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. o8 a4 q+ A7 w1 N
Boy Induced by Indirect Topical3 P+ t# o* ?: A3 v  _
Exposure to Testosterone) j" f4 m4 \0 v! N" \
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
8 P: u% O" z* |2 F3 `and Kenneth R. Rettig, MD1
7 z0 x, ^* A* T5 E6 w0 HClinical Pediatrics$ j& e) ?  f; ~1 i
Volume 46 Number 69 v" b9 V0 ^* B( B( l
July 2007 540-543# c$ I$ H% ]6 U
© 2007 Sage Publications, R: ~9 H6 Y' R+ A
10.1177/00099228062966517 H8 F8 k2 M8 r0 m5 Z2 f
http://clp.sagepub.com; v! ^1 U: D, D! e* ~, l
hosted at
; X/ A) O! A) g5 a! ]http://online.sagepub.com
" U" s. i+ s7 \Precocious puberty in boys, central or peripheral,
% ?! @# `- o; U( A/ Ois a significant concern for physicians. Central
. Z: V( L. s$ Z/ V& W& bprecocious puberty (CPP), which is mediated9 c* H) @; G" }0 p
through the hypothalamic pituitary gonadal axis, has6 \5 G0 o! Z& p
a higher incidence of organic central nervous system
5 I) }) V/ t8 ~  x+ Klesions in boys.1,2 Virilization in boys, as manifested9 Q4 c" y. H7 T) E
by enlargement of the penis, development of pubic) }) Q/ k5 @; L3 K% U0 a1 c
hair, and facial acne without enlargement of testi-: h0 F" O/ `+ Y" \, C
cles, suggests peripheral or pseudopuberty.1-3 We
% Z% R* W2 W/ }! @' A4 R* S1 @report a 16-month-old boy who presented with the
7 k  d% E6 g6 [( [( s- f: _! m  e( w6 y& Yenlargement of the phallus and pubic hair develop-  Y7 P( f4 q% ^  B7 s; {0 {
ment without testicular enlargement, which was due
; \0 a( Y9 k3 C# o8 n3 D# t% Gto the unintentional exposure to androgen gel used by3 x$ c6 d, w6 N/ ^
the father. The family initially concealed this infor-; W# K$ }9 U* q' F) E9 u
mation, resulting in an extensive work-up for this
- h! S+ j( e$ O& l2 G+ hchild. Given the widespread and easy availability of
0 ]; d  D( O3 E4 N6 w8 C. K+ E: dtestosterone gel and cream, we believe this is proba-
2 }6 W& M: q8 z9 m) ^6 @bly more common than the rare case report in the* R6 ]( r, y' S0 {1 d5 Z
literature.4' |+ g1 @; F0 J( E1 F6 k. f+ f& k
Patient Report3 s6 F- W. g1 a1 ~
A 16-month-old white child was referred to the
5 U, k  B4 d9 Q7 o0 R4 m/ x. N1 ]endocrine clinic by his pediatrician with the concern3 Y( R: A! [7 @5 r
of early sexual development. His mother noticed
$ H* R& r# j6 b5 \! Vlight colored pubic hair development when he was5 t: `: p* H8 p; C
From the 1Division of Pediatric Endocrinology, 2University of  \. U! u- Q# F0 M5 Q% J/ _
South Alabama Medical Center, Mobile, Alabama.
; K! R" ~% ^& AAddress correspondence to: Samar K. Bhowmick, MD, FACE,; ]! U. r, n# S6 X' p4 V
Professor of Pediatrics, University of South Alabama, College of
7 s! }9 a  y$ }0 rMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( r4 P6 b  ^, Ee-mail: [email protected].2 A5 U# {% V2 {' v$ A9 I
about 6 to 7 months old, which progressively became
! V- I) k' e5 Y: edarker. She was also concerned about the enlarge-, L  E  Z) A" c
ment of his penis and frequent erections. The child
+ X$ ]3 ?6 v7 y1 Z; }1 \- C3 twas the product of a full-term normal delivery, with
' Y& A% D  f+ s4 ]3 R7 H2 ta birth weight of 7 lb 14 oz, and birth length of( P, o1 \! P9 z# O9 E, n2 r( N
20 inches. He was breast-fed throughout the first year
: D& _$ K5 f# A1 A+ f0 l  \of life and was still receiving breast milk along with
6 {0 m. B' w- i; c1 tsolid food. He had no hospitalizations or surgery,
* V* {; {/ n4 ~+ @" r; E! I7 Pand his psychosocial and psychomotor development6 ]- R$ L+ e5 X4 V' M( B
was age appropriate.
1 b9 _; ~9 u% |* C+ }* {2 \+ }The family history was remarkable for the father,
4 B" x& V" w+ x  C; c7 Ewho was diagnosed with hypothyroidism at age 16,' T. l8 ]1 a- n5 B; k$ f
which was treated with thyroxine. The father’s
/ B3 _9 H& q# K, Q- `height was 6 feet, and he went through a somewhat
% N# T7 j. w* t. w1 L3 ]# m8 kearly puberty and had stopped growing by age 14.; ?! V6 E& Q2 p3 \1 a' e
The father denied taking any other medication. The
( |' y% q: `+ K, n' q3 \1 }child’s mother was in good health. Her menarche
8 p* ?2 N" F5 G! `was at 11 years of age, and her height was at 5 feet1 T) O' X4 y2 f  i* r
5 inches. There was no other family history of pre-
$ J% d! y# N( @9 u- A- Vcocious sexual development in the first-degree rela-1 g9 X4 m1 e2 x2 v
tives. There were no siblings.
5 }5 J! t& X8 p0 DPhysical Examination
6 }: p4 k0 Z+ h" L' J1 z3 e; DThe physical examination revealed a very active,
( b0 I; \9 z! X( G, L( K5 r( vplayful, and healthy boy. The vital signs documented
$ z, i" l9 J2 Z5 I# _, B1 Va blood pressure of 85/50 mm Hg, his length was
9 ?5 L  }8 T) ]( ?+ S7 l90 cm (>97th percentile), and his weight was 14.4 kg% ]  y$ n+ |$ T9 w; l
(also >97th percentile). The observed yearly growth# t5 @0 j3 M/ J
velocity was 30 cm (12 inches). The examination of) A& ]+ U, `8 A' d6 G  v
the neck revealed no thyroid enlargement.
