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
& X! t$ g$ Z$ s! D% h" O* fBoy Induced by Indirect Topical
" \) m: Z5 z8 p+ UExposure to Testosterone
2 S  Z) h! T6 b* ESamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,27 E2 }9 P) O$ Q3 k
and Kenneth R. Rettig, MD11 y9 x# i8 U0 I+ f) Q0 l9 `; s
Clinical Pediatrics9 j: C! H# }' J. P6 m
Volume 46 Number 6
9 @2 w  \* @/ e8 F2 u# CJuly 2007 540-543
" H6 W8 \# A; H6 t: C4 D% h  u© 2007 Sage Publications
" G% e+ N- @4 M, g1 ^10.1177/0009922806296651
+ k/ B% o- J' s1 V# Whttp://clp.sagepub.com# i4 ?4 j$ q1 J7 C- S4 [: P
hosted at
) {. U0 r5 a" Mhttp://online.sagepub.com
5 }0 t. H& K4 [: |* |Precocious puberty in boys, central or peripheral,4 A$ e, h* I2 J$ W! E* Q
is a significant concern for physicians. Central
- O* a( W1 S$ f. l8 X+ |$ Dprecocious puberty (CPP), which is mediated
/ w' j9 K3 @3 a+ _through the hypothalamic pituitary gonadal axis, has# ?' p8 E4 F% |4 Q0 N) V
a higher incidence of organic central nervous system
1 e& _5 b4 L7 O8 d0 d# t- Clesions in boys.1,2 Virilization in boys, as manifested$ P6 m6 q/ J! h2 Y& P2 T& a# |9 S5 E
by enlargement of the penis, development of pubic
( \: q$ l' K8 phair, and facial acne without enlargement of testi-& p2 H* k- |0 X/ e9 W  u6 d
cles, suggests peripheral or pseudopuberty.1-3 We4 Z6 x8 O4 R& m
report a 16-month-old boy who presented with the
, {6 O$ Z+ A3 \% g3 l) a& D) D8 O5 renlargement of the phallus and pubic hair develop-
; h3 l3 g# s' F  Z; a- M! {ment without testicular enlargement, which was due
: t$ ~. Q; W) o, c" ^  C& @0 H. Vto the unintentional exposure to androgen gel used by- P' Y5 F8 Y& B, D+ }
the father. The family initially concealed this infor-9 g* H, T) ~; ?$ o
mation, resulting in an extensive work-up for this. W5 L" l- o+ m; d  A+ H
child. Given the widespread and easy availability of
7 U/ h- c: M0 m7 ]# Ttestosterone gel and cream, we believe this is proba-3 Y2 f. u3 K# h7 I
bly more common than the rare case report in the# k# V# s4 a6 L- B2 s( E6 K
literature.4
8 c; {5 [/ E3 v+ dPatient Report
0 T1 z+ |4 N. y5 S, QA 16-month-old white child was referred to the( Q/ i# v0 L0 E3 E" Q; `
endocrine clinic by his pediatrician with the concern4 W. ^6 t: w# g! @
of early sexual development. His mother noticed
! u: Z" q! n( r5 \! ?5 p. Ulight colored pubic hair development when he was. e3 ^9 T4 x/ D# L6 U- R+ S; }
From the 1Division of Pediatric Endocrinology, 2University of
# _% v4 X$ y' F/ LSouth Alabama Medical Center, Mobile, Alabama.
- c8 V0 t8 c( j4 x1 qAddress correspondence to: Samar K. Bhowmick, MD, FACE,8 M) U3 D  r5 h+ O  s
Professor of Pediatrics, University of South Alabama, College of
0 Y3 ?) b, R6 ]( E& V# PMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  x+ X0 Q! B$ w+ O9 ^e-mail: [email protected].
' J% L, X: x" E0 S. ?about 6 to 7 months old, which progressively became
7 d  e" _, F3 d! k1 m/ X6 P! cdarker. She was also concerned about the enlarge-
' S2 Y! [0 C, ^9 y2 l0 Fment of his penis and frequent erections. The child
* ^( h) v6 m  Twas the product of a full-term normal delivery, with
$ T. u  B+ l$ N7 C2 R5 H. Ea birth weight of 7 lb 14 oz, and birth length of& X3 W% w& ?; e4 v2 A! ?& [
20 inches. He was breast-fed throughout the first year
2 S4 o2 ~/ e" y2 A2 k% s9 Rof life and was still receiving breast milk along with  J0 e  J  K' o3 B
solid food. He had no hospitalizations or surgery,+ r9 ~7 q: x0 m3 i/ A
and his psychosocial and psychomotor development
* v" x  E$ P$ \$ u' Vwas age appropriate.
! }) u. w  u, C/ D  d4 e3 Y$ MThe family history was remarkable for the father,
2 x1 w, N  ~9 x1 W% y0 l0 }who was diagnosed with hypothyroidism at age 16,
# @& O) t) o! ~% X  ^which was treated with thyroxine. The father’s* y. _& [4 L4 K7 r9 ?& n
height was 6 feet, and he went through a somewhat. H0 Q( `$ J* k8 x$ z' e8 ]" O
early puberty and had stopped growing by age 14.
! f; B5 `4 c9 _8 K# [8 ~4 x& s$ RThe father denied taking any other medication. The
* j5 t- H6 }+ t' G3 cchild’s mother was in good health. Her menarche
9 R! y4 l6 p  G6 k& [was at 11 years of age, and her height was at 5 feet& i( }! z% x. b9 E7 @" L
5 inches. There was no other family history of pre-
& b; n+ G+ o$ O7 a: zcocious sexual development in the first-degree rela-. _% M" y: B, K& S! B& k( i9 p
tives. There were no siblings.1 [/ @4 o( j& A
Physical Examination
5 [+ B1 L& r) S4 \* OThe physical examination revealed a very active,: n& d$ c5 g  l) _
playful, and healthy boy. The vital signs documented
/ n' b5 `0 S% A& Pa blood pressure of 85/50 mm Hg, his length was
& n- n4 @! ^2 j8 z90 cm (>97th percentile), and his weight was 14.4 kg! f$ u* E+ u& M  w* Q
(also >97th percentile). The observed yearly growth1 K; G9 Z" A6 t
velocity was 30 cm (12 inches). The examination of
( U4 p' u; f6 h8 |4 p9 Y& x! {7 o& zthe neck revealed no thyroid enlargement.( J. b2 g* b% j- z9 N* b2 F1 R/ X
The genitourinary examination was remarkable for, |5 E1 p0 u0 P. a. @
enlargement of the penis, with a stretched length of# }# f1 ^8 ?) V, d* q/ ~% L; r
8 cm and a width of 2 cm. The glans penis was very well( [1 C  Y; U: C+ h4 z
developed. The pubic hair was Tanner II, mostly around9 s# f' h$ G1 O/ M2 B; c
540# R9 d7 H5 P! T; }* n6 X
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& W# b( s% ^4 O1 G
the base of the phallus and was dark and curled. The# K/ T+ d% \' o) t; _9 G
testicular volume was prepubertal at 2 mL each.
