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Sexual Precocity in a 16-Month-Old+ I% c8 b" d" O9 ]
Boy Induced by Indirect Topical
1 _! f3 e0 b2 g$ u: JExposure to Testosterone
& k- d/ \! D8 wSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; i/ t+ A4 T4 S; j! ?and Kenneth R. Rettig, MD1
, g- n4 s8 j+ c+ R* MClinical Pediatrics( n& S4 w" r0 J" [. d) M- C
Volume 46 Number 6- x8 x/ w. i& K) s, s( T
July 2007 540-543" ^8 l) L& n5 P) X8 F8 u
© 2007 Sage Publications: e$ W: c9 O7 n  z
10.1177/0009922806296651& ~/ e2 c8 h% @4 n, r
http://clp.sagepub.com3 n0 i& y2 n7 h" t
hosted at
! z; K/ Q5 \  G. K4 g/ f0 A$ shttp://online.sagepub.com
/ N' x' e, Q/ v6 e! r: y. o# tPrecocious puberty in boys, central or peripheral,3 x% Y/ r, s7 ?( W- Y1 M
is a significant concern for physicians. Central  V) m3 H* G! s+ ?: L" A
precocious puberty (CPP), which is mediated
% R) s+ P5 V7 [% _6 c' g! W* t% Vthrough the hypothalamic pituitary gonadal axis, has
! d- |) J. d7 `% q/ }a higher incidence of organic central nervous system
, I* j( X( X5 y& r2 U# D# a. slesions in boys.1,2 Virilization in boys, as manifested. L0 Z6 g7 X# `5 \$ Z% K+ I# F
by enlargement of the penis, development of pubic
( a2 g6 Y0 P! W+ _" t# C/ ahair, and facial acne without enlargement of testi-  M/ L+ P. Z& S% C1 o4 f/ t
cles, suggests peripheral or pseudopuberty.1-3 We
8 w3 q/ m+ \# T7 `6 G( p& a' z+ qreport a 16-month-old boy who presented with the0 j, B! D" f4 [' D8 k5 g- m
enlargement of the phallus and pubic hair develop-
0 {! r: ^+ L" Ament without testicular enlargement, which was due
' w- r$ i* h! s- o) r! J" \to the unintentional exposure to androgen gel used by
; ]$ _5 n+ P% V' ]the father. The family initially concealed this infor-
0 ?& L$ j: k6 Z! ]/ M; T( U7 kmation, resulting in an extensive work-up for this
( j9 |# D- [; a- gchild. Given the widespread and easy availability of) {- G/ W% D/ p. \
testosterone gel and cream, we believe this is proba-
0 ?1 Y. E) M# g/ _bly more common than the rare case report in the
2 S% ~' C# _8 c. n+ _literature.4
$ z9 j. k6 @2 _' {Patient Report
. P- k5 ~2 f) L3 S$ G& F0 ]A 16-month-old white child was referred to the0 b9 Z5 J8 a4 i% T& E0 J
endocrine clinic by his pediatrician with the concern  O& |! M+ T( Q  N7 D
of early sexual development. His mother noticed
4 E" i& \; N! n2 |light colored pubic hair development when he was
, B) P1 V2 J1 RFrom the 1Division of Pediatric Endocrinology, 2University of
" l+ d9 E! i2 l! w; g, OSouth Alabama Medical Center, Mobile, Alabama.
. ^8 D2 m, ]( `6 k7 h3 ]Address correspondence to: Samar K. Bhowmick, MD, FACE,
. a4 T+ v8 t: \) h- [' {0 rProfessor of Pediatrics, University of South Alabama, College of0 i, O+ h5 n5 W) d' z8 C7 F( M
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! M4 @" O& w: X3 g/ A' h
e-mail: [email protected].1 a  S6 N( y. t0 P; O8 }
about 6 to 7 months old, which progressively became# y# t7 E+ `, R, F: @) Q5 p
darker. She was also concerned about the enlarge-
7 W% @; }, g3 E1 n- C" Fment of his penis and frequent erections. The child: l" a, ^7 z, I+ Z7 r
was the product of a full-term normal delivery, with
5 \/ e- q& M! M$ B% i5 q9 Ba birth weight of 7 lb 14 oz, and birth length of
9 G; f/ y: m0 r; S# u20 inches. He was breast-fed throughout the first year
, i4 y# H& O, D8 \9 }of life and was still receiving breast milk along with$ w$ ~) z: l" k1 _; j* _9 s! A
solid food. He had no hospitalizations or surgery,6 j' a+ N+ o: ?5 O9 l, D6 u
and his psychosocial and psychomotor development3 L) I8 n) w8 a* w! ]
was age appropriate.
6 d7 [9 W, r! D1 i4 x+ M: fThe family history was remarkable for the father,
9 L- Y' M  v1 ?9 O4 x9 i. B- ^! Swho was diagnosed with hypothyroidism at age 16,1 L- n! Y% @+ `4 W" }! E
which was treated with thyroxine. The father’s
, A8 T  r  J2 |: T+ z) Qheight was 6 feet, and he went through a somewhat! K+ n2 `' l/ z. z
early puberty and had stopped growing by age 14.
4 y, [/ b/ I8 M  m& ?6 g& j( sThe father denied taking any other medication. The
5 g- x( h1 Z; R2 B$ D( [7 }child’s mother was in good health. Her menarche" U' ?: e- N+ i$ d1 G8 z
was at 11 years of age, and her height was at 5 feet" {  O5 d* V' T9 }2 m) @- B
5 inches. There was no other family history of pre-
% A! [# U# f  j: [( c  Z1 Zcocious sexual development in the first-degree rela-
0 L, R1 e" N7 g9 \& ttives. There were no siblings.4 L5 r) D) u! c7 F( p* k/ ^
Physical Examination
' K% m" B1 h  BThe physical examination revealed a very active,
. _! L9 C7 G7 `2 ^% lplayful, and healthy boy. The vital signs documented
' t* Z! A+ O1 n- K3 W. _a blood pressure of 85/50 mm Hg, his length was/ l3 S( _( h  |
90 cm (>97th percentile), and his weight was 14.4 kg
" I4 x( _. R; }(also >97th percentile). The observed yearly growth" v+ o4 ~9 t. A7 ~
velocity was 30 cm (12 inches). The examination of5 d( G+ J; {% g8 C- g+ I& A
the neck revealed no thyroid enlargement.
