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
# ?" d- S, i) ^- uBoy Induced by Indirect Topical
8 ]0 `  v0 ~/ z& N2 c+ iExposure to Testosterone
- X/ t/ }7 H, T5 hSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
* u) y/ @" A4 i, Y' Tand Kenneth R. Rettig, MD1
  g4 ^; }6 `; i% j. k# Y% GClinical Pediatrics
9 P# M0 W0 }1 X  tVolume 46 Number 6/ ]% O. L( T/ ~  k
July 2007 540-543) [" }$ P0 p+ @  }/ A1 R7 q4 K
© 2007 Sage Publications& m) n0 B5 T! X
10.1177/0009922806296651  a0 G! x7 R; r
http://clp.sagepub.com
5 U' R: b8 y$ k1 h4 ~2 Fhosted at% g- z& q+ ^/ A2 d. R6 _+ U
http://online.sagepub.com, P4 n2 c1 v2 G( }4 C9 Y
Precocious puberty in boys, central or peripheral,
- ^( m# J: I# @is a significant concern for physicians. Central
; W! P4 C! p8 s3 S4 jprecocious puberty (CPP), which is mediated; c: `8 w1 J8 R7 P
through the hypothalamic pituitary gonadal axis, has- b8 ~8 v! W: `4 h! U
a higher incidence of organic central nervous system
! ]4 x9 i" }6 P: L( ylesions in boys.1,2 Virilization in boys, as manifested( V3 l5 u4 p. M. @4 U8 s% S
by enlargement of the penis, development of pubic
0 W4 J- p9 T7 A% g8 A; W: v2 shair, and facial acne without enlargement of testi-* a: v5 B5 G' h, B5 p
cles, suggests peripheral or pseudopuberty.1-3 We  b' a( _* Q+ M% l# W
report a 16-month-old boy who presented with the. t6 o5 M- P: `- l1 u: @' y# N
enlargement of the phallus and pubic hair develop-
; S. F4 c2 ^( pment without testicular enlargement, which was due
" J+ U3 W9 m* t9 |to the unintentional exposure to androgen gel used by
- s' y& P9 q8 l6 ~& h/ ]the father. The family initially concealed this infor-
  z; q- p6 |! f" nmation, resulting in an extensive work-up for this# v/ D/ A4 W  G2 I
child. Given the widespread and easy availability of
. G1 }- C9 h4 }4 @testosterone gel and cream, we believe this is proba-' h& Y+ Y. e- f) X
bly more common than the rare case report in the
8 c- K. ]) l% M. X7 Aliterature.40 Y) t: E( U5 \! F: p. S/ m
Patient Report0 e' \( \3 a7 o6 l' ?
A 16-month-old white child was referred to the
* s1 \$ W' c4 i4 g5 Jendocrine clinic by his pediatrician with the concern0 O8 X5 z. E, u& F- A6 E
of early sexual development. His mother noticed
( Y- U$ O+ S0 g/ \! W; D1 R$ b/ A! Alight colored pubic hair development when he was! ~' `& t" O3 z& h
From the 1Division of Pediatric Endocrinology, 2University of# I& p% @- \2 C( {
South Alabama Medical Center, Mobile, Alabama.9 l( a8 Z  Y( }" e+ Q9 |
Address correspondence to: Samar K. Bhowmick, MD, FACE,. q/ l- ]2 G1 \& a+ u: b2 Q
Professor of Pediatrics, University of South Alabama, College of2 z$ m, H2 e! s( H. r4 t8 K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% }( H) d( b7 W
e-mail: [email protected].( t  h) R' K% U' X
about 6 to 7 months old, which progressively became
4 {8 ?; L# M4 j6 G4 d8 q( x# \darker. She was also concerned about the enlarge-1 c! U+ j6 z( J
ment of his penis and frequent erections. The child
  h: N- O  M/ a7 iwas the product of a full-term normal delivery, with
3 _/ M% b9 p+ M8 n7 @! b0 E1 @a birth weight of 7 lb 14 oz, and birth length of
: U3 G% Q% G: |2 V% u9 a20 inches. He was breast-fed throughout the first year( a" K' S$ Q; {: ^4 _- A- r
of life and was still receiving breast milk along with
* g. M% z6 m1 I+ l6 j1 Nsolid food. He had no hospitalizations or surgery,
8 u7 Q" o8 U& F1 xand his psychosocial and psychomotor development  B- o0 A4 J- u; B
was age appropriate.
4 a2 B0 k% }2 \: f  B! Z* y/ I. qThe family history was remarkable for the father,
8 \' A' u( N2 G/ h) u5 Dwho was diagnosed with hypothyroidism at age 16,
% L% o; h# t. ^$ R( S6 X! ^which was treated with thyroxine. The father’s
+ W0 e- F. g1 W, Theight was 6 feet, and he went through a somewhat
: J3 O% \$ F; t) `- f, kearly puberty and had stopped growing by age 14.
& `( p' ~/ ?7 M, E7 F* k# x6 hThe father denied taking any other medication. The
  B/ S' n- v- F9 P) N# nchild’s mother was in good health. Her menarche
9 ]' I# |' D& W9 l7 k2 @was at 11 years of age, and her height was at 5 feet
' j+ l4 v6 f7 O, ]- n5 inches. There was no other family history of pre-
  q) s5 j& ^7 ?+ Q" r) Ycocious sexual development in the first-degree rela-' Y/ C, z* {0 Q
tives. There were no siblings.( C# w0 r; i$ w0 a3 U4 C! j% v
Physical Examination
1 l5 L3 x( E. p; I- ?4 K8 Q5 C( kThe physical examination revealed a very active,
# G  k& |7 T+ b/ g% z- @playful, and healthy boy. The vital signs documented
% T& b! }. U1 sa blood pressure of 85/50 mm Hg, his length was- g) R, V: _1 H# D' ~+ ], g* G) q5 e
90 cm (>97th percentile), and his weight was 14.4 kg
* L# P$ y$ v  Y2 F6 c' t(also >97th percentile). The observed yearly growth& u3 |9 U$ [  W: g7 ^; K
velocity was 30 cm (12 inches). The examination of/ p0 x" z) @1 C1 b% t
the neck revealed no thyroid enlargement.; [; h+ |$ z. |6 P/ ]- @: N9 F
The genitourinary examination was remarkable for* M# K* _: _+ h* m
enlargement of the penis, with a stretched length of' V6 _  i) p' @. {) \
8 cm and a width of 2 cm. The glans penis was very well
! q6 \0 M$ c/ i' N  E% Z( Adeveloped. The pubic hair was Tanner II, mostly around2 F# L. V, ?, K" I
540
# q4 A) K1 e5 W/ h0 J, Z! X; J5 Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 L/ j( ?% o% ?: t5 G% A0 zthe base of the phallus and was dark and curled. The
/ a/ o% Z+ t0 [" @9 Ytesticular volume was prepubertal at 2 mL each.
