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-Old4 H3 q+ H1 j( K1 b, y( l
Boy Induced by Indirect Topical0 n! ]9 D9 f8 G# E9 h  t
Exposure to Testosterone2 J- m( ^- V% T2 q8 E/ O1 A7 o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- p. N3 @) D  {; h7 e
and Kenneth R. Rettig, MD17 {1 a: l; x' u8 L1 V2 H+ x( ~
Clinical Pediatrics+ i& d1 m* H3 d8 V, n' R# m0 f
Volume 46 Number 69 q* q: j" J. ^  ?) V5 e% u
July 2007 540-543
2 @0 q0 D) b/ U! Z2 E0 \, m* _© 2007 Sage Publications# j$ l# f) Q- c& ?$ U: g5 h: ~) X
10.1177/0009922806296651
  U! _" L/ s, i8 i: }http://clp.sagepub.com. S7 h; F2 R$ D! c: I
hosted at
5 d( i% d2 T5 ehttp://online.sagepub.com
+ d: N: E' E7 W5 gPrecocious puberty in boys, central or peripheral,
3 n  W% P7 |# B; h  }6 dis a significant concern for physicians. Central
) ^  T3 H; Y! g/ L1 G' @$ L+ n5 c  hprecocious puberty (CPP), which is mediated
+ Q) z$ S4 {- b( Tthrough the hypothalamic pituitary gonadal axis, has
+ O" M) n+ p# g5 W& W# v% ta higher incidence of organic central nervous system( e6 j! R" E+ w. P/ ^" l1 B
lesions in boys.1,2 Virilization in boys, as manifested
4 W: b4 z+ n$ U7 ^' C9 J# T5 Hby enlargement of the penis, development of pubic! P  i/ u. A& O( |+ W; G
hair, and facial acne without enlargement of testi-) V# \+ j% r5 Q& S
cles, suggests peripheral or pseudopuberty.1-3 We, ~8 q) d. E, b8 n* n# f. n4 ?
report a 16-month-old boy who presented with the/ t) f& a! w- t" E" N5 @) t
enlargement of the phallus and pubic hair develop-# @1 [  }2 Q' a; x7 S" j/ D/ F
ment without testicular enlargement, which was due' v3 U! e$ w9 }, ]
to the unintentional exposure to androgen gel used by
! p& n# a1 l( h, U, Tthe father. The family initially concealed this infor-
7 t) N' G- w( y3 i" lmation, resulting in an extensive work-up for this
0 K( |. A: M% D5 dchild. Given the widespread and easy availability of
3 [8 V& n1 k* _9 A  [testosterone gel and cream, we believe this is proba-
0 ?) \6 y. W: g; R; s/ Jbly more common than the rare case report in the
+ K* o6 O. X+ Z7 Y' Q/ N0 }literature.4
9 F5 o3 z! U# ]5 WPatient Report2 l7 c$ L# a# C: s' \2 ~6 E" E
A 16-month-old white child was referred to the4 K! a% S" v9 L2 O( Z
endocrine clinic by his pediatrician with the concern- @5 o1 J/ l% Q2 S4 y& e  t
of early sexual development. His mother noticed
7 \# B( u6 l3 c" V1 wlight colored pubic hair development when he was) c6 x* _, w$ j  N
From the 1Division of Pediatric Endocrinology, 2University of
* u3 }. d$ H' n2 d: M( I- L, Y5 RSouth Alabama Medical Center, Mobile, Alabama.
% j# @) j8 t; P5 D5 kAddress correspondence to: Samar K. Bhowmick, MD, FACE,
3 K) y+ Y' C3 f6 ^Professor of Pediatrics, University of South Alabama, College of
& e+ m1 [! s& p# j4 GMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 P' W+ u* b9 J/ f# X( D! Se-mail: [email protected]." L4 v9 O3 a: K' D
about 6 to 7 months old, which progressively became/ l% v3 ?! J0 O# @
darker. She was also concerned about the enlarge-+ p; ?( f! \* ]5 L2 s7 y
ment of his penis and frequent erections. The child/ ]$ W# m: i) Y$ m: |5 N4 n$ H
was the product of a full-term normal delivery, with/ P8 t  A# @7 J# a$ E, \) w) O% Z
a birth weight of 7 lb 14 oz, and birth length of
7 p% {( Z0 V8 f& k! n& u$ N; r20 inches. He was breast-fed throughout the first year- Q' G3 x6 N3 i& N3 Z9 O; t
of life and was still receiving breast milk along with# T$ J4 ?4 A* k8 ^. e
solid food. He had no hospitalizations or surgery,' K: [8 c& b  q8 ^# V  B: O0 V
and his psychosocial and psychomotor development
9 h! |- h" r) mwas age appropriate.' M+ @0 Q8 ^/ m) c
The family history was remarkable for the father,
) t, ~5 @& ]5 [0 r; ewho was diagnosed with hypothyroidism at age 16,3 V2 ^+ k% x# \& E6 Q4 |2 `
which was treated with thyroxine. The father’s
. `; }9 T/ I% Yheight was 6 feet, and he went through a somewhat
' I, \* u) b8 j& }6 M& h0 n% R3 xearly puberty and had stopped growing by age 14.
8 q9 M4 g1 P, H. {The father denied taking any other medication. The
( m/ u: c1 {! N0 p5 [% G, f& Mchild’s mother was in good health. Her menarche) o" F# V1 ]9 ^, k9 G& K9 `) A" ]
was at 11 years of age, and her height was at 5 feet
# F) k4 Z/ T$ T5 inches. There was no other family history of pre-
2 @/ ~1 M7 V5 m" Kcocious sexual development in the first-degree rela-% Z; R9 w8 q1 ~5 s
tives. There were no siblings.
, ?7 ^* t  G5 X- A; R# tPhysical Examination
$ h+ @; k7 t" n( p- j9 H: UThe physical examination revealed a very active,
+ Y- H& v3 M  G' r$ w* wplayful, and healthy boy. The vital signs documented( n, P1 D( x% d" I
a blood pressure of 85/50 mm Hg, his length was. G6 Z/ J* D  n: v; @* R
90 cm (>97th percentile), and his weight was 14.4 kg
6 T8 U+ o& T9 g' k9 z(also >97th percentile). The observed yearly growth( r3 F, z5 i, {; a4 w
velocity was 30 cm (12 inches). The examination of( n/ q) S: j5 S2 k6 S* d
the neck revealed no thyroid enlargement.
