WK綜合論壇, WK综合论坛

 找回密碼
 立即注册
樓主: wk007

鄉下的妹子太便宜,一次四個都要了[12P]

[複製鏈接]
發表於 2025-1-4 03:25:35 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
Sexual Precocity in a 16-Month-Old& Q9 Z" C/ I# E
Boy Induced by Indirect Topical4 N7 V* r: i! ^  w& ~4 Q& i- B! u$ _
Exposure to Testosterone% R; ]0 Y: R7 y0 {2 s$ O4 v
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
& W) E' w; P2 _3 Q2 wand Kenneth R. Rettig, MD1, x6 J. s# z% j+ p/ d( W
Clinical Pediatrics
& I6 C7 E: H6 z; EVolume 46 Number 6
& f. X/ J% m) e& h9 cJuly 2007 540-543' N4 A# g+ }: B+ ?/ X- |& v
© 2007 Sage Publications
: e" C: a7 {: s) o! _* ^, q  n10.1177/0009922806296651- l4 [3 ?+ `% _) S" m; W
http://clp.sagepub.com
* z5 ~4 Y9 J  K! n3 a& j4 bhosted at
1 e8 m" z4 \& a& r6 Xhttp://online.sagepub.com- |& H; i2 v2 \% H
Precocious puberty in boys, central or peripheral,
9 _: O  ?# L: a  B. cis a significant concern for physicians. Central# Y2 N$ N" y% @% s& E5 H
precocious puberty (CPP), which is mediated) {& d  M; Q; |1 y6 W
through the hypothalamic pituitary gonadal axis, has
. D9 {7 B9 u( O  U, R$ c, }) f% P- ja higher incidence of organic central nervous system6 b! Z6 J6 _2 I* S) L& f
lesions in boys.1,2 Virilization in boys, as manifested, A7 d* T. v+ c3 B8 `
by enlargement of the penis, development of pubic& G4 P- h7 }2 I0 Q1 x( R/ E0 b" s
hair, and facial acne without enlargement of testi-7 P4 x8 w9 ?4 O) \, j) Y
cles, suggests peripheral or pseudopuberty.1-3 We
: c* n0 M* `# d% ]2 y& oreport a 16-month-old boy who presented with the
& |" B+ @( P" M; y1 U3 Kenlargement of the phallus and pubic hair develop-# Y" d/ h9 [) I  E! I; a9 P, A
ment without testicular enlargement, which was due
( I2 T$ d6 J8 tto the unintentional exposure to androgen gel used by
2 y1 y2 `3 f; P& p" i1 }& Jthe father. The family initially concealed this infor-4 ^7 z( L5 P1 P/ o1 a
mation, resulting in an extensive work-up for this! p# E. Z% v  A4 f: l
child. Given the widespread and easy availability of- Z/ X" _5 ~& H& R0 u
testosterone gel and cream, we believe this is proba-6 g  C* u. l+ y0 f3 q
bly more common than the rare case report in the
+ P# R0 O  i2 n% y" ^' r: Wliterature.4
. a; _6 ]) r7 XPatient Report: E3 I4 z! Y  p# W6 r8 p9 B
A 16-month-old white child was referred to the/ a: O3 v. M# F+ M8 i) A# k7 j$ ]
endocrine clinic by his pediatrician with the concern
3 \' W/ ?! ?0 ], |- t# u, Qof early sexual development. His mother noticed
/ f5 p- \! D, ~8 Blight colored pubic hair development when he was
, C$ L$ G0 q; ^4 r# k; {From the 1Division of Pediatric Endocrinology, 2University of
' K5 t0 ]3 Q% U1 j$ i) PSouth Alabama Medical Center, Mobile, Alabama.2 A) r2 T& f2 T# v4 ~, `
Address correspondence to: Samar K. Bhowmick, MD, FACE,
0 ]' p9 U9 m- H* `. pProfessor of Pediatrics, University of South Alabama, College of
* T. L+ \% ~5 N2 N! H6 |Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 s% ?  d" s1 r! U8 \/ m& ce-mail: [email protected].
0 `. M0 Z! L3 {7 j) cabout 6 to 7 months old, which progressively became8 h; t+ S, ~% ]  W9 ?$ B
darker. She was also concerned about the enlarge-% U! i0 D0 x$ c3 z% O
ment of his penis and frequent erections. The child  z: Q2 j) w8 ~5 E+ T
was the product of a full-term normal delivery, with
% B, @$ K. F" j* na birth weight of 7 lb 14 oz, and birth length of
5 z) `% D* ?5 I( x) Y20 inches. He was breast-fed throughout the first year$ _1 I) T$ ^; y$ [! N7 ^5 N
of life and was still receiving breast milk along with! M: Z# ^" K* \! @7 k! `
solid food. He had no hospitalizations or surgery,
* ^1 j, m5 u$ nand his psychosocial and psychomotor development0 s3 K# L/ h0 w  d
was age appropriate.3 {7 j: t1 C! B9 _. F: ~( D
The family history was remarkable for the father,# O/ T3 S' V8 y& S' F( \
who was diagnosed with hypothyroidism at age 16,+ |" y+ c( z% ^+ P3 |/ h  i
which was treated with thyroxine. The father’s
' P8 ]" @: b+ @9 uheight was 6 feet, and he went through a somewhat
* D. M6 {$ K* v* jearly puberty and had stopped growing by age 14.