! F6 c8 Y1 \' E9 KThe skin was moist and smooth and somewhat( ^/ X# V8 _+ W1 }8 v- U9 Z; h+ N. Z4 R
oily. No axillary hair was noted. There were no
2 F4 X2 p* J4 l1 i! {" i5 xabnormal skin pigmentations or café-au-lait spots.' ?) Y4 R( n/ `, X
Neurologic evaluation showed deep tendon reflex 2+
0 [7 `* [) E1 L" Nbilateral and symmetrical. There was no suggestion
% J/ L) p4 v( }% Cof papilledema.
: [5 G+ ^9 L8 Q9 h3 W1 nLaboratory Evaluation
0 j0 U5 z/ }# q& uThe bone age was consistent with 28 months by
$ n9 d2 z+ L- ~; \/ r) W( fusing the standard of Greulich and Pyle at a chrono-
/ \+ U5 t6 ]6 ~3 _3 g& Alogic age of 16 months (advanced).5 Chromosomal
0 I1 w1 @! j8 \; Z, X& K5 V, Ukaryotype was 46XY. The thyroid function test  c, ~. G* b; N
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
" \/ ]6 `* w; K2 S) rlating hormone level was 1.3 µIU/mL (both normal)./ ^2 H5 m& ]/ v
The concentrations of serum electrolytes, blood: q! C. Y1 I% s. u0 r% P
urea nitrogen, creatinine, and calcium all were
7 G, M3 m, R3 `9 m7 Swithin normal range for his age. The concentration- B  s+ L! p0 x, N3 M  y* \$ [) Z, o
of serum 17-hydroxyprogesterone was 16 ng/dL
  _" W- s0 I5 G$ ?" i; ?+ ^(normal, 3 to 90 ng/dL), androstenedione was 20
+ ?' v# a3 A. x% u8 G/ Z# D6 E+ ung/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. Z- `2 B$ @% N; R4 Vterone was 38 ng/dL (normal, 50 to 760 ng/dL),9 }) G" c/ m% s7 Y3 ]6 {* Q
desoxycorticosterone was 4.3 ng/dL (normal, 7 to( J# k2 P3 @" D  N& Q9 p
49ng/dL), 11-desoxycortisol (specific compound S)
3 ^  @6 C& v' s# l4 `was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( S- Z( j8 w, m; m- D
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ v  p1 Y, c$ [# ]" |% ltestosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 H8 P& \* L4 z/ T/ l
and β-human chorionic gonadotropin was less than/ {  x0 R9 T/ K) @2 K) X* {" g
5 mIU/mL (normal <5 mIU/mL). Serum follicular
: ~6 s) M9 \  ^( ~0 d; C$ Y1 N8 xstimulating hormone and leuteinizing hormone
$ o+ e8 g+ m# z8 A! E& I# {7 Qconcentrations were less than 0.05 mIU/mL8 b" o. L+ m# ^+ \" |1 v5 m# s" ?
(prepubertal).. k' m1 @; T7 N+ l. C0 d
The parents were notified about the laboratory0 u# F* ~3 c7 P: i; h) I7 V
results and were informed that all of the tests were
* g- h$ U+ Q5 z; n, j" cnormal except the testosterone level was high. The
# ?6 Y( z4 a. p4 f5 j8 H* ]follow-up visit was arranged within a few weeks to- s; G8 U  W0 M; Q
obtain testicular and abdominal sonograms; how-' }1 c$ i& f: V' _6 U
ever, the family did not return for 4 months.# ?" d# V' [, R/ L/ D9 H, P6 x. Q
Physical examination at this time revealed that the, N" E) ~# r# i. Y5 d- A' v
child had grown 2.5 cm in 4 months and had gained
% v% W, v7 M6 p* H: |1 w. s$ p# M2 kg of weight. Physical examination remained
4 W1 h5 V& s% O% j' E$ Munchanged. Surprisingly, the pubic hair almost com-! {0 s6 m8 f: a2 N
pletely disappeared except for a few vellous hairs at1 _+ H7 W; f; T, u( B/ }
the base of the phallus. Testicular volume was still 2
' F% `: m- s2 d3 ?* e9 H  PmL, and the size of the penis remained unchanged.
+ |. b1 X& m* f% TThe mother also said that the boy was no longer hav-
; s  z) y0 B% Ring frequent erections.( I( O- j. F3 H+ q2 q" b
Both parents were again questioned about use of! a9 o  T# S" {7 f! |4 o
any ointment/creams that they may have applied to0 W& J6 @5 C/ L2 K
the child’s skin. This time the father admitted the
% b1 ?5 e# o4 k3 mTopical Testosterone Exposure / Bhowmick et al 5410 M  V% j4 m& h4 ~5 m: P) Y* C
use of testosterone gel twice daily that he was apply-
4 X0 |7 ^8 P3 r. [" W, h  Ding over his own shoulders, chest, and back area for7 I& H! F# z% T' T
a year. The father also revealed he was embarrassed
! K/ t7 ^3 `9 X/ c( a9 s  Bto disclose that he was using a testosterone gel pre-
1 h) s! M' ]8 ~3 f+ M, a  E; Pscribed by his family physician for decreased libido
  O2 {7 {: C+ X0 x' e0 csecondary to depression.7 G( z* ?7 D: ]% c( V# w7 z9 G
The child slept in the same bed with parents.
% _$ p4 O$ N% a& b; YThe father would hug the baby and hold him on his; @8 }* ?- |# o* |0 h2 h# T( I
chest for a considerable period of time, causing sig-
: k* M( R8 j# Z, [nificant bare skin contact between baby and father.
