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Sexual Precocity in a 16-Month-Old
7 }4 S6 x/ A$ yBoy Induced by Indirect Topical
9 a) I* O1 t9 d# u+ K( ZExposure to Testosterone
+ e% e8 L1 j1 B! \& _  \Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" e/ \' N& k4 T7 u" z2 jand Kenneth R. Rettig, MD1" d* O9 O1 v. @7 \) l  y: r4 H8 }
Clinical Pediatrics9 q8 d# N' Z3 O' \/ n" u/ w# M
Volume 46 Number 64 H1 Y/ l. D- |
July 2007 540-543
" n1 K6 U! j+ a' _8 x: \: J! G0 b© 2007 Sage Publications
8 ^; b/ L4 A) }$ V5 s/ Y10.1177/0009922806296651, D6 Z+ J! j0 u8 @
http://clp.sagepub.com
, I) L& d$ o2 F) [! `' Ghosted at
, Q- a* ?( Z- S9 r4 ihttp://online.sagepub.com
0 P2 \8 Y! N% Q7 X, y1 R6 ]Precocious puberty in boys, central or peripheral,0 X. W0 y( i/ e! K2 |
is a significant concern for physicians. Central
: }/ T3 d' K5 rprecocious puberty (CPP), which is mediated
) h7 }+ V2 ^% ]1 b. b8 O3 ^through the hypothalamic pituitary gonadal axis, has
! d/ k  Y( M6 S0 ^' ga higher incidence of organic central nervous system
  V& e6 m# C! E  R1 klesions in boys.1,2 Virilization in boys, as manifested7 G+ T/ ]0 R5 f: n4 J
by enlargement of the penis, development of pubic4 i- H- F% g& E
hair, and facial acne without enlargement of testi-
, ]/ w* p3 P+ }& j% jcles, suggests peripheral or pseudopuberty.1-3 We! m/ O/ n4 b/ i# N3 d9 b# C! r
report a 16-month-old boy who presented with the
$ G1 k3 X- v) \$ j5 Q& R+ b+ e" Y, u$ Wenlargement of the phallus and pubic hair develop-
0 w2 x# u* F# F& zment without testicular enlargement, which was due
6 z  b9 z& O  C( Zto the unintentional exposure to androgen gel used by8 p7 @  v' I( N0 d
the father. The family initially concealed this infor-
2 }+ M9 k0 G) q: g2 D# a2 imation, resulting in an extensive work-up for this
* j* I& d- Q6 `  gchild. Given the widespread and easy availability of
% c( X6 _- t( d" gtestosterone gel and cream, we believe this is proba-  ^' f$ R. Z0 C2 Z3 h" {. w
bly more common than the rare case report in the
1 w, r& u- L4 O4 y" g9 gliterature.4% P0 C$ K! a' y, ?" N
Patient Report& S0 r$ g% W% O# m) \  _$ w+ d$ N
A 16-month-old white child was referred to the
1 y, o$ }5 k9 _; U' Zendocrine clinic by his pediatrician with the concern3 V6 X1 Y, k$ ^  I; P) s4 e9 H. A
of early sexual development. His mother noticed
+ t( O2 r2 n* ~2 t, x3 u* U, rlight colored pubic hair development when he was* a& Z6 I$ _: b! o- A/ P& r
From the 1Division of Pediatric Endocrinology, 2University of# |( p2 F3 b. ~' p; W' ^: Q% q
South Alabama Medical Center, Mobile, Alabama.
7 d1 `/ ^; T+ g3 J  oAddress correspondence to: Samar K. Bhowmick, MD, FACE,
! u$ i" c1 Z3 X: \Professor of Pediatrics, University of South Alabama, College of8 o1 G, ^/ v7 _) ^. @
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ D( b/ x* B3 X7 z" Ne-mail: [email protected].
5 U3 r8 ~* g+ [' _- v7 d& S% Habout 6 to 7 months old, which progressively became& o/ G5 q8 ^- Z: b
darker. She was also concerned about the enlarge-, s: u+ }7 ^' c% c9 ]# W- x
ment of his penis and frequent erections. The child5 i$ p1 y7 D5 C# ^
was the product of a full-term normal delivery, with+ W" ~& |" j) f6 r( `0 U
a birth weight of 7 lb 14 oz, and birth length of
- r' o% o0 [5 _1 z" e+ G( P20 inches. He was breast-fed throughout the first year
$ X5 U3 y' ?2 U& B; `! g' z5 @of life and was still receiving breast milk along with3 D1 @* F9 y5 i% i& ~4 S
solid food. He had no hospitalizations or surgery,
6 o% n( b2 I, B) t5 T8 @5 cand his psychosocial and psychomotor development
% {" u0 N) o2 o1 w! _, Twas age appropriate.
4 u% y2 U1 e8 [1 [4 KThe family history was remarkable for the father," r" Z* y3 i% Y' ?, F4 y$ k3 G
who was diagnosed with hypothyroidism at age 16,  G# z; R1 k  d5 T
which was treated with thyroxine. The father’s
2 p) h$ \+ g* C6 o2 P. mheight was 6 feet, and he went through a somewhat
# ~+ o+ C) N0 g& learly puberty and had stopped growing by age 14.8 g( ^) r: r0 V( S2 m
The father denied taking any other medication. The
3 z+ P0 T; F0 m/ z. ]# q: a& Schild’s mother was in good health. Her menarche
& a5 v& Q/ l( X; b0 Z- A9 Twas at 11 years of age, and her height was at 5 feet- |% d- j" s: S2 x, o
5 inches. There was no other family history of pre-
& W2 r8 e: g. j! p; T5 y5 z: ococious sexual development in the first-degree rela-
6 h: p" C* f9 ~! J6 o1 L  jtives. There were no siblings.0 R' P0 H$ n* d! X) u' j7 z! L
Physical Examination; r9 r! E5 L7 `% \6 }
The physical examination revealed a very active,
+ M( G0 e6 c# M4 S& e; }playful, and healthy boy. The vital signs documented3 R- X' M0 s, ?& o- R3 ?
a blood pressure of 85/50 mm Hg, his length was& n# z) Q: I7 I; d1 l1 \
90 cm (>97th percentile), and his weight was 14.4 kg
6 M  d) u! C3 I1 c! ?! u/ m; v* `' `(also >97th percentile). The observed yearly growth4 A. \6 @4 l6 Y' T4 q
velocity was 30 cm (12 inches). The examination of* u) a: ?' W$ D  n5 v& t
the neck revealed no thyroid enlargement.