' E2 `. x; e8 A3 \' m# J  ?% \The father denied taking any other medication. The
* C5 ]7 c9 e+ T% S9 O: vchild’s mother was in good health. Her menarche
7 ~1 w* ~: k* x+ M4 O; Vwas at 11 years of age, and her height was at 5 feet6 S) x: I0 ?" {; I& d6 x
5 inches. There was no other family history of pre-
3 ?( v6 I8 H6 ]) F" O& \5 ucocious sexual development in the first-degree rela-& T2 a1 ]2 Y: f2 y' L& x
tives. There were no siblings.+ G: o6 R5 A+ |( n  K0 y2 w
Physical Examination( a" @& W! P/ L/ a% ^0 D% G
The physical examination revealed a very active,
4 C- L3 m  s; I' s7 Q' Zplayful, and healthy boy. The vital signs documented
$ _9 {/ m! E% i- u& k2 {8 u! K# X- ha blood pressure of 85/50 mm Hg, his length was" D: O6 E% I2 R0 A
90 cm (>97th percentile), and his weight was 14.4 kg
8 Q7 @3 n3 y8 S6 }) o( |3 P(also >97th percentile). The observed yearly growth
9 k" F3 a" m+ i: _8 n$ u9 ^velocity was 30 cm (12 inches). The examination of! A. E0 Q, z9 P& X* ]% v; M% W
the neck revealed no thyroid enlargement.2 }3 Q0 F' P2 w2 u) C. p0 ]
The genitourinary examination was remarkable for
9 |4 E2 [* g; l! s, `+ ]- ~/ Xenlargement of the penis, with a stretched length of
2 y5 Y0 v6 @- t& ^; w8 cm and a width of 2 cm. The glans penis was very well
' S2 a* K" v# f5 }7 q2 C3 O/ Ddeveloped. The pubic hair was Tanner II, mostly around
( _/ p4 M! J6 Z0 p. s8 G2 G540
2 Y0 j" b' F$ M  I# r2 ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: c% g* o( d, T5 B- j& ]5 Ythe base of the phallus and was dark and curled. The
1 o( b0 |6 T; L5 a: P3 ^5 z- Gtesticular volume was prepubertal at 2 mL each.! c3 k& p. Q. Z. ]; _& S  ?! B& c
The skin was moist and smooth and somewhat- [* H$ Y. G/ R' b) q1 I  v
oily. No axillary hair was noted. There were no; X$ S& W6 P. Y: ~7 B" d5 N: Q
abnormal skin pigmentations or café-au-lait spots.% j( J& @0 J7 I$ Q/ C; i1 w
Neurologic evaluation showed deep tendon reflex 2+
) ^! p+ G" r5 h* d. Q9 @/ {bilateral and symmetrical. There was no suggestion
( \' B) g% n- R! ~4 s1 qof papilledema.
( M$ D: x! S4 Y' E  mLaboratory Evaluation
, r+ B! I: ~$ E$ p: wThe bone age was consistent with 28 months by
5 }6 \8 J6 K' b& h% eusing the standard of Greulich and Pyle at a chrono-7 B, _5 J* `8 ?( [. D3 }$ C
logic age of 16 months (advanced).5 Chromosomal
' N0 k& l8 e" c( t! y5 T$ j, ikaryotype was 46XY. The thyroid function test
8 L3 e# {0 ?% ^% W5 K% fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
. S) l5 z- \/ h# rlating hormone level was 1.3 µIU/mL (both normal).( }* t( _- _6 z
The concentrations of serum electrolytes, blood! e* H0 t% m' {- B# c+ O
urea nitrogen, creatinine, and calcium all were
( _/ }7 D6 n2 G' O" Y1 ?within normal range for his age. The concentration1 R, U5 K0 `- Y1 \
of serum 17-hydroxyprogesterone was 16 ng/dL
2 ?4 q0 d+ u/ V$ J! [0 P(normal, 3 to 90 ng/dL), androstenedione was 20
6 ^8 C1 M0 Q7 L: f7 K) m6 png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  n7 Y4 R, I8 J! e; }2 h
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
' {/ }! i* |$ y, Edesoxycorticosterone was 4.3 ng/dL (normal, 7 to
9 s+ R6 h. A, Y4 G" K49ng/dL), 11-desoxycortisol (specific compound S): u5 \6 `% ]* J; M! b
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 F5 Q$ {5 w: T# f' U
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: d6 E3 P: x, d. L$ {: H3 Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),! B- ]7 _( G* {6 I0 n7 j8 v% V; T
and β-human chorionic gonadotropin was less than- V$ G+ e! ^. \+ W% M
5 mIU/mL (normal <5 mIU/mL). Serum follicular7 k8 P- i. |  t% A
stimulating hormone and leuteinizing hormone0 h( B) t) c# W  }' f2 x# R
concentrations were less than 0.05 mIU/mL4 I1 g6 h, ?0 N
(prepubertal).
6 Q1 @) }: [3 X  \' i7 h, \  L# |* t! [The parents were notified about the laboratory
, r8 i8 ^5 _; Z' r# \6 W0 presults and were informed that all of the tests were5 T  n# X6 L3 |2 u0 q7 B6 G
normal except the testosterone level was high. The
- \, \+ n' q! {5 ofollow-up visit was arranged within a few weeks to# t) J3 [- d! b3 H: }
obtain testicular and abdominal sonograms; how-
6 e$ g! d0 }" t/ h8 P( ?ever, the family did not return for 4 months.
: U: S8 q9 K0 g" tPhysical examination at this time revealed that the* n# ^% H: u6 v) L/ O' z
child had grown 2.5 cm in 4 months and had gained
# ^3 x( k$ w2 T2 kg of weight. Physical examination remained5 e& j: l  H" h( r. P
unchanged. Surprisingly, the pubic hair almost com-% o3 H& \- C2 s1 y- Z' N( E
pletely disappeared except for a few vellous hairs at
: i2 H; m- R0 p+ n4 g9 Kthe base of the phallus. Testicular volume was still 2
- Z1 M5 {3 S2 j. y8 f% n% @mL, and the size of the penis remained unchanged.
! d9 `# k; U3 `9 |5 W4 hThe mother also said that the boy was no longer hav-9 N% O( r1 N0 Z$ Q( M
ing frequent erections.+ L1 Q' B  s4 D
Both parents were again questioned about use of5 j+ r+ d  K+ `: `3 l* C1 O  k
any ointment/creams that they may have applied to& u( q. I7 h  R; f4 o( E
the child’s skin. This time the father admitted the
- ?& M1 M6 S2 {3 ^1 FTopical Testosterone Exposure / Bhowmick et al 541
  ]8 m7 L6 c2 o8 X: Kuse of testosterone gel twice daily that he was apply-6 {) [. a% J9 m6 C' n- \
ing over his own shoulders, chest, and back area for, q  t; q) D. N/ n1 w1 J
a year. The father also revealed he was embarrassed
# o7 C$ `' p0 i/ L$ s( Y# p0 \to disclose that he was using a testosterone gel pre-% W1 z: {& j; ?
scribed by his family physician for decreased libido* X2 Z+ o  ^4 h. w& h0 w
secondary to depression.) f/ G  K5 Q# M. u
The child slept in the same bed with parents.
# V0 j9 m6 O3 F5 O: |. mThe father would hug the baby and hold him on his
) j, _3 p; o7 |5 O6 S2 h% z* Hchest for a considerable period of time, causing sig-
% ]' f0 `8 b# R% v4 s3 mnificant bare skin contact between baby and father.
