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/ l% h4 l3 f0 V7 z
Boy Induced by Indirect Topical
( ?+ M" e. S+ i- K% FExposure to Testosterone
- R( B# i* h/ [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! T% ?2 J4 X; z) ]6 eand Kenneth R. Rettig, MD1& ]% B  ~/ U" _$ u3 ?
Clinical Pediatrics
& F7 R" I6 t4 lVolume 46 Number 6
4 s' I) U+ @, G1 F; ?6 n( b5 _July 2007 540-543, o  W, u* h8 B# ~; R- C
© 2007 Sage Publications; Z/ z# \* z/ y, M! t% |3 t, H+ e
10.1177/0009922806296651
$ [2 S7 r3 l% d% q7 uhttp://clp.sagepub.com
- Y9 W$ u; ~1 D% L  P6 `4 Ghosted at
1 |, m+ W/ m# r  G# Phttp://online.sagepub.com
& v: B* x3 n/ G# tPrecocious puberty in boys, central or peripheral,; o7 f. q1 K$ F1 G, ~
is a significant concern for physicians. Central
- T( E- S' r$ H! q1 w) {6 {precocious puberty (CPP), which is mediated
0 `+ z1 U$ r3 j) U$ e& T# ithrough the hypothalamic pituitary gonadal axis, has6 X5 {  D: t" ^8 x4 E
a higher incidence of organic central nervous system
& R2 t1 F7 M) p) [& ?; D) M& h$ klesions in boys.1,2 Virilization in boys, as manifested
4 [/ @2 A( V7 ?. Fby enlargement of the penis, development of pubic+ K+ }2 _# c+ U$ |# r
hair, and facial acne without enlargement of testi-
1 C0 y% b3 M; g3 l6 {cles, suggests peripheral or pseudopuberty.1-3 We# e6 R) I) G: `% V4 z: r; X5 g
report a 16-month-old boy who presented with the; U  i/ d1 l/ [/ O( y8 }9 W1 s, H
enlargement of the phallus and pubic hair develop-  V7 L: V4 r4 c/ y) r  ^& r
ment without testicular enlargement, which was due
5 c' W/ G' r2 k% W2 B" Z9 `to the unintentional exposure to androgen gel used by6 k3 [! e% C2 {1 f3 B1 E9 z
the father. The family initially concealed this infor-
2 Z0 l' j( H: Jmation, resulting in an extensive work-up for this
4 E& S/ h% ]6 O1 i% Y, _! rchild. Given the widespread and easy availability of7 d; m* C6 L& w# T
testosterone gel and cream, we believe this is proba-
0 }& l( i) {* e- A' h) lbly more common than the rare case report in the; l( A) w0 u5 D4 K
literature.4
4 I6 V8 H, i2 p7 B0 E9 j* J7 W, QPatient Report
' \9 ]0 A3 D4 c7 TA 16-month-old white child was referred to the
4 |! _$ T" k3 D. y  eendocrine clinic by his pediatrician with the concern
" P4 g8 r. M9 [* L5 ~of early sexual development. His mother noticed
. Y" ^! K; Y# F1 h* H3 ]light colored pubic hair development when he was
# z6 v8 m3 \# ^8 iFrom the 1Division of Pediatric Endocrinology, 2University of
* N1 l8 I" W( G! C& mSouth Alabama Medical Center, Mobile, Alabama.
% [8 c: l+ B( w) R. H& a' NAddress correspondence to: Samar K. Bhowmick, MD, FACE,# c& n" }2 f; \; r: ^+ Z0 n
Professor of Pediatrics, University of South Alabama, College of
: B3 V: P8 c5 u+ w1 I  Z" RMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;* K, D+ q$ v% G
e-mail: [email protected].
& u6 J  z' S$ C9 Habout 6 to 7 months old, which progressively became
# [2 g' G  m+ |. Y" {2 |% |' fdarker. She was also concerned about the enlarge-5 O& Q8 |1 H7 r8 ]# t: Z; z) ^
ment of his penis and frequent erections. The child
" u1 y4 c2 u8 Y! b+ v. ~5 J% Awas the product of a full-term normal delivery, with9 I. Y" p! d" i# u3 ]) J+ C
a birth weight of 7 lb 14 oz, and birth length of0 y. _7 ?1 ~0 ?4 Y6 L3 _1 P% Z2 K
20 inches. He was breast-fed throughout the first year4 g# X5 A" K" ^1 G9 Z; A
of life and was still receiving breast milk along with
0 I! y- V( i4 csolid food. He had no hospitalizations or surgery,
* g5 F# g) _; s2 X4 f4 w8 cand his psychosocial and psychomotor development- _/ i* d' `3 r; g% e/ j0 `5 {. P
was age appropriate.
, U& A- @* R  Q; [0 R5 v5 a- SThe family history was remarkable for the father,2 K# I3 Y8 U$ l2 L& W- F" I4 ?
who was diagnosed with hypothyroidism at age 16,
3 P! D. H8 F$ K- U* f: ywhich was treated with thyroxine. The father’s8 ~$ c+ k& C0 u; s
height was 6 feet, and he went through a somewhat
; y7 p% o% Q2 Z$ Learly puberty and had stopped growing by age 14.
" w- J( X) d5 t+ uThe father denied taking any other medication. The
/ a! I- r. r) b+ rchild’s mother was in good health. Her menarche
7 h- r  n" p& r5 G0 Dwas at 11 years of age, and her height was at 5 feet+ K4 R8 c5 d  ]2 M
5 inches. There was no other family history of pre-  C$ E3 N/ ]$ }8 k* j
cocious sexual development in the first-degree rela-' r" d: o9 N  W  A3 Z0 m6 ^
tives. There were no siblings.
- F- b3 `9 ^2 ~. OPhysical Examination- X. M* O3 {: w' }  t
The physical examination revealed a very active,
# _, }! Y1 r- Aplayful, and healthy boy. The vital signs documented
; \; F+ V1 p# y& a6 ^2 W- Xa blood pressure of 85/50 mm Hg, his length was
7 H7 m# @9 p( i2 c90 cm (>97th percentile), and his weight was 14.4 kg2 p+ |. P& }$ I! |& c. @/ `
(also >97th percentile). The observed yearly growth$ `* ^6 i; ~5 a7 q! p% f, H
velocity was 30 cm (12 inches). The examination of; i6 c& L7 J" G2 F
the neck revealed no thyroid enlargement.
