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- ~, y2 d. T- U- o) [
Boy Induced by Indirect Topical
5 w3 b$ z/ X6 V9 k2 h! d! FExposure to Testosterone
& C# V& [5 `6 ]2 a, A  w' l/ o8 oSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2+ }) r5 e& Q5 p/ Q: R9 ]. t! K
and Kenneth R. Rettig, MD14 m8 a8 U4 a7 h3 N" }9 ~/ k7 i
Clinical Pediatrics
% P5 F% L$ z0 K9 c" \/ z5 aVolume 46 Number 6" f, ?  F% b  W- V9 Z
July 2007 540-543. V: G9 u3 e4 p7 b# {$ U+ r( q
© 2007 Sage Publications
' s- T; I- [( E6 s' _$ `10.1177/0009922806296651
- K8 ?% U/ ^) S5 D2 u- thttp://clp.sagepub.com
1 h# ^) ]5 I' h: Hhosted at, N) D. [  \! K; K: j, r9 w
http://online.sagepub.com
4 m) ^3 q2 F$ p1 ePrecocious puberty in boys, central or peripheral,+ e1 {  a2 k2 C
is a significant concern for physicians. Central2 E2 I. w% e0 v/ m: r0 X9 @/ o
precocious puberty (CPP), which is mediated' `4 O0 T6 m- t/ T
through the hypothalamic pituitary gonadal axis, has9 `1 S' k2 z8 a8 m
a higher incidence of organic central nervous system9 W; I+ G$ T2 @! W2 ?0 s& e
lesions in boys.1,2 Virilization in boys, as manifested* W  S, q+ G; N
by enlargement of the penis, development of pubic3 ^; u7 \6 N. }7 }# M
hair, and facial acne without enlargement of testi-
$ I8 |; ]0 j! E( `8 f* ocles, suggests peripheral or pseudopuberty.1-3 We
8 x6 [) f' s8 D+ M6 e+ oreport a 16-month-old boy who presented with the
, }* g9 a; r  @% benlargement of the phallus and pubic hair develop-
7 M' w& i, {- _: Q1 ]5 Z- Bment without testicular enlargement, which was due
/ a! D$ O" O) @& ]2 D! m. wto the unintentional exposure to androgen gel used by
( t( n/ `* m2 Dthe father. The family initially concealed this infor-2 b* S7 l& a$ T2 N
mation, resulting in an extensive work-up for this
: k' l( m1 a: J- lchild. Given the widespread and easy availability of3 F; e  G, V, j, \  f
testosterone gel and cream, we believe this is proba-
) \& r) }4 H/ B+ qbly more common than the rare case report in the
! \& Z7 F; z/ |- @literature.4
2 k+ [# g7 G7 [' {# b, F* f3 x' iPatient Report; O- O( E; R2 n  D* l
A 16-month-old white child was referred to the
; S5 [  Z: s+ D0 A! t$ _% B' j0 p/ B; aendocrine clinic by his pediatrician with the concern
) i& k1 e5 V) i2 s6 R1 cof early sexual development. His mother noticed  N) Z5 v) k# c, F4 N3 g) J
light colored pubic hair development when he was* a8 E2 v& m8 z/ ~- m. d
From the 1Division of Pediatric Endocrinology, 2University of
  u) M- ^2 Y! {% @9 g6 R% G! uSouth Alabama Medical Center, Mobile, Alabama.
/ R0 {$ b3 Q' QAddress correspondence to: Samar K. Bhowmick, MD, FACE,+ S( P: d: ]' q7 R
Professor of Pediatrics, University of South Alabama, College of5 y) x, |# m+ T4 S4 |" w
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
' S# ^3 H2 n: E. j4 P2 Y3 ]' Ce-mail: [email protected].6 ^) G# E4 ]! l  v! M8 T
about 6 to 7 months old, which progressively became- W5 D) N5 ?8 F( c1 x
darker. She was also concerned about the enlarge-. y# w5 d6 b# q* |8 w% q
ment of his penis and frequent erections. The child5 j6 ~# y4 L# _& S9 `
was the product of a full-term normal delivery, with) F+ E# c. f& }; c7 m
a birth weight of 7 lb 14 oz, and birth length of- ]# t$ U9 W/ v. ^) b* |
20 inches. He was breast-fed throughout the first year5 Y0 C8 K4 f- ]5 i
of life and was still receiving breast milk along with
9 H( E# N9 B# M/ Z# X6 j1 bsolid food. He had no hospitalizations or surgery,
" V- N3 ~; @$ g- N, V- Uand his psychosocial and psychomotor development
0 m+ a- z9 S/ h) M, A" Qwas age appropriate.# Y8 T7 |* ^0 o, c5 U
The family history was remarkable for the father,
3 D4 O4 f$ w5 o7 g* s" ]5 Cwho was diagnosed with hypothyroidism at age 16,
/ ]" \0 w2 f* W2 e5 L" ^5 \which was treated with thyroxine. The father’s
! M" v: w! V$ G2 I! q" u6 H. `  n4 Zheight was 6 feet, and he went through a somewhat
- R) g) \5 }  n" ]* J0 v0 pearly puberty and had stopped growing by age 14.
  {: s& ~0 g9 v; n  p5 E( bThe father denied taking any other medication. The8 O" M% }4 ^$ x6 V4 M2 x
child’s mother was in good health. Her menarche$ c  g6 w7 X3 @  c$ R2 n7 ]; a2 W
was at 11 years of age, and her height was at 5 feet- `9 P; D+ s* p, {+ M3 Q* W
5 inches. There was no other family history of pre-
) F' Q% ^3 u& U  |cocious sexual development in the first-degree rela-3 \' p. h$ k. A1 d4 [
tives. There were no siblings.