) d( A$ C. Q1 V9 q) _' vThe genitourinary examination was remarkable for' b9 p. r8 N0 q4 v
enlargement of the penis, with a stretched length of  d% k' u8 Z$ L4 ~& x( c8 p
8 cm and a width of 2 cm. The glans penis was very well
2 Y% ~' S: `( a* T" q; @) V; hdeveloped. The pubic hair was Tanner II, mostly around
) w. J# G! e2 O- R: v540
( r5 i5 L4 Q3 |# `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 {# p) }9 g9 l3 |) Mthe base of the phallus and was dark and curled. The. C) A$ N7 j6 V( I
testicular volume was prepubertal at 2 mL each.
1 ^+ a% l# }6 z! q; jThe skin was moist and smooth and somewhat: C  J4 a+ s! v" f5 @' i6 x
oily. No axillary hair was noted. There were no
5 K  R5 S1 U  [3 {7 E0 Kabnormal skin pigmentations or café-au-lait spots.& b. s( x: }4 m3 R8 p
Neurologic evaluation showed deep tendon reflex 2+
" m0 L$ F3 v3 Z$ O/ ?; J5 ]7 ?bilateral and symmetrical. There was no suggestion! T5 i7 U! F7 [0 A! x0 I8 e# k
of papilledema.
" q$ d! }( w/ D& `) @Laboratory Evaluation
7 _4 W; N7 Q( `3 B' JThe bone age was consistent with 28 months by3 O5 _5 F7 D2 f) v" `7 R
using the standard of Greulich and Pyle at a chrono-
" Q2 z1 @  v# g" ~) c+ Z- k: slogic age of 16 months (advanced).5 Chromosomal0 ^) {# f" b% t! i1 Q
karyotype was 46XY. The thyroid function test! N* a, c, L0 `2 m% `! [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-! p- e" d! R6 u1 o& y) m* e
lating hormone level was 1.3 µIU/mL (both normal).
0 O( n6 D: P) u& C% r+ a& F7 YThe concentrations of serum electrolytes, blood& c  K1 k& q8 t. u& |' ~/ Y- N
urea nitrogen, creatinine, and calcium all were
5 n2 [- W4 C4 ~0 wwithin normal range for his age. The concentration5 I8 j2 F7 ?5 h) ]
of serum 17-hydroxyprogesterone was 16 ng/dL
. ~5 G) l7 w7 g, V' `" ^) y2 D- m(normal, 3 to 90 ng/dL), androstenedione was 20
' F  N4 ~/ I4 m! X! l/ c3 h2 L& l* sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 Z) q( e0 I5 T' X1 B7 P
terone was 38 ng/dL (normal, 50 to 760 ng/dL),3 q& N+ d4 L- z3 V0 ~' @
desoxycorticosterone was 4.3 ng/dL (normal, 7 to3 d$ Q% k& [% r& D8 o
49ng/dL), 11-desoxycortisol (specific compound S)3 g; q- J/ n! q5 M
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-' o+ u: N2 i' Y1 N7 T7 X$ Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; Z+ i9 b& n/ C! I! {6 ltestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
6 e. M" z( S% [8 o3 fand β-human chorionic gonadotropin was less than3 c! P& a8 k) R8 g& n; D; Z
5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ x$ k2 v0 ]& Lstimulating hormone and leuteinizing hormone$ K- J* x' H3 M# K6 H
concentrations were less than 0.05 mIU/mL8 z% \4 _& A& g' p
(prepubertal).
4 n" d, C" p& d% iThe parents were notified about the laboratory7 A* B% ]4 v% G8 i
results and were informed that all of the tests were+ e/ |( d3 q% _
normal except the testosterone level was high. The
0 ]6 F* c+ V6 M% Z0 Mfollow-up visit was arranged within a few weeks to* v  L6 p: T8 @
obtain testicular and abdominal sonograms; how-
) e4 Q' C% |( S) y. y+ L- Lever, the family did not return for 4 months.- B) o4 Z: J. x/ v1 C4 b
Physical examination at this time revealed that the4 e! O0 L- Q4 {- F7 V) Y2 o4 a) s
child had grown 2.5 cm in 4 months and had gained* @/ X. N- c2 H  u( L+ c: P
2 kg of weight. Physical examination remained
0 M, K. R1 J1 G0 ?: yunchanged. Surprisingly, the pubic hair almost com-4 u6 m- V1 r1 ?8 s
pletely disappeared except for a few vellous hairs at
* h. ^+ |4 D9 S4 U% H/ _) Ethe base of the phallus. Testicular volume was still 2. h: ]/ D& W- W
mL, and the size of the penis remained unchanged.
, W, L4 [& o# D5 ?: l+ l3 oThe mother also said that the boy was no longer hav-
0 |6 Q7 M9 o4 `* r9 W3 Y/ sing frequent erections.
" {, J2 m+ r1 x9 x+ u- f+ G# ]) K; \Both parents were again questioned about use of
& r% T. H: r, i9 C6 K7 Vany ointment/creams that they may have applied to" r. @7 ~' `6 f& T2 ^2 a' w9 p
the child’s skin. This time the father admitted the
! q# w$ ~3 T+ f! K* @Topical Testosterone Exposure / Bhowmick et al 541* I* f2 T; C1 @6 @! }
use of testosterone gel twice daily that he was apply-
' H. j! k* J2 V* Ning over his own shoulders, chest, and back area for
* d, G: I$ u4 T/ S- [, t1 Pa year. The father also revealed he was embarrassed4 x9 ^% |& k# c0 h7 D: Y4 S+ y  G
to disclose that he was using a testosterone gel pre-
) f8 @" e% d0 ]+ _scribed by his family physician for decreased libido
3 z; u8 W5 P: ]& \4 I4 \secondary to depression.
4 s/ `% ^) s5 OThe child slept in the same bed with parents.4 B3 J  r' I, b
The father would hug the baby and hold him on his
' q: V# G6 W" p1 {: schest for a considerable period of time, causing sig-; Z9 h* E4 L0 X4 s# p
nificant bare skin contact between baby and father.( s: E8 d- K7 z* v6 N( v* W
The father also admitted that after the phone call,5 }: d( v" V+ x+ w- w
when he learned the testosterone level in the baby
, n' L4 J$ B0 w+ d! [was high, he then read the product information& t+ B- I# V% q7 a  J
packet and concluded that it was most likely the rea-# z5 g& H( q6 r4 V- S$ h3 Q# o
son for the child’s virilization. At that time, they
1 K" f  M; }+ A% Rdecided to put the baby in a separate bed, and the( {8 M2 `! R$ j
father was not hugging him with bare skin and had/ B* B' t* X$ g- R  s
been using protective clothing. A repeat testosterone1 I  L* p$ H7 g
test was ordered, but the family did not go to the
% U/ @7 j# Y; z  h* c8 K) C( tlaboratory to obtain the test.