- o( q* ~3 Z% V+ S! Z$ d) ?( Z9 yThe father also admitted that after the phone call,
, x/ L2 P) i- Y, L# ?when he learned the testosterone level in the baby
# q7 u$ X7 X1 A/ uwas high, he then read the product information
: T+ l& ~% \3 t, B, fpacket and concluded that it was most likely the rea-
. c2 ~" ^& S6 W' Yson for the child’s virilization. At that time, they
& M" V( I; J4 d  [2 l/ J7 P" xdecided to put the baby in a separate bed, and the6 J( V0 \5 F6 G6 ^3 ]  _2 Y
father was not hugging him with bare skin and had1 Q: `* t3 Q: `
been using protective clothing. A repeat testosterone
) L, Q1 G2 ~; |% |2 A1 gtest was ordered, but the family did not go to the
# W, y7 X4 V2 R; Xlaboratory to obtain the test./ M! K5 H: g5 {8 i4 m4 d$ g
Discussion
3 ^; j8 g, g" q6 w7 lPrecocious puberty in boys is defined as secondary+ p+ x# s! |( _# Z( l8 p
sexual development before 9 years of age.1,46 H' g( P# f4 m8 R9 ?, T5 a% N& p
Precocious puberty is termed as central (true) when
0 e$ m# \4 R0 Sit is caused by the premature activation of hypo-2 C4 d7 M" P' q0 {0 A, a4 D, o( D! U( }
thalamic pituitary gonadal axis. CPP is more com-. n! K  x" L' }" ^0 v
mon in girls than in boys.1,3 Most boys with CPP2 v5 `; v. ~. [5 I$ A8 x* t2 I
may have a central nervous system lesion that is
8 K! z8 J# X/ K0 n  Xresponsible for the early activation of the hypothal-5 {% e. E! {3 F8 b* r. A! k* _
amic pituitary gonadal axis.1-3 Thus, greater empha-  z6 x( P1 c2 f) d7 h- n+ L$ n' ~  B
sis has been given to neuroradiologic imaging in
! K* J0 S5 k$ d3 I, _" }$ C! Gboys with precocious puberty. In addition to viril-
- D$ A# m, o( kization, the clinical hallmark of CPP is the symmet-8 H/ `5 t! Q3 H# q- [
rical testicular growth secondary to stimulation by1 r1 X' q; [9 m; S! I
gonadotropins.1,37 ]6 b1 V7 K9 f) j3 ^
Gonadotropin-independent peripheral preco-
1 z$ d6 s, s! E' [cious puberty in boys also results from inappropriate/ L* G0 L/ r( A3 ?7 n
androgenic stimulation from either endogenous or
1 ^/ O1 i( A% k( t2 jexogenous sources, nonpituitary gonadotropin stim-- t9 N% Y' {6 F0 ?
ulation, and rare activating mutations.3 Virilizing
% Q6 h: W2 {. ], I0 ncongenital adrenal hyperplasia producing excessive
# A; Y4 R. @" }! P5 yadrenal androgens is a common cause of precocious; S8 ]3 H4 {4 z9 Q. k: k+ z
puberty in boys.3,4" G- y) M- L  d" {& l3 _5 }
The most common form of congenital adrenal
" c3 W+ g  v$ @hyperplasia is the 21-hydroxylase enzyme deficiency.7 o3 g5 o% x+ J8 W6 R" A) d
The 11-β hydroxylase deficiency may also result in
- W  u3 F0 F8 E( u- oexcessive adrenal androgen production, and rarely,
8 l. n' u2 W+ z, Lan adrenal tumor may also cause adrenal androgen4 Z% Q" S! @- a% O7 t
excess.1,3% K2 B+ j) r+ B9 C) ]0 ?" L9 d. v2 |# C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 \- m8 F# F0 [& k
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, p4 }9 F! A( D6 u, {
A unique entity of male-limited gonadotropin-7 p7 F, u0 g6 L- ^: L7 ~
independent precocious puberty, which is also known
+ |: d0 R5 t0 a! O! vas testotoxicosis, may cause precocious puberty at a
7 S: k: p% p1 K8 b$ _very young age. The physical findings in these boys
9 X% ^! O, }0 b! L5 ]4 U  Nwith this disorder are full pubertal development,9 B" K0 F$ Y" W6 C$ \) ?( e- H
including bilateral testicular growth, similar to boys
' Y3 Q. q  A* z) R: n, H+ N* Swith CPP. The gonadotropin levels in this disorder
  N( a! A9 }& H& v. rare suppressed to prepubertal levels and do not show' ]4 @0 G" V* |
pubertal response of gonadotropin after gonadotropin-
  ?  `- E; ~3 ~, _& _8 l1 J" p, y% u3 Ureleasing hormone stimulation. This is a sex-linked4 i/ W0 ~! p) n* Y' ?. z
autosomal dominant disorder that affects only) F# ~4 L! G1 p, P% e
males; therefore, other male members of the family5 z" y% `5 J8 [# g% c* B
may have similar precocious puberty.35 ?; ^& X. j- z% t
In our patient, physical examination was incon-% s$ b& y4 M$ c' a) M6 V
sistent with true precocious puberty since his testi-2 L' f) a2 p" |6 D+ r! G$ K  x8 J# X
cles were prepubertal in size. However, testotoxicosis$ K. L# J( w, F, {0 K! O5 l
was in the differential diagnosis because his father; Q0 o; _- s3 D: t! x' J# F8 |" u
started puberty somewhat early, and occasionally,6 Z; \3 C% K! I6 N- A- N
testicular enlargement is not that evident in the8 d3 H1 T& d; G9 Y4 ~. P! i
beginning of this process.1 In the absence of a neg-
) O7 C( u: K, f$ T: A" j. I5 Bative initial history of androgen exposure, our
. B1 y/ Z- e1 a- U' [/ w3 Ebiggest concern was virilizing adrenal hyperplasia,
$ R7 u; C& f1 O. \# ]! D. |either 21-hydroxylase deficiency or 11-β hydroxylase& `3 N  z3 |) x$ L4 b
deficiency. Those diagnoses were excluded by find-
6 o+ u! b+ U/ L; u; `ing the normal level of adrenal steroids.: o$ p. G4 d' ~
The diagnosis of exogenous androgens was strongly3 @4 G: V9 `# d" c; e1 _
suspected in a follow-up visit after 4 months because
, [& [( a) x* c' K& athe physical examination revealed the complete disap-
/ G' }5 S% g$ m! m  x1 m1 Hpearance of pubic hair, normal growth velocity, and% R, V5 S$ H- m$ R- i- ]6 B6 }
decreased erections. The father admitted using a testos-3 h7 S5 D8 n5 H. V
terone gel, which he concealed at first visit. He was! |0 s+ I- [: S! d* m4 A) m' U
using it rather frequently, twice a day. The Physicians’' c" u' ^0 ?  i. q
Desk Reference, or package insert of this product, gel or
, Y2 l5 a$ ~, A: d% acream, cautions about dermal testosterone transfer to, ]9 ^# ?- |9 K
unprotected females through direct skin exposure.. ]0 {. g3 s0 B- I
Serum testosterone level was found to be 2 times the! r$ H0 T. D1 G" i- E
baseline value in those females who were exposed to
0 ^. k1 ^! s0 B8 ?7 a6 Peven 15 minutes of direct skin contact with their male
* l* W. v; ?8 mpartners.6 However, when a shirt covered the applica-
8 u/ E1 Z1 A3 J+ C! {tion site, this testosterone transfer was prevented.! f, ^0 w4 h2 M6 q5 y# ?5 z! _6 d
Our patient’s testosterone level was 60 ng/mL,
# H9 \: D! V. \- s2 d. Vwhich was clearly high. Some studies suggest that0 d3 S5 @4 Y5 r, F; s* v  W
dermal conversion of testosterone to dihydrotestos-3 `" l6 E; F. \1 E; z! W
terone, which is a more potent metabolite, is more( N2 }; z: ^2 j; n  b: C
active in young children exposed to testosterone$ c* I6 Y% q2 a8 k1 |, b2 P( L; n
exogenously7; however, we did not measure a dihy-
( I, K  R2 ^5 y/ j# q3 p& mdrotestosterone level in our patient. In addition to
" C" }  q$ {7 ]virilization, exposure to exogenous testosterone in* Q7 H6 f. j3 _8 B) M2 d: i) \' a
children results in an increase in growth velocity and
, W! L9 N; ^! |( Cadvanced bone age, as seen in our patient.