5 |: {  e8 I$ ^: a2 V. c8 V5 EThe genitourinary examination was remarkable for
( R. N+ S! T1 Y; @0 Wenlargement of the penis, with a stretched length of
/ g8 P/ m3 e; f* x! {# e/ ~/ O& C8 cm and a width of 2 cm. The glans penis was very well+ ~& y# g& V" q' t/ ^
developed. The pubic hair was Tanner II, mostly around- w( U' y0 z8 b. {# O) H" X
540
, Z) T$ k! v6 K0 C5 y. Zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; i- R% `- a9 s( V( e
the base of the phallus and was dark and curled. The1 l1 K" @& k( Z5 H. {# R8 W6 L  m' V8 l
testicular volume was prepubertal at 2 mL each.
, |: T, d/ Z7 ^0 Q9 X3 PThe skin was moist and smooth and somewhat
& M2 u+ a  S$ c5 Q- r7 x5 j' noily. No axillary hair was noted. There were no
1 X+ p- e8 h) B& m0 {% ^9 _9 R/ {abnormal skin pigmentations or café-au-lait spots.
$ [" ]+ M) M9 U1 lNeurologic evaluation showed deep tendon reflex 2+
* ^# ^0 p' ]; wbilateral and symmetrical. There was no suggestion
+ r0 W) o/ x% P! z7 _) F6 [& p* m+ pof papilledema.& B  z$ O; G& L" |
Laboratory Evaluation$ v# t. _; h& E9 q
The bone age was consistent with 28 months by
8 e# N% W; f# V; _  v8 ^using the standard of Greulich and Pyle at a chrono-
0 h- N$ \4 d, @8 P- v" g8 W0 Dlogic age of 16 months (advanced).5 Chromosomal2 J% k0 ~+ ?. l
karyotype was 46XY. The thyroid function test
% B; q- v4 e# Jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ x3 }6 K7 e; K4 i2 Q, klating hormone level was 1.3 µIU/mL (both normal).
0 U/ ^) U7 W# f# `The concentrations of serum electrolytes, blood" n+ g. n% r% a- {  Y2 V/ V
urea nitrogen, creatinine, and calcium all were
/ {3 o+ }2 f" Twithin normal range for his age. The concentration" ]3 Y. X, a# M3 h% i
of serum 17-hydroxyprogesterone was 16 ng/dL
3 x7 A5 p# G! E1 V- y7 Q$ {/ C8 v8 r(normal, 3 to 90 ng/dL), androstenedione was 20& b7 ~* T9 \, R. ]
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 y( D& `8 x" M  A1 g5 Rterone was 38 ng/dL (normal, 50 to 760 ng/dL),
& d3 l! K+ v# W4 I: D7 e  Odesoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 q& Y% V4 \' _- Y/ r% z, y% Y49ng/dL), 11-desoxycortisol (specific compound S)
( g( R# f0 p( w& l8 Kwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# [: ^3 D6 Y& E
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total2 q5 `8 b) u+ e# k' `) b* N0 ~# A
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),! E2 v' J5 p2 A  E
and β-human chorionic gonadotropin was less than
6 A6 l* i+ d+ E1 J1 `5 mIU/mL (normal <5 mIU/mL). Serum follicular
* L' d: g; O3 R& A0 Astimulating hormone and leuteinizing hormone' r! ?8 ]  ~! Q3 ]  y9 i) i
concentrations were less than 0.05 mIU/mL. y7 n$ X$ K+ \1 }3 `" @
(prepubertal).
# }! \- ^; a0 @+ z" P. q, HThe parents were notified about the laboratory
; X1 N9 U( R& }4 f* ?; L/ X( Y. Vresults and were informed that all of the tests were
, \. C: ]) m6 [9 \; Rnormal except the testosterone level was high. The
8 o8 I! `0 t) H- V3 f2 Q' v+ jfollow-up visit was arranged within a few weeks to
3 \# V8 ^* r  H, b2 j0 }obtain testicular and abdominal sonograms; how-
- ^) t- M' L3 ?* d& F3 cever, the family did not return for 4 months.
- s4 O* u2 z5 \. h' J; IPhysical examination at this time revealed that the! m6 l9 h9 H( A8 P' G
child had grown 2.5 cm in 4 months and had gained
! V9 D& X4 ^, B; p# T% S( ^8 N2 kg of weight. Physical examination remained
+ J' N/ Z# m) I, C- j6 z: F6 Xunchanged. Surprisingly, the pubic hair almost com-
" y% H& m. I% |1 _$ @& b1 o2 G! r; }0 Tpletely disappeared except for a few vellous hairs at  r) |" U: F% E7 Z
the base of the phallus. Testicular volume was still 2
3 x. s: i3 K# j+ lmL, and the size of the penis remained unchanged.
4 [# c, d) |" m" Q4 p3 \2 a1 U9 B, TThe mother also said that the boy was no longer hav-
$ w" M) N# c  X8 V1 e: ving frequent erections.
5 y8 c, v4 f$ \' IBoth parents were again questioned about use of
' p9 N! ?, t( \2 m' ~6 H& O5 oany ointment/creams that they may have applied to
; U3 @4 f8 g( ^4 Gthe child’s skin. This time the father admitted the5 `) J* M$ g( g
Topical Testosterone Exposure / Bhowmick et al 541
. ?$ d2 b9 B& muse of testosterone gel twice daily that he was apply-
9 ^0 G2 n! a! Ling over his own shoulders, chest, and back area for) ~- c7 Q7 S5 H7 g" ]5 z4 A
a year. The father also revealed he was embarrassed
7 Q, w- G* B/ xto disclose that he was using a testosterone gel pre-" R; v& k/ _: x& @8 O% U
scribed by his family physician for decreased libido
# Q8 Z. c. Y- esecondary to depression.9 X& C% K( @  \3 s- L
The child slept in the same bed with parents.( P) i- R1 t, t6 k1 Z9 K
The father would hug the baby and hold him on his; J9 o  D0 ~. `! u% B6 f
chest for a considerable period of time, causing sig-( G3 ]- o: t# f6 A8 E0 T
nificant bare skin contact between baby and father.
