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
) P7 M% N! x/ t: q& m- Y" G, n; aBoy Induced by Indirect Topical
4 g; l5 a  Q' RExposure to Testosterone6 l  X! F: n3 x3 D! E) F7 h
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 A/ [) W# ]9 u6 a) \and Kenneth R. Rettig, MD1/ i6 R! u. v$ m/ I# {3 U# X
Clinical Pediatrics; K% k. I+ C+ s+ ?. ^/ F
Volume 46 Number 6* W. H0 s  z$ i, X+ }# }
July 2007 540-543# R; S$ J  K. i; z9 _/ ]- |
© 2007 Sage Publications# {; \! |. |8 i
10.1177/0009922806296651; u% ]* O6 O5 r9 t' K7 P
http://clp.sagepub.com% Y1 W* ^2 w: K; B  @: Z' }2 k
hosted at, N( j0 p6 c  N/ a! S
http://online.sagepub.com
' O% N: _9 c# r$ x5 fPrecocious puberty in boys, central or peripheral,
7 U6 d0 e4 y  K( bis a significant concern for physicians. Central
. w- t  J+ z/ X  t5 u2 j" \, bprecocious puberty (CPP), which is mediated
7 s3 Z8 L) p& Q, Hthrough the hypothalamic pituitary gonadal axis, has' ]; B; C% y$ C: H
a higher incidence of organic central nervous system$ m' d' d6 b! l3 E; W0 X7 `
lesions in boys.1,2 Virilization in boys, as manifested2 ]  p; j# I2 K* {) N& H
by enlargement of the penis, development of pubic( I: _1 q# a* a8 O2 v7 D
hair, and facial acne without enlargement of testi-7 K9 ?; Y2 V) {6 v) Q9 q* n
cles, suggests peripheral or pseudopuberty.1-3 We+ i- U) j$ L  S5 L: n
report a 16-month-old boy who presented with the
; n* v$ p& K" Y% jenlargement of the phallus and pubic hair develop-
% b, `2 W5 X; B& _8 [" F2 tment without testicular enlargement, which was due( r0 p1 q; u: P' I
to the unintentional exposure to androgen gel used by1 D. Q6 x1 a- Q/ h8 }
the father. The family initially concealed this infor-
7 R0 G) d* [; j' _& p) emation, resulting in an extensive work-up for this
4 U; ^/ p1 V8 d, [* {: Tchild. Given the widespread and easy availability of% U( L! ~7 r, v' ~- O! h. c
testosterone gel and cream, we believe this is proba-
1 @! _, y- S$ S" e# sbly more common than the rare case report in the
, J1 @2 S/ @% \literature.4* L7 L8 r- o5 U+ y5 \- ]" I
Patient Report
* g; u6 T0 e+ ?; O) r, Y- ~6 QA 16-month-old white child was referred to the
* y0 a) d$ W" iendocrine clinic by his pediatrician with the concern5 y( ]% J1 F7 y( q* ?
of early sexual development. His mother noticed
3 ^( a) R7 j3 f0 M  i* E3 O; n7 tlight colored pubic hair development when he was* k6 R" O2 v7 r: q9 F
From the 1Division of Pediatric Endocrinology, 2University of
$ W$ d. {: C5 F: BSouth Alabama Medical Center, Mobile, Alabama.
% y6 @, ~/ j1 i( |/ D: a. |+ MAddress correspondence to: Samar K. Bhowmick, MD, FACE,
* H4 [% R# k  i+ j% n1 z" {8 HProfessor of Pediatrics, University of South Alabama, College of! ~  B: ]7 L6 I
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 P6 w1 \2 |6 \/ }" t1 ee-mail: [email protected].
; w" ~3 A2 C" o  ]+ o# ^about 6 to 7 months old, which progressively became
+ X' o+ W1 y  M3 Ndarker. She was also concerned about the enlarge-
9 a7 F9 M6 \* R9 j# ^4 T% ~ment of his penis and frequent erections. The child& G$ m7 s9 h1 R2 E' i& U$ Z
was the product of a full-term normal delivery, with( v, T) |1 ^6 n5 W: F% X8 I( Y6 {$ {
a birth weight of 7 lb 14 oz, and birth length of- G8 b2 ^* |( C7 y
20 inches. He was breast-fed throughout the first year# r3 a% I6 R* o+ D5 O# J
of life and was still receiving breast milk along with
% N* Z( z1 F5 \7 A7 Z2 w/ D1 i5 qsolid food. He had no hospitalizations or surgery,8 n6 p/ B( q* x" j
and his psychosocial and psychomotor development; r- f3 s( t; r/ i& M
was age appropriate.! S/ q) G; T) x+ f/ W) K5 k1 J
The family history was remarkable for the father,
! z6 C' ?( T* G& \/ rwho was diagnosed with hypothyroidism at age 16,
5 v1 g- S* x& R- ~which was treated with thyroxine. The father’s
) r" a$ k$ n4 I) X- }  sheight was 6 feet, and he went through a somewhat  C- ?1 J* j  b8 l% B4 j1 ]
early puberty and had stopped growing by age 14.
4 ]( w; [* Y; W- {+ t7 c9 sThe father denied taking any other medication. The4 B' b! Q2 ^7 u5 L7 T3 ~
child’s mother was in good health. Her menarche
: G* o5 H) V5 i% m' swas at 11 years of age, and her height was at 5 feet, R1 K& c' _4 X1 E# i' b
5 inches. There was no other family history of pre-$ {7 X  X5 r* q6 x/ W) ]( m! H+ L
cocious sexual development in the first-degree rela-1 M  R/ S. G8 e
tives. There were no siblings.
+ W: X4 B+ V/ l% R0 s4 l; s4 MPhysical Examination. @' V! R* S' u8 {0 N
The physical examination revealed a very active,7 i/ n9 M8 v  N
playful, and healthy boy. The vital signs documented( x; h& K3 }% G8 _6 C" N+ ?* ~- ]4 X
a blood pressure of 85/50 mm Hg, his length was
' v; E9 A' O. v0 h: G/ d90 cm (>97th percentile), and his weight was 14.4 kg
. x: O8 h$ Q- y, l9 [# U  s8 z(also >97th percentile). The observed yearly growth7 L$ x% b: u; [) a/ t: N7 @
velocity was 30 cm (12 inches). The examination of; S7 T  T9 C6 W
the neck revealed no thyroid enlargement.