- e4 s  y7 Z' c4 Y- h( m. O  `6 kThe genitourinary examination was remarkable for
# ]* r& D7 J4 N' H# I: aenlargement of the penis, with a stretched length of
+ T- m' z# `$ r, ?# a- Y8 cm and a width of 2 cm. The glans penis was very well
0 K' r( o/ `9 H6 B5 A$ {developed. The pubic hair was Tanner II, mostly around* ~6 @( W( {/ O+ b9 i4 ~
5405 q1 N$ @. ?$ p! ~! E4 M5 m0 C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ \% s. j0 I8 X' v, vthe base of the phallus and was dark and curled. The" A  ?, d' w* s' J" ~9 ^
testicular volume was prepubertal at 2 mL each.
' Q6 w) a( ^! |. c" W6 h& w% ?  eThe skin was moist and smooth and somewhat6 U3 T' u: a0 g/ D, B$ q4 f5 q# U
oily. No axillary hair was noted. There were no
5 Y7 [  h3 K* t# i1 X8 N0 Kabnormal skin pigmentations or café-au-lait spots." E, U  W9 z3 V8 |% W% ]
Neurologic evaluation showed deep tendon reflex 2+
. y" T% H* {) C$ e* j: J, Ybilateral and symmetrical. There was no suggestion
0 M  B  d, @' y8 P0 V/ l* J1 Wof papilledema.5 {# h/ W& P$ }0 |* R6 S! C
Laboratory Evaluation$ ~' U1 e( ~4 H, I6 I8 c* W* F$ A
The bone age was consistent with 28 months by
3 I% n! V6 h$ X/ y( d7 p$ b* V  xusing the standard of Greulich and Pyle at a chrono-. I, j; W) F6 e3 k6 J5 _
logic age of 16 months (advanced).5 Chromosomal- `* G4 ]4 ]5 Y3 A  `, u
karyotype was 46XY. The thyroid function test+ z6 r5 r1 V" A; H3 j4 t
showed a free T4 of 1.69 ng/dL, and thyroid stimu-. X1 {. X* Y& b8 V: b& M6 \: z( O
lating hormone level was 1.3 µIU/mL (both normal)." x- g0 _! i  k2 p; V
The concentrations of serum electrolytes, blood' t  X" x: u; A- U, T' w% X  w$ I
urea nitrogen, creatinine, and calcium all were
+ G- K+ Y- F4 h" k: dwithin normal range for his age. The concentration
/ f, W$ o& ?: R# P7 G5 a  \of serum 17-hydroxyprogesterone was 16 ng/dL
8 t' z3 P% e) i5 y: O(normal, 3 to 90 ng/dL), androstenedione was 20* x7 l# ^& \4 @- v$ W
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& J/ Q0 j# t1 @terone was 38 ng/dL (normal, 50 to 760 ng/dL),0 z3 Y# n8 Z/ L. u) R4 A! V: X8 o
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 p" z' R6 o2 m+ j: j# I3 P49ng/dL), 11-desoxycortisol (specific compound S)
9 v7 T, A9 H! t; b) ywas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( F0 E! e! @! |
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 a, A8 Z; f3 U0 w( ^% O
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),! v; `' u2 m; J* b3 F+ t
and β-human chorionic gonadotropin was less than$ [; g  y  g) o; t
5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ Y) i$ }1 e, Z3 q0 N% i2 t: Tstimulating hormone and leuteinizing hormone
. z  Q  u. P$ W. Lconcentrations were less than 0.05 mIU/mL
! M4 `. H/ R7 y: a5 w' J(prepubertal).
, r2 x0 q) ~3 f4 o5 B2 ~The parents were notified about the laboratory
, }# |- y7 J- ^4 i& _results and were informed that all of the tests were  ~/ d: d; _0 o1 h
normal except the testosterone level was high. The
. p# z0 c! X5 }& j5 Efollow-up visit was arranged within a few weeks to' m% H; i/ n& K
obtain testicular and abdominal sonograms; how-
! s+ c% q! |& |ever, the family did not return for 4 months.
5 g1 F& Q- m- n  OPhysical examination at this time revealed that the
6 u$ E9 ~4 w% D% Mchild had grown 2.5 cm in 4 months and had gained
, I, j( H0 P* u/ G; _2 kg of weight. Physical examination remained
' H; R6 q4 e4 Eunchanged. Surprisingly, the pubic hair almost com-7 u0 J" F) \0 A  Y* n
pletely disappeared except for a few vellous hairs at
$ q9 K% ?  {$ t! q* ]the base of the phallus. Testicular volume was still 2
& u9 u' T6 f# l$ tmL, and the size of the penis remained unchanged.
