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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old
4 h/ L; p: c( q  j* p0 tBoy Induced by Indirect Topical
7 u' W- U  l5 zExposure to Testosterone
0 z/ @  l* H* ]$ TSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: \, B! }* F  I! tand Kenneth R. Rettig, MD1! \/ i  _7 D9 r) o7 n0 S
Clinical Pediatrics
3 `9 R. D  O; YVolume 46 Number 6
. |1 N2 s( G+ A4 M0 b2 wJuly 2007 540-543
8 m4 O4 Z) d" \5 R© 2007 Sage Publications) C: |7 W$ P5 f1 r+ l2 n
10.1177/0009922806296651- M4 Z2 |: c, x0 l% C" N
http://clp.sagepub.com
8 B( I" W/ v/ ~3 Chosted at, H6 ~8 h3 T$ N7 o# t9 G7 l& Y
http://online.sagepub.com. S) J2 Z( E+ i! g8 P5 ^
Precocious puberty in boys, central or peripheral,: y4 u: z$ h" V- a$ U% f
is a significant concern for physicians. Central$ A$ }* L* q0 U1 x3 v+ V
precocious puberty (CPP), which is mediated- p6 T: m: w' T1 T' a/ I, f' O
through the hypothalamic pituitary gonadal axis, has  p, P" Q3 w+ }+ L! o) d
a higher incidence of organic central nervous system7 w. X) H$ p$ S% d% S
lesions in boys.1,2 Virilization in boys, as manifested7 t$ t3 ]9 s( M' L' s$ b5 X# [+ L
by enlargement of the penis, development of pubic
( [8 E! r7 ^. F4 d, Q# ]; Z( d% Fhair, and facial acne without enlargement of testi-6 Y( n3 C. V  Y; p8 U
cles, suggests peripheral or pseudopuberty.1-3 We  F) L) d! v0 P' M3 q
report a 16-month-old boy who presented with the& v7 K* m* d" A/ c  R6 ]
enlargement of the phallus and pubic hair develop-
4 m0 R2 H  R. r9 ]) ^1 H7 N3 ~ment without testicular enlargement, which was due
% ^/ b5 F, U! S3 R/ Kto the unintentional exposure to androgen gel used by8 g# D9 B! ]/ R: V0 m4 B9 m) t
the father. The family initially concealed this infor-
, g3 T, i* B1 V0 \mation, resulting in an extensive work-up for this
# X5 H: z4 ^) K3 o- Ochild. Given the widespread and easy availability of4 i/ x7 N: p# Q8 G+ b% H) r" f
testosterone gel and cream, we believe this is proba-
9 r7 r5 g" |/ p& d; Obly more common than the rare case report in the4 `: s- [7 y; ^, e% T' n
literature.4
0 D" ?! @4 k4 v  HPatient Report
1 A9 Q8 V- ~7 \A 16-month-old white child was referred to the& H" c, X9 }/ u2 ?9 q- ~' ?
endocrine clinic by his pediatrician with the concern
2 y7 t3 \! W5 P4 x, V! uof early sexual development. His mother noticed' P8 j# l2 V3 C4 A
light colored pubic hair development when he was
) N; @" |6 B- {# h- }3 }! RFrom the 1Division of Pediatric Endocrinology, 2University of7 W4 P: U* ~. i+ F1 o" Z
South Alabama Medical Center, Mobile, Alabama.( b8 e5 K/ ?+ R+ C2 }
Address correspondence to: Samar K. Bhowmick, MD, FACE,; s  J! z: u/ ]
Professor of Pediatrics, University of South Alabama, College of6 c1 C. e4 ]# ?5 H7 u! ]) f- K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 b; l9 m# Q/ ee-mail: [email protected].
$ O) x( C. n# E& O: U% ?0 babout 6 to 7 months old, which progressively became# p( T7 G6 ~* ^
darker. She was also concerned about the enlarge-: M. j" ?  Y; y
ment of his penis and frequent erections. The child  P: ~( U* |2 R4 x
was the product of a full-term normal delivery, with( X: _1 j" K  y+ R4 u, E: t
a birth weight of 7 lb 14 oz, and birth length of$ k! M( o6 K% V, C
20 inches. He was breast-fed throughout the first year, Y: ^5 `( X: b( ^, |$ }
of life and was still receiving breast milk along with* l7 u% O- d3 {! u* G
solid food. He had no hospitalizations or surgery,
% u4 U3 R9 i6 `( Zand his psychosocial and psychomotor development+ R6 V! j; M7 E. s
was age appropriate.