3 ?$ Q2 r% y5 k, ^  g2 A) |0 B' @- FThe genitourinary examination was remarkable for& x( i. \' R8 t/ M9 f
enlargement of the penis, with a stretched length of
" g( G. f' f" b& I8 cm and a width of 2 cm. The glans penis was very well
  H. Z3 R; u  k' t' I  Ydeveloped. The pubic hair was Tanner II, mostly around. B* P% E% ?# I6 I. s4 T4 b
540
: [% \" f. V) g8 F  o  Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 I% @. ^, i+ K) Qthe base of the phallus and was dark and curled. The
6 C) @1 ]- `4 Q7 e6 N4 jtesticular volume was prepubertal at 2 mL each.
4 W- i2 v; b  s( j: p+ VThe skin was moist and smooth and somewhat
: w; {$ I6 ~7 W8 X& W) V( \oily. No axillary hair was noted. There were no; d8 j9 t& ~! [2 b" H
abnormal skin pigmentations or café-au-lait spots.
, z4 M1 L2 E5 k% ~! `. P3 n6 ~Neurologic evaluation showed deep tendon reflex 2+
6 h; N; X( Z9 W! x* zbilateral and symmetrical. There was no suggestion- ~" ?' }% \" ]/ M' w& ^
of papilledema.
. [$ J, S9 i% H3 d2 ^Laboratory Evaluation
. C. i" C4 w& EThe bone age was consistent with 28 months by4 p! G( a% D" U$ a" Q
using the standard of Greulich and Pyle at a chrono-. s/ o! D3 l5 {: V  u: P6 h
logic age of 16 months (advanced).5 Chromosomal
* z' c, n  _/ P% W+ [* Wkaryotype was 46XY. The thyroid function test. C6 P/ O$ Z7 p; r+ R2 G
showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 l9 t( e' p* ?6 d- q, G/ I& T* ~
lating hormone level was 1.3 µIU/mL (both normal).
: B: |1 O  p  C7 u) p. R$ XThe concentrations of serum electrolytes, blood1 ?1 I6 v" Q! }( N# F% {" g
urea nitrogen, creatinine, and calcium all were. a  _: d% V5 l2 q* Q  S" ^( L% J
within normal range for his age. The concentration
7 I& J  c4 n! c2 eof serum 17-hydroxyprogesterone was 16 ng/dL
+ G3 J. }0 x3 g8 _0 O(normal, 3 to 90 ng/dL), androstenedione was 20
8 j; q3 D/ t( Z8 M: jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, ]7 u; g/ U- k; q3 ^# V9 W1 E( s( Wterone was 38 ng/dL (normal, 50 to 760 ng/dL),
9 E- e" }! J( B# t4 Ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 r! Z% a& v& B+ U49ng/dL), 11-desoxycortisol (specific compound S)
; I( y" T, I7 }) N. v3 Dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
# m2 D' ^* P0 f0 u4 L5 V: Y4 A$ J8 u6 otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- {' g4 B$ w! D' h6 N
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),% F/ a# `' @; W( G% V
and β-human chorionic gonadotropin was less than' _, [' V1 D7 Z0 h" c+ |
5 mIU/mL (normal <5 mIU/mL). Serum follicular( m4 E) s# h! v% L) y/ N
stimulating hormone and leuteinizing hormone; n; s3 H) B0 C4 V
concentrations were less than 0.05 mIU/mL
! o' J, s5 k: J2 D  c(prepubertal).
$ N; A* l% q% s* s5 `5 x0 U* uThe parents were notified about the laboratory
7 o* S7 R" s* L! @2 W2 T0 U2 O, L9 ]results and were informed that all of the tests were/ g' c+ ]; g. X3 Z2 ?/ f. B
normal except the testosterone level was high. The
4 M2 f" b0 _5 r$ F3 Nfollow-up visit was arranged within a few weeks to
) L5 @1 P: P2 t- Qobtain testicular and abdominal sonograms; how-
# ~( h% o$ U$ E- jever, the family did not return for 4 months.
: m: {' L1 p& q0 m0 T2 PPhysical examination at this time revealed that the  b5 @, k  w/ u8 R# @; X
child had grown 2.5 cm in 4 months and had gained
- ~) a# N5 D0 w4 l+ A- S7 Y9 K2 kg of weight. Physical examination remained  }% z7 A# b5 [2 l3 F( z
unchanged. Surprisingly, the pubic hair almost com-
! w1 w2 A, E+ D- G2 s* upletely disappeared except for a few vellous hairs at
: ?/ P6 d7 b; S0 Kthe base of the phallus. Testicular volume was still 2
0 f' h0 c- U1 q7 S- ~mL, and the size of the penis remained unchanged.8 Q( Q, K/ [/ O3 R7 i8 ?7 T- L
The mother also said that the boy was no longer hav-
+ q& g2 a; r! w) Ving frequent erections.
+ ^# F- \" N$ B: N- Z1 v. h/ K2 ^, YBoth parents were again questioned about use of
) \: l/ F6 g* L& `$ tany ointment/creams that they may have applied to
: }9 k0 Q: C8 [4 H% z! W/ y* k: athe child’s skin. This time the father admitted the% U# Z% Y+ F2 `( W
Topical Testosterone Exposure / Bhowmick et al 541
& E; }$ ^: E! e  n  L* C& }use of testosterone gel twice daily that he was apply-0 J0 u' G$ B1 f, S
ing over his own shoulders, chest, and back area for/ H" R4 A# J2 s8 g5 y7 w
a year. The father also revealed he was embarrassed, [# Y. J( k+ n1 L2 ~
to disclose that he was using a testosterone gel pre-
* O, T7 J/ Y5 o: {scribed by his family physician for decreased libido# j: O$ e! @8 f2 J# x
secondary to depression.7 n2 }+ K$ N" C; X1 w6 h
The child slept in the same bed with parents.
7 D) x2 Q! l6 D5 R: p: F# U4 f/ vThe father would hug the baby and hold him on his
8 w" w( r9 X* x% ]& C$ @chest for a considerable period of time, causing sig-
0 _( l8 z/ G; pnificant bare skin contact between baby and father.
