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* d4 h6 k2 k8 U5 P. B' j
Boy Induced by Indirect Topical$ w3 K7 j( R9 V: A3 H
Exposure to Testosterone& ?; ?/ Z! X0 ~: d  z; j- j
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: q2 p8 }  f2 `( a8 V' Z8 y
and Kenneth R. Rettig, MD1
! M2 |- Z1 R( ]2 g  J1 O7 T  GClinical Pediatrics+ |6 @1 c# [6 G; V$ k
Volume 46 Number 6
- ~1 r3 R% U& @4 z: qJuly 2007 540-543
9 M0 h/ |+ H1 G/ `% l© 2007 Sage Publications
2 E4 H7 x6 W; r0 |+ F+ O2 s' ~10.1177/0009922806296651" S2 b  D+ O  c8 B3 N
http://clp.sagepub.com$ e8 f5 p* b( T6 u( c6 Y
hosted at8 V2 N6 z9 a. q6 ~0 S7 ]/ |5 I% |7 V
http://online.sagepub.com! x" o% M- `, o$ r/ d
Precocious puberty in boys, central or peripheral,& W! @9 O* D* V5 x+ G& g5 I3 c( ?
is a significant concern for physicians. Central
0 _( |$ X2 p& X5 }- lprecocious puberty (CPP), which is mediated
2 a9 j7 D  J0 t' m& |1 Qthrough the hypothalamic pituitary gonadal axis, has
3 l$ X) |% d" ?a higher incidence of organic central nervous system9 K. c" @7 S1 g3 S1 k
lesions in boys.1,2 Virilization in boys, as manifested+ W6 u4 l# C1 x- T2 Y
by enlargement of the penis, development of pubic
5 Q2 r* p0 T- ~% Whair, and facial acne without enlargement of testi-+ j" B4 a/ S' U
cles, suggests peripheral or pseudopuberty.1-3 We6 c3 _3 S- Z- Z# U2 A
report a 16-month-old boy who presented with the' A7 D* ?, h: R- U# E& Y
enlargement of the phallus and pubic hair develop-
3 y# u+ [. A! u6 r$ ement without testicular enlargement, which was due
: W, C1 y9 t# ~* r% j# K4 M4 f6 v( Mto the unintentional exposure to androgen gel used by
: a! W2 P! y4 @  J( H2 Lthe father. The family initially concealed this infor-
' ~/ ^, C. d( {) I  c. Vmation, resulting in an extensive work-up for this
. c5 p3 ^5 ?$ k. I8 v6 ]child. Given the widespread and easy availability of4 s8 S& a+ |* B, J! i2 F
testosterone gel and cream, we believe this is proba-$ b# @, G6 l, m, k- \. X, v2 ]
bly more common than the rare case report in the  w% t" k" {& z( p+ {
literature.4) w# L& d8 x$ i# c5 p1 I1 }/ \
Patient Report
: ]" p  t. E, S1 I0 X$ x" uA 16-month-old white child was referred to the. H" W- n, @( I; f& K
endocrine clinic by his pediatrician with the concern  N: c5 J/ o  Y6 L0 u% x: R
of early sexual development. His mother noticed5 P" ?) ^2 y0 }" d  V
light colored pubic hair development when he was
# i& q# r7 B6 d0 a# n* ^From the 1Division of Pediatric Endocrinology, 2University of" I) S6 x8 a7 a# c2 X+ ]
South Alabama Medical Center, Mobile, Alabama.% }) Q8 W! t; o
Address correspondence to: Samar K. Bhowmick, MD, FACE,
: o& O4 T, ]+ k, KProfessor of Pediatrics, University of South Alabama, College of
. t8 I. u: e) l4 k: D4 _Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 F) i& d8 _' b% V1 o5 he-mail: [email protected].
7 _+ K. ?, _+ H; pabout 6 to 7 months old, which progressively became
" |; G/ G: d8 Q/ v' Ldarker. She was also concerned about the enlarge-
; M- _. p+ h. }( jment of his penis and frequent erections. The child
3 ?  c( ?1 l1 q2 Q+ E7 `was the product of a full-term normal delivery, with
+ J/ A+ M0 j! i5 i$ J, m! ^a birth weight of 7 lb 14 oz, and birth length of
/ h+ t" _4 n  A! L" b& W% ~& Y& f4 A20 inches. He was breast-fed throughout the first year
8 B) q3 Y9 ^) n8 _( nof life and was still receiving breast milk along with
- z  k: ^( }! |solid food. He had no hospitalizations or surgery,
$ M0 M6 T2 O0 iand his psychosocial and psychomotor development4 F2 W' P  S) ?# E' N
was age appropriate.
, @. [7 y  z! W9 q4 y/ f8 ^4 eThe family history was remarkable for the father,0 V2 t# y7 Y1 A
who was diagnosed with hypothyroidism at age 16,
8 E0 _% _5 ^- G1 ]/ J$ Pwhich was treated with thyroxine. The father’s
$ F3 B% j9 O2 qheight was 6 feet, and he went through a somewhat7 H* o/ n& C1 e6 q" I0 U
early puberty and had stopped growing by age 14.
" T3 r. G2 M  S+ @! i) FThe father denied taking any other medication. The
4 o$ [! |0 a: R' Gchild’s mother was in good health. Her menarche( s7 J9 O6 S- H- g: @7 N- @5 n) s
was at 11 years of age, and her height was at 5 feet
( M3 ]; r3 Q/ x5 C* A0 `6 w1 z5 inches. There was no other family history of pre-0 x  x  x- e; g. U; s0 W
cocious sexual development in the first-degree rela-
0 y) U3 e" n' @8 {2 }5 s! Ctives. There were no siblings.
