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Sexual Precocity in a 16-Month-Old
( Z* d9 n9 ]2 F. g6 ~Boy Induced by Indirect Topical. K" l! _: ?  o. n8 @. Y
Exposure to Testosterone
) @( ]6 d1 M2 o6 r0 rSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2# x3 m! ~, w9 K1 q
and Kenneth R. Rettig, MD15 F2 ^5 k: ?; u% Y
Clinical Pediatrics$ l5 m/ X8 N, y0 d$ e: Q0 x# u
Volume 46 Number 6
3 Q6 U& H" k  @$ O3 C6 X( e; |July 2007 540-543
' b# C4 L# _0 D: q4 `© 2007 Sage Publications
; y$ Y& z' [8 L6 W+ R8 C8 n- Y5 R10.1177/0009922806296651- l% y7 u  |6 D$ X4 C4 m9 \6 J
http://clp.sagepub.com
+ x: L( s0 Y4 w) o4 \$ w/ ahosted at7 }1 u, W$ H8 W
http://online.sagepub.com
7 d7 i& m  ~3 O3 u3 LPrecocious puberty in boys, central or peripheral,
  V& @0 \& x3 }( ?9 V8 Nis a significant concern for physicians. Central) V7 q, O* c1 z( W
precocious puberty (CPP), which is mediated
, d9 ?* n7 S6 A% I: d) mthrough the hypothalamic pituitary gonadal axis, has
- h* K+ J) q) ~5 I# R, Oa higher incidence of organic central nervous system# @; Z* v8 }: b0 ~$ L
lesions in boys.1,2 Virilization in boys, as manifested
  ~  o+ \% q' A& Sby enlargement of the penis, development of pubic
, A8 x1 a( S3 N) i* Q: j# x* rhair, and facial acne without enlargement of testi-
% {2 x5 ~0 y: U6 dcles, suggests peripheral or pseudopuberty.1-3 We
9 I, h8 x# \& s( Greport a 16-month-old boy who presented with the
! m% v; _0 x: {0 I; K4 venlargement of the phallus and pubic hair develop-
8 \! A0 y8 B9 s1 hment without testicular enlargement, which was due
3 C* d+ R6 z7 D- S0 w) A3 Hto the unintentional exposure to androgen gel used by
( t2 N( }+ l; u0 V4 l1 L4 a1 {the father. The family initially concealed this infor-
. X5 ]& e6 W# F0 |8 N# E6 g) Emation, resulting in an extensive work-up for this0 h& d3 x2 i0 r* |+ F' T
child. Given the widespread and easy availability of
" T( W) T, o  ~; wtestosterone gel and cream, we believe this is proba-
) J( i: u3 N& l3 R! Y. K" T( _5 Zbly more common than the rare case report in the! N+ f; O% l/ \: c+ H
literature.4
9 F. [+ }+ b0 Z* D8 O* \9 J+ FPatient Report
) W! P, k. c3 C; e4 qA 16-month-old white child was referred to the
7 _  U" I' @" ]* z3 aendocrine clinic by his pediatrician with the concern
) @3 J" K* z9 i0 Z  }of early sexual development. His mother noticed6 ]6 D6 S, q. c) G- U- ^5 X
light colored pubic hair development when he was9 R7 ^- |0 n8 f  V$ ^- L# y
From the 1Division of Pediatric Endocrinology, 2University of
4 k7 p( B! g4 a, v2 F- ^2 C+ TSouth Alabama Medical Center, Mobile, Alabama.
% n$ W+ Z1 W3 \/ I) WAddress correspondence to: Samar K. Bhowmick, MD, FACE,
7 D5 T7 j) ]! EProfessor of Pediatrics, University of South Alabama, College of
5 j  D3 R0 x6 l. zMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ J; n/ W, d- k9 Q% P2 {e-mail: [email protected].
& D' m- w% {% _! H6 g2 ]0 a! L% Z7 Vabout 6 to 7 months old, which progressively became: h" I; ^' B* Y4 o. h6 Q
darker. She was also concerned about the enlarge-
$ O4 X/ W4 k- Z" Y. b5 ument of his penis and frequent erections. The child% B$ b" l0 i4 g7 d
was the product of a full-term normal delivery, with1 J6 V# N+ ?$ k3 [, t8 u/ x: z
a birth weight of 7 lb 14 oz, and birth length of
7 ]# B5 _$ C3 `2 n8 d) x20 inches. He was breast-fed throughout the first year
7 ~8 u  a, s, @6 _" A6 U5 s& H3 k/ Vof life and was still receiving breast milk along with" E" R- L  G0 o9 r/ n
solid food. He had no hospitalizations or surgery,1 v& O) i1 `/ K+ D' S
and his psychosocial and psychomotor development  h6 u3 A4 z, F
was age appropriate.
( c- J  e: I. Y7 R' \The family history was remarkable for the father,$ d% J. n  k# E
who was diagnosed with hypothyroidism at age 16,
4 u4 [# q. _) n! n: D6 Cwhich was treated with thyroxine. The father’s
, Z: I3 V6 `5 W4 j% r# l' Xheight was 6 feet, and he went through a somewhat+ U$ q5 `2 I6 Z: C
early puberty and had stopped growing by age 14.- Z0 ?( V, T2 W1 U( k# _: u0 o8 T
The father denied taking any other medication. The
  m3 W2 g8 v, e9 F" vchild’s mother was in good health. Her menarche+ y/ U) v5 t/ h  a& s0 ?; t
was at 11 years of age, and her height was at 5 feet
+ f; ?2 o1 a* ]) o% p& L5 inches. There was no other family history of pre-$ \# O7 w; Y9 G2 Z
cocious sexual development in the first-degree rela-
6 B7 p9 n3 J( Ktives. There were no siblings.- ^7 w$ `* V# l2 K
Physical Examination
; I0 F+ n' _- P5 V, ~$ I" `The physical examination revealed a very active,
& [: r% Y$ g, A# i. Z; M& i$ E; dplayful, and healthy boy. The vital signs documented' a& [" J! X+ X6 i  w; [
a blood pressure of 85/50 mm Hg, his length was
) v5 Z% ~  A7 \5 s$ a90 cm (>97th percentile), and his weight was 14.4 kg: c1 f8 J& E/ y' G8 }
(also >97th percentile). The observed yearly growth
  _& {* w5 H5 F6 e3 w( u% Y, _' bvelocity was 30 cm (12 inches). The examination of
$ ]( _4 t) L) ?: ythe neck revealed no thyroid enlargement.
