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) W7 P$ b# ~$ L+ i4 j4 b6 ]
Boy Induced by Indirect Topical, r/ |9 c7 t( C( E# r8 K6 t/ \
Exposure to Testosterone
. Q; Y1 o5 b! S/ ]% r4 a  xSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 f# h% W/ M- f% ^& _; |and Kenneth R. Rettig, MD1
" o" y( k. Z7 W! r( A9 r$ O4 G% DClinical Pediatrics/ S. R! m9 v8 D9 r! u- S
Volume 46 Number 6
% g- V( D5 I7 q  B4 ^) b5 T9 N2 yJuly 2007 540-543
! ?6 P9 Y% R1 p5 c- N© 2007 Sage Publications
" x, a. o* d# ~# a# T/ u10.1177/0009922806296651
0 C) z5 }8 g9 _: ?http://clp.sagepub.com* Y% k, q2 d' [$ q
hosted at
/ q6 W3 `) y6 G0 G6 yhttp://online.sagepub.com
. \7 P; B% x  [0 H  W* A+ g1 APrecocious puberty in boys, central or peripheral,# g0 [& Q. ?* O0 r
is a significant concern for physicians. Central3 [, Q$ u% ~5 m) H
precocious puberty (CPP), which is mediated0 R7 H% Y* S" L9 c+ F$ _
through the hypothalamic pituitary gonadal axis, has
% v2 u0 W, n" R) U3 ?a higher incidence of organic central nervous system
$ _3 G$ @. {8 S) X7 Ulesions in boys.1,2 Virilization in boys, as manifested
$ _  }8 W) h. |+ K$ K  X- Vby enlargement of the penis, development of pubic
0 T" Y0 N2 a. ~6 V- Q9 G+ |% ]% ahair, and facial acne without enlargement of testi-4 B: |4 t) F: J5 S! x2 t# a
cles, suggests peripheral or pseudopuberty.1-3 We7 N' O; z( h! v
report a 16-month-old boy who presented with the" M) e$ b( m. b/ O3 |" g
enlargement of the phallus and pubic hair develop-
( N2 Z) m4 V" M3 H6 J2 \ment without testicular enlargement, which was due
) ~- d  l/ L) u, c) X5 h0 ?1 `% {) Eto the unintentional exposure to androgen gel used by. m5 @4 q) D- J- i, a
the father. The family initially concealed this infor-
3 i/ L2 ?! B4 o2 P, E" `) g  xmation, resulting in an extensive work-up for this
% y* H0 K6 a3 x, H* c' I1 Nchild. Given the widespread and easy availability of! k. g6 d& A% k4 H. |
testosterone gel and cream, we believe this is proba-- z9 S) R% k0 {. G2 ~) G% [
bly more common than the rare case report in the
, Q' I) b7 A8 e8 ^4 G) aliterature.4
- N3 B; X- b9 T1 HPatient Report" {8 E  y) C* e6 b4 B/ D
A 16-month-old white child was referred to the& z6 H9 j% @5 Z+ k! E( W! \% ]
endocrine clinic by his pediatrician with the concern
+ s6 t: S4 g+ T: I7 `6 H9 ?of early sexual development. His mother noticed) U. j0 V1 M# ?  O( ]
light colored pubic hair development when he was
! c0 }: ^  f1 J, R6 oFrom the 1Division of Pediatric Endocrinology, 2University of# h  l8 Q: r5 g
South Alabama Medical Center, Mobile, Alabama.& x6 s$ ]1 o5 G) B, B
Address correspondence to: Samar K. Bhowmick, MD, FACE,, S( |& M$ B9 X  s% \( a& w8 i
Professor of Pediatrics, University of South Alabama, College of( [  e# s4 c4 F$ f5 \
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;: `8 l+ H# z' Y5 m
e-mail: [email protected].: l) X2 ?8 c$ Z. q% Q1 G
about 6 to 7 months old, which progressively became: Z  g" g/ X% J( n- n
darker. She was also concerned about the enlarge-" y9 \* e( m1 {6 p' A0 [
ment of his penis and frequent erections. The child
& o- d0 ^" n: H3 c3 Q' a" y2 Vwas the product of a full-term normal delivery, with$ F) M6 l1 k" [$ a# l
a birth weight of 7 lb 14 oz, and birth length of
, L0 U1 p- r( X20 inches. He was breast-fed throughout the first year8 I7 @" u8 t% F0 {
of life and was still receiving breast milk along with) N# i. t" Y* j5 v
solid food. He had no hospitalizations or surgery,
6 o0 O: T$ ~5 I& {" Zand his psychosocial and psychomotor development2 c. h  ?, p1 H4 k( e: g: d
was age appropriate.! E8 i+ t6 {) L
The family history was remarkable for the father,
% p7 j5 I& n4 awho was diagnosed with hypothyroidism at age 16,1 U' K9 n  K/ x2 x$ M$ H8 J6 `- k1 G- e4 w
which was treated with thyroxine. The father’s
* ?; x+ {* d* e. {4 \8 B7 a3 w6 Uheight was 6 feet, and he went through a somewhat, e' n' u( C( S: M2 {. [
early puberty and had stopped growing by age 14.
1 ~9 J  c& w  I9 F: VThe father denied taking any other medication. The
- b/ x+ G6 Q/ Uchild’s mother was in good health. Her menarche
/ }4 ?, w$ l" P/ awas at 11 years of age, and her height was at 5 feet
4 u5 n8 J1 [4 _# R5 inches. There was no other family history of pre-
% s- h' K/ c: m; mcocious sexual development in the first-degree rela-- f! f; e. {$ y0 n  c; v: C* Z% v8 I$ c
tives. There were no siblings.
- N4 ?* g% k; J1 y- }) \; xPhysical Examination( K- J/ F( r1 e7 ?
The physical examination revealed a very active,, \; P/ G! N+ Z5 }/ u5 [
playful, and healthy boy. The vital signs documented% n" c  F0 z; p8 T+ W" Y
a blood pressure of 85/50 mm Hg, his length was! y! B- l5 u6 ]4 @+ E
90 cm (>97th percentile), and his weight was 14.4 kg
" |+ o) M0 S7 j, ^/ `(also >97th percentile). The observed yearly growth; P8 f- ~7 H- S) r0 h! T% |
velocity was 30 cm (12 inches). The examination of. m1 o- Q( K& u  r$ E6 x
the neck revealed no thyroid enlargement.