& `( l( g8 @) n# y! N8 y+ uThe genitourinary examination was remarkable for! |: v9 z+ `( h2 j" k( }
enlargement of the penis, with a stretched length of" D$ |# d" V8 q9 \
8 cm and a width of 2 cm. The glans penis was very well
  c) S5 c; Y4 v  {/ J- ]: vdeveloped. The pubic hair was Tanner II, mostly around0 }3 p* U+ v9 U/ ]5 J2 T* @
540  @. V# P7 T4 U7 ~. K& \( |& m5 G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 l9 ~  h3 R! j7 c" Z9 \the base of the phallus and was dark and curled. The. q7 `. w$ a2 G% s) j
testicular volume was prepubertal at 2 mL each./ v* p% z: s0 \. X" _$ M
The skin was moist and smooth and somewhat& b/ Q9 F% ?5 Q- Z" W  O2 x
oily. No axillary hair was noted. There were no' y+ m, Z* D- i! i' U1 K+ ~, ]
abnormal skin pigmentations or café-au-lait spots.
$ ]/ D( A- V, _9 b( yNeurologic evaluation showed deep tendon reflex 2+) e0 }$ ^. A, _; l; ?7 F5 U
bilateral and symmetrical. There was no suggestion
! }$ }" |; \2 B8 G' D6 y$ N* qof papilledema.
$ |/ z, o: j2 e, s/ G$ qLaboratory Evaluation
* f: G( ^4 \0 U5 g: sThe bone age was consistent with 28 months by9 c& v4 z! N9 A9 x
using the standard of Greulich and Pyle at a chrono-
# U, y+ h2 J% @logic age of 16 months (advanced).5 Chromosomal6 Z) l* v3 C" j
karyotype was 46XY. The thyroid function test
$ y# h0 u4 C9 v& {% j9 {, Rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
% v; s) U- G; J7 N% E7 F  Plating hormone level was 1.3 µIU/mL (both normal).- A! h0 N) t2 T/ J3 Y# T
The concentrations of serum electrolytes, blood2 H4 |, a, p- J/ e* b/ b) v
urea nitrogen, creatinine, and calcium all were2 ^2 Y7 x. F0 c* A( M' v' I+ s
within normal range for his age. The concentration  J: x. }- F7 m( X, |+ M+ u
of serum 17-hydroxyprogesterone was 16 ng/dL) ?- m+ m2 E# C1 O
(normal, 3 to 90 ng/dL), androstenedione was 20
( U: u& ^- V) e6 _* f/ V6 N) Jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 d1 U( q! m8 Q- @/ u5 b
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 s7 b' D' h' ?3 H4 J2 K3 k) m( adesoxycorticosterone was 4.3 ng/dL (normal, 7 to5 W0 z- a4 `1 g$ y* Z8 j+ @! R
49ng/dL), 11-desoxycortisol (specific compound S)
7 K3 ?- U7 i( h3 hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% X1 T8 c7 y3 Y. \6 w; Btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' L2 v& q4 }7 r8 ?6 H* m& o
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! c. c$ @' o& t# F2 B) iand β-human chorionic gonadotropin was less than) _8 N! t: n  i3 q4 ~) U
5 mIU/mL (normal <5 mIU/mL). Serum follicular
- C5 A7 i' I" s$ H0 K% Vstimulating hormone and leuteinizing hormone
8 H6 n" \$ h8 ^% ?) m7 rconcentrations were less than 0.05 mIU/mL$ y# |8 C3 c8 N' V7 k# y' E, O
(prepubertal).
1 l0 l! v! o9 v; wThe parents were notified about the laboratory! Y" K: Z0 }; C: C5 K
results and were informed that all of the tests were
& m- r/ ?1 n6 e' \normal except the testosterone level was high. The
9 j6 V; h1 U  \* f* |* f* wfollow-up visit was arranged within a few weeks to
7 b5 {2 z- P- Robtain testicular and abdominal sonograms; how-
. Y+ E: n# X5 Oever, the family did not return for 4 months.
5 |  V" l& P2 g" i4 |; WPhysical examination at this time revealed that the
8 Y4 w9 r% I' c' N( e0 m5 e+ ochild had grown 2.5 cm in 4 months and had gained
7 A4 |0 z$ i, s& X; o# ?2 kg of weight. Physical examination remained
" Q" K9 U) W( h6 s- iunchanged. Surprisingly, the pubic hair almost com-' J0 U+ V, }2 S* ?" |
pletely disappeared except for a few vellous hairs at
' Y# V+ m% p. S/ u: J8 _$ ~the base of the phallus. Testicular volume was still 2; t: `5 ?5 \. k$ V: Q; g4 M
mL, and the size of the penis remained unchanged.
) a1 h" C8 A& V4 x* V5 cThe mother also said that the boy was no longer hav-
- U; R3 J' R4 n7 ping frequent erections.
& t, k& }, w$ j! e; V5 vBoth parents were again questioned about use of; e: x; {- K( A5 }4 V! b! w3 x8 P
any ointment/creams that they may have applied to) Y. Y6 T: y3 g$ s+ I+ \3 ^
the child’s skin. This time the father admitted the
' o- }) z; N" d6 RTopical Testosterone Exposure / Bhowmick et al 541* i6 y7 s3 A0 Z  z
use of testosterone gel twice daily that he was apply-
, z% |9 N+ a8 u/ E, }6 H. R- R. b! king over his own shoulders, chest, and back area for
$ i9 G" K! N( Ga year. The father also revealed he was embarrassed6 i( m0 |* x+ M; c4 h
to disclose that he was using a testosterone gel pre-
0 P) M3 X, Z& d- p& rscribed by his family physician for decreased libido
4 C, T% p0 Q. b8 j! h" ?secondary to depression.' w( N2 q% _5 Q# F
The child slept in the same bed with parents.