! k( b' L+ s0 ~6 Z8 FDiscussion0 |2 t) H! B  C3 s$ t2 v' ]
Precocious puberty in boys is defined as secondary
# n/ I. i, {; I5 ~5 lsexual development before 9 years of age.1,4
3 C6 t5 O, V: n9 OPrecocious puberty is termed as central (true) when
& q5 g" m7 C8 h; L: n2 D  D, cit is caused by the premature activation of hypo-% R# M) \& ]1 _- ^( @: a) f5 j
thalamic pituitary gonadal axis. CPP is more com-
2 Q1 z& v/ ?# omon in girls than in boys.1,3 Most boys with CPP
  P+ V- K0 P. e& o7 }0 p8 c1 r, imay have a central nervous system lesion that is
" n2 {  M3 j; T- aresponsible for the early activation of the hypothal-
  O& b. ~6 g& ^amic pituitary gonadal axis.1-3 Thus, greater empha-
- s/ h" B6 N% t! a! R5 psis has been given to neuroradiologic imaging in+ o* ]2 k+ P6 s: h
boys with precocious puberty. In addition to viril-
% ~$ Y; `  s- B$ I% T- r' x: U7 _, Kization, the clinical hallmark of CPP is the symmet-
( ~# b$ q" e0 F2 V7 O! Frical testicular growth secondary to stimulation by9 l' i. F5 Q1 g% m! `) A* m
gonadotropins.1,3
2 R+ b/ h' g+ M5 ]' ^& N* _, zGonadotropin-independent peripheral preco-3 I" Q: T8 u7 k
cious puberty in boys also results from inappropriate
* w0 N& G  A+ Z- O0 wandrogenic stimulation from either endogenous or7 X0 j$ @, W9 O8 ~& Z+ C
exogenous sources, nonpituitary gonadotropin stim-9 h5 J+ _& m; d9 r6 T6 f
ulation, and rare activating mutations.3 Virilizing
& V4 J& R9 i' |congenital adrenal hyperplasia producing excessive1 r" y6 Z  ^; o7 D" q/ a! Y/ n
adrenal androgens is a common cause of precocious: V+ d' S: ]8 S% v4 `% l& M
puberty in boys.3,4
" {+ l( E7 l  P' iThe most common form of congenital adrenal
: r) D' W% A  A( Q* A2 Q' `hyperplasia is the 21-hydroxylase enzyme deficiency.
' e' V4 q' s' Z7 KThe 11-β hydroxylase deficiency may also result in
2 e. e/ a7 }; ~excessive adrenal androgen production, and rarely,) r& T- E+ T- i5 n! K
an adrenal tumor may also cause adrenal androgen' q6 D8 b' w" F3 ^- }
excess.1,3# ~- J$ w, o* L5 b/ Y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 y+ U  D# ?$ C" t542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
# r  i2 \" @2 j  K0 cA unique entity of male-limited gonadotropin-: X  T8 ?/ X0 a3 c
independent precocious puberty, which is also known
5 Z+ t* Z0 t$ S* g! ?as testotoxicosis, may cause precocious puberty at a
8 S# P$ i  I5 Uvery young age. The physical findings in these boys% h' L; @/ H. G* q7 B
with this disorder are full pubertal development,* V4 e' ~: i  j" \6 T- i6 i
including bilateral testicular growth, similar to boys  a' V# X$ q8 h, u7 {# Q" j$ }
with CPP. The gonadotropin levels in this disorder
) g" s& }7 l6 S- i- Iare suppressed to prepubertal levels and do not show+ B2 L- e5 V) r/ G; U9 }- v& U
pubertal response of gonadotropin after gonadotropin-6 ?. y& g2 f6 ?$ a
releasing hormone stimulation. This is a sex-linked
: l& r" W! ?) U/ r: s6 Q6 Zautosomal dominant disorder that affects only
1 h6 t4 A* g& N6 s, Hmales; therefore, other male members of the family$ E& ]3 L: O& ~) R
may have similar precocious puberty.3
& B: H: B7 p2 \1 {# @' sIn our patient, physical examination was incon-2 P) |# {5 V. q( |
sistent with true precocious puberty since his testi-+ A0 j# Y  P/ _( G% m! d! P6 }
cles were prepubertal in size. However, testotoxicosis+ g$ ?; Z; G! D) ~* S4 v! k
was in the differential diagnosis because his father
" \+ j: r4 c( f7 u+ Z; G6 }started puberty somewhat early, and occasionally,
7 _( n, a: ]; C. stesticular enlargement is not that evident in the
5 F5 b1 \! X- M' @beginning of this process.1 In the absence of a neg-
' f' {8 |' R9 z" Y9 R/ Z$ W8 |+ z; ~ative initial history of androgen exposure, our7 B5 w: W' i: l/ t1 |4 g
biggest concern was virilizing adrenal hyperplasia,
- L/ A" h9 b, zeither 21-hydroxylase deficiency or 11-β hydroxylase/ e% `6 r  t2 B7 b9 [
deficiency. Those diagnoses were excluded by find-, M" a- ~3 ?# o
ing the normal level of adrenal steroids.' _. M$ j' S; W% ]+ e5 N$ E9 `/ U" d
The diagnosis of exogenous androgens was strongly% m% O& w7 j+ {: s; O' T2 {
suspected in a follow-up visit after 4 months because
6 V' J1 S$ P9 f4 c" z3 kthe physical examination revealed the complete disap-- H9 Y& m0 _/ z# U: g7 Y/ g' m
pearance of pubic hair, normal growth velocity, and- C1 ^9 A, b4 _  u, m5 A
decreased erections. The father admitted using a testos-; ]% l/ f/ _, I5 z
terone gel, which he concealed at first visit. He was
) H& m4 r  e9 p1 s9 g0 Musing it rather frequently, twice a day. The Physicians’- b7 R/ U9 k6 L$ m) \& q
Desk Reference, or package insert of this product, gel or
1 _+ B8 t0 k# h; g8 I. K7 @! Rcream, cautions about dermal testosterone transfer to& a3 e. M" H4 \# L) w7 ]2 e
unprotected females through direct skin exposure.