/ _* l( m  z8 {7 DThe father also admitted that after the phone call,' w6 |; ^. E: o' h- e2 D# J
when he learned the testosterone level in the baby. [$ _; {* K2 ]9 C9 I$ i, z4 V1 ~
was high, he then read the product information
9 q1 w7 z; d8 l! ^packet and concluded that it was most likely the rea-) r7 ^9 E2 Q) @( p# N2 d
son for the child’s virilization. At that time, they! F5 K) k+ M& w; ~$ N
decided to put the baby in a separate bed, and the& ]3 B- V3 w. A$ v+ L7 B6 p
father was not hugging him with bare skin and had1 V- u  j) t$ |2 `4 B
been using protective clothing. A repeat testosterone
9 K& U5 w- w' n" {# Itest was ordered, but the family did not go to the
4 x+ S6 D+ E3 ^9 ~4 ?7 n2 J$ @laboratory to obtain the test.* E4 f) @8 b1 L) @  E) E$ ]
Discussion% _" c; u) F2 l5 H- X- g
Precocious puberty in boys is defined as secondary$ K/ G) H! b8 r6 Y3 Z. _- O
sexual development before 9 years of age.1,4. e: m& v/ a1 y' B- E
Precocious puberty is termed as central (true) when5 w$ l: y) d" N8 g
it is caused by the premature activation of hypo-
  m/ P1 t( V+ n- x* }# w  f. w! ~thalamic pituitary gonadal axis. CPP is more com-
3 J1 `. }: R  K8 X+ H* R7 q. M/ a5 O  F3 Imon in girls than in boys.1,3 Most boys with CPP
6 f; s' C, P8 X% D" {may have a central nervous system lesion that is( Q* X) W% P9 n2 Y3 X1 D8 S
responsible for the early activation of the hypothal-% O# g9 ~+ I( m3 O! m: B, W
amic pituitary gonadal axis.1-3 Thus, greater empha-- R4 f1 T" r& K
sis has been given to neuroradiologic imaging in  |4 S* ^5 k7 n5 ]
boys with precocious puberty. In addition to viril-' F- u$ s8 Y& ~
ization, the clinical hallmark of CPP is the symmet-$ O  z- D, o' Y3 M3 v
rical testicular growth secondary to stimulation by  S8 C% j. j; A$ w+ S1 O" N' I1 o
gonadotropins.1,3/ S- O  i, M8 t; P! @
Gonadotropin-independent peripheral preco-/ K) ?/ a" n9 E" e6 l1 b* O
cious puberty in boys also results from inappropriate
5 Y% }9 O, T1 D" \. Kandrogenic stimulation from either endogenous or, A9 O5 ^$ l1 V: B) }( I0 [7 a
exogenous sources, nonpituitary gonadotropin stim-
' F& k, J! u; Q/ P. culation, and rare activating mutations.3 Virilizing
% h. U6 e( o7 d1 K) econgenital adrenal hyperplasia producing excessive5 Y2 m* m4 {5 l' T" r
adrenal androgens is a common cause of precocious7 L* _9 g" M* v- v! G
puberty in boys.3,4) C  R; |3 r3 j
The most common form of congenital adrenal: g% Q. r( f; r2 M4 ]) |
hyperplasia is the 21-hydroxylase enzyme deficiency.9 j4 g# B* _& [4 |
The 11-β hydroxylase deficiency may also result in
- f" Q$ V" c$ Q; Bexcessive adrenal androgen production, and rarely,0 w, J* W8 X- l( y
an adrenal tumor may also cause adrenal androgen* ?( E1 O% L8 H6 c8 l, x
excess.1,3* k- l$ d4 c) L' ^& s# C  @% p
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 S' H% O/ W4 Z% a
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007% U( Q. R  ?2 K! k* t2 M
A unique entity of male-limited gonadotropin-
9 z% ^6 o% I2 bindependent precocious puberty, which is also known
/ f! m# b/ m: Z# N; O0 q/ Z# B" xas testotoxicosis, may cause precocious puberty at a! k) Y& b* f; g- T- j
very young age. The physical findings in these boys
  t% o3 K) u" L( d- vwith this disorder are full pubertal development,
. ~- i+ C4 J3 Iincluding bilateral testicular growth, similar to boys' K5 f% P- \7 i* F$ l$ \
with CPP. The gonadotropin levels in this disorder! e4 G, \- o! L! G9 D9 S
are suppressed to prepubertal levels and do not show* P# i0 x4 q0 G9 M" Z" \
pubertal response of gonadotropin after gonadotropin-8 r7 U2 S2 M( F
releasing hormone stimulation. This is a sex-linked' q* R# W' n- \* @  Y
autosomal dominant disorder that affects only
, |) R3 d0 t* bmales; therefore, other male members of the family7 i4 B9 p3 r" i) S) _8 G
may have similar precocious puberty.34 m% _; K# q8 d% }; ?' D
In our patient, physical examination was incon-4 ^) c' Z- u/ c! F. c0 n4 _
sistent with true precocious puberty since his testi-. T& C6 U( u  u7 g5 I: s: o
cles were prepubertal in size. However, testotoxicosis$ W. \! @+ Z) z
was in the differential diagnosis because his father) c- W6 d) ^5 g
started puberty somewhat early, and occasionally,
% e; h+ I9 e; D/ mtesticular enlargement is not that evident in the
; t+ h$ \% |* `% ?beginning of this process.1 In the absence of a neg-
0 O& p+ z" u* m! e7 n- ?. f: fative initial history of androgen exposure, our8 s2 p* s: G! e4 {) c# {$ L1 G
biggest concern was virilizing adrenal hyperplasia,
4 u& @& S# \, Q5 r8 \- D4 Deither 21-hydroxylase deficiency or 11-β hydroxylase: S) ~0 B: ?$ H# B
deficiency. Those diagnoses were excluded by find-
3 o* I; {0 _1 x1 Q/ f7 Aing the normal level of adrenal steroids.