) q- n: r/ w/ e: \% C' C& iThe skin was moist and smooth and somewhat5 b0 j& l  V5 Q6 A1 X+ ]" X
oily. No axillary hair was noted. There were no
6 j; E9 p3 q$ ^. A: K$ E/ ]" x7 l% oabnormal skin pigmentations or café-au-lait spots.5 Y6 o# h; B& ~, B* O7 Q0 |$ p
Neurologic evaluation showed deep tendon reflex 2+
+ u. t% N4 p( L8 Ybilateral and symmetrical. There was no suggestion
1 S+ D6 S0 v2 x; `/ qof papilledema.( I8 d/ f! W* F! n6 F% m" O
Laboratory Evaluation
* z, \. p& W* {/ n( @3 PThe bone age was consistent with 28 months by3 Y# W; h. h: c! x2 Q4 }
using the standard of Greulich and Pyle at a chrono-+ \- f4 ]" t1 P+ n
logic age of 16 months (advanced).5 Chromosomal
5 ?* O, P! k1 E/ Jkaryotype was 46XY. The thyroid function test
3 f8 c# E" w! n$ X  nshowed a free T4 of 1.69 ng/dL, and thyroid stimu-' S8 r( o1 w6 o/ j4 o
lating hormone level was 1.3 µIU/mL (both normal).. y6 m9 j7 ?, w. o
The concentrations of serum electrolytes, blood9 C+ ?0 u1 b( m3 n3 F
urea nitrogen, creatinine, and calcium all were
: B0 a/ y$ ^% Y( a+ Kwithin normal range for his age. The concentration! l3 A; c% f/ C0 e, b" Z0 R& k
of serum 17-hydroxyprogesterone was 16 ng/dL% v) Q1 B' J! h, g  j* D
(normal, 3 to 90 ng/dL), androstenedione was 20- ~7 L6 E' G: M" R/ p  v* \
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
: W' q8 u$ K; |  P+ g8 I9 [6 b: C# G% Wterone was 38 ng/dL (normal, 50 to 760 ng/dL),- e6 a/ e1 Z/ H1 X  l
desoxycorticosterone was 4.3 ng/dL (normal, 7 to6 ]+ t- L6 Q, t! }
49ng/dL), 11-desoxycortisol (specific compound S)
* `) _! C6 i) q) bwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& t- U. G* q6 U# N& T; ^/ x* ^tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
8 i% M, q$ b' A% Q5 i  E5 ?testosterone was 60 ng/dL (normal <3 to 10 ng/dL),* C2 o5 G6 B/ n" u4 q
and β-human chorionic gonadotropin was less than. T5 _7 t7 w8 Q0 t* e
5 mIU/mL (normal <5 mIU/mL). Serum follicular  R/ V7 B+ z$ G/ A
stimulating hormone and leuteinizing hormone
. C4 z. F3 T6 Aconcentrations were less than 0.05 mIU/mL, L: E1 y! L- T- V! O
(prepubertal).
+ E% J& T8 T( M7 w9 EThe parents were notified about the laboratory) Q1 D0 x4 \, x# g' v
results and were informed that all of the tests were/ W- |1 O0 l  {' K% p
normal except the testosterone level was high. The
8 y' v3 A6 p: zfollow-up visit was arranged within a few weeks to3 c) c' \  w1 K% \9 e
obtain testicular and abdominal sonograms; how-0 X' M& Y9 r- i0 W: Y, m  S* A" s
ever, the family did not return for 4 months.8 d+ W5 z# B! ^* t
Physical examination at this time revealed that the' b% ~% h' ?! \# \: ?* u( \& K
child had grown 2.5 cm in 4 months and had gained
  [9 o& T' k2 r: F  x/ \2 kg of weight. Physical examination remained' g& ~8 o! g. J- G* B
unchanged. Surprisingly, the pubic hair almost com-
! q4 }+ c! g- `# n+ |- mpletely disappeared except for a few vellous hairs at4 B3 q& q, h/ W( ]" Y8 ~; O; r
the base of the phallus. Testicular volume was still 2
& F' w; c1 `7 h6 k3 C! |mL, and the size of the penis remained unchanged.
- ~, H, d) i& _, m0 O' S9 p% CThe mother also said that the boy was no longer hav-
9 d: u: }% I& Zing frequent erections.
2 ]. Q: [$ V$ yBoth parents were again questioned about use of
/ O/ v* l% h! G2 {, E; ?! ^any ointment/creams that they may have applied to+ V  q6 e4 Q4 W" ?) P; a& P
the child’s skin. This time the father admitted the' V9 O0 F3 V' j/ a4 y5 A" f
Topical Testosterone Exposure / Bhowmick et al 5415 h& [$ n7 o9 A% T& J" d0 }
use of testosterone gel twice daily that he was apply-5 q- y" ?- E3 P6 O! d# j
ing over his own shoulders, chest, and back area for
7 z( U# t2 t& x) q* |. t' `6 O5 i, Ya year. The father also revealed he was embarrassed: }0 X2 T' E5 N' ~4 V6 c; P- I
to disclose that he was using a testosterone gel pre-1 h5 S' P' O0 t3 p/ V6 @
scribed by his family physician for decreased libido
% L" m0 f  A9 w$ Xsecondary to depression.
4 z4 m1 `5 \8 d2 A3 D  z# c, AThe child slept in the same bed with parents.
( e- v7 Z: b3 p. EThe father would hug the baby and hold him on his
0 b, q2 e; g2 L4 kchest for a considerable period of time, causing sig-0 }1 `/ D/ G& T* _' H' C2 B; L* \$ u1 C
nificant bare skin contact between baby and father.