  E! `+ U) S4 f, U. v* H  X+ ?8 J) tThe father also admitted that after the phone call,
, D& k6 x- P) r% y2 e6 Qwhen he learned the testosterone level in the baby
: }3 W. G. @/ N6 xwas high, he then read the product information8 ]# S! T6 A5 F' ^" b
packet and concluded that it was most likely the rea-( ~& I$ ~- P, z4 G! N6 G+ |3 N
son for the child’s virilization. At that time, they8 }$ L2 ^8 U% _9 u6 |& T
decided to put the baby in a separate bed, and the3 Z9 f& A. `; D5 w1 s; K
father was not hugging him with bare skin and had
$ v$ o# q0 v& abeen using protective clothing. A repeat testosterone, d' w7 h& T8 D
test was ordered, but the family did not go to the) r. Z& s# A- E3 B$ }0 H
laboratory to obtain the test.
/ p& Z# W1 X% q5 tDiscussion
  C4 Q; K! a2 Z: m* ZPrecocious puberty in boys is defined as secondary+ U3 ]2 R1 [3 U. T; V$ ~1 p
sexual development before 9 years of age.1,4
0 H% \( w8 N4 F' b5 d7 ]( `Precocious puberty is termed as central (true) when
4 J! ~) ?2 h) Y  ait is caused by the premature activation of hypo-
: a! r- W) a$ z- A1 D6 V1 P% s0 dthalamic pituitary gonadal axis. CPP is more com-2 J9 v0 O6 ?# [( F. A
mon in girls than in boys.1,3 Most boys with CPP5 E" f5 f  w: f3 |6 L
may have a central nervous system lesion that is3 i9 k$ x" R0 U5 y$ [6 ?
responsible for the early activation of the hypothal-
, ~/ ?1 P2 P8 I! l5 wamic pituitary gonadal axis.1-3 Thus, greater empha-
* l8 F$ n: F( y( i( O; osis has been given to neuroradiologic imaging in% d1 g2 f# D! D" h
boys with precocious puberty. In addition to viril-+ D) R+ K, ~( e9 Y7 ]9 e2 P+ N% `
ization, the clinical hallmark of CPP is the symmet-
6 V$ M' }$ x8 k3 r: R! j0 k  wrical testicular growth secondary to stimulation by
2 L) M5 A5 r$ F6 a) t3 Sgonadotropins.1,3  E2 o& r- u2 g3 C" p/ T" ?
Gonadotropin-independent peripheral preco-. i- v1 g* @2 h( h
cious puberty in boys also results from inappropriate
3 v% m$ j$ [( Q( F  Zandrogenic stimulation from either endogenous or$ S: R& U7 K0 V  _
exogenous sources, nonpituitary gonadotropin stim-, _7 W3 K. M3 P$ G5 D3 l
ulation, and rare activating mutations.3 Virilizing, e& d- K% d7 H# q+ L! p$ K
congenital adrenal hyperplasia producing excessive
4 m' `: u2 }" \5 Q5 E8 l$ q4 Sadrenal androgens is a common cause of precocious
1 d7 f: A5 |- ~- `& Xpuberty in boys.3,4
- g  d2 ~% G% |* ~The most common form of congenital adrenal; S% k, A2 t8 ^1 T2 Q, N0 W
hyperplasia is the 21-hydroxylase enzyme deficiency.
& W9 q* K" Y. ~The 11-β hydroxylase deficiency may also result in
/ b( U% i2 z% ?  kexcessive adrenal androgen production, and rarely,
# _2 a, D  o7 Ran adrenal tumor may also cause adrenal androgen
6 l: A4 l9 ~+ b# Iexcess.1,3, w. W' V/ g/ B9 m
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 p! V* c- S. U! [, S1 J( B542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 N9 {8 T7 E4 s9 jA unique entity of male-limited gonadotropin-
' N) G3 f1 a7 ?; t: v, Y+ \independent precocious puberty, which is also known
3 \/ k% W  H- ]as testotoxicosis, may cause precocious puberty at a3 h5 }8 n% l* J$ r# p1 p: w
very young age. The physical findings in these boys* g8 s& |: n$ [; R
with this disorder are full pubertal development,
: l- u) h% ?5 e: N# j3 bincluding bilateral testicular growth, similar to boys0 _4 W( t, l9 A5 ?; h" G8 Z9 q
with CPP. The gonadotropin levels in this disorder: `# Y( z* E% D
are suppressed to prepubertal levels and do not show( j) \2 _2 w* |( H( Q* i; j
pubertal response of gonadotropin after gonadotropin-# S* w7 [: f4 n2 K7 m2 h/ A
releasing hormone stimulation. This is a sex-linked
8 K& H7 [5 F: [" Iautosomal dominant disorder that affects only
1 R9 S$ J: a% U6 Pmales; therefore, other male members of the family
& s' D5 F, t9 W- w1 k& kmay have similar precocious puberty.3
& k; _* W# ^; {$ m2 Q5 b2 `In our patient, physical examination was incon-0 h4 v( p& |4 Q* S
sistent with true precocious puberty since his testi-, `; j! X- D; G% G( p  J6 S
cles were prepubertal in size. However, testotoxicosis7 C2 }7 w! d! L2 f. {" D( }
was in the differential diagnosis because his father" M. @- ]+ c' n+ U/ n
started puberty somewhat early, and occasionally,1 s6 u' W; H3 X5 O  q; |/ m
testicular enlargement is not that evident in the
+ e, ?: S7 P" j) T2 R. Ubeginning of this process.1 In the absence of a neg-1 z7 c9 u6 x  [$ _7 S+ i
ative initial history of androgen exposure, our
: F/ \: I2 G5 [biggest concern was virilizing adrenal hyperplasia,+ B, m$ C3 T9 l. F" F+ i! D
either 21-hydroxylase deficiency or 11-β hydroxylase
/ a+ G# I& a& @# Vdeficiency. Those diagnoses were excluded by find-
. K- Q- _) z* k& ping the normal level of adrenal steroids.# U  [6 B. b7 n3 X$ M2 V
The diagnosis of exogenous androgens was strongly1 r1 I( S7 Z; `9 `( c4 F% _" F( Y
suspected in a follow-up visit after 4 months because
: z, b" S; r7 M5 Wthe physical examination revealed the complete disap-) W2 n" j9 I# P' m6 c
pearance of pubic hair, normal growth velocity, and
9 l2 L2 y. @* u' {, H# `decreased erections. The father admitted using a testos-$ F& a% e  `7 H, a8 G
terone gel, which he concealed at first visit. He was
$ s- |* m; N4 _- E$ k3 pusing it rather frequently, twice a day. The Physicians’8 x2 t/ X% Q' \" T/ M4 t
Desk Reference, or package insert of this product, gel or$ V- m  y, X9 `$ D) p7 F) Z/ S
cream, cautions about dermal testosterone transfer to6 T8 I7 ^* g. W: m& ?
unprotected females through direct skin exposure.