6 D+ p: F9 h  ]% JThe father also admitted that after the phone call,
; y! u4 j% l5 F. [2 t8 s6 q% U3 x! twhen he learned the testosterone level in the baby# M# D2 p) _0 K  c- J
was high, he then read the product information) p4 z" [' j0 W8 _) K* ]! u  O0 S
packet and concluded that it was most likely the rea-/ F( T' _& N) D/ N  s8 @5 @
son for the child’s virilization. At that time, they% m$ D5 A0 `9 a
decided to put the baby in a separate bed, and the
5 L. ~: n! j+ H' p7 u% J) kfather was not hugging him with bare skin and had
0 w" h' z* O3 z+ q7 k1 _$ qbeen using protective clothing. A repeat testosterone
5 F" F1 i) Z6 _9 _. y' Rtest was ordered, but the family did not go to the0 }8 X; v$ h0 r2 ^, a* ?% l( W0 ^. c
laboratory to obtain the test.
0 z/ s# P& S; jDiscussion6 g1 A7 H6 c- ~. l
Precocious puberty in boys is defined as secondary
$ y% \0 E+ v& O# tsexual development before 9 years of age.1,4
' L. H4 m, s8 P! L, O  c3 q( kPrecocious puberty is termed as central (true) when6 Q0 h& F8 x, ^. f$ j
it is caused by the premature activation of hypo-
# a' O* M" U2 V5 S. W2 G" j* Cthalamic pituitary gonadal axis. CPP is more com-4 d- l" @+ X2 U3 \4 e
mon in girls than in boys.1,3 Most boys with CPP! Y; {" @  C& I6 ]- Y7 H
may have a central nervous system lesion that is' b$ T& Y0 o* C$ ]/ h; U. t
responsible for the early activation of the hypothal-7 q+ ^; Z5 a5 d: B8 Y5 R% h, W9 r
amic pituitary gonadal axis.1-3 Thus, greater empha-
' l; \; h6 [, _+ P9 g% msis has been given to neuroradiologic imaging in
: y; q0 |2 q: ~* u/ ]boys with precocious puberty. In addition to viril-
; |# Y: S9 @  gization, the clinical hallmark of CPP is the symmet-
- |5 O7 `7 |% G  @5 Vrical testicular growth secondary to stimulation by
% M4 L& j( B( w; e) J2 I/ u! Pgonadotropins.1,3
$ r  q! P& i; O) b% [Gonadotropin-independent peripheral preco-3 c0 ?/ V9 p; v( q+ E
cious puberty in boys also results from inappropriate
; {, G$ |$ \! candrogenic stimulation from either endogenous or
+ }0 z) [& I1 m' {' B1 gexogenous sources, nonpituitary gonadotropin stim-
& p6 c' b" w8 \% t$ julation, and rare activating mutations.3 Virilizing
  G$ u- H/ w, I  T1 icongenital adrenal hyperplasia producing excessive
7 b' k  C6 g4 n$ a8 h1 Oadrenal androgens is a common cause of precocious
( u% q1 F7 A6 B% Q; w3 L( J: O& a4 dpuberty in boys.3,4+ D. l- q6 ]# I  g5 K
The most common form of congenital adrenal
- s6 f$ l2 w0 _0 g! Hhyperplasia is the 21-hydroxylase enzyme deficiency.
6 n9 @8 J$ G) X- I5 P8 rThe 11-β hydroxylase deficiency may also result in6 ^: r: d" [/ i1 j$ J
excessive adrenal androgen production, and rarely,
8 N4 q" ~7 o. |& f" {9 ?an adrenal tumor may also cause adrenal androgen
% s, A$ v' `+ yexcess.1,3
+ z" H" X: Z% d  T+ h  Tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' q; o0 H% A* U( |542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 F$ m! U9 t6 I3 RA unique entity of male-limited gonadotropin-
  ]# I* {8 O0 H3 }: r4 zindependent precocious puberty, which is also known
. S9 q; m. V9 has testotoxicosis, may cause precocious puberty at a% \, F. Z: g6 ~  Z7 I, l: T# e: B
very young age. The physical findings in these boys
- D' B* r9 ~9 f/ }with this disorder are full pubertal development,- D0 v' U5 E1 O, A- D
including bilateral testicular growth, similar to boys4 y9 d$ T* l; i+ {2 T" [+ i( }
with CPP. The gonadotropin levels in this disorder
4 ?0 ~- Y/ L0 c$ ?$ q/ bare suppressed to prepubertal levels and do not show
/ U/ V2 T3 Z6 i  |# X3 [  {pubertal response of gonadotropin after gonadotropin-2 Z$ n0 e1 V3 E3 c
releasing hormone stimulation. This is a sex-linked
0 w. Z4 y2 c: Y) X+ t1 U( nautosomal dominant disorder that affects only" Q" q& c, \- B8 I# L
males; therefore, other male members of the family* X1 X. x/ A. T: _
may have similar precocious puberty.3: G( n/ q! Y& P1 D, G: R
In our patient, physical examination was incon-' p) a0 a/ o/ v% B2 W* A
sistent with true precocious puberty since his testi-" G! {" ~9 ^# T  q
cles were prepubertal in size. However, testotoxicosis
. x: h/ J% |% n, h5 kwas in the differential diagnosis because his father
6 T2 _* H, n8 d8 C- x9 Rstarted puberty somewhat early, and occasionally,) W+ d0 `1 {& J: r( u5 C# y
testicular enlargement is not that evident in the
2 U" D2 s' B% [5 O; J7 `2 nbeginning of this process.1 In the absence of a neg-
4 t5 E% b7 j! K& Sative initial history of androgen exposure, our
8 H' x% [4 E* }  ~' r# b3 ]biggest concern was virilizing adrenal hyperplasia,& ]. L, Z6 W& X7 Y1 i9 \( v
either 21-hydroxylase deficiency or 11-β hydroxylase3 n+ X. l' G/ J# x2 q1 i
deficiency. Those diagnoses were excluded by find-/ [6 _" q: h) x& b, Z
ing the normal level of adrenal steroids.: w8 d9 p' Z3 E7 k5 v, C
The diagnosis of exogenous androgens was strongly
$ h+ Q3 ?4 q! o3 |0 Y1 lsuspected in a follow-up visit after 4 months because  X- m9 p% x% s! O; [5 o
the physical examination revealed the complete disap-3 w) w2 U* U7 s0 g6 P: w
pearance of pubic hair, normal growth velocity, and
$ Q/ h0 I; i+ @8 J  O9 Vdecreased erections. The father admitted using a testos-& Y4 Z% w1 ]7 F# r) h