. E- Q: D) \0 F- DSerum testosterone level was found to be 2 times the* ^8 d/ P8 X+ A; j" `2 X, M4 h
baseline value in those females who were exposed to
* n: l$ E0 n/ {# Feven 15 minutes of direct skin contact with their male
6 E! X. U( M, k0 Y; ~$ Spartners.6 However, when a shirt covered the applica-8 O% C+ q, X! \% _  W( z. w
tion site, this testosterone transfer was prevented.
; d+ x- b! k4 o) G! aOur patient’s testosterone level was 60 ng/mL,
2 `* P2 J2 g+ ?+ `which was clearly high. Some studies suggest that
% J* E! V, V2 O6 [0 {- ~+ P0 odermal conversion of testosterone to dihydrotestos-2 h5 z+ D# t6 K# `2 w  e: n/ `% r
terone, which is a more potent metabolite, is more
$ I2 ]/ @: a) G; Cactive in young children exposed to testosterone
, @* C" r& I  h+ g9 ]3 _exogenously7; however, we did not measure a dihy-% N$ s$ p% p6 D- q) f' ]7 P' a* }# e
drotestosterone level in our patient. In addition to
9 S" `/ P) h$ g! p- a; T* ]2 _  A' q$ fvirilization, exposure to exogenous testosterone in
9 J% t! Q7 E$ qchildren results in an increase in growth velocity and% L6 z2 f' @2 F3 T' D
advanced bone age, as seen in our patient.
2 q% b1 X4 u, ^The long-term effect of androgen exposure during
1 A+ ~! T, J/ x4 z) T& R1 hearly childhood on pubertal development and final
* }, ^/ t6 e% E( C. {% x3 z  ]adult height are not fully known and always remain, K- \- P! t6 D# A  I( a" A
a concern. Children treated with short-term testos-/ ]/ @4 g, t* U# G( j/ @4 v9 }) R
terone injection or topical androgen may exhibit some
1 Q) `4 M: U" e& P. A. h0 ^0 Dacceleration of the skeletal maturation; however, after: K  p9 l3 l' ]0 b$ O
cessation of treatment, the rate of bone maturation
9 X! l& n% H$ k, i, sdecelerates and gradually returns to normal.8,9
% ^( R, y9 |) Z  V: }: G1 yThere are conflicting reports and controversy. j1 j* n( R4 d% h1 j( G
over the effect of early androgen exposure on adult$ t) b, D/ \6 d' h) c/ R
penile length.10,11 Some reports suggest subnormal
8 z, p! E4 R! o! hadult penile length, apparently because of downreg-
) W4 D9 r+ x/ A7 `$ l" w" k3 Aulation of androgen receptor number.10,12 However,
! k% h0 r! Z: B* }Sutherland et al13 did not find a correlation between1 Z4 l) S7 O- `% H+ @
childhood testosterone exposure and reduced adult
& R9 }" U- F: O+ Z9 X  ipenile length in clinical studies.9 q7 l$ x/ S4 z2 R( N* X" K$ s( D) V
Nonetheless, we do not believe our patient is
% [/ W" ^5 [- A& W( Egoing to experience any of the untoward effects from
7 ?4 l- S. l8 ktestosterone exposure as mentioned earlier because8 v( F7 Q/ Y7 Q2 S
the exposure was not for a prolonged period of time.
7 R  x, l( ?# P& gAlthough the bone age was advanced at the time of8 k$ S) {6 \' w7 ~& C
diagnosis, the child had a normal growth velocity at
* z/ H/ ?, A5 s! j$ _the follow-up visit. It is hoped that his final adult
' x8 g$ w- @) h& Oheight will not be affected.* q7 G- ?  w7 W% v
Although rarely reported, the widespread avail-  j9 B9 N& t6 X4 U: b- x$ Z
ability of androgen products in our society may
% `2 ^1 n! |0 P& u* ~- V) z' [9 aindeed cause more virilization in male or female6 Q% u+ J) R5 y5 n- [( n% s
children than one would realize. Exposure to andro-" n9 T. k- G& b) T5 ?& \# N
gen products must be considered and specific ques-9 ]& y6 p" c/ [2 j5 [% ]
tioning about the use of a testosterone product or
4 t: l- p3 {( ]1 ]; |& z0 l# \gel should be asked of the family members during  h/ @# w" I, u) c) c( ~6 Q
the evaluation of any children who present with vir-  `: c* _; O$ \2 B/ d
ilization or peripheral precocious puberty. The diag-+ b/ X. }) \% Y! l0 @
nosis can be established by just a few tests and by; S: F+ u* g% @
appropriate history. The inability to obtain such a/ M6 R9 Y/ q) k. z' }+ Q0 {! D
history, or failure to ask the specific questions, may8 O1 K+ X. l  p$ Z. [! J
result in extensive, unnecessary, and expensive
" @0 m' o2 ~' ^+ |# v9 `! z4 ?investigation. The primary care physician should be
9 \/ c3 T6 C; T( j  F) t% ?aware of this fact, because most of these children2 R: H- z; N3 k+ {  E- m( [
may initially present in their practice. The Physicians’
9 N. l9 G& w2 o2 f5 S5 I* mDesk Reference and package insert should also put a
, Q4 d/ R9 {% G9 P7 cwarning about the virilizing effect on a male or2 y/ V5 S( u; s/ b2 H9 I; O7 Z
female child who might come in contact with some-
: ]+ z' p0 D. M2 Kone using any of these products.) G7 W  D# ~8 `, {2 T8 W7 P+ q1 ~% j
References
- ]' n, `$ G3 K. b' m1. Styne DM. The testes: disorder of sexual differentiation0 \1 ?4 C4 D! g0 H. B  a! t
and puberty in the male. In: Sperling MA, ed. Pediatric  J7 Y+ K! w, i9 W3 N
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, J2 _5 p9 U0 t) o' o4 r2002: 565-628.