% S0 E% ?" a( Q) M: t9 l( uThe family history was remarkable for the father,9 S- S5 ~5 p! }5 W' j
who was diagnosed with hypothyroidism at age 16,
+ l% R5 U: b# _+ Lwhich was treated with thyroxine. The father’s4 r- e& o7 m3 i; f) {! o. s- W
height was 6 feet, and he went through a somewhat8 t1 Y6 t# _; \3 }& x3 i  c# L
early puberty and had stopped growing by age 14.3 O" a# B0 ]9 ?' G
The father denied taking any other medication. The  q5 m9 j' f1 n% `5 Y
child’s mother was in good health. Her menarche$ N+ ~9 ^. K6 Y
was at 11 years of age, and her height was at 5 feet
$ e9 S( V( n0 t4 S/ a: O( |% n5 inches. There was no other family history of pre-% ]/ Y6 @, r- }* N8 E
cocious sexual development in the first-degree rela-' D: x& \/ d2 m
tives. There were no siblings.
' W5 F/ @! Y" E9 fPhysical Examination/ N8 ^* i+ u: ~9 D2 l
The physical examination revealed a very active,
; Q$ e2 y7 ~: F1 |* dplayful, and healthy boy. The vital signs documented+ j7 ]1 y2 ?7 B6 r& z
a blood pressure of 85/50 mm Hg, his length was( V- I) F2 F2 V0 o& H8 b4 K
90 cm (>97th percentile), and his weight was 14.4 kg8 A! W+ L8 F8 s) V
(also >97th percentile). The observed yearly growth
% x6 Q9 a" l( Svelocity was 30 cm (12 inches). The examination of. ^# |5 z/ x) j+ Z, H) K
the neck revealed no thyroid enlargement.# [, g0 A% l( R: C
The genitourinary examination was remarkable for
4 m' n' ^" l- g8 d' w& `enlargement of the penis, with a stretched length of
6 E) X. c1 D: H5 @8 {8 cm and a width of 2 cm. The glans penis was very well
. V. ^6 z0 f& I* ndeveloped. The pubic hair was Tanner II, mostly around; Y+ y7 W4 R8 @' f# M
540
/ p6 |  |) L/ L  n( i7 E% J! y# Zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  r( Z  _3 r  J. n% J* r
the base of the phallus and was dark and curled. The
4 k4 Z: i3 H" _0 Atesticular volume was prepubertal at 2 mL each.
4 {2 b: S( c  z# N1 FThe skin was moist and smooth and somewhat" }$ f) f: ?/ B/ E
oily. No axillary hair was noted. There were no" H3 }$ c6 B2 f) N8 `& H8 r- B! }
abnormal skin pigmentations or café-au-lait spots.