; C9 V. S) ^5 N  \4 s% J0 A- bThe genitourinary examination was remarkable for3 @% v) Y0 x: y* d) z
enlargement of the penis, with a stretched length of
8 {" L$ }7 d" j, z$ ^) P: S1 t2 g8 cm and a width of 2 cm. The glans penis was very well
& i- L/ \; l: o- C( ydeveloped. The pubic hair was Tanner II, mostly around; c# o# j, C4 \
540
4 G* C' B% X0 P" D  I, oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- b/ K. x4 j4 D
the base of the phallus and was dark and curled. The
6 _- e# |# f( z  J) R# o. Atesticular volume was prepubertal at 2 mL each.
1 y5 H6 J* ]# K) n0 F( vThe skin was moist and smooth and somewhat
/ s# U& H( Y% y/ L' m( Y/ D( y2 uoily. No axillary hair was noted. There were no
6 `8 s* {  H. X* y: r1 ]abnormal skin pigmentations or café-au-lait spots.
+ N" u* _8 p5 N3 w0 y( rNeurologic evaluation showed deep tendon reflex 2+' W& H! M1 i2 T: w8 d
bilateral and symmetrical. There was no suggestion# A$ l2 e9 L8 _0 h; I
of papilledema.
# z( e3 k+ Y( z. K& n+ B4 }7 QLaboratory Evaluation
- e4 w, {9 K  y% [8 G3 \The bone age was consistent with 28 months by
) h( K% D2 b/ [) e1 k5 k% ], Nusing the standard of Greulich and Pyle at a chrono-% B* T+ Z" Y# q8 R' X1 m6 U$ ]) c
logic age of 16 months (advanced).5 Chromosomal
. P& J" M* e; V7 j5 }, k* J& T" ukaryotype was 46XY. The thyroid function test
' O5 [2 ?" ~+ d+ u/ l& k& B( fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-7 P5 [8 G  w- e2 k" I. b
lating hormone level was 1.3 µIU/mL (both normal).
4 w' L4 p' l* d$ V) u$ BThe concentrations of serum electrolytes, blood, I% |) W6 |( v5 X- y" x
urea nitrogen, creatinine, and calcium all were
! _8 ~( j9 {4 Mwithin normal range for his age. The concentration& E# A0 X4 L4 u5 E9 k/ k% f7 T
of serum 17-hydroxyprogesterone was 16 ng/dL( j& V0 G8 O' ^$ ]( c
(normal, 3 to 90 ng/dL), androstenedione was 20
" [9 R- |( Q: t! a+ @ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 Z$ x* j/ ~4 Z; [$ p, Aterone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 S& f9 m$ b+ Wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to' {3 r, u( Z, }# L
49ng/dL), 11-desoxycortisol (specific compound S)
. g- s5 g/ y% ~was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ w5 v, q. Z9 i8 D6 R$ M
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) B9 }, O& @! ^
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 {% W% o5 q& l0 |; u! z6 N
and β-human chorionic gonadotropin was less than
- Z1 ^7 o2 B  s( P9 A# w6 U6 B5 mIU/mL (normal <5 mIU/mL). Serum follicular
. S+ i2 O; J1 a+ ]. ustimulating hormone and leuteinizing hormone
* m9 D9 Q  t& C/ d: Zconcentrations were less than 0.05 mIU/mL( T5 W2 ~) {* z. H! ]
(prepubertal).' G  ~: m  M' I! p: u" i9 _- ]
The parents were notified about the laboratory
2 N$ x! \6 v4 J( presults and were informed that all of the tests were3 {. m  c1 y3 c
normal except the testosterone level was high. The
* v! a+ O  E/ E1 W6 xfollow-up visit was arranged within a few weeks to
5 t1 q( x3 }, n7 o- pobtain testicular and abdominal sonograms; how-
: }& H, Y7 [* H9 vever, the family did not return for 4 months.5 J2 s: J9 C! {
Physical examination at this time revealed that the( u% c. z# U1 u2 o/ c: E0 Q
child had grown 2.5 cm in 4 months and had gained
  r% `6 `1 i4 J' k2 kg of weight. Physical examination remained% P' D! ]4 V! D* F# J
unchanged. Surprisingly, the pubic hair almost com-$ b+ H% z8 B  I) y+ y" H2 e
pletely disappeared except for a few vellous hairs at
. C8 f3 K( w7 t! Pthe base of the phallus. Testicular volume was still 2* `3 g& e# I, g% Y8 @. y, I
mL, and the size of the penis remained unchanged." N0 R7 z* c. Y
The mother also said that the boy was no longer hav-/ R8 q, M" C  G& T
ing frequent erections.( v% m2 v( N% L5 p% B' ]
Both parents were again questioned about use of
8 x8 V6 z% h& @, s( `8 vany ointment/creams that they may have applied to
  s  U4 T% V$ j& l4 \the child’s skin. This time the father admitted the: V5 T) l. E" t
Topical Testosterone Exposure / Bhowmick et al 5410 |5 y6 V3 m( k8 R) L; \7 O" P# L
use of testosterone gel twice daily that he was apply-
9 n5 Y6 T3 |& H3 king over his own shoulders, chest, and back area for
* t! |( {  L% z) [) Z$ sa year. The father also revealed he was embarrassed
( H, {/ J0 t6 }+ X6 S! m: p/ nto disclose that he was using a testosterone gel pre-# e+ r9 v" j0 f- b6 t) D3 t  q/ t
scribed by his family physician for decreased libido
) y$ \5 r; O$ csecondary to depression.
$ H& D8 U$ B6 _# }' zThe child slept in the same bed with parents.
( f) I, T- f' g$ K5 jThe father would hug the baby and hold him on his$ P) W. C; q3 s: K" J  q
chest for a considerable period of time, causing sig-
+ C8 u5 ], \6 R2 d; H2 \0 E) S) }nificant bare skin contact between baby and father.