4 B- H: w& @. VThe long-term effect of androgen exposure during; ]3 F' r/ A- \( d( Y# P
early childhood on pubertal development and final; q$ d( U! u, W& J( c7 i0 d; I" d
adult height are not fully known and always remain
! b; n6 S2 f' \+ e0 ?6 c. Da concern. Children treated with short-term testos-0 W' J4 |. e& f$ L
terone injection or topical androgen may exhibit some
9 [4 p; w! m9 d( x7 m. [, Oacceleration of the skeletal maturation; however, after$ T. o6 ~# f1 I' |5 A
cessation of treatment, the rate of bone maturation" |  B: H  q3 F* N: ~
decelerates and gradually returns to normal.8,9
* |1 E$ x$ R) Q4 u& nThere are conflicting reports and controversy9 L& f% ^% P2 W% K
over the effect of early androgen exposure on adult
% Q" z, W9 v* }4 J9 Kpenile length.10,11 Some reports suggest subnormal
  K3 C) u2 m! Y2 p5 f. o( Kadult penile length, apparently because of downreg-# u2 [* B4 n3 N+ t% b) {$ w# ^) f3 T
ulation of androgen receptor number.10,12 However,
/ V: a" |# k; a( y( @2 W$ t5 R" S3 p. USutherland et al13 did not find a correlation between8 _7 S% C: z+ |2 g# n; `9 w" Q5 j
childhood testosterone exposure and reduced adult
) Y6 B, [# h/ w) @) B  |" mpenile length in clinical studies.
* p- G% m& B( E  i' G" A' TNonetheless, we do not believe our patient is
) F, Q& C* O! Lgoing to experience any of the untoward effects from: O! d5 r0 |/ O, z" ]$ [; o1 I
testosterone exposure as mentioned earlier because
7 |# b  y' y- R* ^7 Kthe exposure was not for a prolonged period of time.8 R9 ]  @( m, I0 u% L$ J+ i+ q
Although the bone age was advanced at the time of
+ C3 K! _( K6 Rdiagnosis, the child had a normal growth velocity at8 S( L( [# w* G; e' S8 Z  S
the follow-up visit. It is hoped that his final adult& p- a* V8 u9 D! h
height will not be affected.
+ R2 O6 {9 R8 T3 P7 a5 yAlthough rarely reported, the widespread avail-
& z' P* b0 K! ~9 a/ p% d# |, zability of androgen products in our society may
! b6 s2 |, G) n* K4 r! P+ yindeed cause more virilization in male or female/ l( m7 q( ~3 @# c' @$ b- n9 X0 U
children than one would realize. Exposure to andro-
4 O9 V! o5 u9 _- p, M/ q. f! Ugen products must be considered and specific ques-* `: h) U- K$ L7 p1 |' x
tioning about the use of a testosterone product or7 l$ F' g3 s, ?' B. ~& T# M7 ^
gel should be asked of the family members during( }% P; ^, q8 P  P
the evaluation of any children who present with vir-8 X3 J5 \% d; h9 w' p
ilization or peripheral precocious puberty. The diag-
* U  [. t3 }( W: B% E# [nosis can be established by just a few tests and by
3 P* i  g& R' ]4 g* aappropriate history. The inability to obtain such a
. K2 S# t" y$ o/ [, s* ohistory, or failure to ask the specific questions, may
% f$ D6 N5 H3 Uresult in extensive, unnecessary, and expensive
) ^/ g# ?! ^7 [- c/ x3 xinvestigation. The primary care physician should be
: m) O1 R* r6 F) q0 ]4 Oaware of this fact, because most of these children) m) h" [7 b4 I# n; ^7 S: ~
may initially present in their practice. The Physicians’
5 {3 k1 }/ K& i) x" fDesk Reference and package insert should also put a6 D) m6 ^  }8 H+ A6 Y% ^0 Y) V
warning about the virilizing effect on a male or
! c+ s& |! X! Afemale child who might come in contact with some-, h: ~7 z) `# l( W9 Q- a
one using any of these products.- I) l% Y( Z( [4 ]# H$ u# W5 c" j
References
# v6 W. d9 S6 u7 w: K1. Styne DM. The testes: disorder of sexual differentiation
/ H" F& r! @& L; fand puberty in the male. In: Sperling MA, ed. Pediatric
( b0 W" c/ c; n$ O, WEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ \2 {0 `& T+ a+ e4 a5 H
2002: 565-628.
