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: Q; L4 l* k2 @% R' |0 t4 P
Boy Induced by Indirect Topical" j/ P) t3 ?% F9 F+ D
Exposure to Testosterone
! `' ?3 `6 ]( R7 i# R, RSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( _* n/ D) R9 ]+ J
and Kenneth R. Rettig, MD14 |( P$ ^) _2 c3 a0 |5 X
Clinical Pediatrics& y9 a9 _6 ]! W" c+ ^' O
Volume 46 Number 6
4 R- ?) |1 [+ OJuly 2007 540-543
# G0 u7 L" K$ i7 e0 u* v© 2007 Sage Publications9 D) k$ M/ ~- U' |2 K9 f" q
10.1177/0009922806296651
$ x8 e0 |+ x  g: W: q: B% Ihttp://clp.sagepub.com$ b. S( E0 m! c) K
hosted at
! U" l3 ]4 m- }4 j( b# y+ [) Bhttp://online.sagepub.com6 o/ O. w! `# S
Precocious puberty in boys, central or peripheral,
. o6 C+ k. }& {. y; X1 |# fis a significant concern for physicians. Central( r8 C4 e% G0 T9 w9 J
precocious puberty (CPP), which is mediated
/ t2 O! E/ \3 w9 Q& q5 wthrough the hypothalamic pituitary gonadal axis, has" m! _& Y% O/ m' V
a higher incidence of organic central nervous system! |. `. S. w5 {) v1 D$ G
lesions in boys.1,2 Virilization in boys, as manifested
1 M1 D# e1 w" \+ f) x% w. Sby enlargement of the penis, development of pubic
! W( L2 N2 b' U5 x- z8 ~- X3 Ehair, and facial acne without enlargement of testi-1 Q, x5 T* D4 H6 c% `) ~4 F
cles, suggests peripheral or pseudopuberty.1-3 We
# y) f* m* M$ r& J1 G5 Kreport a 16-month-old boy who presented with the! X5 A+ y- A% e1 b5 Q
enlargement of the phallus and pubic hair develop-
& s* V$ Z" M9 D! V0 u5 V" qment without testicular enlargement, which was due
* H  a. U- X; q! M2 Z6 pto the unintentional exposure to androgen gel used by
7 K; g* D8 d- A/ j7 ?the father. The family initially concealed this infor-+ x9 L/ I  ^7 A% S5 ~7 h$ p$ L. y
mation, resulting in an extensive work-up for this
! B: x7 T. H: J. Echild. Given the widespread and easy availability of
% e* b0 C6 ~" X$ B: T" Y& Itestosterone gel and cream, we believe this is proba-1 I" T/ z& o5 y7 [- ^
bly more common than the rare case report in the3 M. y% d# |  [* P5 s4 [
literature.4
$ g; Z5 W, @- V- B9 NPatient Report7 m7 X% O. g# e' Q! W0 G
A 16-month-old white child was referred to the- T! b6 I9 Z% `0 d6 Q9 Q
endocrine clinic by his pediatrician with the concern  P9 o" v6 g- T6 `
of early sexual development. His mother noticed/ J: u; |, h8 o  T2 [
light colored pubic hair development when he was2 o9 E: G$ e6 s5 F
From the 1Division of Pediatric Endocrinology, 2University of+ H- h" m: ?" T* Y4 L) e# C8 H
South Alabama Medical Center, Mobile, Alabama.2 ]( \+ Y0 g- G! F; k
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 W8 \3 U8 ]$ i( D; Z% q8 `% X
Professor of Pediatrics, University of South Alabama, College of
1 P: x# @9 z2 E0 rMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;- O$ e$ i- y% h; @* p8 S; i: k2 ^
e-mail: [email protected].
/ _* l" a, C. g- t4 yabout 6 to 7 months old, which progressively became- y7 \+ w- ^0 j4 t7 q9 _8 t
darker. She was also concerned about the enlarge-
8 d" ~+ t- p$ i4 f) a# dment of his penis and frequent erections. The child( f* f- D0 r1 V8 {) B3 D
was the product of a full-term normal delivery, with8 r- h5 F+ x0 d8 i6 Q
a birth weight of 7 lb 14 oz, and birth length of
* |) E) e0 z$ I" t, y20 inches. He was breast-fed throughout the first year
- `2 }9 h' o! a/ F" hof life and was still receiving breast milk along with2 l  i% t* ]1 P
solid food. He had no hospitalizations or surgery,+ `' K# w' Q/ ]) j! \
and his psychosocial and psychomotor development; _( n3 T$ A7 A
was age appropriate.( _, }' x0 B: o9 ~
The family history was remarkable for the father,
- P* D+ M2 ~8 S; ]. V4 b9 ]5 A6 @1 Dwho was diagnosed with hypothyroidism at age 16,
" ?. W& _/ ]. \8 x$ _, pwhich was treated with thyroxine. The father’s3 t7 o- n2 p& X
height was 6 feet, and he went through a somewhat
% _- G. z6 f/ S2 d4 s0 R5 `3 S# \early puberty and had stopped growing by age 14.  t9 r( c' [# f& a3 i+ S* z  |, t
The father denied taking any other medication. The
) m' q/ r+ k3 Qchild’s mother was in good health. Her menarche& Z& U$ T* j; Q, m/ |1 X8 e
was at 11 years of age, and her height was at 5 feet7 G" f4 R& `8 B  }0 X) L! d* _- S
5 inches. There was no other family history of pre-) u7 j$ r# K2 r. F8 y" P
cocious sexual development in the first-degree rela-
/ q& ^+ ?) O5 v. E) k2 x# rtives. There were no siblings.0 r: r% p- r2 ?$ A1 ]+ z5 v! @
Physical Examination( q" x% c( i+ J4 l' _$ P4 r5 G
The physical examination revealed a very active,! h2 u5 c. ^# Q
playful, and healthy boy. The vital signs documented
; h5 n) S2 Z/ ]7 L6 {7 B5 sa blood pressure of 85/50 mm Hg, his length was
0 J# t; l9 H" o90 cm (>97th percentile), and his weight was 14.4 kg
2 t% l4 [) I- t% c: J& G, P$ ^(also >97th percentile). The observed yearly growth$ G1 [+ \( e' U. \$ u) y5 Y' a- g# l" T
velocity was 30 cm (12 inches). The examination of
* }0 B7 `# r1 S# |% l3 c* Bthe neck revealed no thyroid enlargement.