1 b4 H* |  M9 i$ J, O5 A. y# n( |Physical Examination; M" u3 w9 l5 z
The physical examination revealed a very active,
( s0 k, j- V8 O7 B- _  |playful, and healthy boy. The vital signs documented9 ~, C) w9 K( d$ }, T# @6 M8 b, C
a blood pressure of 85/50 mm Hg, his length was0 e. N/ N  X+ w& L; [& R4 m
90 cm (>97th percentile), and his weight was 14.4 kg
3 F) ~  U; d" t4 L! d(also >97th percentile). The observed yearly growth
+ O- y! g% B; u& y3 W8 {- P* bvelocity was 30 cm (12 inches). The examination of! ]2 o: ~. h. P, p) K
the neck revealed no thyroid enlargement.. T! S) Q1 @6 Z  ~' m
The genitourinary examination was remarkable for
* ~  A% h+ S9 r" d; G/ |+ Benlargement of the penis, with a stretched length of
8 i0 r! K- H' i5 P$ k8 cm and a width of 2 cm. The glans penis was very well
2 i: [% i9 a- n9 Tdeveloped. The pubic hair was Tanner II, mostly around
, m7 H% w: }& O5 v% @! K: S5405 }. V7 `! |. a% d" Q) e* l$ m
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 v9 I; [' i- o6 o
the base of the phallus and was dark and curled. The
1 H9 _6 n$ |  y6 ktesticular volume was prepubertal at 2 mL each.5 z0 ~$ V4 \' L0 W3 Y3 v9 T5 X
The skin was moist and smooth and somewhat3 K5 X% q' i; E" G( p
oily. No axillary hair was noted. There were no- V0 i) b; {2 {/ `
abnormal skin pigmentations or café-au-lait spots.
) @2 D+ B$ F5 w  v/ O+ V$ lNeurologic evaluation showed deep tendon reflex 2+  X# m2 I, a* ]. s! x
bilateral and symmetrical. There was no suggestion8 u" [- d# Q0 b- i$ _4 ^' T
of papilledema.
* g/ y: {2 i5 G+ y) T* x2 L+ `Laboratory Evaluation
" A% l/ ^+ i7 d6 ]The bone age was consistent with 28 months by
( y: ]& h6 l) L) V- X3 Uusing the standard of Greulich and Pyle at a chrono-
$ K% [: m; S6 A5 V9 Vlogic age of 16 months (advanced).5 Chromosomal
% n8 O; I! u: w- vkaryotype was 46XY. The thyroid function test
" V. J+ m: @( f+ d; ?  @showed a free T4 of 1.69 ng/dL, and thyroid stimu-
% f: l7 ^" J8 w( p1 A/ Dlating hormone level was 1.3 µIU/mL (both normal).
. R% a3 a7 E+ IThe concentrations of serum electrolytes, blood
7 I  O7 A' k7 Y: r2 p# u3 j. p5 Xurea nitrogen, creatinine, and calcium all were
5 m- U9 v9 J) j/ xwithin normal range for his age. The concentration0 p: L' v  h9 [- W3 F
of serum 17-hydroxyprogesterone was 16 ng/dL% s. }* p7 z" H' \% k
(normal, 3 to 90 ng/dL), androstenedione was 20  o: Z( Z7 E8 m! p9 j
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 h, C/ U* |- I' _/ _9 [& X- zterone was 38 ng/dL (normal, 50 to 760 ng/dL),; {. L. N1 f9 h) I- ^
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
% e0 F1 |( j. x% _49ng/dL), 11-desoxycortisol (specific compound S)7 y+ E7 F4 S3 g5 G3 @  c
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# O  B3 G6 ~4 @& i( N8 \
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* x1 P+ V0 H1 R) B) i
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; o; [2 Y: G1 Xand β-human chorionic gonadotropin was less than" z' B8 o6 B4 U( B; M' n
5 mIU/mL (normal <5 mIU/mL). Serum follicular
% l. l/ Z  g$ Q& ~3 P7 O; |0 lstimulating hormone and leuteinizing hormone
6 I$ v2 h/ A3 I! S+ r" [6 O6 j: ]concentrations were less than 0.05 mIU/mL' u6 V  L* X5 P# H# f1 S
(prepubertal).
3 T7 \& T+ t& Y) _% iThe parents were notified about the laboratory! {' j' c, Y  y
results and were informed that all of the tests were2 l+ T0 Z" D8 g' w) z+ d  {% y9 R0 Z
normal except the testosterone level was high. The
, G- B4 g9 E7 w; }* Z" S4 ofollow-up visit was arranged within a few weeks to+ e2 ?+ V8 M. s3 V
obtain testicular and abdominal sonograms; how-, n/ ^; `6 @0 U0 X( A& `
ever, the family did not return for 4 months.; e$ r7 w% y8 j$ |
Physical examination at this time revealed that the$ @* k  E7 u( _# A1 w: J
child had grown 2.5 cm in 4 months and had gained
6 ?+ X/ P$ ^# k0 T" k  x2 kg of weight. Physical examination remained. F, Z& [/ @) o3 c+ ?0 X' `
unchanged. Surprisingly, the pubic hair almost com-# y1 P  p3 K! u, G; w
pletely disappeared except for a few vellous hairs at
4 W* t8 q3 D% g2 r: s: y7 ethe base of the phallus. Testicular volume was still 2
, }8 q4 J5 F& R6 F$ Z+ m" TmL, and the size of the penis remained unchanged.2 O9 Y5 D4 k2 |$ X* v" e
The mother also said that the boy was no longer hav-$ T/ @& C2 C8 Q& _/ B+ Z9 P
ing frequent erections.; X2 t6 K  u& @, F' E
Both parents were again questioned about use of
) q  R1 U% Z( Tany ointment/creams that they may have applied to
1 k- l( ?5 Q* X- o, P4 Ythe child’s skin. This time the father admitted the
3 a0 d' J( `. G' g' ^# kTopical Testosterone Exposure / Bhowmick et al 541
7 m/ v" {  X1 @' z& _* Fuse of testosterone gel twice daily that he was apply-
2 [* W% w- F8 ^5 E# ]% c" Ying over his own shoulders, chest, and back area for
: G1 u# H8 _0 U1 Ja year. The father also revealed he was embarrassed3 e/ F* T! i3 \# T2 o3 \
to disclose that he was using a testosterone gel pre-) O' |3 E5 h$ w2 T% D, `2 f" \
scribed by his family physician for decreased libido  _7 b5 T, y& A! {5 N: @1 R
secondary to depression.- j. J" Y: ?# t  o  H, q
The child slept in the same bed with parents.' {& e3 k& a+ b4 E. H
The father would hug the baby and hold him on his
" h" ]/ t' p) s5 B8 Hchest for a considerable period of time, causing sig-
0 S3 j) l, {5 znificant bare skin contact between baby and father.6 d- _( M6 ~7 U5 F" _0 `
The father also admitted that after the phone call,: B; r9 @( ?2 g, n6 F
when he learned the testosterone level in the baby4 E3 t" {% [; `4 a5 E, g, M
was high, he then read the product information
# U4 @/ |" A6 r* ~9 Z& ?$ E) Spacket and concluded that it was most likely the rea-
! R* {8 a9 f* Q, w% c& Z- yson for the child’s virilization. At that time, they- \& j: l) K2 d1 M, s; d
decided to put the baby in a separate bed, and the
: Q: c6 _) D5 }9 i4 ]* Afather was not hugging him with bare skin and had
. y, t, e, ]" Ibeen using protective clothing. A repeat testosterone) \. r0 M# T7 @, O5 ?- a  A
test was ordered, but the family did not go to the0 ^) E% W) A/ B8 j/ x
laboratory to obtain the test.