+ a* c5 T* N/ Q  L* `The father also admitted that after the phone call,
, I' t0 \) {. X: v. d5 V3 v. t% ?: Gwhen he learned the testosterone level in the baby4 N5 d: N4 h, p+ G2 p: {- D0 t
was high, he then read the product information* z3 F( h7 r1 j6 h* c3 K
packet and concluded that it was most likely the rea-; @* N1 @/ Q6 l, y) n% F1 Q5 x
son for the child’s virilization. At that time, they
5 V; i. V8 A$ |- g  Edecided to put the baby in a separate bed, and the
- z2 j8 l( f8 ?, `father was not hugging him with bare skin and had
$ s, G; ]7 `: v8 g  Ybeen using protective clothing. A repeat testosterone4 h$ M! d8 k5 ?2 c
test was ordered, but the family did not go to the: z5 R# M: R) y- j* Q: u
laboratory to obtain the test., l3 ~6 S9 `0 V% C
Discussion7 V* Q( V+ v( b7 l2 e
Precocious puberty in boys is defined as secondary
5 \/ v% d5 L; _# X) M# fsexual development before 9 years of age.1,4
1 `0 g9 P8 y3 V4 y7 P* n$ ]3 APrecocious puberty is termed as central (true) when
/ j! u1 P! V6 j8 B' K- r& Uit is caused by the premature activation of hypo-! [8 I, C' A; e$ ?( O0 e' K8 X) f* G0 q
thalamic pituitary gonadal axis. CPP is more com-: j9 h3 K3 a" \9 y% }+ Q% g& o  M
mon in girls than in boys.1,3 Most boys with CPP
0 I2 e; G- _; O9 u! b* d" j6 ^2 f& n0 r, Tmay have a central nervous system lesion that is5 v4 D. l, t* N1 X
responsible for the early activation of the hypothal-! _' C1 P& O/ z, n
amic pituitary gonadal axis.1-3 Thus, greater empha-
0 |0 G7 i9 }2 ?+ v4 psis has been given to neuroradiologic imaging in
7 }% [  e. j! Vboys with precocious puberty. In addition to viril-8 B2 v; b; \* V. C1 [+ o. I
ization, the clinical hallmark of CPP is the symmet-
( S, v% ~- D* J# Z; ~8 [) g6 Frical testicular growth secondary to stimulation by2 [! R9 O7 ?5 ~5 p7 T9 [$ Q) `$ h
gonadotropins.1,3
/ t4 ]7 N- k* O& k% eGonadotropin-independent peripheral preco-
% \7 z0 e- l1 K8 O* G4 ~8 u- Ucious puberty in boys also results from inappropriate1 ]! a% P1 e' Y; F  P9 n
androgenic stimulation from either endogenous or
/ H; i: e% _6 c: b+ w4 k# xexogenous sources, nonpituitary gonadotropin stim-5 h1 Y3 D% s# s7 X
ulation, and rare activating mutations.3 Virilizing. t' m% z( g) Y
congenital adrenal hyperplasia producing excessive
5 d* P' _8 Z' aadrenal androgens is a common cause of precocious
0 U& I, X( r! {6 i4 H. bpuberty in boys.3,4
, x# `5 f  `; N- L, a$ L6 YThe most common form of congenital adrenal+ {4 d; h) t+ o
hyperplasia is the 21-hydroxylase enzyme deficiency.
' @, @4 @, ~+ R6 BThe 11-β hydroxylase deficiency may also result in& Q# l1 P! \5 p/ K) O
excessive adrenal androgen production, and rarely,4 X# ~# b5 |3 M) o" T' _/ H: V* n
an adrenal tumor may also cause adrenal androgen
6 c% X( ~1 Q& ?( h1 n: oexcess.1,30 X$ n& j/ m3 X* I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' h3 p: `# C0 a3 y# \5 q8 E% ?
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 E, P' p$ J& }+ LA unique entity of male-limited gonadotropin-
$ f) r8 p( Z3 O' o5 o/ Qindependent precocious puberty, which is also known
# i" L7 Z4 n: kas testotoxicosis, may cause precocious puberty at a
( D- M4 i* T; G9 Qvery young age. The physical findings in these boys& ^$ m1 a- X- b& ^& S; ]
with this disorder are full pubertal development,
4 `: e) U7 o+ I! kincluding bilateral testicular growth, similar to boys
5 [, |8 H/ v. A: F; {4 {with CPP. The gonadotropin levels in this disorder
' e7 ^2 F& B$ k+ Qare suppressed to prepubertal levels and do not show1 R& t! D! J/ m* A5 w# N- A
pubertal response of gonadotropin after gonadotropin-
# z6 y9 [( P- Vreleasing hormone stimulation. This is a sex-linked
% Y$ s+ G" [9 ?( [& U# Kautosomal dominant disorder that affects only% g& i" Q- y# [
males; therefore, other male members of the family) ?' |, b7 y7 [$ C
may have similar precocious puberty.3  t* V( y; f1 L1 R9 l" W7 c
In our patient, physical examination was incon-; c/ ^& k0 k9 W. l
sistent with true precocious puberty since his testi-
: n# X; u( p. N* i9 Bcles were prepubertal in size. However, testotoxicosis
6 |. _9 e% J* |, ]* P! h. n: ywas in the differential diagnosis because his father
! I% m9 g/ \) L" sstarted puberty somewhat early, and occasionally,
1 x9 a( s/ G  Y4 |, t; D! j; mtesticular enlargement is not that evident in the- N; u8 w3 D3 e1 r+ ~: Z) X8 [3 I
beginning of this process.1 In the absence of a neg-
* X7 Z* Y6 l9 x+ ?ative initial history of androgen exposure, our
5 _% B; j, I. I4 {' ~* h! B4 p$ ?biggest concern was virilizing adrenal hyperplasia,3 T5 l2 p2 h# C; V
either 21-hydroxylase deficiency or 11-β hydroxylase" C' d4 o3 N7 G% r% ^% U
deficiency. Those diagnoses were excluded by find-) y6 u* D" V$ s  I8 b' x* P
ing the normal level of adrenal steroids.