8 V0 J1 X3 S) N+ _2 l& Q5 ]The genitourinary examination was remarkable for1 @6 _% P* F. T( {
enlargement of the penis, with a stretched length of
& S  t* F4 ]" F& O3 N8 cm and a width of 2 cm. The glans penis was very well
# P4 v/ _! y# D# L2 T& b  ~  Ydeveloped. The pubic hair was Tanner II, mostly around
% F, F3 U, _' c0 M$ k! i1 B+ D540
( {" V! C3 M) Z6 K$ Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* i7 E; |0 B, Y1 P+ g* t  a- J! E0 i* Z
the base of the phallus and was dark and curled. The5 k; j+ p" U2 y$ U) D" Y
testicular volume was prepubertal at 2 mL each.
- ^( a8 S9 V8 h- ]/ k, ^3 [The skin was moist and smooth and somewhat
" d. z4 k% `6 J+ [. I% foily. No axillary hair was noted. There were no
8 a+ I5 [. K4 ?" z* \abnormal skin pigmentations or café-au-lait spots.9 D; e5 {/ E) f, w5 p" R4 y8 I  a
Neurologic evaluation showed deep tendon reflex 2+7 Z8 \! u1 l( `$ W7 U+ ^0 Z  L
bilateral and symmetrical. There was no suggestion* t0 [) b; O: z' y
of papilledema.. b- s( h0 y2 b# F: T6 N5 E
Laboratory Evaluation, g$ B* ^' U! x6 H
The bone age was consistent with 28 months by5 p; P% Z8 S( E8 d! I1 J
using the standard of Greulich and Pyle at a chrono-* `' i; w9 u% u6 Q% C' }
logic age of 16 months (advanced).5 Chromosomal
' ]% O1 p" P! d3 [karyotype was 46XY. The thyroid function test& a% S7 J7 g2 w3 x) o) L" `, `# F; S2 _1 q
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, A4 Q; g1 t: K/ y# B0 F
lating hormone level was 1.3 µIU/mL (both normal).6 V: z" Y5 y9 u) u1 w! D
The concentrations of serum electrolytes, blood
$ b6 E" @. n* K" F$ @1 n2 Iurea nitrogen, creatinine, and calcium all were  F4 S5 E- r* G6 _" |- Z
within normal range for his age. The concentration
& L  S9 r# G) p3 v3 dof serum 17-hydroxyprogesterone was 16 ng/dL1 K& R9 F' P1 z- P+ T
(normal, 3 to 90 ng/dL), androstenedione was 20
$ b3 n/ P; K! q# i0 i' z9 Qng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 F  x6 _- n+ y* S( ?terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. u7 l) {$ G0 V, ^8 odesoxycorticosterone was 4.3 ng/dL (normal, 7 to
% K0 z" O0 m: y0 B% `+ w49ng/dL), 11-desoxycortisol (specific compound S)$ W6 I7 T/ Z/ j5 m
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
5 L4 `: T1 I+ F6 _8 h4 ]tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" x4 l) `/ _: o9 Otestosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 g1 F) C$ l, j0 S" m6 w+ g! v
and β-human chorionic gonadotropin was less than
; `- g3 r/ e4 \& B/ D5 mIU/mL (normal <5 mIU/mL). Serum follicular
1 R4 ~( ^! D" J" R; `stimulating hormone and leuteinizing hormone
& O) h* W% M  e8 D% Qconcentrations were less than 0.05 mIU/mL
/ V- L' \! J/ s) T( B/ P6 U/ Z- Q(prepubertal).7 |  f7 ]5 i& m
The parents were notified about the laboratory
6 h$ t# F" U/ X2 C$ n( Hresults and were informed that all of the tests were8 L" _" L' Q; {
normal except the testosterone level was high. The
1 W5 Y6 B- X! N! z0 ~  h- Xfollow-up visit was arranged within a few weeks to
; ~. `# M' V( S$ |8 w: cobtain testicular and abdominal sonograms; how-
$ q9 r' ^  n4 V1 }1 {+ [+ uever, the family did not return for 4 months.& ~) s; X  U' E2 V6 t' t8 T7 q- V
Physical examination at this time revealed that the
% p7 @- ?( k" J: }child had grown 2.5 cm in 4 months and had gained1 m# B7 I& [; ]" _  r0 P
2 kg of weight. Physical examination remained0 |! J% i0 H% r) n8 A6 c* L
unchanged. Surprisingly, the pubic hair almost com-! S4 j; J2 _0 P" Q6 ?/ q2 f$ `
pletely disappeared except for a few vellous hairs at  d0 k% d( X4 Y! w" G0 E7 l
the base of the phallus. Testicular volume was still 2* i+ i4 W' a: C" B% D; e
mL, and the size of the penis remained unchanged.2 j2 t. t. U$ t& w% O
The mother also said that the boy was no longer hav-( {  o# u4 K1 X- a
ing frequent erections.
* k' n% E& k5 w; _# YBoth parents were again questioned about use of
. ^: @  ?1 I$ \( Jany ointment/creams that they may have applied to3 j, c; H+ y* R; N& M- H
the child’s skin. This time the father admitted the
9 X; G( }7 h' WTopical Testosterone Exposure / Bhowmick et al 541' u6 w  g" C* t
use of testosterone gel twice daily that he was apply-
1 c4 |, A" F, \' }ing over his own shoulders, chest, and back area for; h& Y% _4 k5 d/ _* t: K
a year. The father also revealed he was embarrassed% j5 I) L6 E- M
to disclose that he was using a testosterone gel pre-
8 g- ?) u% r/ T  g4 v% Xscribed by his family physician for decreased libido
- `1 x9 j/ Y1 r5 o' u; }secondary to depression.+ B6 j: R2 F- C$ D+ W# u0 ]
The child slept in the same bed with parents.
2 e, v) f1 L1 j2 b7 HThe father would hug the baby and hold him on his: A; [4 b2 r3 |& _* @: W
chest for a considerable period of time, causing sig-
5 g$ U8 r. A; q2 E0 a# S2 rnificant bare skin contact between baby and father.