# M; y" V" c. cThe genitourinary examination was remarkable for
, K/ Y' Z" T$ D3 \9 r7 y0 Genlargement of the penis, with a stretched length of9 i% Z. R4 ]8 @" y1 T. U
8 cm and a width of 2 cm. The glans penis was very well
  I# V/ N! Z; _8 u) d8 Q: r1 Zdeveloped. The pubic hair was Tanner II, mostly around
) ^: p  X: z$ J: l2 [7 G" p1 @540. O- r8 w' [2 s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 P- g7 D. x2 I* }7 E# n5 C, B. {* ethe base of the phallus and was dark and curled. The
# c$ q* `7 ]9 y3 \0 Mtesticular volume was prepubertal at 2 mL each.) [7 H! e$ c- k1 ^+ q0 C
The skin was moist and smooth and somewhat
% d6 B" d' X" G  w6 J4 p1 Doily. No axillary hair was noted. There were no
( O" V: g! q4 N2 E! B/ |abnormal skin pigmentations or café-au-lait spots.! I( [+ u( X: l0 s: n1 |
Neurologic evaluation showed deep tendon reflex 2+
" N+ ]$ Y$ a% a) @" A$ P$ l7 Zbilateral and symmetrical. There was no suggestion
: Z# ]: z) G! Aof papilledema.* ^9 ]- ~% y: J
Laboratory Evaluation
* @; ~1 ^4 i8 L& zThe bone age was consistent with 28 months by
! `$ i, G/ o) ~6 h" o2 g3 k& O' F6 Uusing the standard of Greulich and Pyle at a chrono-8 p+ @* @: v2 F. N: x
logic age of 16 months (advanced).5 Chromosomal% K+ n# g4 j, B, f! `  B/ E
karyotype was 46XY. The thyroid function test( d- ~1 {* ?- `
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
$ W" X- a2 H4 M) U# D; `3 Blating hormone level was 1.3 µIU/mL (both normal).
# c: r4 |4 q' c. p6 `The concentrations of serum electrolytes, blood
2 B1 B% Z% L1 G" L* H+ O9 E8 Y- K5 h9 surea nitrogen, creatinine, and calcium all were
1 K- t( i9 ?1 e; u7 J# @! twithin normal range for his age. The concentration! N! p( W3 y" |  v5 S
of serum 17-hydroxyprogesterone was 16 ng/dL! t& l- t4 T: d6 D8 T0 ]6 b
(normal, 3 to 90 ng/dL), androstenedione was 20: D" o7 [8 c! |/ W2 }5 k
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
+ U. x# d( A8 K) m' gterone was 38 ng/dL (normal, 50 to 760 ng/dL),
) s% _: J5 s' d$ ^8 s. p* F1 Adesoxycorticosterone was 4.3 ng/dL (normal, 7 to
; n& }) u6 f$ y& Z6 n. [49ng/dL), 11-desoxycortisol (specific compound S)6 A# P3 F$ A. R0 [, K# E
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; l$ t) g7 g. t) I4 q% S
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* _# ^' D7 f* w& J6 P6 Otestosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 m5 x) S" H1 K" v
and β-human chorionic gonadotropin was less than
6 r2 R) a8 F$ e% s5 R5 mIU/mL (normal <5 mIU/mL). Serum follicular% a, C4 S6 Z. k7 u
stimulating hormone and leuteinizing hormone' C+ B/ d; X7 V3 X8 A
concentrations were less than 0.05 mIU/mL- D. c% S& z* z) \
(prepubertal).* J. b2 R9 \9 W7 N1 G, Y  \
The parents were notified about the laboratory3 B: k) j1 l. e) ~
results and were informed that all of the tests were3 x5 |# }5 a' D) H# _9 h+ e  `0 W
normal except the testosterone level was high. The2 l& o+ z4 K8 d- ?% d
follow-up visit was arranged within a few weeks to
1 J) V% M( H1 a! sobtain testicular and abdominal sonograms; how-
* j& _9 b5 r/ X: L6 i; k0 Yever, the family did not return for 4 months.( ?' t, O& O" V& Y2 @
Physical examination at this time revealed that the
1 l; c% Y- u1 p. h$ I- Z4 Cchild had grown 2.5 cm in 4 months and had gained
! }& k* y% r# O, M7 e9 H4 P2 kg of weight. Physical examination remained
; Q3 c! c# M7 a5 `9 ]' a: B0 M* munchanged. Surprisingly, the pubic hair almost com-
. n. s" R8 P. {2 ?pletely disappeared except for a few vellous hairs at4 \6 U+ Q) b" H( o. l) b: T
the base of the phallus. Testicular volume was still 2: m9 [  O, ?2 D7 B+ i* d% b
mL, and the size of the penis remained unchanged.
6 j, f, B+ R/ Z4 t8 bThe mother also said that the boy was no longer hav-% {7 d' S1 w! Y3 t" w& E9 w
ing frequent erections.
" a7 G* J$ E( ^% G  X5 O6 RBoth parents were again questioned about use of1 ]9 @6 o6 @; |( I/ h$ z, i
any ointment/creams that they may have applied to0 S4 j2 D! ]6 V- k& c
the child’s skin. This time the father admitted the" P2 X! d! `0 r
Topical Testosterone Exposure / Bhowmick et al 541
2 t4 Y  a6 g* h2 Zuse of testosterone gel twice daily that he was apply-
+ y1 y4 ~8 n5 `& _8 Wing over his own shoulders, chest, and back area for
5 S7 h/ t% \" x$ |, m: [8 `a year. The father also revealed he was embarrassed
+ e( G9 O5 c3 Mto disclose that he was using a testosterone gel pre-) c7 g7 j$ C$ G
scribed by his family physician for decreased libido
/ H9 m2 G$ A) P; x+ ?) ?/ s+ K! vsecondary to depression.  O* i8 x$ L+ T& J% V
The child slept in the same bed with parents.
! J% c* x6 T1 i! YThe father would hug the baby and hold him on his! y' @% I- O% n1 T
chest for a considerable period of time, causing sig-
% i5 R5 N4 U# _2 N. b# lnificant bare skin contact between baby and father.