& `: D+ x: v% S0 Q& bThe father also admitted that after the phone call,
7 \2 @4 H& F# p! a- hwhen he learned the testosterone level in the baby" V  Y6 M0 J* Y0 d  [. ]
was high, he then read the product information
0 _0 a' W4 |0 F/ ^packet and concluded that it was most likely the rea-
, K& `: @" j  M1 W$ _' oson for the child’s virilization. At that time, they# m. O7 l) j$ S9 N6 D+ l& ~1 |2 `$ _
decided to put the baby in a separate bed, and the3 q5 ?8 X& o7 v, n) l8 G
father was not hugging him with bare skin and had$ J; K3 C6 S( p4 K, r3 C0 f
been using protective clothing. A repeat testosterone
9 T7 B- ^1 F+ ]# h& D( @test was ordered, but the family did not go to the
! I9 @& |9 m- V8 ]laboratory to obtain the test.5 G$ \) O8 Q1 R0 p. |
Discussion
% Q7 M" @& j0 i. k/ S" s% w! `( j( HPrecocious puberty in boys is defined as secondary7 v) X' d! o: j2 B& x4 f2 [
sexual development before 9 years of age.1,4
1 _$ g/ @! v( W' G3 dPrecocious puberty is termed as central (true) when0 A. p4 E3 `* w
it is caused by the premature activation of hypo-
# s( V; J5 Z1 u0 C8 ]thalamic pituitary gonadal axis. CPP is more com-4 T  z( X4 U3 C; d+ R
mon in girls than in boys.1,3 Most boys with CPP$ c, m) I9 ]1 h, L
may have a central nervous system lesion that is  t' u" d( v8 m8 U# G2 S1 v  r
responsible for the early activation of the hypothal-/ T# @1 b! q) k* |
amic pituitary gonadal axis.1-3 Thus, greater empha-6 e% B9 E7 q$ p( L9 S( q
sis has been given to neuroradiologic imaging in
4 @) O; j8 L! D$ fboys with precocious puberty. In addition to viril-3 C3 c6 L* D$ n5 N* {0 S
ization, the clinical hallmark of CPP is the symmet-
7 ]4 \& o% K  K% `8 H. ?rical testicular growth secondary to stimulation by
6 ^/ y  R7 H/ g5 |gonadotropins.1,3+ m7 W+ x3 F6 G5 b% i" e1 X
Gonadotropin-independent peripheral preco-; E7 X* b, J9 b3 i0 M3 Q4 s
cious puberty in boys also results from inappropriate# ~6 v: B9 j6 h' Z; s" g. m/ D
androgenic stimulation from either endogenous or' ~  o! x7 M. l6 G4 O1 k
exogenous sources, nonpituitary gonadotropin stim-
: ~1 a  s* K  _ulation, and rare activating mutations.3 Virilizing' p7 Y0 w: j1 g. X9 R! Q
congenital adrenal hyperplasia producing excessive
) T0 [& L. d$ N, \: Sadrenal androgens is a common cause of precocious
9 F7 s$ C! j: @$ X" R2 A( tpuberty in boys.3,4& R: z0 E% k( O) h3 O
The most common form of congenital adrenal) a7 q4 G/ n& m- d7 H9 ~& |9 H
hyperplasia is the 21-hydroxylase enzyme deficiency.
& @) ?. {' O. a) j* JThe 11-β hydroxylase deficiency may also result in& W& J+ v& Y: g* x
excessive adrenal androgen production, and rarely,7 ~" H; b7 S/ q+ g! H) x1 |
an adrenal tumor may also cause adrenal androgen  A' d* Y* q& g7 G5 u6 U+ ~
excess.1,36 `9 n1 {! M7 w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# E5 U1 V# ^: V0 i; G- d0 E1 A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ ?9 O/ X5 L2 A7 K- g* G  b
A unique entity of male-limited gonadotropin-
) S* G" g( J. C" C; Eindependent precocious puberty, which is also known" P7 U: C+ _$ @/ _# C2 T. K
as testotoxicosis, may cause precocious puberty at a  }# v/ Z, P) P4 q
very young age. The physical findings in these boys
6 N/ A1 U0 y4 ]2 @. D3 ~with this disorder are full pubertal development,
, h6 w) n5 C8 m- x3 E; hincluding bilateral testicular growth, similar to boys
0 ~3 i7 [) @9 ?3 nwith CPP. The gonadotropin levels in this disorder( ~# Y" j8 `/ M+ `( B
are suppressed to prepubertal levels and do not show7 D1 G# D$ \& G6 c! L* A/ W  P  I
pubertal response of gonadotropin after gonadotropin-
" X, J+ ?+ B0 F4 F3 F+ ereleasing hormone stimulation. This is a sex-linked
2 z% u. ^' R. _2 V) _4 u, S" E' b( |autosomal dominant disorder that affects only
) \4 g) T, g. ]: k8 q) Hmales; therefore, other male members of the family# Z: u: Z+ Y7 \; D. {: L
may have similar precocious puberty.3! C# Y, Y% c  [, ^9 l
In our patient, physical examination was incon-% l+ K+ ?" l2 K5 ?  \. e9 c
sistent with true precocious puberty since his testi-
) z$ t1 {+ G2 G% ncles were prepubertal in size. However, testotoxicosis/ n8 O; l0 B0 G% A4 |4 ?, a
was in the differential diagnosis because his father" G9 @$ _; Z  o, z) w. x, |
started puberty somewhat early, and occasionally,
0 q) E2 s  ]4 _7 Etesticular enlargement is not that evident in the
9 Q: l6 B' V% ^. P. Kbeginning of this process.1 In the absence of a neg-
4 C* ]6 `+ o1 ~; n+ o# l( z) g) wative initial history of androgen exposure, our4 O0 ]* X  a6 a+ j5 {
biggest concern was virilizing adrenal hyperplasia,+ b8 u" E8 X& B( l
either 21-hydroxylase deficiency or 11-β hydroxylase
  n8 G2 [: n6 l; O2 {deficiency. Those diagnoses were excluded by find-
8 s" t2 ?# ^8 I  U6 I' Q4 Uing the normal level of adrenal steroids.
- n- c/ z; e( }The diagnosis of exogenous androgens was strongly/ R2 ^5 w5 S6 D+ w0 H: J' N
suspected in a follow-up visit after 4 months because
' m( M% t# R6 B9 s8 ^the physical examination revealed the complete disap-
& H- s" Q: D- M: Y- U3 [, N- @pearance of pubic hair, normal growth velocity, and
( E3 Z" P2 o! D1 z2 `9 _+ k- z5 udecreased erections. The father admitted using a testos-1 s* N) y6 P, a* h" W
terone gel, which he concealed at first visit. He was
# D8 I2 w: d, {) _  i9 e  Yusing it rather frequently, twice a day. The Physicians’( C, i* _* X2 K& M
Desk Reference, or package insert of this product, gel or9 S5 `- p1 m4 Y
cream, cautions about dermal testosterone transfer to' b. o- Y, h) o1 F, A1 P
unprotected females through direct skin exposure.