' |& P% L& Y( S( @! vDiscussion
8 c' x$ q) ~3 u1 D( N9 J( zPrecocious puberty in boys is defined as secondary
! q3 [2 y# ?) isexual development before 9 years of age.1,4
" v" ?1 f/ m6 ^( QPrecocious puberty is termed as central (true) when
0 }, Y3 a  y% @it is caused by the premature activation of hypo-4 h5 B6 v5 O$ F. a/ b( h
thalamic pituitary gonadal axis. CPP is more com-
! A0 C" o- p* G6 d& q4 w+ a8 h6 S8 Wmon in girls than in boys.1,3 Most boys with CPP
9 H; k5 q/ O% Smay have a central nervous system lesion that is
( Y" T' x5 H( r( X8 yresponsible for the early activation of the hypothal-
! R1 [+ F4 F  s5 ~& E6 vamic pituitary gonadal axis.1-3 Thus, greater empha-
, H, p  |; Y  S( ^sis has been given to neuroradiologic imaging in% G1 E( H0 X6 L6 x/ ^, ~
boys with precocious puberty. In addition to viril-& X% c* J1 L3 Y) [
ization, the clinical hallmark of CPP is the symmet-
% ?$ k5 k! p: o0 `rical testicular growth secondary to stimulation by% \4 J: |, _. M, n
gonadotropins.1,3/ ?+ s4 k7 ^4 N9 H, q. a
Gonadotropin-independent peripheral preco-
* U# g; h/ ]* Y$ k) M5 _0 jcious puberty in boys also results from inappropriate
* H  v; l8 O6 U5 g/ i6 V# S0 ?androgenic stimulation from either endogenous or2 t; d4 l8 q% \" G( Q/ `3 J
exogenous sources, nonpituitary gonadotropin stim-- u1 U2 I9 @2 R" C+ Y  a8 p  _5 f
ulation, and rare activating mutations.3 Virilizing
2 k  m9 X. k6 |1 X. k$ `congenital adrenal hyperplasia producing excessive$ ]0 ]2 q! ?7 c( j6 Y* @3 v: T
adrenal androgens is a common cause of precocious! h2 n* [+ \% h1 f: @" X+ R$ }. m( Q
puberty in boys.3,48 J+ f0 V% R5 d6 g' S' x) a
The most common form of congenital adrenal
8 d2 U* e2 O5 G" m' u0 s- Xhyperplasia is the 21-hydroxylase enzyme deficiency.
7 F& b7 U: U1 |! w* g" U+ AThe 11-β hydroxylase deficiency may also result in" @3 X9 Y$ f, V3 J, k1 N  O, F, w  }
excessive adrenal androgen production, and rarely,/ l4 o3 h  l4 U% t
an adrenal tumor may also cause adrenal androgen
+ ~$ ~" J- w" Z) j$ j# P( x5 bexcess.1,3
9 e* I. `/ h; o1 O. v# N" Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* y! \+ L1 `+ ~$ f6 i& d* [" k! r
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, V0 ~: M; z- {A unique entity of male-limited gonadotropin-
& e# c' t. I1 bindependent precocious puberty, which is also known
/ |0 m* z' e! \3 Q5 w) Das testotoxicosis, may cause precocious puberty at a
4 d9 z) s$ @4 [* }4 U$ vvery young age. The physical findings in these boys; a4 U0 N4 B: n( W: h2 m
with this disorder are full pubertal development,. z8 k/ Z* o0 k+ b
including bilateral testicular growth, similar to boys
4 b1 P; g9 a! O5 Twith CPP. The gonadotropin levels in this disorder
5 I$ A- `0 ?& }3 z" ]are suppressed to prepubertal levels and do not show
: _. u! [+ C" K9 H& d# X* ]3 }pubertal response of gonadotropin after gonadotropin-
! _2 B% l% t  g) }; A" D: \9 \releasing hormone stimulation. This is a sex-linked
6 M8 _) X5 _9 W' x9 }autosomal dominant disorder that affects only8 H* K4 ^- o' a: c, {
males; therefore, other male members of the family  h; p8 z4 L+ l
may have similar precocious puberty.3
" F0 E! }# R0 J) D( l! bIn our patient, physical examination was incon-
7 j* E8 W& |) U0 R* Rsistent with true precocious puberty since his testi-
- f" [$ P/ c% t: [8 |cles were prepubertal in size. However, testotoxicosis8 n% O, o' d/ Q
was in the differential diagnosis because his father
! t8 d. {$ o5 ?: m1 F% ^started puberty somewhat early, and occasionally,
1 P# o( ?7 o! g: \testicular enlargement is not that evident in the
4 X+ `) z' O4 o5 n$ r0 k0 jbeginning of this process.1 In the absence of a neg-, _- }) \7 g* U- K# \7 a0 L
ative initial history of androgen exposure, our
* j+ [4 u% {- R" ybiggest concern was virilizing adrenal hyperplasia,# ?: r8 x& {& E* E- c8 Q2 T
either 21-hydroxylase deficiency or 11-β hydroxylase
- f, d/ t. F0 Q% s- C2 zdeficiency. Those diagnoses were excluded by find-7 V- A: p9 u0 I: ^  d) |
ing the normal level of adrenal steroids.