( T  f; v/ g0 P" ~! Y; ^Serum testosterone level was found to be 2 times the
) M! K- P0 M3 f0 b4 Mbaseline value in those females who were exposed to
. T7 d, y' j7 ?even 15 minutes of direct skin contact with their male
- C8 o8 i' ^0 `1 Npartners.6 However, when a shirt covered the applica-
. D8 }+ k% d& f3 }tion site, this testosterone transfer was prevented.
( d9 ~* D: b( v1 I! a! YOur patient’s testosterone level was 60 ng/mL,0 Z7 A0 f4 p- [* w
which was clearly high. Some studies suggest that
. `, L/ ?  N& p9 |% [& ndermal conversion of testosterone to dihydrotestos-
+ X; @6 U5 x. m& G0 X% D# @terone, which is a more potent metabolite, is more
/ g- |# ~& U. N6 U7 x3 factive in young children exposed to testosterone
  ]: o1 `9 L+ f; J; @- jexogenously7; however, we did not measure a dihy-
* {, ~9 V; f& Y9 F& U  r" @5 Pdrotestosterone level in our patient. In addition to+ e3 o) `/ m/ q; ]+ f$ W
virilization, exposure to exogenous testosterone in
2 S  A: O- Y0 I/ Z0 U4 ?* Vchildren results in an increase in growth velocity and+ T( [) n* ~* q: o+ d6 f; K! u
advanced bone age, as seen in our patient.
3 G6 |0 ]3 ~! v6 M, AThe long-term effect of androgen exposure during
9 M6 j% i( E( {& g" J4 O$ |early childhood on pubertal development and final
, U4 o, J' ?0 `5 y) Nadult height are not fully known and always remain, y/ D9 w# u6 q7 \
a concern. Children treated with short-term testos-
+ {) O* L$ [2 j% i0 E; Uterone injection or topical androgen may exhibit some
& ^8 a( l( ]* I& H8 n0 W+ Xacceleration of the skeletal maturation; however, after
' J" f  w# Y8 u; q- O: Dcessation of treatment, the rate of bone maturation4 G' s& R! _9 B: a) O3 _7 g3 N8 x
decelerates and gradually returns to normal.8,98 C2 _0 A2 H/ x" {
There are conflicting reports and controversy
: d5 Q: P) H$ D- t2 \1 P" Lover the effect of early androgen exposure on adult' S, w' q/ q; H: B/ h( G/ n
penile length.10,11 Some reports suggest subnormal
2 x% i* h/ |3 P* v8 c: ?8 j! ladult penile length, apparently because of downreg-& T# }' ]9 v) ^' Q: e5 H
ulation of androgen receptor number.10,12 However,
' X: `0 u- G* Q$ I5 MSutherland et al13 did not find a correlation between5 w: g& F1 r4 u+ t* d2 }
childhood testosterone exposure and reduced adult# N$ z; X- n9 U, ^: C; W
penile length in clinical studies.
: e  n, |7 T/ [8 ~$ _Nonetheless, we do not believe our patient is
2 e7 D0 M: u1 p# Kgoing to experience any of the untoward effects from
3 h( p: u) x5 P( u* E- _5 A9 \testosterone exposure as mentioned earlier because
8 W- q* x, L" I5 Ithe exposure was not for a prolonged period of time.
; _: x7 o  `6 e9 C; H0 K- ]Although the bone age was advanced at the time of
) M$ P8 ]" @2 m. |. t+ W2 }& pdiagnosis, the child had a normal growth velocity at) O* t; r( w" _7 C7 S" |- R
the follow-up visit. It is hoped that his final adult, I) m- f* A' k" H
height will not be affected.
8 D* P9 k2 ]( x: OAlthough rarely reported, the widespread avail-
9 z. ^4 r) U& D# Y: B# P* g+ Iability of androgen products in our society may
) t( L) i9 T- H+ B* Z9 h* m. `indeed cause more virilization in male or female
4 I- ^5 ]# k0 b3 uchildren than one would realize. Exposure to andro-
0 h; K  [! x$ E) l8 Y# Xgen products must be considered and specific ques-
. n# ]% W4 v; _1 Rtioning about the use of a testosterone product or  A( I  F# r8 r& |, M$ W
gel should be asked of the family members during& C8 X2 k: k, B- L8 A; I# {
the evaluation of any children who present with vir-
9 `. q% R2 F5 ?" |4 f; milization or peripheral precocious puberty. The diag-
; e; F, O" w$ `$ [: v/ a- gnosis can be established by just a few tests and by
9 I$ s& z+ U( ~5 eappropriate history. The inability to obtain such a
( P' ^, K; f+ K& ]' J& J0 \. Y7 k; c- ehistory, or failure to ask the specific questions, may
; W2 T1 t" ~/ @/ D1 q$ nresult in extensive, unnecessary, and expensive& w" V" g& z1 `
investigation. The primary care physician should be
5 y8 g' O( L# m0 Eaware of this fact, because most of these children: U- W3 n0 z3 l1 H. [6 Y
may initially present in their practice. The Physicians’7 a/ H6 ^7 q! w
Desk Reference and package insert should also put a5 F2 F5 b( s! l/ v) Z
warning about the virilizing effect on a male or
9 _8 D$ z6 `4 j6 U: sfemale child who might come in contact with some-6 W; K9 V, v! L/ T) W- ?
one using any of these products.
3 F3 @  K6 _$ F1 gReferences
# V# W" i1 d1 w) j4 B1. Styne DM. The testes: disorder of sexual differentiation& m/ z; e( Z! o* @- ?
and puberty in the male. In: Sperling MA, ed. Pediatric
' i9 p2 x  ]/ REndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% _* V& a4 E1 o% m2002: 565-628.