8 e) r4 U1 J" r1 j2 N8 [Serum testosterone level was found to be 2 times the! ]9 l" i! @% u" b3 E1 j- O0 C
baseline value in those females who were exposed to
" R0 R% j9 i) l+ L5 W  `% v/ Teven 15 minutes of direct skin contact with their male
2 E5 ^& b; J  cpartners.6 However, when a shirt covered the applica-% \% M; B" ^: A; g" f
tion site, this testosterone transfer was prevented.  A7 y# C  G1 z: l
Our patient’s testosterone level was 60 ng/mL,
# Q3 P/ ~9 K) C5 T* e5 V& _/ ?which was clearly high. Some studies suggest that
3 n$ P4 Y: t9 h( o9 {6 g9 idermal conversion of testosterone to dihydrotestos-
4 ~+ R% M1 Y$ D4 o8 w6 T% \terone, which is a more potent metabolite, is more: G8 o  b8 z8 T+ z+ ~; C
active in young children exposed to testosterone
, @! ?' f) ]. z* ~exogenously7; however, we did not measure a dihy-5 a1 w! ]( C3 A/ T' E4 k) E
drotestosterone level in our patient. In addition to
* s, u' y' i+ u5 J' Q; U5 Nvirilization, exposure to exogenous testosterone in+ T. H/ o# i& I( a1 m
children results in an increase in growth velocity and2 e/ X1 \. @( B2 \3 T. N
advanced bone age, as seen in our patient.! s9 I' e/ ~" _) f
The long-term effect of androgen exposure during+ k6 `1 _. u3 ?
early childhood on pubertal development and final: \4 s( Z  P9 c6 f; {+ Z8 C
adult height are not fully known and always remain+ H& H! U) C2 z% D, m( D3 u
a concern. Children treated with short-term testos-- l. f! T" c2 B- ~% b
terone injection or topical androgen may exhibit some
; G/ k: [6 L3 ?" A/ O# Xacceleration of the skeletal maturation; however, after
  ~3 c% ]4 }" {4 Q" s) ecessation of treatment, the rate of bone maturation
  T) y8 n! p: y: @decelerates and gradually returns to normal.8,9! g/ S# |" `9 K5 D
There are conflicting reports and controversy
3 x, N% Q, y5 ]3 I6 M1 ]" Sover the effect of early androgen exposure on adult
4 V. n) s+ z  ipenile length.10,11 Some reports suggest subnormal
7 |3 P& R+ M) x5 A8 Vadult penile length, apparently because of downreg-+ J! P. l, d5 ]3 |
ulation of androgen receptor number.10,12 However,# T. W. J) U8 g
Sutherland et al13 did not find a correlation between
( Y" v2 }  ]6 ?" z  d8 f1 jchildhood testosterone exposure and reduced adult+ K- b2 B1 @9 {/ ^
penile length in clinical studies.' [* I! o4 |% m# S+ u) b
Nonetheless, we do not believe our patient is
3 a  X6 d. R$ n% z& k5 Ogoing to experience any of the untoward effects from# x- N5 z, f. D, c
testosterone exposure as mentioned earlier because+ C0 ]! v1 Q* H) p6 P$ _) I: Z$ l
the exposure was not for a prolonged period of time.. C' r# w3 a4 r( r8 }* i
Although the bone age was advanced at the time of
' z* P2 M$ d4 h/ z+ L3 Vdiagnosis, the child had a normal growth velocity at0 |" K+ H: h' b) o9 r9 k
the follow-up visit. It is hoped that his final adult
1 U) y' J( _; e/ r% i* ?2 D/ F# P1 hheight will not be affected.
: S8 N" F' g9 J/ |Although rarely reported, the widespread avail-: C' Y3 _; x* L' }6 _( U$ E
ability of androgen products in our society may/ F& _2 Y. I: e# W! o, a. y1 D
indeed cause more virilization in male or female
  g, V0 M! F( zchildren than one would realize. Exposure to andro-4 P, c6 U9 V4 B$ |' K, L
gen products must be considered and specific ques-
/ {" u8 g! Z" s9 |3 @" m" z  ftioning about the use of a testosterone product or
* ^4 }' ]- v" M, Vgel should be asked of the family members during0 M4 z% j8 k- h* \: V
the evaluation of any children who present with vir-9 x; n8 v9 q  \: q$ c! M, O  o9 q7 ^
ilization or peripheral precocious puberty. The diag-5 Z. ?) o9 X8 p. L
nosis can be established by just a few tests and by
9 [$ w$ T& s$ v* eappropriate history. The inability to obtain such a
# z4 U! B' m" H6 Whistory, or failure to ask the specific questions, may* ^: C: |6 |1 W! b% _' `! q
result in extensive, unnecessary, and expensive, w( D4 G) s3 r9 s; @5 v) Q. r
investigation. The primary care physician should be
+ O- J  R% M9 {- W. I; M+ V) saware of this fact, because most of these children
( s$ c. k' t3 L& @& f: Ymay initially present in their practice. The Physicians’
. I( ~+ ^# Q- YDesk Reference and package insert should also put a
  m" m, m4 r, u4 x9 m, g( n+ E1 hwarning about the virilizing effect on a male or
4 F4 x3 b- C0 Y1 g9 a) gfemale child who might come in contact with some-
- U6 d0 e- f. B" ]+ c" G1 l, d; Fone using any of these products.
7 z9 Y0 w2 u+ C& c- a/ [References0 m: }# F2 W% F5 S* J% ~4 R8 j
1. Styne DM. The testes: disorder of sexual differentiation2 p3 y8 \+ G) D3 {
and puberty in the male. In: Sperling MA, ed. Pediatric4 D( q7 W+ b8 Z1 W) n$ N+ C( G8 ^
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& Z: H* N  ?/ U4 a' w2002: 565-628.( f. {  W; Q2 R% ?
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. C" s# g5 _$ z' {0 `# K% ?