+ d) D  J0 t  d$ ZThe father would hug the baby and hold him on his9 w) F5 F  C9 A) V( Y" W  f
chest for a considerable period of time, causing sig-
. |4 V) K, d, e& Q& Z6 I- Wnificant bare skin contact between baby and father.( e* J1 ?: o' ^' D2 G8 B5 ?" M
The father also admitted that after the phone call,2 E9 P7 p: S  E( k* x4 p
when he learned the testosterone level in the baby+ F( R1 k& e3 b* l, m% U) u! ?
was high, he then read the product information
9 W2 T9 a5 U+ s' ~5 o6 ~3 }packet and concluded that it was most likely the rea-
4 [2 e" {# n9 ^) t! Y( a2 V* [& Bson for the child’s virilization. At that time, they8 q  J4 M( Y, }! `5 d, k- b" y
decided to put the baby in a separate bed, and the  @! a6 A7 l# W) N  N  b
father was not hugging him with bare skin and had/ r: w* v9 A: Z" o  |  a2 u& |& p$ ^3 M
been using protective clothing. A repeat testosterone
+ q7 _, v1 k$ A+ L+ w6 D) |( ^test was ordered, but the family did not go to the
& A9 Z! |" F# Flaboratory to obtain the test.- T/ C, X; b# Z& }8 A# k0 X3 p
Discussion
( a- s9 n; S. w2 B) LPrecocious puberty in boys is defined as secondary8 W2 t. j1 h/ g" C% k/ Y' Z
sexual development before 9 years of age.1,4
, D2 k3 H, H, @( j" q# j3 R' APrecocious puberty is termed as central (true) when
/ E& a' L* ^5 P/ Q' wit is caused by the premature activation of hypo-5 P# U6 i: K/ a% S) [
thalamic pituitary gonadal axis. CPP is more com-1 t  k* ~7 z) [4 d" J
mon in girls than in boys.1,3 Most boys with CPP, B$ g/ G) M0 g4 r4 C
may have a central nervous system lesion that is
: h5 [6 n- `* e3 Q3 rresponsible for the early activation of the hypothal-$ B* _4 C+ }* D& Z) A2 {. [& A
amic pituitary gonadal axis.1-3 Thus, greater empha-+ ?0 ]- Y! Q/ O- Y
sis has been given to neuroradiologic imaging in
% X0 ^7 z+ D3 r) c1 Cboys with precocious puberty. In addition to viril-! T. h- ]$ R! G6 G
ization, the clinical hallmark of CPP is the symmet-/ R/ b: J- e' K& |" w
rical testicular growth secondary to stimulation by
1 [0 V) X) |2 C: Q$ b8 Ugonadotropins.1,3
; f7 T# {" p% j* Z7 s& `1 M# `9 hGonadotropin-independent peripheral preco-
1 B$ u! j- d/ s3 V2 c% {; q, Icious puberty in boys also results from inappropriate
, C0 ~! r( [7 j: ~7 l0 M& e8 K1 [androgenic stimulation from either endogenous or
& M# {9 B) {1 @' Jexogenous sources, nonpituitary gonadotropin stim-
2 x9 m* g# u/ Q- E' p3 G2 g& Oulation, and rare activating mutations.3 Virilizing
/ d$ T" |0 ?8 `# J9 |( \congenital adrenal hyperplasia producing excessive8 u. ^) b5 v- z) `0 t: s& Z
adrenal androgens is a common cause of precocious9 \: p8 |) e) j3 p& C1 g; p# Y+ b
puberty in boys.3,4
" e! C8 c+ ^( f( D0 C' _The most common form of congenital adrenal
" N: ~/ Z* T7 r6 E. Bhyperplasia is the 21-hydroxylase enzyme deficiency.  v; u7 @3 j+ g7 C+ ^  d$ ?' A
The 11-β hydroxylase deficiency may also result in
9 ?# s5 z6 @6 s& h! ^5 I7 Oexcessive adrenal androgen production, and rarely,
) @, h' s$ d2 b7 d9 D4 Dan adrenal tumor may also cause adrenal androgen% r4 ^2 B+ r% c' y- @6 E/ d
excess.1,38 D; u6 j: j9 L0 A$ x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% B7 F1 V! g* P% y  }" g+ z542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 j( i  A6 x' Y/ I" rA unique entity of male-limited gonadotropin-7 v' t& r( w/ f1 f
independent precocious puberty, which is also known
/ v1 T4 p0 T3 Ras testotoxicosis, may cause precocious puberty at a1 K! Z9 ]  _* M5 T% z8 ^
very young age. The physical findings in these boys
+ o& l* d: j& q- `! f. g* Awith this disorder are full pubertal development,, z6 |9 e' g6 V
including bilateral testicular growth, similar to boys
9 T$ R2 e8 J; y1 C8 k$ r! `, W6 A6 hwith CPP. The gonadotropin levels in this disorder# G9 t9 R$ a) d, u
are suppressed to prepubertal levels and do not show$ g0 g" u$ X7 K0 Z* p' H' t% x0 V
pubertal response of gonadotropin after gonadotropin-, e* N4 f, \8 F  p0 Q& r8 W' p
releasing hormone stimulation. This is a sex-linked2 D1 _* k7 r& [& j% P# f, {' d
autosomal dominant disorder that affects only0 |9 P' @! k" B
males; therefore, other male members of the family1 S1 t! j8 r* j
may have similar precocious puberty.3; J+ z4 a1 M- p/ g
In our patient, physical examination was incon-
; n4 \& D! k' ?2 R% _4 _sistent with true precocious puberty since his testi-
) p  h) a+ D5 U- S, x# {cles were prepubertal in size. However, testotoxicosis
4 t" d7 u. Y% o. Y( Rwas in the differential diagnosis because his father
, _0 [7 m& T6 |5 k$ [& K# pstarted puberty somewhat early, and occasionally,  p2 n) W1 N4 e4 ]% s; ^9 E$ \
testicular enlargement is not that evident in the4 S: z2 L9 @( a
beginning of this process.1 In the absence of a neg-5 }$ e% R( _# Z3 Y/ ]3 O  c# y
ative initial history of androgen exposure, our
% m2 R! e7 y2 W. K  r+ j0 v$ xbiggest concern was virilizing adrenal hyperplasia,5 ^! g+ A8 g! [' D7 N- N, `3 v3 l
either 21-hydroxylase deficiency or 11-β hydroxylase* Y* w3 t  ]. w, G5 {3 F8 Z. G
deficiency. Those diagnoses were excluded by find-& N9 ^; Q# ^# E" O' m( q) B9 h
ing the normal level of adrenal steroids.