- }. V; a% Q3 l, ?2 T# S% R/ _" e- `The father also admitted that after the phone call,
0 u9 N& v, `  M  V8 T* Y; c2 uwhen he learned the testosterone level in the baby
2 Y. B* L$ L$ ^/ b+ a6 V$ g$ Owas high, he then read the product information% w/ i# y' y" `8 o- ]* p
packet and concluded that it was most likely the rea-# T* u2 i& [0 M3 `6 y5 n" A5 m/ _% }
son for the child’s virilization. At that time, they
8 n# q# q7 u8 n/ l; i' B0 Adecided to put the baby in a separate bed, and the+ U( p& v  J/ K7 L; G
father was not hugging him with bare skin and had, C7 [( G% i% `( [( _, ]1 n1 K
been using protective clothing. A repeat testosterone2 W$ {' Q% W% `1 [
test was ordered, but the family did not go to the% A- I" `3 O( ^& J1 Z  v, L
laboratory to obtain the test.1 ?3 p4 x0 S# A- F# F" f2 R; P" O
Discussion; E' D3 J/ C7 t. L7 N( b3 }
Precocious puberty in boys is defined as secondary
0 Y9 k  C% I- Y0 N( U5 Rsexual development before 9 years of age.1,4
0 d9 Z( l; N2 N: `. y4 [Precocious puberty is termed as central (true) when
0 J$ L. |5 Z. @1 |it is caused by the premature activation of hypo-/ V$ v4 E6 t, Z# |1 Q; o
thalamic pituitary gonadal axis. CPP is more com-
/ m& i5 Z: c6 _% c1 A9 |mon in girls than in boys.1,3 Most boys with CPP
' n" h2 t1 H4 qmay have a central nervous system lesion that is
& `( Y0 H, w% x% o- \+ Kresponsible for the early activation of the hypothal-" h$ q4 O* v% a  z% y4 O
amic pituitary gonadal axis.1-3 Thus, greater empha-1 a( X% ]3 k4 w( v7 R7 J8 Q
sis has been given to neuroradiologic imaging in4 i- }+ |, _2 h9 W3 x1 _  x0 D  e/ ?
boys with precocious puberty. In addition to viril-2 g' s, C7 r7 I; J  Y) U3 W  P
ization, the clinical hallmark of CPP is the symmet-
1 S+ W  R% H8 N$ s9 Urical testicular growth secondary to stimulation by/ C/ N( W. W" r, q* `
gonadotropins.1,39 n. U9 Q% `% ~; v
Gonadotropin-independent peripheral preco-& |% e0 k0 {9 r9 h8 G
cious puberty in boys also results from inappropriate
0 d0 a* S8 B2 kandrogenic stimulation from either endogenous or, T2 P$ ?* p/ R7 J( E
exogenous sources, nonpituitary gonadotropin stim-
: C; S4 Z' j. j8 g) `; Lulation, and rare activating mutations.3 Virilizing
( |, ~$ c8 b# O5 ocongenital adrenal hyperplasia producing excessive
5 {4 Y# ?! Z7 K! \  G6 B) ?- f8 U5 Padrenal androgens is a common cause of precocious
9 @$ H( D. ?9 Mpuberty in boys.3,4
( h5 H1 R) w. S! V- m5 ?" PThe most common form of congenital adrenal
/ M: b) B) S% u) c% thyperplasia is the 21-hydroxylase enzyme deficiency.
: i+ p! ^! z" |. h% F  B! f4 S& QThe 11-β hydroxylase deficiency may also result in
  R* S/ E, W6 {( x& nexcessive adrenal androgen production, and rarely,
9 H  n$ U7 G6 P8 N* z4 i; |3 X; q1 Pan adrenal tumor may also cause adrenal androgen4 T$ y9 y! A7 F
excess.1,3% k) {" C; q" u6 l
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 u( N1 O  f5 n! c
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007  z" T' N$ o: g8 W+ S; h! {
A unique entity of male-limited gonadotropin-( W/ f9 t6 E/ c+ ?& r
independent precocious puberty, which is also known
2 z7 W8 q# q0 H( V7 B3 s. j  `as testotoxicosis, may cause precocious puberty at a
. A# y: q. Z9 N8 C+ F$ n) [( C) p" Qvery young age. The physical findings in these boys
! Y7 c" C4 y/ ^2 Z; q9 S% ~with this disorder are full pubertal development,
+ }) M( j+ c# z; X; Wincluding bilateral testicular growth, similar to boys3 @  z& e/ ~  u( I1 W2 m! l
with CPP. The gonadotropin levels in this disorder
! n' Q! U% Y( _+ ^4 p7 Tare suppressed to prepubertal levels and do not show3 m  W0 N- {; k0 C+ A
pubertal response of gonadotropin after gonadotropin-
' f- J$ @2 J# H' V7 d5 F9 z- yreleasing hormone stimulation. This is a sex-linked2 ^" }6 X) N( q( z
autosomal dominant disorder that affects only) r4 w  N* c, A  P2 w1 i3 x
males; therefore, other male members of the family
# d+ n8 m) `" rmay have similar precocious puberty.3, l2 E: @" x  s8 _
In our patient, physical examination was incon-
' N- p, v0 R% C& g; esistent with true precocious puberty since his testi-$ W0 A. }' g0 A! l$ L; h& B
cles were prepubertal in size. However, testotoxicosis
  L7 @4 p  C6 Nwas in the differential diagnosis because his father
, _% Z0 [! M7 A3 |- z9 W: |: fstarted puberty somewhat early, and occasionally,
- D7 \: V; U3 o5 ?7 n5 P0 ttesticular enlargement is not that evident in the
0 d7 g" A1 L) I# a9 ]6 l  t: ubeginning of this process.1 In the absence of a neg-
8 o* q$ S* d/ X* f9 Aative initial history of androgen exposure, our# L  f$ P' s+ {; E. d9 ?
biggest concern was virilizing adrenal hyperplasia,
0 j% J  ~" Y: I4 y* qeither 21-hydroxylase deficiency or 11-β hydroxylase
/ p! h0 }. N0 N. l$ Ldeficiency. Those diagnoses were excluded by find-
% J' B7 a* l9 A3 c+ ying the normal level of adrenal steroids.