' \9 H! H& e# S% HThe genitourinary examination was remarkable for9 J4 s0 _5 n# j$ H, U( i4 e
enlargement of the penis, with a stretched length of  W+ K# ]3 Q7 @- Z, C
8 cm and a width of 2 cm. The glans penis was very well
8 T- S8 u# Y7 x% N: C1 [' `developed. The pubic hair was Tanner II, mostly around  M8 {. W3 I' Q9 C) Z% b
540
, b3 V- {/ W' i4 |- ~9 Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- e* e7 \  _' W/ S0 Z' p
the base of the phallus and was dark and curled. The
" d' V; b: T! r7 h% l8 xtesticular volume was prepubertal at 2 mL each.* \* _% {6 t1 N8 P. m  \, v
The skin was moist and smooth and somewhat8 T  B( a9 G  k( j8 g5 K+ G: @
oily. No axillary hair was noted. There were no
5 ^7 R& ]6 M9 z2 ^9 I4 Eabnormal skin pigmentations or café-au-lait spots.& `! [+ A4 y3 i& o5 j/ b- h
Neurologic evaluation showed deep tendon reflex 2+/ t+ n" e: a' T& s) y; a% q
bilateral and symmetrical. There was no suggestion
  l6 l3 R" p; @) Nof papilledema.
- f6 U- m/ ]8 n9 r4 |$ b( BLaboratory Evaluation3 _1 C) a" n+ V. {
The bone age was consistent with 28 months by
* s1 Z7 Q9 |' D2 d* D7 S0 G8 busing the standard of Greulich and Pyle at a chrono-
/ l# C' g0 X7 h; i( b- dlogic age of 16 months (advanced).5 Chromosomal6 a& D  S% C, P  ~
karyotype was 46XY. The thyroid function test
$ L' r5 {9 L: nshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 u! b; U9 p/ n, j5 e- i; K/ jlating hormone level was 1.3 µIU/mL (both normal).7 R9 b* T8 J' w$ |5 z( l/ `
The concentrations of serum electrolytes, blood
5 D" z8 ?6 c% P4 V# e$ c; n  p' m) qurea nitrogen, creatinine, and calcium all were
& x  V: B' |0 {, Z4 Y1 F# pwithin normal range for his age. The concentration
2 l0 a5 a, h, X' f$ x; F# E4 ^+ g" J0 Jof serum 17-hydroxyprogesterone was 16 ng/dL
+ j7 {* E3 A0 w(normal, 3 to 90 ng/dL), androstenedione was 20
- q$ g" u+ O* ?8 [4 ]8 ^- @7 b& Bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  R& v7 P6 U* q4 H
terone was 38 ng/dL (normal, 50 to 760 ng/dL),  Q% s9 T- S0 T' U" A- U
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 s6 {( }) \: g; I. E% n7 g49ng/dL), 11-desoxycortisol (specific compound S)4 P% ?1 y: C$ t) y; v% d4 D) r2 x
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
" p, l/ K# F9 H) [" ~: ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 i" C4 X' v3 N
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( B4 }" D" h* j! {. g& Q: O& m
and β-human chorionic gonadotropin was less than' Q4 r6 b& C% ?$ z( X; [; @
5 mIU/mL (normal <5 mIU/mL). Serum follicular* {4 L+ B9 Z2 p+ t& `7 B7 S+ {) D
stimulating hormone and leuteinizing hormone
; J4 x# n8 [/ r2 F0 _4 Iconcentrations were less than 0.05 mIU/mL# y- X% n4 i: h7 L2 e! T' o3 W, g& G
(prepubertal).
3 ~; w/ y7 n2 ?: }* i8 ]. h% \The parents were notified about the laboratory
5 t8 L& x7 L8 z2 Y8 Oresults and were informed that all of the tests were
* p' e! U, Q, Q. O; ^$ E+ knormal except the testosterone level was high. The
6 g1 k5 X& O2 D, B/ ~, Ofollow-up visit was arranged within a few weeks to) M  _, M9 ^& c3 i( `( D
obtain testicular and abdominal sonograms; how-
5 e; o" ^2 H9 b7 Dever, the family did not return for 4 months.
" z& x, O$ {/ R: j* _6 ^0 yPhysical examination at this time revealed that the
7 }0 F8 ~0 l. G6 X! W  Hchild had grown 2.5 cm in 4 months and had gained
3 K" B8 m# |- c2 kg of weight. Physical examination remained9 D. p" S7 p/ K3 r8 b1 A2 m, S2 B
unchanged. Surprisingly, the pubic hair almost com-
, q2 z, a/ P) }* q4 Opletely disappeared except for a few vellous hairs at$ I" s; Q: c+ m" }
the base of the phallus. Testicular volume was still 2/ ^' J5 ^7 K9 h+ @5 g7 X
mL, and the size of the penis remained unchanged.
- i7 K9 `/ R6 u5 x9 m2 _; g8 TThe mother also said that the boy was no longer hav-
1 e. m* m5 [. _1 D. Ving frequent erections.0 n) g2 p9 m: T1 J: C0 J: l7 j! u5 V
Both parents were again questioned about use of3 {& s. e/ W' n) Y; j6 t1 q: R2 a5 D# P
any ointment/creams that they may have applied to
! m( V( ^- s$ d, L( A+ R) X2 ^6 l3 Wthe child’s skin. This time the father admitted the
5 x- ], ^3 ]: [Topical Testosterone Exposure / Bhowmick et al 541
$ s+ P6 t* A6 v! [0 ruse of testosterone gel twice daily that he was apply-7 J' Q, W4 |% T$ Y+ C5 N1 E3 V
ing over his own shoulders, chest, and back area for4 s1 m# A: ~$ u! T7 l
a year. The father also revealed he was embarrassed
( }; r8 p- B  C" [to disclose that he was using a testosterone gel pre-
! `  l+ n6 z2 ?2 q: \+ }scribed by his family physician for decreased libido
" D) D/ V) [9 b- w/ {secondary to depression.