( X8 x  L" e% O2 [9 F) T$ c- yThe diagnosis of exogenous androgens was strongly2 V) Z% w% O, L; K' {
suspected in a follow-up visit after 4 months because
9 b6 M5 r8 N# C+ D; K# Gthe physical examination revealed the complete disap-! x$ e9 j! C6 F# m& q$ K0 Y
pearance of pubic hair, normal growth velocity, and( m+ w% m& R& {) O
decreased erections. The father admitted using a testos-; s7 \% e: c5 j& b* \, }: M" I
terone gel, which he concealed at first visit. He was
, o0 A# x& A2 ]. q4 lusing it rather frequently, twice a day. The Physicians’# s# p/ {( z, L; G2 C5 B& u9 r
Desk Reference, or package insert of this product, gel or3 d, B3 a5 F- c# V, `4 F
cream, cautions about dermal testosterone transfer to0 b$ T/ K2 i0 g) F
unprotected females through direct skin exposure.7 ^: x  Q( Q3 n6 k; ?
Serum testosterone level was found to be 2 times the
+ @' u0 J- q# p( }4 [baseline value in those females who were exposed to
0 ^0 Y+ ~! Z* y0 x6 j; ?even 15 minutes of direct skin contact with their male
6 N. G# B6 t; `* K' C7 wpartners.6 However, when a shirt covered the applica-
8 P4 I; s' @& a# b; ]/ ^tion site, this testosterone transfer was prevented.
. T: ~! u  W0 K  ^Our patient’s testosterone level was 60 ng/mL,1 O/ k/ _& Z3 s' f
which was clearly high. Some studies suggest that
+ H4 R- \6 h5 v' x& f* Hdermal conversion of testosterone to dihydrotestos-
* p9 @/ T' }1 o: l$ d: Aterone, which is a more potent metabolite, is more- {# ~0 r. h- m! X+ f% o
active in young children exposed to testosterone
3 @  s6 z/ ]4 F2 Z; sexogenously7; however, we did not measure a dihy-: s2 S6 C" {: [& v- ?! y9 x2 P
drotestosterone level in our patient. In addition to
9 q# L- R7 F+ |9 O: v( Zvirilization, exposure to exogenous testosterone in
2 V" f$ Q. g" i9 j3 R# |* L6 x& uchildren results in an increase in growth velocity and% v5 g$ f0 W  d+ z; E: Y, F+ b
advanced bone age, as seen in our patient.
& l- l* J  S5 XThe long-term effect of androgen exposure during
, H9 i/ z7 O9 u3 `5 z1 j; a; iearly childhood on pubertal development and final
: l: {2 x" A7 t" I  ~" u( U! V: radult height are not fully known and always remain7 Z5 }. t) Y+ r* a% j3 v
a concern. Children treated with short-term testos-4 B: [4 A  A$ `4 s8 m* g
terone injection or topical androgen may exhibit some0 u9 ~6 M8 }8 f; u
acceleration of the skeletal maturation; however, after
! z; q: [$ p/ J1 Y7 b1 W; J3 Pcessation of treatment, the rate of bone maturation
4 ?% |3 s3 X5 }  C0 u# f- Jdecelerates and gradually returns to normal.8,9* X3 Z; w9 Z- W4 C+ m. X4 s5 ]
There are conflicting reports and controversy' P; C' `" q6 d; _9 u4 N
over the effect of early androgen exposure on adult2 @9 z/ I# B2 O& i& n% t
penile length.10,11 Some reports suggest subnormal
( |% u# c0 H( n, E' Gadult penile length, apparently because of downreg-
9 B1 l* F! a! a' U: kulation of androgen receptor number.10,12 However,
( m' g7 Y# H8 M; f& B) F9 k' R5 a! q/ `$ ZSutherland et al13 did not find a correlation between7 R4 r! l6 f& J/ n( C% V' K( q  n# q
childhood testosterone exposure and reduced adult
$ ~' z+ b% g+ w2 m( npenile length in clinical studies.
2 \! `* @6 u6 V& ?' G1 a; iNonetheless, we do not believe our patient is+ H" g3 F6 C' J- N( r
going to experience any of the untoward effects from' r1 P5 e6 \2 Y& ^' C8 u! ~* z
testosterone exposure as mentioned earlier because
4 {/ ]: C* C# V+ H, v# _the exposure was not for a prolonged period of time.
! F) h; H0 Y: Z# A9 l1 vAlthough the bone age was advanced at the time of
4 h: `/ |$ ]2 b6 r& ^" F2 r* bdiagnosis, the child had a normal growth velocity at! ?+ T' b+ f. d: ^
the follow-up visit. It is hoped that his final adult4 m: A) B7 y- e7 h- y! h
height will not be affected.
, |; ]; I% t, s: c# N; XAlthough rarely reported, the widespread avail-
3 i5 y( ~) L/ o6 b1 F. L! P2 B2 ]ability of androgen products in our society may3 G8 @  }( z8 j: g
indeed cause more virilization in male or female
" n  ^8 ]% j6 I/ K6 h6 ]& {children than one would realize. Exposure to andro-
# u8 w& L' w* }% l! ogen products must be considered and specific ques-
: j+ K% {/ G% Btioning about the use of a testosterone product or
" C" [8 q: Z( @$ f; L7 h5 I- sgel should be asked of the family members during0 d# y( @# q- D# ~
the evaluation of any children who present with vir-: R! ^( o9 g- a/ g' z1 [
ilization or peripheral precocious puberty. The diag-
  s9 \7 ~0 j/ g$ o" h  h# s: hnosis can be established by just a few tests and by6 c9 O4 n/ t/ c  {0 M
appropriate history. The inability to obtain such a
/ Z( Q3 `. {- p$ d. L6 [history, or failure to ask the specific questions, may7 L% f9 P4 u7 \0 F& q# N
result in extensive, unnecessary, and expensive
$ w; i& J8 d5 ^investigation. The primary care physician should be
% r7 g$ _3 S9 s! U: h6 oaware of this fact, because most of these children
. |3 A* X; Z4 Z% T3 b/ Cmay initially present in their practice. The Physicians’0 z7 k+ c" Z4 _' g5 P0 q6 o6 w0 R
Desk Reference and package insert should also put a4 X& L3 O" t- x, {2 u* V% H
warning about the virilizing effect on a male or
% M+ ?$ l" P( Q2 r$ ]$ ]' L9 Zfemale child who might come in contact with some-
$ Q) x* L& r/ r5 C/ g3 a* r. x' Hone using any of these products.  O' U6 W9 M0 e/ i
References
- N, y4 H+ V2 M! ^" Y% W1. Styne DM. The testes: disorder of sexual differentiation
6 O1 O- {3 t1 Z! j7 M. Tand puberty in the male. In: Sperling MA, ed. Pediatric
1 P) N7 e. ?# JEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
! C1 @2 g+ g/ S4 W" s* D: M6 D2002: 565-628.9 r3 }4 y/ f9 n
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- W1 S% d% y6 ~8 O6 ^3 npuberty 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
: s: Y) v6 d2 r2 u4 }9 yBoy Induced by Indirect Topical: ]" B( O1 _) o5 ^% f
Exposure to Testosterone7 k" U" K- {3 L2 c
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 r9 f' S& `: H. S0 `: r
and Kenneth R. Rettig, MD1. e: ^- u- l2 @2 K
Clinical Pediatrics/ |  e# Z' F% a5 T; l! n/ e
Volume 46 Number 6
1 m4 z2 o+ _& \4 v- @July 2007 540-543
; S! l# s6 B2 D1 ^$ o© 2007 Sage Publications
' [' q* R7 k6 H* h# n9 ]0 g4 g10.1177/00099228062966513 M  s; [0 A4 ~& ?