' t6 I0 W/ ^! M7 h8 n3 SPhysical Examination
1 S% L+ G! O1 \# D7 T: T, d( }8 A4 eThe physical examination revealed a very active,9 q- _) D% r6 U" u. t( ~
playful, and healthy boy. The vital signs documented* A% j8 X) t/ @& {8 h) E
a blood pressure of 85/50 mm Hg, his length was+ ~) D( e! n3 p9 s2 J: R. w+ [8 C
90 cm (>97th percentile), and his weight was 14.4 kg% a# l7 X2 l" j5 `' }
(also >97th percentile). The observed yearly growth6 a1 c: c# C9 b: B% u% I* M' }
velocity was 30 cm (12 inches). The examination of1 H: |3 p/ f- a6 j
the neck revealed no thyroid enlargement.8 F5 ?* P# ^: U! T+ l
The genitourinary examination was remarkable for2 }" M6 |: b' S1 Y, {( [5 t, t
enlargement of the penis, with a stretched length of3 _; j* {" |+ @3 C  |# ~& L# p- I
8 cm and a width of 2 cm. The glans penis was very well8 F5 e8 c& O) W9 d. v  P% @  G9 P
developed. The pubic hair was Tanner II, mostly around* r6 g$ e: w! Z4 I
540% x1 N% l" E6 l9 x$ @- X
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( C$ R* s! M( A% ?% ]0 E; Z4 W# \the base of the phallus and was dark and curled. The7 @0 g. b/ W6 D, U' p+ h0 }0 i/ M
testicular volume was prepubertal at 2 mL each.
% W* `& l5 S2 h9 M& u' `The skin was moist and smooth and somewhat
+ t, O0 u9 c+ J' U# F8 w2 hoily. No axillary hair was noted. There were no& M5 b$ y1 p& {! q7 b
abnormal skin pigmentations or café-au-lait spots., L1 t5 k0 c( _
Neurologic evaluation showed deep tendon reflex 2+
7 ?0 J; d5 {* k  z9 Z) @bilateral and symmetrical. There was no suggestion7 H/ P% x4 g* d9 r; U- b
of papilledema.1 H8 t6 Y1 j9 M+ J: O* A7 v5 r# T
Laboratory Evaluation
# Y4 J2 b$ P3 D- Z; ?) O& t: l; Z8 RThe bone age was consistent with 28 months by
+ K. M1 Z' U, w, busing the standard of Greulich and Pyle at a chrono-
) J# k2 i* f  m, R# ~* elogic age of 16 months (advanced).5 Chromosomal
8 v7 ^9 q/ Y0 A2 X; d7 X* k# |( X( b& \karyotype was 46XY. The thyroid function test* G. e9 z7 R# i  _6 z& m& x  n
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
  ^3 }; K, d$ ~% \' ilating hormone level was 1.3 µIU/mL (both normal).
5 |+ }" T$ q$ |The concentrations of serum electrolytes, blood
  ~) e# _* q. H6 Xurea nitrogen, creatinine, and calcium all were
& L" S5 `# a. S* Q1 M9 f0 N1 v5 Awithin normal range for his age. The concentration
& [" |: Z0 e' r4 x1 y8 L( uof serum 17-hydroxyprogesterone was 16 ng/dL
6 T* j& x$ m4 O* G- q(normal, 3 to 90 ng/dL), androstenedione was 20" L  t5 j3 _( L7 ~( s. U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 L8 ]& Y" s1 e* V! P+ H( X: |terone was 38 ng/dL (normal, 50 to 760 ng/dL),
* d' U4 A% R& u" k2 R) i( xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 s  X- `1 l* ^49ng/dL), 11-desoxycortisol (specific compound S)3 ^3 R8 {  e6 f; [
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
; j" K9 @# @, c9 K7 etisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 q( f, p. B' w* _1 {  G. btestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( Q6 }2 \  a5 j  wand β-human chorionic gonadotropin was less than
% T$ H6 Q5 s) y7 Y& f, |5 x5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 ^' ~$ g; e- f3 V3 R1 |$ ]* E. Zstimulating hormone and leuteinizing hormone
# [7 e0 Q2 A) r+ {9 O6 \, p  X  ?  N5 {concentrations were less than 0.05 mIU/mL
! b( P; K, ~5 K! q(prepubertal)./ e" m% W2 U! f; f& Q
The parents were notified about the laboratory
9 }" c+ ~9 N8 z! L! [results and were informed that all of the tests were6 U5 `7 j0 `. x/ B# A
normal except the testosterone level was high. The
; C0 H! y$ K  l6 Y" s/ U% s) Nfollow-up visit was arranged within a few weeks to
. q: _# A3 W  L0 dobtain testicular and abdominal sonograms; how-
, q6 N; E* P# L1 D* m: ]& Y8 Q9 Pever, the family did not return for 4 months.& o0 N) `- {# {: g
Physical examination at this time revealed that the
* n1 z% M( p0 z# _child had grown 2.5 cm in 4 months and had gained
, o) q2 S7 L% l6 r3 p2 kg of weight. Physical examination remained/ U- Z: ~7 p2 Y" A" V
unchanged. Surprisingly, the pubic hair almost com-' Z/ }, L& q2 L) k
pletely disappeared except for a few vellous hairs at+ L4 \1 E% P: n& e. I1 ]7 j- I+ h
the base of the phallus. Testicular volume was still 24 K- u& I1 \% D9 G2 P7 d
mL, and the size of the penis remained unchanged.& C; a, o" Y' q# h6 p7 }
The mother also said that the boy was no longer hav-  H2 r. D" ?0 u' l9 ~- L
ing frequent erections.
% r: J! S9 a9 OBoth parents were again questioned about use of, F& @0 Y& y+ [
any ointment/creams that they may have applied to+ k* e. ?6 m1 ^8 {2 b
the child’s skin. This time the father admitted the1 {/ ^. ?) z* {( f% d% Y
Topical Testosterone Exposure / Bhowmick et al 541
& L( s1 K2 b4 I" I; vuse of testosterone gel twice daily that he was apply-
3 B/ w7 x0 N. J. @# c8 A: _- fing over his own shoulders, chest, and back area for
* _9 Q; ?  ]! G6 P! I9 K0 la year. The father also revealed he was embarrassed
7 V* E# y0 _) U5 g3 y! x# q- |* o  @to disclose that he was using a testosterone gel pre-
4 ]5 j+ F+ X+ x( D6 Q( B9 cscribed by his family physician for decreased libido
  B+ t, Y: `( W$ ysecondary to depression.