2 A+ T+ u( `2 W# |( J$ m0 f1 n$ N' V+ U2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( v% m, t' u  ~, g% i# Lpuberty 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/ E0 j, w! K7 F) z# T) E  p
Boy Induced by Indirect Topical2 x, Y2 l- A, b
Exposure to Testosterone: Y" M" k# Q- {$ S$ f$ H0 @
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. K2 T: |6 r0 i5 p- f  band Kenneth R. Rettig, MD1
+ c' @; A; G& k9 ~* oClinical Pediatrics
: O. S7 H4 U+ ]& j' d+ vVolume 46 Number 6
$ Q0 \$ @/ B% X. |7 }) r- [July 2007 540-543
) [) R" J3 q# \, L. n© 2007 Sage Publications
9 f" y, x7 X; c3 g- y/ z10.1177/0009922806296651
; o# }" }3 [1 dhttp://clp.sagepub.com2 @* [% U$ t, j5 i& {1 ?
hosted at
& Z% Q7 N4 l0 _' R+ ?4 yhttp://online.sagepub.com
& X9 v1 t/ _$ x6 g0 }Precocious puberty in boys, central or peripheral,
2 |# N+ _  v3 _* C" @is a significant concern for physicians. Central# K: Q+ \# w5 e' ~1 s9 G
precocious puberty (CPP), which is mediated- M/ k7 Y9 v  E. z6 w$ N
through the hypothalamic pituitary gonadal axis, has
/ D( S% y  M" a$ K/ C4 ~6 Ra higher incidence of organic central nervous system$ \0 F0 b! T! K9 o1 O2 V: l- t2 c* Z
lesions in boys.1,2 Virilization in boys, as manifested
5 B% K4 K9 ?2 P4 K. B, h, |" G- Lby enlargement of the penis, development of pubic
2 I3 R7 f9 @! r' S& r1 Ghair, and facial acne without enlargement of testi-
, L9 X0 D4 L+ M5 @cles, suggests peripheral or pseudopuberty.1-3 We7 b: i' B& P# F0 R
report a 16-month-old boy who presented with the
0 N9 ?7 d% H  f& {" k0 U! Henlargement of the phallus and pubic hair develop-
0 W; B9 O/ ~! j* F# H* bment without testicular enlargement, which was due; h. V4 e. Q; i& ?: r) Q
to the unintentional exposure to androgen gel used by
- G; R! I2 i! |the father. The family initially concealed this infor-$ L6 u. R! l" C
mation, resulting in an extensive work-up for this. r' i5 Q, I( b, a. ], T% o$ p: N
child. Given the widespread and easy availability of: `! E& K+ H1 y8 e- {- x6 r
testosterone gel and cream, we believe this is proba-3 J0 R+ Z4 p) {& {9 m/ x+ G! R
bly more common than the rare case report in the0 T0 z: p7 i, h9 |
literature.4& T0 t. i# \) o6 c# _. k, o
Patient Report
  [$ b3 g( E) |8 u; D8 w; J2 bA 16-month-old white child was referred to the" c1 \5 V7 c5 x) G5 k
endocrine clinic by his pediatrician with the concern
: k! J: Z) P8 I* D# O3 mof early sexual development. His mother noticed
' N# m8 e2 \% }/ plight colored pubic hair development when he was
# L( ~3 K3 x( D) m0 JFrom the 1Division of Pediatric Endocrinology, 2University of
" s2 H+ B+ q- J5 A0 RSouth Alabama Medical Center, Mobile, Alabama.
7 N3 f* p+ \7 A, }% d$ @+ vAddress correspondence to: Samar K. Bhowmick, MD, FACE,
4 _" U/ s+ I  Q/ T. t1 f9 NProfessor of Pediatrics, University of South Alabama, College of4 C+ N2 y2 P3 K2 W% A" D
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;5 [6 Q4 _( u5 T5 R
e-mail: [email protected].1 j) {/ F; Y9 J" V% {
about 6 to 7 months old, which progressively became
+ J( O) _* @$ r, M2 udarker. She was also concerned about the enlarge-4 L- D" E: b6 b" L# M0 X8 m
ment of his penis and frequent erections. The child1 {3 g1 |5 ~# ^  Z* w9 k
was the product of a full-term normal delivery, with
- o& i8 i% u/ C) Q2 k2 |0 }a birth weight of 7 lb 14 oz, and birth length of4 ]1 j* L7 Y% \0 [, w/ p
20 inches. He was breast-fed throughout the first year
% f4 T! z) U7 u; X& `; p7 ?% w. X# xof life and was still receiving breast milk along with/ x7 J3 j, J; V) [  a5 H) y% y
solid food. He had no hospitalizations or surgery,
' g) h9 U/ \4 q. l* S$ h3 C* Nand his psychosocial and psychomotor development9 x6 ~; D0 c8 @- Z2 o! A. S
was age appropriate.
% v$ G; r- Y, D4 LThe family history was remarkable for the father,7 C  K$ O3 i8 m2 ]. @
who was diagnosed with hypothyroidism at age 16,
7 L: D3 U3 X. h" B9 lwhich was treated with thyroxine. The father’s
2 k; z$ P3 L8 x/ @height was 6 feet, and he went through a somewhat
6 e1 _. b8 d" w; Z$ Gearly puberty and had stopped growing by age 14.
/ B/ w7 p! |1 @' ~6 ]4 i5 kThe father denied taking any other medication. The
) d) ]: {2 D+ x3 @5 p# K) dchild’s mother was in good health. Her menarche
( [% U0 ~) k' B  U5 cwas at 11 years of age, and her height was at 5 feet
9 y" n5 I0 }0 u' d5 \5 inches. There was no other family history of pre-
2 b' f9 p  U- k& s2 A$ x( z8 lcocious sexual development in the first-degree rela-
* g! W! z2 p6 {6 Ktives. There were no siblings.' J' o5 w3 ?5 f  a( `' J
Physical Examination
/ n: Y  o, N9 R/ dThe physical examination revealed a very active,
: _* i4 ?" N) ]% M4 N7 h  X' eplayful, and healthy boy. The vital signs documented
6 R, \- D& `. O1 Ga blood pressure of 85/50 mm Hg, his length was- r1 g. S1 m& s+ l: [
90 cm (>97th percentile), and his weight was 14.4 kg
8 f1 Z' F0 ~' ](also >97th percentile). The observed yearly growth* \3 I! b$ n- m& U' L
velocity was 30 cm (12 inches). The examination of4 G# w' l& _& s# P4 M/ q
the neck revealed no thyroid enlargement./ T- U. @7 Y! n( Q' Z1 j! m
The genitourinary examination was remarkable for& O" u0 x6 j/ [4 O" }
enlargement of the penis, with a stretched length of
! q; X% b8 n; Z' \- H8 cm and a width of 2 cm. The glans penis was very well
; M+ g  J( k& g& r' ~: rdeveloped. The pubic hair was Tanner II, mostly around
, K0 T7 ]( ?  O8 [8 m% G540
' ^2 U4 [( Z2 D! \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' e% [& W4 w- Jthe base of the phallus and was dark and curled. The) @" K! q$ h* L4 E% ?, j6 ?# K
testicular volume was prepubertal at 2 mL each.( P+ ?6 n5 T1 B+ C8 G$ g! H
The skin was moist and smooth and somewhat" D! B" `0 H, c$ B
oily. No axillary hair was noted. There were no
* P( I2 e- ^- Yabnormal skin pigmentations or café-au-lait spots.