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old. e7 }+ f# _6 r7 V$ X# u) D
Boy Induced by Indirect Topical4 g( l# F( E" G0 ~
Exposure to Testosterone, x. ^  g0 j5 E0 A: |
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 |/ \# V& Y" q4 A6 `1 Q. C( `, z3 n
and Kenneth R. Rettig, MD1& ]) `) N. `  k3 N& S! b' |
Clinical Pediatrics5 h6 d& a+ Q. ~: j
Volume 46 Number 6
  m- C! V9 G! n* jJuly 2007 540-5436 n7 J4 E% m7 N3 h# [4 _# I# M: C
© 2007 Sage Publications
5 v% T9 f3 B$ }2 k$ N3 H/ l10.1177/0009922806296651* r0 |4 u. X4 r1 c" J- \" \' c
http://clp.sagepub.com
/ Y5 l5 X# p6 S3 q$ Y- Ihosted at
! U1 h7 X2 e: X' c. y( Rhttp://online.sagepub.com9 r8 B- J1 c; ]2 ^5 b
Precocious puberty in boys, central or peripheral,, ^# y/ c9 C" {  C/ Z* j
is a significant concern for physicians. Central9 X% }+ G3 J( i/ }: y7 u0 j5 f
precocious puberty (CPP), which is mediated2 B. r4 {1 g% ]: |6 a" k+ @
through the hypothalamic pituitary gonadal axis, has. t3 g9 b1 P, K3 T
a higher incidence of organic central nervous system' L/ j8 {) z, q2 n6 S
lesions in boys.1,2 Virilization in boys, as manifested
( l0 C- x! L; v* Q5 j$ [1 A. Oby enlargement of the penis, development of pubic
: g  E  o1 Y) Zhair, and facial acne without enlargement of testi-
- [8 G1 Q( F* P5 O$ ?  Jcles, suggests peripheral or pseudopuberty.1-3 We
- e. u5 H; U  N5 r- Rreport a 16-month-old boy who presented with the+ S* X  N- ]( X. N: r, I- b6 N* y
enlargement of the phallus and pubic hair develop-
6 }! c- [- Z$ ^9 Vment without testicular enlargement, which was due
% Y; ?2 F- E; @to the unintentional exposure to androgen gel used by
8 `2 I+ M, s! X0 w& m) W- j6 q8 Qthe father. The family initially concealed this infor-$ \+ H; {2 ?8 d- N' a
mation, resulting in an extensive work-up for this
% Q! F& Y6 Y$ k6 I/ y& a6 h; d' ^child. Given the widespread and easy availability of6 h3 \+ ~" O) V8 V# I0 N
testosterone gel and cream, we believe this is proba-0 @# X  q; J0 \& I( H2 O
bly more common than the rare case report in the
3 {# z9 J7 m# S* a4 z; M! gliterature.48 C! ]6 H" A$ E  \% a: B- {  U/ {+ ^
Patient Report
" u6 h9 ~1 z: G5 WA 16-month-old white child was referred to the5 F0 z! R+ J# J8 l6 n& M& h6 ]# v+ q
endocrine clinic by his pediatrician with the concern% i; `4 r7 }: y: X3 j& c
of early sexual development. His mother noticed' A: @. ]3 S/ }: O: ]
light colored pubic hair development when he was
6 @3 V  P8 f: N* CFrom the 1Division of Pediatric Endocrinology, 2University of5 ?& d; E2 n9 g
South Alabama Medical Center, Mobile, Alabama.3 ^; c* r8 k4 Y
Address correspondence to: Samar K. Bhowmick, MD, FACE,& r: e: G2 P' _4 E. P
Professor of Pediatrics, University of South Alabama, College of$ i& b( c! u7 U  E% C
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 l+ l/ O3 ?8 v5 \6 }! j( G% [
e-mail: [email protected].4 Z3 _* \& ?7 G/ B
about 6 to 7 months old, which progressively became' R% }# g) w! m) n) Z* Q
darker. She was also concerned about the enlarge-* W( ?- v* V, P9 G' Y
ment of his penis and frequent erections. The child/ g7 j* o+ t( C: A6 D' f! G
was the product of a full-term normal delivery, with7 p6 y$ x# I* R8 M& H& O  _
a birth weight of 7 lb 14 oz, and birth length of' c; B* g7 A7 Q3 V& i( J6 g
20 inches. He was breast-fed throughout the first year9 R7 \, Z& G' r$ [# }
of life and was still receiving breast milk along with
. r7 z: a  D- p8 j: Fsolid food. He had no hospitalizations or surgery,
; W" y8 y3 B3 C2 R2 gand his psychosocial and psychomotor development" K& Q+ `  z1 P9 Z( [
was age appropriate." V* ^+ l+ u5 ?& A3 l) f4 w
The family history was remarkable for the father,, I) v5 R) Z: |* t' _! t$ Z4 u
who was diagnosed with hypothyroidism at age 16,
5 H1 q9 E: x) x* T2 A9 Q& j& [& q, Nwhich was treated with thyroxine. The father’s
! B% S) X4 r1 l" k- }' _height was 6 feet, and he went through a somewhat  r4 C7 @/ _; l
early puberty and had stopped growing by age 14.
3 L$ \/ G% u  C4 h+ k- ^The father denied taking any other medication. The" p0 K/ B: g( i, w* y
child’s mother was in good health. Her menarche2 ]8 \* _9 e! F4 m% N0 n. d7 M
was at 11 years of age, and her height was at 5 feet
. Z) p7 O( [2 ~: v, a5 inches. There was no other family history of pre-
( `# X! n# l. N# ccocious sexual development in the first-degree rela-9 Y4 w( t/ ^/ A1 `8 l5 Z
tives. There were no siblings.+ A( D* g, C6 h: e$ Z' H/ d
Physical Examination6 Y* e; \+ s" i2 v2 A/ O" o
The physical examination revealed a very active,6 N5 T6 l8 _8 D2 j# _6 @
playful, and healthy boy. The vital signs documented" R( B+ R' i) I: Y, U% [1 f
a blood pressure of 85/50 mm Hg, his length was, o* Y$ Q( s( c
90 cm (>97th percentile), and his weight was 14.4 kg
) e% d8 W( E/ {; _(also >97th percentile). The observed yearly growth
8 D% i# R, B+ C' G2 Nvelocity was 30 cm (12 inches). The examination of+ [' ?3 z, s1 \6 T8 d$ z
the neck revealed no thyroid enlargement.2 C. o$ Y* f! U3 l- I2 H; g
The genitourinary examination was remarkable for
5 T. v1 l- X. l7 kenlargement of the penis, with a stretched length of
7 g0 M1 }2 {# s- W/ `2 v8 cm and a width of 2 cm. The glans penis was very well+ _! ~! V6 _2 O& C( g2 A+ C$ d
developed. The pubic hair was Tanner II, mostly around
2 Y. i( E# l# ^1 f+ ]540
- n+ v2 K0 A1 m( c0 ^/ y. tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ J, a7 |  _1 n1 t7 othe base of the phallus and was dark and curled. The. Q- s8 p/ ^5 s& b
testicular volume was prepubertal at 2 mL each.