3 c# O9 h' j6 c7 oThe child slept in the same bed with parents.; b& n  K2 M2 L* d" N" ]3 s
The father would hug the baby and hold him on his% u' r+ \. I& ~
chest for a considerable period of time, causing sig-
0 D% v# F3 j. m) \; R/ ]nificant bare skin contact between baby and father.
+ F# W  ^( G; D0 bThe father also admitted that after the phone call,7 e" W  l; W) \, f& }
when he learned the testosterone level in the baby
. W" J0 x" D% T" Y2 j& s8 k5 Fwas high, he then read the product information
0 R6 E; ~7 y/ H( W$ {6 o9 B, k) B2 \+ Dpacket and concluded that it was most likely the rea-1 c9 W6 D7 D8 O( [5 d# y: G
son for the child’s virilization. At that time, they- l5 x, D: q! F3 K
decided to put the baby in a separate bed, and the
" Q) m, E" ^* N. [9 h7 O2 p& ifather was not hugging him with bare skin and had
! n! r$ h9 P2 L, abeen using protective clothing. A repeat testosterone
6 r* q2 d7 @# K# M6 F8 ktest was ordered, but the family did not go to the
/ U3 e6 Q) v, n5 A3 F% l$ t: J! v  zlaboratory to obtain the test.
! A# g4 f  m+ |  WDiscussion" E" M9 H0 V0 e
Precocious puberty in boys is defined as secondary
; l; K3 ]1 I/ w7 @' Wsexual development before 9 years of age.1,4
  t- i9 I4 ~0 w! \) SPrecocious puberty is termed as central (true) when
" Z% r* D- E# P7 t, nit is caused by the premature activation of hypo-% L+ R$ F0 d2 M3 n2 j& d9 A  {( {7 h. P
thalamic pituitary gonadal axis. CPP is more com-
. z* X% W5 S" c2 {2 zmon in girls than in boys.1,3 Most boys with CPP2 Y: |0 M. K0 ^, i1 R
may have a central nervous system lesion that is
4 ~6 }  w6 P8 z* v/ wresponsible for the early activation of the hypothal-( _& F# h9 x$ Y6 A7 J2 y
amic pituitary gonadal axis.1-3 Thus, greater empha-
4 W8 c" t  ]7 Usis has been given to neuroradiologic imaging in- Q+ s7 _1 n* a3 B2 d' s" Q8 K8 w4 b
boys with precocious puberty. In addition to viril-
' Y/ ~! t# R- }( o, v6 }7 Z- g! nization, the clinical hallmark of CPP is the symmet-
5 t& t4 A) i0 ]+ ]! Z7 E" W$ Krical testicular growth secondary to stimulation by
; K8 I  Z$ g  I( N" T  X% g+ pgonadotropins.1,3& J* }# M5 p  P; O) S
Gonadotropin-independent peripheral preco-
" h5 Q' O* `9 Q0 Lcious puberty in boys also results from inappropriate5 a0 n8 A: @% P7 |
androgenic stimulation from either endogenous or
( w: p, ~( z( ~/ H- `exogenous sources, nonpituitary gonadotropin stim-( D# e, K5 z1 G; e. U
ulation, and rare activating mutations.3 Virilizing
0 ]! _7 Y' S; S$ b4 jcongenital adrenal hyperplasia producing excessive, q) z3 _1 D1 |$ {/ C% r1 s3 ~
adrenal androgens is a common cause of precocious; `: Q0 Z7 }' @! v( v  P/ \
puberty in boys.3,46 l7 y2 R. s" S' K. _4 k3 b6 J
The most common form of congenital adrenal
; d4 m( p& q+ F, @1 j0 d* Ihyperplasia is the 21-hydroxylase enzyme deficiency./ O( g* ^: t( h3 D. r, g. l: `
The 11-β hydroxylase deficiency may also result in
! [- P  u, \9 n/ `* a8 k" E- g( gexcessive adrenal androgen production, and rarely,/ ?" p. c$ H  \" p# i
an adrenal tumor may also cause adrenal androgen* o( e/ s$ J* O+ c& z% }; B7 V8 _/ u
excess.1,3
- q4 F- b/ u( n, [; ?- \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# O. j5 b9 _8 H$ {* y- J+ g
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 O' h+ f* W2 L7 Y7 R- K2 M8 VA unique entity of male-limited gonadotropin-+ s2 ~/ i* e& I
independent precocious puberty, which is also known& N7 f5 x/ g' P$ a. d, x( s- I) u/ g
as testotoxicosis, may cause precocious puberty at a
; E! n' n" V- f7 R4 a; B. Wvery young age. The physical findings in these boys! j$ m3 u6 f( L0 z* t
with this disorder are full pubertal development,/ V2 n, z: q4 a4 \# N
including bilateral testicular growth, similar to boys
( E, l1 H3 C- f7 N" l4 _with CPP. The gonadotropin levels in this disorder9 I; n; E' c- v
are suppressed to prepubertal levels and do not show' J3 j+ P% h" X
pubertal response of gonadotropin after gonadotropin-
* s/ |: k. _3 P8 g# X) |4 g8 N9 Nreleasing hormone stimulation. This is a sex-linked$ Y+ ]/ D# ]) O, c
autosomal dominant disorder that affects only
8 Y, t' Q* _6 e* v2 A% v9 umales; therefore, other male members of the family8 e5 Z. @. A* o/ b
may have similar precocious puberty.3
+ i: q) H7 Q$ WIn our patient, physical examination was incon-2 K5 N- o6 T7 \1 R3 Y) N' Z
sistent with true precocious puberty since his testi-6 f- K/ C" o6 X1 P7 U
cles were prepubertal in size. However, testotoxicosis
6 l5 A5 V% H0 E" S0 nwas in the differential diagnosis because his father9 d6 r! ?, b% _+ Z1 [. y# P
started puberty somewhat early, and occasionally,
% D! k+ s" X" d3 Q6 ctesticular enlargement is not that evident in the$ ]( @: U. F2 }' R# X1 ?
beginning of this process.1 In the absence of a neg-
8 e8 s/ l. F& l- h/ Jative initial history of androgen exposure, our
5 T4 m5 O' y0 ?& ^  l8 C3 W, _* Dbiggest concern was virilizing adrenal hyperplasia,: o* G) n+ s3 ^- [
either 21-hydroxylase deficiency or 11-β hydroxylase
% H( r$ d0 y/ Xdeficiency. Those diagnoses were excluded by find-$ ?( i# ?9 E+ X
ing the normal level of adrenal steroids.9 U# O2 d2 L& r. {
The diagnosis of exogenous androgens was strongly
9 ?4 x; r7 c2 w+ r# t; Vsuspected in a follow-up visit after 4 months because
, `! \/ ?" g  B" v: W2 R2 Xthe physical examination revealed the complete disap-
. G2 T5 L% D% V/ I1 y/ E: G0 qpearance of pubic hair, normal growth velocity, and5 ?& B: m2 v' X9 i9 s& x
decreased erections. The father admitted using a testos-
$ e: O& T: o1 Eterone gel, which he concealed at first visit. He was
9 A5 o2 H- E( |; x: Qusing it rather frequently, twice a day. The Physicians’
5 _" m% j& ?$ ^Desk Reference, or package insert of this product, gel or
; `" Q- B+ B5 x5 Q: |( qcream, cautions about dermal testosterone transfer to
* s' w; t6 E- junprotected females through direct skin exposure.