! ]- d5 t$ [5 M  s; tNeurologic evaluation showed deep tendon reflex 2+
  }, x" Z' i+ f/ \bilateral and symmetrical. There was no suggestion
  S9 P6 D# |0 s( ^: f& jof papilledema.& q  g1 n# k, R/ }( m4 B
Laboratory Evaluation1 _9 G7 I' ~" y" D) _$ [! k* A
The bone age was consistent with 28 months by
% z$ o6 J, |( H3 [( tusing the standard of Greulich and Pyle at a chrono-) j' {4 Z3 x8 v- P( G
logic age of 16 months (advanced).5 Chromosomal
, H7 b9 e) {* j- [$ v5 y+ Tkaryotype was 46XY. The thyroid function test
, v( D7 n- n' [) zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-- e0 F1 T; F/ f0 G( U! ]
lating hormone level was 1.3 µIU/mL (both normal)., T# k+ F* b9 |" D) B
The concentrations of serum electrolytes, blood8 }  A4 N2 o( P) d/ J  E
urea nitrogen, creatinine, and calcium all were1 B* ?) I! j- V( U5 {# u( q
within normal range for his age. The concentration
# U# i: E: z; B/ P2 x* P5 gof serum 17-hydroxyprogesterone was 16 ng/dL$ _* ~& C. y5 W6 x( w, N+ ]; E
(normal, 3 to 90 ng/dL), androstenedione was 20
" s/ g8 ^  ^& Q* @" ?ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  @) e& F; V, K  `: x8 \2 ]6 Q2 gterone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 s) H8 ]: Z. U$ y7 L; j3 Udesoxycorticosterone was 4.3 ng/dL (normal, 7 to
4 h, o, h7 Y. q9 |* m49ng/dL), 11-desoxycortisol (specific compound S)2 w' N: q' g: R; I. J
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% A# \9 S. q+ v
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 J0 S/ b4 @% u- stestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
- Q6 R% y" H" t% |( j4 @1 D- Tand β-human chorionic gonadotropin was less than  y4 Q0 r- v& w
5 mIU/mL (normal <5 mIU/mL). Serum follicular/ s. f: o4 I% f0 U$ T
stimulating hormone and leuteinizing hormone8 z! B. _' u+ G* ~6 K2 H
concentrations were less than 0.05 mIU/mL
* R/ k9 j: R- l1 }( j  ^5 F(prepubertal).
9 ~, m$ R) k6 F1 E" ?: x4 A5 P9 {The parents were notified about the laboratory( P# K- N# K# _4 c$ N: P2 b
results and were informed that all of the tests were. V5 c  k3 {9 B: R3 x( \* t
normal except the testosterone level was high. The
9 M" o' G6 @6 v- [follow-up visit was arranged within a few weeks to  e( W+ p0 C; d3 l0 \
obtain testicular and abdominal sonograms; how-
2 l( d8 u5 F1 aever, the family did not return for 4 months.
1 G7 H/ I# z# F8 i% J' ]1 W5 M" CPhysical examination at this time revealed that the
( s* Q0 N) I6 ]: ~child had grown 2.5 cm in 4 months and had gained
5 J* P9 X$ I# O& W- A" F2 kg of weight. Physical examination remained; I+ w5 o( z! D8 Z6 o! l% O
unchanged. Surprisingly, the pubic hair almost com-
! q- R& g, ?6 {7 I1 j5 Spletely disappeared except for a few vellous hairs at
, T) ~$ O* L$ C' H# x# cthe base of the phallus. Testicular volume was still 2- I/ Y: _8 r/ \/ m
mL, and the size of the penis remained unchanged.
# R4 e& G& y( ^7 |The mother also said that the boy was no longer hav-
, x- f- ?; Y0 ~- n2 \ing frequent erections.$ v, J  q$ Z) j0 t8 Z$ z) \0 P
Both parents were again questioned about use of
. A( |7 l4 p% Q8 ?& c/ M. bany ointment/creams that they may have applied to
! {) {6 L! S4 D- b  ^the child’s skin. This time the father admitted the
. E7 o/ N; P$ U' }8 B, M; b  Y- gTopical Testosterone Exposure / Bhowmick et al 5411 V+ e6 A; E8 h! m$ k
use of testosterone gel twice daily that he was apply-, L" U3 k6 c7 b$ r
ing over his own shoulders, chest, and back area for5 ~/ i0 V! }4 u
a year. The father also revealed he was embarrassed+ N2 c& M; N7 X# I% S- P, @1 K
to disclose that he was using a testosterone gel pre-) n% w, [* {, I) _; i
scribed by his family physician for decreased libido
4 `3 b! y* E) g( j9 ^, f% X: C' `+ M( Psecondary to depression.
5 L  }; b  g- X  @1 f$ \, EThe child slept in the same bed with parents.
+ l  ]* n9 a3 {$ K" A8 x4 uThe father would hug the baby and hold him on his; T0 d" l/ f; h( E  r( ~; D, e
chest for a considerable period of time, causing sig-
3 n( l* N7 S$ [% enificant bare skin contact between baby and father.