8 h; r: v( Z: ?$ y" ZThe skin was moist and smooth and somewhat. _( g7 _, w" H/ d& f- F
oily. No axillary hair was noted. There were no
( d. A' x4 S% C2 N4 `! Mabnormal skin pigmentations or café-au-lait spots.
$ R1 S8 j6 c$ Z+ s; {: S( ZNeurologic evaluation showed deep tendon reflex 2+
, W! d* ]% q2 @( {# R& G/ Q" sbilateral and symmetrical. There was no suggestion
. v* s2 n. w  U4 j1 z, e) V; nof papilledema.6 k, V1 |+ n! w' c  s
Laboratory Evaluation
# o3 t6 G2 r, }; m2 s; P5 |4 cThe bone age was consistent with 28 months by
1 z8 y6 p; |5 l6 tusing the standard of Greulich and Pyle at a chrono-
3 M* F4 l" V: w" Y. Xlogic age of 16 months (advanced).5 Chromosomal  @: r$ {1 s" D4 T9 x
karyotype was 46XY. The thyroid function test) p$ b6 W7 B+ ^* Y) l8 q) t, Y; ]" {8 n
showed a free T4 of 1.69 ng/dL, and thyroid stimu-' n) ?) `% ~- A) z$ c( i
lating hormone level was 1.3 µIU/mL (both normal).
: j7 V! g" r) T- E. G0 u! I9 G" }/ NThe concentrations of serum electrolytes, blood& Q/ f$ w) b! @' s
urea nitrogen, creatinine, and calcium all were
4 B. A- z, v% H: X  \within normal range for his age. The concentration
2 e: Z( N) ^1 a# ?+ c" fof serum 17-hydroxyprogesterone was 16 ng/dL7 A' b% p$ R- P1 u( K' U
(normal, 3 to 90 ng/dL), androstenedione was 20
: L7 y; N, b  Z' O) eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-" h6 v/ X7 D& o8 U
terone was 38 ng/dL (normal, 50 to 760 ng/dL),/ p: f  p2 P9 _7 O# `& B
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
, A  P. s4 _3 w' U) H49ng/dL), 11-desoxycortisol (specific compound S)9 r( ?0 A! Q7 {! x
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# Y6 O: l7 v* g
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total  M) @6 }, R8 a+ c  b
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 F" j4 d& c) _9 h) \2 c% T
and β-human chorionic gonadotropin was less than7 z1 V) z4 J" A! I* g: c
5 mIU/mL (normal <5 mIU/mL). Serum follicular
" \5 g$ n5 }- s! U, ?2 Dstimulating hormone and leuteinizing hormone
+ B8 \! K: e2 \% W, Q8 oconcentrations were less than 0.05 mIU/mL
. Y5 [% v. s5 H4 X; p. ?(prepubertal).  u2 D1 e9 `; d
The parents were notified about the laboratory! D1 P& [# H, N/ L' }$ r, }6 y3 F
results and were informed that all of the tests were
: I' j  G" b- snormal except the testosterone level was high. The
8 @3 X& M3 Z9 rfollow-up visit was arranged within a few weeks to
& E+ B2 r: f6 A# g- d5 Pobtain testicular and abdominal sonograms; how-2 _+ d0 W6 W" K7 c1 U  R1 K
ever, the family did not return for 4 months.
, D& G9 i& }/ p& t4 F4 n. APhysical examination at this time revealed that the
7 |, b8 g4 P4 V3 u; Ichild had grown 2.5 cm in 4 months and had gained
. ]# ~9 }- X+ {0 a2 kg of weight. Physical examination remained1 p2 ^) L& z6 I- s3 h& D7 u
unchanged. Surprisingly, the pubic hair almost com-
. B0 o0 B3 S$ |+ G& g0 x9 zpletely disappeared except for a few vellous hairs at
" k8 w7 o5 d# \& Q# l$ K$ Athe base of the phallus. Testicular volume was still 29 m9 r! B  G' t* N
mL, and the size of the penis remained unchanged.
8 ]6 @% m" G7 PThe mother also said that the boy was no longer hav-
- D" f- y3 r# o9 ~ing frequent erections.
' F# U8 v6 C! Q; T; mBoth parents were again questioned about use of  ]! F8 d" ]! Q; p! j; [$ P) ]" p
any ointment/creams that they may have applied to
- m1 I7 _. J3 u7 c3 othe child’s skin. This time the father admitted the' x+ j7 v1 A2 L; \& w
Topical Testosterone Exposure / Bhowmick et al 5419 C" n) P- X/ e/ Z
use of testosterone gel twice daily that he was apply-
- N% \* {. W' H" R* Q  ding over his own shoulders, chest, and back area for
) _+ \9 _* `6 e1 t# \a year. The father also revealed he was embarrassed
3 z3 @$ z( K  |( `, Ato disclose that he was using a testosterone gel pre-
* }  \8 D5 j1 S/ }4 u7 {scribed by his family physician for decreased libido
3 G& h5 w& d' o( hsecondary to depression.: B4 S( X2 A2 w, x0 A
The child slept in the same bed with parents.
3 `7 Q+ P+ Q5 j; n2 e6 b, `/ Y4 mThe father would hug the baby and hold him on his
# u& z' q5 g/ Y  T8 Gchest for a considerable period of time, causing sig-2 i7 z. |. `. l  |' ?
nificant bare skin contact between baby and father.