2 q) @8 e7 Y, MSerum testosterone level was found to be 2 times the" D8 v, p* G7 @
baseline value in those females who were exposed to
0 O- b; z# H  p) [4 Y* G- @even 15 minutes of direct skin contact with their male
3 H: G7 c1 p% v4 H5 W. ?' i9 ^; wpartners.6 However, when a shirt covered the applica-3 X% v! O+ s; S& [' ^
tion site, this testosterone transfer was prevented.; S6 [' d( k8 B! b. ~) `$ `/ a
Our patient’s testosterone level was 60 ng/mL,+ O! ?6 K* t4 d  M, ]! |# i
which was clearly high. Some studies suggest that
! T% v$ _2 J& x0 u( tdermal conversion of testosterone to dihydrotestos-
2 j1 ^5 U# z1 Xterone, which is a more potent metabolite, is more
7 R6 \( V6 ^' u4 P/ {3 m- [active in young children exposed to testosterone/ v; Z. n; N" w  N3 p" }
exogenously7; however, we did not measure a dihy-7 p$ U; r7 G* D; H' _0 z3 d, C
drotestosterone level in our patient. In addition to9 i, e6 [, i* U8 w( K+ S
virilization, exposure to exogenous testosterone in6 }! z. [. C; ^  w9 \
children results in an increase in growth velocity and, r- O0 T& G  B; o. A
advanced bone age, as seen in our patient.
6 t. @5 q1 R/ T3 _The long-term effect of androgen exposure during
7 R2 T, T+ G2 [- s$ n- Fearly childhood on pubertal development and final
$ k' k4 v7 {" d  I( S( V" ladult height are not fully known and always remain+ Z8 _) Z) A9 M$ e
a concern. Children treated with short-term testos-
! y: G/ C9 @9 R1 e( ~" _terone injection or topical androgen may exhibit some! t: X8 @% w& O- C3 B7 X
acceleration of the skeletal maturation; however, after) s+ D/ P- K1 G5 L4 V2 ^
cessation of treatment, the rate of bone maturation$ G* `; ~; B5 d$ H  [
decelerates and gradually returns to normal.8,97 f6 ]$ F5 A% P5 r
There are conflicting reports and controversy0 u% V; Y' U& d5 C( P
over the effect of early androgen exposure on adult
" c( C. A6 }6 z- vpenile length.10,11 Some reports suggest subnormal4 `- x4 A3 J) q* w0 I! u% k# S
adult penile length, apparently because of downreg-, Q! {/ {# n+ w; u2 q$ l' x
ulation of androgen receptor number.10,12 However,% U* A, \4 |' M! ~
Sutherland et al13 did not find a correlation between
. ^4 E$ h  p6 }% T+ \, Q9 Fchildhood testosterone exposure and reduced adult
" Z2 C6 |3 k% N- p7 w/ wpenile length in clinical studies.
! ]6 a- I* }$ `  H. L6 ANonetheless, we do not believe our patient is
9 B) D: S7 S; @: ~2 E) ?) Agoing to experience any of the untoward effects from
: T" s4 Z( [8 n9 v$ i4 w* k3 @testosterone exposure as mentioned earlier because
) Y3 a6 j) `) p% A/ r, A0 Rthe exposure was not for a prolonged period of time.
) W& v9 r% m; u- A) A8 G5 PAlthough the bone age was advanced at the time of8 y6 [$ Q0 G  M( q+ T+ v
diagnosis, the child had a normal growth velocity at9 K# E  x; s! `: ^
the follow-up visit. It is hoped that his final adult8 ^! `: n# D! n. ^6 _- s8 q5 m
height will not be affected.
0 Y1 K" S8 s; F( D$ Y4 q7 I6 a; l. DAlthough rarely reported, the widespread avail-
, V. L3 i& Y4 o- u7 Rability of androgen products in our society may
7 |% K: z8 c& T+ @8 Jindeed cause more virilization in male or female4 M* Z+ G9 o1 [& ]% J! B
children than one would realize. Exposure to andro-
0 z* a" v4 g. T7 b4 \) ^1 w9 O/ Fgen products must be considered and specific ques-
" r) i6 R3 Z/ q5 i9 X; Ltioning about the use of a testosterone product or
& Z% S  f7 @  g1 H0 egel should be asked of the family members during& @. v0 h$ Y8 {* y! J0 |
the evaluation of any children who present with vir-
0 x) t% I; d5 r3 tilization or peripheral precocious puberty. The diag-
$ R* O1 `; ?# V" e% s* z8 @" l! jnosis can be established by just a few tests and by/ f) J2 _4 B. |
appropriate history. The inability to obtain such a, G$ a3 O" \& h
history, or failure to ask the specific questions, may. {& ~, k/ z  `
result in extensive, unnecessary, and expensive
/ G! x, b( V3 Vinvestigation. The primary care physician should be
, ~1 x3 z( ]4 k: [+ o; [- K/ |aware of this fact, because most of these children  _, P8 ?1 G8 X
may initially present in their practice. The Physicians’
- F( _7 {  J; [( U& Z/ t, s+ bDesk Reference and package insert should also put a
  ?* {; ~; k9 q% l7 F9 \, ~1 W0 p- dwarning about the virilizing effect on a male or/ w9 z0 p' D) ]" \% H* Q$ l( k8 i! R+ b
female child who might come in contact with some-
, O' n$ S1 N$ \3 Hone using any of these products.
+ }$ [- N' F& a% PReferences
+ f6 ?. p$ M( Q% Z' c0 X1. Styne DM. The testes: disorder of sexual differentiation
7 `' R6 Y* ?1 Q! L# T5 l" J: x% ]and puberty in the male. In: Sperling MA, ed. Pediatric
$ n# a1 f7 \* j3 ~Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- o+ [" U  d9 ^/ @3 o+ o. J2002: 565-628.