" W* ^2 h2 ^  Z" zThe diagnosis of exogenous androgens was strongly1 G. ^5 F! f# L5 G7 _  u! n9 q# e
suspected in a follow-up visit after 4 months because
' `6 U3 u% e0 _) U: I: ~) o. M( h4 fthe physical examination revealed the complete disap-: s! k& r( B( j9 o7 o/ H: V& A& A( o
pearance of pubic hair, normal growth velocity, and  R1 i/ S( C1 l! T2 ^
decreased erections. The father admitted using a testos-
4 \, K. [$ H# m! b1 m/ ^- l* h; q" ?terone gel, which he concealed at first visit. He was
9 s1 D$ A+ [" N) U' @using it rather frequently, twice a day. The Physicians’
  @* d3 V1 F8 W8 }. j) ]Desk Reference, or package insert of this product, gel or0 R- V$ ~7 l+ v- k
cream, cautions about dermal testosterone transfer to5 u2 N2 c4 ?$ |* ^
unprotected females through direct skin exposure.! Z' Q4 r6 m2 F3 ^( K" c! J; M& q
Serum testosterone level was found to be 2 times the- H" D& S  z4 ]  k' W5 D! }
baseline value in those females who were exposed to
0 F: ]. ^& n: w9 S  a; j( \even 15 minutes of direct skin contact with their male6 D# B! N. d# l: e" F( M
partners.6 However, when a shirt covered the applica-
) O# d' i9 U" Z* ]7 w; otion site, this testosterone transfer was prevented.
8 A6 d; I# {' r8 R4 n% NOur patient’s testosterone level was 60 ng/mL,
) C$ u* |) n9 N. }which was clearly high. Some studies suggest that
9 x  s: U7 F" P+ b5 o, E, Mdermal conversion of testosterone to dihydrotestos-' [2 e6 r% C% ?# U; y# D' ^' o
terone, which is a more potent metabolite, is more
9 y3 D: h4 `- ^. ^  a+ `active in young children exposed to testosterone" o' f# X3 N- U5 a6 N! e
exogenously7; however, we did not measure a dihy-
* x' k. J& d7 E5 q$ r9 k, mdrotestosterone level in our patient. In addition to) }% @" `. W( @9 p! o5 H
virilization, exposure to exogenous testosterone in
1 {, G) r( U4 ?( y0 P/ `/ Mchildren results in an increase in growth velocity and
. p! ?1 ]6 V% D# c5 Iadvanced bone age, as seen in our patient., a* T0 ~  k) Q7 ?3 Z8 p! ^
The long-term effect of androgen exposure during
  g5 M' ~$ Z- @% wearly childhood on pubertal development and final9 }+ H' ]' u% }+ [, m( d' K
adult height are not fully known and always remain
6 H6 c. K1 r- Y" X# da concern. Children treated with short-term testos-, E* S; V' H' u6 X/ b# Y) x
terone injection or topical androgen may exhibit some
' V# p" G& G) |: u4 E2 z. i4 n9 Macceleration of the skeletal maturation; however, after
) K* C; a' R1 {" Dcessation of treatment, the rate of bone maturation
" g* c* O$ ~0 `" g. z& P8 K; A* |decelerates and gradually returns to normal.8,9' r* K3 f! [/ M* n  n* E8 R# c
There are conflicting reports and controversy; ^  [6 L  F7 w7 e1 c
over the effect of early androgen exposure on adult: R* z& ^2 B0 J2 Q9 i
penile length.10,11 Some reports suggest subnormal
( c7 \0 T0 f) f2 p& qadult penile length, apparently because of downreg-  X- C0 P& Y8 b  W% S5 I
ulation of androgen receptor number.10,12 However,
: }  D- E* m* k7 v6 _Sutherland et al13 did not find a correlation between
* J7 K  u/ k$ zchildhood testosterone exposure and reduced adult% f# |' N* H4 T' v- Q& ~
penile length in clinical studies.' V  ?1 |8 h/ q5 _5 U: X# l7 v
Nonetheless, we do not believe our patient is
. P4 t) l2 \: g+ K/ I3 ugoing to experience any of the untoward effects from
4 [6 {1 }8 S2 `, r; Ktestosterone exposure as mentioned earlier because
2 y7 Y0 U% d8 j% H9 s8 l- Kthe exposure was not for a prolonged period of time.
& M; Q8 @0 |+ F$ S. T/ OAlthough the bone age was advanced at the time of
& w, ~9 Q6 n1 c& C2 N8 |diagnosis, the child had a normal growth velocity at
2 F( |! J6 f9 Ythe follow-up visit. It is hoped that his final adult4 I7 e& P& [4 Y5 H: x8 U
height will not be affected.. ?9 r( o. I' B# w- H8 Y
Although rarely reported, the widespread avail-9 N3 m2 u3 V4 G+ n
ability of androgen products in our society may
$ n% j' m5 g  w+ {0 U/ E, a" Vindeed cause more virilization in male or female
* a* O; E- b6 j, S  p+ T# N/ ychildren than one would realize. Exposure to andro-% G- X) b! P* f: A  y$ f3 O
gen products must be considered and specific ques-9 p6 Z# s: R; e: V9 \0 O- _
tioning about the use of a testosterone product or
& e) @, e& t# @( ygel should be asked of the family members during- l' n$ Q$ l4 U9 `
the evaluation of any children who present with vir-
: b9 B# b; `* N: @  c7 d9 wilization or peripheral precocious puberty. The diag-3 u' h! o% T- V0 r; g  C) R
nosis can be established by just a few tests and by
: }& o% H5 |, L3 S" g. qappropriate history. The inability to obtain such a4 J: y# e- {- S
history, or failure to ask the specific questions, may
4 n- R6 j8 C0 Q) X/ xresult in extensive, unnecessary, and expensive
- n8 Y) M4 K" S0 X$ vinvestigation. The primary care physician should be
7 @/ N- n0 L0 z( h& N# aaware of this fact, because most of these children
6 s+ ?: c1 D& b& Jmay initially present in their practice. The Physicians’# ^" Y. _% f+ @. J  V
Desk Reference and package insert should also put a0 V8 F: H, r& O$ a/ A8 ~" N
warning about the virilizing effect on a male or
1 b: Z4 ?# x/ W2 c' h( e+ zfemale child who might come in contact with some-' s1 d8 ?' r0 g) l$ D
one using any of these products.
" u6 O* |" J" Q. lReferences0 x' z+ {# {# I
1. Styne DM. The testes: disorder of sexual differentiation4 Y% m3 e* }+ W; v; k- ~# a
and puberty in the male. In: Sperling MA, ed. Pediatric; b; p2 e! m# }
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. e3 k: M) e5 B
2002: 565-628.