http://clp.sagepub.com
. ^+ f% a( C9 }2 ]% G! Ihosted at
" z1 ~! |' H9 P9 `4 m/ Nhttp://online.sagepub.com8 [& l9 V0 U# i2 c6 n+ U" a
Precocious puberty in boys, central or peripheral,/ f6 w/ Z: z. Z$ E; Z5 S
is a significant concern for physicians. Central
  g, h$ p, J6 \* v: P# D& tprecocious puberty (CPP), which is mediated5 i3 `  g& ^! r/ U; M+ i
through the hypothalamic pituitary gonadal axis, has8 @6 d. ~; F3 S: X
a higher incidence of organic central nervous system6 z% G) R7 D# n  k
lesions in boys.1,2 Virilization in boys, as manifested
7 A6 J8 u. ^2 S# z6 U0 Rby enlargement of the penis, development of pubic- |# u! x. e" V1 M
hair, and facial acne without enlargement of testi-7 ?9 G7 h8 k# ~, g
cles, suggests peripheral or pseudopuberty.1-3 We
& ]3 A. l+ `: I* t! G( treport a 16-month-old boy who presented with the0 B  s' t3 ~6 z3 ~2 a) R. _
enlargement of the phallus and pubic hair develop-3 M! T  V8 W' l
ment without testicular enlargement, which was due! r# J& |' C: s% f* p
to the unintentional exposure to androgen gel used by4 A1 z: u, V% v8 n0 u% f
the father. The family initially concealed this infor-
: G% ~. ^9 h9 ~' T! zmation, resulting in an extensive work-up for this& |3 c8 g$ H5 G( j
child. Given the widespread and easy availability of. d6 h2 [' J1 a  T( K5 r3 n
testosterone gel and cream, we believe this is proba-7 _. D) r. T) }; o
bly more common than the rare case report in the
& R2 }# W: Y* _' v* a: N- V, dliterature.4: K8 e" a# ^8 T4 V, e- |
Patient Report6 ~2 q) O5 Z2 ^
A 16-month-old white child was referred to the
9 _/ c* t% G/ J8 P( F$ E" Nendocrine clinic by his pediatrician with the concern/ R- A5 d1 L( f2 w
of early sexual development. His mother noticed8 _# U5 @( }" Q+ y: q
light colored pubic hair development when he was' j- E" U! b8 a7 `$ W9 w
From the 1Division of Pediatric Endocrinology, 2University of
) s$ F- s* a( w# T$ l% e/ l! }. hSouth Alabama Medical Center, Mobile, Alabama.
; y7 n+ A1 _' P* n, iAddress correspondence to: Samar K. Bhowmick, MD, FACE,
+ J) \: n! X( h, X/ ^Professor of Pediatrics, University of South Alabama, College of
9 F* N$ F1 j( ]3 mMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ o, A4 k$ {1 }3 R) S  ?" \; |
e-mail: [email protected].
1 E! V, r& G; a! a: j6 {about 6 to 7 months old, which progressively became
; S: J" l6 r" f6 r! ^. @darker. She was also concerned about the enlarge-
& i( O6 m5 m- x1 C" W) ]* `& `ment of his penis and frequent erections. The child# [" n1 C1 {6 m' B
was the product of a full-term normal delivery, with
4 f# u# e$ B& U1 v/ g) k+ W. xa birth weight of 7 lb 14 oz, and birth length of) N7 \8 u. N- r9 c1 _9 Q' Q  N
20 inches. He was breast-fed throughout the first year2 Q+ D0 V  e3 D) c/ A
of life and was still receiving breast milk along with
% R( a/ K0 X( P5 k5 hsolid food. He had no hospitalizations or surgery,0 x& G( i1 b+ a1 O- v3 L1 D* }4 u
and his psychosocial and psychomotor development
, l! r* F) u; lwas age appropriate.; l! V4 M* _; {6 F) R; H
The family history was remarkable for the father,9 S. t8 J- Y( A+ I+ G
who was diagnosed with hypothyroidism at age 16,
; W- i  o+ K* v9 qwhich was treated with thyroxine. The father’s
6 r, V, ]' m. C6 |. yheight was 6 feet, and he went through a somewhat
. f6 X" u3 }  E+ e0 ~6 @( G! qearly puberty and had stopped growing by age 14.
6 {3 [! W0 |; x9 a- HThe father denied taking any other medication. The
- G8 Y  f+ v8 Jchild’s mother was in good health. Her menarche
5 X7 Z5 n+ \5 V. M9 ^: N* i9 Qwas at 11 years of age, and her height was at 5 feet
1 @- _  A+ F' ^- d0 X6 k5 inches. There was no other family history of pre-$ s" v; Y, }" B6 w# ^! _3 ]
cocious sexual development in the first-degree rela-& z" v, M. p, y0 }- d% w# a
tives. There were no siblings.6 j0 a0 `. \/ A. S
Physical Examination
5 @6 L! O8 L. Y8 k1 O8 ZThe physical examination revealed a very active,/ X# l4 p4 q% r
playful, and healthy boy. The vital signs documented3 h1 R3 J) A/ T
a blood pressure of 85/50 mm Hg, his length was2 Y/ W- ^2 g7 Q( `
90 cm (>97th percentile), and his weight was 14.4 kg
, |( \. |7 ^2 @  O- R(also >97th percentile). The observed yearly growth
- h8 F' S9 u( L/ ?- ~% r/ Cvelocity was 30 cm (12 inches). The examination of! l+ S* {0 D5 Z
the neck revealed no thyroid enlargement.