terone gel, which he concealed at first visit. He was
+ e7 W! R0 _% z/ i4 Pusing it rather frequently, twice a day. The Physicians’
$ ^9 C( T' V: z0 c: q5 u7 `Desk Reference, or package insert of this product, gel or1 e6 d; {9 C- {1 W8 [
cream, cautions about dermal testosterone transfer to+ O9 T. R0 A4 E/ C0 v
unprotected females through direct skin exposure." h% p4 ]5 z' P' H9 s
Serum testosterone level was found to be 2 times the3 G0 A. U- l4 v+ l& u4 l/ U6 t
baseline value in those females who were exposed to
9 k' v) W. V: |4 }& k8 Zeven 15 minutes of direct skin contact with their male
4 K* K, r- E# N- s# W& i/ Opartners.6 However, when a shirt covered the applica-  d8 [1 Q* |. {/ ^& w# b
tion site, this testosterone transfer was prevented.0 D/ x$ p* w& t0 u1 C" z
Our patient’s testosterone level was 60 ng/mL,
8 C; u; M8 t# D& ~1 c/ p1 m- D3 d/ fwhich was clearly high. Some studies suggest that
1 B" m  O( x8 H! B( \dermal conversion of testosterone to dihydrotestos-+ M! {; y+ d( l8 g
terone, which is a more potent metabolite, is more
; v3 _' v4 ]) I1 G- Uactive in young children exposed to testosterone
: @# o2 ^3 n2 D5 E0 A. jexogenously7; however, we did not measure a dihy-! ?; R. d7 |  ]6 _9 b" e6 \* ~
drotestosterone level in our patient. In addition to
9 ]2 e& f* y3 K! Jvirilization, exposure to exogenous testosterone in
, n) B+ q. x" _children results in an increase in growth velocity and
8 Y5 y5 L5 ]0 q8 ?- j5 ^, G9 i  tadvanced bone age, as seen in our patient.( ]" q9 e) g0 S, P" t/ H2 `9 s7 u& b
The long-term effect of androgen exposure during) h+ V9 X; ?1 |3 F
early childhood on pubertal development and final
% N0 t2 \' F% K  g) X( \" cadult height are not fully known and always remain- J: N$ ]5 \1 c  D6 P7 h
a concern. Children treated with short-term testos-1 M0 z0 J2 U0 p* [5 v7 ~
terone injection or topical androgen may exhibit some. L" H# y) ?, k% R( `
acceleration of the skeletal maturation; however, after
, k" s! [) o( B3 O2 Ucessation of treatment, the rate of bone maturation5 j% F& z* q& A7 E" @
decelerates and gradually returns to normal.8,9
" B3 a) ^6 Z4 d! t0 iThere are conflicting reports and controversy
& _5 S) Y+ G0 p' A7 f8 `* ?. Aover the effect of early androgen exposure on adult9 m2 P6 L7 z: l
penile length.10,11 Some reports suggest subnormal
# O& V. Y. _; }9 Nadult penile length, apparently because of downreg-
, S" u9 Z" P+ X4 W4 ?ulation of androgen receptor number.10,12 However,
% j# u/ S3 Q+ N& ASutherland et al13 did not find a correlation between
. L& @! i; y; {* q/ O) Bchildhood testosterone exposure and reduced adult: M; ~: X- @- w5 q; E8 M$ D- x
penile length in clinical studies.
3 S( o1 t, N+ H5 S+ S7 g* C6 ONonetheless, we do not believe our patient is
' [! W; U9 Y9 D+ v$ m! Rgoing to experience any of the untoward effects from( ]3 E1 ~" y9 \+ z
testosterone exposure as mentioned earlier because
5 X7 m* F+ o% W' h0 W% y- Ythe exposure was not for a prolonged period of time.& n+ k, ?; n: ]& H
Although the bone age was advanced at the time of  F% |8 F. x& X; D6 J8 B4 i9 Z
diagnosis, the child had a normal growth velocity at
7 ?; ]. _  c7 W! e2 C! Bthe follow-up visit. It is hoped that his final adult
9 k  N% z; e& ^& C8 ?height will not be affected.
+ M1 y' Z/ {( X3 l% l- i2 w1 _" _Although rarely reported, the widespread avail-  k( Z8 `* ~5 O) U2 M1 F% N, O) Z
ability of androgen products in our society may9 Q- ]& |3 I; ]% F3 A
indeed cause more virilization in male or female
( Z' r8 ?* ?0 a) @, L9 zchildren than one would realize. Exposure to andro-
' i7 W, i& U) J# d* X7 C& X: ngen products must be considered and specific ques-
" C- m# S8 H' ]( `. \tioning about the use of a testosterone product or8 b0 c% h. i0 o( r0 O
gel should be asked of the family members during
7 {! P* z5 x) n: vthe evaluation of any children who present with vir-
( g& C8 T* [# m6 v0 U- f8 I8 W7 Lilization or peripheral precocious puberty. The diag-$ i# v* [0 F+ x0 ^. w# z# z+ Q
nosis can be established by just a few tests and by
! a+ T" L% S1 d/ v7 u& A$ Aappropriate history. The inability to obtain such a+ V- y7 Y& m: l: P2 C1 ^3 v
history, or failure to ask the specific questions, may
' {3 O& ~1 B6 O# r) T' Mresult in extensive, unnecessary, and expensive" P# S5 S1 g( ?" v, ^6 g2 L  O; a  _: V: m
investigation. The primary care physician should be0 L' T% d/ \- _
aware of this fact, because most of these children% G' N& B+ G/ s% g9 S8 u3 {
may initially present in their practice. The Physicians’
- _6 f4 C  V% O( tDesk Reference and package insert should also put a
! y1 J4 f4 n7 Q( q2 Dwarning about the virilizing effect on a male or" S- @' B/ \0 T% ^( I
female child who might come in contact with some-- }- W( E6 S  N2 e7 |# w
one using any of these products.
" Z: [+ U* g2 |9 j2 n  x# ~References. p0 @' Q4 d; |* Q  @- G
1. Styne DM. The testes: disorder of sexual differentiation
1 t% ?% e# b' y/ }; V8 Kand puberty in the male. In: Sperling MA, ed. Pediatric
" Z  _( k3 G2 Z5 @- Q6 l8 \) TEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& Y' b" m' ~8 Q. k2002: 565-628.