( ^+ y2 `$ a- Y* Q+ O, B2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 g7 h% u" Q5 F5 d
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
; }( O3 l  z! `: `+ |Boy Induced by Indirect Topical
) ]+ Q: q# i! |8 |3 r" PExposure to Testosterone
2 m5 i' I% U, K' qSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 \8 L* }, v8 M, P% B; eand Kenneth R. Rettig, MD1  a$ o4 B1 f- R) x3 N4 [/ L, b
Clinical Pediatrics+ Y' \. \  x5 h* z7 J: a
Volume 46 Number 6# H1 ]7 x' ?- [& w0 \- }! g
July 2007 540-543
& K" t6 o( v1 p" X/ W- N; m0 ~© 2007 Sage Publications% q1 J1 ~7 m! s1 N
10.1177/0009922806296651
9 }+ S: N1 d; H$ m' yhttp://clp.sagepub.com
9 ~% D0 e, @* jhosted at1 I' Z+ d4 a; A4 G/ v
http://online.sagepub.com  |* |- f" n; Q! c0 W
Precocious puberty in boys, central or peripheral,4 I0 ?. C- j( q3 d) L
is a significant concern for physicians. Central
7 g- ^* g. Q' W3 ^2 gprecocious puberty (CPP), which is mediated( @9 f0 R" H& m4 n; b% C
through the hypothalamic pituitary gonadal axis, has
5 k: c2 I; ]+ i. d% G0 D" ua higher incidence of organic central nervous system
( y5 W4 V9 V  ]4 C/ Tlesions in boys.1,2 Virilization in boys, as manifested+ W0 F8 [& ^& _6 `5 T& b' P
by enlargement of the penis, development of pubic5 m' l' U' R: }6 P+ @
hair, and facial acne without enlargement of testi-
+ C5 s+ D9 f# Z7 j& G0 l2 ^' s. vcles, suggests peripheral or pseudopuberty.1-3 We
. K! }5 g/ i0 g. q  sreport a 16-month-old boy who presented with the
% \# ?2 P( m2 G( ?1 eenlargement of the phallus and pubic hair develop-
4 f. t$ o! L7 v9 _4 q. g5 F& [ment without testicular enlargement, which was due. k  l: e7 N8 {* ^, c8 V8 b8 k0 N
to the unintentional exposure to androgen gel used by: S, X- r$ S' ^
the father. The family initially concealed this infor-& J' J8 N$ A( W, [
mation, resulting in an extensive work-up for this4 A. A* l9 b0 J, T) P) r
child. Given the widespread and easy availability of3 N0 e5 V/ \) _+ G. p0 l
testosterone gel and cream, we believe this is proba-9 {6 k. |* O  ?4 h2 D, K0 u" y& b
bly more common than the rare case report in the  |% Z; w" G: R6 m  X6 c* k' f
literature.40 m0 ^) l2 D0 x/ v
Patient Report' J1 v7 M/ {& f* A
A 16-month-old white child was referred to the/ r% |4 i/ y# z& B
endocrine clinic by his pediatrician with the concern
% d* P0 ~$ t& }0 L) bof early sexual development. His mother noticed
% s7 |6 X! e$ I- G7 dlight colored pubic hair development when he was
: ?5 Z* t5 r" y' p: ~From the 1Division of Pediatric Endocrinology, 2University of
; G( A. j3 l) j% t8 _+ H% [* l) LSouth Alabama Medical Center, Mobile, Alabama.6 }  c1 r9 C3 z  f
Address correspondence to: Samar K. Bhowmick, MD, FACE,
  N! j+ V( }- i" nProfessor of Pediatrics, University of South Alabama, College of
2 w% z; }$ \* iMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
* A0 W9 G) y# e2 ?: Ie-mail: [email protected].! M% \8 B5 T4 |# e: B! P, d0 N7 T
about 6 to 7 months old, which progressively became
' R* E' p. K& A, t9 l& Sdarker. She was also concerned about the enlarge-
+ \- J5 S# @& h- I: b8 g' E* iment of his penis and frequent erections. The child
6 `# W8 V9 T. X7 |3 x. T2 xwas the product of a full-term normal delivery, with% z0 X; c( }) {. V' Y5 {- Q
a birth weight of 7 lb 14 oz, and birth length of) s' B, |" E: I$ H! {" P* {
20 inches. He was breast-fed throughout the first year
% N2 l3 X7 s4 q' y5 F: ]( [- wof life and was still receiving breast milk along with9 @/ k0 {, {% T- ^
solid food. He had no hospitalizations or surgery,) T8 U) b, P: \9 D- s# ]
and his psychosocial and psychomotor development
. p, l8 ~+ A9 z4 `  ^( Jwas age appropriate.
7 L. W" _7 M% B* g; Q* n# WThe family history was remarkable for the father,: d$ [2 ^5 q5 F' h
who was diagnosed with hypothyroidism at age 16,
8 ?9 M9 D2 M1 W# k  d; [which was treated with thyroxine. The father’s
6 w; O' Y, Y. }: Oheight was 6 feet, and he went through a somewhat8 w4 T) l9 ^9 |# b' k3 C' \
early puberty and had stopped growing by age 14.
- j0 h" k$ D) c: R9 y8 SThe father denied taking any other medication. The
  }/ Y: a" }8 m1 u$ f, w& J: Mchild’s mother was in good health. Her menarche9 v( g( K3 w4 B
was at 11 years of age, and her height was at 5 feet+ t- }( ^; D7 S- H
5 inches. There was no other family history of pre-
! Z/ P$ P( E3 @3 ]) x$ d- H4 Fcocious sexual development in the first-degree rela-7 ^" I* [9 L1 }4 {1 X3 D) D$ P3 h
tives. There were no siblings.
6 X) {6 I5 L" i$ D* K  P0 d8 KPhysical Examination
& \* P" q# F+ z2 nThe physical examination revealed a very active,- a4 ?+ F* c! q5 I# t% T8 |
playful, and healthy boy. The vital signs documented6 Q7 v( d+ s/ [
a blood pressure of 85/50 mm Hg, his length was
% y! M9 l8 y0 D9 i5 X% n: h90 cm (>97th percentile), and his weight was 14.4 kg: Q1 Q$ c* F8 O& |0 t  k1 l
(also >97th percentile). The observed yearly growth5 b( z$ G7 ]0 o
velocity was 30 cm (12 inches). The examination of& D7 `7 F! ]- J& ]! w
the neck revealed no thyroid enlargement.