. }; P( T' n: S( Q% wThe mother also said that the boy was no longer hav-
- P' V3 E; p1 ^ing frequent erections., Z2 z0 [+ e( s$ a: E# x
Both parents were again questioned about use of$ x' O. c& q5 ?0 X: e. C
any ointment/creams that they may have applied to5 z: }7 O- c. a
the child’s skin. This time the father admitted the
% K6 {5 [% W7 k- \' [( ^Topical Testosterone Exposure / Bhowmick et al 541
6 g7 p1 B2 a. O$ Kuse of testosterone gel twice daily that he was apply-
  O2 F. }3 W7 a7 q* F9 Z2 a) ning over his own shoulders, chest, and back area for
. L+ o! B( f0 ?! G  q- F+ N/ h8 D# Xa year. The father also revealed he was embarrassed
% P) n' j' ~, \* B5 M; J$ Eto disclose that he was using a testosterone gel pre-9 p! v( L( P3 l* J) J; |8 i
scribed by his family physician for decreased libido
' g' {9 S3 C+ `6 k; D: Qsecondary to depression.2 U6 o5 V" z4 s. G% }$ `% F( E
The child slept in the same bed with parents.  M- J+ d$ e- s( n3 O) Q: y% t- c
The father would hug the baby and hold him on his
* r9 P' W8 H0 |; I. K3 M0 dchest for a considerable period of time, causing sig-
7 @$ N; z+ {, N# H7 Nnificant bare skin contact between baby and father." r, b* U/ s" j- A9 j3 s+ L+ D
The father also admitted that after the phone call,
( [2 w: @2 s! M6 S5 Zwhen he learned the testosterone level in the baby
" U6 D) C* L) O  d. swas high, he then read the product information. ~# Z$ Z, G3 Z$ q8 K
packet and concluded that it was most likely the rea-$ @# Z+ b: w5 I( G9 h0 ^3 h6 E
son for the child’s virilization. At that time, they
; a1 I4 q7 d! B$ Edecided to put the baby in a separate bed, and the
3 R! K: N3 i/ \" U6 Y8 v( bfather was not hugging him with bare skin and had
# H% l5 T# \% `+ K2 Rbeen using protective clothing. A repeat testosterone
. W! {" D  k. s5 Atest was ordered, but the family did not go to the
; `' ?" E- t% k6 `laboratory to obtain the test.$ y' q2 A/ K* @+ R
Discussion
+ ?( ?( [' G1 I( m, b% n. _' K* l* dPrecocious puberty in boys is defined as secondary
1 u# a5 o) q3 g) `sexual development before 9 years of age.1,4
% w4 n9 d- V0 l/ p, E7 s% tPrecocious puberty is termed as central (true) when' W5 W$ |% t3 s" C/ }; e
it is caused by the premature activation of hypo-
: F3 d5 K$ B. }1 W3 qthalamic pituitary gonadal axis. CPP is more com-+ a( j; x; \; t$ N# T9 v" Q, v% v
mon in girls than in boys.1,3 Most boys with CPP" o4 M8 i+ O' m5 q
may have a central nervous system lesion that is
5 \$ I: @; L. A9 O' [! e% kresponsible for the early activation of the hypothal-
! C/ v  ^; e4 \2 \# gamic pituitary gonadal axis.1-3 Thus, greater empha-
; f5 Z, [& L! a8 ysis has been given to neuroradiologic imaging in
) V( ?' U% d8 {+ U  O. Y; N1 Yboys with precocious puberty. In addition to viril-0 V9 u, j! i7 w; D  k$ G; V1 s
ization, the clinical hallmark of CPP is the symmet-% n  m$ C! I+ U8 d1 T- \9 ^9 a7 a2 ^
rical testicular growth secondary to stimulation by
. J2 H6 B7 X; D& Q0 {gonadotropins.1,3
7 [& S9 @8 f, ?Gonadotropin-independent peripheral preco-$ h: x) _1 U- G' H& C: r
cious puberty in boys also results from inappropriate! F! \9 @7 ?  U- G1 A9 m
androgenic stimulation from either endogenous or
0 q( J7 \3 S% W& h- \exogenous sources, nonpituitary gonadotropin stim-
% K; o$ y4 T, a' @* I9 m) X6 ?# Dulation, and rare activating mutations.3 Virilizing: l# s+ j5 q& o, D
congenital adrenal hyperplasia producing excessive* l  W" ~9 d( W# a; G
adrenal androgens is a common cause of precocious) l5 g6 P& N+ z( S3 m  c7 e
puberty in boys.3,4" l! a4 G* ?3 ]
The most common form of congenital adrenal+ o6 S8 `1 j5 R
hyperplasia is the 21-hydroxylase enzyme deficiency.1 x# i' j$ {6 l0 o: ^
The 11-β hydroxylase deficiency may also result in
2 P5 o) t0 k% M1 `  H9 Cexcessive adrenal androgen production, and rarely,
3 v. `- J% J6 D7 a2 b) Ian adrenal tumor may also cause adrenal androgen
6 s" \, G% M) Y; B2 C2 e* a% ^excess.1,34 e" T% c! E( v: W+ T" r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% {4 W7 j+ E% j, N1 w4 g1 e542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. \0 z5 N# p3 N. E* CA unique entity of male-limited gonadotropin-( z3 ]& b) e% {9 ~9 t# a& l: S7 t
independent precocious puberty, which is also known# h5 t; ^% r& _
as testotoxicosis, may cause precocious puberty at a
" z' c4 m2 F  P3 A4 T% p# Uvery young age. The physical findings in these boys
% X  J; v  \/ W) r! T- ^with this disorder are full pubertal development,
7 y/ x$ E. q) K$ H! Y0 R5 m+ h+ yincluding bilateral testicular growth, similar to boys
( o4 I2 O1 I  l; u9 Xwith CPP. The gonadotropin levels in this disorder" {. a0 [$ ], ?  Q5 P
are suppressed to prepubertal levels and do not show
: @. U+ }" q! |0 ~: l8 `6 f4 hpubertal response of gonadotropin after gonadotropin-7 A; W  h  @6 }0 h3 A4 }# v6 b; t; W
releasing hormone stimulation. This is a sex-linked, b: b. O4 G& P2 z
autosomal dominant disorder that affects only
# K6 c) z' b1 _( y3 ?9 d' ^males; therefore, other male members of the family$ o# e; k9 i7 |! {- [
may have similar precocious puberty.32 q5 Q/ N' P8 d9 S- M
In our patient, physical examination was incon-
, J$ a' \% l: {  w, I" ]. Msistent with true precocious puberty since his testi-1 d+ }2 l; I' Q* d
cles were prepubertal in size. However, testotoxicosis
3 a) G0 l3 ^. o0 nwas in the differential diagnosis because his father1 c" G$ U. `( c# W* a) t( P# _
started puberty somewhat early, and occasionally,
* e1 c8 T7 }  e" B! Qtesticular enlargement is not that evident in the
; {* C7 `; N" l  y5 A& [beginning of this process.1 In the absence of a neg-
3 D! h) A, w7 c6 @- F% @5 Fative initial history of androgen exposure, our
! G; ^: V" N! d6 L# {3 ^biggest concern was virilizing adrenal hyperplasia,
% H6 B; t' b* e7 L4 M0 M8 Keither 21-hydroxylase deficiency or 11-β hydroxylase& z- g( j, [6 @+ ~' ]
deficiency. Those diagnoses were excluded by find-6 u9 {2 x1 T3 ?4 p
ing the normal level of adrenal steroids.