0 I1 Z4 w6 O4 k3 G( |2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ M% _+ t/ [2 T6 D' Qpuberty 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
) `2 t- r8 f3 l6 LBoy Induced by Indirect Topical- D" d6 F% V7 b, F6 H# z# r) @
Exposure to Testosterone
/ _$ s2 @, N2 ?2 n3 F9 x+ MSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) @9 j6 b, i- g; o
and Kenneth R. Rettig, MD1
7 L" W6 [9 O1 T' ?0 J, bClinical Pediatrics/ P0 _- [6 r) y4 y4 ^/ F/ p3 D
Volume 46 Number 6' E1 X+ F& Z/ M# O1 k0 `' W" L
July 2007 540-543# p, Q, |- m. W' d# I
© 2007 Sage Publications
& v$ m4 z% B. H, v10.1177/0009922806296651
# ^$ W( _. }0 r" l. A# Uhttp://clp.sagepub.com7 X7 A+ m# e4 }: \" f
hosted at
& ~$ Y' l2 o& m2 }, J* N  |8 xhttp://online.sagepub.com0 @4 C( `' r5 h/ x. R, J  ?+ |1 v
Precocious puberty in boys, central or peripheral,
# ?& E; J. V3 s" T- B; o( c' G( \4 ais a significant concern for physicians. Central* k" Y5 b7 c' A/ v
precocious puberty (CPP), which is mediated
3 s( x0 N+ j5 Y0 r7 s' z& o" o: s& T" C0 \through the hypothalamic pituitary gonadal axis, has
6 I0 `& f2 e0 O/ t: F9 E2 na higher incidence of organic central nervous system9 D: m  G) H* y- f2 y2 U* _
lesions in boys.1,2 Virilization in boys, as manifested$ [- k8 L! y% U6 J) q! H% c8 w
by enlargement of the penis, development of pubic/ T6 l- D; R7 E) c* u. l9 B8 o
hair, and facial acne without enlargement of testi-
' A! ^* v7 G. |8 W) D4 f$ B) Ccles, suggests peripheral or pseudopuberty.1-3 We2 ]4 L, Y6 H6 V% ^6 r8 o: ^
report a 16-month-old boy who presented with the3 \5 I( y# F* [( M( g
enlargement of the phallus and pubic hair develop-8 c$ b2 N$ H, E' {
ment without testicular enlargement, which was due$ `! D8 W2 L- \8 e
to the unintentional exposure to androgen gel used by
. F8 s9 I, @1 l' G) N, o6 wthe father. The family initially concealed this infor-
9 S4 c5 Z' G  Z( q6 T9 y9 zmation, resulting in an extensive work-up for this4 T0 `  _0 E- Q& f  i6 d
child. Given the widespread and easy availability of
% _* {$ Y: ]& L7 Q; Otestosterone gel and cream, we believe this is proba-
' P4 [' _/ x8 w7 h( X; ^bly more common than the rare case report in the- e3 ?4 c6 ^! |! [
literature.4( @: ?7 ~% N" ~; L( ?' ?5 z
Patient Report- [) S9 M, S/ V5 B4 T
A 16-month-old white child was referred to the
5 I$ I+ R; s  f$ b# b8 Pendocrine clinic by his pediatrician with the concern
" J" V" N  Z, }) ~of early sexual development. His mother noticed8 u  ]! [: K2 ~. T8 R
light colored pubic hair development when he was
1 H( `: I: q1 s1 [- DFrom the 1Division of Pediatric Endocrinology, 2University of6 `% K7 y/ }6 m# Z
South Alabama Medical Center, Mobile, Alabama.
0 ~8 ^" l8 \1 W- k8 ~$ I9 u3 }4 \4 @Address correspondence to: Samar K. Bhowmick, MD, FACE,' r( ~- h4 q' Y; k/ c
Professor of Pediatrics, University of South Alabama, College of. ^$ i: a% H2 y+ N
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 k5 d6 e! O7 n3 E' W  o- me-mail: [email protected].
+ n4 }7 J" P* J, l, v/ `about 6 to 7 months old, which progressively became6 d9 g; C2 c7 k5 W# Y
darker. She was also concerned about the enlarge-
9 G! K/ J5 B1 T! N+ ament of his penis and frequent erections. The child
5 ]9 e8 D% [% N2 p6 x7 S+ L6 Mwas the product of a full-term normal delivery, with
* E1 y; E6 e4 e  U) H* [$ K5 J) Ha birth weight of 7 lb 14 oz, and birth length of
& w' f) d& M( `20 inches. He was breast-fed throughout the first year
- g4 ]9 l& m8 G) n& g3 ]2 L" J8 cof life and was still receiving breast milk along with
. i% Y2 t3 a8 v# Y/ osolid food. He had no hospitalizations or surgery,: M; p6 B" f- J4 p; F& F. u3 U
and his psychosocial and psychomotor development
8 K% ?$ K9 U8 J( \. h5 Fwas age appropriate.
: U4 _9 g7 i; \) m) }The family history was remarkable for the father,
: J7 [6 w4 z3 `/ Y( f6 B; nwho was diagnosed with hypothyroidism at age 16,
$ f6 G% P$ i; ^' q/ {which was treated with thyroxine. The father’s
# q1 v  B* Q% h7 @+ n# [height was 6 feet, and he went through a somewhat" u# g! \  J' m$ N( A7 b
early puberty and had stopped growing by age 14.# E+ `3 ?+ H! P. d" |
The father denied taking any other medication. The
- O. z+ y" m2 U- y) Ychild’s mother was in good health. Her menarche
# X( j; \) l, f+ z/ Cwas at 11 years of age, and her height was at 5 feet
( I/ Q# N6 R  ~+ S5 inches. There was no other family history of pre-
! O6 _# s" E9 ^9 ^1 mcocious sexual development in the first-degree rela-
$ X9 T! k" `3 w+ utives. There were no siblings.6 K1 G7 }: k+ R4 r) C7 N
Physical Examination
% e$ S% I' P8 VThe physical examination revealed a very active,
5 d+ A" M$ \& V% o; Xplayful, and healthy boy. The vital signs documented) B6 _' R3 A0 y! h( \
a blood pressure of 85/50 mm Hg, his length was
) o# P) Y  u' }/ u8 L& }90 cm (>97th percentile), and his weight was 14.4 kg
2 o# S  D2 d, n(also >97th percentile). The observed yearly growth5 @/ a. X! E9 U4 E
velocity was 30 cm (12 inches). The examination of. a. n/ [. h- O6 W5 }8 n3 I; C
the neck revealed no thyroid enlargement.