4 b  e4 ?9 ^' K$ M- L, D' S2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
0 Z  y  f% [, C  c8 Z) o' vpuberty 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  c4 E& H% f4 z1 d- l" X
Boy Induced by Indirect Topical9 W7 Z3 ~/ s, p$ L' v
Exposure to Testosterone3 J: c  c+ G1 f& y$ s# j
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: x/ |6 }. v% aand Kenneth R. Rettig, MD1
; c) f% V% {3 v$ G, eClinical Pediatrics
5 U3 _- C9 t* ^' E" ?) |& dVolume 46 Number 6. s' h8 _$ S5 b% p9 Y% t% d% W
July 2007 540-543
. ]7 K7 t, S  u4 N/ F© 2007 Sage Publications6 g, Y; G( r$ o8 W+ S
10.1177/0009922806296651& {. }+ K0 N8 Q8 z. |
http://clp.sagepub.com: G( g: s$ P& Y6 f6 _, w" d: o% i4 t! s
hosted at
  \5 D6 I1 N9 t, b) P3 [http://online.sagepub.com
6 l. ^/ ]% J( p* }, |& }0 XPrecocious puberty in boys, central or peripheral,9 i/ N6 ]+ ]6 S4 F, ^& r1 l
is a significant concern for physicians. Central9 |" a0 s- j$ G
precocious puberty (CPP), which is mediated
0 u8 d7 V+ \' ^2 qthrough the hypothalamic pituitary gonadal axis, has
/ J3 F  X$ r' y& @! o$ c0 s1 U) Ga higher incidence of organic central nervous system7 o3 m  @: [6 h) n' [
lesions in boys.1,2 Virilization in boys, as manifested
$ @# F( L- C: B1 _9 K$ ]* Mby enlargement of the penis, development of pubic8 m+ Q$ A9 @- Z5 q* _
hair, and facial acne without enlargement of testi-
% r+ x7 y) S/ Z/ W" Rcles, suggests peripheral or pseudopuberty.1-3 We
' n5 I, {) i$ m0 e" H* k, R  n; Preport a 16-month-old boy who presented with the
/ n( L( Z2 {' |0 t8 n% e/ Kenlargement of the phallus and pubic hair develop-, L7 g/ @. s1 {
ment without testicular enlargement, which was due9 q, s3 p1 {3 T* u5 R
to the unintentional exposure to androgen gel used by1 ^/ c: [& h) o$ O2 L" f* l" K5 |1 I
the father. The family initially concealed this infor-
& ~$ C6 _$ X5 T/ c, ymation, resulting in an extensive work-up for this4 L7 F: a3 u6 n
child. Given the widespread and easy availability of$ e6 [- }* ?% d+ L
testosterone gel and cream, we believe this is proba-2 H. A  {; s. P* ?' w5 s+ r7 Z7 A
bly more common than the rare case report in the
# i+ O- f* U, `( @literature.4
" x0 K- O/ A( j! D8 O. bPatient Report
0 X! D& U: `8 F, d7 FA 16-month-old white child was referred to the' J2 B# z! _8 \
endocrine clinic by his pediatrician with the concern9 F8 B, u4 N; u7 E$ p* S
of early sexual development. His mother noticed
, d) ], Y/ s5 }3 F2 W; Xlight colored pubic hair development when he was
( g! `2 z9 W& i& ]. @9 wFrom the 1Division of Pediatric Endocrinology, 2University of
$ N( I' x. R& x7 K3 L5 \South Alabama Medical Center, Mobile, Alabama.
7 \! b% e8 g9 Z; iAddress correspondence to: Samar K. Bhowmick, MD, FACE,
- `' J! p4 M) U3 @, J/ b$ XProfessor of Pediatrics, University of South Alabama, College of
# X9 R9 b+ l+ Z3 ~Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 D, Z' l% s3 K
e-mail: [email protected].
) N# T! Y: t$ d7 sabout 6 to 7 months old, which progressively became! R; |' Z" h% m  S5 a
darker. She was also concerned about the enlarge-2 I" r1 u' M+ \7 q
ment of his penis and frequent erections. The child9 e* Q& Y; v4 w" t" q  F, K
was the product of a full-term normal delivery, with
$ h! r* m. B. z+ E- C  Y' Ya birth weight of 7 lb 14 oz, and birth length of
- g0 ^% g0 n$ J5 H: G20 inches. He was breast-fed throughout the first year7 F" e# W$ m5 S
of life and was still receiving breast milk along with
- m8 U9 O- V4 i$ e: E( osolid food. He had no hospitalizations or surgery,' ^# ~% R, x  [. _8 ]& b
and his psychosocial and psychomotor development6 Z( p* i% f5 f( s+ ]" ^
was age appropriate.* B' F' O, l; U2 ?, h9 M
The family history was remarkable for the father,
6 D% U* g9 k$ ?8 ~" R% Y! R. hwho was diagnosed with hypothyroidism at age 16,, z$ \) I; T& p8 r
which was treated with thyroxine. The father’s
# t& L) {/ k# ?5 aheight was 6 feet, and he went through a somewhat* V! V" ?) G! o9 H3 Z
early puberty and had stopped growing by age 14.4 D0 Y$ Y# I* K2 {
The father denied taking any other medication. The
. x3 F# ^0 I( W8 H1 Ochild’s mother was in good health. Her menarche
3 P3 K$ e4 P( T1 f! cwas at 11 years of age, and her height was at 5 feet3 S- l% L) F1 p5 N& g( H: a
5 inches. There was no other family history of pre-
2 K. b. T; p6 u1 A6 M% Kcocious sexual development in the first-degree rela-6 r9 L) S1 _6 A2 z3 b
tives. There were no siblings.% X( |, \' P% F5 N
Physical Examination" [, W+ Q/ N+ @* z  R1 o
The physical examination revealed a very active,
( g# j; ~4 _1 p; Iplayful, and healthy boy. The vital signs documented
; U* B/ T$ ?) r+ R( j% ~a blood pressure of 85/50 mm Hg, his length was
9 b: Z1 x6 w! c# g5 g, d8 g+ [+ r90 cm (>97th percentile), and his weight was 14.4 kg
0 `" s/ D3 o7 n% c(also >97th percentile). The observed yearly growth
. |5 S, w- C( U( W0 P1 y9 N. X; jvelocity was 30 cm (12 inches). The examination of  s, b1 |# N( E
the neck revealed no thyroid enlargement.. v" F; q4 t: X4 W
The genitourinary examination was remarkable for
. J3 v9 ]5 f, ?# Z! Q) Menlargement of the penis, with a stretched length of
7 Y: U3 F, s6 f% r- o8 cm and a width of 2 cm. The glans penis was very well# r- Q/ Z1 {3 L& z% }$ |" X
developed. The pubic hair was Tanner II, mostly around- O' }3 b1 p; E  a  @
5404 o+ m- J2 g% X; d2 _& l5 E
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ O& Z* x3 ~0 H8 `& `  k( s( Uthe base of the phallus and was dark and curled. The0 r$ t1 T8 J2 n$ u9 ]3 \, ]& S/ \7 u
testicular volume was prepubertal at 2 mL each., O2 O% x% V% ?, T, T
The skin was moist and smooth and somewhat6 R' U9 ^* O( n& d
oily. No axillary hair was noted. There were no) P3 [# j$ @7 g
abnormal skin pigmentations or café-au-lait spots./ {6 T1 }4 e3 y3 @  n  i% T
Neurologic evaluation showed deep tendon reflex 2+
8 k9 \4 Z7 q/ Sbilateral and symmetrical. There was no suggestion( e* q; D' T9 |6 o5 y- T
of papilledema.3 H9 j! E7 v, a6 l( \, f8 w
Laboratory Evaluation
, i8 v! \, g: F4 ^  IThe bone age was consistent with 28 months by
& L3 U" W; G, I# [% N2 w3 Musing the standard of Greulich and Pyle at a chrono-7 d9 `1 G' H0 V& [7 u: S, d* l