) R/ f. p- g, t! O, G. z9 O  @The father also admitted that after the phone call,
4 L- g# d  ^8 Q! L$ }! vwhen he learned the testosterone level in the baby
5 j8 @) Q/ _0 K" E5 H" Twas high, he then read the product information0 r, o7 |+ N7 u
packet and concluded that it was most likely the rea-1 d) B7 J" w# f: s, d
son for the child’s virilization. At that time, they% y; t& r5 Y: o
decided to put the baby in a separate bed, and the
, A7 N% i' o8 c; C% Hfather was not hugging him with bare skin and had
: S7 V9 T9 ~8 M3 i, ^* tbeen using protective clothing. A repeat testosterone
  |" ]( B" F9 G  c4 Y/ T- Otest was ordered, but the family did not go to the
& G  {: B% g5 Llaboratory to obtain the test.
8 T* N, v% b! n$ LDiscussion8 L# X, M9 N% I5 h' D3 R3 E
Precocious puberty in boys is defined as secondary" ~$ s  Y% j- g5 ]( S
sexual development before 9 years of age.1,4
0 l2 f  I) [9 vPrecocious puberty is termed as central (true) when+ Q1 d5 n: h3 G* r9 h
it is caused by the premature activation of hypo-
0 \! K+ d" F: n- E: kthalamic pituitary gonadal axis. CPP is more com-
; N7 P  }6 v9 N4 b5 Jmon in girls than in boys.1,3 Most boys with CPP$ P5 R" e" C% i# [( `" L
may have a central nervous system lesion that is
! _* K' \- o6 s6 R! i4 v1 ~responsible for the early activation of the hypothal-6 i3 L3 t" Y: ^$ g  W
amic pituitary gonadal axis.1-3 Thus, greater empha-2 V) d3 u/ B3 }! c/ U2 X
sis has been given to neuroradiologic imaging in: X  X, J4 u1 ^/ ?
boys with precocious puberty. In addition to viril-% z8 }, |( V2 Z- H1 H5 ~2 k
ization, the clinical hallmark of CPP is the symmet-
* F& u) e/ N& Z# z/ G: rrical testicular growth secondary to stimulation by1 M- G0 l1 y8 G; P
gonadotropins.1,3
6 O" s$ P3 e/ V8 {6 d7 W, Y( G% ZGonadotropin-independent peripheral preco-
% \' M% d8 n6 f( t. W0 d0 acious puberty in boys also results from inappropriate
9 N3 \' o3 u# ?: g: ~$ I6 q8 Iandrogenic stimulation from either endogenous or$ y) B6 |) x! f4 k  H
exogenous sources, nonpituitary gonadotropin stim-( O; Y$ a% H% q- t& V" j
ulation, and rare activating mutations.3 Virilizing: e5 V4 T% G3 r3 _# N# k+ b
congenital adrenal hyperplasia producing excessive( S, y" U1 k/ T/ X% q2 g" A
adrenal androgens is a common cause of precocious% j: Z! z# I/ \1 ^  p1 @( C
puberty in boys.3,4
, m: F$ V, ?+ W/ WThe most common form of congenital adrenal" y* A# I2 F6 Z$ F  \7 j- c+ q
hyperplasia is the 21-hydroxylase enzyme deficiency.
0 O. L+ h# y; \) ~: E7 I& r+ {* FThe 11-β hydroxylase deficiency may also result in
, A* ~- R7 }, e. gexcessive adrenal androgen production, and rarely,
- `5 J9 g2 [* s" x- zan adrenal tumor may also cause adrenal androgen
0 e8 a0 R( w' q) p! bexcess.1,3$ j& i8 A5 R) B, u4 [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 L  o; q: M7 m& Z
542 Clinical Pediatrics / Vol. 46, No. 6, July 20071 s+ C0 d( g. I( b# c4 U9 \
A unique entity of male-limited gonadotropin-# _9 s! `$ _6 Q5 a0 ]
independent precocious puberty, which is also known
" j* \2 N) N( @. V1 b7 V6 ]as testotoxicosis, may cause precocious puberty at a
$ Y" f& f, [; p0 w! a/ z: p# A& dvery young age. The physical findings in these boys
! P6 _  ?* s3 _( s' J  B$ S0 O4 Mwith this disorder are full pubertal development,
. V( q7 O" W. X% E2 ?, pincluding bilateral testicular growth, similar to boys, B9 n- j; j! ]2 r2 N3 q
with CPP. The gonadotropin levels in this disorder) E" }; c! w4 E% P# Z
are suppressed to prepubertal levels and do not show
( {4 {: N5 a: x: c" j: Cpubertal response of gonadotropin after gonadotropin-4 N0 g0 n6 b* S! M4 g& o
releasing hormone stimulation. This is a sex-linked
  u9 s5 Z" q' A$ C: X* Wautosomal dominant disorder that affects only6 i3 L+ b$ h2 T6 [# g7 x
males; therefore, other male members of the family
9 s8 Z* n/ @7 V& Y8 D' h2 umay have similar precocious puberty.3" S* A# ^2 R0 ^
In our patient, physical examination was incon-
; o) W# T1 j3 o5 E: s9 o" usistent with true precocious puberty since his testi-; l1 K( N+ a0 _: C9 B
cles were prepubertal in size. However, testotoxicosis3 s; l, ~4 a9 j3 C- b/ `  A" [
was in the differential diagnosis because his father' N1 S* w$ v) `4 Q+ B/ n; Y
started puberty somewhat early, and occasionally,- Q$ v5 ~; q- y' O$ b8 J1 ~
testicular enlargement is not that evident in the" f2 S5 s5 t" d
beginning of this process.1 In the absence of a neg-
) w9 d2 B  x% F/ g+ _ative initial history of androgen exposure, our8 u6 d" k0 ]+ }
biggest concern was virilizing adrenal hyperplasia,5 ^9 D2 _- {7 ?/ y6 y# z! ~& l
either 21-hydroxylase deficiency or 11-β hydroxylase
( ~7 s9 v! ~) U. @deficiency. Those diagnoses were excluded by find-
0 q  L$ L9 l2 A( P1 Z& m- ming the normal level of adrenal steroids.' \# P) K1 N: z& X, m7 ~1 _
The diagnosis of exogenous androgens was strongly% X7 V" {; f' [& j" ~# `4 W
suspected in a follow-up visit after 4 months because
# M# Z; ^( R( O: Gthe physical examination revealed the complete disap-
! G# w& ?7 B- w/ z: i8 npearance of pubic hair, normal growth velocity, and% r5 f/ V% V. u# O$ C: K5 o# K
decreased erections. The father admitted using a testos-
( D; P5 E7 u# p) O/ X4 Pterone gel, which he concealed at first visit. He was
$ T; G8 g; q: v5 Vusing it rather frequently, twice a day. The Physicians’
4 S* a  w" T9 A6 D0 qDesk Reference, or package insert of this product, gel or
1 ~' W# Q# M1 u7 i5 Mcream, cautions about dermal testosterone transfer to
. Q6 A! Z) r) O1 a) ~unprotected females through direct skin exposure.7 y. j, I4 j, @9 @" @8 \" {& t
Serum testosterone level was found to be 2 times the
" U* C; r6 E$ j- Bbaseline value in those females who were exposed to1 m& \! F* x: ~8 k$ Y
even 15 minutes of direct skin contact with their male0 W  y% m, V" o/ p) d
partners.6 However, when a shirt covered the applica-
! D( W" Y, M* ~" xtion site, this testosterone transfer was prevented.7 z, t9 P3 ]  R: \4 o
Our patient’s testosterone level was 60 ng/mL,! M' V1 }' Y" J3 x
which was clearly high. Some studies suggest that
, s' r, S+ [" s4 ydermal conversion of testosterone to dihydrotestos-9 I4 L4 j, U$ f
terone, which is a more potent metabolite, is more2 d* G. K  T. L7 x8 `; l
active in young children exposed to testosterone
' V8 Y% m* m6 Z( Sexogenously7; however, we did not measure a dihy-* e- V/ M: \( V6 N: }
drotestosterone level in our patient. In addition to3 o* r/ U' L/ G: M- `  I% p5 m$ M0 ^
virilization, exposure to exogenous testosterone in( ]0 y3 E' K, A- h$ w
children results in an increase in growth velocity and& z& o+ J  d8 A5 I! b, K2 v
advanced bone age, as seen in our patient.