2 ?# J; V. p; b/ d) uThe genitourinary examination was remarkable for
" L6 x4 F" |- X5 g; u0 \enlargement of the penis, with a stretched length of
) @2 L: Q, \1 E: X5 H+ j8 cm and a width of 2 cm. The glans penis was very well
/ x9 F# N' f  H: K. `8 ydeveloped. The pubic hair was Tanner II, mostly around
% N$ s% X1 n8 |+ _  k, Q: g+ L7 g0 O540+ S( O: z' f6 s4 J$ ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, Y2 x) r5 c3 x6 X( o" dthe base of the phallus and was dark and curled. The9 j" v. [8 e/ s
testicular volume was prepubertal at 2 mL each./ s6 W8 r' i6 c& H7 \/ L' g) d
The skin was moist and smooth and somewhat
; B0 {4 L) [2 Q' k. V* Goily. No axillary hair was noted. There were no: D6 H/ b# O6 L' w4 D* N" }( J
abnormal skin pigmentations or café-au-lait spots.
4 ~3 ~. C( _% d" JNeurologic evaluation showed deep tendon reflex 2+
: L4 l- u# H3 v5 |$ A- }bilateral and symmetrical. There was no suggestion- V3 c6 }. E$ L: E
of papilledema.- r/ p. J8 T) g! H/ Y3 O# r
Laboratory Evaluation: e. w/ ?3 n$ R0 `
The bone age was consistent with 28 months by+ e) ^8 A$ J: V  i9 u5 Q5 {
using the standard of Greulich and Pyle at a chrono-4 U( x+ c4 u0 R+ f! Z
logic age of 16 months (advanced).5 Chromosomal
+ N, m& x3 h; ^# q7 H% skaryotype was 46XY. The thyroid function test
& ]2 `  @  g  F  I- l+ Ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-2 L9 F$ B, M/ c: ~( ?& Y' y2 Z
lating hormone level was 1.3 µIU/mL (both normal).
0 V' x; y* x. D3 I* pThe concentrations of serum electrolytes, blood
9 e2 O9 E9 R' @) |1 S3 L  [# Curea nitrogen, creatinine, and calcium all were/ I9 A7 T5 s  @" F
within normal range for his age. The concentration5 N! p+ O2 ?: Z- V# {
of serum 17-hydroxyprogesterone was 16 ng/dL( P: k: Y& t) T1 _
(normal, 3 to 90 ng/dL), androstenedione was 20
7 p9 {6 [3 g4 M" E3 N6 x$ c) Xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
* P4 H- ^6 B/ }! L/ ~: Yterone was 38 ng/dL (normal, 50 to 760 ng/dL),& `" [6 Q8 v9 b# \0 ]/ u; j0 i. G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 |/ g1 |8 x" p, h4 O" j8 v49ng/dL), 11-desoxycortisol (specific compound S)# [9 E" ]/ V$ \! o9 A3 k0 Z
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 M: V8 x9 ]5 c. i4 U6 L
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, _4 u  X5 |$ `- m& X
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 p  k( Q3 u4 Band β-human chorionic gonadotropin was less than
- J! ?( p$ k7 ]. p0 X& G! j5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 U; F" l0 z; b5 estimulating hormone and leuteinizing hormone
- U( o$ q- U& cconcentrations were less than 0.05 mIU/mL; N0 ]1 f& b7 W7 c2 Y, h
(prepubertal)., d, A5 ?4 I$ G( j7 Y5 h
The parents were notified about the laboratory
" o1 ~0 w$ F9 ~6 r. fresults and were informed that all of the tests were
5 u% A; R. t+ |8 J$ Vnormal except the testosterone level was high. The6 I% }3 ~- K0 S7 a$ p& E
follow-up visit was arranged within a few weeks to; C) T  `# p* y# }1 v& p
obtain testicular and abdominal sonograms; how-8 m" i9 ^6 A/ _8 S, E" S- S% A
ever, the family did not return for 4 months.# H' r- j! c# u* u. z
Physical examination at this time revealed that the
3 I/ J( w" G4 e" V- t  ?child had grown 2.5 cm in 4 months and had gained7 m- b  \: C9 @; m6 f3 ?! V- i$ q
2 kg of weight. Physical examination remained
$ N6 t/ E0 `" Z4 H0 k! t4 L% i0 Zunchanged. Surprisingly, the pubic hair almost com-$ M9 f' ^' E+ e! y
pletely disappeared except for a few vellous hairs at
5 w1 P6 L" |! I  G& ]the base of the phallus. Testicular volume was still 24 X; }( a7 i' x( H2 L! r8 c! n: m
mL, and the size of the penis remained unchanged.1 ?( N" t. Y; {6 T% n
The mother also said that the boy was no longer hav-
, w# i0 T/ Q. Ging frequent erections.2 i* y% k. y; N$ b. j  u
Both parents were again questioned about use of) V+ E- J, m. `& m: @
any ointment/creams that they may have applied to0 V/ M) B) P+ D5 _. U* J# C
the child’s skin. This time the father admitted the! e1 }, M" V6 L+ w9 ]9 ]) o
Topical Testosterone Exposure / Bhowmick et al 541! F* x% J/ X) i1 s  k3 D. P0 ^; n
use of testosterone gel twice daily that he was apply-2 n( m, Y* T, N7 z" H( M) V
ing over his own shoulders, chest, and back area for# H8 C1 B! Z, ~/ S: {, p
a year. The father also revealed he was embarrassed
% x! K) J" i3 g) O7 ~5 ito disclose that he was using a testosterone gel pre-; y  T4 j6 V* W9 h" @. I
scribed by his family physician for decreased libido
) Q0 a6 l0 `5 Z. n) T9 e" z/ ?secondary to depression.& U# ~4 B9 V% t6 m) l* W! B
The child slept in the same bed with parents.
) f7 A9 j1 d5 o7 [2 F( I" hThe father would hug the baby and hold him on his
, o; c2 G3 w5 Vchest for a considerable period of time, causing sig-
9 j: g2 A8 ~/ anificant bare skin contact between baby and father.) Y# M8 q5 N9 y' I; s6 N
The father also admitted that after the phone call,
. p" ~6 R2 B  Y* Z& bwhen he learned the testosterone level in the baby
9 [1 S  f! r5 w. g3 W/ s: Nwas high, he then read the product information' _' g( L* ?3 V6 `9 B7 o- r
packet and concluded that it was most likely the rea-4 T" K" B" a+ G( Z( i9 ]& j4 |) E
son for the child’s virilization. At that time, they
3 {0 h  a& [3 tdecided to put the baby in a separate bed, and the  }+ @8 [' d0 R& N+ U- s  b! c
father was not hugging him with bare skin and had8 B! n* V1 s) x. F9 P3 ^. o; e) G! N
been using protective clothing. A repeat testosterone  J  H/ k" z! \& o) ^
test was ordered, but the family did not go to the
( e/ N8 G2 t% O3 e4 g  }. k$ @6 xlaboratory to obtain the test.