5 r9 N& o. `" C) H: c) E2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: t; f% N- b" ^* s+ n
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-4 03:27:02 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
Sexual Precocity in a 16-Month-Old
: p  ~, q$ @! M! A( eBoy Induced by Indirect Topical
; x+ c. G4 {, L5 F7 W) ZExposure to Testosterone
- x- f* B8 t: ]+ \Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: w& I0 K- x) N6 X+ ?: X! Q
and Kenneth R. Rettig, MD1
4 @, _' e7 b' s2 _  {+ iClinical Pediatrics
% B/ q* b0 z" QVolume 46 Number 6
/ ^% B" A9 L/ J( W) O& iJuly 2007 540-543
# ~" _4 B7 H7 _3 p- a- r5 \© 2007 Sage Publications5 d3 F+ X: n; y4 W6 q2 C' q! P0 Y
10.1177/00099228062966512 g, x/ m. ?& {. |
http://clp.sagepub.com2 n9 _, _: C0 r3 }2 M; ]
hosted at
$ I9 b8 `5 z" `" b2 [1 @, y8 Yhttp://online.sagepub.com
: P# g2 i. D9 c( v' U  q5 a8 VPrecocious puberty in boys, central or peripheral," y, [6 Y% K& W8 Z! Z
is a significant concern for physicians. Central
* v8 R1 m% `0 g( J1 ?+ h) ]precocious puberty (CPP), which is mediated
( s: W2 n4 u4 h+ U1 U3 Ithrough the hypothalamic pituitary gonadal axis, has
- F! ^6 X3 V. k! x$ j4 j9 ma higher incidence of organic central nervous system# @) H+ s0 |4 K2 e/ N, N( m8 I
lesions in boys.1,2 Virilization in boys, as manifested
% \+ H( S9 I( j, Mby enlargement of the penis, development of pubic+ p) h8 s3 w' }* i
hair, and facial acne without enlargement of testi-) t$ {( h7 M) K9 h4 g6 `
cles, suggests peripheral or pseudopuberty.1-3 We
, H8 }/ b" A/ x, vreport a 16-month-old boy who presented with the$ [, X! a% F1 @
enlargement of the phallus and pubic hair develop-# a' o/ K2 c2 G4 L  j6 L/ o
ment without testicular enlargement, which was due
: \+ Q6 @( H, u( O5 q% w( Nto the unintentional exposure to androgen gel used by
. I$ F% H0 w# Uthe father. The family initially concealed this infor-
5 e2 K& S: ]5 L4 o4 N1 D9 Kmation, resulting in an extensive work-up for this
) |4 Y+ R; D  k: c7 |- p; w. H3 Gchild. Given the widespread and easy availability of
: v" N2 ^% T$ G( Ytestosterone gel and cream, we believe this is proba-* V7 m5 U7 p, v8 v: V
bly more common than the rare case report in the- G/ i; a% m# ?
literature.4. s. e0 w7 [5 ?5 H8 h, G' ?
Patient Report! G( v/ t" e* v1 p
A 16-month-old white child was referred to the! O4 L- ~' y( o9 R( |9 y0 z, |  Q! E
endocrine clinic by his pediatrician with the concern
9 j) n& ?9 j# ?& pof early sexual development. His mother noticed( F$ Q1 |( z$ H; X2 d$ u# w- O
light colored pubic hair development when he was) N, T9 W; L4 M  G, w
From the 1Division of Pediatric Endocrinology, 2University of) m% h; K& R, H3 z) J' r- [
South Alabama Medical Center, Mobile, Alabama.7 |5 U0 m; N9 J
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* X" x& d; I* [  oProfessor of Pediatrics, University of South Alabama, College of
# P! \& B. @: l* H1 gMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
* X7 J1 Y( k- g' O; A2 ]7 We-mail: [email protected].
' l8 X& n5 @/ Fabout 6 to 7 months old, which progressively became
# @" Y0 n" F. |8 d( G5 t; Qdarker. She was also concerned about the enlarge-
, l( D, U9 E! e4 e2 E1 {% Ament of his penis and frequent erections. The child& U) F9 x1 B: w* F" ?
was the product of a full-term normal delivery, with9 v( b, m) Z/ U) W7 X6 W1 }4 R' `# w
a birth weight of 7 lb 14 oz, and birth length of$ ?1 q; H8 ]9 W$ Z
20 inches. He was breast-fed throughout the first year
2 L) u" y1 Y2 l6 \( ^0 Uof life and was still receiving breast milk along with" k$ k$ A- |! P  e3 H. b
solid food. He had no hospitalizations or surgery,
# s* x8 z0 v: u5 {5 [and his psychosocial and psychomotor development+ ?( {7 |) B9 P2 |$ a- y
was age appropriate." B  |" {: R5 p7 e
The family history was remarkable for the father,
5 l; m% Z7 w6 X! I* v0 `who was diagnosed with hypothyroidism at age 16,& p% p7 i8 N2 q- {4 c/ K
which was treated with thyroxine. The father’s
' {: Q( I! r  K: x2 w/ Lheight was 6 feet, and he went through a somewhat
( p) ^2 l+ j) Z1 learly puberty and had stopped growing by age 14." x. Q) s8 t/ C4 \
The father denied taking any other medication. The$ Z" D( G; ^7 u
child’s mother was in good health. Her menarche
5 }. a: N5 D+ ?# Y4 S) w  v+ Pwas at 11 years of age, and her height was at 5 feet1 F' a7 V$ K3 \
5 inches. There was no other family history of pre-
2 C6 q' U7 b. V# o% e+ G( c; l6 |cocious sexual development in the first-degree rela-
& y6 B' q# {1 Z& M  s% btives. There were no siblings./ G/ Q* ]( N0 V) v% I) D! y
Physical Examination
, q) h; ^& A$ V( L9 zThe physical examination revealed a very active,
+ `& p7 k7 n3 F$ q5 f1 b6 Z1 M0 Oplayful, and healthy boy. The vital signs documented
' J5 N! \& Q* ]" r& Xa blood pressure of 85/50 mm Hg, his length was
' {4 V2 ~3 E- ?* {90 cm (>97th percentile), and his weight was 14.4 kg
9 P8 Y$ a- E( M0 ^6 j+ z: k4 p(also >97th percentile). The observed yearly growth
: [5 |# Q8 C1 I  y1 b! Evelocity was 30 cm (12 inches). The examination of! A: ^  A" n$ j! {; i
the neck revealed no thyroid enlargement.. E$ u$ b% W9 ?* B! N% u5 M
The genitourinary examination was remarkable for" Y9 ?& W: Q' ]/ }7 E
enlargement of the penis, with a stretched length of
+ n1 N1 U- T4 Y( d% P* q( b8 cm and a width of 2 cm. The glans penis was very well
& Z% N7 z  q: X1 p/ ?! Odeveloped. The pubic hair was Tanner II, mostly around
. g7 V% z& _0 t- Y5408 @6 V4 _0 B- T8 G7 X9 V
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 |& F% w5 O6 B7 o: K9 V4 @, z9 g
the base of the phallus and was dark and curled. The2 A/ z- q" k7 D0 u) t; I9 e
testicular volume was prepubertal at 2 mL each., @$ b  i& }) }8 X# L/ N, {
The skin was moist and smooth and somewhat
( }1 W4 r; Z) eoily. No axillary hair was noted. There were no5 S( {) i  @, i0 C/ v5 F
abnormal skin pigmentations or café-au-lait spots.