% P8 ^: h! T/ i/ n8 mThe diagnosis of exogenous androgens was strongly
: T$ X  H3 X5 {& y$ Ususpected in a follow-up visit after 4 months because
/ t' e3 n9 {0 g9 H  L+ A: nthe physical examination revealed the complete disap-8 }1 H" ~- y6 X( k3 C; ]
pearance of pubic hair, normal growth velocity, and
: Z6 O+ z) v- ]/ U9 ^decreased erections. The father admitted using a testos-6 X$ G: f; S* }: Z/ `
terone gel, which he concealed at first visit. He was/ N7 O) T" U4 _. h) s: C' D5 R
using it rather frequently, twice a day. The Physicians’- P, P4 I0 N- H4 N) ^
Desk Reference, or package insert of this product, gel or
6 X  B) z/ Q6 S# n  V6 a% X6 {# Fcream, cautions about dermal testosterone transfer to
2 C/ z7 `8 s6 ^& x% _( j& iunprotected females through direct skin exposure.
$ U( F! r) Y( C5 A% eSerum testosterone level was found to be 2 times the
2 b$ t- V, g6 {. w! I8 Dbaseline value in those females who were exposed to& t2 [- g( N/ ^6 v
even 15 minutes of direct skin contact with their male9 y( c  ^3 R( p3 _  M; c
partners.6 However, when a shirt covered the applica-
6 r+ P& g* b2 d/ Z4 {1 qtion site, this testosterone transfer was prevented.; j2 R% Q& \. R3 m# S
Our patient’s testosterone level was 60 ng/mL,
5 U) H6 o/ g, N( f8 D5 Vwhich was clearly high. Some studies suggest that
/ B5 l1 ~/ Y/ Xdermal conversion of testosterone to dihydrotestos-; T7 Y. r" c! M% x7 [5 e9 R
terone, which is a more potent metabolite, is more
* J" V) ~' f0 ?0 @) Yactive in young children exposed to testosterone
) I1 [& y; G# C+ X( T: Jexogenously7; however, we did not measure a dihy-- G- A: v4 U. w0 O1 j
drotestosterone level in our patient. In addition to
; P) m) C" [$ }7 E/ Lvirilization, exposure to exogenous testosterone in5 s- p5 ~8 Z7 c8 z5 w4 z/ k$ ]
children results in an increase in growth velocity and
: }' p$ J/ w6 ~+ jadvanced bone age, as seen in our patient.0 F: Y' ~' ~6 k, |0 N
The long-term effect of androgen exposure during
! Y! ^8 {1 ?  u/ g" M: L3 F- |early childhood on pubertal development and final
$ k; U' l8 Z* A" e  ?adult height are not fully known and always remain5 k7 b, ~2 @! J5 p! j: i8 n
a concern. Children treated with short-term testos-
) u/ }. ~( {- t) {# x* aterone injection or topical androgen may exhibit some1 o0 @" l' p3 I0 ?0 _. L  B4 \/ O
acceleration of the skeletal maturation; however, after  S4 x7 p  F% Y  y  V' F% U' ~
cessation of treatment, the rate of bone maturation
3 c2 b- m' J, ^- }% j" _2 _5 wdecelerates and gradually returns to normal.8,9
4 _5 C- D6 |4 eThere are conflicting reports and controversy
$ _: ^5 i7 E; W" E9 K' mover the effect of early androgen exposure on adult6 f  U7 M9 _% z- a9 x- e7 A! Y
penile length.10,11 Some reports suggest subnormal# p0 G$ |2 g5 a9 o
adult penile length, apparently because of downreg-5 |: m0 l$ `, h# P) ]; ~/ Z
ulation of androgen receptor number.10,12 However,
. h" y1 d5 m( j2 }0 s" H# L# [Sutherland et al13 did not find a correlation between
& f( d4 l* W3 }# ~8 Wchildhood testosterone exposure and reduced adult5 w& r3 A. w3 b8 F; K8 W5 M
penile length in clinical studies.
% X% d0 Q; j& o) t5 j. J( z* ^3 P5 TNonetheless, we do not believe our patient is
" N7 S. }' K) m, h! w6 dgoing to experience any of the untoward effects from
: A. I; L  z- }+ O  mtestosterone exposure as mentioned earlier because- @6 }5 K, P& g; n) C. m( @
the exposure was not for a prolonged period of time.
! e1 @6 {4 R8 {, n% @9 d3 N& |! CAlthough the bone age was advanced at the time of
! z+ X$ q- U4 _& [( Wdiagnosis, the child had a normal growth velocity at, k5 q  X$ x+ T0 ^9 S
the follow-up visit. It is hoped that his final adult6 P, a/ I% `+ {
height will not be affected.; N6 x) K9 S2 @9 t, H
Although rarely reported, the widespread avail-% ]# p2 G4 b- K# Z, R2 ]1 b. l0 f
ability of androgen products in our society may
2 @. \: D# q. \; h* Jindeed cause more virilization in male or female
: V/ H  s: |& R8 fchildren than one would realize. Exposure to andro-
, Y% q3 Y" U- egen products must be considered and specific ques-
- S3 c; P/ e1 s- o. W- Z+ Ationing about the use of a testosterone product or: X3 c) r, ~/ }, c
gel should be asked of the family members during
$ H! H1 {( q! q$ l# ~5 N9 nthe evaluation of any children who present with vir-: ]3 o  M$ n0 }+ O$ |3 o1 q6 Q
ilization or peripheral precocious puberty. The diag-
. S8 G9 @3 e7 G5 h# dnosis can be established by just a few tests and by& v, B8 q! L+ s( p0 R) u/ K
appropriate history. The inability to obtain such a& J* N* R3 U0 _' r* `$ ^
history, or failure to ask the specific questions, may! d3 v' a+ ^* C: g/ `/ [4 q( h
result in extensive, unnecessary, and expensive$ p. r! d6 Z  ?3 Z, P6 f3 Q
investigation. The primary care physician should be+ T0 M* [* n3 c% U% V
aware of this fact, because most of these children+ `' D1 `  V8 O$ F
may initially present in their practice. The Physicians’) f1 D8 O% S4 e* h+ r/ ^
Desk Reference and package insert should also put a
1 z2 y# I3 n/ ^5 V' E  ^7 B6 X& `& Fwarning about the virilizing effect on a male or
/ w& ~7 s, X$ Y3 f# ]female child who might come in contact with some-% `. ~  e2 J2 H$ O" ~
one using any of these products.