5 Q0 `9 f1 Q0 U$ |  g& qDiscussion
% p/ X4 t8 Q" Z1 dPrecocious puberty in boys is defined as secondary3 o4 N4 [* P+ ^# U$ ^
sexual development before 9 years of age.1,4
: k$ o' y9 B$ I% zPrecocious puberty is termed as central (true) when
7 Z9 c& ]7 @0 M# Ait is caused by the premature activation of hypo-4 h& |2 K. d& U3 m+ Y& C
thalamic pituitary gonadal axis. CPP is more com-. i( ]/ e! Y, M. g. V
mon in girls than in boys.1,3 Most boys with CPP
, [% L3 X$ G. I, q  Umay have a central nervous system lesion that is
. C8 Y7 N" f1 M7 p0 q% A2 B; Nresponsible for the early activation of the hypothal-
( {8 m9 c+ F& Wamic pituitary gonadal axis.1-3 Thus, greater empha-
/ n) s( u" f" F& a1 zsis has been given to neuroradiologic imaging in
1 ]8 H* n, w+ d, p/ Jboys with precocious puberty. In addition to viril-
, L/ r' l1 N; ?$ G! t9 hization, the clinical hallmark of CPP is the symmet-- Y# s4 k2 k/ d! }
rical testicular growth secondary to stimulation by3 B8 H. d* p; c9 F1 ?$ H1 F) F
gonadotropins.1,3$ M6 D# t; ]7 ?9 p, w4 X0 ^
Gonadotropin-independent peripheral preco-( L* ]7 r) x5 h1 L  t6 Z
cious puberty in boys also results from inappropriate( Y* l' K+ ]: C% E6 L( _
androgenic stimulation from either endogenous or, c% l/ n1 }7 f0 s* ]
exogenous sources, nonpituitary gonadotropin stim-: ^2 B. t: k" P* `; D  ^
ulation, and rare activating mutations.3 Virilizing
$ _4 m* [4 y' t$ v7 k+ @2 \congenital adrenal hyperplasia producing excessive
. Y) r# C2 C) j) \8 xadrenal androgens is a common cause of precocious5 [& w+ Y* F  j7 X& r7 H) h8 \
puberty in boys.3,4: b7 G, p9 q3 [. l/ u: a0 I
The most common form of congenital adrenal0 Z' }0 S) C6 f4 w$ r$ |* \
hyperplasia is the 21-hydroxylase enzyme deficiency.# ~8 I# z4 W8 j2 D3 R: g
The 11-β hydroxylase deficiency may also result in. f% K" l  ]$ T
excessive adrenal androgen production, and rarely,
* a! V; X$ D7 e7 x. e/ \7 s( Ean adrenal tumor may also cause adrenal androgen9 r' a9 [3 S' a1 o+ x2 i& |( e
excess.1,3
3 e. R3 S$ Z. Y) K0 d$ nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* ^; h# ~+ d  M0 }  C542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 P; ^7 Z* b1 S+ u9 ~6 q8 R3 e
A unique entity of male-limited gonadotropin-2 s6 F1 Z: M& ?* i  G& g; o
independent precocious puberty, which is also known
4 z1 B: j1 _5 Q& R4 f7 v+ ?as testotoxicosis, may cause precocious puberty at a
! t3 n, C+ d/ \; Xvery young age. The physical findings in these boys
# ~4 D% r4 S* Swith this disorder are full pubertal development,
/ r/ g$ n+ L0 A4 x* z, @2 }# {including bilateral testicular growth, similar to boys3 i! O" ^" P7 f7 @  f; _
with CPP. The gonadotropin levels in this disorder  S3 E$ ?% L" l( u
are suppressed to prepubertal levels and do not show  `1 @! `5 c3 [$ a! Z* Z* r
pubertal response of gonadotropin after gonadotropin-
, Q! E3 U. x0 D& z! _releasing hormone stimulation. This is a sex-linked
% L* P. s& c: m* w/ Aautosomal dominant disorder that affects only
9 l* v9 ~% @& R. C& q8 Y& M7 q/ f) [males; therefore, other male members of the family
3 B# _$ ^' a# `" x( I/ umay have similar precocious puberty.3
( v' C& u) s0 wIn our patient, physical examination was incon-& E4 T; x7 n& L- D
sistent with true precocious puberty since his testi-+ d# i# }  |: g$ ^
cles were prepubertal in size. However, testotoxicosis: K$ I+ t- {" h8 J- j" C( ]& w. D
was in the differential diagnosis because his father. @8 G2 c1 Y7 L- m; X3 z
started puberty somewhat early, and occasionally,
7 M4 F5 y- K3 j; m* ftesticular enlargement is not that evident in the& i* v, @4 H' n# J+ c( R9 m2 f6 q
beginning of this process.1 In the absence of a neg-
6 i9 t5 d9 E: r* ~# e& kative initial history of androgen exposure, our
/ z" q; x5 S1 c# \# o9 X) Abiggest concern was virilizing adrenal hyperplasia,/ `3 c" K2 }& T" X  `
either 21-hydroxylase deficiency or 11-β hydroxylase0 I. z! e$ r1 B6 ^& G7 t5 i3 Z
deficiency. Those diagnoses were excluded by find-
+ [, }3 K! e: g3 w8 `! B: {. bing the normal level of adrenal steroids.$ S0 g3 T2 B; R7 a; I  J8 S: F
The diagnosis of exogenous androgens was strongly
1 R3 x4 m1 w5 w# f4 z. Nsuspected in a follow-up visit after 4 months because0 R5 R1 M' Y4 Q9 ~! ~* D+ _+ F: @
the physical examination revealed the complete disap-& v1 b9 |5 @, |( r+ `8 S2 c$ ]4 @
pearance of pubic hair, normal growth velocity, and
6 X5 E5 P2 i- A" Jdecreased erections. The father admitted using a testos-+ L8 L, X, m# r) r
terone gel, which he concealed at first visit. He was
5 Q' M; q1 ^7 \! P( O$ husing it rather frequently, twice a day. The Physicians’/ k- \  v! d% c3 H1 ~; u/ W+ N7 g
Desk Reference, or package insert of this product, gel or
  Z: q3 R2 c# Q4 Hcream, cautions about dermal testosterone transfer to
$ i8 f) \! q6 \0 A% Lunprotected females through direct skin exposure.  w8 M7 N, d( r5 E
Serum testosterone level was found to be 2 times the( [/ X1 a, H) m+ O
baseline value in those females who were exposed to
  s$ w: Z/ l3 t8 ueven 15 minutes of direct skin contact with their male
& c" X. t2 x7 F1 W  `6 C( opartners.6 However, when a shirt covered the applica-
; N) \9 B1 j  M7 v9 X5 T6 c, Z" \/ ~tion site, this testosterone transfer was prevented.