" |# v5 C- s4 i- l' X% i, k  xThe long-term effect of androgen exposure during
$ W! [9 Z4 O6 P, M$ M3 |early childhood on pubertal development and final% H" T7 s+ Y' j8 r
adult height are not fully known and always remain
/ R: Z* F/ N7 K, u# qa concern. Children treated with short-term testos-3 e. ^: {) V. v8 R. c3 j
terone injection or topical androgen may exhibit some0 }9 O) C$ @4 f# G, x/ N6 p' ~' y8 q
acceleration of the skeletal maturation; however, after- U: C0 V0 _. V' M
cessation of treatment, the rate of bone maturation7 w0 n  z: n0 D1 t' g
decelerates and gradually returns to normal.8,9% p7 d* ^3 u. `: ?( f+ _$ c. G
There are conflicting reports and controversy
* `0 Z/ g* F8 e! L, Iover the effect of early androgen exposure on adult0 m9 h$ ^% n8 B
penile length.10,11 Some reports suggest subnormal# n0 O) x$ [" J
adult penile length, apparently because of downreg-  s. m1 H* N. V. m; Q% y4 G0 g
ulation of androgen receptor number.10,12 However,3 ?* H& E+ N1 D1 {6 g3 u
Sutherland et al13 did not find a correlation between
2 b5 D# R% a/ F' K. ochildhood testosterone exposure and reduced adult6 R2 l6 o% b/ ^9 C& U
penile length in clinical studies.
+ @, ]+ O  d: J# P( t# r# rNonetheless, we do not believe our patient is
0 t" g! w! j1 G+ ~5 [( P) Lgoing to experience any of the untoward effects from* |# Y: Z% q/ e6 f) w) i( d$ }, T1 V
testosterone exposure as mentioned earlier because4 N1 o9 I. V% u& U2 {
the exposure was not for a prolonged period of time.0 y" `! z; R+ V' \" @
Although the bone age was advanced at the time of
. J+ {7 e2 l8 p2 q1 Pdiagnosis, the child had a normal growth velocity at/ u- Z9 ?& K2 Y# W' s/ I$ }
the follow-up visit. It is hoped that his final adult8 H6 Y/ w8 R; I
height will not be affected.
" y7 _$ n/ Z0 {6 p+ t0 HAlthough rarely reported, the widespread avail-
, D3 x# ^$ B, |  j- n2 L7 mability of androgen products in our society may3 N! G6 X3 `) @5 O% n' x, `
indeed cause more virilization in male or female" R! q( X& w5 O" Y9 q- c3 q7 F
children than one would realize. Exposure to andro-. ^  G6 f- n; w+ N( t/ y/ I* K  X( k5 u
gen products must be considered and specific ques-
! c+ r6 n# J+ B5 s& Ftioning about the use of a testosterone product or
1 ^+ B! P9 V0 A8 [gel should be asked of the family members during
6 i, v/ T8 I! Q- g# }) Rthe evaluation of any children who present with vir-
1 `! C( A; C3 b# p4 z# \ilization or peripheral precocious puberty. The diag-
/ \! `" q4 A; p6 ^1 Jnosis can be established by just a few tests and by
7 |3 X2 j/ z% Pappropriate history. The inability to obtain such a" z3 j% Z1 e  X& t
history, or failure to ask the specific questions, may# {" r$ l! j) s" G3 L# {3 }
result in extensive, unnecessary, and expensive
" `8 ^- m: l  E8 B) Uinvestigation. The primary care physician should be/ Q' r$ {9 u& K$ J
aware of this fact, because most of these children  n, {' @8 ^8 ]! i; `1 r0 b
may initially present in their practice. The Physicians’- C0 }+ x- h% N* K; D
Desk Reference and package insert should also put a: ^' a# k  [7 ~1 p
warning about the virilizing effect on a male or! u& D! V' E0 A( |3 n- h2 f3 c
female child who might come in contact with some-
( A: b! z4 ^3 p, ione using any of these products.
7 Y2 {/ C- H2 F8 i% jReferences
1 j% O" |; Z' h; \' X1. Styne DM. The testes: disorder of sexual differentiation' H$ @' _- y1 j9 ?4 [4 X/ m8 R
and puberty in the male. In: Sperling MA, ed. Pediatric0 L5 ?# \& m. q$ {
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
$ x3 J7 v* B' h) o! Q5 p( ^2002: 565-628.