3 ^7 l% d, v2 YThe diagnosis of exogenous androgens was strongly
" ]: s8 p* x% d5 N" wsuspected in a follow-up visit after 4 months because
0 \% C5 Z2 _$ K. r5 {; ethe physical examination revealed the complete disap-: q+ m6 n. v1 g! t1 t
pearance of pubic hair, normal growth velocity, and5 ?; Q2 K& {, ^* Z% U0 d# o, K
decreased erections. The father admitted using a testos-
$ L7 m  X9 O0 Z  o  K7 t! {  I$ rterone gel, which he concealed at first visit. He was% N! }$ Y0 ^. e9 n0 A
using it rather frequently, twice a day. The Physicians’& E6 b3 z/ w/ T
Desk Reference, or package insert of this product, gel or$ U( a  g; G" _7 o
cream, cautions about dermal testosterone transfer to
  `+ U/ \7 S( [4 r/ `1 q7 D) Ounprotected females through direct skin exposure.2 m7 y+ R: P+ K
Serum testosterone level was found to be 2 times the7 v3 N9 F; Z# V0 X5 w
baseline value in those females who were exposed to
4 ]  K1 ~) T$ L; x: [$ x6 Jeven 15 minutes of direct skin contact with their male/ }& k1 `; E* O/ A' d3 s
partners.6 However, when a shirt covered the applica-
  s* Y# x! X& ztion site, this testosterone transfer was prevented., ^) h4 B. L' d
Our patient’s testosterone level was 60 ng/mL,& S# h2 d) v& q- M$ K$ L8 D; A  [3 x
which was clearly high. Some studies suggest that  j( A4 |$ U: t, Q- W; ]+ s
dermal conversion of testosterone to dihydrotestos-) B7 l; k$ P" s3 l
terone, which is a more potent metabolite, is more
0 A4 r) J/ @1 q8 o) i+ [; {1 gactive in young children exposed to testosterone
$ q5 F& v7 H6 F$ aexogenously7; however, we did not measure a dihy-/ @. T) @" y! Z: z8 Y, j
drotestosterone level in our patient. In addition to
% a9 U5 x& [4 ?7 P1 Yvirilization, exposure to exogenous testosterone in
1 T" k9 e) Y5 N* G3 o$ vchildren results in an increase in growth velocity and8 l4 o% d% e  a# u
advanced bone age, as seen in our patient.
2 f0 ]7 @# N0 e* HThe long-term effect of androgen exposure during
; C( A' a9 k% h1 r1 jearly childhood on pubertal development and final) S5 h( ~3 A2 j5 A. P0 z
adult height are not fully known and always remain
5 S8 g9 w/ B- l8 t( l/ X( `a concern. Children treated with short-term testos-
+ o2 V+ X6 ]. n4 J) zterone injection or topical androgen may exhibit some: J, V5 J8 f/ g! @7 D
acceleration of the skeletal maturation; however, after+ ]0 I5 s: d4 P' u" @6 E
cessation of treatment, the rate of bone maturation: S% t7 M" y; G7 d
decelerates and gradually returns to normal.8,9( ~, F7 ^! c9 e
There are conflicting reports and controversy
# C1 e0 P: N' F* \over the effect of early androgen exposure on adult& O/ d  v) Z/ m( g
penile length.10,11 Some reports suggest subnormal
! q8 ^0 N! e& e6 _* S" Fadult penile length, apparently because of downreg-$ ?; f: P6 q7 F9 d
ulation of androgen receptor number.10,12 However,
) G( {! v0 [' |Sutherland et al13 did not find a correlation between4 t7 A0 X9 d* I! d" H
childhood testosterone exposure and reduced adult
* e3 m( N  v0 C  P' `penile length in clinical studies.- D- B5 n% _/ [) ?4 Q
Nonetheless, we do not believe our patient is
  i( y8 l. [: ^8 j* X' Mgoing to experience any of the untoward effects from5 L" Q/ C, E2 Z( F! W1 o2 t0 z* ^9 I
testosterone exposure as mentioned earlier because2 S! f* h3 C) a8 w2 B
the exposure was not for a prolonged period of time.5 r8 m0 n6 R% C5 p7 a$ Z
Although the bone age was advanced at the time of
2 _4 ]* c4 c& @! Z1 I% [; Ediagnosis, the child had a normal growth velocity at5 {4 o! p: t4 o/ }4 V" O# c
the follow-up visit. It is hoped that his final adult
& w7 L7 G+ |) K3 vheight will not be affected.4 S" ^4 r2 w/ `- V
Although rarely reported, the widespread avail-
( F. x* b) w1 Z/ v# cability of androgen products in our society may
7 S* S) i/ e* |' E, E) a1 `. O9 cindeed cause more virilization in male or female7 m3 i$ |1 x5 ]1 T- j
children than one would realize. Exposure to andro-+ W, y6 M  \( P( I" p8 C
gen products must be considered and specific ques-& ?3 E" O0 b  t4 `2 G# \0 H
tioning about the use of a testosterone product or' N: v5 n2 F1 F4 N6 v0 A( d
gel should be asked of the family members during
" L- m' j$ x$ U+ }! Hthe evaluation of any children who present with vir-0 N5 H" S! L, N; G5 P, v1 T" k: D
ilization or peripheral precocious puberty. The diag-
8 p6 O7 i4 G& P, S" x0 ?nosis can be established by just a few tests and by
  |3 n7 q& U0 G4 O$ p: q4 J" Gappropriate history. The inability to obtain such a
/ u. m  n; C) ?! C1 zhistory, or failure to ask the specific questions, may
/ q( e" z2 g  Hresult in extensive, unnecessary, and expensive
2 p$ `5 w' i" s5 I. o3 c3 X8 finvestigation. The primary care physician should be. b8 |+ _1 H: [
aware of this fact, because most of these children; q! a0 k& D% Y- a1 F$ v
may initially present in their practice. The Physicians’. x# q# C$ ]' h+ F
Desk Reference and package insert should also put a5 x; z" J( @8 F0 L( b, z, g) m
warning about the virilizing effect on a male or! a  Z9 l, ?4 l2 t
female child who might come in contact with some-
; s4 e3 O6 Q6 Z5 ~7 cone using any of these products.' y% t8 w$ J: K7 R, _
References' m/ X3 \& i$ ^: I$ ^2 g, \8 f% U
1. Styne DM. The testes: disorder of sexual differentiation9 c( G7 @' c+ z2 k* j+ p
and puberty in the male. In: Sperling MA, ed. Pediatric
6 z) {/ s5 @, [4 k# ~2 z4 JEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. c, T6 J. N9 N% R; }
2002: 565-628.