# ~6 Q- f8 E0 n2 D4 u- KThe diagnosis of exogenous androgens was strongly
, P, i- O$ c4 J6 E/ s' N4 U/ e1 q5 Asuspected in a follow-up visit after 4 months because- q$ }4 E) q+ x5 N
the physical examination revealed the complete disap-
) r1 f1 J: y" x% U- g0 ~. xpearance of pubic hair, normal growth velocity, and
9 G2 H) |8 _8 |$ Mdecreased erections. The father admitted using a testos-
, D5 E- g3 T) M- G( Rterone gel, which he concealed at first visit. He was
! ]( c* J7 R0 Z. _using it rather frequently, twice a day. The Physicians’
0 b' g% F4 J, |$ R, h( `Desk Reference, or package insert of this product, gel or) @; ]0 F4 ^. E- \6 d3 d3 r
cream, cautions about dermal testosterone transfer to/ K5 v8 Y' b4 b, p3 v5 a/ s. |, W
unprotected females through direct skin exposure.
& R6 S" U5 h8 X+ t$ `+ eSerum testosterone level was found to be 2 times the+ f3 o" m6 Y3 v' c/ Z! M9 p
baseline value in those females who were exposed to
6 {8 b$ Z! E8 i5 f. b: P" zeven 15 minutes of direct skin contact with their male0 T$ Z6 p' K/ R5 @0 Q
partners.6 However, when a shirt covered the applica-) @) K( I# h9 S) m# n8 u( q
tion site, this testosterone transfer was prevented.0 A* c4 d/ r( N1 G% A$ s- m, I. L0 b
Our patient’s testosterone level was 60 ng/mL," W, w/ O" }( g
which was clearly high. Some studies suggest that
! ?; b7 z1 w' o* Gdermal conversion of testosterone to dihydrotestos-
$ c. c4 }7 f5 kterone, which is a more potent metabolite, is more
; t# F# ~$ v: ^$ Kactive in young children exposed to testosterone" b3 ^" E% w0 d
exogenously7; however, we did not measure a dihy-
& Q& C( H' a& B: I' A9 W8 W6 wdrotestosterone level in our patient. In addition to/ u' i: E, @2 m4 P$ o/ E
virilization, exposure to exogenous testosterone in
9 y  [, z. L. I0 Xchildren results in an increase in growth velocity and
) K( N' Z5 y& uadvanced bone age, as seen in our patient.: I% l" z0 z8 _( A* Y
The long-term effect of androgen exposure during
2 Q: l+ M( o5 [! n' p7 nearly childhood on pubertal development and final0 d2 Z% r6 |4 `1 f9 R
adult height are not fully known and always remain
( }/ Z1 e+ v+ b5 |1 i6 s6 d/ \a concern. Children treated with short-term testos-
; ?5 }+ D% O9 Uterone injection or topical androgen may exhibit some
5 Q' r1 j3 M4 @6 u+ Oacceleration of the skeletal maturation; however, after
1 K, _# h, g  q! l* Ecessation of treatment, the rate of bone maturation& X% B/ _, Q$ z+ C. g/ S
decelerates and gradually returns to normal.8,9' t/ J( D1 Y( Z
There are conflicting reports and controversy
' o# f# g2 l- [over the effect of early androgen exposure on adult$ ?- e. G6 w: x- n
penile length.10,11 Some reports suggest subnormal
# H  X( ~& F. ]adult penile length, apparently because of downreg-
/ ?' U4 k- q$ b. @ulation of androgen receptor number.10,12 However,% Y' u( A8 s9 L; `( d7 e
Sutherland et al13 did not find a correlation between
) l' Y( Y6 `5 p5 G: s4 R, {- v% Kchildhood testosterone exposure and reduced adult
4 b5 r6 d2 y' w$ |& v$ rpenile length in clinical studies.
/ R8 \) X! F! M7 v. g2 C  lNonetheless, we do not believe our patient is
7 I- t9 I! s5 G. \- \8 z7 Ggoing to experience any of the untoward effects from% v- j! E; X2 B
testosterone exposure as mentioned earlier because) M6 _1 N/ f$ W# s6 A4 L
the exposure was not for a prolonged period of time.( C7 e5 g9 z! O* K6 l, N
Although the bone age was advanced at the time of% d1 K% ^- H% d; i* F4 \+ l# g7 k1 I
diagnosis, the child had a normal growth velocity at. r, {* @1 L0 |$ ~: q
the follow-up visit. It is hoped that his final adult- R* [6 R1 W% l! y  Y. }9 V
height will not be affected.
6 w3 y1 x) {3 k' B9 ]Although rarely reported, the widespread avail-- e  Z! B, k, ?& [  g- s/ |
ability of androgen products in our society may
( c9 _& |- y  I  pindeed cause more virilization in male or female
! g$ t# J# @/ f3 J; q0 gchildren than one would realize. Exposure to andro-! o7 O$ x& q4 _& P+ Z0 x. w
gen products must be considered and specific ques-
$ j" F2 @$ G3 m; I$ N$ htioning about the use of a testosterone product or. D2 w1 I- d' _
gel should be asked of the family members during' J7 S4 d1 H& R" s& i
the evaluation of any children who present with vir-
5 N/ W6 O; ]# [7 {& f! M! Vilization or peripheral precocious puberty. The diag-7 [( a4 A" ]8 k0 R( |/ N
nosis can be established by just a few tests and by3 q; [% n  [3 r& _4 j, k
appropriate history. The inability to obtain such a+ \# w  k5 M( ^& _0 r0 E
history, or failure to ask the specific questions, may
" R: X& v' A' I0 X  i. Z- H2 Rresult in extensive, unnecessary, and expensive+ D6 ?- E# C' S, K, R% {; j
investigation. The primary care physician should be  X8 ~' l4 z# m) t+ L$ a) z6 `
aware of this fact, because most of these children& c6 I2 X' z4 A& t- {( @% m
may initially present in their practice. The Physicians’
$ b. x7 d- p6 d# r) D* SDesk Reference and package insert should also put a
5 n8 Q. u# M6 Zwarning about the virilizing effect on a male or
/ [9 k' a9 H/ P: q9 E9 b; U7 J7 F3 nfemale child who might come in contact with some-1 c5 U' |" i+ h2 L  {& K0 Y
one using any of these products.; ?& [* p7 g: z2 e: ]* Z+ J8 p2 f
References
  a! Q- A/ x8 B1. Styne DM. The testes: disorder of sexual differentiation- {4 }1 _+ a7 A& D8 q
and puberty in the male. In: Sperling MA, ed. Pediatric
% t* B5 O- i2 V0 V$ K; ~1 X# |Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- I( y2 i& R2 B6 ^( Z2002: 565-628.* X( _0 U! \# t0 D! f0 t