% @4 _) S( X0 @( C- [: A( W; KReferences8 i1 I+ J5 O) G
1. Styne DM. The testes: disorder of sexual differentiation
% ^6 h3 X8 Z+ ]& P% `( X! J! |and puberty in the male. In: Sperling MA, ed. Pediatric! B; h8 z& o- W3 W' `7 ?9 B
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- F  A; Z: z8 M' N+ q  N2002: 565-628.. ?6 }: p3 `. u
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% N9 H2 R7 {7 K' t% l& B& Bpuberty 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-Old0 j, c; g' t) i- e6 o, u
Boy Induced by Indirect Topical
. h0 A. E1 m. w0 Q& ?6 a) kExposure to Testosterone
' w5 h! }; z5 `; h" P  n! M" Q2 @$ ]Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
$ u% ^$ p: d3 A" h( Rand Kenneth R. Rettig, MD1. ]8 K; e$ I- V" B0 C4 M
Clinical Pediatrics
+ b' o  L2 F0 L5 `9 n7 rVolume 46 Number 67 [" g, c7 L4 ^0 F+ ?! u
July 2007 540-543
4 m; i) E/ U+ Q- Z- w7 B2 t/ {© 2007 Sage Publications: K' y" x! M( g& ]' P! B8 f: k4 n. E
10.1177/0009922806296651
) [  i, u' I$ M( S) Y. H  Uhttp://clp.sagepub.com. a9 u9 T. U  h9 L) i( R/ V
hosted at
3 V( z" m5 D# Uhttp://online.sagepub.com
3 j' F7 {! H9 b1 \Precocious puberty in boys, central or peripheral,
# ^" `0 l+ j4 _3 eis a significant concern for physicians. Central
1 s, s( O" K, Y, W, `! U- v3 x8 p$ Yprecocious puberty (CPP), which is mediated) ?: m+ x) d3 d8 h4 R+ e# W
through the hypothalamic pituitary gonadal axis, has5 U* M5 r1 e; c/ Y& o
a higher incidence of organic central nervous system
& K4 ]9 R4 J$ N' }) Vlesions in boys.1,2 Virilization in boys, as manifested
* d! q1 }4 l& O6 Y/ Yby enlargement of the penis, development of pubic/ y2 [6 z6 o7 X! x6 u! c1 u5 y7 ~( e
hair, and facial acne without enlargement of testi-
% {) a" B9 w  Jcles, suggests peripheral or pseudopuberty.1-3 We1 T0 W  G; ^) ?( ?- ~. e' F% L
report a 16-month-old boy who presented with the6 w0 e+ i4 n6 ]0 R5 a* m
enlargement of the phallus and pubic hair develop-/ l3 Z" G7 _: @" ~% T) T
ment without testicular enlargement, which was due
. [' L2 x8 S8 [! |' t* c" _to the unintentional exposure to androgen gel used by0 D# |# a; A* g7 W( ~' T
the father. The family initially concealed this infor-
& Y+ V/ ]# t. V  m: o9 dmation, resulting in an extensive work-up for this
' a3 |& J# f6 {% [6 m8 P" xchild. Given the widespread and easy availability of, `" G* t  v2 G8 r( L
testosterone gel and cream, we believe this is proba-6 g# E5 U  p) o, n1 p
bly more common than the rare case report in the: d2 w# ^3 j5 q  W) ~# x2 u
literature.4
) ~6 o: z0 y8 s9 g3 g7 ]. r6 _- BPatient Report
. O4 _2 L0 \# Z. [. ]7 J% AA 16-month-old white child was referred to the
) M& j0 \2 V- u6 N% V# Z. T8 L# u: kendocrine clinic by his pediatrician with the concern' s" i2 k8 M0 |  K8 J  Y
of early sexual development. His mother noticed
3 x( `; c* @$ f, j  Nlight colored pubic hair development when he was9 P; m$ \! \* @- O7 N$ z( j# {
From the 1Division of Pediatric Endocrinology, 2University of
3 Y; K& J3 U$ j; i* L" C( i& t( KSouth Alabama Medical Center, Mobile, Alabama.
/ k* k7 t# f( B3 B/ W3 E2 zAddress correspondence to: Samar K. Bhowmick, MD, FACE,
1 Y' w- y/ g* L# z0 y/ ^" iProfessor of Pediatrics, University of South Alabama, College of; H0 B3 }. G; z) e
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 P) b3 G  L, V. a
e-mail: [email protected].6 |- I9 _5 c9 S( M; P& P" M# r6 V2 [
about 6 to 7 months old, which progressively became
8 R. F% k' J/ P) D* C& {# N- edarker. She was also concerned about the enlarge-
- D; q- x6 ]& _; Ument of his penis and frequent erections. The child; |- a) v1 R, f* C. T- A
was the product of a full-term normal delivery, with4 B4 c: R* ^; D" \4 z% e
a birth weight of 7 lb 14 oz, and birth length of
2 T$ b4 @8 x7 m( ~" \20 inches. He was breast-fed throughout the first year
  ~+ G' x( u, W$ `of life and was still receiving breast milk along with
& V1 M; H' N5 U, {! w4 L- psolid food. He had no hospitalizations or surgery,
5 g1 _- k2 ]: x- L1 q: o' Vand his psychosocial and psychomotor development# q1 r+ W  M3 y- J: k! z8 @
was age appropriate.! O2 K. C0 N' u. i* n
The family history was remarkable for the father,
7 Y9 o; ~! o5 x2 Q" Awho was diagnosed with hypothyroidism at age 16,
! G. W0 I6 L( u, {/ ]2 vwhich was treated with thyroxine. The father’s
9 L6 h# S  N$ Q0 F! [* J! {height was 6 feet, and he went through a somewhat
% k6 E# U9 J' _; p; U! Fearly puberty and had stopped growing by age 14.
0 V; l3 V" u/ A  zThe father denied taking any other medication. The
7 e& I! J. V" F+ L+ {+ n; E; Uchild’s mother was in good health. Her menarche9 S0 M  \: `, a& J, Q& Q
was at 11 years of age, and her height was at 5 feet8 z3 Z3 V4 d+ O) M
5 inches. There was no other family history of pre-; L: E- c! G# U; A$ _2 d
cocious sexual development in the first-degree rela-
$ V* i( s3 e! x0 p  n6 }tives. There were no siblings.5 [9 _  h' w" Z9 N' |. H
Physical Examination
* Y! H( V2 H) N# g+ V! N6 g6 d2 {" MThe physical examination revealed a very active,
2 v( |. I& V% a0 _) T# O2 b; F% _playful, and healthy boy. The vital signs documented
/ E/ W3 Z# t( O8 L4 P* t" Ja blood pressure of 85/50 mm Hg, his length was: d3 {& l. \- e/ r
90 cm (>97th percentile), and his weight was 14.4 kg7 m3 U5 ~+ ?$ a; ^; u4 t6 t5 a
(also >97th percentile). The observed yearly growth
, n! b: l" Y; O. C. Tvelocity was 30 cm (12 inches). The examination of
( r/ o% X& ^/ p' M6 G. nthe neck revealed no thyroid enlargement.) ^3 z1 I& M$ H$ E4 ~
The genitourinary examination was remarkable for; k4 m3 X# i7 K& a
enlargement of the penis, with a stretched length of9 v/ ]$ M% q1 V7 H
8 cm and a width of 2 cm. The glans penis was very well
( ~6 s8 ~2 E& v% {3 ^5 \* K; c3 Xdeveloped. The pubic hair was Tanner II, mostly around
; M* E3 N' O. F! C) k  f) E  T7 ?5401 @2 R2 m  H  \
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 }! n; Z, Y/ b9 F& i5 q! t) T2 u1 cthe base of the phallus and was dark and curled. The