5 k5 j! u# {- `& n  uThe genitourinary examination was remarkable for
  S0 z! T/ N, p$ N! F2 e/ L  [/ Tenlargement of the penis, with a stretched length of
; `( V  B# h6 ~+ }8 cm and a width of 2 cm. The glans penis was very well# r8 Y* P3 ?/ \" a1 P) a
developed. The pubic hair was Tanner II, mostly around% y* i0 Q5 L) M& p  {5 U
5403 R5 _8 b' J- S& e0 l9 `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  e+ k% b) F+ a; t+ `( x4 ?, w- V2 ]the base of the phallus and was dark and curled. The
# n+ v6 J; A) h* Z! x: }testicular volume was prepubertal at 2 mL each.
5 l' k+ s2 b% m7 l; h6 uThe skin was moist and smooth and somewhat
/ R/ Y2 T( X- c, c, d; e4 j# r0 Xoily. No axillary hair was noted. There were no
* D8 r! }  d2 K+ Z9 zabnormal skin pigmentations or café-au-lait spots.( Y: R! q" q; l! y
Neurologic evaluation showed deep tendon reflex 2+4 U# b; m. x# d9 x9 I  o( v8 s
bilateral and symmetrical. There was no suggestion! R/ e7 I- n/ |0 k8 s3 A6 K9 M* p
of papilledema.
( m1 F0 h% w5 h4 MLaboratory Evaluation! N& s6 y( b; k- m5 y
The bone age was consistent with 28 months by
1 F" j9 U6 l1 g; C% `using the standard of Greulich and Pyle at a chrono-6 h/ `; N3 y) a( o8 @. l2 P% @
logic age of 16 months (advanced).5 Chromosomal7 R9 n! @# q5 o, ?5 Z
karyotype was 46XY. The thyroid function test
9 z  N7 }' f0 M0 y0 r: mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
, ?, F6 k0 `0 R8 M- r5 S2 u! [lating hormone level was 1.3 µIU/mL (both normal).- h5 v+ V7 u. M; x" \8 z, U: K
The concentrations of serum electrolytes, blood# W  {# B* n8 M; l' q
urea nitrogen, creatinine, and calcium all were
) Q7 N( `# j1 C  k& w) fwithin normal range for his age. The concentration
6 x/ O1 z. H! ]. l! O2 d2 @5 B, d: Pof serum 17-hydroxyprogesterone was 16 ng/dL
, D" L: |5 O4 d+ {' A$ `(normal, 3 to 90 ng/dL), androstenedione was 20
# m! w) k2 x( ?0 r5 l5 lng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 Y( a; {& [% d! a& A# S5 O) D  Rterone was 38 ng/dL (normal, 50 to 760 ng/dL),
# M) |, H6 U4 E" @" _: L8 mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to" j, ?( i. ]% R# f& W0 Q! F8 y
49ng/dL), 11-desoxycortisol (specific compound S)+ l& E7 k1 a, I
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, ^. P4 Q* c: `2 Stisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 ^* {- Q. }0 Q, q1 L  Y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 u3 K$ _; Y5 K4 u. l
and β-human chorionic gonadotropin was less than
; C' W3 e6 L  u/ m5 mIU/mL (normal <5 mIU/mL). Serum follicular$ U6 Q5 {: [, A2 i- \6 c0 o
stimulating hormone and leuteinizing hormone
* b8 ~% h3 x2 K- e. C* C+ Vconcentrations were less than 0.05 mIU/mL
' O  v+ ^) F7 A: }2 k  r(prepubertal).+ A, {3 r& o( b
The parents were notified about the laboratory
8 h$ I2 o/ b6 ~9 ~) g: M' u5 b6 K. xresults and were informed that all of the tests were
4 a( v9 [$ ^& p$ wnormal except the testosterone level was high. The
+ V: a# W7 X" tfollow-up visit was arranged within a few weeks to
: S* E5 ?8 K2 T$ ]9 P6 l/ Xobtain testicular and abdominal sonograms; how-$ f4 _+ L; v! _# f
ever, the family did not return for 4 months.( f* r. [1 n4 w9 V6 Z
Physical examination at this time revealed that the
% @' Z1 J% p6 Vchild had grown 2.5 cm in 4 months and had gained. s) q6 x. P3 y- ?" \
2 kg of weight. Physical examination remained
" K/ v6 Q; r) Punchanged. Surprisingly, the pubic hair almost com-
5 f+ {0 }% R' i9 k3 v0 L% a3 Kpletely disappeared except for a few vellous hairs at
* B& s' R! F7 \* d1 D% Gthe base of the phallus. Testicular volume was still 2
2 ^0 ?! d: A* e+ q0 v5 t* ^mL, and the size of the penis remained unchanged.
# L- h5 `$ B9 e, T" Q  k4 N3 JThe mother also said that the boy was no longer hav-# H5 `, r2 M3 {: y
ing frequent erections.7 Q3 I. G* y* M5 |0 C
Both parents were again questioned about use of+ K1 x+ A8 L& C! {5 b4 W4 H
any ointment/creams that they may have applied to+ U$ G( d  T; q/ w1 q. t4 A9 _
the child’s skin. This time the father admitted the
! `8 D! I: f) Z: y5 t9 uTopical Testosterone Exposure / Bhowmick et al 541* v, h* ~9 N! ~, p: Z4 L) l
use of testosterone gel twice daily that he was apply-
+ N; ?/ R+ s& |- B# Ring over his own shoulders, chest, and back area for
- t, T4 B: \8 j. }a year. The father also revealed he was embarrassed, m3 M1 {; v2 \
to disclose that he was using a testosterone gel pre-
0 X( P4 m* e7 c! Q2 H5 y- B0 K. d! x! y) Zscribed by his family physician for decreased libido% M9 Q* F6 g2 s1 s  W
secondary to depression.8 c! h& [( U4 s( q: d6 f
The child slept in the same bed with parents.