4 W2 N; K- n- ]Neurologic evaluation showed deep tendon reflex 2+  U, r8 R( |# T
bilateral and symmetrical. There was no suggestion* P& N5 O# y1 e! Y! w' ?1 d; L
of papilledema.% |. u2 P7 n2 h. C* i
Laboratory Evaluation
& M3 R, z1 Q' L" t8 SThe bone age was consistent with 28 months by3 e5 y. P9 S0 |3 k
using the standard of Greulich and Pyle at a chrono-
3 Q# ~/ W0 k" ^9 qlogic age of 16 months (advanced).5 Chromosomal. K- l+ ~: z; Q2 i+ t
karyotype was 46XY. The thyroid function test9 q( a* C" U% S" n
showed a free T4 of 1.69 ng/dL, and thyroid stimu-+ ]/ q# c, a* j" m3 }
lating hormone level was 1.3 µIU/mL (both normal).* j5 [9 t! W9 `
The concentrations of serum electrolytes, blood- q) O; c3 ?! L8 b5 `. q  S4 L# ^
urea nitrogen, creatinine, and calcium all were0 d4 m3 j/ O8 q* k  @: {
within normal range for his age. The concentration, z2 d- y; h/ H6 x% g+ d
of serum 17-hydroxyprogesterone was 16 ng/dL
) z5 u) P) Q0 b2 p(normal, 3 to 90 ng/dL), androstenedione was 20
, d+ S/ ~% Q: y* J# _' }2 L# W; b+ hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) }/ Z5 g1 C) ]( Y  ]" }
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 o% u) N! o$ X0 Ddesoxycorticosterone was 4.3 ng/dL (normal, 7 to2 T  z2 F; I& |, y8 R# J
49ng/dL), 11-desoxycortisol (specific compound S)
7 u0 I; P% N1 m& k$ R2 x  Z5 t7 `was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 ]. C0 ~# |7 [4 d9 g, W* K
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 h% z: R. M& P/ \1 ptestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 S8 F( e# x" H) p: Q. Oand β-human chorionic gonadotropin was less than
; {$ o. `9 Y' g5 mIU/mL (normal <5 mIU/mL). Serum follicular. u) g/ v- B) t, Z
stimulating hormone and leuteinizing hormone( g" _, m- B, W' }0 P5 ^4 G
concentrations were less than 0.05 mIU/mL# h4 m9 K& o8 ?
(prepubertal).
. E; ?- u! k0 _7 V) r9 [The parents were notified about the laboratory
/ _! B' u3 a7 X- Z9 R3 R: E$ ~4 Yresults and were informed that all of the tests were
" m+ Z( @1 C8 H# B5 G9 @normal except the testosterone level was high. The
+ t4 g! H- r6 q6 C. D$ ifollow-up visit was arranged within a few weeks to
" g7 Q% r4 s( X: Pobtain testicular and abdominal sonograms; how-9 v1 p2 C# a7 G
ever, the family did not return for 4 months.' ]" l6 O: `' |6 S* a+ g6 \( L
Physical examination at this time revealed that the2 N/ y3 c/ W: _* u* J( w3 E. ]
child had grown 2.5 cm in 4 months and had gained
4 ]( V+ ^0 s- o/ `( |2 kg of weight. Physical examination remained, m) d4 u2 k0 a3 q
unchanged. Surprisingly, the pubic hair almost com-
% R1 T, v% b: n1 J0 C2 }7 X! Bpletely disappeared except for a few vellous hairs at5 y2 d6 @2 U# ~+ h9 O4 _* k
the base of the phallus. Testicular volume was still 2
, @7 Q0 ~" [) A: a/ r. GmL, and the size of the penis remained unchanged.& Y4 O- h7 h1 `- s
The mother also said that the boy was no longer hav-
+ \: y+ i% [" ]2 }3 ring frequent erections.
! i7 C3 }  C- G: T+ tBoth parents were again questioned about use of
! r; u$ M# P8 Cany ointment/creams that they may have applied to
+ t7 r& G3 A, _/ }* q" x  Sthe child’s skin. This time the father admitted the
9 h1 z$ d5 b3 B3 Q: ]Topical Testosterone Exposure / Bhowmick et al 541
( \- A  a: d4 V: j' ause of testosterone gel twice daily that he was apply-
  P" D( m/ K" _. `1 a$ s. ring over his own shoulders, chest, and back area for
' p: B% S5 \0 _9 y  `+ Ja year. The father also revealed he was embarrassed
- p) S: X/ F' m  W1 p4 @to disclose that he was using a testosterone gel pre-
5 H, G# c6 c$ c/ C( h& cscribed by his family physician for decreased libido/ B) r0 R0 n9 Z8 ~: P8 M! W9 o5 C1 v
secondary to depression.( V4 R+ d' e  v
The child slept in the same bed with parents.
1 H; ]0 [& z0 hThe father would hug the baby and hold him on his- I( x9 p, V. `: H& A6 p+ ~8 a7 `
chest for a considerable period of time, causing sig-
6 y: w+ Q& ^, u/ [" pnificant bare skin contact between baby and father.
