$ q# \/ N1 n7 F) q0 J  }4 @including bilateral testicular growth, similar to boys. b$ f9 y7 Y) R9 z
with CPP. The gonadotropin levels in this disorder
8 G4 X- h, s  F* G% @4 Ware suppressed to prepubertal levels and do not show! a5 S  J) j- `: O, E
pubertal response of gonadotropin after gonadotropin-) i3 k+ E( [4 F7 N: g7 R4 Z3 a
releasing hormone stimulation. This is a sex-linked; N3 ]$ |) P; A& G: z8 Z: y
autosomal dominant disorder that affects only
5 Z; \: Q  V6 F1 O; Q+ omales; therefore, other male members of the family
' r4 N* g+ [$ W) y% t4 q& Xmay have similar precocious puberty.37 h) M  `, t0 }3 ?0 E) D; ]
In our patient, physical examination was incon-
  Q3 W, H- V2 |sistent with true precocious puberty since his testi-
4 Y* u+ m' z$ U( R8 w( B# ncles were prepubertal in size. However, testotoxicosis+ \: |0 E& K* N* b5 [; L* ?
was in the differential diagnosis because his father
& C9 t) R0 k5 ~4 h& b* estarted puberty somewhat early, and occasionally,
/ p2 w' P9 L& O; E' ?: d. W2 Z2 ktesticular enlargement is not that evident in the" `8 y- c5 O: Q8 e  S' C7 ]
beginning of this process.1 In the absence of a neg-
7 g+ m6 b6 F* c. ~, ^% @ative initial history of androgen exposure, our
" g5 h, _8 V6 y/ o# {2 G: {biggest concern was virilizing adrenal hyperplasia,$ N1 W# }% f% l# k
either 21-hydroxylase deficiency or 11-β hydroxylase
& ?% g! E: R5 j5 t+ [deficiency. Those diagnoses were excluded by find-
- i; q6 t. h) @7 _- U$ s5 C) ling the normal level of adrenal steroids.) i- A' P8 @% G( Q- x8 }2 {
The diagnosis of exogenous androgens was strongly
8 N2 \( l1 H5 j8 P% y, osuspected in a follow-up visit after 4 months because9 v# [: U- N7 g- Y0 V
the physical examination revealed the complete disap-$ V3 o; A8 ]: I, a) T
pearance of pubic hair, normal growth velocity, and
4 l4 G+ M. g! `: T( H2 Z  A7 [decreased erections. The father admitted using a testos-
9 b' I  y2 C4 i+ u, ^7 F# q+ uterone gel, which he concealed at first visit. He was- p0 X0 H0 p3 c4 F3 J) L* H0 `0 ]' k
using it rather frequently, twice a day. The Physicians’  Q1 H" s6 M3 u) }7 f
Desk Reference, or package insert of this product, gel or) w- ?! x: Z* f* a6 }* E( Y8 m' W
cream, cautions about dermal testosterone transfer to
4 f# G8 y2 ^& j, D. Tunprotected females through direct skin exposure.
! `  G/ u6 h% LSerum testosterone level was found to be 2 times the3 t! w* E( b0 Q
baseline value in those females who were exposed to
8 R0 W( H; ?$ X" A8 b8 B8 D% Veven 15 minutes of direct skin contact with their male% n9 ?2 ~6 T' R4 h' q: F
partners.6 However, when a shirt covered the applica-
  l5 Q( \) T2 `& j+ ^tion site, this testosterone transfer was prevented.3 b* E. ?7 m' g( v' |# l! _
Our patient’s testosterone level was 60 ng/mL,
  V/ R! W9 k: K$ {which was clearly high. Some studies suggest that
$ n$ i1 D' [6 I; _7 d3 sdermal conversion of testosterone to dihydrotestos-/ p/ r7 G. u% ?; `! a3 ?. z: d
terone, which is a more potent metabolite, is more
) s8 G0 P+ p6 X0 }: I9 ?active in young children exposed to testosterone/ \: V  P0 l% X+ B6 c+ K
exogenously7; however, we did not measure a dihy-
2 ~7 d/ U8 I; W( ?; x0 M4 n7 Qdrotestosterone level in our patient. In addition to3 [0 ?6 R  H. |
virilization, exposure to exogenous testosterone in  z& J  j1 P9 Q* B1 ~! O/ n
children results in an increase in growth velocity and8 e  |  G/ }/ i% v
advanced bone age, as seen in our patient.