: D4 B' m: N: Z1 ?; Y/ m1 P5 ]2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  O( `" n* t. S/ Kpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old, {1 v- Q! a* f  n* p7 H
Boy Induced by Indirect Topical1 g* L: w) l8 T: Y# h- R% I" k) [+ F
Exposure to Testosterone
) L0 [; G+ e' ^9 a+ e1 D; GSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,23 I* U3 m( v# d' D- ~
and Kenneth R. Rettig, MD1
, Q) H* H% u  s  W* t5 AClinical Pediatrics
% O! `  ?2 v% z' Z) n+ zVolume 46 Number 6
6 ^& t( P4 C- m" [July 2007 540-5430 ^3 \0 E9 Z0 z. G! `
© 2007 Sage Publications
; w' f! P6 A$ V7 n7 Z10.1177/0009922806296651
: r- Z' G: Z) n. s1 ~6 w7 V$ e3 Ahttp://clp.sagepub.com, R3 w( b# K; @; Q! u+ [
hosted at
$ m5 c& z+ c: G3 _/ @( u" H2 ohttp://online.sagepub.com
5 A( W6 |( Q, JPrecocious puberty in boys, central or peripheral,$ y. l2 f7 g6 f1 d2 k. e
is a significant concern for physicians. Central
9 S# x6 y/ L* lprecocious puberty (CPP), which is mediated
5 x" j  r1 @  ?. K2 Z. Xthrough the hypothalamic pituitary gonadal axis, has
8 O& w: g0 p3 o3 D/ {: ha higher incidence of organic central nervous system1 A+ o5 w% E" l3 X5 w$ z
lesions in boys.1,2 Virilization in boys, as manifested3 y0 {2 E+ O3 t
by enlargement of the penis, development of pubic0 O% f" m! F2 g/ b6 [
hair, and facial acne without enlargement of testi-
$ M+ i/ M+ n+ y' fcles, suggests peripheral or pseudopuberty.1-3 We8 p9 r; h6 D) K3 n+ r, h
report a 16-month-old boy who presented with the- U$ K& O9 B! V# O
enlargement of the phallus and pubic hair develop-  K" G$ k& }) h2 D( o
ment without testicular enlargement, which was due# L" d% q( p8 E
to the unintentional exposure to androgen gel used by
# e8 K2 s- {8 M: ythe father. The family initially concealed this infor-
. M* C( W. C. j; ?6 }mation, resulting in an extensive work-up for this
4 v$ H& h5 ]$ U! H) [child. Given the widespread and easy availability of
# W1 O/ }  ~' l6 o2 Vtestosterone gel and cream, we believe this is proba-% A5 H* I0 \4 Q
bly more common than the rare case report in the1 t! P0 U- e2 ]+ @% i! u/ z
literature.4) E. ?9 ~/ F2 ~3 J( F
Patient Report
  R. y' y. }& \0 LA 16-month-old white child was referred to the) i$ o! V2 ~. t8 v3 }9 I$ t
endocrine clinic by his pediatrician with the concern# Q# B% D9 D; H8 B: H4 u
of early sexual development. His mother noticed# _8 C' t) v, z) r. S1 C7 c
light colored pubic hair development when he was0 E$ A& Z( Z4 e( c& {8 y2 X0 a
From the 1Division of Pediatric Endocrinology, 2University of
0 x" P/ w( |0 L) Z' mSouth Alabama Medical Center, Mobile, Alabama.
- t7 }4 y, I. K8 x& MAddress correspondence to: Samar K. Bhowmick, MD, FACE,
/ ]$ w9 {4 {4 s" e6 t8 p" cProfessor of Pediatrics, University of South Alabama, College of
0 J7 O7 S+ g0 {3 V. c. z* v* _4 sMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ N% |+ n- r0 |2 C: F( D' w; De-mail: [email protected].
; l2 E3 s, j  ?* R2 C" P" e- tabout 6 to 7 months old, which progressively became) P* h) R/ u/ g2 w
darker. She was also concerned about the enlarge-  ?% g/ |9 T$ P' a" }. c
ment of his penis and frequent erections. The child
# t' s4 C9 l/ x" fwas the product of a full-term normal delivery, with/ a2 V% U3 {& s5 }' ^; L/ R
a birth weight of 7 lb 14 oz, and birth length of
& i; ?( M1 z" P/ ^20 inches. He was breast-fed throughout the first year
2 x' ?' X. l( [  Lof life and was still receiving breast milk along with
8 T  E. N. [. B* B) q5 msolid food. He had no hospitalizations or surgery,
( |3 H# ~$ Q! {& p. E& w4 r! b, p9 iand his psychosocial and psychomotor development
4 ]5 p5 C$ l, Ywas age appropriate.
( G- ~4 s7 L, J) ~5 F& VThe family history was remarkable for the father,! H! T% T9 s4 I0 e
who was diagnosed with hypothyroidism at age 16,$ H  ]( V0 i; r8 h
which was treated with thyroxine. The father’s9 S+ u& S) `7 Y2 h: Z  Y1 X6 b
height was 6 feet, and he went through a somewhat
) f  [+ f; x8 z8 c1 l0 q/ Searly puberty and had stopped growing by age 14.
/ _  v) a) u2 iThe father denied taking any other medication. The7 l  n: \1 C+ V5 g
child’s mother was in good health. Her menarche
8 \! _# t+ T: H# C; ~6 \* ]4 R( j( Kwas at 11 years of age, and her height was at 5 feet
; i+ @$ Z5 H4 k- V$ P& R- D5 inches. There was no other family history of pre-
! D/ O/ f2 B9 F0 W- e( Pcocious sexual development in the first-degree rela-
0 `6 `! Y& ~9 v6 I9 E( vtives. There were no siblings.
! z5 q4 p  F2 s  C" LPhysical Examination
7 ~: t9 j5 ~( u8 y, W8 |! mThe physical examination revealed a very active,
- ]8 p: \# I- E$ ]$ s: f3 xplayful, and healthy boy. The vital signs documented  z$ ^. N" o7 J7 G: ?! I- r8 n7 R; n4 C
a blood pressure of 85/50 mm Hg, his length was: a% [+ G0 K0 k- ?" K: D
90 cm (>97th percentile), and his weight was 14.4 kg
, t) I" X5 F5 o; y0 f5 F(also >97th percentile). The observed yearly growth6 v1 F2 T0 w( L/ x& o
velocity was 30 cm (12 inches). The examination of
/ H( U' [; T  Jthe neck revealed no thyroid enlargement.