# ^2 E8 M: P" m* e( `The father also admitted that after the phone call,
* f+ U& `0 [/ v7 [9 ]; U# ywhen he learned the testosterone level in the baby
: Z" s% X8 S2 [! n" f8 z; Lwas high, he then read the product information, ^) v& x% ]+ [: t( v5 W
packet and concluded that it was most likely the rea-
, V( X/ z) K" }son for the child’s virilization. At that time, they2 U" R+ B$ k, \
decided to put the baby in a separate bed, and the
6 f9 d# [% c: S7 S1 b; gfather was not hugging him with bare skin and had
' Q2 Z& E$ b( F* E+ c9 Cbeen using protective clothing. A repeat testosterone& k9 @. V- H; M# v% v
test was ordered, but the family did not go to the2 U$ Q# i3 g1 e3 S& {: C
laboratory to obtain the test.6 D% K( H5 x* V
Discussion
! z! M) K* u2 x2 F1 m  x5 q/ _' |( TPrecocious puberty in boys is defined as secondary+ e% c- `5 z  R4 P( w- Q& _  B$ o
sexual development before 9 years of age.1,42 K) {1 x4 n3 T
Precocious puberty is termed as central (true) when2 W% N8 q9 [( Z/ B( y( c
it is caused by the premature activation of hypo-7 B: [3 k! J& @) X. y5 ^
thalamic pituitary gonadal axis. CPP is more com-
8 F( L- T' ?) W% c; g. Hmon in girls than in boys.1,3 Most boys with CPP
, Q8 h: f; p$ Z3 E- E0 Rmay have a central nervous system lesion that is
, v3 P' |1 h5 Jresponsible for the early activation of the hypothal-& _& M1 o: ]* b: K7 k; G" Y* U
amic pituitary gonadal axis.1-3 Thus, greater empha-8 B$ R; K" b. m* Z9 W7 S
sis has been given to neuroradiologic imaging in+ T4 ?& W1 d2 q4 [9 W6 w! z
boys with precocious puberty. In addition to viril-* S$ X5 ^" `/ w6 j8 `& \& {/ U
ization, the clinical hallmark of CPP is the symmet-' N. `7 X9 W  Z8 V
rical testicular growth secondary to stimulation by5 A; v" i+ S0 O/ J' R
gonadotropins.1,3* Q7 g: p9 X  [9 t0 R
Gonadotropin-independent peripheral preco-
1 L0 ~% J  K; Y+ O; o. u) r5 gcious puberty in boys also results from inappropriate' @' B5 x/ {# g4 c) U+ @6 h# Z
androgenic stimulation from either endogenous or8 y& A) p+ o# N
exogenous sources, nonpituitary gonadotropin stim-( }' l4 z+ D7 T! o
ulation, and rare activating mutations.3 Virilizing  T2 z; X* M/ H4 [2 {! ]
congenital adrenal hyperplasia producing excessive
$ n7 E+ r; c$ ^+ N4 N! V# c( G. Vadrenal androgens is a common cause of precocious
# ?7 p8 u  `; G6 ^puberty in boys.3,4
, t1 d# K: M0 M  lThe most common form of congenital adrenal/ F0 K4 e: I; f' k9 [
hyperplasia is the 21-hydroxylase enzyme deficiency.
: ~! F- ?! @" U' \3 U1 n% XThe 11-β hydroxylase deficiency may also result in
, X" Y7 o$ M0 [' Q7 g3 P; a- m7 Uexcessive adrenal androgen production, and rarely,
9 N1 U. @: X; N  `! xan adrenal tumor may also cause adrenal androgen
9 K9 x- b. Q1 _  Sexcess.1,3' `% ~# c6 C. t9 e0 L  ~  N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ w6 m  y# V/ X  r1 K0 a
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
# r) F  w: v4 i: CA unique entity of male-limited gonadotropin-( W) \' J  P6 g7 x
independent precocious puberty, which is also known
0 Z; w: n, \+ G  r' n( Cas testotoxicosis, may cause precocious puberty at a
( D# G  m# t7 Q4 c/ v2 z" M3 hvery young age. The physical findings in these boys
' V  S4 ~! j  [+ d6 n" H0 iwith this disorder are full pubertal development,1 q1 {- j) ]+ i8 V
including bilateral testicular growth, similar to boys
# ?0 J# i5 [; G& Zwith CPP. The gonadotropin levels in this disorder; A( f0 Q6 U: D/ h+ \- }5 |
are suppressed to prepubertal levels and do not show
( m) Z8 j0 O- @/ D  k  x6 g  F# spubertal response of gonadotropin after gonadotropin-* m: H9 \7 j: I! a
releasing hormone stimulation. This is a sex-linked; A. l+ N. H- n/ F% d
autosomal dominant disorder that affects only7 u: v# e- U& K0 j8 n
males; therefore, other male members of the family1 }* C) A$ P: ~$ q$ R9 x# r
may have similar precocious puberty.3
+ ]" T9 Y4 n" f( X* YIn our patient, physical examination was incon-
  I/ k4 J5 t+ R4 ssistent with true precocious puberty since his testi-% a4 N4 Z( h; ^6 c2 B1 v' O
cles were prepubertal in size. However, testotoxicosis- [: H$ A6 h% m! A" w
was in the differential diagnosis because his father7 Y0 Y0 b1 l4 a" g
started puberty somewhat early, and occasionally,
  U! y4 a5 |$ c* X: Ftesticular enlargement is not that evident in the
# S+ f' x* ~) y$ L& i/ ?! Pbeginning of this process.1 In the absence of a neg-: U& |8 k  \# ~9 f
ative initial history of androgen exposure, our7 j* {  }; \; G1 B9 Y3 M# E
biggest concern was virilizing adrenal hyperplasia,
7 w4 v" d& k5 D; I/ ^% l5 c) heither 21-hydroxylase deficiency or 11-β hydroxylase
4 y% E+ E) p" K7 m- Ddeficiency. Those diagnoses were excluded by find-
* U9 A1 A* P" x4 Eing the normal level of adrenal steroids.
& l( D6 W4 m: }/ qThe diagnosis of exogenous androgens was strongly$ Q# {& Z! Z8 s+ S2 M# O* @
suspected in a follow-up visit after 4 months because
+ r2 d  D2 R# D5 r" K4 Ethe physical examination revealed the complete disap-
1 @1 \8 T, y# q4 Jpearance of pubic hair, normal growth velocity, and* K; \) ?# o9 }- p1 K3 y
decreased erections. The father admitted using a testos-1 s' i1 V/ r* f7 v* W
terone gel, which he concealed at first visit. He was, d' d# G1 \/ ~7 }# k9 C
using it rather frequently, twice a day. The Physicians’
# W5 K8 g( k4 t! kDesk Reference, or package insert of this product, gel or/ f' N- \2 ]7 z
cream, cautions about dermal testosterone transfer to
( E9 J- C+ ]7 n+ k( `unprotected females through direct skin exposure.