" R+ ^* m! y0 N( uThe child slept in the same bed with parents.4 @& y1 c1 E- Y
The father would hug the baby and hold him on his: y! b2 Z% J; q" h0 T- _, ]
chest for a considerable period of time, causing sig-
! I. l5 ^: U7 f- L/ E% hnificant bare skin contact between baby and father.' z( [7 R, k& v' \- a- s
The father also admitted that after the phone call,. y9 G$ p, [9 B" y4 l; g: M0 q, Q
when he learned the testosterone level in the baby8 u" s9 P+ L3 a% |; K- g  j
was high, he then read the product information
" [9 V% ~' e8 b- B7 ]packet and concluded that it was most likely the rea-
# R" G, \1 S$ P7 I9 _son for the child’s virilization. At that time, they/ }* ^+ {( b+ c1 s" {  x6 v
decided to put the baby in a separate bed, and the: V4 R2 r, |5 ?6 a" D, y9 F
father was not hugging him with bare skin and had
* Z" n9 [& \. }9 Hbeen using protective clothing. A repeat testosterone" K+ a4 [/ E! J& e
test was ordered, but the family did not go to the
8 H( t5 o) E8 Y  f9 |; y% K( S2 slaboratory to obtain the test.
5 r. g) N; P2 v) i) @+ S" VDiscussion
, J. X/ p' l1 z3 F+ e7 v" `Precocious puberty in boys is defined as secondary
1 i) f$ W5 ]- U' S6 M# Psexual development before 9 years of age.1,4& J  U7 H* c- q' b0 L
Precocious puberty is termed as central (true) when) Y0 H  ]7 }9 B
it is caused by the premature activation of hypo-
7 M/ E5 E# R# I1 x2 R: c. Cthalamic pituitary gonadal axis. CPP is more com-
9 R+ B# D0 Z% b5 cmon in girls than in boys.1,3 Most boys with CPP/ i( W+ Z8 d  C: y! L  i
may have a central nervous system lesion that is
* t6 Y7 v7 m3 a7 }7 Bresponsible for the early activation of the hypothal-! G9 u7 q) ^5 G/ g! y7 X3 t
amic pituitary gonadal axis.1-3 Thus, greater empha-
8 F! u  s& ]$ O; osis has been given to neuroradiologic imaging in: C+ a, c: X3 O& B$ g
boys with precocious puberty. In addition to viril-7 h" H& i- Z6 R8 ~
ization, the clinical hallmark of CPP is the symmet-
0 X' Y, F1 ^4 frical testicular growth secondary to stimulation by
, ], N8 a4 d: l- }  Y" t7 @$ L! Bgonadotropins.1,3
% r. o, e/ I$ H, O* BGonadotropin-independent peripheral preco-7 M' H5 Y/ I5 O5 b
cious puberty in boys also results from inappropriate
- ?2 b  ~, [- j5 xandrogenic stimulation from either endogenous or5 L- f9 D7 B6 z0 A2 {, c
exogenous sources, nonpituitary gonadotropin stim-
" ~) j0 |) |1 O" Xulation, and rare activating mutations.3 Virilizing
# e+ x: d9 S, v0 lcongenital adrenal hyperplasia producing excessive" f  j: N; C2 \9 p5 z4 i
adrenal androgens is a common cause of precocious
: _7 L# p' K% n. x% g) o( u; D! A% tpuberty in boys.3,4
7 Z* `6 b5 Z0 U) b/ h2 bThe most common form of congenital adrenal
3 x; h# G  Q5 m, o' f- v# Bhyperplasia is the 21-hydroxylase enzyme deficiency.
' n4 i* f. V2 y) ~! xThe 11-β hydroxylase deficiency may also result in  V% U" Z2 R3 [; }' R' Z0 S9 ^4 e, R5 h
excessive adrenal androgen production, and rarely,
7 j) p# D. h( w, o  b& I, Kan adrenal tumor may also cause adrenal androgen
7 p; \& E% y" r( P, `# ?excess.1,3: E% a% B  u# K% p- R* b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) }% G, O9 [" E" _' B5 s
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 Z. ?' p6 H( t  o, |A unique entity of male-limited gonadotropin-
$ d9 M; g- \* K3 ~- q- U+ \independent precocious puberty, which is also known
% A, {$ @) k- I$ A4 X" eas testotoxicosis, may cause precocious puberty at a0 _, X4 i, F9 J; @, Q- H
very young age. The physical findings in these boys: a& a" y3 I! T' c' [7 e* f
with this disorder are full pubertal development,$ Q! c6 S2 A& D5 @% o
including bilateral testicular growth, similar to boys& d5 x8 P' r$ T3 |5 y- @
with CPP. The gonadotropin levels in this disorder- R  k  T; |  ~
are suppressed to prepubertal levels and do not show
& w$ s( U1 r/ h# Z" Apubertal response of gonadotropin after gonadotropin-( d7 z. r8 c  |, ^9 y8 t: e2 o
releasing hormone stimulation. This is a sex-linked* R% \# A/ C/ J( }* A" ~
autosomal dominant disorder that affects only
4 O! Y0 L0 F9 K6 {" dmales; therefore, other male members of the family
- T8 r, f4 m7 u& hmay have similar precocious puberty.3
2 f& p. U, O$ F- o+ s/ `In our patient, physical examination was incon-
: t' Y! W" N$ Z+ Q' ?: xsistent with true precocious puberty since his testi-
& ^6 f) c9 d# k+ {- `. R8 q( Lcles were prepubertal in size. However, testotoxicosis
  e$ }7 D8 `! Q6 g5 Qwas in the differential diagnosis because his father5 v1 x+ c* J3 y0 r" I
started puberty somewhat early, and occasionally,
8 [; U  Y4 D2 f- {) t, Gtesticular enlargement is not that evident in the
9 l: c2 q" A8 r7 l3 h: u0 K- Sbeginning of this process.1 In the absence of a neg-
2 `0 c# Y# z9 Cative initial history of androgen exposure, our+ |+ ]7 y, G' m! E, c: k: U
biggest concern was virilizing adrenal hyperplasia,8 M7 U! j+ q0 k* f7 a1 X+ N
either 21-hydroxylase deficiency or 11-β hydroxylase
, i% G3 o- J7 q7 @* sdeficiency. Those diagnoses were excluded by find-
( e, t/ I( F  p$ g$ ding the normal level of adrenal steroids.! B7 p) V; h+ U2 [) D: f  y
The diagnosis of exogenous androgens was strongly
2 `! U; H( x* \suspected in a follow-up visit after 4 months because( o: K: E  x) b/ G0 K, J
the physical examination revealed the complete disap-; P* R. @! r* ?8 R, m9 {
pearance of pubic hair, normal growth velocity, and
5 S' t3 ^6 w+ n4 Y* [2 m5 E* ^decreased erections. The father admitted using a testos-
, _# e8 M/ t( ]- Y; kterone gel, which he concealed at first visit. He was
8 A- h0 ]. t% ~; r1 V9 D8 ^using it rather frequently, twice a day. The Physicians’1 L% [6 ]5 q* \5 k& A" m
Desk Reference, or package insert of this product, gel or3 e# y6 z' T, s/ T$ w6 a0 |& z# Y
cream, cautions about dermal testosterone transfer to" W2 x/ i+ ]8 Z5 n  D! E) c! c* n
unprotected females through direct skin exposure.& r; z: d) d0 O% `% q3 M
Serum testosterone level was found to be 2 times the
& O5 B; c# ?0 f& k# F% W9 k! _% Abaseline value in those females who were exposed to
+ C6 c: M  ]' W/ B7 c+ [6 Reven 15 minutes of direct skin contact with their male8 b3 p1 S0 I1 a$ |# r! k
partners.6 However, when a shirt covered the applica-5 u' q3 S& c* T# r5 P& y
tion site, this testosterone transfer was prevented.+ v& }  Z8 G# H1 n9 _7 b, Q: {
Our patient’s testosterone level was 60 ng/mL,
  b6 l# S! L3 Z1 T5 X, w  F1 Z' dwhich was clearly high. Some studies suggest that
9 t8 Q6 q5 ^8 v6 a! m9 _dermal conversion of testosterone to dihydrotestos-
; A1 R( i+ q2 P& s  qterone, which is a more potent metabolite, is more9 s8 e1 D/ a$ Q* y# |( u& e/ O
active in young children exposed to testosterone$ A- h4 b6 h7 O/ n' s
exogenously7; however, we did not measure a dihy-
- h1 w) p3 j4 [  v7 n3 E7 ^drotestosterone level in our patient. In addition to2 e0 }- K# Y# ?