) U7 V9 F- \  P" `( SThe genitourinary examination was remarkable for
7 ^  h2 [8 x  i( |- E% Nenlargement of the penis, with a stretched length of
  P1 g" r# ?& w2 T, W8 cm and a width of 2 cm. The glans penis was very well; O" H4 H' n- {- j- f# \7 {
developed. The pubic hair was Tanner II, mostly around) \( r0 H. A1 Q- d4 ?
540
( z9 x* @7 I; m! A6 |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 Z0 H$ u# ~8 Y. z3 b: ~the base of the phallus and was dark and curled. The! m5 B) ]; m) Z. n
testicular volume was prepubertal at 2 mL each.# v2 i* N7 H0 I( z
The skin was moist and smooth and somewhat
6 y) W% _( p9 T8 D, ]& }4 ]* w0 eoily. No axillary hair was noted. There were no
2 I9 C3 L& I# Qabnormal skin pigmentations or café-au-lait spots.
- o! M6 n2 n! U; t3 n6 bNeurologic evaluation showed deep tendon reflex 2+
5 W1 Z( N( A. \& o4 Z: \bilateral and symmetrical. There was no suggestion
" B7 {; J" J/ C4 q* Jof papilledema.. [/ @; T4 T# q- \
Laboratory Evaluation$ I- W3 w& f# e
The bone age was consistent with 28 months by
( J, @8 G) q  rusing the standard of Greulich and Pyle at a chrono-
1 I$ J6 i( J9 P" Elogic age of 16 months (advanced).5 Chromosomal
/ w+ V& X# d6 I$ e  lkaryotype was 46XY. The thyroid function test: o0 h' _) l" {+ ~* g* m
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
* r! N" u# i* ^' |. flating hormone level was 1.3 µIU/mL (both normal).
" r3 C! R1 E( d5 U1 M, RThe concentrations of serum electrolytes, blood" r; X" _  i$ K) D$ {& ?- V
urea nitrogen, creatinine, and calcium all were
% ]1 B( |8 Y( ]% dwithin normal range for his age. The concentration4 x7 e1 k8 y5 i; c5 Q3 X/ p) `% b; K
of serum 17-hydroxyprogesterone was 16 ng/dL. k- A) |: y* ~
(normal, 3 to 90 ng/dL), androstenedione was 20: X- x$ Q0 O2 V  p) T/ `
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& {$ |, M" K' _, M  Cterone was 38 ng/dL (normal, 50 to 760 ng/dL),2 N. M3 q4 [5 E. H
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 Z3 r; J" G0 \49ng/dL), 11-desoxycortisol (specific compound S)
6 m9 {1 \% i* q; s9 m' Owas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- G& ^# N+ X  \2 N7 Q' R
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total6 F7 b1 {+ ]  r. e2 a0 R  E
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 b" U( q  j1 e7 {and β-human chorionic gonadotropin was less than
5 e( O4 E: l5 M" S: J5 mIU/mL (normal <5 mIU/mL). Serum follicular$ J4 ]: F. v3 F$ D
stimulating hormone and leuteinizing hormone
) Y0 E9 Z5 \& nconcentrations were less than 0.05 mIU/mL
- `7 B" B1 \2 t' g(prepubertal).
$ c' r' ~9 Z# \1 T( b: D$ ZThe parents were notified about the laboratory
4 @2 [) u9 L" ^4 n+ K. Tresults and were informed that all of the tests were
+ m+ s6 z9 ~$ k: _2 xnormal except the testosterone level was high. The: H. g" x: t: c: l- D! R
follow-up visit was arranged within a few weeks to- Q( z4 c! ?5 D( g% c5 K
obtain testicular and abdominal sonograms; how-
+ b! w9 A( ?* u  aever, the family did not return for 4 months.* n' G8 j3 E. @8 W. [) g2 d
Physical examination at this time revealed that the
) n4 [+ O% C* bchild had grown 2.5 cm in 4 months and had gained7 o5 j, Z# q+ e" }0 Z! L
2 kg of weight. Physical examination remained
' o4 p6 F8 P9 k! w  ]6 E$ gunchanged. Surprisingly, the pubic hair almost com-
: |. m! o7 D( i7 Y- d- I% bpletely disappeared except for a few vellous hairs at/ `6 j7 P  M3 }
the base of the phallus. Testicular volume was still 2# e) r  g8 E" C' ]
mL, and the size of the penis remained unchanged.; l1 E4 o3 b4 m5 O% [
The mother also said that the boy was no longer hav-. f6 [1 X- ]/ G. ~" o# n
ing frequent erections.
* T9 o  i+ w3 `/ N+ C9 @Both parents were again questioned about use of+ C& G) K, f2 q6 I; F% I4 x
any ointment/creams that they may have applied to/ c- D6 }+ ~% i$ d& h
the child’s skin. This time the father admitted the
- T, v. `- b9 M$ D( p6 `Topical Testosterone Exposure / Bhowmick et al 541$ x7 Y" y; h1 F) q- F2 h0 w
use of testosterone gel twice daily that he was apply-8 R& Y! X& ~3 B
ing over his own shoulders, chest, and back area for+ y# m" Y5 ?# l3 F) o
a year. The father also revealed he was embarrassed! r: ^: i) m" b" h9 k1 q
to disclose that he was using a testosterone gel pre-
5 I) A6 z* l0 s; ascribed by his family physician for decreased libido
( ?+ q! f3 t- e# X. q. Jsecondary to depression.
9 u/ S8 W# x) h' |# E7 q$ GThe child slept in the same bed with parents.