& ]2 `) O9 r9 T( S4 n; IThe father would hug the baby and hold him on his
7 o2 P/ m# Z, `' q7 Ychest for a considerable period of time, causing sig-7 @2 ~0 V1 |. s; J* _$ l$ I
nificant bare skin contact between baby and father.+ Y+ v  z" k% {, q+ y+ D" Z6 }
The father also admitted that after the phone call,9 A+ v: R$ F4 f  Q
when he learned the testosterone level in the baby
' a7 [* d8 A) g; r" \& Kwas high, he then read the product information
8 B/ Y  [  N4 i% B( z& opacket and concluded that it was most likely the rea-# q- j1 Y& L3 \5 t4 ?& P, ~. w5 _
son for the child’s virilization. At that time, they
2 |" D6 B1 G( |3 j. fdecided to put the baby in a separate bed, and the
7 |$ [, ~/ E/ o* vfather was not hugging him with bare skin and had2 Q* [+ B' F4 y! r) L5 I
been using protective clothing. A repeat testosterone9 [) J' U0 T& h7 L
test was ordered, but the family did not go to the2 h+ f( m5 }" |
laboratory to obtain the test.
6 b$ Y' i4 f% y& o. g% ODiscussion4 m# q3 Q# Q$ |  w1 A1 }
Precocious puberty in boys is defined as secondary
  s* L/ w( e1 P$ h- Y$ nsexual development before 9 years of age.1,4, z6 q6 `3 N& [5 E6 I9 I
Precocious puberty is termed as central (true) when
( E' w  l! \$ V; B7 S: P# eit is caused by the premature activation of hypo-
& l6 a8 {5 b2 f* W; d" Mthalamic pituitary gonadal axis. CPP is more com-& m2 o# a& `' N/ R! x
mon in girls than in boys.1,3 Most boys with CPP
9 u8 R) F8 s* D$ y; Rmay have a central nervous system lesion that is
* t* F8 d9 v( d3 [! Tresponsible for the early activation of the hypothal-
% t: O- q- h( v4 Hamic pituitary gonadal axis.1-3 Thus, greater empha-
* n1 ]' e$ [; Q9 p& fsis has been given to neuroradiologic imaging in
; z1 q% Z2 V$ n; N5 sboys with precocious puberty. In addition to viril-
. T8 t1 @% y/ Y3 c) F; G; Fization, the clinical hallmark of CPP is the symmet-
# e) a, g2 |1 w5 u" q- \rical testicular growth secondary to stimulation by
7 g9 r8 J$ F5 D8 ~) }# \gonadotropins.1,3
8 X5 b- U8 w. r) h& ^# DGonadotropin-independent peripheral preco-
* J) n6 l( d6 P" O& gcious puberty in boys also results from inappropriate+ r& ^: P  @0 W0 ?) a" D
androgenic stimulation from either endogenous or4 t0 x& r7 M: }8 @
exogenous sources, nonpituitary gonadotropin stim-' u2 C, D& t* L% N4 W
ulation, and rare activating mutations.3 Virilizing
  e; J$ A$ _: h& o$ k( @congenital adrenal hyperplasia producing excessive3 D" W4 @0 P$ P9 l1 A1 Z! C
adrenal androgens is a common cause of precocious
  y+ r! L8 ?2 C9 D3 d4 A- d3 Z$ tpuberty in boys.3,4
) {1 Z2 _% R2 ]% \( m' [' J8 t6 kThe most common form of congenital adrenal5 ?* }- E# @: H/ Z1 v* r
hyperplasia is the 21-hydroxylase enzyme deficiency.
% o: h  f$ N/ T6 oThe 11-β hydroxylase deficiency may also result in
. ?% u% r9 V. Kexcessive adrenal androgen production, and rarely,
6 E: {) ^: i: g7 t6 y! }an adrenal tumor may also cause adrenal androgen
7 e6 i  L, ]- e) ^5 Z* n8 kexcess.1,3/ I2 M$ S( v: k: E, ?  b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" N- |; s3 q+ i( Z* W" x! \542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 o5 p) ]/ B& C* E! e# V- L# U! I
A unique entity of male-limited gonadotropin-, p. J# l* J& w& n, G& |
independent precocious puberty, which is also known
& A" e# W1 ]" {4 u" t2 jas testotoxicosis, may cause precocious puberty at a8 x' L: s; b0 ^, Y) Q8 _
very young age. The physical findings in these boys
- \4 T0 I. m! \8 ?; ]( I1 P3 dwith this disorder are full pubertal development,
' D2 ^& K4 F0 N. [1 T1 d$ s& tincluding bilateral testicular growth, similar to boys
( Y0 o4 P: b% [$ x: {, R9 gwith CPP. The gonadotropin levels in this disorder& ^* V% }! o/ s. y2 s! D
are suppressed to prepubertal levels and do not show7 c0 |% I- \% ?
pubertal response of gonadotropin after gonadotropin-+ C5 l& {6 A- e7 x" N7 e
releasing hormone stimulation. This is a sex-linked7 W$ z8 J! x( b$ `  m, s5 u3 n
autosomal dominant disorder that affects only% U% d$ c6 c, X- X1 Y
males; therefore, other male members of the family
( \( Q" ~& X3 \- \2 Y' W& umay have similar precocious puberty.3
' L4 M3 q  e0 V& e8 k  AIn our patient, physical examination was incon-& b8 S- h6 i' F
sistent with true precocious puberty since his testi-, v  k! A, j' J5 p$ m
cles were prepubertal in size. However, testotoxicosis5 F" K6 V" r' F/ W7 ~' L+ @1 Y
was in the differential diagnosis because his father
; m0 {8 }. \! |2 cstarted puberty somewhat early, and occasionally,8 d+ ~  i9 ~# M# E
testicular enlargement is not that evident in the; ]! q# ?( M4 D8 S- k8 `7 F* t# k
beginning of this process.1 In the absence of a neg-. T: B  u5 G3 p; s
ative initial history of androgen exposure, our: V: s( M  I. r! O
biggest concern was virilizing adrenal hyperplasia,
! G$ K' w4 V" `: b0 A, |either 21-hydroxylase deficiency or 11-β hydroxylase, x7 u1 \1 U9 `8 ]$ x3 _: ^
deficiency. Those diagnoses were excluded by find-' K( E8 t  m; J; e" s3 ~; u
ing the normal level of adrenal steroids.