$ g( e- C$ z  z) O, e5 z% u2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  X8 l1 a$ W- l* X& k  t; B: B
puberty 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
! b; x2 o* }! f, e0 }Boy Induced by Indirect Topical
" h# s; i; ^7 A+ UExposure to Testosterone
$ J' S1 b7 ]: c0 U3 }- ?; t; ASamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
3 _' m% ~* i* N/ Fand Kenneth R. Rettig, MD1
* m  K& Q$ S. c6 }$ \Clinical Pediatrics' v5 T1 o+ B' i, s& i
Volume 46 Number 6
' l4 g" t! S# n+ Y: T8 X% I0 ^July 2007 540-543
0 P2 H4 h. U: x© 2007 Sage Publications& V; \% W) Y/ }& W0 C0 F/ v
10.1177/00099228062966511 K" m/ t8 S, K( T3 ?
http://clp.sagepub.com
: b7 _1 l3 X+ N7 F$ k1 T* k# ahosted at
% m1 I1 z: b1 N& m- ghttp://online.sagepub.com
: Q' i" q" G8 x% Y% BPrecocious puberty in boys, central or peripheral," h# i% v' T, o) x; i
is a significant concern for physicians. Central7 v" p* S5 o$ X0 x7 `  p8 m3 x3 P
precocious puberty (CPP), which is mediated! I) p7 O  Q7 G7 W* P; E5 B
through the hypothalamic pituitary gonadal axis, has
- o" T/ v8 i7 Q5 I3 F$ }$ h  ka higher incidence of organic central nervous system
8 ~" m6 u$ B! ]' a/ u+ F- ylesions in boys.1,2 Virilization in boys, as manifested5 }9 j" B  M+ n
by enlargement of the penis, development of pubic
; z" X$ O* J: h) l+ }" w# @hair, and facial acne without enlargement of testi-: q( w$ k* Z) I
cles, suggests peripheral or pseudopuberty.1-3 We
9 g+ n& ~- m4 D& _) |" X! kreport a 16-month-old boy who presented with the
  z0 J9 [" G# Q2 Senlargement of the phallus and pubic hair develop-
2 `6 a3 P, Y# T9 E! F. Yment without testicular enlargement, which was due$ p0 Q7 s0 Y3 w7 f( d1 A( m
to the unintentional exposure to androgen gel used by+ g0 N% [2 E! R+ v* ~  K
the father. The family initially concealed this infor-& U& N  e# b* `
mation, resulting in an extensive work-up for this" n& h, y* f* c
child. Given the widespread and easy availability of
* ?' c$ |# [0 J& e* q+ ctestosterone gel and cream, we believe this is proba-
2 g3 @' _% {6 r/ b8 X" Fbly more common than the rare case report in the
# y# ^5 W+ m6 Z2 Yliterature.45 A  C  H  x, |$ i
Patient Report
. \. E8 A1 z' D2 G6 J4 ?A 16-month-old white child was referred to the- Y& u8 L1 r' X- O
endocrine clinic by his pediatrician with the concern  e+ z+ q3 Q7 R
of early sexual development. His mother noticed2 _) l( E8 c4 [( _- A0 u
light colored pubic hair development when he was! S/ m8 |7 M8 }4 A
From the 1Division of Pediatric Endocrinology, 2University of
7 Z( A4 x, ~$ D% v1 W' CSouth Alabama Medical Center, Mobile, Alabama.
8 q6 r# e) }; \; C# a& A% yAddress correspondence to: Samar K. Bhowmick, MD, FACE,1 ]! D) Z0 Y" x. l/ ]7 V* w
Professor of Pediatrics, University of South Alabama, College of
2 s3 H& D# r! i4 DMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! O  m+ y" \* s$ [4 {1 V7 [- V$ pe-mail: [email protected].
' {% P% S: Q! }7 S' J$ L9 _about 6 to 7 months old, which progressively became
6 O& x  I- ^7 F+ Cdarker. She was also concerned about the enlarge-. E) C" g7 J' \  E3 G0 K
ment of his penis and frequent erections. The child  I% o8 _5 q/ a& H% D2 S( W
was the product of a full-term normal delivery, with
- q4 h% k* I' O2 ^7 o% Qa birth weight of 7 lb 14 oz, and birth length of
7 A( e3 [% N1 K7 I: n. c20 inches. He was breast-fed throughout the first year( b9 V6 q/ A( M
of life and was still receiving breast milk along with2 F7 [6 {. G7 b5 o' \' ]4 h& J
solid food. He had no hospitalizations or surgery,
6 m! e) a) I" u  i1 Yand his psychosocial and psychomotor development9 Q; `, N- I) o+ F+ J' S' b9 V
was age appropriate.
6 e2 _2 U& M8 d  GThe family history was remarkable for the father,
8 u2 K3 h) v% `  R( \1 awho was diagnosed with hypothyroidism at age 16,) w% r1 z" f  A6 w) Y3 o
which was treated with thyroxine. The father’s
: n) u9 S9 H3 g* j0 jheight was 6 feet, and he went through a somewhat
8 g0 \7 P/ f/ T1 Y! \3 bearly puberty and had stopped growing by age 14.
4 m$ l1 y9 T: L5 E/ dThe father denied taking any other medication. The# ?' @7 B7 S! p: d
child’s mother was in good health. Her menarche
% s' V- X! @9 |2 v# _* cwas at 11 years of age, and her height was at 5 feet4 O' B3 ~, Q! E- V* e" o7 r
5 inches. There was no other family history of pre-, Q. o8 E; [' P, r+ \2 [
cocious sexual development in the first-degree rela-
# Q) k! `- ^3 O& M# H+ r8 f% |; jtives. There were no siblings.* e% {$ R. W$ I( b0 m5 B, F
Physical Examination8 K7 i" U. V4 s5 Z
The physical examination revealed a very active,$ d1 g3 \6 E7 u/ U  n! G1 E6 u
playful, and healthy boy. The vital signs documented
, D4 L( r: M* Y. p" \1 B! ]: \7 ia blood pressure of 85/50 mm Hg, his length was3 V; b; o7 R% u/ ?! C. W3 f
90 cm (>97th percentile), and his weight was 14.4 kg
3 O2 Z; h- [8 b% J- `(also >97th percentile). The observed yearly growth
1 d) o/ k( F$ pvelocity was 30 cm (12 inches). The examination of
0 ^0 @: @& I5 Dthe neck revealed no thyroid enlargement.! q3 N5 w7 ^! I8 l9 Y- H# [, z
The genitourinary examination was remarkable for: A% u2 [( d) \9 p( r; A! T
enlargement of the penis, with a stretched length of
" Q! k/ e: r8 p. C/ _+ r/ d5 T8 cm and a width of 2 cm. The glans penis was very well
+ U2 w$ e; n5 l( }/ |1 Z$ B7 J2 u2 edeveloped. The pubic hair was Tanner II, mostly around# n, Q/ j/ p1 b/ v) b4 C# a2 {& D$ h: i
540) F. F* s" G) O* K  k; `* }& ?8 `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) A+ Z* h* ~8 N( n! O% |the base of the phallus and was dark and curled. The. W0 v* p. O8 u: _
testicular volume was prepubertal at 2 mL each.