, m7 E, _2 |6 U" c  M) WThe father also admitted that after the phone call,
/ ^" Z& [! A6 M3 e% qwhen he learned the testosterone level in the baby
# Y2 e; T0 b9 Q! S+ U9 T# Twas high, he then read the product information
# i' ^. K7 E5 c; V% Xpacket and concluded that it was most likely the rea-% h9 ~5 _3 N8 k( g) w- t
son for the child’s virilization. At that time, they5 O$ |2 S/ H% n) e% A7 z0 ^+ `
decided to put the baby in a separate bed, and the4 ]4 ?3 I1 N8 F0 V8 d1 }
father was not hugging him with bare skin and had; u% {$ S: ~4 z& \
been using protective clothing. A repeat testosterone' u+ R) Z. l% x7 ~: ]  A) X6 k
test was ordered, but the family did not go to the
* q4 ]: a* p8 K) V1 s# }laboratory to obtain the test.
! M3 i0 C, ^5 Y* xDiscussion
* v8 v4 [5 O4 w3 oPrecocious puberty in boys is defined as secondary- e; v" V; K( Q4 }8 b4 @/ i$ `3 G
sexual development before 9 years of age.1,4
, V+ X9 q' Y/ s! E* NPrecocious puberty is termed as central (true) when# J2 k9 v. t6 ~3 C0 n; B
it is caused by the premature activation of hypo-
4 ^( t$ `9 l/ Z. E( @0 Kthalamic pituitary gonadal axis. CPP is more com-
6 l! e6 g& [% |' ]mon in girls than in boys.1,3 Most boys with CPP7 \$ v6 e/ I! c9 e8 c
may have a central nervous system lesion that is* i" e" }7 N7 c6 Q3 J, A5 n
responsible for the early activation of the hypothal-
7 W0 @6 j: U* P; G: lamic pituitary gonadal axis.1-3 Thus, greater empha-
9 L$ j; x3 q( C2 zsis has been given to neuroradiologic imaging in( x, s: ?7 @" s+ P- F
boys with precocious puberty. In addition to viril-
- d& J& v" V* Y* E* k( ~- K2 |' uization, the clinical hallmark of CPP is the symmet-
/ \$ w1 D6 l4 g2 X3 Krical testicular growth secondary to stimulation by  @- ~% d3 T! f. ^& X
gonadotropins.1,3
9 V1 S7 P9 U/ o$ y2 C6 x7 o+ s( qGonadotropin-independent peripheral preco-$ t* B; P; D8 G! l$ G& W- [
cious puberty in boys also results from inappropriate
) W( G7 Y1 k( Wandrogenic stimulation from either endogenous or
0 B4 f$ m7 P+ b; U7 O. c0 h( F) T5 ^exogenous sources, nonpituitary gonadotropin stim-' A4 K! k( [& p/ C. l# O
ulation, and rare activating mutations.3 Virilizing: M5 J! c: p4 Y  q
congenital adrenal hyperplasia producing excessive" ^0 ]1 t+ s" c: S, s+ R6 E
adrenal androgens is a common cause of precocious7 p- _( z+ W- t# ^
puberty in boys.3,4
3 u# y- [  M0 b6 }: N8 P: S! KThe most common form of congenital adrenal
. U% u( w4 J- B: @- A( shyperplasia is the 21-hydroxylase enzyme deficiency.) P+ O! _, o% m
The 11-β hydroxylase deficiency may also result in
) G" ]6 z7 Z/ I0 V. p( R2 ^) y. eexcessive adrenal androgen production, and rarely,
# j8 o4 m/ ^$ J+ Z' `! gan adrenal tumor may also cause adrenal androgen
! Y9 ~7 r0 y( W( \: lexcess.1,3
7 t' a% X- e. }. Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' a# \$ J  Q4 P" c0 N8 {; z
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; s. z+ f7 t) G, S7 O7 D: ?A unique entity of male-limited gonadotropin-" [" M/ z& A6 {# F
independent precocious puberty, which is also known
# Y* ]; s! u2 o! Q7 sas testotoxicosis, may cause precocious puberty at a
, h1 r' p8 h' _+ k, zvery young age. The physical findings in these boys) `! O0 t2 g* B1 A
with this disorder are full pubertal development,
. V- g8 \& H) E& B0 Uincluding bilateral testicular growth, similar to boys
* ]7 N# |! x( ^; z! T/ C- xwith CPP. The gonadotropin levels in this disorder
+ ^" J  n0 {3 z2 z! V4 c  `are suppressed to prepubertal levels and do not show$ l" e1 M. Z) ], n2 a. r
pubertal response of gonadotropin after gonadotropin-
1 _4 O. l& q/ m: A9 }$ E* d, Breleasing hormone stimulation. This is a sex-linked/ B' ]) W$ Q! @% j! \% q& R
autosomal dominant disorder that affects only; s2 z1 `, I9 N
males; therefore, other male members of the family
- W" w2 U1 V' L; j9 omay have similar precocious puberty.3
' @: J8 f6 Y( ZIn our patient, physical examination was incon-
9 B9 D9 a8 ^6 T& V, hsistent with true precocious puberty since his testi-
4 h( e3 q- P% S6 }cles were prepubertal in size. However, testotoxicosis! Z- Z4 e& g; ^
was in the differential diagnosis because his father8 Z5 _/ p' B1 A& o
started puberty somewhat early, and occasionally,
/ W+ a( D7 E; z& S- P# Jtesticular enlargement is not that evident in the
: g( h! Q, v+ ^  R1 }beginning of this process.1 In the absence of a neg-
8 O6 Q9 F4 V. U2 Native initial history of androgen exposure, our
# U9 A' c1 o7 S, M! V" f9 tbiggest concern was virilizing adrenal hyperplasia,* i! p3 E% k- M- ]! D' w9 p$ k: [- v* R
either 21-hydroxylase deficiency or 11-β hydroxylase
: Q. l' L  A9 A5 N& G' H! v8 Cdeficiency. Those diagnoses were excluded by find-* v- q  J7 B% i' W% w
ing the normal level of adrenal steroids.
( p6 K5 }% a. {$ u; U4 |3 DThe diagnosis of exogenous androgens was strongly- z, J# ]! s, a; B
suspected in a follow-up visit after 4 months because( b! u* T1 S3 D0 A$ s2 y& V
the physical examination revealed the complete disap-
; i; g9 N% E: F; T2 Jpearance of pubic hair, normal growth velocity, and
- K' |" u7 v" jdecreased erections. The father admitted using a testos-
% D1 f; R2 E$ S! L9 H" w. yterone gel, which he concealed at first visit. He was+ s2 ?* y9 {- l1 J
using it rather frequently, twice a day. The Physicians’
% E4 r9 w  U% ^3 ?) k/ ZDesk Reference, or package insert of this product, gel or
2 p) |8 `4 a5 J+ j! O! rcream, cautions about dermal testosterone transfer to0 F& U, [- ^, k4 w/ v& q
unprotected females through direct skin exposure.