2 o# I" B9 u8 M5 ]2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& b) z* Z2 }. e& b" A4 G$ ipuberty in children with tumours of the suprasellar pineal
發表於 2025-1-4 03:27:02 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
Sexual Precocity in a 16-Month-Old
$ |( S1 r* o1 \2 m5 r. ~Boy Induced by Indirect Topical7 t& i# Y& j8 d/ H
Exposure to Testosterone
2 z+ F& k2 c. T- uSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! Y6 d4 _% W& y! i# @
and Kenneth R. Rettig, MD11 P0 z5 @" @& ]3 |
Clinical Pediatrics5 k$ n  P$ z% t$ J4 p
Volume 46 Number 6
3 H' i1 N. g4 c+ v4 [July 2007 540-5439 u9 g( l' [, W: r5 `6 z
© 2007 Sage Publications; ?) N+ `/ m. u2 x% Z
10.1177/0009922806296651
! @" y4 W! V0 P5 u' L1 S# ?http://clp.sagepub.com
! `7 F% \& k' z  vhosted at
6 i1 _) l/ o  T! vhttp://online.sagepub.com
. z% ~) E# i1 G7 A& ?8 T* zPrecocious puberty in boys, central or peripheral,2 b! J/ e) E1 G$ Y1 n
is a significant concern for physicians. Central
- n, W. y: Q% a7 k9 f2 J8 |/ Xprecocious puberty (CPP), which is mediated
0 c6 X6 a+ I' Y$ _. Z* a+ P' ~through the hypothalamic pituitary gonadal axis, has
$ X3 K7 M- D: H& R. M9 E0 s1 {1 Q5 Wa higher incidence of organic central nervous system
) I  z" v" c; d2 x5 o  Nlesions in boys.1,2 Virilization in boys, as manifested
& p0 c8 F" o3 C( Cby enlargement of the penis, development of pubic
* }, F- B3 I& R9 z5 @: shair, and facial acne without enlargement of testi-
& x$ }7 H! N5 `2 b! Wcles, suggests peripheral or pseudopuberty.1-3 We
1 {% A& p3 a  w7 E3 E. kreport a 16-month-old boy who presented with the- \& @! T, z- o- P" V
enlargement of the phallus and pubic hair develop-
0 F- _8 F0 Z. K5 A8 ument without testicular enlargement, which was due/ c6 s, a, H1 o; V4 \$ C8 K
to the unintentional exposure to androgen gel used by" ^/ q6 H& e+ K7 g1 F/ n
the father. The family initially concealed this infor-% b8 {+ o2 k; W- \" n. ]5 W* f
mation, resulting in an extensive work-up for this
; K; e) ^5 A+ Z- Z( M! x, qchild. Given the widespread and easy availability of5 P: S6 f0 ~' [! r/ U5 E
testosterone gel and cream, we believe this is proba-
" f+ R- y, }8 [0 d! m" u- Ably more common than the rare case report in the
# v- b* ^' Q7 ~; u( @literature.4
6 |4 q$ `1 I1 m, |3 D! H' o$ S; JPatient Report
% e# w( t  |! qA 16-month-old white child was referred to the" ?6 Q# m# M' v( j1 d: N  g
endocrine clinic by his pediatrician with the concern
! o4 ?8 o8 X: `- c2 I# x0 I' tof early sexual development. His mother noticed
% E- c9 ?' z6 X5 z5 hlight colored pubic hair development when he was
- O+ m/ ^# G9 C! Q( _From the 1Division of Pediatric Endocrinology, 2University of
; ?) R& ?* ?! s! [3 pSouth Alabama Medical Center, Mobile, Alabama.8 C4 w7 Z6 ]8 o* L7 S
Address correspondence to: Samar K. Bhowmick, MD, FACE,
# L1 I/ s! ]; p5 o, IProfessor of Pediatrics, University of South Alabama, College of5 w/ Z9 ]* ]2 F! u5 E  a
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! H) v8 n) ~1 ?: Q1 ~8 oe-mail: [email protected].- P: T1 ]; F/ b& P
about 6 to 7 months old, which progressively became
2 w! b/ A- P9 K; }+ Z1 Y" m7 d- |1 rdarker. She was also concerned about the enlarge-
% p; o0 W% m. J! B. dment of his penis and frequent erections. The child* ^0 M$ ~' e- {* U7 ~7 L; L2 E
was the product of a full-term normal delivery, with, ]' q4 D3 K: F& c2 k) P7 Q
a birth weight of 7 lb 14 oz, and birth length of) x1 [( p) b/ f9 n" v
20 inches. He was breast-fed throughout the first year# y  X6 K, X1 L4 |0 _6 A5 a
of life and was still receiving breast milk along with
, A* x! t# t# z+ g. X6 V7 R8 e* tsolid food. He had no hospitalizations or surgery,- \0 Y' b) D/ S1 ~# U, R: I
and his psychosocial and psychomotor development
0 }* ^" d3 }* a% W! uwas age appropriate." d9 p* w9 k, o' S) e- V
The family history was remarkable for the father,
- [$ k* V/ z9 H# m9 [' J' I6 ywho was diagnosed with hypothyroidism at age 16,
5 N1 K/ `  D9 T9 y! O/ swhich was treated with thyroxine. The father’s3 o/ j2 W! v" R* E
height was 6 feet, and he went through a somewhat5 M& O; u0 E! ^( z
early puberty and had stopped growing by age 14.
+ H* V# [# f& ~/ DThe father denied taking any other medication. The% o$ L3 ]+ ^* l& a5 Z# z
child’s mother was in good health. Her menarche+ i' Q  c3 J# D, Q2 }9 b
was at 11 years of age, and her height was at 5 feet
" ~+ R5 [% g4 q* ^$ w# c( i6 [5 inches. There was no other family history of pre-2 m% b' U: A% k% \% ?! P: J" z
cocious sexual development in the first-degree rela-
! Z3 |1 P! {3 s( Ptives. There were no siblings.
% t4 Q0 R0 j. s* X% S1 QPhysical Examination; J: U, u3 q" H4 N( c; j' N
The physical examination revealed a very active,
+ E, P  D4 J; u. ^0 T. Nplayful, and healthy boy. The vital signs documented, d# U' x+ g) F7 e3 A) V8 t+ D
a blood pressure of 85/50 mm Hg, his length was" W$ u( u- N8 k6 M5 a3 F
90 cm (>97th percentile), and his weight was 14.4 kg
( R. h" {: o3 R4 T+ \5 v7 l(also >97th percentile). The observed yearly growth* V5 d' \7 T  ]
velocity was 30 cm (12 inches). The examination of# Q3 H& @9 V. u0 O1 `8 k+ [
the neck revealed no thyroid enlargement.