2 \# @* t3 T" z- a1 ^The father also admitted that after the phone call,; g% s  T2 ], v$ G
when he learned the testosterone level in the baby
4 W( N9 L) m, y5 n! z0 H7 Zwas high, he then read the product information
5 d. z* x1 x. e! g0 U# Rpacket and concluded that it was most likely the rea-
/ W$ l' d8 Q. E5 V" Z, pson for the child’s virilization. At that time, they
& y5 ~! @( @! _, s7 O8 r4 {decided to put the baby in a separate bed, and the* a# i. s; i9 g$ r% n+ b2 \
father was not hugging him with bare skin and had
( P& \; D8 |$ y) K& h" i2 @been using protective clothing. A repeat testosterone7 W4 W8 k9 [) I5 c& w, M
test was ordered, but the family did not go to the
( D, e  [6 \- b# [% l& V4 Alaboratory to obtain the test./ d% E0 a) s6 _
Discussion
  F; C1 V5 p$ t5 G" aPrecocious puberty in boys is defined as secondary
& B% @# |" S/ Esexual development before 9 years of age.1,45 X0 v1 d4 @5 L; T2 ?5 A- d
Precocious puberty is termed as central (true) when9 `* l7 p& _- x  l& w6 C  P
it is caused by the premature activation of hypo-
/ W" L  l+ S" x3 Fthalamic pituitary gonadal axis. CPP is more com-& q& t8 Q# u8 L* l& c" C1 K
mon in girls than in boys.1,3 Most boys with CPP
6 N; Q" D. P( C7 k& @/ Hmay have a central nervous system lesion that is
$ o9 K6 J0 _7 C3 M2 ]3 F0 T: Cresponsible for the early activation of the hypothal-$ P7 o. L* N( ~9 A, L: q1 \
amic pituitary gonadal axis.1-3 Thus, greater empha-- {( k7 V# b! D: I/ t: e
sis has been given to neuroradiologic imaging in  ?) ?, Y* c7 G: y* E3 G4 {
boys with precocious puberty. In addition to viril-
8 |3 T  X4 M$ Q5 F) p- B7 Wization, the clinical hallmark of CPP is the symmet-
# A# C6 ^1 t5 e6 B, M! brical testicular growth secondary to stimulation by
( p0 m( A9 J, V: ~6 Pgonadotropins.1,3+ r4 F, k$ q1 s+ t2 y( i
Gonadotropin-independent peripheral preco-! v& k$ ]# J' T6 K
cious puberty in boys also results from inappropriate
! B7 e# ~* {8 A3 r' Candrogenic stimulation from either endogenous or
& e/ Z$ y8 V" Q+ `  jexogenous sources, nonpituitary gonadotropin stim-6 C% J& A: h3 N, d/ D3 j+ m
ulation, and rare activating mutations.3 Virilizing# {- a  E/ P( S# @* B, U$ @# H* L2 o
congenital adrenal hyperplasia producing excessive" ~# z9 F% }, n. u$ T) H
adrenal androgens is a common cause of precocious* G* C3 Y( X0 ~4 q6 [! X3 B1 L( `
puberty in boys.3,4
# i% u, m0 [+ C2 P3 A! [The most common form of congenital adrenal
2 d0 R) c, v1 _7 x$ Shyperplasia is the 21-hydroxylase enzyme deficiency.! E2 w# g: m9 D; O2 p. z
The 11-β hydroxylase deficiency may also result in
/ l. P8 h9 e' S" Y* V) p/ W  t/ Mexcessive adrenal androgen production, and rarely,+ N" \, }9 X# a' c* D4 j. h+ v
an adrenal tumor may also cause adrenal androgen
) f; u4 O# a  {  w. ?excess.1,3& m- N+ n+ U& z  F5 j# O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; L! x* E; C, L: R$ b( F  O/ _
542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 X) Q! d$ q% `/ L' t
A unique entity of male-limited gonadotropin-
5 v9 A2 G. |  zindependent precocious puberty, which is also known6 {5 ]% ^; u5 }) u2 _0 u( h$ M
as testotoxicosis, may cause precocious puberty at a