' M' P) s& D5 `) q! P+ S) \$ GSerum testosterone level was found to be 2 times the
- t- {5 w1 a+ Xbaseline value in those females who were exposed to
; c, p  V% t( J! z  r; deven 15 minutes of direct skin contact with their male! Z% E* y* |6 \* T0 b. r* R
partners.6 However, when a shirt covered the applica-# s. N) `4 U0 B' L: D
tion site, this testosterone transfer was prevented., U3 c6 h9 U$ P/ a" s
Our patient’s testosterone level was 60 ng/mL,
+ D1 e7 _" O$ }9 d2 }% swhich was clearly high. Some studies suggest that, w0 e6 e4 }( Z" G" G2 ~8 g
dermal conversion of testosterone to dihydrotestos-
/ t$ K9 J! k2 o) p* I1 `; O" p$ Cterone, which is a more potent metabolite, is more4 @$ M( Y2 I$ m5 ^& u/ B3 u, z
active in young children exposed to testosterone9 S/ p2 S( Q" ~0 ^! X
exogenously7; however, we did not measure a dihy-
0 f$ R: x, W! B" Zdrotestosterone level in our patient. In addition to; x) L6 W& y! m: S3 `
virilization, exposure to exogenous testosterone in
( d  x0 Y. A+ }children results in an increase in growth velocity and
# K1 E4 U8 f2 C, cadvanced bone age, as seen in our patient.
3 w( X! Q, o6 x+ M- H0 p' mThe long-term effect of androgen exposure during
  K) {. O  |: G& {# z1 X. ^; \early childhood on pubertal development and final7 B3 |1 m9 H, j3 o% E
adult height are not fully known and always remain* C$ t  v7 _- h; L9 a$ v' B, X
a concern. Children treated with short-term testos-
# q. ]& |5 w. J9 M+ R3 S' l" Wterone injection or topical androgen may exhibit some4 Y/ H3 {, o: t' w
acceleration of the skeletal maturation; however, after
/ o6 E) l  U% r# n6 R7 A# l2 p$ S8 kcessation of treatment, the rate of bone maturation% l6 F) a# E  m; Z# z$ O
decelerates and gradually returns to normal.8,9/ a2 `3 Z1 T* k+ A3 s7 U- w/ }
There are conflicting reports and controversy4 D2 F  f0 b& b
over the effect of early androgen exposure on adult3 ?. `4 {$ r1 p7 ~7 l5 @; G* L
penile length.10,11 Some reports suggest subnormal& w2 t1 q: M/ v9 m: {
adult penile length, apparently because of downreg-* P# m3 z. ]7 M* c
ulation of androgen receptor number.10,12 However,
2 q0 c4 y1 |4 l) i8 m4 p1 }Sutherland et al13 did not find a correlation between8 N% A& K. c8 F6 {0 _+ m
childhood testosterone exposure and reduced adult6 p' x& l1 f) k7 R; _" N
penile length in clinical studies.
! K7 r: N/ |! x9 \5 t8 nNonetheless, we do not believe our patient is
" l$ K, J+ I2 k" A0 [# sgoing to experience any of the untoward effects from7 W3 t( R7 P3 ]
testosterone exposure as mentioned earlier because: i* p2 [, O+ l, u+ S
the exposure was not for a prolonged period of time.
/ @; _0 ~9 }% ~# ^; n9 N) J! hAlthough the bone age was advanced at the time of. `. r/ \1 U5 O7 q4 q4 c. K6 Q
diagnosis, the child had a normal growth velocity at
5 |& F/ g* @' h( @the follow-up visit. It is hoped that his final adult" a$ o5 m; U9 J" L! g3 H) \
height will not be affected.
6 z2 O8 S" `. M7 s/ DAlthough rarely reported, the widespread avail-
; Q& O" b; a% N5 z5 [ability of androgen products in our society may
/ M, ?$ ^% P- L' b" Eindeed cause more virilization in male or female4 S9 P  z+ L! m+ x) W
children than one would realize. Exposure to andro-
: Y' Z0 }' d/ Q3 p( ?9 u; o- o/ Zgen products must be considered and specific ques-
! W9 @  K- h( C- B. _tioning about the use of a testosterone product or
# C. ~) N, b7 r3 @! `8 Mgel should be asked of the family members during
3 j' k! y/ H/ {& ~, ^# K6 ]0 Fthe evaluation of any children who present with vir-0 d$ z* D3 c# w/ ~+ [9 j# d1 V
ilization or peripheral precocious puberty. The diag-: [' `, q& k8 H1 `; k
nosis can be established by just a few tests and by
2 V4 v, _  H5 Z4 M2 i8 jappropriate history. The inability to obtain such a- u  x9 b# J/ f. S, q1 |1 f
history, or failure to ask the specific questions, may
5 d' [; T; P2 w4 Hresult in extensive, unnecessary, and expensive
( _/ \8 \* B. X  y$ oinvestigation. The primary care physician should be- [1 d# K( J% m% \  f
aware of this fact, because most of these children
5 _# ^: {( \. h3 ~1 p5 hmay initially present in their practice. The Physicians’
! L& g2 T0 P9 L; i. [6 d) GDesk Reference and package insert should also put a
0 h8 z1 e7 I3 ?3 f& zwarning about the virilizing effect on a male or
0 y  Z6 E* }5 I2 t, Rfemale child who might come in contact with some-; o$ {; y# ?' P8 z0 s+ y! E% R
one using any of these products.4 x7 h2 J1 d; i) L3 L6 i( b. R
References
7 Y6 K3 L1 T" z' p( b& U; k' q: x1. Styne DM. The testes: disorder of sexual differentiation
3 D1 b  Q4 |' b9 m0 I& H! G0 {4 |and puberty in the male. In: Sperling MA, ed. Pediatric
% ?- L7 F( A' oEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  Z) a6 h: W5 j/ ?- `0 ~/ U9 m* ^2002: 565-628." p+ F' M) K4 J8 g9 r4 J! ?: ]9 w
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  P1 N7 ^; v5 t% o8 Upuberty 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
& P; I7 K# t  X$ _% \( z  @6 ~
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