9 {4 \( A" Y+ IThe genitourinary examination was remarkable for
7 U! S3 Z5 v+ l9 K! ]; t; q2 venlargement of the penis, with a stretched length of2 I2 a% \1 c; x/ q. _
8 cm and a width of 2 cm. The glans penis was very well
6 e" g3 G; e, f! J4 H( wdeveloped. The pubic hair was Tanner II, mostly around
. t# K" _5 o2 _; Q3 P5 ^1 x540/ r3 o" E& x- F, O' r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 I1 i* N6 |7 Q5 h3 ?: @7 O3 Qthe base of the phallus and was dark and curled. The: o: \5 b6 [1 e2 l+ @4 i$ @% m# q/ m
testicular volume was prepubertal at 2 mL each.
5 W1 o8 p3 C8 a) {The skin was moist and smooth and somewhat- r% o% {- H" M/ I, H" Q  K2 N
oily. No axillary hair was noted. There were no; X* d5 s8 B+ ]. t- @+ A  l& j
abnormal skin pigmentations or café-au-lait spots.
6 n8 @2 j% t& K6 a0 oNeurologic evaluation showed deep tendon reflex 2+
7 H3 k6 I1 \7 n8 q( b9 Ibilateral and symmetrical. There was no suggestion# O# k# c0 Z- K1 P
of papilledema.! q6 D2 \9 ]- j* m
Laboratory Evaluation
. j/ _/ n# e) ]. C+ PThe bone age was consistent with 28 months by
. Q8 \- ]# e# K9 J1 V: m' tusing the standard of Greulich and Pyle at a chrono-2 P2 X' k% U! u4 G1 B7 a! u2 L
logic age of 16 months (advanced).5 Chromosomal
- c" w) B- A2 d' e) i% Ukaryotype was 46XY. The thyroid function test
3 J) N: t: k3 x' M. Nshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
/ Q7 ]/ k2 I( Vlating hormone level was 1.3 µIU/mL (both normal).
, l8 H$ h* Z4 x9 ]2 c: CThe concentrations of serum electrolytes, blood
1 Y- ?* R% @; v& y( E* ?1 [2 \urea nitrogen, creatinine, and calcium all were
! _( f, z- s& d' t9 uwithin normal range for his age. The concentration  S: }& j; m0 v8 U3 k; S
of serum 17-hydroxyprogesterone was 16 ng/dL
/ z: b+ F* N5 c. ]: p$ P& P% K(normal, 3 to 90 ng/dL), androstenedione was 20
& R0 w& h4 U2 c. Lng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& q+ G6 H' R) ^& U8 Y5 H! p
terone was 38 ng/dL (normal, 50 to 760 ng/dL),2 ^) N% C6 g* H$ W2 y2 d
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
. r" c) }% a0 E! A4 y49ng/dL), 11-desoxycortisol (specific compound S)
- Z) ?, g: ^2 T4 v) qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) v7 I3 p5 }' q3 b" y
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 q( r1 e6 g5 q& U6 [; Ltestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
. X/ ?6 f; x8 \7 c  c$ ]! N! Y4 J. c2 band β-human chorionic gonadotropin was less than/ [5 H/ [$ b2 h$ r3 ?* p/ o
5 mIU/mL (normal <5 mIU/mL). Serum follicular
/ a$ p8 ?" }: i$ U5 \/ S6 C5 _stimulating hormone and leuteinizing hormone/ I7 }% w  V- }: w+ T
concentrations were less than 0.05 mIU/mL
* C- K: \: C/ E0 @" H: |(prepubertal).
/ s* _. v9 F3 x1 E2 E% v6 o: J: IThe parents were notified about the laboratory% f9 P9 b# V4 x! X) l& ]* m# k6 g
results and were informed that all of the tests were( i0 W6 v5 ~" H$ B/ D
normal except the testosterone level was high. The
8 R2 M2 z, Y5 m/ n" _4 dfollow-up visit was arranged within a few weeks to% G9 J0 G, u6 W) R2 i# A' l- e
obtain testicular and abdominal sonograms; how-; ^. q7 m" q4 K# F0 _6 v3 [9 J
ever, the family did not return for 4 months.0 A2 f, t. y3 @% H
Physical examination at this time revealed that the( `, Q; ?* y& a* Y4 N( l$ G
child had grown 2.5 cm in 4 months and had gained( [' X) P# W0 s. \' q
2 kg of weight. Physical examination remained: F+ ~3 @! r8 j0 n+ x
unchanged. Surprisingly, the pubic hair almost com-7 y. _0 Z! E/ \8 o/ I$ _
pletely disappeared except for a few vellous hairs at
2 f! Q6 Y; f" u. d9 a: @the base of the phallus. Testicular volume was still 2
" M! B2 F0 J% G3 I- |/ ^mL, and the size of the penis remained unchanged.6 ]. Z0 ]  M5 H5 Q
The mother also said that the boy was no longer hav-
' d: _* l" u5 j6 [# H  ?6 }ing frequent erections.3 I. l3 H# L6 N& G# K4 X
Both parents were again questioned about use of, }; k* K- |8 N& r
any ointment/creams that they may have applied to
% |2 l. @4 k+ |0 u8 C9 Mthe child’s skin. This time the father admitted the) N, |% _! S, q, q0 m: l% U
Topical Testosterone Exposure / Bhowmick et al 541
) s, H9 {: l4 c+ R' N, ^, xuse of testosterone gel twice daily that he was apply-
" j5 m+ }: m4 H" z5 U, Wing over his own shoulders, chest, and back area for
. m9 Z" J% I1 h; v3 o! f, m& la year. The father also revealed he was embarrassed+ a6 [( s0 |& V# g% z: ?7 G' P) O
to disclose that he was using a testosterone gel pre-
" c- ?' E. [. K0 {& H2 Z, }scribed by his family physician for decreased libido
1 q$ l! F% A7 [8 {  w- _! H2 n& vsecondary to depression.& V. d7 z: R" ^* J! G& u
The child slept in the same bed with parents.2 E/ s" e/ X0 Y# W: l
The father would hug the baby and hold him on his
) l% E: X: ^- r) C5 I& h8 Nchest for a considerable period of time, causing sig-) {4 X1 }- }, P
nificant bare skin contact between baby and father., b6 w8 a6 K# A1 j) G
The father also admitted that after the phone call,- i, X/ P7 `) C8 N8 F6 t
when he learned the testosterone level in the baby
1 |% c9 L: Q7 P4 jwas high, he then read the product information
; L2 ?& R- A# t& p9 Ypacket and concluded that it was most likely the rea-
6 b& ^8 b+ l) @& C! q. gson for the child’s virilization. At that time, they
  }( X8 L2 o' J- J+ idecided to put the baby in a separate bed, and the2 ^& W. k' e, \
father was not hugging him with bare skin and had
- a4 l' ~# Z3 P  i; s4 Q; obeen using protective clothing. A repeat testosterone
1 o4 s6 L$ S$ }5 H+ Y" A1 itest was ordered, but the family did not go to the
0 t. l0 ?1 F1 q& u- Llaboratory to obtain the test.