  g, v# L1 y% I* @, A4 lNeurologic evaluation showed deep tendon reflex 2+! {  O9 C" V( @7 T; O
bilateral and symmetrical. There was no suggestion
% T: B# t' |+ d* A9 j5 Qof papilledema.
# D5 D( g4 B. s3 [6 LLaboratory Evaluation7 |) c. k( e- k" |. P  d$ E
The bone age was consistent with 28 months by0 I+ g3 U* V8 g0 E
using the standard of Greulich and Pyle at a chrono-2 r% x$ J: P4 A7 i$ l3 s5 r  i
logic age of 16 months (advanced).5 Chromosomal4 t/ |& @; ^; z% z; O
karyotype was 46XY. The thyroid function test$ x# a$ m5 u3 a
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
: U  [7 r5 @1 m6 e" q1 blating hormone level was 1.3 µIU/mL (both normal)., J. o; r. |: @  I: Y& Q1 }6 K6 z
The concentrations of serum electrolytes, blood% c! s& A; B$ `4 U4 L
urea nitrogen, creatinine, and calcium all were0 }- w- B  J8 q& U
within normal range for his age. The concentration( ]. X' w1 B; b; j6 p
of serum 17-hydroxyprogesterone was 16 ng/dL* H. I0 e3 {3 t/ ]
(normal, 3 to 90 ng/dL), androstenedione was 20" v) `" e5 q8 Z' n: {  r9 c# E
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-. T4 Q9 C3 y2 `% k$ k
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 o, m8 A9 k+ r  j/ cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ t8 Z% _/ g. @3 ?, |  m49ng/dL), 11-desoxycortisol (specific compound S)
( I4 ?  U/ `& ^; \9 g. ^. ~  ~5 Awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* y% K4 d# C) L  l" Ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 x" u# u: |8 W& M+ K
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 j3 a8 h( v& ]& Cand β-human chorionic gonadotropin was less than
% C8 u7 v5 r4 R- W1 O5 mIU/mL (normal <5 mIU/mL). Serum follicular
# w- b$ c! [4 L. v! hstimulating hormone and leuteinizing hormone, c' F8 _$ v! M; B
concentrations were less than 0.05 mIU/mL1 Y& e" w: z5 I( O
(prepubertal).
9 }' c2 C& O8 S7 N) y# ~The parents were notified about the laboratory2 h) G6 o6 g& C' l  U  z* e) |
results and were informed that all of the tests were2 \9 s8 A7 d0 }4 v9 S1 ~' n
normal except the testosterone level was high. The
1 ]0 {) g* Q7 |, d8 _/ ffollow-up visit was arranged within a few weeks to
8 d# {% O: _7 O, O3 Mobtain testicular and abdominal sonograms; how-
0 s3 M: L# A# t+ ?% k! O; }ever, the family did not return for 4 months.
, \8 Y- }4 V+ g% G5 jPhysical examination at this time revealed that the
; [* V3 }3 f! vchild had grown 2.5 cm in 4 months and had gained
! t# x( U% ~% a+ s/ d5 e2 kg of weight. Physical examination remained. e0 C0 q/ n: n% e1 y
unchanged. Surprisingly, the pubic hair almost com-
$ H$ Y5 W7 @" y; K* E' I8 I# h0 \pletely disappeared except for a few vellous hairs at! t5 @0 w! ^# }4 F
the base of the phallus. Testicular volume was still 2
2 D) ~+ E* u. Q! V( W2 i& ^1 d6 fmL, and the size of the penis remained unchanged., p$ {4 E  e0 d& F
The mother also said that the boy was no longer hav-9 C" H' X5 g8 p) S8 G5 {- t( s& M
ing frequent erections.
. R; ?4 \8 y' H- l8 QBoth parents were again questioned about use of: ^9 T' w$ B5 K9 K2 H
any ointment/creams that they may have applied to
+ \! H" S1 }! l7 M& P9 d6 p0 O' bthe child’s skin. This time the father admitted the
3 {% i' B, I7 R- V, B& mTopical Testosterone Exposure / Bhowmick et al 541
1 M: @& Q( R1 ]( E- [0 k5 Tuse of testosterone gel twice daily that he was apply-
! ?8 M) a- D  g8 C9 E+ Xing over his own shoulders, chest, and back area for# h2 V. w: q7 B" |) y7 {
a year. The father also revealed he was embarrassed, w' N- {& {, o6 t
to disclose that he was using a testosterone gel pre-& n) B' [8 H9 a% o
scribed by his family physician for decreased libido
9 W- O. M9 N' f" Osecondary to depression.
4 @7 |" Q7 \% _: IThe child slept in the same bed with parents.
: E% U5 k* G1 Y+ w" G% \/ fThe father would hug the baby and hold him on his; t& y7 K; j# [7 C' r
chest for a considerable period of time, causing sig-- O; t$ ?& ~) S% y! d. b$ `# O
nificant bare skin contact between baby and father.