/ D8 U+ `: Z7 ]The genitourinary examination was remarkable for
2 f2 E1 M5 i6 ^# q+ Jenlargement of the penis, with a stretched length of
$ g& Z3 H8 d: V- F( w. \4 Q8 cm and a width of 2 cm. The glans penis was very well
# N  W' J/ D( X$ h: Q7 ^1 qdeveloped. The pubic hair was Tanner II, mostly around  E) Q7 _+ `6 d9 \3 I: v4 A8 [0 e
5403 L9 m: f: e2 A! D; ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( K$ Q% k) N/ l3 {the base of the phallus and was dark and curled. The( n% Q+ w+ W1 ~# j9 x/ G
testicular volume was prepubertal at 2 mL each.
4 d# Z4 R4 ~5 z" HThe skin was moist and smooth and somewhat
2 r: @  @( w" f# j1 U6 Foily. No axillary hair was noted. There were no2 W! C3 P9 [5 a  u
abnormal skin pigmentations or café-au-lait spots.
3 W3 x& @4 A- D6 zNeurologic evaluation showed deep tendon reflex 2+: x& T1 }! s( l4 l# Z1 b  U: n* `
bilateral and symmetrical. There was no suggestion
0 M& j. I3 C0 B4 S1 l# Vof papilledema.
+ B- C4 y! F( o3 ~( fLaboratory Evaluation) E! N" i' e) S7 O" E* ~/ A; L
The bone age was consistent with 28 months by6 O8 x. L! m; J9 [' q# k
using the standard of Greulich and Pyle at a chrono-
4 d1 M" A8 e" I( R6 I0 }logic age of 16 months (advanced).5 Chromosomal* L6 P' z/ H( }8 d5 O0 y4 X+ }  Q
karyotype was 46XY. The thyroid function test
& q% I5 }& Y& I8 V; P( Y1 M* Fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
* F9 g& b* w1 j2 D: zlating hormone level was 1.3 µIU/mL (both normal).
4 M. a1 m* f+ t- J8 }& L- _The concentrations of serum electrolytes, blood6 t0 D6 y; n5 H" o; m; h
urea nitrogen, creatinine, and calcium all were
2 Z2 Y0 H. t" y- i# K& r$ F" Zwithin normal range for his age. The concentration
8 p- U; x! j3 H$ P) aof serum 17-hydroxyprogesterone was 16 ng/dL8 Z4 b; T. T/ h" b4 [3 X
(normal, 3 to 90 ng/dL), androstenedione was 205 _* T9 C* V& `
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  l4 x% l4 _8 b4 C% ^$ E* D
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 o/ I6 Q$ F  [5 [% v# o; v  vdesoxycorticosterone was 4.3 ng/dL (normal, 7 to. y. b6 H/ m# x' K8 i, y
49ng/dL), 11-desoxycortisol (specific compound S)( G, l" h$ _) N- ]8 c% I
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
# _- e; e0 L5 c1 k5 k- n) f7 rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ }2 P( E6 J8 U% I
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ \* l! Q1 m  m$ _) g. Sand β-human chorionic gonadotropin was less than
& y8 @0 i& N+ \9 g8 I+ g, n9 B5 mIU/mL (normal <5 mIU/mL). Serum follicular$ h- C( F* P. |2 C# H+ P. c& y$ T
stimulating hormone and leuteinizing hormone
/ q; f( G& `, Z0 M( @  yconcentrations were less than 0.05 mIU/mL/ W3 C9 I: P( ]8 u$ z, n$ }
(prepubertal).
  q' c6 v8 w4 D. A- \: t3 S0 EThe parents were notified about the laboratory
+ y' @2 r$ W3 e, |2 S) _) Oresults and were informed that all of the tests were# n/ S+ k# V6 I/ V- d! M" J' M
normal except the testosterone level was high. The  ]* ~# O7 M" j, ^. z, |; C: s
follow-up visit was arranged within a few weeks to; s2 z, O/ ?' M2 F! q2 a8 ]% j# v
obtain testicular and abdominal sonograms; how-* E6 K3 K: v9 t4 f# `; r0 x; |
ever, the family did not return for 4 months.
' ^& B1 E% t0 s4 y- |Physical examination at this time revealed that the, u0 m* U: \8 W/ A8 u2 T1 C, e
child had grown 2.5 cm in 4 months and had gained
- E  ~7 f& Z: q& r2 kg of weight. Physical examination remained0 N) I& P2 A$ F
unchanged. Surprisingly, the pubic hair almost com-
' I$ G2 Y6 [9 s  P2 c% D+ Y9 apletely disappeared except for a few vellous hairs at' Q  K+ u! i, L& v
the base of the phallus. Testicular volume was still 20 P; O# ?1 v1 i  w
mL, and the size of the penis remained unchanged.( Y+ Y' \( @$ P. w, x6 V/ R
The mother also said that the boy was no longer hav-
" S. g: L9 _3 |$ }8 i" m) ming frequent erections.# P% q) s2 q( \. }
Both parents were again questioned about use of
- G9 [; [% v( b8 Q7 ^9 Hany ointment/creams that they may have applied to
/ z" ~: K& W2 ^. Rthe child’s skin. This time the father admitted the
4 ]4 a/ u7 B3 W, v! @* M$ dTopical Testosterone Exposure / Bhowmick et al 541
# l, I+ K0 i/ q, H2 }use of testosterone gel twice daily that he was apply-
2 K; {! B3 _. V: Hing over his own shoulders, chest, and back area for4 j1 R8 [' C0 f% }5 c5 I3 k
a year. The father also revealed he was embarrassed! @+ a( Z2 J% }5 [# Z# ~8 L
to disclose that he was using a testosterone gel pre-) h6 ~- ~4 f$ o' W
scribed by his family physician for decreased libido) e9 L* r8 |/ K1 Z
secondary to depression.; C2 |  ?3 ~' @4 |, S
The child slept in the same bed with parents.  H6 d2 ^' M! m3 d0 M4 S
The father would hug the baby and hold him on his8 F  j; Y. h6 n: {
chest for a considerable period of time, causing sig-
/ L: P  H/ e2 o) d8 ]nificant bare skin contact between baby and father.