/ x8 q) A2 J" l* C9 w5 g! sThe diagnosis of exogenous androgens was strongly' u1 v( Z) E3 c) J+ g2 L
suspected in a follow-up visit after 4 months because
9 j$ D9 s, Z  j. D, A4 ?' Ethe physical examination revealed the complete disap-
6 r7 `& i- i- r1 K+ y: }% s" `) e' x, ?pearance of pubic hair, normal growth velocity, and( I8 N9 ^+ D( ]- Q/ i3 n
decreased erections. The father admitted using a testos-
8 [& M/ @% r3 V: kterone gel, which he concealed at first visit. He was
$ j7 I5 h: f; Tusing it rather frequently, twice a day. The Physicians’2 Q/ V0 v+ x% J5 Z) [; g8 m! n" h
Desk Reference, or package insert of this product, gel or
  d/ }3 H2 z9 l4 U; m: O6 U; Ccream, cautions about dermal testosterone transfer to! X; k/ ^- H2 x! B9 d* u2 V5 f
unprotected females through direct skin exposure.. K! J( h+ y$ I
Serum testosterone level was found to be 2 times the+ M! ]; \0 U2 p# a$ S6 X- N
baseline value in those females who were exposed to
/ [1 \2 ?! K# }1 }1 [- weven 15 minutes of direct skin contact with their male1 L) M2 K! k% \) l* g- L7 u" e* q
partners.6 However, when a shirt covered the applica-
6 k1 D( [/ h' O; M. `' X. x) \tion site, this testosterone transfer was prevented.
3 h% B- Y1 I% s8 g  p2 f% ]Our patient’s testosterone level was 60 ng/mL," P# t2 w( w$ |4 W$ i* T. a
which was clearly high. Some studies suggest that. w) u1 _4 ^. {( P* v2 ?0 V* K0 x0 f
dermal conversion of testosterone to dihydrotestos-
2 k8 {4 w" o4 j/ A4 F3 Gterone, which is a more potent metabolite, is more6 a" c( x* `! V! _# [9 o! b8 X
active in young children exposed to testosterone1 y" `: u& V5 F- a1 j
exogenously7; however, we did not measure a dihy-9 M2 R, S0 ^& {9 d* {. V5 G
drotestosterone level in our patient. In addition to
! i( L9 a% {$ g* [" E! ^virilization, exposure to exogenous testosterone in
0 z. T8 z9 w0 Cchildren results in an increase in growth velocity and
5 j& R  O+ r" @: e6 ]( G/ m3 V1 madvanced bone age, as seen in our patient.  U8 Q! ?. X6 D4 P" L& ~& @2 R
The long-term effect of androgen exposure during5 _9 A9 M/ Q6 t# \6 F" i) _4 s5 @
early childhood on pubertal development and final
. F- ~* A! O6 ^7 H' k1 Hadult height are not fully known and always remain
) `! J) z7 N% E; {  j/ F) G% ea concern. Children treated with short-term testos-
9 y, O4 E/ E3 ~  O- iterone injection or topical androgen may exhibit some, C: a: b# D$ @4 L' @& ?! ]
acceleration of the skeletal maturation; however, after
0 u) n7 J; J8 [' U' vcessation of treatment, the rate of bone maturation! m& M1 w0 Q1 F3 }
decelerates and gradually returns to normal.8,93 p# B$ S% y% s. I# R5 p+ {2 D% H
There are conflicting reports and controversy( h0 h/ }( h8 V3 V7 Y
over the effect of early androgen exposure on adult! f$ V* W& m" d1 X& x: M; c# Y2 e
penile length.10,11 Some reports suggest subnormal
0 I' {& V  o) badult penile length, apparently because of downreg-
. [3 _% o2 L( Y* J. Hulation of androgen receptor number.10,12 However,
; K& z7 s3 f0 J+ K, |Sutherland et al13 did not find a correlation between% Z5 r3 l3 \' ~* T# T
childhood testosterone exposure and reduced adult& k* B9 Y# v" x7 Z
penile length in clinical studies.2 ~+ _( U, Z4 ?( y1 k
Nonetheless, we do not believe our patient is  D" K+ b- f# m
going to experience any of the untoward effects from# ]" Z# `" I3 `- b/ j& z% J
testosterone exposure as mentioned earlier because
& f1 C  V% K/ W; Qthe exposure was not for a prolonged period of time.
  A0 x9 o8 p3 \9 W4 T( _Although the bone age was advanced at the time of
2 W9 G9 G* t. e: _: z$ z5 xdiagnosis, the child had a normal growth velocity at
( W" d2 b& t5 M. ~5 T2 f0 \the follow-up visit. It is hoped that his final adult
  i; Z7 r7 L1 q' `1 B( Dheight will not be affected.
7 {+ X1 F+ T4 N- p5 I1 `/ U, o) r: r8 Z2 UAlthough rarely reported, the widespread avail-5 Q9 u( _- C4 [1 O* Q4 A
ability of androgen products in our society may
& l' M$ a, o% Q: F" o, ^7 q, jindeed cause more virilization in male or female
' \5 _7 R( n' a2 f: tchildren than one would realize. Exposure to andro-
& t0 Z: h+ U2 [" P1 ]5 I/ @gen products must be considered and specific ques-
. Q$ ?- N/ Z+ Z2 {tioning about the use of a testosterone product or, ?7 L. [: T( M2 ]7 i
gel should be asked of the family members during) P# y4 ]4 x/ j: d
the evaluation of any children who present with vir-  E% M" v! |$ J
ilization or peripheral precocious puberty. The diag-$ i2 _' N$ G6 G% u, e( i& j" w
nosis can be established by just a few tests and by% b+ t8 N1 o5 b7 S: V5 f% c' n/ B. Z% f
appropriate history. The inability to obtain such a
8 [/ M, O2 j8 I9 ahistory, or failure to ask the specific questions, may
  N8 }5 t: g! Uresult in extensive, unnecessary, and expensive
: d- v$ R# M% e1 x$ l# sinvestigation. The primary care physician should be; G7 Z2 g  V0 G2 S0 k
aware of this fact, because most of these children7 L$ F4 d& X2 k
may initially present in their practice. The Physicians’
% ~2 n$ Z& C" f, e! [% rDesk Reference and package insert should also put a
, L3 Y; ~: n9 P* q# j  }8 F! I' G( v/ Kwarning about the virilizing effect on a male or
9 N' s* J9 _  h9 ~, z: Afemale child who might come in contact with some-
' M% T. A% f2 eone using any of these products.+ s2 M8 M  y4 J1 R: R( d! |3 S! R
References2 l; _6 }8 `( Q, T9 @
1. Styne DM. The testes: disorder of sexual differentiation
5 D2 {8 v1 X, J+ }- `and puberty in the male. In: Sperling MA, ed. Pediatric
; V" m4 D' H) ^5 W4 v( ZEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- o% Q" e" w# M. X- e
2002: 565-628.