4 N& X9 ?6 s; W1 W  H: btesticular volume was prepubertal at 2 mL each.
  g  g+ O0 z- _The skin was moist and smooth and somewhat
% m2 H: ~7 W4 c8 w' W) noily. No axillary hair was noted. There were no: ~# v2 B6 s0 s4 q( K; |' O
abnormal skin pigmentations or café-au-lait spots.( G! E  T, R( G
Neurologic evaluation showed deep tendon reflex 2+
: _- |0 |2 R0 k; V6 @bilateral and symmetrical. There was no suggestion( g6 D! F$ W  a
of papilledema.
) q4 c; T# }" ~5 N5 vLaboratory Evaluation+ B$ N" S" K! l& j
The bone age was consistent with 28 months by
# [0 ?+ G& ~" v% l6 R. A6 Dusing the standard of Greulich and Pyle at a chrono-
  T* q9 G0 L1 E2 |3 F: Glogic age of 16 months (advanced).5 Chromosomal$ c! t- d# K" T
karyotype was 46XY. The thyroid function test' a1 ^' N: h" Y8 x% w. B% R( v
showed a free T4 of 1.69 ng/dL, and thyroid stimu-: \# f; G! M8 J6 X  h/ n
lating hormone level was 1.3 µIU/mL (both normal)., j, D/ H; |4 \& ^; z0 ~+ i
The concentrations of serum electrolytes, blood; r; M; ]) e4 }7 I+ Z7 k$ h
urea nitrogen, creatinine, and calcium all were6 O- a; E1 Y$ ^
within normal range for his age. The concentration: t  y% s- U. Z9 F$ M) S
of serum 17-hydroxyprogesterone was 16 ng/dL
2 q& W' r6 I) U9 C, U(normal, 3 to 90 ng/dL), androstenedione was 206 p; _& ~/ x+ W7 i0 B2 E
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) ?! r# P& o# u
terone was 38 ng/dL (normal, 50 to 760 ng/dL),+ C. {# n% M, s  x
desoxycorticosterone was 4.3 ng/dL (normal, 7 to( R+ e- {- b$ E2 x: ?4 c: E( i
49ng/dL), 11-desoxycortisol (specific compound S)* I* `( n1 K) ?: R) t
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 O: }9 J2 C3 h4 k' P! o) R! L8 Xtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' o$ `: h0 _- f( K3 M
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, H6 C% M5 l" q5 y3 dand β-human chorionic gonadotropin was less than5 h! [, I0 q. ^, n! p
5 mIU/mL (normal <5 mIU/mL). Serum follicular$ W# i2 o( K. J
stimulating hormone and leuteinizing hormone
& U$ Y8 F) d, c' U- h% Nconcentrations were less than 0.05 mIU/mL; I* f$ _1 R* t6 j) d/ c+ r; e0 m
(prepubertal).
0 J3 _6 R" k7 ~; U" n! vThe parents were notified about the laboratory
- A1 C% _- d' Q. gresults and were informed that all of the tests were
$ S0 s. u" C! Lnormal except the testosterone level was high. The$ q5 Z% s0 A1 O+ R5 B9 w+ O4 f
follow-up visit was arranged within a few weeks to) B' m4 e7 O5 L
obtain testicular and abdominal sonograms; how-
' ^8 V+ H& Q8 s& s. ]ever, the family did not return for 4 months.2 z9 j  O: q' k0 B. Y
Physical examination at this time revealed that the2 e! G6 v* q: q  z
child had grown 2.5 cm in 4 months and had gained
% f! k  W5 l# h2 kg of weight. Physical examination remained7 q" A  U+ f! @2 K
unchanged. Surprisingly, the pubic hair almost com-, X) t( s; e+ _0 g& W
pletely disappeared except for a few vellous hairs at
/ C" ?' B; J. M/ U0 ~" t: [1 uthe base of the phallus. Testicular volume was still 2
, f! P1 B) f% a1 I6 [mL, and the size of the penis remained unchanged.' U4 l/ P# _! I  g% G
The mother also said that the boy was no longer hav-
3 _. U" V) a& eing frequent erections.. H# r. A$ N2 b1 [( q# u6 @
Both parents were again questioned about use of' X+ o$ S. P+ K1 q
any ointment/creams that they may have applied to& V$ w( ~0 N( I4 t
the child’s skin. This time the father admitted the
7 I5 ^# r/ v6 y' iTopical Testosterone Exposure / Bhowmick et al 541& K" d5 N- a& Y
use of testosterone gel twice daily that he was apply-
) h8 D  n9 \+ }  ~# d: B3 Z9 N. Ting over his own shoulders, chest, and back area for
( C2 k- k9 b3 c$ Q  h# J* x9 [3 Aa year. The father also revealed he was embarrassed
6 I$ `9 ]2 F6 |4 Gto disclose that he was using a testosterone gel pre-
& u3 [: V3 i% r' X; I( F$ g$ u( G, ?scribed by his family physician for decreased libido
' C% g2 ^0 O8 s1 r/ ksecondary to depression.
8 K6 D. b1 D& f' K1 A- a1 D+ A' LThe child slept in the same bed with parents.$ p, h* e! b4 v) B# ~: h
The father would hug the baby and hold him on his
% k* L  S" N" e1 a% y4 b' Q5 Gchest for a considerable period of time, causing sig-8 o1 t$ w7 ]) K0 c
nificant bare skin contact between baby and father.