virilization, exposure to exogenous testosterone in
, i* I/ Z- @9 [. C) ~4 h8 ?0 ~children results in an increase in growth velocity and
7 x) h  w( e. S4 |* j- G+ |advanced bone age, as seen in our patient.
, L: o. e4 _4 _The long-term effect of androgen exposure during
1 b9 g( {9 k7 J8 j% J2 z# P0 i1 yearly childhood on pubertal development and final3 Z* G0 U, ]5 ^, t& Y' A% E
adult height are not fully known and always remain4 {0 U/ s7 _! D+ J; n0 U( O
a concern. Children treated with short-term testos-+ W$ Y( k+ i  C; S2 x5 ^
terone injection or topical androgen may exhibit some
9 C! t' M8 I+ v- ?, H* }+ Q' Zacceleration of the skeletal maturation; however, after
2 q* [- c" d; w. d  @. Pcessation of treatment, the rate of bone maturation( N8 I& l" Z/ Y& D% Z
decelerates and gradually returns to normal.8,9
  X' V' I7 q7 e0 B6 P2 ?There are conflicting reports and controversy
" o5 ^" P* b3 K& a( l' ^over the effect of early androgen exposure on adult+ j" Q& E. N5 @. h
penile length.10,11 Some reports suggest subnormal
& u+ z8 ?) ]: n" M  Jadult penile length, apparently because of downreg-& Z' s, Z0 Z7 j* x& N1 s
ulation of androgen receptor number.10,12 However,4 i$ B3 ]" `+ d
Sutherland et al13 did not find a correlation between
, Q$ K. N& C! Q7 gchildhood testosterone exposure and reduced adult
1 D# E: {1 y6 U4 C8 ?/ Cpenile length in clinical studies.7 o' W! q8 S3 l4 I' E2 q
Nonetheless, we do not believe our patient is
2 G( R! q% j( j; q- d$ Q  {going to experience any of the untoward effects from
% t. a7 D* n. g6 I" btestosterone exposure as mentioned earlier because
, ], Z3 k! U8 N; athe exposure was not for a prolonged period of time., o4 v* S+ ]5 B* K) \
Although the bone age was advanced at the time of
( _- i6 E8 J# M; `diagnosis, the child had a normal growth velocity at. J3 Q& |  A: Z" D
the follow-up visit. It is hoped that his final adult- P# h; B$ l. O0 m/ u4 i
height will not be affected.
. @' _) P3 b6 x6 f* GAlthough rarely reported, the widespread avail-
+ s  T0 _% v3 Y  F3 }ability of androgen products in our society may- q4 Z$ |8 C. I, ]
indeed cause more virilization in male or female, U$ c7 o7 [7 D% C
children than one would realize. Exposure to andro-
$ w& J/ d- J7 S4 }* y% ogen products must be considered and specific ques-
' y; _* y8 ~# u! t% utioning about the use of a testosterone product or
* z5 e5 x) L" t( ]4 p5 `gel should be asked of the family members during
0 _: D. F- [0 i% H9 r3 H% T( Zthe evaluation of any children who present with vir-
8 D# l% y3 i' X! [ilization or peripheral precocious puberty. The diag-
" `; |5 Q' S) j5 ]* y  pnosis can be established by just a few tests and by, s  I/ T6 R: t8 s* ?
appropriate history. The inability to obtain such a
+ Z& X2 L! X4 E5 b/ ~9 yhistory, or failure to ask the specific questions, may1 s/ y  b4 {# q8 z' {
result in extensive, unnecessary, and expensive
4 U6 ~; j: {& b. f/ finvestigation. The primary care physician should be
' v" E8 _9 I. K* Taware of this fact, because most of these children
& }/ p3 a% o; a* |5 k: jmay initially present in their practice. The Physicians’! b5 B. N4 L5 v9 {
Desk Reference and package insert should also put a
) L# T' d2 m% x! y) }. j7 D  [1 |warning about the virilizing effect on a male or; \2 ~0 i0 A6 j7 S- q/ ^' S+ J6 h
female child who might come in contact with some-
5 _/ _6 H8 j1 V& r; {one using any of these products.