( P9 x3 G: o( U+ @  b# C, K* \2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 Z( c7 u2 \0 Zpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old3 j: f. l- h8 n3 ^
Boy Induced by Indirect Topical3 t+ H; q, y! x  S6 ^
Exposure to Testosterone4 K1 ~$ g, x* }8 b6 e
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# v1 z6 T* P  Xand Kenneth R. Rettig, MD1" S& r. r+ R. z9 p
Clinical Pediatrics4 l% ~, n  ^1 K: n0 m/ I
Volume 46 Number 6: u( V5 k, q; T9 y+ ]% L' l3 F
July 2007 540-5435 b$ b4 m+ v; R; F+ V
© 2007 Sage Publications
, j, w. I0 z% M) W% r! c0 n0 W  Z10.1177/00099228062966513 V  U" u: E- T" `1 y
http://clp.sagepub.com0 f- _. V8 u1 \( C! h
hosted at
3 C# w" W" z  J% }1 u0 v* Nhttp://online.sagepub.com
1 [6 t; [( c9 XPrecocious puberty in boys, central or peripheral,
* J' P$ K% h8 f( i% ]# m" Ais a significant concern for physicians. Central: m$ O8 l4 U$ k8 F( g! ^* h
precocious puberty (CPP), which is mediated
$ b  W# e' n$ I8 u3 y  H; }through the hypothalamic pituitary gonadal axis, has5 t/ y2 U4 p/ G) `" r" }
a higher incidence of organic central nervous system
7 A+ F: s% m3 x+ b/ A/ ?lesions in boys.1,2 Virilization in boys, as manifested
4 @5 G6 U% x! i( m* N. }, E9 pby enlargement of the penis, development of pubic
( D# A2 C7 A- D  n$ thair, and facial acne without enlargement of testi-* T5 X- H: f& E# K) B  E7 @7 S+ t
cles, suggests peripheral or pseudopuberty.1-3 We2 d! `  |& ]# b' |
report a 16-month-old boy who presented with the
4 B/ w! V6 F7 W: Z  U) n3 tenlargement of the phallus and pubic hair develop-
" Y* |8 }' \+ d: O) gment without testicular enlargement, which was due; L7 U7 {* s% S% U
to the unintentional exposure to androgen gel used by
: K& ]! a  T2 h/ \& s: Pthe father. The family initially concealed this infor-
2 @# k* W& C1 k: ]mation, resulting in an extensive work-up for this# F0 @2 p. ^! L5 U) |2 U
child. Given the widespread and easy availability of
, }7 G) H& S" G8 ztestosterone gel and cream, we believe this is proba-0 C( ?* ~0 m  K/ f5 m7 s
bly more common than the rare case report in the
3 w7 {! q1 R6 Y' `- iliterature.4
7 S* Y) s; y# T9 i. [0 B/ _* sPatient Report! k& A0 J/ r, u% _9 T0 y
A 16-month-old white child was referred to the
4 G) V- L* ]% Qendocrine clinic by his pediatrician with the concern
% f! J) g! q# e1 E9 Y0 d) w4 b8 N- y' Vof early sexual development. His mother noticed
3 r2 P- D; V, t# j3 `" dlight colored pubic hair development when he was
( \/ s" p( [$ y. G" \$ `From the 1Division of Pediatric Endocrinology, 2University of
2 S0 O/ `9 i: P& c- B$ S% oSouth Alabama Medical Center, Mobile, Alabama.
' w+ ~& `! S$ ~5 I  N2 d  fAddress correspondence to: Samar K. Bhowmick, MD, FACE,
8 K7 u  Q+ {2 {3 N4 nProfessor of Pediatrics, University of South Alabama, College of9 C3 a& i$ C' y" ~
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 U( G) Q) O; |9 I3 ^$ k
e-mail: [email protected].
$ h. `* X1 q- n$ l0 J: N! ]$ Qabout 6 to 7 months old, which progressively became
) b. z0 C9 t6 p9 _4 T4 T: Fdarker. She was also concerned about the enlarge-
6 K+ X3 h8 q, K: f: L: m' Yment of his penis and frequent erections. The child+ g: l4 P0 u2 f& z8 X- }0 v. m$ `' V- p
was the product of a full-term normal delivery, with
4 u- g. N/ t/ C8 W4 xa birth weight of 7 lb 14 oz, and birth length of
2 ~/ s" t% ~1 u8 _20 inches. He was breast-fed throughout the first year
; n+ C- u5 Z9 i- t1 ]2 z% H# Xof life and was still receiving breast milk along with
8 }# |) u& O- \: ~3 a% [solid food. He had no hospitalizations or surgery,+ M1 N9 b7 \% A$ e4 S
and his psychosocial and psychomotor development( n( H# @$ J7 U  D5 R* O
was age appropriate.
; G  Q- C9 n9 Z. _  tThe family history was remarkable for the father,7 ^# |1 z; U& _/ ~
who was diagnosed with hypothyroidism at age 16,
* C/ ^7 Q# {8 B9 Nwhich was treated with thyroxine. The father’s; j& q: M8 n2 k4 ?# R4 B
height was 6 feet, and he went through a somewhat- n8 l. U& \5 b% ?
early puberty and had stopped growing by age 14.
/ V: N; C: j8 E% J$ o  zThe father denied taking any other medication. The/ y3 O! r* j; ]$ Z
child’s mother was in good health. Her menarche% B+ W4 \& A: R, s  T
was at 11 years of age, and her height was at 5 feet
! r. s' c2 [4 j5 inches. There was no other family history of pre-
) ]1 e3 Q3 j9 G  `6 X  W) jcocious sexual development in the first-degree rela-
5 K% [7 T2 H; h6 u4 ]6 T9 Y5 Htives. There were no siblings.
  O5 D+ B+ U5 @8 F+ P1 J/ z/ yPhysical Examination0 B7 Y6 k. G+ N$ u2 c
The physical examination revealed a very active,6 b8 w+ T* X  }# L5 g* w
playful, and healthy boy. The vital signs documented
4 n/ z/ f/ L8 c) F" `6 D. S( ~a blood pressure of 85/50 mm Hg, his length was& ]& m3 d- Q: {( U! U
90 cm (>97th percentile), and his weight was 14.4 kg+ k8 T- i! {& m/ I5 X
(also >97th percentile). The observed yearly growth
# F* d% z& p3 X5 q+ r6 yvelocity was 30 cm (12 inches). The examination of* y7 z- b& U# N) B
the neck revealed no thyroid enlargement.6 ^+ _& i0 [* c: |. i( |: ?