logic age of 16 months (advanced).5 Chromosomal9 P8 [2 A0 b; Q+ g3 n' [4 F$ G
karyotype was 46XY. The thyroid function test+ q1 B" c% E. ?" G) c
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
2 W% M% d1 A. l0 slating hormone level was 1.3 µIU/mL (both normal).
0 C3 n6 E1 n0 X; B  \9 f; M3 k7 U/ [The concentrations of serum electrolytes, blood
& v+ |4 J1 V+ Durea nitrogen, creatinine, and calcium all were
: |4 n' f# {" Twithin normal range for his age. The concentration
# L$ G" f. P) I- S( y( iof serum 17-hydroxyprogesterone was 16 ng/dL
: w3 g' W1 x. T; f6 @(normal, 3 to 90 ng/dL), androstenedione was 20
2 K6 h9 }! f- h( n0 B  `# c  v8 k9 Z. |ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, p  e; d' F$ g$ Y! tterone was 38 ng/dL (normal, 50 to 760 ng/dL),
; \" F5 W. I7 ~2 o( Cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to" u: j) P( ]3 P+ A) e$ P
49ng/dL), 11-desoxycortisol (specific compound S)
2 Q9 Z/ F" T4 ~( ]; e; Zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 d- K. o7 m- K( p7 U' e
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 @* i0 ]5 {1 a' T
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# S9 N% ]5 f2 h  n; M4 Oand β-human chorionic gonadotropin was less than* n& ?7 G, z) G
5 mIU/mL (normal <5 mIU/mL). Serum follicular' Y- }- ~7 f* R
stimulating hormone and leuteinizing hormone7 o" o$ c4 Y. D$ K( u, G6 a5 k% q* m9 o
concentrations were less than 0.05 mIU/mL
8 e0 k) r) t* L, O, k  w(prepubertal)." @3 L* B; n9 Q
The parents were notified about the laboratory/ q% c% T# C: Z
results and were informed that all of the tests were; P' o! x' N* B
normal except the testosterone level was high. The3 B) S2 e, p" k/ f- _0 r
follow-up visit was arranged within a few weeks to
6 U% s- c! d. sobtain testicular and abdominal sonograms; how-7 _, G1 q5 j- s* B$ O
ever, the family did not return for 4 months.
, s+ Z  H8 a2 g8 H" F9 [4 [# mPhysical examination at this time revealed that the& ?, `/ J6 J* y( ]
child had grown 2.5 cm in 4 months and had gained
. }- i6 M3 K5 [3 d2 kg of weight. Physical examination remained' V# i6 R/ Y" h' o/ R1 P- @
unchanged. Surprisingly, the pubic hair almost com-
. x- S  ], I' {' {2 Ipletely disappeared except for a few vellous hairs at5 O$ x# B& V9 b4 C, p
the base of the phallus. Testicular volume was still 2( v: F! g5 @- k+ `& W) [/ @% b& K0 z& N
mL, and the size of the penis remained unchanged.
- h. o7 y$ R6 I1 WThe mother also said that the boy was no longer hav-
  R6 O& u* M+ A  z5 Iing frequent erections.( ?/ g+ a1 [) q' Q# L1 K5 h$ R
Both parents were again questioned about use of# W  ?" o9 |& @1 ?/ O7 g
any ointment/creams that they may have applied to4 f* O; }% Z* Q' \7 f$ c' J: |
the child’s skin. This time the father admitted the5 D6 M& ?- s! E: B9 _1 p! ~
Topical Testosterone Exposure / Bhowmick et al 541
9 Q! u7 q5 w2 v; m$ q; Vuse of testosterone gel twice daily that he was apply-
" l9 U; Q7 z/ E0 z: H' ^4 wing over his own shoulders, chest, and back area for
7 _# ]- s, Y8 ~( _" @- ja year. The father also revealed he was embarrassed
6 s: I/ E( g" c$ x6 M* y- v8 cto disclose that he was using a testosterone gel pre-
$ C" B% @  S' r0 z, K. Wscribed by his family physician for decreased libido5 n" ], j, X" u) d
secondary to depression.
: P$ E8 o& V( c0 |* rThe child slept in the same bed with parents.# y+ M( T& c3 t! F- j2 n6 Q& x
The father would hug the baby and hold him on his
% \/ ~/ I2 K+ D! L3 o) e7 o0 s8 p  g# Jchest for a considerable period of time, causing sig-& T$ [7 r2 h, `! Z; D. ~
nificant bare skin contact between baby and father.