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 e2 o4 n& f3 d) z1 F  ^3 gpuberty 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( K- u! G/ [+ p! I3 Q4 `
Boy Induced by Indirect Topical5 s6 D: V. c5 x5 J3 q9 O+ O) a  r
Exposure to Testosterone7 R$ I, h8 C! Q: ^0 Y# u1 d6 ?5 B( K8 R
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,27 A9 R- a1 B7 N
and Kenneth R. Rettig, MD1
* N3 W. e2 m, mClinical Pediatrics. _4 ?4 I( B+ [9 e/ w
Volume 46 Number 6% G3 U+ h+ D' ~' l/ W5 P$ K) J% S
July 2007 540-5434 b0 y' C) R# s* \. y. O
© 2007 Sage Publications
8 D) ?6 ]$ F* q, U& G' S4 o10.1177/0009922806296651% h9 t' q& N; i% f2 g3 R6 h- K' D
http://clp.sagepub.com
9 M' c9 q6 W! N4 ihosted at( ]/ B' D. w' v
http://online.sagepub.com
. F4 j+ D6 A4 F# W1 |+ v9 KPrecocious puberty in boys, central or peripheral,
# O0 ]! Y: q4 P4 Zis a significant concern for physicians. Central
/ k$ a: l9 p5 X( @precocious puberty (CPP), which is mediated. z4 _7 u3 a% K
through the hypothalamic pituitary gonadal axis, has9 K# k# j6 q2 w, Q. K* w: Y! {6 N
a higher incidence of organic central nervous system
3 c. ^& m5 _' S9 q" B7 Jlesions in boys.1,2 Virilization in boys, as manifested
, N9 Z0 N8 P9 i2 {by enlargement of the penis, development of pubic
  C3 n4 F  p: lhair, and facial acne without enlargement of testi-
" P* d: ^0 _2 _( _1 Y5 ecles, suggests peripheral or pseudopuberty.1-3 We
7 \# ^( x3 @7 R& q( w1 N2 Areport a 16-month-old boy who presented with the6 x3 k6 u+ R8 |! E( j
enlargement of the phallus and pubic hair develop-, }1 n# o0 J: [) J* }: G# [
ment without testicular enlargement, which was due
( z3 ^/ L7 t) x- A+ f% N2 O! `to the unintentional exposure to androgen gel used by
* V: f( i; `, q2 U2 y9 Bthe father. The family initially concealed this infor-# \. o4 E+ G1 [0 w" Y
mation, resulting in an extensive work-up for this) @9 `- k# ]3 }0 y7 t. a
child. Given the widespread and easy availability of
. I7 [9 v* r% N4 y7 C$ c) }! u% Ttestosterone gel and cream, we believe this is proba-: V7 ^& @9 C" E* L
bly more common than the rare case report in the
  T! G  G) m& d# q+ `+ ]literature.47 Y% _5 R: i  V7 F! X% D
Patient Report: x. Y6 x3 @7 N, v
A 16-month-old white child was referred to the
# P) D. O+ J! b8 Y' ^+ Wendocrine clinic by his pediatrician with the concern
8 O# w7 I7 y: I! }of early sexual development. His mother noticed
8 j1 D$ ?% @. |1 Llight colored pubic hair development when he was' f. }; u# C' ~2 X+ _6 h- P6 n
From the 1Division of Pediatric Endocrinology, 2University of$ C3 j9 `" _& r1 m1 u" H" h
South Alabama Medical Center, Mobile, Alabama./ G, }+ ~& k: ?
Address correspondence to: Samar K. Bhowmick, MD, FACE,
  K/ e7 r! G- f. v  b& o2 kProfessor of Pediatrics, University of South Alabama, College of
( i, D6 E# C; }2 B9 N# T# N' kMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
* e) w" M5 O+ f1 S$ de-mail: [email protected].- D; J, w8 |4 _
about 6 to 7 months old, which progressively became6 `& e6 Y) M, ~* _2 c
darker. She was also concerned about the enlarge-
, H7 G- y) [( T" y2 c& R, Sment of his penis and frequent erections. The child
) U- m9 K" F3 a8 c2 z  j9 mwas the product of a full-term normal delivery, with
' a' w: L3 }% ^. W. M- la birth weight of 7 lb 14 oz, and birth length of4 n9 N9 k$ x& T5 _2 b! t- O
20 inches. He was breast-fed throughout the first year
! n8 j, I1 X4 X8 l  T# rof life and was still receiving breast milk along with
4 B% ]3 ?9 ?) _5 J2 Xsolid food. He had no hospitalizations or surgery,: D3 i6 W8 l+ o- X2 J' e
and his psychosocial and psychomotor development# k9 a& t' U0 Z6 j
was age appropriate.
( K& h$ G- ~' l. f4 J: m+ c7 JThe family history was remarkable for the father,. ]# Q2 }7 Y3 x" D
who was diagnosed with hypothyroidism at age 16,
3 s' w* h) m' l2 o0 [( n& Wwhich was treated with thyroxine. The father’s
1 r% i1 I% R% z0 W8 g- Q- u8 w% Dheight was 6 feet, and he went through a somewhat
0 m2 A% E7 e6 W' A$ E5 ~early puberty and had stopped growing by age 14.
2 w' ~% I, T7 O# _1 e' F& y/ y/ |The father denied taking any other medication. The8 m) r: B  |2 t1 ~  U% L
child’s mother was in good health. Her menarche" ]4 A4 W, e7 N
was at 11 years of age, and her height was at 5 feet
% b+ R0 V5 K; m6 i5 inches. There was no other family history of pre-
. O5 h, A; W1 }' icocious sexual development in the first-degree rela-+ I" E- W6 D) c& n* D4 r
tives. There were no siblings." y: a& b4 T1 |7 j. c
Physical Examination! r7 u: Y+ e) |% _8 C
The physical examination revealed a very active,
: b! d5 K5 x# f) Z5 pplayful, and healthy boy. The vital signs documented: P. n, ~( @4 o" \
a blood pressure of 85/50 mm Hg, his length was
, `, P! n* D0 E+ c7 x. Y90 cm (>97th percentile), and his weight was 14.4 kg, y6 Z7 b. X1 B) o  T
(also >97th percentile). The observed yearly growth
1 ?! _8 O/ k. _2 M' Q# P& W$ ^velocity was 30 cm (12 inches). The examination of
" O" G* b7 ^/ V) w+ G6 ithe neck revealed no thyroid enlargement.% H1 [6 f+ `- a' @& i
The genitourinary examination was remarkable for3 B5 t/ ~+ b: m% L% j
enlargement of the penis, with a stretched length of
! i2 _1 K; P: m5 E2 t$ K8 cm and a width of 2 cm. The glans penis was very well
. D  Q9 ?+ v9 tdeveloped. The pubic hair was Tanner II, mostly around% X0 u; A7 m5 H, i  u7 H/ I6 I
540
7 I0 r4 l2 f/ w$ q8 L' P8 x6 iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) P& O6 q& d9 O4 Z
the base of the phallus and was dark and curled. The
! t' |0 q! G- L, u* \5 Qtesticular volume was prepubertal at 2 mL each.