The genitourinary examination was remarkable for4 g: v( S" Y- F* J' F( I( |+ I
enlargement of the penis, with a stretched length of2 v# Q5 V# R: N  h) b
8 cm and a width of 2 cm. The glans penis was very well4 G" s4 T# O0 N3 Q; O, z' b
developed. The pubic hair was Tanner II, mostly around* x8 G+ @0 @% j2 j& B% V. K" z
5404 c4 a: J5 z/ C
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the base of the phallus and was dark and curled. The
$ E* G. x  U; h- S! C* Ptesticular volume was prepubertal at 2 mL each.2 F; Y4 Y9 q) a; K0 t' ^
The skin was moist and smooth and somewhat6 n4 @7 ^3 z6 Q1 n9 F* b/ J
oily. No axillary hair was noted. There were no" B4 u$ d0 [; I! N9 e/ c2 B1 `
abnormal skin pigmentations or café-au-lait spots.
+ H7 K3 ^: ^. D1 t4 r) FNeurologic evaluation showed deep tendon reflex 2+2 B$ H7 B" u) @4 n/ ]
bilateral and symmetrical. There was no suggestion. @# d6 B" `- j/ S" h- v4 V
of papilledema.
& c5 q/ n7 v+ O9 i% B! @  V, L4 YLaboratory Evaluation
9 b( l5 a1 [, K1 F- c% @' e# [) JThe bone age was consistent with 28 months by! v! S  s4 r: K- a9 M6 b( P, `
using the standard of Greulich and Pyle at a chrono-% f4 V; C4 {# d
logic age of 16 months (advanced).5 Chromosomal
( u0 @, n+ q/ j1 dkaryotype was 46XY. The thyroid function test
* l1 B( t% {7 H+ Y- h3 Ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-
" a; Y# u7 C) w" Slating hormone level was 1.3 µIU/mL (both normal).
0 O+ h% T. a1 B/ _- w" `- OThe concentrations of serum electrolytes, blood
$ n+ x  W; L9 l6 {: F$ M, Jurea nitrogen, creatinine, and calcium all were* a7 m! ]  a1 O. M$ U
within normal range for his age. The concentration# I0 R% c' C! u3 W5 E
of serum 17-hydroxyprogesterone was 16 ng/dL
  \2 k8 i- O. y(normal, 3 to 90 ng/dL), androstenedione was 20
8 \7 q/ F( p* p, p* ^& ]6 jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& h; d: O$ _1 n# _" U5 Vterone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 Z. l! C6 c1 o& w4 Wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
% X. }/ {: B' i1 E8 A% P8 l49ng/dL), 11-desoxycortisol (specific compound S)
+ y4 H" \3 R- ~+ R4 zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* x5 _8 G/ E( |$ gtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% P+ ?, @3 U7 t6 W8 t  v8 Ytestosterone was 60 ng/dL (normal <3 to 10 ng/dL),4 g. h, _7 ?) x4 t
and β-human chorionic gonadotropin was less than
9 G5 }5 a0 U: U6 @& q5 mIU/mL (normal <5 mIU/mL). Serum follicular- Z+ q$ r9 \8 ^# j6 E0 I( }
stimulating hormone and leuteinizing hormone
( ]! b+ O. j3 l" j- M; jconcentrations were less than 0.05 mIU/mL
) I2 J7 P' N5 g' I* T8 ~7 n(prepubertal)./ o; p3 s, O3 H8 U
The parents were notified about the laboratory
# y* i' r& T$ k. Kresults and were informed that all of the tests were0 T* V3 c8 y: m" F) W, T/ y. N
normal except the testosterone level was high. The
- z- o$ m5 p, t8 G- pfollow-up visit was arranged within a few weeks to+ n% B' b3 O, f7 Q: r6 s
obtain testicular and abdominal sonograms; how-
  d2 V7 O4 s, y6 ]" yever, the family did not return for 4 months.; |3 B+ R" g9 g. G" \$ s$ d' o7 N
Physical examination at this time revealed that the) F/ }1 L* T& ~; R
child had grown 2.5 cm in 4 months and had gained6 q2 M& s5 [/ I- E8 h
2 kg of weight. Physical examination remained
; r# X' g1 g3 _* @$ Lunchanged. Surprisingly, the pubic hair almost com-8 ]' X4 G3 H" s
pletely disappeared except for a few vellous hairs at
. A6 M) H  y5 _) E, s! x5 Tthe base of the phallus. Testicular volume was still 2* l  {+ j1 C: h0 ~1 w; I" S
mL, and the size of the penis remained unchanged.! D9 b9 E  K) D- \4 r9 @0 i
The mother also said that the boy was no longer hav-3 d1 x* Q! Z9 `- H4 q8 h6 }
ing frequent erections.
- j+ Z- J2 k3 ~! UBoth parents were again questioned about use of7 ]% f7 {; t' y( \3 h4 u7 q( t0 T
any ointment/creams that they may have applied to7 m/ }. b" J4 y, x, G
the child’s skin. This time the father admitted the. |. B! P2 U; u+ N/ v
Topical Testosterone Exposure / Bhowmick et al 5418 f8 w, r3 t6 {
use of testosterone gel twice daily that he was apply-- u8 H3 t# i5 U7 V, M
ing over his own shoulders, chest, and back area for
& e! C: M/ y/ l: i9 ha year. The father also revealed he was embarrassed
# q( G9 k0 I( B; Tto disclose that he was using a testosterone gel pre-9 r: `+ |/ j% ]( d
scribed by his family physician for decreased libido
- B; v% }7 k) |8 x5 xsecondary to depression.
% X2 L1 w9 {+ ]9 K- b3 QThe child slept in the same bed with parents.
* r* w; b* J) M4 eThe father would hug the baby and hold him on his
; f& E5 R3 q2 h/ [# tchest for a considerable period of time, causing sig-
) s  |6 B/ J% p8 j5 q9 A. Lnificant bare skin contact between baby and father.