1 @* ~9 Y1 Z- Y0 g3 w$ I  eThe father also admitted that after the phone call,
# f2 ?. `6 K0 Z4 B- Rwhen he learned the testosterone level in the baby! Y% E1 W2 ]8 K1 B3 g4 t
was high, he then read the product information$ u) e- C  D4 w$ n! y% t1 x
packet and concluded that it was most likely the rea-
9 A2 ^" h, `. tson for the child’s virilization. At that time, they
2 `0 x' v* N- x, U& _/ G4 fdecided to put the baby in a separate bed, and the
3 z! @3 u, C3 H- r0 `) D, Bfather was not hugging him with bare skin and had  i/ k. q( s7 G. @2 s. r; J
been using protective clothing. A repeat testosterone& n6 f0 Z& A# x. [8 L8 j
test was ordered, but the family did not go to the
  k; i4 E. ]- K0 H  m2 m, wlaboratory to obtain the test.
) ?% }, Q. O2 k0 L" VDiscussion
, m  m; Q* S6 t7 v: ePrecocious puberty in boys is defined as secondary. U6 t# k  o/ ^7 y; \; o6 x' Y
sexual development before 9 years of age.1,4. X! a; F# w# L7 p( `
Precocious puberty is termed as central (true) when
6 q/ P5 ]! p& W) |. e: j# A' [it is caused by the premature activation of hypo-
2 m1 Q0 U, t4 \' Rthalamic pituitary gonadal axis. CPP is more com-* ^! e* W& F2 ?4 R/ f
mon in girls than in boys.1,3 Most boys with CPP  R  e  h4 s3 ~8 I
may have a central nervous system lesion that is
5 x; b# p: l% e- i2 ]responsible for the early activation of the hypothal-
1 O/ g5 v/ P* n% Y- Q2 g5 famic pituitary gonadal axis.1-3 Thus, greater empha-. J/ e  F: o5 |+ J, [4 K5 _9 q" r
sis has been given to neuroradiologic imaging in5 ~6 F) d% G+ o( l  t
boys with precocious puberty. In addition to viril-6 l/ e. J+ W  b
ization, the clinical hallmark of CPP is the symmet-9 ^0 r" x1 N+ U: C
rical testicular growth secondary to stimulation by3 l: g* N0 K+ j2 d) c, A
gonadotropins.1,30 W+ R" b2 Z3 O! A1 o. d
Gonadotropin-independent peripheral preco-
' |! V# M. V: _* q4 ~9 C/ }+ V# y/ ^cious puberty in boys also results from inappropriate, R/ R9 j7 u+ {9 i& c) R
androgenic stimulation from either endogenous or$ g8 C, ?4 w" ~. c; H  B- C9 F
exogenous sources, nonpituitary gonadotropin stim-  Q4 ]& W! [7 {5 @
ulation, and rare activating mutations.3 Virilizing- t1 W2 w5 G3 A! C
congenital adrenal hyperplasia producing excessive( S% ~3 n7 C% T, y+ p
adrenal androgens is a common cause of precocious/ ~4 U6 @: d5 Y/ n& F1 G: z9 u" c# I
puberty in boys.3,4
, M% V* a- I: Z  ~4 DThe most common form of congenital adrenal( a- ]* U# ~0 G. {( I% L/ z/ j
hyperplasia is the 21-hydroxylase enzyme deficiency.
; ]: w+ u) G* J, V: \The 11-β hydroxylase deficiency may also result in, T+ s* X! R1 r) A" m
excessive adrenal androgen production, and rarely,6 D. o# w; m" Y0 n$ y5 X
an adrenal tumor may also cause adrenal androgen; S$ Z1 p& w  ~+ Z+ W% b
excess.1,3
6 Z/ M2 ]4 Z  w2 C8 ~8 ~$ V0 fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# l* b2 s2 c% @: w7 s) X
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007  K0 n/ H4 r, H. T  N" R
A unique entity of male-limited gonadotropin-$ N+ ], Y1 Q. a
independent precocious puberty, which is also known
+ y9 A1 k# v+ Yas testotoxicosis, may cause precocious puberty at a
! ]) S, h0 _, Z: l0 ]very young age. The physical findings in these boys
1 u; H4 }% M  h- w. Iwith this disorder are full pubertal development,
4 q- D) \; k2 ^5 M3 W, T- Dincluding bilateral testicular growth, similar to boys1 v( l: U- ?6 @+ R
with CPP. The gonadotropin levels in this disorder
: E, ^3 H: x+ ]2 J/ kare suppressed to prepubertal levels and do not show
) Z. e; q' D' c( npubertal response of gonadotropin after gonadotropin-
; T9 p$ h$ r$ |0 U7 Treleasing hormone stimulation. This is a sex-linked  h: w( g6 G5 ^
autosomal dominant disorder that affects only
" r+ T; L7 G: J, t2 Vmales; therefore, other male members of the family
7 Y5 ]/ b2 h2 Mmay have similar precocious puberty.3
4 A7 |/ ~, Q1 t2 ]7 ]' YIn our patient, physical examination was incon-
8 O. j  R0 e$ X  ^' Rsistent with true precocious puberty since his testi-) c( A  i" n7 l
cles were prepubertal in size. However, testotoxicosis' ~1 Z3 ~. `0 J" Q4 y" S) b% ]) D
was in the differential diagnosis because his father" z* H$ H9 G+ @% W1 Z) N% ~
started puberty somewhat early, and occasionally,
! ]( Z# o+ [# e2 o( u" O" ctesticular enlargement is not that evident in the, |/ r1 @3 Y+ c" G/ v% O; |
beginning of this process.1 In the absence of a neg-
# X9 L/ W0 s  }1 a* F. vative initial history of androgen exposure, our6 u& Q1 H  k$ V$ N' w: t3 J
biggest concern was virilizing adrenal hyperplasia,
7 |3 w" _3 P; y% `' peither 21-hydroxylase deficiency or 11-β hydroxylase
5 i& u  E# O: {+ |/ gdeficiency. Those diagnoses were excluded by find-5 L, L& R, h! G& K: i
ing the normal level of adrenal steroids.. V' z$ ?, t/ [+ Q
The diagnosis of exogenous androgens was strongly& s! T, r2 X% J4 n1 o% p
suspected in a follow-up visit after 4 months because
5 Q; [5 D- o; k/ k; Uthe physical examination revealed the complete disap-
' G/ Y; s0 C0 _+ upearance of pubic hair, normal growth velocity, and
: ^3 F: }) x+ n9 M1 @: gdecreased erections. The father admitted using a testos-
& i" \7 W& t3 {terone gel, which he concealed at first visit. He was
1 d& N" v; H; ^1 r; cusing it rather frequently, twice a day. The Physicians’
% Y3 L/ J4 u* @$ N  L- y2 v1 HDesk Reference, or package insert of this product, gel or. i5 ~# q1 f% R5 p4 S
cream, cautions about dermal testosterone transfer to- v* V; O5 f9 Y1 o2 h/ P" d
unprotected females through direct skin exposure.