( _  }2 s% x6 s# W) }The skin was moist and smooth and somewhat
8 f! ~  M& R* L( poily. No axillary hair was noted. There were no
* k; C6 c! B4 a6 h3 {. g7 cabnormal skin pigmentations or café-au-lait spots.
' s. }, [8 N8 F" F: V* c; H7 \2 HNeurologic evaluation showed deep tendon reflex 2+
% s( ]" ~% C/ j& dbilateral and symmetrical. There was no suggestion
' M: T% c$ H: x& A9 @of papilledema.7 @! d" J, p) `" a, }: X3 e
Laboratory Evaluation
2 D, e, J* p5 d6 @9 X1 S  \The bone age was consistent with 28 months by; h9 X6 {" t; a; E" e( C9 N
using the standard of Greulich and Pyle at a chrono-- y0 J$ c9 Z  \
logic age of 16 months (advanced).5 Chromosomal
" e  _; O  P" ^& ckaryotype was 46XY. The thyroid function test& k/ F$ _$ j" t
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 e. f, k) e( M: h& d
lating hormone level was 1.3 µIU/mL (both normal).
5 n, x6 V1 q2 U; h! y$ {The concentrations of serum electrolytes, blood
; h" H' g' w* m/ Vurea nitrogen, creatinine, and calcium all were
! u# b9 W7 g% l+ e5 o3 q$ F$ z5 kwithin normal range for his age. The concentration
0 ?# ?: e' S8 q  ~( ?2 wof serum 17-hydroxyprogesterone was 16 ng/dL
5 B  ?! j( a  Q# u6 \  u(normal, 3 to 90 ng/dL), androstenedione was 20% i0 H4 b8 I( D; x8 R  @& v( C4 b
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& C1 C' n' ~* [  C+ I) mterone was 38 ng/dL (normal, 50 to 760 ng/dL),0 A2 n0 D6 }8 O; V( I5 F
desoxycorticosterone was 4.3 ng/dL (normal, 7 to& X8 y- E8 \+ ~
49ng/dL), 11-desoxycortisol (specific compound S)
/ E5 n  s0 E6 }4 V/ Lwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- i( N: ]; I! j; t& z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. N$ b; G# T( d* k# I6 v" X9 o) K: Qtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 J' H$ z% c/ l/ G" N5 i
and β-human chorionic gonadotropin was less than
) \5 A& _1 Z; A$ X8 W. f$ a  l5 mIU/mL (normal <5 mIU/mL). Serum follicular8 ?5 f1 [9 m: ~
stimulating hormone and leuteinizing hormone- U( q3 ]7 ~! K9 _. Q/ a; [+ a
concentrations were less than 0.05 mIU/mL" {$ g$ ]1 h  J4 B
(prepubertal).  V# q- t4 W6 _) B/ j
The parents were notified about the laboratory
6 ~% s$ d7 S, Qresults and were informed that all of the tests were9 W4 I; D0 Y7 J$ A
normal except the testosterone level was high. The9 M, k7 _# O) U# o. N# a/ @8 b7 D: v
follow-up visit was arranged within a few weeks to
# n( I) b2 R2 H4 {) {) }& robtain testicular and abdominal sonograms; how-1 |* }5 K$ C# U( l% y+ ^* w5 }; s
ever, the family did not return for 4 months.
$ e, ~9 I( T1 L/ u: O8 `9 xPhysical examination at this time revealed that the
2 X& C! e2 R& L, a) d1 q! _5 r; O! lchild had grown 2.5 cm in 4 months and had gained
: }* @. C: W9 Q+ v2 kg of weight. Physical examination remained! i4 O2 j6 Z* U: R, }, c6 n4 q
unchanged. Surprisingly, the pubic hair almost com-
' |2 c/ Z# _) I+ D' O: e* p# Opletely disappeared except for a few vellous hairs at/ n1 F* D% k& c. V2 o
the base of the phallus. Testicular volume was still 2- I1 I" V# b$ s8 c4 ^6 Z/ G; ~
mL, and the size of the penis remained unchanged.1 z4 ~0 `3 m; d" [
The mother also said that the boy was no longer hav-
! B) |" R8 m4 `8 h, Q+ i, Eing frequent erections.
: F7 R( M+ X- J4 oBoth parents were again questioned about use of
3 o  V4 L  O* k- p* ^" c* Yany ointment/creams that they may have applied to
. E8 o: y' M2 y4 p# M; @5 P5 a. Rthe child’s skin. This time the father admitted the# Z% L9 k! w) A  O8 M0 ]/ X, A
Topical Testosterone Exposure / Bhowmick et al 541
  X& _5 g, ~0 H2 K+ Z" [use of testosterone gel twice daily that he was apply-
. m% J2 M# ~) x, Cing over his own shoulders, chest, and back area for+ E5 x! y4 X1 n# z4 x$ s: U
a year. The father also revealed he was embarrassed, @, j5 s5 f9 x6 \! u3 W  |
to disclose that he was using a testosterone gel pre-6 S  `/ @% ?5 x! m
scribed by his family physician for decreased libido  N8 i1 r9 H9 C. j; e1 k$ Z% ]
secondary to depression.
7 E' o1 \; C1 p# o* b% Q4 qThe child slept in the same bed with parents./ V9 B) o6 v( ?4 R& x2 w
The father would hug the baby and hold him on his
  H1 v. U0 o% c* ]chest for a considerable period of time, causing sig-, d& _/ s; i. Q* O7 ]
nificant bare skin contact between baby and father.