8 o' @0 k& t+ X& _References, W( K/ `  s5 F+ z: o& z
1. Styne DM. The testes: disorder of sexual differentiation
6 C) w1 }6 E3 U  rand puberty in the male. In: Sperling MA, ed. Pediatric9 y! Z# r/ z+ w% C/ Z* i3 N
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, U2 Z7 }0 ]: K3 g$ t3 y
2002: 565-628.# P( J8 n% q! D' D
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! k+ x$ o. L" l- dpuberty 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-Old7 j( x3 Y; N- L' V0 W  ?: ?; L
Boy Induced by Indirect Topical5 w5 |1 r  f. B2 J4 o5 u+ i( v$ M/ l
Exposure to Testosterone. U; ?3 {# m' U8 ?! `4 m
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 ~9 k& [' A7 a$ d$ J" L9 V$ R
and Kenneth R. Rettig, MD1
7 W+ X% C$ L8 R; d3 B% hClinical Pediatrics
9 f, G, y# p; K7 }4 i0 T2 i  o% R8 |$ N  DVolume 46 Number 68 j- w0 V2 x, k& S1 c
July 2007 540-5433 N3 N7 P* n" R  v  P* q
© 2007 Sage Publications; T* q' F$ _8 g) p
10.1177/0009922806296651' C" X. m5 s( d* F$ N8 d! g& v
http://clp.sagepub.com# b& U$ B+ R0 M) ], _: U
hosted at
. _& A7 H) a, J; a1 g1 K! o1 V* Uhttp://online.sagepub.com
9 x4 U- S, `( nPrecocious puberty in boys, central or peripheral,2 E  w+ U3 N* h# e
is a significant concern for physicians. Central
8 ?* r- K2 U: }. b1 H* f4 P" B% ?precocious puberty (CPP), which is mediated
; d  L- g' Z+ Q; c) c) g! Q" F' N' Q3 r5 f' ?through the hypothalamic pituitary gonadal axis, has4 c$ F/ F& J& q0 L# e- `9 d
a higher incidence of organic central nervous system
5 V* i1 p1 d: `3 R( ^1 _lesions in boys.1,2 Virilization in boys, as manifested9 e' B6 t: E: f
by enlargement of the penis, development of pubic
" C: f. U) u+ n3 o! Ahair, and facial acne without enlargement of testi-) B1 E& x9 G6 _% Z- A6 O8 H+ N
cles, suggests peripheral or pseudopuberty.1-3 We
0 u+ Y! l1 z/ j9 _report a 16-month-old boy who presented with the
5 k" a( M/ y# zenlargement of the phallus and pubic hair develop-6 M* A! ^7 i, d1 ^) `  s: [0 [
ment without testicular enlargement, which was due) o: u. [! x$ N" f- \0 X, p' t
to the unintentional exposure to androgen gel used by
) T& I6 f6 f+ O& r. o7 Gthe father. The family initially concealed this infor-( h5 |3 b3 J1 x) Z: o# E% L
mation, resulting in an extensive work-up for this
' a9 {9 s+ b& Ichild. Given the widespread and easy availability of
. b; k; F1 I' d  X- M; c$ }testosterone gel and cream, we believe this is proba-
4 p  x  q" U; F* x6 ?' ybly more common than the rare case report in the  @2 C, p, d! v, g
literature.4& d1 s  c. F+ G( H
Patient Report
- v8 ~+ b: \6 H/ z- z* xA 16-month-old white child was referred to the
: G7 t. y/ L6 i- @9 b" `& q- h  _3 aendocrine clinic by his pediatrician with the concern
8 ^. y; C( Z# {$ Z( Q- Vof early sexual development. His mother noticed
4 i4 P3 |1 s/ X7 i2 F. H* Hlight colored pubic hair development when he was
, y$ j; O4 c2 C0 |From the 1Division of Pediatric Endocrinology, 2University of
  y0 I8 W/ q7 I; }South Alabama Medical Center, Mobile, Alabama.& J  d2 @# _8 h1 q+ ^  O+ B: d
Address correspondence to: Samar K. Bhowmick, MD, FACE,1 q* r$ h, M: n$ t6 [" f
Professor of Pediatrics, University of South Alabama, College of
' [+ D- B& K# v- KMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 g* d2 R: f* M" Y: N; ~/ C5 Qe-mail: [email protected].
3 U2 T9 a9 g  W# I% W. Z" v0 Pabout 6 to 7 months old, which progressively became* F  b- u! j, [3 I: W+ \4 l& f
darker. She was also concerned about the enlarge-  f. G/ v8 Z! p& o$ I; T+ e0 P
ment of his penis and frequent erections. The child* }# `2 S, k" _) `9 v/ d
was the product of a full-term normal delivery, with
0 O- ]# s& @9 R% ?+ ha birth weight of 7 lb 14 oz, and birth length of
7 L" h6 ]" A  [, d1 A. p0 Y20 inches. He was breast-fed throughout the first year
/ o1 [9 ^' n, T* g: ~3 }of life and was still receiving breast milk along with7 b4 n" b% U- R8 u$ o+ D* G; r1 W
solid food. He had no hospitalizations or surgery,7 z$ ^4 c+ ^- p
and his psychosocial and psychomotor development: z" ]! y$ q  J/ t7 r6 P
was age appropriate.. L. @0 `) t" S' h0 _& L
The family history was remarkable for the father,  S9 H# S9 L3 @1 x, s
who was diagnosed with hypothyroidism at age 16,
6 l. C7 w# x7 _) [2 Kwhich was treated with thyroxine. The father’s
5 f" p) d. F5 d$ T) sheight was 6 feet, and he went through a somewhat3 T: r5 h" q+ n. Z9 w3 s
early puberty and had stopped growing by age 14.
. q1 }1 D. j" d9 a: EThe father denied taking any other medication. The; w" N# E. A  L+ ], L! r% M
child’s mother was in good health. Her menarche
' R2 o; l( R1 ^was at 11 years of age, and her height was at 5 feet% H+ y% ~2 e( e4 j6 ?. \/ p8 H5 I
5 inches. There was no other family history of pre-
7 W% p  o1 ^+ d7 Q1 ~cocious sexual development in the first-degree rela-
, u% F, d( x( K$ ftives. There were no siblings.% A) K2 I! e! k7 }) z9 G/ u
Physical Examination
! I. [/ `7 |$ A/ A3 oThe physical examination revealed a very active,% E8 r+ W, \/ F; j' ^6 T
playful, and healthy boy. The vital signs documented$ u( F* X! W, X5 n
a blood pressure of 85/50 mm Hg, his length was
8 Y$ s- o0 G' h% _90 cm (>97th percentile), and his weight was 14.4 kg
& @. \' e6 F! ]3 X0 l(also >97th percentile). The observed yearly growth
4 P  s* a2 X' Z' |# c2 e! `velocity was 30 cm (12 inches). The examination of
8 e% T- D1 ?8 f9 Y. kthe neck revealed no thyroid enlargement.5 {, b0 r! ~& o' _1 ~: N
The genitourinary examination was remarkable for/ D* E7 j- f  e+ P  }- m
enlargement of the penis, with a stretched length of
( a4 j3 r, B4 K  P; ^* [/ h8 cm and a width of 2 cm. The glans penis was very well
- S& z1 \5 T' T. {9 o9 ndeveloped. The pubic hair was Tanner II, mostly around
0 T* D) W$ E) m7 f. i  W5402 N4 g: z, p! x8 v. `3 Z% I8 n  g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 Q! S8 h$ x* }) J% T. P" g& wthe base of the phallus and was dark and curled. The* H: q; u& l, N; @7 Z0 p3 Y( a9 d
testicular volume was prepubertal at 2 mL each.8 T3 |; W9 a0 @+ f4 U1 r1 [
The skin was moist and smooth and somewhat/ O! r2 v- v9 W8 R- ~# V
oily. No axillary hair was noted. There were no
% k) ^$ I0 H; G9 F* o$ Yabnormal skin pigmentations or café-au-lait spots.