& b& V9 `# ~/ X- g( v' _; sOur patient’s testosterone level was 60 ng/mL,
2 x! @+ I! ^: @" }0 B" twhich was clearly high. Some studies suggest that5 F% n4 K, g& C" ]; N
dermal conversion of testosterone to dihydrotestos-
& V2 L5 ~$ |+ B' F4 g/ a9 aterone, which is a more potent metabolite, is more3 p# E5 d2 u5 @) R
active in young children exposed to testosterone+ _! h$ ]" O* p2 j6 H. \1 ^
exogenously7; however, we did not measure a dihy-
; S0 h! d& L5 E& U7 h+ ?: H" F' gdrotestosterone level in our patient. In addition to5 s. e, k; f$ r
virilization, exposure to exogenous testosterone in2 H; q$ T4 M! o; Y) S5 I. S
children results in an increase in growth velocity and
, |% L' K; Z) Zadvanced bone age, as seen in our patient.9 O" K0 @/ C( p: `$ y
The long-term effect of androgen exposure during& l) y2 ^4 t4 M/ l8 U7 X
early childhood on pubertal development and final
5 H/ S7 G- K! u5 Uadult height are not fully known and always remain" ?$ x& ?4 Z# I, M) x, K6 D
a concern. Children treated with short-term testos-1 S% R8 t3 o) I4 s* h# A
terone injection or topical androgen may exhibit some, J; x: S3 X6 C0 N
acceleration of the skeletal maturation; however, after* _1 m5 X9 i4 u" P
cessation of treatment, the rate of bone maturation9 j: v' G9 \) x' L( z6 E* n
decelerates and gradually returns to normal.8,9
) }0 u, m; ~; b. k9 eThere are conflicting reports and controversy( M: M% r: Q6 J3 i* q4 D1 R" [  {
over the effect of early androgen exposure on adult
2 z- \: U' A( ]. b# fpenile length.10,11 Some reports suggest subnormal9 f  K3 C3 o  \# |+ E, \) X
adult penile length, apparently because of downreg-
6 z6 ?( ]' X% Q1 b, b2 [+ Mulation of androgen receptor number.10,12 However,  J: I) A+ @, O2 l3 {5 [% d/ t
Sutherland et al13 did not find a correlation between+ j  `8 P+ u/ a
childhood testosterone exposure and reduced adult
0 A" D& m+ U3 P+ K" R) B8 i: W: d* Upenile length in clinical studies.# n% L6 ~$ x$ f( k6 i
Nonetheless, we do not believe our patient is  S" r) m% O2 H5 C: m
going to experience any of the untoward effects from  |4 T  s* I5 r, E
testosterone exposure as mentioned earlier because
6 i4 s3 Q  h( F( U. Tthe exposure was not for a prolonged period of time.0 o: y; U/ q1 t8 X
Although the bone age was advanced at the time of& f" p( M) a4 N7 s
diagnosis, the child had a normal growth velocity at7 [; O; J# C# T" J6 A
the follow-up visit. It is hoped that his final adult
, {' E" O7 K; f! J; @& Q" _height will not be affected.
  x; X* Y" H. sAlthough rarely reported, the widespread avail-
6 a% W  ]: N. I3 `: L0 C2 zability of androgen products in our society may
0 N6 ~$ c& F8 ]* m: _5 X5 |" mindeed cause more virilization in male or female2 ]' Y0 l' o7 h0 N; R7 p$ r
children than one would realize. Exposure to andro-
1 R8 S& g5 @' ^% Wgen products must be considered and specific ques-
- i. B6 D, u& O" Y# A' o- ]$ jtioning about the use of a testosterone product or
  L4 x8 h% L/ p: J% {gel should be asked of the family members during0 m/ Y( }9 L0 k$ H
the evaluation of any children who present with vir-( k0 [' \9 V# b( B9 W0 N+ M, O
ilization or peripheral precocious puberty. The diag-
+ J0 o2 C$ y9 s* gnosis can be established by just a few tests and by& E2 e, I2 k; ^7 T
appropriate history. The inability to obtain such a
& e' {$ H* N: O6 w; m7 bhistory, or failure to ask the specific questions, may
2 C0 z! J, |0 Hresult in extensive, unnecessary, and expensive
8 z8 M$ }& E  j4 i2 iinvestigation. The primary care physician should be# y  Z+ z, P3 \& E  p1 E" L  b5 j
aware of this fact, because most of these children6 s2 @7 }3 j. }) ?5 W6 M
may initially present in their practice. The Physicians’
7 n' H$ ~1 p6 B  u: }2 {Desk Reference and package insert should also put a
; f5 E( n; t' m9 K1 O7 Ewarning about the virilizing effect on a male or
4 W' _- V. N9 z4 k9 e. mfemale child who might come in contact with some-& m: Q" O1 _, P4 r
one using any of these products.6 j% j+ \2 n0 x2 C: w/ G
References* f, Z7 @9 v( R$ e5 d! D
1. Styne DM. The testes: disorder of sexual differentiation
% D& p$ a9 S5 b$ ^; ~and puberty in the male. In: Sperling MA, ed. Pediatric
) F. x" E# Q8 H2 y- d. T! pEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 @  t6 R5 d4 }# K2002: 565-628.
' a- L5 e6 Z. L. m7 j2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. f; {3 u. N, Q6 C# O5 [/ K2 _0 lpuberty 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

% t+ @; `5 N# I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