7 U6 u' z1 F1 y8 [0 g. t) Q+ ]The father also admitted that after the phone call,
- E0 }" q# a9 {when he learned the testosterone level in the baby% l/ P# k+ S# T' i
was high, he then read the product information
" ~& _% x! |. v' {! m! \packet and concluded that it was most likely the rea-
: z. v( W, M) M; p" m) o9 yson for the child’s virilization. At that time, they; X* `8 u2 N5 N9 o7 \  X4 T
decided to put the baby in a separate bed, and the
3 W5 W& B# x% s; \% J' t  o& m% ?father was not hugging him with bare skin and had) a( J- b9 P: z
been using protective clothing. A repeat testosterone
  q) |& J. z% g: w1 S8 Q3 ltest was ordered, but the family did not go to the5 J) t* e2 e* }& c  a0 x- K
laboratory to obtain the test.- |% _1 a5 F5 m  E" m3 q( I7 u
Discussion7 e; e' _: ~6 Y2 @; a7 e5 o9 r
Precocious puberty in boys is defined as secondary, @6 S) [# v7 |6 o9 r( L. O+ u
sexual development before 9 years of age.1,4, J; D- y/ G2 f5 a
Precocious puberty is termed as central (true) when
4 l7 n. }4 }4 H' Eit is caused by the premature activation of hypo-
3 `  ]. u3 e8 `/ y0 i$ R2 F) h5 }  Z( G2 Pthalamic pituitary gonadal axis. CPP is more com-
1 b  u& h: H( b( n9 V+ R/ _mon in girls than in boys.1,3 Most boys with CPP
6 P4 |  m  H1 A. l, i" dmay have a central nervous system lesion that is
, s7 a- E8 U0 N0 Sresponsible for the early activation of the hypothal-" g. X* n: e: y) T; s
amic pituitary gonadal axis.1-3 Thus, greater empha-
$ R/ M! S9 ?% Osis has been given to neuroradiologic imaging in
: E; Z" L, q: ~" n. ^boys with precocious puberty. In addition to viril-* P1 H: A( F6 h5 {2 p/ r
ization, the clinical hallmark of CPP is the symmet-& i& C  `( h( e
rical testicular growth secondary to stimulation by
6 V7 Q: W/ `3 Kgonadotropins.1,3
! L& T2 Y+ ~% f; U( I& H4 hGonadotropin-independent peripheral preco-6 f/ u3 y, y; f" f# ?" B5 H
cious puberty in boys also results from inappropriate
/ r; H! j, ^7 ~% V1 v) Y& Kandrogenic stimulation from either endogenous or& Y+ i- ~% [5 v) d! f
exogenous sources, nonpituitary gonadotropin stim-6 i' X. f' \* ^3 Y9 ]
ulation, and rare activating mutations.3 Virilizing
) i" X/ a- X& E% G$ ?congenital adrenal hyperplasia producing excessive
$ M) E% q( h4 o1 cadrenal androgens is a common cause of precocious
  [( }* Y, u1 p+ V# Opuberty in boys.3,4
3 Q- n. H" M5 Q! Z9 h0 N7 ]& m8 k2 F  UThe most common form of congenital adrenal
+ p) }2 j0 ~3 {. m5 o  O$ W$ phyperplasia is the 21-hydroxylase enzyme deficiency.
# [' E! A1 S& rThe 11-β hydroxylase deficiency may also result in' @3 Z+ d- `5 P  v( H6 M
excessive adrenal androgen production, and rarely,/ \9 o# l+ s6 c2 }$ }' i! b3 M) K
an adrenal tumor may also cause adrenal androgen
; s+ ~, D9 D0 f5 Qexcess.1,3
7 v# q: q8 ^# C& xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 M* l% ]1 a' z' L: p2 l542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 d9 e1 Z! T. \) E
A unique entity of male-limited gonadotropin-1 |8 l3 j7 Q' u. X. L2 S8 |
independent precocious puberty, which is also known
$ R, S7 b4 ?/ n! t" yas testotoxicosis, may cause precocious puberty at a
+ H3 l# d0 ]& u9 x. q+ p( t/ k+ Bvery young age. The physical findings in these boys5 k- L1 O4 c/ ?- h
with this disorder are full pubertal development,
7 m* e% F! d6 |4 n  S3 g3 Tincluding bilateral testicular growth, similar to boys
, O( m6 K; c3 T3 Dwith CPP. The gonadotropin levels in this disorder
' k( m+ L. g! D  g5 K) j7 C5 I( j* D8 aare suppressed to prepubertal levels and do not show
8 L! g6 V- P# ^3 G8 Tpubertal response of gonadotropin after gonadotropin-
& |, f2 Y2 @, @& l& d4 O) Lreleasing hormone stimulation. This is a sex-linked* s* @/ Y+ e) D# E3 W6 L5 C
autosomal dominant disorder that affects only; ^$ R# x9 E& k4 i2 a
males; therefore, other male members of the family+ _% X6 A; H% m$ l( E
may have similar precocious puberty.3% }3 ~4 c# `9 ~3 c1 R; l7 E
In our patient, physical examination was incon-
; n. K  o0 m* ]# J; e' [8 hsistent with true precocious puberty since his testi-" r7 w" @' o! B9 T4 k+ n% _, [
cles were prepubertal in size. However, testotoxicosis+ J7 a9 x- ]: m' `/ U' ]
was in the differential diagnosis because his father  _' [3 f1 q0 [2 n0 a
started puberty somewhat early, and occasionally,9 W1 s! A* n: c" j
testicular enlargement is not that evident in the8 ~) M0 [2 L; O7 W! i3 O
beginning of this process.1 In the absence of a neg-6 B% {9 R/ W( c' k) }1 Q
ative initial history of androgen exposure, our  w- g2 C+ z  R/ ?
biggest concern was virilizing adrenal hyperplasia,
& n& l! }" b  b/ O8 d) l/ beither 21-hydroxylase deficiency or 11-β hydroxylase
2 {; g8 g7 b9 W& b' s5 Ddeficiency. Those diagnoses were excluded by find-! h4 B) i/ w: O* s( }: Y
ing the normal level of adrenal steroids.* U  y" o. j/ M
The diagnosis of exogenous androgens was strongly  F3 F4 |! e8 @7 m. n8 C
suspected in a follow-up visit after 4 months because
; F( V; R# ^+ B; {! B. s0 @the physical examination revealed the complete disap-$ {/ w+ B2 V' H# i& u/ `4 X) D
pearance of pubic hair, normal growth velocity, and9 m( n1 C6 B( c5 \  d
decreased erections. The father admitted using a testos-* _/ s$ m6 O3 {( N8 k
terone gel, which he concealed at first visit. He was8 E* e0 N) _! Q" f' s; _2 M
using it rather frequently, twice a day. The Physicians’
! h0 F# C. A  _& R5 ?( ?  i/ d6 y" h  _Desk Reference, or package insert of this product, gel or
; M1 f0 v' U4 `+ U, ncream, cautions about dermal testosterone transfer to
7 l  [1 Q, d" {% j3 dunprotected females through direct skin exposure.