$ \& l7 D) F( k1 h5 ]- kThe skin was moist and smooth and somewhat
7 M% `. Q8 j0 N' x, toily. No axillary hair was noted. There were no" Q& ?( F5 n$ y. T
abnormal skin pigmentations or café-au-lait spots.: S& y$ h5 U7 `. B5 F& l6 a
Neurologic evaluation showed deep tendon reflex 2+
4 E  p# k4 a4 a1 F' T& Nbilateral and symmetrical. There was no suggestion
. j' a* ~. V- F- j) _( qof papilledema.
% X$ z; |( R7 i& H" |) U1 j1 q) \# HLaboratory Evaluation
6 d' g% b, @5 Y6 {1 \The bone age was consistent with 28 months by3 s* u% F+ ~" P% o% n3 y
using the standard of Greulich and Pyle at a chrono-
9 V: J3 {/ M) Blogic age of 16 months (advanced).5 Chromosomal3 b$ \8 c3 p9 N4 ~  b
karyotype was 46XY. The thyroid function test$ s$ L9 ^+ ?7 y9 q
showed a free T4 of 1.69 ng/dL, and thyroid stimu-$ P. p! |) t, j3 H; |
lating hormone level was 1.3 µIU/mL (both normal).7 {7 z, Y$ u$ m
The concentrations of serum electrolytes, blood# K9 {+ x. u  V( F; r0 C
urea nitrogen, creatinine, and calcium all were
3 ?" d" X1 `8 V1 I( Y! }" dwithin normal range for his age. The concentration
) F8 ~: {& X* ~: \% _& sof serum 17-hydroxyprogesterone was 16 ng/dL
. Y" d7 P2 Z* g% b(normal, 3 to 90 ng/dL), androstenedione was 20# @, ~* l8 k8 T* k1 h. m
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 p+ {5 X5 U9 s6 n' p" e* |, fterone was 38 ng/dL (normal, 50 to 760 ng/dL),. D  s" T, P9 [, g3 ~- s6 _
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
9 ~2 S1 J1 X& p( X7 M; P- n: T3 v49ng/dL), 11-desoxycortisol (specific compound S)+ ~! z. v6 G/ {: B
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# W5 l  c6 h. a4 D8 N
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 r/ m& H& l+ H1 G
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),) X* v$ p2 u0 b0 {0 H
and β-human chorionic gonadotropin was less than
" f% z7 B% o" i' L. U- H5 mIU/mL (normal <5 mIU/mL). Serum follicular
! N$ }8 X+ c- G! H3 e6 Gstimulating hormone and leuteinizing hormone' p$ w2 I. Y) ^5 k
concentrations were less than 0.05 mIU/mL, T0 g! T+ X* q6 x* y
(prepubertal).! m; p' n0 G$ o* ?0 E
The parents were notified about the laboratory
7 ~+ e$ f5 G: ~. Wresults and were informed that all of the tests were7 G  s" {5 D( ]6 `
normal except the testosterone level was high. The( h6 X6 }; q$ r. O0 L
follow-up visit was arranged within a few weeks to+ z  x; o* h8 W- r% K
obtain testicular and abdominal sonograms; how-8 t/ ~; D" d8 I
ever, the family did not return for 4 months.
. ]- u& v  C- r* i, h1 O* VPhysical examination at this time revealed that the3 ~* b; T1 l! M" L* |0 L
child had grown 2.5 cm in 4 months and had gained- h' x1 G* g* W. u& H; v: W3 r
2 kg of weight. Physical examination remained, D* w0 k: @, h' \
unchanged. Surprisingly, the pubic hair almost com-$ H# g3 U8 E  n- F: f7 Q) ~
pletely disappeared except for a few vellous hairs at" ^1 @" Y+ n3 H2 V4 ^
the base of the phallus. Testicular volume was still 2
+ O8 j0 r8 _9 k  q7 l2 O2 ~mL, and the size of the penis remained unchanged.' K' u) F: B$ o) x" C9 W
The mother also said that the boy was no longer hav-0 y4 H" M: R7 G1 f  f; b
ing frequent erections.& y" q, Z/ h' r6 i
Both parents were again questioned about use of& l& P0 D8 w5 ^& N0 y; g2 U
any ointment/creams that they may have applied to# l* K3 C2 p" s' f
the child’s skin. This time the father admitted the
& H8 m) g* ^0 J5 b  qTopical Testosterone Exposure / Bhowmick et al 541
; w4 u: P5 q5 L" s% Wuse of testosterone gel twice daily that he was apply-
. y7 R5 t- _. z, [; y9 king over his own shoulders, chest, and back area for
. _" q# _% _: B  S# o$ S! J+ f0 Ta year. The father also revealed he was embarrassed! b' a8 ^. v9 [/ f; e
to disclose that he was using a testosterone gel pre-
! u0 j0 \# k5 ]4 fscribed by his family physician for decreased libido
) I1 [) _) t- Qsecondary to depression.
' @2 s: v- D. s' aThe child slept in the same bed with parents.
* B' a8 p: p5 r" ^. ~The father would hug the baby and hold him on his
, Q) g1 n; h+ B  p9 h' ~chest for a considerable period of time, causing sig-
; ]# s- C3 t* m0 E$ }nificant bare skin contact between baby and father.