8 \5 G5 x; u) {' x0 O, dThe father also admitted that after the phone call,4 c0 \; [9 b5 s+ t; Z
when he learned the testosterone level in the baby- k6 d) s3 P* D6 E5 b  T0 R* @! B
was high, he then read the product information
1 C$ n" x6 K' I8 wpacket and concluded that it was most likely the rea-
- b# c6 ?3 P$ P" ^0 Kson for the child’s virilization. At that time, they
# \  g* N. ?$ Ydecided to put the baby in a separate bed, and the
5 c& w* a; @! o$ `" V$ hfather was not hugging him with bare skin and had
2 [/ J8 x) p5 h+ L8 Y6 B- ?; Q6 abeen using protective clothing. A repeat testosterone0 V" [, Y& v  D6 N
test was ordered, but the family did not go to the
+ M" v  d3 U/ R% Vlaboratory to obtain the test.
: P# o& s+ Y# |8 o+ DDiscussion
; _, L1 o# [; Z8 b; JPrecocious puberty in boys is defined as secondary
& a- y( g$ {/ v6 X8 O- osexual development before 9 years of age.1,44 F7 o8 f& Q9 r( M2 I- W
Precocious puberty is termed as central (true) when
0 A- a- |( q+ F0 {  J% P2 @% E% R1 Q0 Rit is caused by the premature activation of hypo-
  X; P6 P0 s% g/ O5 w, rthalamic pituitary gonadal axis. CPP is more com-
, u3 t& F) |+ p' m5 w. o) Kmon in girls than in boys.1,3 Most boys with CPP
) k" K) T& c( {3 W% b  A1 Wmay have a central nervous system lesion that is
  v- O- H" ?' m4 ]2 r- tresponsible for the early activation of the hypothal-* M' Z8 ^- k- k. T& Y' [( s
amic pituitary gonadal axis.1-3 Thus, greater empha-1 X7 G& ]2 ^/ a
sis has been given to neuroradiologic imaging in
' P; t' }% a: Z0 L* U6 v( Xboys with precocious puberty. In addition to viril-
9 N. J, x/ @6 F0 Z! {5 m/ Hization, the clinical hallmark of CPP is the symmet-
0 u; O* R0 M; [9 v) ?rical testicular growth secondary to stimulation by
. \- q; S: h+ P5 a5 zgonadotropins.1,3( y. r- W  P. C8 f5 X  }) c
Gonadotropin-independent peripheral preco-
, ?( R( [; \4 o$ _- {/ R& E7 v3 gcious puberty in boys also results from inappropriate
# l. W  A% |% Handrogenic stimulation from either endogenous or* `$ V8 T, w( y/ n% b' |
exogenous sources, nonpituitary gonadotropin stim-
" w& k$ f0 v, \ulation, and rare activating mutations.3 Virilizing6 ~; r! W; g7 O
congenital adrenal hyperplasia producing excessive# i  Q/ M: A8 i: a7 {2 H; L
adrenal androgens is a common cause of precocious# s" }) B7 n0 O; t* r& f1 ?
puberty in boys.3,4! k; N% A0 G; k9 `& X9 ~! R
The most common form of congenital adrenal
* c, z. y8 g! z% h. L$ @& xhyperplasia is the 21-hydroxylase enzyme deficiency.2 V- p- e: X6 n; q+ p
The 11-β hydroxylase deficiency may also result in( b$ ^' n5 N" Q: j
excessive adrenal androgen production, and rarely,
, O; `* a1 O2 L9 Z; |5 S( y9 b( M/ han adrenal tumor may also cause adrenal androgen
) U" ?$ l# }  {9 G+ H1 texcess.1,34 s- Q0 H: n8 Z( [8 ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 A. C+ v2 R$ [. M# V9 @/ {
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
  @, M1 o% y! G. n4 a. M" @A unique entity of male-limited gonadotropin-+ j4 T. D# k( o% ]( s; f
independent precocious puberty, which is also known( ]% F6 e  J4 `0 ?
as testotoxicosis, may cause precocious puberty at a" M" b' y' }$ h% [/ N: A2 \8 W
very young age. The physical findings in these boys
4 Q$ @( p5 j1 t" X# X" ~: nwith this disorder are full pubertal development,
# g& |0 ^6 D: n4 C$ W( Kincluding bilateral testicular growth, similar to boys* g( m4 I2 x5 C; ?
with CPP. The gonadotropin levels in this disorder
+ c" T: c: _4 ?9 j# w0 A/ t% P% Care suppressed to prepubertal levels and do not show
1 }3 S* r2 x( F+ f- vpubertal response of gonadotropin after gonadotropin-
2 `1 [* U* z' |1 p) breleasing hormone stimulation. This is a sex-linked
, d% f3 u" E# F, O3 R6 U- lautosomal dominant disorder that affects only/ P% ]$ p$ ?0 z
males; therefore, other male members of the family. }! P8 K& |6 S3 h* D
may have similar precocious puberty.3
; N  P; h; P4 o7 c% F# O: DIn our patient, physical examination was incon-
# x, h7 [" x7 ysistent with true precocious puberty since his testi-
  l1 t: o5 \! `; Ocles were prepubertal in size. However, testotoxicosis
* w8 F4 N5 `9 mwas in the differential diagnosis because his father
) C2 L$ c; b& C+ \started puberty somewhat early, and occasionally,
# I: K+ o+ y' E5 f1 g( E; Xtesticular enlargement is not that evident in the7 s9 T. v5 B+ c, X
beginning of this process.1 In the absence of a neg-
6 B5 N$ [$ f1 t. j! t$ g# v; t) Xative initial history of androgen exposure, our7 @  e$ u; s3 e* G% @  _
biggest concern was virilizing adrenal hyperplasia,. \9 ~9 F; c+ b  m8 N) V* Q
either 21-hydroxylase deficiency or 11-β hydroxylase
% ^* M* e9 e2 W2 X  tdeficiency. Those diagnoses were excluded by find-4 A% J; D8 I# R* J* [0 D4 `
ing the normal level of adrenal steroids.