. m$ n- u! q3 o' dThe father also admitted that after the phone call,7 x' q/ z: |4 t( P
when he learned the testosterone level in the baby
- s6 u5 m' o0 J; P6 B* Uwas high, he then read the product information/ {6 ?, Q% ~1 n7 X$ ]
packet and concluded that it was most likely the rea-
5 T2 b, w  g$ x. e+ [/ S# l$ V5 ~2 G' _son for the child’s virilization. At that time, they
  M' ~7 n8 R" Y" O& b" Hdecided to put the baby in a separate bed, and the
) W; R9 }2 d5 b+ A4 A9 Z, Z1 efather was not hugging him with bare skin and had+ [( l  T- V; f  `  V
been using protective clothing. A repeat testosterone
% y# j' F6 ?! r2 Q4 u- qtest was ordered, but the family did not go to the& S/ E0 T8 d/ _; z+ n
laboratory to obtain the test.* H  G# }; t0 j7 O: n
Discussion
5 X/ m7 a6 n) G4 t6 lPrecocious puberty in boys is defined as secondary( i4 l: A/ z; k
sexual development before 9 years of age.1,4: _$ U- _" }( Q7 w# D: k# E
Precocious puberty is termed as central (true) when$ s$ l# \: x' ]2 J) T8 a( y
it is caused by the premature activation of hypo-
! t6 N7 ]! W/ `! g# P6 w- Ithalamic pituitary gonadal axis. CPP is more com-
; Z! X0 T+ _$ ~0 G5 R  P+ ymon in girls than in boys.1,3 Most boys with CPP
4 w5 W$ n/ u& tmay have a central nervous system lesion that is9 R+ U5 u8 {5 k  t5 a
responsible for the early activation of the hypothal-5 t9 D" R# W, e1 _1 n5 r
amic pituitary gonadal axis.1-3 Thus, greater empha-6 G4 f0 Q9 x& Q" V4 s. r5 D
sis has been given to neuroradiologic imaging in
2 z1 |& i& a2 v) q: zboys with precocious puberty. In addition to viril-
% @/ j: R- u5 Q5 fization, the clinical hallmark of CPP is the symmet-
6 S" T! ~5 A- }- Y& ?& Urical testicular growth secondary to stimulation by
& s+ b5 K! m6 C0 D( b8 l+ Jgonadotropins.1,3
/ @8 s9 F+ Q) q0 W: }Gonadotropin-independent peripheral preco-
. S0 v$ ?" ]/ t: ecious puberty in boys also results from inappropriate9 R* a$ j2 }  [7 j
androgenic stimulation from either endogenous or6 n" |: K6 d1 P1 v" q
exogenous sources, nonpituitary gonadotropin stim-
0 W, g0 i, p& f+ F; r" ^6 ^ulation, and rare activating mutations.3 Virilizing
& N. \. v4 m( a7 U% w$ h) Kcongenital adrenal hyperplasia producing excessive
4 v& |" o5 `) P5 f4 o( Sadrenal androgens is a common cause of precocious% q- E" [4 y  T" n! ~
puberty in boys.3,4
4 w! M( T4 G; k9 Q2 sThe most common form of congenital adrenal
. ^; x3 j! W3 Q7 ~hyperplasia is the 21-hydroxylase enzyme deficiency., O% O3 o$ L5 x6 N- s% |$ x" r
The 11-β hydroxylase deficiency may also result in8 s4 P) U$ l9 x" w+ t
excessive adrenal androgen production, and rarely,. }3 o4 F$ D* W  A
an adrenal tumor may also cause adrenal androgen! q- V; T2 x3 I6 b4 Z
excess.1,3% ~5 p( u0 J  H9 p5 |2 ~3 o
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ h1 X: i. v3 o1 C) H3 F542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 y; z: P5 |( \* d* o/ P; Q: jA unique entity of male-limited gonadotropin-
+ _7 d4 h5 a* {$ K% d1 Cindependent precocious puberty, which is also known% b  j0 m8 e& }6 f7 H
as testotoxicosis, may cause precocious puberty at a9 C4 T) c  I; |$ U! |6 V
very young age. The physical findings in these boys( o0 W. g. @- G" P+ S
with this disorder are full pubertal development,
+ y# h" D, b+ K, zincluding bilateral testicular growth, similar to boys
% K# F- a  ^- A; [! gwith CPP. The gonadotropin levels in this disorder
+ i- W7 ^. S4 i2 d. U- {- o9 {are suppressed to prepubertal levels and do not show
/ s8 u. T, k% \( L4 [+ Qpubertal response of gonadotropin after gonadotropin-4 x4 K: J- w9 q# K9 d% B
releasing hormone stimulation. This is a sex-linked
- s) g( `' o+ k9 c1 }7 W$ Hautosomal dominant disorder that affects only2 P4 r8 u+ d( F7 o# z& O6 U! c+ t
males; therefore, other male members of the family
- [: y6 Z, |, F9 s* rmay have similar precocious puberty.3" D- z) e. n: D0 h; w( p
In our patient, physical examination was incon-
* G9 a3 Y1 [. K. o$ l6 psistent with true precocious puberty since his testi-
) p- F. q: d3 g) I( C) Kcles were prepubertal in size. However, testotoxicosis" n$ z' a. i6 M/ v; A& [
was in the differential diagnosis because his father
: H; `! |" e6 Z" O0 T  |started puberty somewhat early, and occasionally,3 J% Y2 N- V0 J6 ^
testicular enlargement is not that evident in the
( l. h' K+ }0 y) T2 f0 Y! Ybeginning of this process.1 In the absence of a neg-6 c; W4 @% o' K
ative initial history of androgen exposure, our
: Y  G! ]# H/ b  `9 \0 u5 s6 ybiggest concern was virilizing adrenal hyperplasia,6 l# p4 Z+ C( C% x
either 21-hydroxylase deficiency or 11-β hydroxylase
) I8 x( I, B0 [  sdeficiency. Those diagnoses were excluded by find-' K; p  C6 t- _3 v0 a8 \/ L
ing the normal level of adrenal steroids.