/ ~' b) }$ p: B  z9 s9 NThe father also admitted that after the phone call,! Z) V' b/ B) D$ v" E8 d
when he learned the testosterone level in the baby
7 D! q; z- b8 b/ N, q* mwas high, he then read the product information
% m1 A/ v! s# F( h' _7 ]. y* ypacket and concluded that it was most likely the rea-
& U* {/ n7 a- }+ d  r- l) H. oson for the child’s virilization. At that time, they: H/ F) z0 s4 v) p3 w. ^
decided to put the baby in a separate bed, and the
6 r+ W, e' A4 e& K1 dfather was not hugging him with bare skin and had
, E0 H+ ~; j3 ?been using protective clothing. A repeat testosterone
( b- i" s5 ~! M5 z* P% r2 c! W  stest was ordered, but the family did not go to the! `6 \! E% r5 ?) k5 S
laboratory to obtain the test.
9 j' S+ o6 O* R& u' v7 Z" gDiscussion
7 P. j* v3 ]* J2 y$ qPrecocious puberty in boys is defined as secondary
& Y. N6 D! M" m2 ?6 T5 y5 T  usexual development before 9 years of age.1,49 c( e' m3 X; f3 l6 G
Precocious puberty is termed as central (true) when
7 y1 L' |  O8 R8 E' W: Fit is caused by the premature activation of hypo-
7 K0 k' N7 W. Qthalamic pituitary gonadal axis. CPP is more com-
. s, F' A( F: _mon in girls than in boys.1,3 Most boys with CPP. a& [3 D, v7 |0 {. R: M
may have a central nervous system lesion that is2 I; J( x; r/ y" Z
responsible for the early activation of the hypothal-
- i- U5 f% e3 O! j6 tamic pituitary gonadal axis.1-3 Thus, greater empha-
. M2 X* F6 B3 _9 U% R, V" H; bsis has been given to neuroradiologic imaging in4 y7 \$ B- ?' |7 B" U; b/ v7 i
boys with precocious puberty. In addition to viril-
2 H  s/ O7 S  k- iization, the clinical hallmark of CPP is the symmet-+ w9 `1 N- @) ^) s7 M
rical testicular growth secondary to stimulation by
) [. g* E. m9 P& ~% U& A# Ggonadotropins.1,3
- T. `" \. _' QGonadotropin-independent peripheral preco-& t) ~+ ~" q9 W
cious puberty in boys also results from inappropriate
: m7 I1 @. w! J4 ]  ?* candrogenic stimulation from either endogenous or
8 n% E% O+ B$ y/ r; Dexogenous sources, nonpituitary gonadotropin stim-' y) T9 ^3 `3 b+ X1 s" T2 u
ulation, and rare activating mutations.3 Virilizing
# t2 e0 |0 f) ^congenital adrenal hyperplasia producing excessive
1 H' e: q) s$ Sadrenal androgens is a common cause of precocious$ s: V; K: L; T4 H- o/ b
puberty in boys.3,4
( E2 _8 |4 G& {- q: g# P: VThe most common form of congenital adrenal. B* l/ W8 _+ v; p5 w' q1 k
hyperplasia is the 21-hydroxylase enzyme deficiency.
% y- Z% h5 Q' f0 ]! z* qThe 11-β hydroxylase deficiency may also result in! s& x: Z0 L3 U1 F( T
excessive adrenal androgen production, and rarely,
/ }- z4 f$ e. Ran adrenal tumor may also cause adrenal androgen
" R- R; c2 C0 N+ o# o# X- {excess.1,3% l' p2 e1 H& ~0 F0 T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 J5 o" g; V; f) `
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. ?2 s# R! z3 [* }0 L7 b8 n
A unique entity of male-limited gonadotropin-( \" u  D! p, s, q, w! @
independent precocious puberty, which is also known) U/ u3 O0 Q9 ~1 ~
as testotoxicosis, may cause precocious puberty at a) X5 B; G, {. v! \9 l# J/ [7 z' h% N
very young age. The physical findings in these boys- b' X6 ~* P6 ~
with this disorder are full pubertal development,
; H# e' z: J2 Sincluding bilateral testicular growth, similar to boys
! T. |0 o/ E& ^3 H) Q0 O6 S/ P: Awith CPP. The gonadotropin levels in this disorder2 q3 o4 Q9 k( t/ z& _( q9 n  t% t
are suppressed to prepubertal levels and do not show1 {5 s4 Y5 [2 g0 a" q
pubertal response of gonadotropin after gonadotropin-$ w  H7 i/ M7 O' ?
releasing hormone stimulation. This is a sex-linked% T  z+ y6 Q4 N- W" v
autosomal dominant disorder that affects only
* H3 D6 G# {# G  W: J; d6 M! mmales; therefore, other male members of the family
$ ^$ K9 {: [. S5 G. Umay have similar precocious puberty.3
8 Q5 o' n8 o1 r5 R( s, @1 pIn our patient, physical examination was incon-! [5 m; m. m4 c; @  H& p) }
sistent with true precocious puberty since his testi-
5 ~- q) t0 C: N' @8 N6 e* zcles were prepubertal in size. However, testotoxicosis
' s9 x) T( C# R+ G0 v! f) _was in the differential diagnosis because his father
: {3 [8 q! W  `1 D! [5 Qstarted puberty somewhat early, and occasionally,
& r6 r+ d, M! }3 ptesticular enlargement is not that evident in the( `0 R- y$ x+ c
beginning of this process.1 In the absence of a neg-* f: Z. @% q; Z2 P  Y
ative initial history of androgen exposure, our
1 w2 T' w) T, P! z& t6 w& p# ubiggest concern was virilizing adrenal hyperplasia,# F+ j6 ?# k; D( e/ F6 K9 y
either 21-hydroxylase deficiency or 11-β hydroxylase# ?/ b/ g2 m" n; Z
deficiency. Those diagnoses were excluded by find-7 E! V  ?6 {% P4 u
ing the normal level of adrenal steroids.