* C) E5 T3 {8 V$ ]2 ^  ], u# O! zSerum testosterone level was found to be 2 times the! K5 P3 [( q/ @' O
baseline value in those females who were exposed to
1 \& E7 k, E6 ?, r3 j# E) Ieven 15 minutes of direct skin contact with their male2 V" |/ ~/ O7 E% O3 S, ~
partners.6 However, when a shirt covered the applica-
6 a( O7 _% f. Gtion site, this testosterone transfer was prevented.
2 _! T9 S3 X8 y, D6 n( y4 fOur patient’s testosterone level was 60 ng/mL,4 X  V, V/ D1 b
which was clearly high. Some studies suggest that% s, h# F/ b+ _: K
dermal conversion of testosterone to dihydrotestos-" k8 }$ t1 b) ?; y  d
terone, which is a more potent metabolite, is more: o& T7 n8 _( Z) `
active in young children exposed to testosterone, M: `& `5 r. `: l8 N
exogenously7; however, we did not measure a dihy-
$ a0 C+ [! _5 B! ^7 D3 _9 s/ n) ~+ [drotestosterone level in our patient. In addition to
/ D/ L+ [* M" rvirilization, exposure to exogenous testosterone in
* ?$ {+ m8 p/ n5 L( A  X2 Y+ achildren results in an increase in growth velocity and  z7 c8 t' C% v+ C) s
advanced bone age, as seen in our patient.1 [  A3 [6 v, I' X6 H1 O- h
The long-term effect of androgen exposure during
8 k  a5 M) a7 b) r3 A, [& Pearly childhood on pubertal development and final
9 y1 U0 O, p  @6 C) y4 zadult height are not fully known and always remain
6 h! K' z0 n( e' L6 M0 s; {8 g$ ~a concern. Children treated with short-term testos-
( h3 y4 N  ^( f8 j3 F9 Bterone injection or topical androgen may exhibit some
& B% |2 v5 U' v3 facceleration of the skeletal maturation; however, after
" [" ~+ F8 Q2 q4 wcessation of treatment, the rate of bone maturation( E6 r( }3 b+ H  j5 @4 X! {
decelerates and gradually returns to normal.8,9% r/ q* |0 Y* b/ Q
There are conflicting reports and controversy2 z2 e- Y5 T" W7 j( {, O: u' c
over the effect of early androgen exposure on adult3 {, I4 ~1 k  X" I3 J
penile length.10,11 Some reports suggest subnormal
! g& s$ B6 ?, F; u5 c6 Yadult penile length, apparently because of downreg-
: S3 |. h6 w+ u, kulation of androgen receptor number.10,12 However,
! s1 c1 T7 K, D, u4 K* K$ a& r: lSutherland et al13 did not find a correlation between$ L. \0 B8 f- Y' H- S% s
childhood testosterone exposure and reduced adult; J. o: I* M' j6 V/ N
penile length in clinical studies.
8 m9 o5 B# z. e6 XNonetheless, we do not believe our patient is
: H4 t  `6 k* p( ^" b0 R+ Bgoing to experience any of the untoward effects from
( h' K: P5 N; D5 ^testosterone exposure as mentioned earlier because
5 S7 U3 I1 c& }& ]0 Wthe exposure was not for a prolonged period of time.7 T2 i) o) _" C! x1 d9 J
Although the bone age was advanced at the time of
8 b" V; w2 G3 t; n  _$ W$ Bdiagnosis, the child had a normal growth velocity at
+ l  Z6 j: `( u) ?6 i# N& m1 ^' Zthe follow-up visit. It is hoped that his final adult
4 y1 t: z4 \( s' m' \* t) Oheight will not be affected." {5 D9 G2 Y2 V# k
Although rarely reported, the widespread avail-0 n; a. @* u2 `  z1 m5 S: w0 p7 O
ability of androgen products in our society may, T# M( {+ F) D( _/ _3 q. c. N
indeed cause more virilization in male or female
$ r2 v& f9 g) j$ i" W6 z% vchildren than one would realize. Exposure to andro-) Q9 d/ h4 l( h
gen products must be considered and specific ques-
8 U" d5 Z$ F; J4 P# D/ k& m( ytioning about the use of a testosterone product or
) B* L- w# p5 o6 @* Egel should be asked of the family members during  R, \, G$ _0 D+ ^% }
the evaluation of any children who present with vir-# o& ~& A" T2 [
ilization or peripheral precocious puberty. The diag-1 d; t9 n6 _$ F; \7 M1 S" Q
nosis can be established by just a few tests and by
8 s. d4 u& ]# a, P: F, P; C8 fappropriate history. The inability to obtain such a8 F3 e4 K# L! v3 j$ D
history, or failure to ask the specific questions, may
2 J5 T4 w. H; N- k! sresult in extensive, unnecessary, and expensive
8 y! X' w1 g4 E- minvestigation. The primary care physician should be5 ^4 n7 a; n4 ?/ x
aware of this fact, because most of these children: |$ v- z& G1 U. X; n
may initially present in their practice. The Physicians’" F9 k5 Q! z3 f. I
Desk Reference and package insert should also put a
/ Y* u9 t; H3 v0 s6 fwarning about the virilizing effect on a male or: _& D6 m9 B: x* @
female child who might come in contact with some-' i2 A2 C/ Q5 s( M0 `8 r: b' O
one using any of these products.3 t6 ?$ O6 t( G% Z! m" |( W5 l
References
' e& z  t4 m! j% X8 D1. Styne DM. The testes: disorder of sexual differentiation
7 T1 ?+ R( B7 X$ H- K& eand puberty in the male. In: Sperling MA, ed. Pediatric
( T; [7 a! Q# k6 [" b+ N2 }5 r8 n( ?Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* U0 A7 W5 B5 U6 d
2002: 565-628., i: h8 H: V, r. R% l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  T. O( h: q8 c5 v; k) m; Z5 c1 k" \
puberty in children with tumours of the suprasellar pineal
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女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
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4个什么样的?
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/ g" N; u7 G0 m
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
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么好吧v进化过程就回国参加发uft成就和;哦i回来就好v科技股份兄弟人的 路由公开vu个v库每年b
發表於 2025-4-8 11:10:25 | 顯示全部樓層
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
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