2 _1 x% a# a0 B; w! T, t1 KDiscussion
% P3 R6 `( s% e. B$ Z+ {4 yPrecocious puberty in boys is defined as secondary& }- V% b5 \' g- A% M0 k
sexual development before 9 years of age.1,4
- s4 h, F" S% X$ R/ VPrecocious puberty is termed as central (true) when
6 E+ {2 r! F/ l1 c" h% y4 J, r7 b; I; \$ lit is caused by the premature activation of hypo-# Y; A- |8 I% i* S6 s% x7 n' Y7 E
thalamic pituitary gonadal axis. CPP is more com-
$ D# ~3 _6 Z7 |. V0 Bmon in girls than in boys.1,3 Most boys with CPP
# T7 o* W( _9 v( n  J4 M3 Qmay have a central nervous system lesion that is
% P0 |4 X" o# t! N. V. Lresponsible for the early activation of the hypothal-
2 ^/ p) v1 B& pamic pituitary gonadal axis.1-3 Thus, greater empha-
, N% c, }( _7 T. Xsis has been given to neuroradiologic imaging in
* G$ m$ W4 S, W+ t( [' a$ n. }* hboys with precocious puberty. In addition to viril-2 w$ T$ ]. \; Z4 t1 Q8 ]4 B
ization, the clinical hallmark of CPP is the symmet-
+ ^& N; d* T# u6 o+ t3 w9 X" U  j9 O- Drical testicular growth secondary to stimulation by& |$ o* }, R* w, g. t
gonadotropins.1,3) ]7 A  d3 b# j( a
Gonadotropin-independent peripheral preco-
: F) ^; v" w" Z. xcious puberty in boys also results from inappropriate
3 o4 D9 W5 u+ M( M- L! Qandrogenic stimulation from either endogenous or  y, ^; b# U  @
exogenous sources, nonpituitary gonadotropin stim-9 {: z3 b" f) W9 }9 u- y
ulation, and rare activating mutations.3 Virilizing
6 b- q7 F6 M! x3 F. |congenital adrenal hyperplasia producing excessive! k: e# Q4 y! ^3 `2 i: G
adrenal androgens is a common cause of precocious
5 W' i7 K2 M8 @3 Tpuberty in boys.3,4
1 M: B  n0 v; N7 Q7 aThe most common form of congenital adrenal  F$ E- r5 R& Q2 t# e& q
hyperplasia is the 21-hydroxylase enzyme deficiency.0 a+ K/ |7 G9 z
The 11-β hydroxylase deficiency may also result in( R$ u7 @( ?3 A& H
excessive adrenal androgen production, and rarely,
9 p, p" Z! B( v  \! _( qan adrenal tumor may also cause adrenal androgen- X$ A1 w2 L0 E- ?) i3 R
excess.1,30 }7 ^3 x. H3 Z/ z; f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 A0 ?' e. F# T% v542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 M  S0 u6 ]3 R8 c; p
A unique entity of male-limited gonadotropin-
& g6 H9 j4 \7 o' Lindependent precocious puberty, which is also known
- A# k. @% S; ^. X0 Zas testotoxicosis, may cause precocious puberty at a6 d; R/ S7 `/ u* @
very young age. The physical findings in these boys
- s) G. v' i8 Y: r5 b2 z. d) U9 n2 l) U- lwith this disorder are full pubertal development,
7 ~$ ?- s7 e2 K% H4 s7 Dincluding bilateral testicular growth, similar to boys
5 H$ V. {, b* K* r4 }# i* A" hwith CPP. The gonadotropin levels in this disorder
1 ^3 i, H! y% Q+ k, t' \' d9 [+ Oare suppressed to prepubertal levels and do not show
" [5 ?4 M3 z* z2 a3 Qpubertal response of gonadotropin after gonadotropin-
2 R! Y) l3 q% U4 O0 A: U- S2 kreleasing hormone stimulation. This is a sex-linked
3 c1 u& t; B( N9 f: u" i) zautosomal dominant disorder that affects only
- J4 j+ Y! K# P- A6 V' Mmales; therefore, other male members of the family+ g, p! P& T! Q& ?2 [" \
may have similar precocious puberty.3$ V; v3 R& \4 g) v3 T5 r& I; V# }3 Z
In our patient, physical examination was incon-
3 }( ?2 S4 Q) q' x$ rsistent with true precocious puberty since his testi-$ @$ L/ ^4 g$ v8 ?2 c' ~
cles were prepubertal in size. However, testotoxicosis
1 U# Y6 g2 n: p( hwas in the differential diagnosis because his father5 F$ e6 E! v1 w# {5 r
started puberty somewhat early, and occasionally,
0 F4 @6 s$ `) f* ?' |1 dtesticular enlargement is not that evident in the
7 T1 h8 E0 A- O9 tbeginning of this process.1 In the absence of a neg-% W# r( T) R6 e9 f9 |, Q
ative initial history of androgen exposure, our4 b6 m$ m) e+ P& I
biggest concern was virilizing adrenal hyperplasia,
+ J" I& I# H$ J' ~! ]either 21-hydroxylase deficiency or 11-β hydroxylase
: o# P1 S( D& Bdeficiency. Those diagnoses were excluded by find-5 U0 y3 ^  R9 B! e$ G  d( X  Q
ing the normal level of adrenal steroids.) f: X1 E% m# M8 L( U8 b4 e
The diagnosis of exogenous androgens was strongly
) \7 o! D, ?: p4 p1 m8 Fsuspected in a follow-up visit after 4 months because4 \# X2 ~$ ^6 K% `& g
the physical examination revealed the complete disap-9 Q/ B- i( h& E4 v9 L' D( {2 |7 W, `
pearance of pubic hair, normal growth velocity, and2 J* J9 P7 m. x) d# R
decreased erections. The father admitted using a testos-
# L. O( a; h  e9 R4 _& Gterone gel, which he concealed at first visit. He was
# s6 i) Z$ c4 e$ Kusing it rather frequently, twice a day. The Physicians’
9 A* {& Z6 f3 X# W4 d9 aDesk Reference, or package insert of this product, gel or0 |3 i3 j; u0 W3 s6 M5 M6 w
cream, cautions about dermal testosterone transfer to% [) r1 L2 Q' ?, I3 c$ H; y% e
unprotected females through direct skin exposure.