, X5 e; i* w6 A4 B9 U& cThe diagnosis of exogenous androgens was strongly, i  ]8 c: ~7 n3 O1 {& ^# g* ?
suspected in a follow-up visit after 4 months because( ~. k+ Z" ?4 B+ F
the physical examination revealed the complete disap-
! y* Y: ~. T2 Spearance of pubic hair, normal growth velocity, and
1 ]7 d# N- w3 g: Cdecreased erections. The father admitted using a testos-, `7 H4 @1 H/ X: S9 F% e+ {: `
terone gel, which he concealed at first visit. He was' F. o. P. G4 x" _
using it rather frequently, twice a day. The Physicians’
  l% s# R: y/ G% ~Desk Reference, or package insert of this product, gel or% {3 u" E. F1 {
cream, cautions about dermal testosterone transfer to* T3 Y" M- S8 P1 Z2 G8 b9 C
unprotected females through direct skin exposure.
% u4 o, A. V0 H3 DSerum testosterone level was found to be 2 times the; h0 u/ {# M) A1 g' d& S% f
baseline value in those females who were exposed to5 A) X2 \: r4 e5 O8 t
even 15 minutes of direct skin contact with their male- p' q  k5 a/ T# _% `
partners.6 However, when a shirt covered the applica-  e- ]" |0 b& j' z8 M! P$ G
tion site, this testosterone transfer was prevented.) |7 ^. F* Z. X0 ~. V
Our patient’s testosterone level was 60 ng/mL,
9 N+ b/ E0 n" l" ]which was clearly high. Some studies suggest that
, t: t1 K0 k- L( O, ]' bdermal conversion of testosterone to dihydrotestos-1 D8 P: @* v. b4 J. o& u
terone, which is a more potent metabolite, is more
3 Q2 m9 u4 \' D# eactive in young children exposed to testosterone8 U) X& k4 a. D7 i9 j  G
exogenously7; however, we did not measure a dihy-  E  {% m& g  |6 g
drotestosterone level in our patient. In addition to$ q3 `5 f! S0 z
virilization, exposure to exogenous testosterone in+ d: y. H, w: e8 L( V; e7 \
children results in an increase in growth velocity and
( l0 b0 J6 r) i8 c4 E) q7 qadvanced bone age, as seen in our patient.7 ^1 m. T3 h8 a0 ?
The long-term effect of androgen exposure during) _2 Z' p! m2 n' ]4 C$ H
early childhood on pubertal development and final4 j, F+ S) Q6 [3 j: X- R
adult height are not fully known and always remain6 h! C8 c% J3 x: y7 h
a concern. Children treated with short-term testos-' M& `" }* j6 ?% ]& @+ n3 m2 `# l
terone injection or topical androgen may exhibit some
2 z! ~9 \+ Y7 A$ _/ Bacceleration of the skeletal maturation; however, after
, J* N- ]6 t% |- U& P# Kcessation of treatment, the rate of bone maturation2 M1 v  B+ }- {4 X
decelerates and gradually returns to normal.8,9
8 n! P3 e0 \8 D7 k$ D# R1 zThere are conflicting reports and controversy* U+ r7 g5 i, z( ~, ~$ n
over the effect of early androgen exposure on adult
% H* i+ B* F9 R. z. J* V4 [penile length.10,11 Some reports suggest subnormal- n' I+ A9 W* [' B9 _
adult penile length, apparently because of downreg-2 {! k& V- T/ a& `, a& X4 P
ulation of androgen receptor number.10,12 However,2 c: t2 _7 V7 J+ h5 w( ^  C
Sutherland et al13 did not find a correlation between7 X0 ]) M9 T- h6 z8 ]- R- t
childhood testosterone exposure and reduced adult, v  T3 E- [  Q3 S6 H( B
penile length in clinical studies.' E/ G9 j# p; J# k: v+ M: X) _) o
Nonetheless, we do not believe our patient is& }+ ~. g; t5 ~* b! H! X
going to experience any of the untoward effects from
! |, b1 w, Q- s& R  Q9 |testosterone exposure as mentioned earlier because; R) A! h" {9 Y' _6 _
the exposure was not for a prolonged period of time.
7 x: w. m% R+ O5 \2 M- o8 xAlthough the bone age was advanced at the time of& p6 A+ O7 `/ b4 ]
diagnosis, the child had a normal growth velocity at5 e5 F! P5 j' i# h7 e) B0 G  J
the follow-up visit. It is hoped that his final adult( ^. m0 R% ^& L" X2 b. ^% |0 i
height will not be affected.5 d' R% U! D# ~$ O: b, u
Although rarely reported, the widespread avail-. e, B2 \' r9 D8 q
ability of androgen products in our society may3 h, B  L8 _7 d- `6 I8 p5 u  b
indeed cause more virilization in male or female
3 L1 F: m2 {3 I1 J1 M5 @% y) @children than one would realize. Exposure to andro-& Y  X2 [" U! j- A
gen products must be considered and specific ques-
+ F! T, y' P6 |, M+ ktioning about the use of a testosterone product or
$ L/ j8 S. K0 f' Ygel should be asked of the family members during' k* ?  ^) `! q' {$ t$ z, A
the evaluation of any children who present with vir-" ~! s# T2 n# `, [- T
ilization or peripheral precocious puberty. The diag-
& r9 B' i/ H' G3 Knosis can be established by just a few tests and by
6 i" `/ V8 R- O8 lappropriate history. The inability to obtain such a
: `- F9 E* ^* ihistory, or failure to ask the specific questions, may. w0 p# c$ B+ ~. V  U6 J( p
result in extensive, unnecessary, and expensive0 h; V3 w. h( s0 d: U& ^
investigation. The primary care physician should be% M+ c( l& s" K- L: a( f! n( h# m
aware of this fact, because most of these children
5 c/ W: p9 ?! w/ x, q. j1 mmay initially present in their practice. The Physicians’4 \2 ]* I5 x: J
Desk Reference and package insert should also put a
  M$ l* h+ ^3 n& C2 ~! o+ Z# hwarning about the virilizing effect on a male or
: F  ^1 r# I  A0 ~8 F$ Ffemale child who might come in contact with some-
: `6 o: y$ S6 q3 f  l! b7 ~6 K. B# rone using any of these products.
3 T( g( ], y( A* ~References8 h; _/ T  [, m$ @2 G& Z  o$ v' h# ^
1. Styne DM. The testes: disorder of sexual differentiation' ?0 Z- e2 r9 L& v6 z2 _, ]2 A
and puberty in the male. In: Sperling MA, ed. Pediatric$ C- r% h  `& }8 R4 w" Q- `
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. v; g  x, x# \) D
2002: 565-628., T9 R" Z  K$ u1 M) I
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
" u: p4 Z' A$ Ppuberty 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
8 l6 S2 I. g" x3 G
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