( N0 ?4 b# h3 r) g; ^7 }6 ^' xNeurologic evaluation showed deep tendon reflex 2+
. P5 G" {8 s. b. y8 C+ {bilateral and symmetrical. There was no suggestion
" u* i& F* O' I8 Nof papilledema./ w# O! }' k: A9 u3 C' W" R) s
Laboratory Evaluation& B0 T4 T8 Z* n5 v3 n0 |4 i7 E$ H
The bone age was consistent with 28 months by
1 c- h1 x9 q# b% d) @$ h* J" ^using the standard of Greulich and Pyle at a chrono-
0 n$ ^. P: ]2 N2 z: Elogic age of 16 months (advanced).5 Chromosomal6 a- ?( `# V# ~# u0 S2 c
karyotype was 46XY. The thyroid function test
. }8 _3 F4 K8 a0 [! q& C1 p" d# hshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
& H8 g5 o( Y" g1 E. d) Glating hormone level was 1.3 µIU/mL (both normal).( S( f' a  S# D; ^2 K& x
The concentrations of serum electrolytes, blood% K7 c9 L8 j( z: v. D
urea nitrogen, creatinine, and calcium all were( U- b* b# \/ p; v4 h$ U; P
within normal range for his age. The concentration
2 N! x7 {$ o, M, g5 ~of serum 17-hydroxyprogesterone was 16 ng/dL
- M; n$ q7 K$ Z% n(normal, 3 to 90 ng/dL), androstenedione was 20
0 j$ t2 d- f& y% P( Lng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, W7 {! ~9 k0 B& U/ N
terone was 38 ng/dL (normal, 50 to 760 ng/dL),% B. j# J  v3 D3 w- y
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 v3 h$ c6 @8 j9 v8 \' H49ng/dL), 11-desoxycortisol (specific compound S)
! |5 m; Q4 m+ Q, m( t+ L& cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
6 A. [! C  r4 t' Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* S* J/ j1 z2 r" s1 dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 S8 w! x( b% |  D  ]0 g6 M! w
and β-human chorionic gonadotropin was less than' u5 o% V# G2 n" ]/ f9 ~$ \
5 mIU/mL (normal <5 mIU/mL). Serum follicular$ N: V! L6 @) V
stimulating hormone and leuteinizing hormone3 X% @) s3 ?6 L. U" I! N
concentrations were less than 0.05 mIU/mL  `; n- S( H# \7 K, f* F, m; R
(prepubertal).$ W; r: g, J" `+ G6 g
The parents were notified about the laboratory4 D9 @: H  _+ ~+ ?6 |4 Z
results and were informed that all of the tests were3 ?2 ?" B4 C8 N4 |  T9 c/ f
normal except the testosterone level was high. The7 L  W# K9 p2 O: O
follow-up visit was arranged within a few weeks to$ F6 U: D6 Q' l5 R8 N
obtain testicular and abdominal sonograms; how-7 E% r! E" x' ^+ }& i2 g! Y- [
ever, the family did not return for 4 months.1 _& x" L( r+ a, x+ w% n
Physical examination at this time revealed that the
# I" N# I& `: l+ p* Xchild had grown 2.5 cm in 4 months and had gained9 T' G7 X: p7 M$ ]
2 kg of weight. Physical examination remained
* D0 G! Y; v8 l  gunchanged. Surprisingly, the pubic hair almost com-' ?1 z. f1 P! g
pletely disappeared except for a few vellous hairs at
2 c0 \  s1 }& C3 Kthe base of the phallus. Testicular volume was still 25 s6 M' `1 ^$ y% k/ C1 N
mL, and the size of the penis remained unchanged.( |0 W6 x! S1 M% Q* |7 |4 _
The mother also said that the boy was no longer hav-
, H% Q2 V& R+ `# |3 [/ \2 W0 ^ing frequent erections.# S# [0 E8 r0 h; ~
Both parents were again questioned about use of7 x8 z8 i2 s! R1 Z. r# y0 |; k) |
any ointment/creams that they may have applied to
& R* L- s  |, b2 Pthe child’s skin. This time the father admitted the: l: W" E3 G" o$ u. j
Topical Testosterone Exposure / Bhowmick et al 541
* ?0 K- m" V4 I  Quse of testosterone gel twice daily that he was apply-
' ^& h+ B8 ^0 w7 ]9 ]3 Xing over his own shoulders, chest, and back area for
4 q1 R8 W7 g3 q% g2 Ea year. The father also revealed he was embarrassed
  I/ I$ u2 b! l9 D! n  ~8 ]. Hto disclose that he was using a testosterone gel pre-
* J. B2 P9 C9 l; i' N" J& Sscribed by his family physician for decreased libido
! o5 p% p2 ]  M3 k6 E# [" Asecondary to depression.
9 |6 C8 N! d# A1 TThe child slept in the same bed with parents.
! Z$ Q' s! ]9 F# s; c; E( b1 YThe father would hug the baby and hold him on his/ a9 c% R- A8 J8 b  O0 Z" t
chest for a considerable period of time, causing sig-  \6 j$ O: x: S) a4 b, v
nificant bare skin contact between baby and father.