1 p! M  A4 y7 q3 E, X7 YThe diagnosis of exogenous androgens was strongly/ y, r: e! n' e% F. n8 z1 @# o
suspected in a follow-up visit after 4 months because
1 _; ^; \6 B7 h# athe physical examination revealed the complete disap-
( g" S8 d6 u3 G+ Lpearance of pubic hair, normal growth velocity, and
; S; P+ b+ j0 I6 K$ W, g' ~decreased erections. The father admitted using a testos-! ^+ g# {8 v8 Y) I5 \: q
terone gel, which he concealed at first visit. He was
( F4 P/ I7 r% b- N, t+ c9 Pusing it rather frequently, twice a day. The Physicians’! \9 w+ I' d- e* X8 g2 L
Desk Reference, or package insert of this product, gel or
9 B! @0 p& J7 g5 l* Ycream, cautions about dermal testosterone transfer to
+ m8 P) Y& o; _- G4 }unprotected females through direct skin exposure.* `7 I2 p' U! `; J* O. U, |6 q
Serum testosterone level was found to be 2 times the
3 D' _4 Z5 U" t0 T! Jbaseline value in those females who were exposed to2 h2 Q4 T, e% Y
even 15 minutes of direct skin contact with their male# T. v( B/ F2 u6 b) m+ f% _( l
partners.6 However, when a shirt covered the applica-# ~" [/ b3 j' y4 ^: {' R( m( g. [: }
tion site, this testosterone transfer was prevented.
3 `4 L; g; r% A# m' g- tOur patient’s testosterone level was 60 ng/mL,
) J  T* g' W2 ?* G2 N& Nwhich was clearly high. Some studies suggest that
0 t; q, w4 h8 b" k& B3 ?dermal conversion of testosterone to dihydrotestos-
: Y" g: S3 `8 Y" Z. g  H/ Rterone, which is a more potent metabolite, is more
; \7 j, u- u; U8 G6 z* R1 l- `active in young children exposed to testosterone7 Y: Y/ E9 t* q% V. P5 D
exogenously7; however, we did not measure a dihy-
: E2 v7 |8 T3 b1 C7 W, sdrotestosterone level in our patient. In addition to
" |: i/ `+ |$ F4 |7 U* Vvirilization, exposure to exogenous testosterone in" k3 f4 m5 u) T2 x  l# W
children results in an increase in growth velocity and5 A, \  k) g1 x  r6 c
advanced bone age, as seen in our patient.) ?& X& Z. [+ g+ j# X. V( Q6 r
The long-term effect of androgen exposure during* F- q. ?$ g5 @& \4 \
early childhood on pubertal development and final7 i( B- E8 Y$ ?# G' H- z% S+ Y
adult height are not fully known and always remain
8 K1 o) |' {! P% X9 ma concern. Children treated with short-term testos-) a: A; O# r$ p' D3 `
terone injection or topical androgen may exhibit some
' M" r$ L& V$ v1 J! oacceleration of the skeletal maturation; however, after5 ^0 [. L0 W1 m2 c0 R
cessation of treatment, the rate of bone maturation+ w9 f) z1 j7 f. V; f; K4 m# t/ x# r
decelerates and gradually returns to normal.8,9
$ B! y8 \- ~7 V* R. w7 n3 ^: cThere are conflicting reports and controversy7 [! o6 ?$ Y0 c
over the effect of early androgen exposure on adult$ ]$ ~; w( {1 [& q
penile length.10,11 Some reports suggest subnormal
* |; V8 F) a$ G8 ~adult penile length, apparently because of downreg-. a2 W9 i9 ^1 b/ h* u. t" S
ulation of androgen receptor number.10,12 However,3 a! G% H) t0 ?0 @$ j& j
Sutherland et al13 did not find a correlation between. `$ `# A4 I7 r: @" M) m
childhood testosterone exposure and reduced adult: v/ j. u( d3 V' L& Q/ r0 M' C
penile length in clinical studies.
# ^1 L! g. J/ f7 bNonetheless, we do not believe our patient is$ y! Z8 Z" C/ X& c0 Y7 O
going to experience any of the untoward effects from2 x: \& j9 E. m8 p
testosterone exposure as mentioned earlier because& q# _" F' m( y8 k9 I
the exposure was not for a prolonged period of time.' o( r+ V" u1 D' {8 }; P
Although the bone age was advanced at the time of
* G* h& ~+ Y& Q( v0 s& ]  ?$ b* mdiagnosis, the child had a normal growth velocity at) U7 J0 E5 H$ B* g$ f5 C
the follow-up visit. It is hoped that his final adult/ f) [: ^8 y# d4 f
height will not be affected.6 s9 v( k+ B8 @  d3 P, U9 B0 H( k
Although rarely reported, the widespread avail-
( Q4 ?7 x; k6 F* X9 u  M& Sability of androgen products in our society may& j0 o5 Y% v( O1 o
indeed cause more virilization in male or female) g) l& e, I; D
children than one would realize. Exposure to andro-
* f6 d5 L5 J7 C, L$ H6 P, y9 Zgen products must be considered and specific ques-
9 ~6 f! @! C+ l; }6 W1 i- e5 g+ V1 Gtioning about the use of a testosterone product or
) y9 ^2 W  p! T+ ~8 T: }% i& I, Jgel should be asked of the family members during
5 T' w! d: J, {% B) v7 lthe evaluation of any children who present with vir-- N6 W: v4 U! H3 k; {& Q( b6 G
ilization or peripheral precocious puberty. The diag-
" ^* _( g1 J& f) J1 A% l, knosis can be established by just a few tests and by6 T5 G1 @9 P: F, U
appropriate history. The inability to obtain such a
( d8 l) l' r5 X+ t& v0 Uhistory, or failure to ask the specific questions, may
0 O" B. ^0 u( ^( zresult in extensive, unnecessary, and expensive
" H! [8 f' ~. Oinvestigation. The primary care physician should be
0 ^" X8 I4 h! maware of this fact, because most of these children0 n2 s* X: I2 j0 R- V+ ~
may initially present in their practice. The Physicians’
3 P) H4 S/ n6 ?3 y& k, B: K) C' VDesk Reference and package insert should also put a
5 [: a$ y% O! ?. g9 o* W2 Qwarning about the virilizing effect on a male or, T& q2 H( {9 A3 N9 \. [
female child who might come in contact with some-) z- `( M( P* y4 I; N' a
one using any of these products.
( C- |- O* J0 q. o$ y; I4 rReferences
7 u! F8 e' Q% D5 b' i1. Styne DM. The testes: disorder of sexual differentiation
6 s  @" h- j. G! j0 y$ I2 C9 e/ Land puberty in the male. In: Sperling MA, ed. Pediatric
$ `0 a" o. U: V4 t& a$ a. T: sEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 v# }# _$ M) w& j! {$ z+ a2 A
2002: 565-628.
" ~0 U8 \0 C2 g# \- D2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 d/ x& B! `& u4 r
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
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

& g, I* q3 u, B. a, E# e/ E2 f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