& B" S, x$ T' x/ Z5 i- N1 p& r& xSerum testosterone level was found to be 2 times the
$ c0 v# X' m) c8 N% O) Mbaseline value in those females who were exposed to% P, n- g/ E6 A# _% N- N- d  E
even 15 minutes of direct skin contact with their male3 Q3 Q1 g& O, Y1 y$ b! K$ a
partners.6 However, when a shirt covered the applica-6 L  @& a7 `. ?0 I8 p
tion site, this testosterone transfer was prevented.3 S( h) D5 B& z8 r! S
Our patient’s testosterone level was 60 ng/mL,! e: w6 [  Y7 Y: @" ~
which was clearly high. Some studies suggest that
5 A. `( r: d& n$ D7 Fdermal conversion of testosterone to dihydrotestos-
6 T0 P% H' m9 d; \+ \terone, which is a more potent metabolite, is more( A4 K+ y; u: c) c9 O
active in young children exposed to testosterone
( \' f. @6 M; Z$ \  e6 Z5 a7 bexogenously7; however, we did not measure a dihy-
& L, w+ T1 H& ?9 ]% p8 j0 Udrotestosterone level in our patient. In addition to
' E, H- K! O. n$ c9 d  Kvirilization, exposure to exogenous testosterone in' K5 \: A% G2 O' s- v! k$ H$ ~
children results in an increase in growth velocity and* r# [5 K6 n4 P. s
advanced bone age, as seen in our patient.
# p" c# i, }! D0 cThe long-term effect of androgen exposure during- h( W8 y# G& f" e$ w  R
early childhood on pubertal development and final+ U/ n. @- B- e: o
adult height are not fully known and always remain
' U: Q- `: h: d6 b/ Pa concern. Children treated with short-term testos-6 _4 d- ]6 _) Q: n
terone injection or topical androgen may exhibit some9 E  J- e6 H5 K2 T1 m& _7 A
acceleration of the skeletal maturation; however, after
! T  Y+ @; f( A+ S$ Fcessation of treatment, the rate of bone maturation0 e; U5 ]0 K& i" j" w
decelerates and gradually returns to normal.8,9
6 j6 R1 r! @: b# AThere are conflicting reports and controversy! G+ S6 a$ Y' `2 t# Y
over the effect of early androgen exposure on adult
8 X' {* ]# Y! C5 U/ Kpenile length.10,11 Some reports suggest subnormal/ b3 G/ F' T" q- |
adult penile length, apparently because of downreg-2 v# f5 e* M8 B: L6 i+ H
ulation of androgen receptor number.10,12 However,
1 _) M: P( t6 u: k1 bSutherland et al13 did not find a correlation between9 C6 A" S+ `3 C6 G
childhood testosterone exposure and reduced adult# `% Q& S9 a4 q% |' ^" T( Y
penile length in clinical studies.
# G; \: }4 @7 |1 o' j5 H3 zNonetheless, we do not believe our patient is" i* |& }' u( O/ D; m* a" Q1 l
going to experience any of the untoward effects from7 v: X, e  J1 q# S$ V4 b/ j! e
testosterone exposure as mentioned earlier because
( }: x+ G4 }+ N/ g, U1 Xthe exposure was not for a prolonged period of time.
: y9 I% I" m6 W% T8 YAlthough the bone age was advanced at the time of
' ]. g, Y/ T5 `) ?1 w- ^diagnosis, the child had a normal growth velocity at
9 u6 c- g6 Z5 hthe follow-up visit. It is hoped that his final adult  m" m2 S4 b; C6 B3 p# Q
height will not be affected.
1 O! I( C! S8 |% @9 I: BAlthough rarely reported, the widespread avail-4 Q% U/ z7 B: m. ~
ability of androgen products in our society may1 E/ a! ?& D; e8 d8 p
indeed cause more virilization in male or female- ^4 |) M5 s- c! z) u
children than one would realize. Exposure to andro-
' j0 x" i! \2 p( n' S6 m5 dgen products must be considered and specific ques-
& C) t& S% O& W7 u, `tioning about the use of a testosterone product or
* q7 H1 {! Y! c' c/ t) hgel should be asked of the family members during/ I5 k2 h  F4 \# P. y, I' Q$ Y$ ^
the evaluation of any children who present with vir-
  e  u; E1 T0 u, c% U! dilization or peripheral precocious puberty. The diag-
, V2 o* w9 z! rnosis can be established by just a few tests and by/ d" n" f7 L$ H, s1 T
appropriate history. The inability to obtain such a
' E' ?8 U! A) G/ H/ b. ]6 t) S4 Z8 bhistory, or failure to ask the specific questions, may
, @$ U0 Q* c$ ^1 G$ Q1 V* lresult in extensive, unnecessary, and expensive7 L" g1 M- Q% x: X  J# x
investigation. The primary care physician should be
+ Y$ x3 P  E0 V" P/ vaware of this fact, because most of these children" ~  x0 F! _: G" G9 }' Z3 Z6 j
may initially present in their practice. The Physicians’
; M# {9 K! ^1 u- V1 V( L: pDesk Reference and package insert should also put a7 F) I9 x8 c# K- |. z
warning about the virilizing effect on a male or
# i) n; n2 a" P' w. Z5 b4 bfemale child who might come in contact with some-
: Q! t% ]# A4 h0 d4 qone using any of these products.
. H: W: K  K' g/ ~* jReferences
7 z  t6 J: d; R3 x' Y1. Styne DM. The testes: disorder of sexual differentiation* K( z( R+ K8 U- S6 X& g; y
and puberty in the male. In: Sperling MA, ed. Pediatric2 Z; v' f( L2 j
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ ~' W  _0 Y4 ^2002: 565-628.) u3 o; [+ q: O% R& y+ r* q# z
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ o  R4 w4 P" V  t; Ipuberty 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

# X# c$ Y4 o  A+ M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