7 R2 t1 e0 U& s: I5 Q+ [The father also admitted that after the phone call,; ^0 k' k! R/ c
when he learned the testosterone level in the baby% _  P, l7 R) b+ H
was high, he then read the product information5 ^, P! ~6 p6 E! j
packet and concluded that it was most likely the rea-+ }4 Q& F; L2 m) x+ l
son for the child’s virilization. At that time, they+ Q* Q1 Z, q$ }' E9 z" l, b
decided to put the baby in a separate bed, and the) \0 h! B( Z& C1 z" q
father was not hugging him with bare skin and had
. q/ a! L: i  B% @8 obeen using protective clothing. A repeat testosterone
9 h6 j/ D& U5 g$ H( `( w2 gtest was ordered, but the family did not go to the
$ w6 |, X9 Y7 {5 dlaboratory to obtain the test.
2 `  k( M+ L0 v' ~1 I8 q. J7 HDiscussion* q7 n+ L% z, I8 o/ D+ A
Precocious puberty in boys is defined as secondary
2 D7 T9 g+ o& y8 Q8 B: xsexual development before 9 years of age.1,4
3 M) |" }6 Z0 L, B" gPrecocious puberty is termed as central (true) when
! ?% H# z$ E  \it is caused by the premature activation of hypo-
) P! I: E: x6 @* r+ K/ |( {thalamic pituitary gonadal axis. CPP is more com-& g# O: p( I0 u1 p. N% f5 E
mon in girls than in boys.1,3 Most boys with CPP: a8 X8 C2 ^. @: j0 [, h7 ]
may have a central nervous system lesion that is
/ a; s. Y' ~1 W2 [# `responsible for the early activation of the hypothal-
$ h  Z, d4 g; m. p/ ~amic pituitary gonadal axis.1-3 Thus, greater empha-
; \$ u/ i; @4 h) |" msis has been given to neuroradiologic imaging in) E1 N, Z$ D8 l( h4 m2 S' n1 T
boys with precocious puberty. In addition to viril-8 {0 k5 f; F! }
ization, the clinical hallmark of CPP is the symmet-
0 w; q2 M0 [0 v- h$ Jrical testicular growth secondary to stimulation by
8 {# j# O( T: Fgonadotropins.1,3! f  I( x! G1 L# z6 I1 B+ a
Gonadotropin-independent peripheral preco-9 J& R6 T# @& B% y0 l3 W0 b
cious puberty in boys also results from inappropriate
4 |; s; Z$ ~& n' N, randrogenic stimulation from either endogenous or
/ H' S# }$ W! M- [2 X+ rexogenous sources, nonpituitary gonadotropin stim-# c( B% y! I7 \3 n
ulation, and rare activating mutations.3 Virilizing
- w6 ?! e& q4 O1 I5 W6 Lcongenital adrenal hyperplasia producing excessive
) Y+ g$ `7 l& ?1 ?/ d% B- }$ v) z/ Padrenal androgens is a common cause of precocious
0 I0 ^2 f8 ]2 Z( ~1 g) Epuberty in boys.3,4
# {; E7 o8 M: i1 k9 u4 N9 w4 d5 kThe most common form of congenital adrenal
" W' M' w* v* k' Phyperplasia is the 21-hydroxylase enzyme deficiency.
4 u. D+ i4 k  C: WThe 11-β hydroxylase deficiency may also result in
+ H. t5 C  i- p- J* e* V' ^  o  ^excessive adrenal androgen production, and rarely," N5 K  S  o9 z+ j
an adrenal tumor may also cause adrenal androgen
6 F/ E- M1 T  S  M" |9 |excess.1,3. s6 B) w! v! b5 P# O1 {
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& _. E5 x) H6 |% y2 ]" f0 S542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
) i- |7 p: p/ b* QA unique entity of male-limited gonadotropin-  [" w4 X6 \# E( D% {! g: ]! r% `% Y
independent precocious puberty, which is also known
+ W$ t2 q6 A3 {+ }* }as testotoxicosis, may cause precocious puberty at a
# \' ~& t; u# k; h3 K3 Overy young age. The physical findings in these boys
  ~# h% }6 e9 B' ]% x4 ywith this disorder are full pubertal development,
9 ?# i0 G" l" _/ i6 [! B1 Y/ tincluding bilateral testicular growth, similar to boys
* t$ D2 c0 h, }+ x& J7 s% Wwith CPP. The gonadotropin levels in this disorder9 N! x1 p- w4 o5 X2 m/ r9 d6 m) P
are suppressed to prepubertal levels and do not show
, N$ i! n: Y1 H" U# j3 L6 G4 [pubertal response of gonadotropin after gonadotropin-  D: ~! l) {5 J; Q3 \  k
releasing hormone stimulation. This is a sex-linked
! ]/ y& T( h7 f  e  l( ?( A  v& Pautosomal dominant disorder that affects only/ G$ n- Q% B/ Y+ ?