. \- E2 N3 C6 KThe diagnosis of exogenous androgens was strongly
: I# P0 {5 r# Q, B( o& `suspected in a follow-up visit after 4 months because
7 \7 p- @3 M) s# jthe physical examination revealed the complete disap-2 x" h. |2 J' Y+ Z+ L5 |3 s- ]  u
pearance of pubic hair, normal growth velocity, and
" h% Q: m7 z4 M" w) D) D# z. idecreased erections. The father admitted using a testos-. H/ K! V& t2 b3 \
terone gel, which he concealed at first visit. He was
7 a$ b$ C& J% ~; ?- ~using it rather frequently, twice a day. The Physicians’4 G1 L  e( ^% B
Desk Reference, or package insert of this product, gel or6 Z1 b' N5 `: {
cream, cautions about dermal testosterone transfer to
/ d8 x, U5 z0 M5 n/ s' H) \) ounprotected females through direct skin exposure.2 d' `3 v) d5 C# z* R: h
Serum testosterone level was found to be 2 times the! L4 u8 e. W, m# Z$ \; p$ [  ]
baseline value in those females who were exposed to1 |! w2 M& W0 w8 I3 j" |
even 15 minutes of direct skin contact with their male
% ?7 N' }# i; V, ?2 Z/ M; Mpartners.6 However, when a shirt covered the applica-! d9 }, B: d) M. z# {  C
tion site, this testosterone transfer was prevented.8 ?5 m' e1 {3 E
Our patient’s testosterone level was 60 ng/mL,8 i6 ~/ T3 P' |# D4 ?% X
which was clearly high. Some studies suggest that
3 I$ S3 x1 a! ^- edermal conversion of testosterone to dihydrotestos-6 M. h- w- k/ W5 ^
terone, which is a more potent metabolite, is more% }! }' o* t; i' ^, R8 M: e& ^
active in young children exposed to testosterone
( E4 d0 Q- y  p, W6 u8 I& o- aexogenously7; however, we did not measure a dihy-
2 `. E6 d. A8 [0 J7 T6 Jdrotestosterone level in our patient. In addition to
- x, Y1 y# V0 C- ?: Bvirilization, exposure to exogenous testosterone in
; D' B  |0 A! {+ b- u$ r% o# Zchildren results in an increase in growth velocity and" a3 H4 L! z" |# h
advanced bone age, as seen in our patient.
2 k  p# y$ N( dThe long-term effect of androgen exposure during
+ {/ Q* z1 U' p- I' i+ I0 m# {early childhood on pubertal development and final) `& o, t# U& ~, d1 Y5 V- w+ T, u5 [) t
adult height are not fully known and always remain+ C8 h# n% p" m0 w. B' ^  {
a concern. Children treated with short-term testos-9 n: Z7 Z. S" t0 N- }% t: l8 I0 q
terone injection or topical androgen may exhibit some
- Q9 U, Q9 R% V, tacceleration of the skeletal maturation; however, after. n8 x- t6 Q9 E7 }! b+ i8 u
cessation of treatment, the rate of bone maturation
* h+ o$ {. M1 o- Ddecelerates and gradually returns to normal.8,9
. y8 x  B! l; TThere are conflicting reports and controversy
5 s8 K3 V9 }  [' F: hover the effect of early androgen exposure on adult
- S$ C: B8 a% F* m4 d( c* A7 Y' Rpenile length.10,11 Some reports suggest subnormal3 x! G( o" W; A3 }4 D. D* i
adult penile length, apparently because of downreg-
& p( y  n9 S0 W* T. qulation of androgen receptor number.10,12 However,
+ P8 `- n6 x2 J# T' D, tSutherland et al13 did not find a correlation between
' G! J! e3 h: B  T8 wchildhood testosterone exposure and reduced adult
. `. [1 d3 C2 A+ Openile length in clinical studies.
7 z; K9 k: {, }) l& a: p: f  sNonetheless, we do not believe our patient is6 t) f8 L- b9 P" l6 [; k+ f6 K
going to experience any of the untoward effects from
& e+ j, L4 N" G% s# k% Gtestosterone exposure as mentioned earlier because
1 d: P: {: r3 |# P% V& {: Q' Y/ n  [the exposure was not for a prolonged period of time.6 ~' R3 J3 p8 p$ i* @1 z) b( E
Although the bone age was advanced at the time of
# ]5 e  A8 j6 I5 {" X0 Idiagnosis, the child had a normal growth velocity at
7 P8 Q9 m2 U2 B0 k& [! cthe follow-up visit. It is hoped that his final adult% z$ o, `* D, y  ]
height will not be affected.
9 [% u  Y- h, ^) O8 ]( H9 s, bAlthough rarely reported, the widespread avail-
3 f( G/ j  O0 c5 G: p2 q+ Z7 I1 ~1 `ability of androgen products in our society may2 w2 P3 J1 ^! t4 M# t/ E0 l$ j3 _5 G$ v
indeed cause more virilization in male or female( P  C9 B7 w6 G" X  P$ K/ y, h
children than one would realize. Exposure to andro-
- P9 n6 D+ Z6 A& j4 u4 bgen products must be considered and specific ques-. K( d! n, \- k& N6 s0 ]  e3 o
tioning about the use of a testosterone product or
; O0 q! c+ ^0 p( D  y' u: h: @gel should be asked of the family members during
$ Q$ w/ ?; F8 |6 x! ~the evaluation of any children who present with vir-! A; x2 z. v$ l3 N3 }" I1 a% N8 `
ilization or peripheral precocious puberty. The diag-
2 L& C- U+ C7 J) j$ Y6 y4 }nosis can be established by just a few tests and by; P" }( V% O- }/ \
appropriate history. The inability to obtain such a
" P. \5 B1 b: [: S7 Z4 R( }history, or failure to ask the specific questions, may
: T* I0 c7 l4 \1 {+ @! }. G: Iresult in extensive, unnecessary, and expensive
8 k$ o; J+ R' Q5 c% C. Hinvestigation. The primary care physician should be# e' M6 ?8 L2 E% W4 T
aware of this fact, because most of these children* G- q8 ?0 k' _+ M
may initially present in their practice. The Physicians’4 k$ [6 q% e' D- M
Desk Reference and package insert should also put a2 m! f5 x0 _1 i9 K* B
warning about the virilizing effect on a male or
) Z- P% r# A* h) S) F; Efemale child who might come in contact with some-& s" k- N0 s& z3 [! M, U
one using any of these products.
6 {; x# I% F$ ?. r4 a% B0 q) ?. [References" S" b/ I( ~$ J6 y2 X1 g5 Y6 j/ Y
1. Styne DM. The testes: disorder of sexual differentiation0 a5 x5 j' W- H; m) C
and puberty in the male. In: Sperling MA, ed. Pediatric5 k6 x) V, R& b2 U
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 U% {% {& S5 N; m0 R! u- e. t2002: 565-628.
5 g) @7 H1 b, F  h2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" t4 b9 A3 E) \  B5 j. o$ S
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

8 E3 U/ U8 c! u$ R7 h5 @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