) F2 Y. S, O: G. P( cSerum testosterone level was found to be 2 times the
- |2 L' I( A7 B- w/ `baseline value in those females who were exposed to" l9 q* K# w# V9 r
even 15 minutes of direct skin contact with their male0 y5 \2 W' k8 b* G
partners.6 However, when a shirt covered the applica-
9 \# e9 J( ]2 M$ Ntion site, this testosterone transfer was prevented.
9 V, z7 Z3 v, H5 t- r3 o% H6 a: sOur patient’s testosterone level was 60 ng/mL,
7 Q, b$ m6 O, Bwhich was clearly high. Some studies suggest that0 v5 |3 Z3 K3 e/ ], m6 z- Z1 q
dermal conversion of testosterone to dihydrotestos-, |, q% ]9 k6 G% D+ q, m! C
terone, which is a more potent metabolite, is more
' C3 O9 m4 R8 b; f; ractive in young children exposed to testosterone% a: i$ M' i( z2 b* x8 R* d9 F4 M, i
exogenously7; however, we did not measure a dihy-4 g) U4 a* x1 e( B; s- j
drotestosterone level in our patient. In addition to) @% R1 Y0 H1 [( L7 R6 w
virilization, exposure to exogenous testosterone in
6 p1 P& p/ M4 Y2 v. R6 \/ W& q9 tchildren results in an increase in growth velocity and) c( l$ ^' z4 ?' |& h
advanced bone age, as seen in our patient.( J$ L& k: k* M& @
The long-term effect of androgen exposure during: m, d$ t- d3 D' w; _2 K
early childhood on pubertal development and final
$ S8 _' t6 v6 kadult height are not fully known and always remain
" _8 h, ]& c% b/ l' Ea concern. Children treated with short-term testos-+ j0 f/ N) C: W+ b5 |
terone injection or topical androgen may exhibit some" `0 E8 E7 m* W% t7 R6 t# A- ?
acceleration of the skeletal maturation; however, after2 L/ T  g6 t" _2 L, E
cessation of treatment, the rate of bone maturation" j3 b& d, R- x- n$ E
decelerates and gradually returns to normal.8,99 l& O6 i( D+ {* d. i+ z' X
There are conflicting reports and controversy* D' o' i# H' Q, k5 o( a1 m
over the effect of early androgen exposure on adult
. T- X1 G! R, `' k1 V) Cpenile length.10,11 Some reports suggest subnormal9 W8 o( G# L# I' U; Q# d+ j5 ~$ g, `5 |! R
adult penile length, apparently because of downreg-
/ k) \$ l  E: [  M; i, B0 _ulation of androgen receptor number.10,12 However,0 u% y- Y& c& b& x% h, C: f
Sutherland et al13 did not find a correlation between
! U& U* _$ B) M9 W* F# A9 wchildhood testosterone exposure and reduced adult
1 n( g. c2 v! U" E$ a# D: Y0 hpenile length in clinical studies.9 s8 f9 u4 R0 S3 z* b
Nonetheless, we do not believe our patient is4 }7 j( o2 {- w2 B3 g
going to experience any of the untoward effects from
1 V. l6 H& F+ M) x5 O1 ttestosterone exposure as mentioned earlier because: f, N# A8 x: Z( G
the exposure was not for a prolonged period of time.
, F1 W9 \" r# o) I5 E' T- DAlthough the bone age was advanced at the time of
& `1 {; Z0 l0 d9 `9 S; L2 |0 Pdiagnosis, the child had a normal growth velocity at
2 e: a, |( A$ Q6 p# xthe follow-up visit. It is hoped that his final adult
: H# v6 Z* Y) l# ~4 ^/ ?height will not be affected.
5 V. j9 }4 X, _6 _; o1 RAlthough rarely reported, the widespread avail-
7 I8 A/ Q! E# c% e, @2 jability of androgen products in our society may
4 Z; x: Z* K6 B% S4 lindeed cause more virilization in male or female% w9 ~0 \& Y) D! W6 @
children than one would realize. Exposure to andro-2 X9 M0 y1 u7 e" x6 y3 X& d
gen products must be considered and specific ques-% L! {: M( O5 F* I* H, u
tioning about the use of a testosterone product or
2 }6 i- M8 x8 h, c5 c% v4 G3 Fgel should be asked of the family members during: \0 f% x, H6 ?9 I
the evaluation of any children who present with vir-
5 Q: a  I; T, b, F1 }3 X. Lilization or peripheral precocious puberty. The diag-
& p4 A# `2 Q7 |2 I' d  fnosis can be established by just a few tests and by
  {* y$ V' h( L2 e; v& Yappropriate history. The inability to obtain such a
  g  j, `6 {6 T3 m4 _5 T8 Q! A% qhistory, or failure to ask the specific questions, may$ c" v* |& d$ l6 l. \- Q% y
result in extensive, unnecessary, and expensive
  y7 x. c& [$ X: e3 Qinvestigation. The primary care physician should be
+ T' _* x# N2 D) R$ v  laware of this fact, because most of these children
* U3 L9 d: g3 c+ g) M7 O# A  Emay initially present in their practice. The Physicians’
1 e. R3 a# O( C3 A6 aDesk Reference and package insert should also put a( E' I/ F" _0 C) U4 q
warning about the virilizing effect on a male or
0 a4 X5 D$ C- t. l7 Ifemale child who might come in contact with some-
. G* r2 D& ]& a1 d0 d: mone using any of these products.3 z# Z; |. S6 A: k* y3 Z
References
6 q' Q. G" n5 R" ?6 g9 i: r8 y. I: {9 b1. Styne DM. The testes: disorder of sexual differentiation/ O8 `2 r+ f( T$ R8 j
and puberty in the male. In: Sperling MA, ed. Pediatric0 _6 i. W  q  H) k
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 H) [- p4 W0 C9 A2 P# J- W. H. G+ I! ^/ {
2002: 565-628.# m" p1 a5 y7 m7 G) }: J# Q& G4 x
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 Q# Y8 w' e. ypuberty 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

8 r# N, g+ D8 B. R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