+ R2 R* ?, r% Q* o) }6 y8 B  p8 nThe father would hug the baby and hold him on his
( t* j/ b1 t2 B& ]chest for a considerable period of time, causing sig-
3 ^; v; G6 k  W) I3 nnificant bare skin contact between baby and father.* O' X0 b# l! H0 H$ @9 x/ ]3 L
The father also admitted that after the phone call,
4 }6 ~1 o4 n* M7 ^. j- A$ Swhen he learned the testosterone level in the baby% I3 q; M2 g# c3 j8 H
was high, he then read the product information
* ]- V% }0 V. k' Y$ G& hpacket and concluded that it was most likely the rea-! t$ M7 j1 |7 x' Q. G! ?, \
son for the child’s virilization. At that time, they
3 {. k: I; R/ L; J# I4 Cdecided to put the baby in a separate bed, and the$ o- b% ?5 r! X! x
father was not hugging him with bare skin and had
6 V) b0 n$ p5 r7 B: fbeen using protective clothing. A repeat testosterone
! I. ?# w( [( W4 x2 C+ F" W) Ztest was ordered, but the family did not go to the
- X; N: }6 j* B+ U' T6 F, C0 `laboratory to obtain the test.  v0 G$ `7 f# \' D' E
Discussion) ~( o2 o. I  H- c3 S  ^9 G3 f
Precocious puberty in boys is defined as secondary
1 y5 {9 T8 Q* `" Y6 Qsexual development before 9 years of age.1,4- ?. O$ k8 ^  q7 {, Y+ e
Precocious puberty is termed as central (true) when; z$ q# s6 m! I& B- G( h
it is caused by the premature activation of hypo-" p1 n) P8 g. e# v2 r
thalamic pituitary gonadal axis. CPP is more com-" j: G. u8 n6 t9 l9 G
mon in girls than in boys.1,3 Most boys with CPP3 T) c0 V2 U  @+ m# N
may have a central nervous system lesion that is
/ B& d5 v+ p7 h: U$ F2 Y* u4 O( nresponsible for the early activation of the hypothal-9 ~8 {4 Z8 x5 _: }: u- |
amic pituitary gonadal axis.1-3 Thus, greater empha-; B0 J' w+ s" `( Y
sis has been given to neuroradiologic imaging in+ \0 o% R4 M$ j6 X/ J, o
boys with precocious puberty. In addition to viril-. D+ B2 B3 [7 f3 O
ization, the clinical hallmark of CPP is the symmet-, L' d$ L4 }7 s, K" }2 Y* a
rical testicular growth secondary to stimulation by
4 D: i% Q0 H, w- z5 ggonadotropins.1,3. ^9 |) @0 v8 \
Gonadotropin-independent peripheral preco-
: [; V: O. r9 H2 o# ?# d9 Ycious puberty in boys also results from inappropriate* [; k2 Q+ f" B4 c* |& F  v
androgenic stimulation from either endogenous or
; l9 Z5 y4 ?) C" U' }exogenous sources, nonpituitary gonadotropin stim-
3 T, z' Z4 I: h. w( Mulation, and rare activating mutations.3 Virilizing
5 s7 s/ V8 B4 J- p" d3 J  econgenital adrenal hyperplasia producing excessive2 ]6 n- B+ f/ d6 H) f+ J, t
adrenal androgens is a common cause of precocious
0 m6 L* G+ H, spuberty in boys.3,4
$ K: n0 H& P, v8 |3 dThe most common form of congenital adrenal+ a: T( |+ m# }+ g% B
hyperplasia is the 21-hydroxylase enzyme deficiency.. @( f: u. n6 n
The 11-β hydroxylase deficiency may also result in
6 S% N% `3 l; R6 hexcessive adrenal androgen production, and rarely,
$ z8 s. n% @$ b+ q& aan adrenal tumor may also cause adrenal androgen
7 g7 m* B6 K' ^7 \( \) nexcess.1,3
% }/ R! ]) z, P  [  A. x& iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 l' K% e( r) [" w% w9 S" J$ f542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; b3 f2 m% _7 l% U8 O; H' jA unique entity of male-limited gonadotropin-" m1 ~5 [6 r8 ]; X4 n# B& v
independent precocious puberty, which is also known, k' m1 O; S& G/ |% J% R
as testotoxicosis, may cause precocious puberty at a
* G5 k& B) M+ I" u. k9 ^very young age. The physical findings in these boys1 I( {+ s/ G4 X' X
with this disorder are full pubertal development,( ?% j8 ~2 _4 M2 X! u  `0 a
including bilateral testicular growth, similar to boys
$ t6 e2 G& S( e- h- pwith CPP. The gonadotropin levels in this disorder" u7 W* I; d) n9 L$ G0 i
are suppressed to prepubertal levels and do not show0 X2 i9 o0 f; I6 d; s. s4 ?
pubertal response of gonadotropin after gonadotropin-( s( o; @/ q9 i4 B) e* J
releasing hormone stimulation. This is a sex-linked3 P1 @: _" y; f2 E# Z) P- u
autosomal dominant disorder that affects only* p4 d( G6 R2 L8 g: `2 W
males; therefore, other male members of the family
& N- @1 Z/ [! F  L& y8 [may have similar precocious puberty.33 ?% \% ^) m# M! L1 M4 w
In our patient, physical examination was incon-
2 `4 V9 Z- ?1 t# e' Nsistent with true precocious puberty since his testi-, N% z- U* y. E( \3 F
cles were prepubertal in size. However, testotoxicosis
0 X6 @- o8 g( K: S# _$ M! a: ewas in the differential diagnosis because his father7 S7 i; X# T# h0 q7 y6 O; y- [' b
started puberty somewhat early, and occasionally,% {3 C# |: K: J: F- S" h) ~
testicular enlargement is not that evident in the+ ]7 T6 b7 X0 v. m% `
beginning of this process.1 In the absence of a neg-7 m# _5 V: C! _" Y, u
ative initial history of androgen exposure, our
: P4 a& p. I" r: P  z! ebiggest concern was virilizing adrenal hyperplasia,5 _9 K" m- R3 ]! ~# n* r5 J
either 21-hydroxylase deficiency or 11-β hydroxylase
$ S6 u- [" B1 K# [0 S/ Qdeficiency. Those diagnoses were excluded by find-& b6 i" m* I# r: }$ R$ g
ing the normal level of adrenal steroids.) ~  ?* C; a: J4 E2 I
The diagnosis of exogenous androgens was strongly
7 o: V# s, w6 H2 ksuspected in a follow-up visit after 4 months because# w/ M/ o! f% U- t+ S2 K
the physical examination revealed the complete disap-
1 o' F4 I0 ]2 u: l' lpearance of pubic hair, normal growth velocity, and
& g  t& }4 p$ v/ h, O) H2 \2 ^decreased erections. The father admitted using a testos-
0 }- L( K0 }& o$ t* r* jterone gel, which he concealed at first visit. He was3 z5 j& @$ i' D+ u
using it rather frequently, twice a day. The Physicians’3 y7 B, K% B, N/ Q% t% j6 V
Desk Reference, or package insert of this product, gel or
7 N. V2 N  r3 R9 _0 U: \cream, cautions about dermal testosterone transfer to
4 o( V3 {  L( w% b' Gunprotected females through direct skin exposure.