$ ~6 i* v4 [% s/ f" mThe father also admitted that after the phone call,
# v7 k. U/ W$ o6 {% awhen he learned the testosterone level in the baby
; E# \' r& K( A7 ~$ @was high, he then read the product information
; F/ o; Y6 e% Y3 Rpacket and concluded that it was most likely the rea-) y. p* f# Y. u6 ^8 I! x
son for the child’s virilization. At that time, they, w+ R$ j! Y% |: A( [
decided to put the baby in a separate bed, and the
1 _4 Z8 ]- P" r6 F) U2 vfather was not hugging him with bare skin and had
3 X6 J- ^' f/ n4 N4 Fbeen using protective clothing. A repeat testosterone
, r8 |2 F& R( wtest was ordered, but the family did not go to the8 x5 H; _. n5 g' I
laboratory to obtain the test.
# E/ Z* S+ |/ v$ K' w! wDiscussion5 R/ b; I$ F& `5 i
Precocious puberty in boys is defined as secondary. S0 P0 }, S) Z8 G# p" q
sexual development before 9 years of age.1,4& o' X$ }( b8 I2 f
Precocious puberty is termed as central (true) when
. }9 J+ d$ s1 F9 ~it is caused by the premature activation of hypo-
7 \& Z9 ~$ v( w0 u2 I+ T# W  [, Gthalamic pituitary gonadal axis. CPP is more com-
4 W2 l8 `* t% O3 `; rmon in girls than in boys.1,3 Most boys with CPP
9 e& L2 Z6 y  _" bmay have a central nervous system lesion that is$ [" l+ V  W. \: F+ |# m
responsible for the early activation of the hypothal-
* x# l% l$ f2 L6 b7 ^amic pituitary gonadal axis.1-3 Thus, greater empha-8 z5 B$ ?) X3 M" j# m) L9 n6 p
sis has been given to neuroradiologic imaging in4 A" f; @6 D8 ^
boys with precocious puberty. In addition to viril-
3 A2 s5 B- M. F/ u5 U' \" g8 m/ Fization, the clinical hallmark of CPP is the symmet-
  _& N/ n# f: `1 H* jrical testicular growth secondary to stimulation by
7 D$ k. o: n# Tgonadotropins.1,3  d8 p( r8 i: v: t/ y
Gonadotropin-independent peripheral preco-8 J, Y* w1 k6 ]: E% F# x. ]
cious puberty in boys also results from inappropriate
% L- }) T$ b1 Tandrogenic stimulation from either endogenous or7 p) Z) m' O; L& j
exogenous sources, nonpituitary gonadotropin stim-
/ p3 g. E4 |' o* ?ulation, and rare activating mutations.3 Virilizing: [( m1 W7 l+ @$ e% f5 m, U1 K
congenital adrenal hyperplasia producing excessive; R% Y9 K. Z5 K: Q6 ?8 [3 a
adrenal androgens is a common cause of precocious% ]- x: u" ]! t/ f
puberty in boys.3,41 u5 T4 U4 J+ P9 v) k3 {4 M/ s/ q
The most common form of congenital adrenal" u& L9 @. A6 M" P
hyperplasia is the 21-hydroxylase enzyme deficiency.
& D: H4 \# T+ p- P0 Z* y+ mThe 11-β hydroxylase deficiency may also result in
! w2 x& B" q4 p4 u. c& Xexcessive adrenal androgen production, and rarely,6 s$ U+ I( J3 d# @+ P6 y+ B( ]
an adrenal tumor may also cause adrenal androgen
, i8 A" q- ~3 K% }' n8 K2 M: Hexcess.1,3
' a8 {1 M+ X5 x9 @. Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! j) b9 e) |( L: t542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- c+ {" m+ @9 ^6 _
A unique entity of male-limited gonadotropin-
' u8 C( \4 r+ H4 r7 C* ?independent precocious puberty, which is also known% t4 S9 {( a& g( ]% }
as testotoxicosis, may cause precocious puberty at a
0 O- T7 r( p* ?; L6 m' @3 \: D: bvery young age. The physical findings in these boys
+ Q& ?- Y! S3 c5 o9 U8 f. iwith this disorder are full pubertal development,
3 y0 N' W3 y' [+ T. V# {6 b8 I7 Yincluding bilateral testicular growth, similar to boys
, R1 W- L; }3 Y( g0 {# g5 Dwith CPP. The gonadotropin levels in this disorder
& y7 N+ O; S! vare suppressed to prepubertal levels and do not show
2 e: x1 ^1 @) j, |pubertal response of gonadotropin after gonadotropin-" Q: R* a! I5 b
releasing hormone stimulation. This is a sex-linked
/ k4 |! F& E- T4 Tautosomal dominant disorder that affects only( r  M6 J. y( K( v3 V, |
males; therefore, other male members of the family
1 j6 P" s6 l9 c, ]2 Z$ c; n3 G, tmay have similar precocious puberty.30 ]) B: I" o- w7 p1 R) O
In our patient, physical examination was incon-+ F0 C* O3 E, N. p# {
sistent with true precocious puberty since his testi-! W" _. {8 m$ u  B
cles were prepubertal in size. However, testotoxicosis6 s+ B, z* P2 A, w. Q% h0 P
was in the differential diagnosis because his father
: |6 M* ^" t2 O4 J; d) [started puberty somewhat early, and occasionally,
. E3 X+ R4 J1 h, O' y0 p9 `testicular enlargement is not that evident in the
' L2 \) D8 |! Y1 H& a, ]beginning of this process.1 In the absence of a neg-: `. V; U1 O, i/ T* e9 ^
ative initial history of androgen exposure, our) |8 O. J4 K# C) M
biggest concern was virilizing adrenal hyperplasia,
+ b# g+ g9 J+ p: p0 F- peither 21-hydroxylase deficiency or 11-β hydroxylase& V9 {) i* y: R% ]2 B) m
deficiency. Those diagnoses were excluded by find-
+ O# C/ J: o1 E+ B8 u* u, p, Ging the normal level of adrenal steroids.9 z6 l- ~; `3 i: s+ s- J
The diagnosis of exogenous androgens was strongly
5 y! K/ x2 D$ ?) ssuspected in a follow-up visit after 4 months because
9 Z  z8 i# X/ c7 ]" l, Dthe physical examination revealed the complete disap-6 a4 m: ]  t! Q' t" b4 R, q
pearance of pubic hair, normal growth velocity, and0 J" l5 x8 r+ M6 Y! a) f
decreased erections. The father admitted using a testos-
5 j( l, p- V0 O7 Z7 yterone gel, which he concealed at first visit. He was
" b$ F2 C  K& S6 @using it rather frequently, twice a day. The Physicians’
3 d4 Q% r, o9 Y$ j3 K2 M5 Y$ n( uDesk Reference, or package insert of this product, gel or
) D& C" ?8 u% O8 ?  |cream, cautions about dermal testosterone transfer to
; ^: M* ~* F0 a- O7 O8 P" L: N" |unprotected females through direct skin exposure.