7 J% N* L6 o0 B2 z  l2 ~" fThe diagnosis of exogenous androgens was strongly
2 c# e" d: {; w2 K* b  Tsuspected in a follow-up visit after 4 months because
& \; W  E/ J# H0 H: z0 H: Athe physical examination revealed the complete disap-
4 E: X9 |7 F& W+ d# N4 epearance of pubic hair, normal growth velocity, and
* g$ u7 v2 K# J$ [; ~decreased erections. The father admitted using a testos-
. c2 \6 a& M; ^  l( E) b( Zterone gel, which he concealed at first visit. He was- a) O' a# A! o1 b
using it rather frequently, twice a day. The Physicians’. _7 ^; |( L6 Z- m& o! [& v
Desk Reference, or package insert of this product, gel or
# _- u; i6 V1 T* v& t& S  Zcream, cautions about dermal testosterone transfer to
; D+ i6 k# @4 F6 o4 Gunprotected females through direct skin exposure.  j2 _' G, G4 ^+ |0 \0 B% }
Serum testosterone level was found to be 2 times the$ a6 ~, e5 n8 t* |0 M
baseline value in those females who were exposed to, b$ d  R- [: h+ Y5 n0 ?
even 15 minutes of direct skin contact with their male' g, C. N- x; c  E8 R. G
partners.6 However, when a shirt covered the applica-
) }7 D$ {  q0 `+ S( D# Z; I* `tion site, this testosterone transfer was prevented.9 M. q- B5 t" t4 p7 E
Our patient’s testosterone level was 60 ng/mL,
8 y. g4 J! s" g. Z/ twhich was clearly high. Some studies suggest that+ L4 _6 V) k6 n4 N
dermal conversion of testosterone to dihydrotestos-
  d' h. f/ B" u  J1 Q* e0 I5 Q3 Mterone, which is a more potent metabolite, is more/ q) l$ P3 q' q4 o% h
active in young children exposed to testosterone0 A0 M. ^$ x. j3 v3 g' R. m  v
exogenously7; however, we did not measure a dihy-: |4 o! W2 A; s4 g$ j
drotestosterone level in our patient. In addition to) \! |! h& S8 M* ^) G
virilization, exposure to exogenous testosterone in
/ u$ }9 ]9 r4 Q1 L( uchildren results in an increase in growth velocity and, }" \3 r, ]8 R
advanced bone age, as seen in our patient.
1 T" }+ y5 S/ P4 g4 UThe long-term effect of androgen exposure during
: _% Z! Q% Y1 Searly childhood on pubertal development and final
+ X9 \! Z% X* `) P1 ]adult height are not fully known and always remain
0 p  t3 P2 K- W* t3 T0 b+ ba concern. Children treated with short-term testos-
; T; B0 ~) ~8 ]3 W3 |terone injection or topical androgen may exhibit some+ b9 B% |: ^3 B/ H" v: F
acceleration of the skeletal maturation; however, after
7 ^6 g6 N, {5 ^1 ocessation of treatment, the rate of bone maturation
( @* c' @$ j6 Zdecelerates and gradually returns to normal.8,9* U! t% Y. n( I( c& a3 |; u
There are conflicting reports and controversy
8 r5 m/ s& A! k- L% u- S8 cover the effect of early androgen exposure on adult0 G& p3 q8 F. e& |- C7 ^, l
penile length.10,11 Some reports suggest subnormal
' }6 q( I# L+ W( |' Z: P) qadult penile length, apparently because of downreg-
8 v$ s8 c0 P! D3 e; nulation of androgen receptor number.10,12 However,9 z0 M" G* L% y
Sutherland et al13 did not find a correlation between, B; X0 F5 w7 X2 I' H
childhood testosterone exposure and reduced adult: N$ U: ~- |3 I. k
penile length in clinical studies.
; R) V! r/ k2 m: F; TNonetheless, we do not believe our patient is+ j5 m- W# L9 d! }* q
going to experience any of the untoward effects from0 t' T8 J# y+ \0 G
testosterone exposure as mentioned earlier because
: w' i3 u# N1 j# v6 _, G; jthe exposure was not for a prolonged period of time.5 ?0 ~/ S& i6 C5 v) M! G9 f
Although the bone age was advanced at the time of$ C, G) a' d0 \8 a
diagnosis, the child had a normal growth velocity at
( X$ r- J, A+ ], ]6 u0 Ithe follow-up visit. It is hoped that his final adult
* |1 j3 r5 g5 ^height will not be affected.  ?" H1 P# k8 p. A% A
Although rarely reported, the widespread avail-
: k& Y6 b  J& t/ wability of androgen products in our society may. S  q2 q+ q: m- j
indeed cause more virilization in male or female$ C' \2 q7 c! ~5 _. g
children than one would realize. Exposure to andro-
2 V/ n; `  U! lgen products must be considered and specific ques-6 R3 }6 _$ V/ N; m1 N' J
tioning about the use of a testosterone product or' d. `9 n  k$ A7 v* w( {
gel should be asked of the family members during
+ g$ ]7 m! [( b4 U7 z4 }the evaluation of any children who present with vir-
; i: a- S4 k% ]& M/ W, \ilization or peripheral precocious puberty. The diag-
1 E9 r8 M& H/ U. ynosis can be established by just a few tests and by8 t( `! n6 q+ \( g) x/ E
appropriate history. The inability to obtain such a% s- M3 F% }% |5 y) I. F# }7 X
history, or failure to ask the specific questions, may
6 j4 x! O8 E: D! r5 ]* zresult in extensive, unnecessary, and expensive
1 \# @* z' N: t+ @, o( Zinvestigation. The primary care physician should be9 s, y! c4 {, P9 [3 x
aware of this fact, because most of these children
( e. h$ P' y9 V# xmay initially present in their practice. The Physicians’6 `! ^  b  e5 F& t) f8 L1 |+ w2 f4 ^
Desk Reference and package insert should also put a* S2 C2 r7 {# V& L7 ]+ Z3 t
warning about the virilizing effect on a male or
' G; n; E* M3 G+ J: Nfemale child who might come in contact with some-
; s# h, ]+ Z  p/ Eone using any of these products.) ?# x& \2 j  I, H4 m3 q6 l
References' _  {9 e: @' I7 p% _6 \# V
1. Styne DM. The testes: disorder of sexual differentiation
: Z$ t, e% k  b" i# n+ |1 D+ Dand puberty in the male. In: Sperling MA, ed. Pediatric, V1 p3 ?# W, T$ `& V  n
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 G" [# v* b, G# j6 B$ }- N2002: 565-628.' s9 B2 @. t- {/ G' f+ ]9 B
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 o4 @1 k# @. c+ h, ?& k  D/ C
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
# }: b5 {7 h! q; [
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