+ b: b! t, r' B0 G) b! D8 }Serum testosterone level was found to be 2 times the
+ {7 G2 T$ h+ A6 ^. O( E3 Xbaseline value in those females who were exposed to
* h$ |; p5 v9 Meven 15 minutes of direct skin contact with their male
0 q) x# G& Z& y& W2 |6 Zpartners.6 However, when a shirt covered the applica-: |! C! e* ^% i  I+ K4 C
tion site, this testosterone transfer was prevented.
! W, g) Q+ p: b0 t: DOur patient’s testosterone level was 60 ng/mL,% I8 r7 `9 k! U& K+ {% L2 s
which was clearly high. Some studies suggest that
& ~# U+ l* u' _) W# f% K. qdermal conversion of testosterone to dihydrotestos-& w' g4 g0 m, ]- V9 n
terone, which is a more potent metabolite, is more' s# e; }0 g* D1 g4 V$ J7 x! F
active in young children exposed to testosterone. O. O5 S" z$ R' {& x% D
exogenously7; however, we did not measure a dihy-
% D9 Y/ j( e1 a; ~drotestosterone level in our patient. In addition to
) C% a6 W# y! E6 yvirilization, exposure to exogenous testosterone in! W/ N6 S" a0 h4 I; Q0 ?4 b
children results in an increase in growth velocity and
7 F5 G, H$ I) `1 X0 k) V& ]advanced bone age, as seen in our patient., L' z" x0 u" s4 f1 _% I* X7 r  V. g
The long-term effect of androgen exposure during& y$ V) t) [' t, g, c+ c3 y
early childhood on pubertal development and final) y& }8 _, [1 j3 ^& v! D9 o) z
adult height are not fully known and always remain
" v4 M0 }* p" k  za concern. Children treated with short-term testos-" m% i9 N: {' Z/ L, K
terone injection or topical androgen may exhibit some
& i' t1 P5 C/ r. O+ S' Aacceleration of the skeletal maturation; however, after2 s  Y% O" D/ W( C/ |# \3 Q
cessation of treatment, the rate of bone maturation3 T+ h  K2 ?% T' Q( Z5 D
decelerates and gradually returns to normal.8,9
+ e3 S' C, }( ~, R+ dThere are conflicting reports and controversy7 l3 h- m0 o) W& R5 e4 p  s
over the effect of early androgen exposure on adult& L* `7 U7 ^. o5 }! f
penile length.10,11 Some reports suggest subnormal
& g; x2 I( {# s3 K' b4 b# Gadult penile length, apparently because of downreg-( ]' A/ z$ Q4 t/ V% |& L( S$ H# J
ulation of androgen receptor number.10,12 However,, D$ `+ d- |4 S# w  g( j9 f
Sutherland et al13 did not find a correlation between' S! z3 g2 S0 e. T- j& t2 X! m
childhood testosterone exposure and reduced adult' W- C/ n: Z. f- J/ C5 X- J
penile length in clinical studies.
$ S  Q7 t; o( c6 f+ pNonetheless, we do not believe our patient is
0 }) O7 v1 h" Z- A1 z( dgoing to experience any of the untoward effects from' \' @0 v3 J  V. u: z
testosterone exposure as mentioned earlier because1 O* Q: U. `% R( f+ u1 X, i% T
the exposure was not for a prolonged period of time.
8 \% l6 Z: F5 _" I% U# J1 ZAlthough the bone age was advanced at the time of9 L/ c' o0 o, h; M" V% [+ |+ Y. l
diagnosis, the child had a normal growth velocity at
1 k. @" X$ W: X) c  \the follow-up visit. It is hoped that his final adult9 t" ~, ]8 f/ q' E
height will not be affected.
5 L) J2 C' g9 N# R) `Although rarely reported, the widespread avail-
) j6 B- n" \* p+ @/ ?% b: Jability of androgen products in our society may- ~' Q+ A- _6 I  ]; g7 P: _
indeed cause more virilization in male or female
+ D: r# j2 t% e" ]( d, q5 l2 ^8 achildren than one would realize. Exposure to andro-  }7 }) @) F3 @0 p, J; o
gen products must be considered and specific ques-
; N& E5 x" P7 w# p; F4 p" Stioning about the use of a testosterone product or* c1 s) x2 S- \% H5 J' Y
gel should be asked of the family members during
4 y" U$ w9 b$ S' mthe evaluation of any children who present with vir-
) W- `, l3 z& w- b% ?: n4 xilization or peripheral precocious puberty. The diag-
/ M3 d* Z. X- [& h; Pnosis can be established by just a few tests and by
  s* D" i% ]3 `% R2 Y( F# }appropriate history. The inability to obtain such a! y+ |! X1 @# h% `9 S
history, or failure to ask the specific questions, may
4 w* b& ]/ v! t9 |9 uresult in extensive, unnecessary, and expensive5 j4 r. O. D/ r9 L
investigation. The primary care physician should be3 [: i( V4 n. e; ~1 }
aware of this fact, because most of these children; G# h# A9 s8 f6 o% D  B% q
may initially present in their practice. The Physicians’
( |5 r$ }- }3 Q+ B- cDesk Reference and package insert should also put a: D+ M/ [7 |7 b) b! h; h% p
warning about the virilizing effect on a male or6 B0 I# W; l# d" t9 f2 `
female child who might come in contact with some-
+ Q, P- K# I1 i& p4 ]* g0 a- jone using any of these products.
1 K6 y! P0 S  F1 ?1 y7 `& ~References
: W: r& c8 y4 G% W% K1. Styne DM. The testes: disorder of sexual differentiation
8 D7 D8 p+ u3 W" ^, yand puberty in the male. In: Sperling MA, ed. Pediatric; _. q' l+ `9 C' }
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, }! Z) W" K0 b7 \# G+ A& l- J2002: 565-628.
* R+ [3 X1 c! a2 v2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  x) o% P  R  Q5 V8 S7 Gpuberty in children with tumours of the suprasellar pineal
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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
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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

/ G2 y( N9 w+ _' j/ u& i) ~( o4 Y8 r4 u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!
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