( T  `7 j/ }) A. LThe father also admitted that after the phone call,5 C+ Y0 M9 H' n0 ?: z$ G2 K9 z1 u2 I
when he learned the testosterone level in the baby
# R- H" c# e; l9 }was high, he then read the product information
0 _5 b7 _+ D: cpacket and concluded that it was most likely the rea-4 M- g$ [/ I, x$ c% q
son for the child’s virilization. At that time, they
2 [2 H: h- Z7 B# i7 G* edecided to put the baby in a separate bed, and the
0 E, U1 r/ b. ^father was not hugging him with bare skin and had+ X4 |3 V$ O4 J0 Q" }
been using protective clothing. A repeat testosterone4 }, l1 {  P0 N; b7 j( A! ?
test was ordered, but the family did not go to the# \+ D& s7 o! G% a/ ?
laboratory to obtain the test.3 g2 S4 I7 ~4 O; D  R0 p* O
Discussion3 {- I0 Q# Q( z, o2 m8 F. A
Precocious puberty in boys is defined as secondary
, X- p9 [4 _2 S" z) _% [  ksexual development before 9 years of age.1,4
" F  ]2 [7 _6 P- C: q5 @Precocious puberty is termed as central (true) when0 L# R7 H. h6 p! r8 T
it is caused by the premature activation of hypo-
0 ]1 V; N- y% h/ ~thalamic pituitary gonadal axis. CPP is more com-
5 d- E) A* I8 ?8 `8 \- E, _1 O9 cmon in girls than in boys.1,3 Most boys with CPP
7 _  [' j% z5 H. s2 T# D0 M5 ]may have a central nervous system lesion that is
, Y- t2 K0 g- _; q6 Q" Presponsible for the early activation of the hypothal-6 r( G1 I% a4 K
amic pituitary gonadal axis.1-3 Thus, greater empha-
! o3 _- t/ X  X: v4 I# ^7 J/ _sis has been given to neuroradiologic imaging in
  {5 |. R: T9 R1 aboys with precocious puberty. In addition to viril-1 y6 b1 S8 s9 ]4 R4 C( N7 l) W
ization, the clinical hallmark of CPP is the symmet-" O/ C, \" u: F9 H
rical testicular growth secondary to stimulation by
6 I/ l3 S( x3 F; c4 i  z$ L1 n, y) Hgonadotropins.1,3
$ W# u" u/ M4 i' bGonadotropin-independent peripheral preco-( ?1 d5 u1 a0 o
cious puberty in boys also results from inappropriate
; f3 g9 e4 j0 O( Y% \; W  Vandrogenic stimulation from either endogenous or! I6 v9 O3 _* C' j4 Q
exogenous sources, nonpituitary gonadotropin stim-
+ p8 e. T0 n& k1 }2 |# Lulation, and rare activating mutations.3 Virilizing
8 Q3 C' o0 `1 o2 Hcongenital adrenal hyperplasia producing excessive
. I( o2 |; X& h: c; Padrenal androgens is a common cause of precocious
' A9 t/ I( c2 O# wpuberty in boys.3,4! s& a+ F" U; A% h! E
The most common form of congenital adrenal. b" ?6 C2 A; y0 h2 D. Q& q
hyperplasia is the 21-hydroxylase enzyme deficiency.8 A2 j- Q0 c$ N! \+ k4 F' J8 ]
The 11-β hydroxylase deficiency may also result in. R8 v4 J" g' @0 U( v; C3 f8 n
excessive adrenal androgen production, and rarely,
& Z: ?: ?: v2 s. `( ?; Van adrenal tumor may also cause adrenal androgen' y/ c) w4 E' T4 b- N: t/ R
excess.1,3$ b* s9 Q: d7 ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 v1 L" N+ q- l
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
* z) f2 D/ Z7 P8 z. b$ aA unique entity of male-limited gonadotropin-
# h3 ~* c& \' U; e3 s/ U* Oindependent precocious puberty, which is also known
/ @/ s$ J* v3 Q, O" jas testotoxicosis, may cause precocious puberty at a% H& p5 C! @3 A2 z- }0 L7 N
very young age. The physical findings in these boys
8 g; X/ Q) p" H% Y6 twith this disorder are full pubertal development,
: Q8 C3 v  h$ fincluding bilateral testicular growth, similar to boys5 {. k9 F8 H1 x9 a6 Z) x
with CPP. The gonadotropin levels in this disorder2 ]$ {% K6 d$ U2 M1 b1 C) Z
are suppressed to prepubertal levels and do not show% e1 V  E1 S6 O7 N  O
pubertal response of gonadotropin after gonadotropin-! j7 N* E) t6 u' G+ A) g
releasing hormone stimulation. This is a sex-linked: d0 |. P6 `- b& }/ e. ~2 P9 R( F
autosomal dominant disorder that affects only* m8 I; G' [+ z3 [% e  I
males; therefore, other male members of the family
& u' t1 P# o. G0 ~% P; c$ jmay have similar precocious puberty.32 ~- c, I/ S# V& m, @$ n0 ^
In our patient, physical examination was incon-% X9 h) t$ l! g( U1 B* e8 Y3 K
sistent with true precocious puberty since his testi-% j; d# P6 U: [7 @
cles were prepubertal in size. However, testotoxicosis/ h, I/ Z. _! u3 q5 h" O$ q( i
was in the differential diagnosis because his father0 H  l& D1 Y- H0 V0 y1 l) Y; {
started puberty somewhat early, and occasionally,
0 R  n7 b" e& Dtesticular enlargement is not that evident in the
& Q% x% g- |* m( r0 o, X( obeginning of this process.1 In the absence of a neg-
) f* m! v# ]+ Y$ v% h. }: Eative initial history of androgen exposure, our
" F) A5 l" }5 w5 a9 b- |; o* Ebiggest concern was virilizing adrenal hyperplasia,& S8 {! @% k0 ]9 U4 i% G2 M8 C4 O/ c
either 21-hydroxylase deficiency or 11-β hydroxylase+ q0 X* k8 b$ J* H* @2 q' G. ?
deficiency. Those diagnoses were excluded by find-
: l! @- h: v8 s5 {; q0 Ting the normal level of adrenal steroids.0 R) p( s3 o. s# \" V# g
The diagnosis of exogenous androgens was strongly
5 ^# C2 Z4 C* \) T2 H0 i; m8 Ysuspected in a follow-up visit after 4 months because. }' G9 I# X$ X8 Z" ]/ G- j9 g2 Q
the physical examination revealed the complete disap-+ `- N( ^, N3 Q4 |& q% U' _
pearance of pubic hair, normal growth velocity, and
- |" f8 j' d% P7 q+ M9 udecreased erections. The father admitted using a testos-
, a- n# e" o% Y6 a# H1 Fterone gel, which he concealed at first visit. He was; l! U$ ?  Z4 t- D
using it rather frequently, twice a day. The Physicians’
$ x4 Z' P( I; O( z* lDesk Reference, or package insert of this product, gel or8 J5 \8 I( c7 K; D4 \
cream, cautions about dermal testosterone transfer to! x" G3 n8 L3 P* j
unprotected females through direct skin exposure.& y( S$ G6 w# J! |- v' q* n, u
Serum testosterone level was found to be 2 times the
9 p1 W6 [% ~3 C$ R5 l8 ~baseline value in those females who were exposed to2 [& p1 u) F9 e/ ^1 T
even 15 minutes of direct skin contact with their male# F! H8 |/ a3 C. N0 z2 ~
partners.6 However, when a shirt covered the applica-' j0 a6 Z* i9 V6 w/ p+ e
tion site, this testosterone transfer was prevented.