2 h+ p" C2 U3 R* c0 a3 C: DSerum testosterone level was found to be 2 times the* h9 y- u, I  X) ?2 C
baseline value in those females who were exposed to% @9 w9 J1 m& G$ e
even 15 minutes of direct skin contact with their male  B3 I. |& m8 C$ H( c+ b& u
partners.6 However, when a shirt covered the applica-
4 t7 f# t3 l$ `! e3 R" Stion site, this testosterone transfer was prevented.6 b% J! o' j( o+ q- `$ Q
Our patient’s testosterone level was 60 ng/mL,1 w5 y; _& |; O- `0 C( ?
which was clearly high. Some studies suggest that
. k1 B( z" }1 |+ C) r2 G; Kdermal conversion of testosterone to dihydrotestos-  }9 Q5 t9 @- D: [' ]7 D
terone, which is a more potent metabolite, is more% {6 Q; s5 W, p9 i5 A
active in young children exposed to testosterone2 Q7 }& `" p) Y/ Y; |+ ^
exogenously7; however, we did not measure a dihy-
0 ]- U/ a( V# R8 i; ?: Gdrotestosterone level in our patient. In addition to
5 s8 N, {( p. O4 |/ }virilization, exposure to exogenous testosterone in% C4 G; w' `3 j) t- D+ t$ x
children results in an increase in growth velocity and: j8 b: h" J+ w$ y* }3 {
advanced bone age, as seen in our patient.* Q) m# i$ I; j4 x7 [7 D7 C, d0 U
The long-term effect of androgen exposure during7 M/ f7 V# c# J9 X
early childhood on pubertal development and final" Z! v+ e9 I. Y0 B
adult height are not fully known and always remain1 j" h, E9 u3 Y5 _. F' e
a concern. Children treated with short-term testos-% e% }7 A' |% r, a9 M
terone injection or topical androgen may exhibit some
/ S( z6 I( O0 u. Iacceleration of the skeletal maturation; however, after1 m, N' G8 ]/ ~' U
cessation of treatment, the rate of bone maturation: z6 f3 j) }' M1 ^$ R
decelerates and gradually returns to normal.8,9( z: R% h7 i! J0 F: L: a2 ^; `- M
There are conflicting reports and controversy* W1 Y/ C; l5 S  u! U6 l
over the effect of early androgen exposure on adult) ?- S: ?, u/ m; U, J
penile length.10,11 Some reports suggest subnormal" U2 x8 f+ P8 u% V- |  K
adult penile length, apparently because of downreg-' D" k8 z- _2 W3 `
ulation of androgen receptor number.10,12 However,+ t- v# e  o/ _2 u* q
Sutherland et al13 did not find a correlation between
. B  [) ]( e, s; U; A' hchildhood testosterone exposure and reduced adult
: h$ j& q, C& N& @1 p% U$ Cpenile length in clinical studies.
% i6 O5 Q* u& m2 v! yNonetheless, we do not believe our patient is& o3 e* u2 x7 h/ p
going to experience any of the untoward effects from9 |  `# Y: u* m
testosterone exposure as mentioned earlier because7 D" e/ y& [( F0 e9 Z. C
the exposure was not for a prolonged period of time.9 ^/ f( j3 G5 A; h
Although the bone age was advanced at the time of! A; F/ U0 b% a
diagnosis, the child had a normal growth velocity at
  N* i. Z; \7 n% b6 J, |the follow-up visit. It is hoped that his final adult
4 b2 u$ X& V" @+ V$ `height will not be affected.0 J3 W" P, \' f1 s6 S$ c" O& ^
Although rarely reported, the widespread avail-1 [2 ]3 q& i/ l8 i+ `$ h
ability of androgen products in our society may
% M2 x: H+ L% V3 m$ r! Pindeed cause more virilization in male or female, q' C1 A. W) j. O# t; Q; j- K
children than one would realize. Exposure to andro-
# ]+ I3 Y( i' B3 vgen products must be considered and specific ques-
3 |5 f! _5 I& h# r5 Stioning about the use of a testosterone product or% P7 a9 ]3 X: G( G7 y) F* r! X2 A! }/ ^8 i
gel should be asked of the family members during7 U9 _. n( f3 g' m' s$ c
the evaluation of any children who present with vir-5 L7 i, D* j1 {! R: ?
ilization or peripheral precocious puberty. The diag-  B  \7 r$ l8 B/ [" D. E
nosis can be established by just a few tests and by
1 k4 O7 i; V* c% F/ K. R) fappropriate history. The inability to obtain such a) b* n( ^9 f% K3 T
history, or failure to ask the specific questions, may
9 @3 C/ p5 k) Tresult in extensive, unnecessary, and expensive$ Y7 L, [; o9 D4 |( K5 u: l, K" N2 i( l
investigation. The primary care physician should be6 q1 V5 |* _1 }1 a
aware of this fact, because most of these children5 W& {, \7 s3 W9 r- r  L6 l- ^
may initially present in their practice. The Physicians’, Q$ f0 R5 |2 F( V# J
Desk Reference and package insert should also put a/ c8 ?& s* n* R/ S) ~' J+ A
warning about the virilizing effect on a male or
; T, [: k, `% \: b0 p; Hfemale child who might come in contact with some-" y3 Q* I0 r% R- o" Q
one using any of these products.7 P& y( R' _! B  y2 F9 G- E
References
1 F# m: P* \4 G& V/ v1. Styne DM. The testes: disorder of sexual differentiation
7 R  I1 P' @1 ~and puberty in the male. In: Sperling MA, ed. Pediatric
( a2 `9 B, y& M& WEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' ?( ^% d# T- @/ V3 \8 a2002: 565-628.
- h+ x& K# Z0 q+ e9 a2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' {% S3 F* {& C, e% j( Z& C; l+ 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
% Z9 i  R" D) l- }& d% U& E9 @% m
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
您需要登錄後才可以回帖 登錄 | 立即注册

本版積分規則


快速回復 返回頂部 返回列表