males; therefore, other male members of the family
1 t9 c$ h9 D4 t4 ~  g( hmay have similar precocious puberty.38 ~# z$ Y0 P  a! \: G# X
In our patient, physical examination was incon-2 C. {( F& U3 K5 @, t. S
sistent with true precocious puberty since his testi-8 i/ x. X+ G9 r3 K# v
cles were prepubertal in size. However, testotoxicosis
8 n4 t$ ?# j8 b' K. Gwas in the differential diagnosis because his father7 ?+ r, j! V5 s0 ]
started puberty somewhat early, and occasionally,/ y8 M; b" Q1 |, u. o
testicular enlargement is not that evident in the! q* H6 A: W+ ?- Y
beginning of this process.1 In the absence of a neg-
* X4 j  q! P7 ~ative initial history of androgen exposure, our
* k) [. T2 x1 T4 g# Kbiggest concern was virilizing adrenal hyperplasia,( y0 c0 z7 V5 M2 ], V
either 21-hydroxylase deficiency or 11-β hydroxylase: W7 e& T8 \: v5 A! F
deficiency. Those diagnoses were excluded by find-. v( x0 m9 K8 }4 @+ G+ z+ f" N
ing the normal level of adrenal steroids.1 w/ \" |- q3 T0 B
The diagnosis of exogenous androgens was strongly1 p: `5 ~* C% A3 c! e" Y$ V; v' G
suspected in a follow-up visit after 4 months because5 `/ j$ q. `/ r# k0 c
the physical examination revealed the complete disap-
: L- e5 r, j$ C- j" m$ Upearance of pubic hair, normal growth velocity, and" s: I/ B2 c; h- g. X& g
decreased erections. The father admitted using a testos-' f  i0 i) b4 n; I  C3 Y* g
terone gel, which he concealed at first visit. He was) C) }& H% E" E8 t
using it rather frequently, twice a day. The Physicians’/ g: a+ b( d/ H2 `5 l+ Y4 f0 x
Desk Reference, or package insert of this product, gel or
: K5 O) `1 Z: U8 `cream, cautions about dermal testosterone transfer to# J) ^6 P  d! ~  b
unprotected females through direct skin exposure.( P! e+ V0 Z. E# \7 K
Serum testosterone level was found to be 2 times the6 l3 n4 V7 _  l; v& R
baseline value in those females who were exposed to
$ n' c, S$ H" z7 u& Meven 15 minutes of direct skin contact with their male0 f  ^. `" a& Q$ W! D# i
partners.6 However, when a shirt covered the applica-
. O9 i2 Q. e- q7 j3 g' {tion site, this testosterone transfer was prevented.* v' a+ d# i* ]& \3 R$ P
Our patient’s testosterone level was 60 ng/mL,
" M. S9 C$ p; t' N# N$ ]& w0 Qwhich was clearly high. Some studies suggest that
+ s; w$ G' m; l. Q- D2 cdermal conversion of testosterone to dihydrotestos-
/ P4 b7 K3 u( O2 N) O5 mterone, which is a more potent metabolite, is more# \  `! B$ h6 i6 @2 e
active in young children exposed to testosterone1 R; R: Q2 q, B
exogenously7; however, we did not measure a dihy-
8 O% [4 p6 m* k3 `/ O3 Y' jdrotestosterone level in our patient. In addition to
8 c0 x& J$ `: y5 g$ j. \4 mvirilization, exposure to exogenous testosterone in
! E9 |: y& h. j+ y. j1 Lchildren results in an increase in growth velocity and5 R. |9 Z! Z- q6 b8 w& Z4 D7 a
advanced bone age, as seen in our patient.2 c9 ]2 O* ?3 e: n1 K. Q
The long-term effect of androgen exposure during
: S# M4 c# Q1 w( q1 d, Vearly childhood on pubertal development and final
& ]' U6 z# E( K& ]* K) Uadult height are not fully known and always remain
& \3 Q4 h) \6 O" D/ aa concern. Children treated with short-term testos-
, j% ], G' J* jterone injection or topical androgen may exhibit some
2 c" V/ C5 U) Iacceleration of the skeletal maturation; however, after+ J0 [( }& T. U, R/ N, G" q3 ]
cessation of treatment, the rate of bone maturation
2 H' r& q. R- c/ idecelerates and gradually returns to normal.8,93 R* a! Q4 Y3 [/ H& [, {
There are conflicting reports and controversy! `- ]& O) U4 X3 q/ p- y5 t
over the effect of early androgen exposure on adult9 m0 ]9 m3 C5 N" R
penile length.10,11 Some reports suggest subnormal
" E2 A$ b' L7 Hadult penile length, apparently because of downreg-  h- P7 O, n7 S
ulation of androgen receptor number.10,12 However,
" C3 f) @1 c9 }Sutherland et al13 did not find a correlation between
9 C" r+ x; Z' W* ?' D9 y+ H  l3 cchildhood testosterone exposure and reduced adult
& m! Y$ u. H4 Y% N  jpenile length in clinical studies.* _. [" F( z3 W( s2 ?
Nonetheless, we do not believe our patient is0 ?  z. j6 d6 d% H$ y: g; E0 g
going to experience any of the untoward effects from$ Z4 v* h4 g% T- h/ f* A
testosterone exposure as mentioned earlier because
2 y. \& j. `; |" i+ W; e1 Othe exposure was not for a prolonged period of time.
  {" d! p- A1 v! b) o+ c3 HAlthough the bone age was advanced at the time of7 F* c/ Y& Z5 ^& r
diagnosis, the child had a normal growth velocity at: z, M) t) ~. U# N: i# |0 F
the follow-up visit. It is hoped that his final adult
" e. M/ b! I& h, i2 P, c# a0 hheight will not be affected.
  k+ o* F9 m% p! Q0 E- D1 e4 qAlthough rarely reported, the widespread avail-  E3 F- j  l( z0 H) a6 Q' B
ability of androgen products in our society may' h7 Y) O1 c0 i: r! p
indeed cause more virilization in male or female
+ s: ]: u$ U+ V* {* u9 [children than one would realize. Exposure to andro-6 ~% h% c$ S3 m* l2 V  r
gen products must be considered and specific ques-+ U) D6 n) W7 P- ~; P) c' j
tioning about the use of a testosterone product or
( l  h3 d1 P- ?7 [' Ggel should be asked of the family members during
  {9 C& Q! c9 U. v# k* S1 H9 hthe evaluation of any children who present with vir-+ t- y9 c, ~+ l0 p3 g$ e
ilization or peripheral precocious puberty. The diag-! x, m# p' \4 Q& r
nosis can be established by just a few tests and by( q  a# c3 l3 m( e! J: j$ i  H3 _
appropriate history. The inability to obtain such a
' H$ T4 K/ k' W! Z& X! `  u0 k' P% Chistory, or failure to ask the specific questions, may7 W' z2 t8 d( M& z
result in extensive, unnecessary, and expensive  r% n% T! {1 ]+ ?7 t
investigation. The primary care physician should be0 L1 k5 ~1 g- N1 U5 m
aware of this fact, because most of these children# `* j1 k: N0 j" J  P
may initially present in their practice. The Physicians’
+ i0 k- W9 u3 C# YDesk Reference and package insert should also put a
+ C) N. e) V' {$ I. U1 rwarning about the virilizing effect on a male or
$ D. M8 s0 n/ K2 g8 t$ c' Efemale child who might come in contact with some-
. u/ v* z# t3 j& q& \' k8 L# Mone using any of these products./ ~) V4 g$ l9 \- c, W* a; v
References6 f' G) e) R' o+ l/ _
1. Styne DM. The testes: disorder of sexual differentiation4 y: L$ e. K" ^  P6 \% a4 o- n$ E
and puberty in the male. In: Sperling MA, ed. Pediatric: P4 `- r$ x$ e4 `6 [7 G
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. i- p- _) u1 w0 f' t. Y7 ?2002: 565-628.
7 B" u3 {# `! q/ T! N2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* U/ ?& R2 ]& o$ r1 H3 }& Y0 |
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
- C; f8 l4 |1 r" {7 c& p
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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