+ _6 U+ x+ T/ jThe long-term effect of androgen exposure during
1 N( d( L; P% c. ~* D8 g6 m2 s3 |0 qearly childhood on pubertal development and final4 h/ W& u. v) H1 A" |1 ]* R0 b
adult height are not fully known and always remain
/ v, Y6 m7 K# ^! j+ m6 A* \: z6 Ma concern. Children treated with short-term testos-$ L" \8 W: U% N& N. e
terone injection or topical androgen may exhibit some/ V. ?! {6 S4 r" d6 c! x6 b$ H+ _  {
acceleration of the skeletal maturation; however, after. w8 z5 q" n) W- {9 Y1 l6 t
cessation of treatment, the rate of bone maturation  p4 B2 c& h9 g9 m: {" r
decelerates and gradually returns to normal.8,97 y( y& V% }6 F
There are conflicting reports and controversy: p) }% E  e* \) P' N+ q6 [
over the effect of early androgen exposure on adult: u! F+ V9 y. q, d
penile length.10,11 Some reports suggest subnormal# a  e/ N, k7 G
adult penile length, apparently because of downreg-
8 Y( K8 U. u% a# x1 tulation of androgen receptor number.10,12 However,
0 i0 n: U4 _1 q1 \  GSutherland et al13 did not find a correlation between$ z0 W. K; X. M- ~
childhood testosterone exposure and reduced adult
% k8 y- G+ k- H# ^' V/ openile length in clinical studies.2 J) y; ^6 P& \
Nonetheless, we do not believe our patient is
+ \) t& f- p1 x# Jgoing to experience any of the untoward effects from
4 |) o" u2 u8 h) A0 c2 _; ]testosterone exposure as mentioned earlier because
- a" y; g+ A" G! N/ Nthe exposure was not for a prolonged period of time.
+ o9 d7 d& R$ V: _4 \5 z% J9 |Although the bone age was advanced at the time of
/ O( z0 d( y3 ~' q1 S6 Ddiagnosis, the child had a normal growth velocity at
8 q4 h4 P9 H8 ?0 v( P7 \6 {the follow-up visit. It is hoped that his final adult
1 n$ q& d7 b% z& wheight will not be affected.9 P0 g( G+ Y* x2 c8 H7 W. ~) j
Although rarely reported, the widespread avail-& c1 @6 r6 X9 d& m" B
ability of androgen products in our society may% q% I$ }, x  N) Y8 d! y2 L
indeed cause more virilization in male or female
/ Q8 @& r  _+ W' U) ]  f" @children than one would realize. Exposure to andro-
0 {" m3 D4 |' g4 pgen products must be considered and specific ques-0 F& w- f# E: w
tioning about the use of a testosterone product or& V. |. M3 K2 E8 k3 z. t2 M4 w
gel should be asked of the family members during* n  T! z) E( w! ]9 T6 o7 {
the evaluation of any children who present with vir-
" R8 J% I' [- r5 b& w! xilization or peripheral precocious puberty. The diag-, o. v( C1 Y2 }5 x
nosis can be established by just a few tests and by
* ]  \3 M1 c- C" V5 ]appropriate history. The inability to obtain such a9 k1 G( B  r& P8 F
history, or failure to ask the specific questions, may
/ ~5 ]' G6 x) u8 ?* A9 @! Hresult in extensive, unnecessary, and expensive
+ M2 f) L2 o8 Z% j+ h+ Iinvestigation. The primary care physician should be; T8 ~8 g  V: F7 n) N2 A
aware of this fact, because most of these children/ x( h# u9 u* M& t0 `* u
may initially present in their practice. The Physicians’
# R0 M9 x+ t- V# Z# EDesk Reference and package insert should also put a- W: [! \& q: \; w8 y% L
warning about the virilizing effect on a male or0 g. F2 O% E# l$ {$ F9 h
female child who might come in contact with some-: c* p$ @4 N4 d' ]% i% G1 Z. }1 b, i4 ^+ e
one using any of these products.! z' O9 O+ {5 F# E5 \6 e+ V% }2 ]
References
- j. v; y6 z: U9 [( }( n- X6 P6 a7 y8 Y1. Styne DM. The testes: disorder of sexual differentiation* A* w& N: S; \  @. t6 I5 K, d8 D
and puberty in the male. In: Sperling MA, ed. Pediatric
2 L* Y5 a1 T/ ]- QEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* ^* E" G& V" _% w/ g* l0 j
2002: 565-628.2 u5 C- n6 z. n' U3 w& t  q
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! d* o8 P. e# v4 [/ L& [4 s
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
! s- ~& D7 X' C* b7 d1 P
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