( d% B  E, ^" @$ p+ e6 t% SOur patient’s testosterone level was 60 ng/mL,; P0 e6 D+ n3 h3 H8 B! `
which was clearly high. Some studies suggest that
! ?5 G& r5 ]3 Y1 Kdermal conversion of testosterone to dihydrotestos-& E) i! i- M& E: ?# W
terone, which is a more potent metabolite, is more! w& ~9 C, _5 B# s% z
active in young children exposed to testosterone" l3 Z; @" k# [* u6 E
exogenously7; however, we did not measure a dihy-, I! O4 ^. W. P$ Y5 M: d+ g
drotestosterone level in our patient. In addition to
1 ]: l- D% L1 w6 `* S6 _: D( d% Zvirilization, exposure to exogenous testosterone in
3 A6 o5 A9 {8 t- }. L: G- gchildren results in an increase in growth velocity and
. B& O8 e6 _4 W2 ]! b( Fadvanced bone age, as seen in our patient./ O* A  |, ^' k* N3 c7 ~
The long-term effect of androgen exposure during$ A# e. _% w1 E; K8 B- p
early childhood on pubertal development and final
; p$ G% L1 Y5 V; }! {* k, I7 |adult height are not fully known and always remain7 i9 L( D; e7 T% |% r( ?- O
a concern. Children treated with short-term testos-1 @$ t: O2 I  [8 \
terone injection or topical androgen may exhibit some
3 l$ k" N& X2 v2 v& Sacceleration of the skeletal maturation; however, after
% i& m6 q# I$ C2 Qcessation of treatment, the rate of bone maturation2 L8 U* @! Z0 R6 b( N' g
decelerates and gradually returns to normal.8,9/ A% `% M/ T  i5 `8 u# t& X2 t
There are conflicting reports and controversy" {3 F4 f& C6 m# s1 Q# A
over the effect of early androgen exposure on adult
" m8 i$ w* m  N0 Bpenile length.10,11 Some reports suggest subnormal
  D' V" S8 Y/ Y. O& {adult penile length, apparently because of downreg-
' e3 \! n7 [  |6 O& d  oulation of androgen receptor number.10,12 However,
- ^- P5 M$ d0 H1 b& vSutherland et al13 did not find a correlation between
$ t! c& v+ P% ^9 J  Schildhood testosterone exposure and reduced adult
% T/ q4 @0 n$ S4 e8 g3 Dpenile length in clinical studies.
2 M3 Y% |3 N1 z# k" e- ?' \7 fNonetheless, we do not believe our patient is' Q! q1 o. z) B* D1 M
going to experience any of the untoward effects from
( N7 Q+ D! O/ y& s' }testosterone exposure as mentioned earlier because
2 p. v  f* i4 u. L  ?+ o5 I  kthe exposure was not for a prolonged period of time.
. d/ t( t/ `! K' v+ BAlthough the bone age was advanced at the time of, u7 x0 g4 E' Y
diagnosis, the child had a normal growth velocity at
: A1 i% C4 u8 h9 V5 gthe follow-up visit. It is hoped that his final adult* V3 N1 _$ P5 s7 t5 \( m% B; H
height will not be affected.0 w9 q8 @6 @7 G6 K; d( l
Although rarely reported, the widespread avail-
; B" M. [( M. p' _, hability of androgen products in our society may
. F, `* `0 w" t: ]+ Nindeed cause more virilization in male or female/ B6 M8 U# Q5 o  _, X2 B: D8 r, P, b. \
children than one would realize. Exposure to andro-8 @0 \5 Q, s1 B' ?- T% p3 S
gen products must be considered and specific ques-- X* N, f: {) p5 X- j1 ^  m
tioning about the use of a testosterone product or
8 h8 r* N- Q& egel should be asked of the family members during. `  p5 L' v0 k; Y* K: V7 C
the evaluation of any children who present with vir-: N( C% _& h2 x# n
ilization or peripheral precocious puberty. The diag-: V! T* h- [" C8 ?2 ^- s
nosis can be established by just a few tests and by- ^+ ?9 j; S* W3 T9 h
appropriate history. The inability to obtain such a6 `2 z1 p6 A! l; U5 G
history, or failure to ask the specific questions, may% a+ n" h0 B4 F
result in extensive, unnecessary, and expensive
( W$ `/ g" Z9 v/ c& E, Winvestigation. The primary care physician should be
& c0 ^5 M+ O" P" Aaware of this fact, because most of these children
5 o8 G  o3 H* i. G$ dmay initially present in their practice. The Physicians’
3 h2 I$ b$ w3 g, v/ B# \5 jDesk Reference and package insert should also put a  I, U, \3 u9 g& t+ r
warning about the virilizing effect on a male or
; Z/ m& |; b# Bfemale child who might come in contact with some-+ n* u2 L: |# ]" A* k
one using any of these products.1 j3 e6 y2 B  H, _/ ~
References
1 E8 A4 e% j7 d1. Styne DM. The testes: disorder of sexual differentiation0 H5 w* x# }' v' G$ ^4 N
and puberty in the male. In: Sperling MA, ed. Pediatric# {8 \$ A1 n& V0 ~6 \
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 H$ O- r9 u3 R- K- @. W. C' T4 N2002: 565-628.
+ F7 I- s- m' T6 n1 l) a2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 N' O( ]8 _! x+ p7 N0 ?% m# [: A
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

' W% M1 K: D0 l* ?$ G精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
您需要登錄後才可以回帖 登錄 | 立即注册

本版積分規則


快速回復 返回頂部 返回列表