: t: `' i6 {, U# ]* a% [, q0 fSerum testosterone level was found to be 2 times the: _% M( }: @! F) |5 c$ r( C/ G
baseline value in those females who were exposed to$ O, }* O, U2 q
even 15 minutes of direct skin contact with their male
8 F5 f& t7 x* [6 i, Vpartners.6 However, when a shirt covered the applica-& T% [* d" s' B0 p& m  H! u1 o
tion site, this testosterone transfer was prevented.& W+ [  l* x* _$ ?( P$ S& P
Our patient’s testosterone level was 60 ng/mL,
/ U" G' q' D7 @" P2 ]3 W8 ewhich was clearly high. Some studies suggest that
4 `" R8 l5 R. t5 U$ S4 G, R. Xdermal conversion of testosterone to dihydrotestos-6 L1 T0 r+ S, ], {0 a4 `/ S9 c
terone, which is a more potent metabolite, is more  r- J* H6 B0 x6 l& R' r! n
active in young children exposed to testosterone/ @" u$ h2 y4 ]0 K9 O/ O! k+ N4 I
exogenously7; however, we did not measure a dihy-/ T  E( Z; \3 R4 ], W
drotestosterone level in our patient. In addition to- Q1 Z3 L' j3 s7 L
virilization, exposure to exogenous testosterone in
1 P+ n. }. F; X# Lchildren results in an increase in growth velocity and
7 k2 F$ i+ {4 R, }) N- R! Madvanced bone age, as seen in our patient., O& P- s" D5 i
The long-term effect of androgen exposure during
0 F5 }/ V) G, z/ Cearly childhood on pubertal development and final: ]9 i1 S5 t, t. p& g* P
adult height are not fully known and always remain
# c* ]! B) i* r8 @! D$ ]4 O$ Ha concern. Children treated with short-term testos-+ ^7 W7 ~# ]: m& T* D8 x* V' n# L- k
terone injection or topical androgen may exhibit some
3 N) C9 V1 \# b: c8 r% R0 h% Wacceleration of the skeletal maturation; however, after
2 d0 m7 r: k$ W. Y- B4 tcessation of treatment, the rate of bone maturation
% e' u: K6 m$ w5 ydecelerates and gradually returns to normal.8,9' C" V( y0 C  o. t6 P
There are conflicting reports and controversy
+ `/ ?# K& b5 ]  c2 b  rover the effect of early androgen exposure on adult' G: j* x+ I- T( H2 |5 T: [
penile length.10,11 Some reports suggest subnormal
" i8 Q0 ?; x( g9 I( }adult penile length, apparently because of downreg-9 S: o6 z, ~% F9 D! R" X2 v$ [' N
ulation of androgen receptor number.10,12 However,
2 G  M% ]" i" [$ G7 M! KSutherland et al13 did not find a correlation between" X% w; y( I: Q. W
childhood testosterone exposure and reduced adult
1 c' g5 l4 d# [* O5 B& [2 \penile length in clinical studies.+ i% ?0 x- v1 |) \
Nonetheless, we do not believe our patient is
7 d( R2 \6 N4 Sgoing to experience any of the untoward effects from6 b! n! R: w: N; @$ ]% o8 E8 @
testosterone exposure as mentioned earlier because
1 u) w/ m- C( D" }/ o0 G1 kthe exposure was not for a prolonged period of time.* |1 W* X* u/ `3 K5 J. _( z
Although the bone age was advanced at the time of
9 N$ U6 D# d  q7 w  c+ k2 q. D" pdiagnosis, the child had a normal growth velocity at
! D) w9 Q  [% {$ ^3 X3 ~' Bthe follow-up visit. It is hoped that his final adult6 T3 p' x: k9 {8 n% Z5 b& c8 S
height will not be affected.' C# ]: m+ J. E1 Z$ b$ n) T
Although rarely reported, the widespread avail-
1 x) q$ \" U1 Mability of androgen products in our society may
- r" P2 y% x8 ?' k; Xindeed cause more virilization in male or female
; D& u: E( D9 H/ j$ o! r( n0 Qchildren than one would realize. Exposure to andro-+ I; Z5 |! t1 l5 Y2 M' e) I
gen products must be considered and specific ques-5 {8 U7 k! ^/ a3 a. F
tioning about the use of a testosterone product or) K1 H; f: {) L) M+ f
gel should be asked of the family members during4 D+ w- i/ A0 P9 w9 r# h# F
the evaluation of any children who present with vir-5 p9 Q- R6 w8 X* r' E) ?
ilization or peripheral precocious puberty. The diag-
8 v( O  ?( t  f/ [nosis can be established by just a few tests and by
$ q, f3 B8 c4 G, u6 d  q8 ?; nappropriate history. The inability to obtain such a
% p0 `. E9 a/ [5 Jhistory, or failure to ask the specific questions, may
6 ?2 n9 r) x8 Q7 ~result in extensive, unnecessary, and expensive
/ N4 T) B* ~) ?) g, h( X9 l0 Ainvestigation. The primary care physician should be
4 |, F6 c' H8 u: ^" A" Xaware of this fact, because most of these children
$ q/ `& H& i- K3 C) Tmay initially present in their practice. The Physicians’$ x" m: d/ ^. v
Desk Reference and package insert should also put a! ~7 `7 p. O2 r4 [+ I* N
warning about the virilizing effect on a male or
- m/ V8 y# p. jfemale child who might come in contact with some-- a2 z4 Z: U6 z9 q- |1 K# @
one using any of these products.
. Q; W0 r7 o* p$ t9 |- R- U3 AReferences/ C; w3 n, w% {
1. Styne DM. The testes: disorder of sexual differentiation
3 W% T5 k5 a& Jand puberty in the male. In: Sperling MA, ed. Pediatric% g1 V" L: T  ^: w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- H! R0 D  I4 k; v) ~2002: 565-628.7 Q, p2 O" h, d
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& P* W3 r: o( b" B: @1 J
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
' U8 P4 B- s% G5 n* j& q& T
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