! C% \4 U+ D+ q; K* Kvery young age. The physical findings in these boys2 h- y! ?. w$ k
with this disorder are full pubertal development,$ }- t7 I- `8 Q* t6 I4 R9 Y, ]
including bilateral testicular growth, similar to boys
' g1 R. T! a1 fwith CPP. The gonadotropin levels in this disorder
8 J/ o% h. Q4 A) Y2 W; P" Mare suppressed to prepubertal levels and do not show6 E5 M( |: o4 H9 b: k: V1 j
pubertal response of gonadotropin after gonadotropin-
1 W/ o9 ?6 q9 P4 `releasing hormone stimulation. This is a sex-linked3 y3 t2 t/ X2 w- }* o9 r( w, g
autosomal dominant disorder that affects only
, ^6 F: G( r- u0 B* ~males; therefore, other male members of the family
1 e: ^5 }' y8 ]: Z/ i7 L9 a1 X  \* T9 \may have similar precocious puberty.3" t8 B* _. i' e5 N! H% Q
In our patient, physical examination was incon-  a* t* x5 |, y" |
sistent with true precocious puberty since his testi-
: e  r3 |* t" n/ K7 S( Kcles were prepubertal in size. However, testotoxicosis
$ l" m! Q  _; T2 e0 O. i5 t. jwas in the differential diagnosis because his father
+ i+ F4 u7 Z) gstarted puberty somewhat early, and occasionally,
5 }4 t& m0 G1 i+ A' h4 Y/ g) ~testicular enlargement is not that evident in the$ m. z/ [1 b) ~7 [- R5 ]& D- F2 f
beginning of this process.1 In the absence of a neg-0 G3 o( g( {7 h5 a
ative initial history of androgen exposure, our) G  w, g' u  _/ m# N& d: J5 d5 ^
biggest concern was virilizing adrenal hyperplasia,
$ ], v0 h/ `' `& A: neither 21-hydroxylase deficiency or 11-β hydroxylase* B( Y1 ]  P- N  s8 A# D( X: E) y
deficiency. Those diagnoses were excluded by find-; u6 V" Q. [4 N6 C
ing the normal level of adrenal steroids.
( z' r) B3 ?5 y0 L6 L( CThe diagnosis of exogenous androgens was strongly$ g) v/ m' _- F
suspected in a follow-up visit after 4 months because
9 H$ M7 ~. c' r0 p) a8 S4 Mthe physical examination revealed the complete disap-$ R( f) d5 P3 g1 C) X$ n9 K
pearance of pubic hair, normal growth velocity, and
% ]1 o0 a6 W' H& H& rdecreased erections. The father admitted using a testos-
* z* }# s) I1 n. yterone gel, which he concealed at first visit. He was0 l' ?+ y3 l8 v( n7 C4 g8 }
using it rather frequently, twice a day. The Physicians’! D$ ~1 s3 L+ ?0 Q/ @# [, |
Desk Reference, or package insert of this product, gel or- ^4 E5 a* W  E* J) W
cream, cautions about dermal testosterone transfer to( f( w* x9 G. t, Q1 X3 r! J
unprotected females through direct skin exposure.  E+ D0 b7 I* `' L3 D" G9 C, E
Serum testosterone level was found to be 2 times the
( [1 R, B3 D2 A1 \7 ~baseline value in those females who were exposed to7 M% a9 z7 O; y# _4 e
even 15 minutes of direct skin contact with their male
0 q$ o8 i4 D8 |partners.6 However, when a shirt covered the applica-: q' m) ^% Y5 l1 Q* T) n$ F: N* d
tion site, this testosterone transfer was prevented.
4 F! a3 u4 D) j. K3 S+ ~! {Our patient’s testosterone level was 60 ng/mL,
% H  g/ o3 S+ a6 n4 \& Awhich was clearly high. Some studies suggest that
6 ]' c! P6 M6 }! Pdermal conversion of testosterone to dihydrotestos-
# w9 N! w5 M2 F  Z. d7 ]terone, which is a more potent metabolite, is more
" F0 @# w: a2 [+ o# j4 l! p( hactive in young children exposed to testosterone" F& o) O3 S  o! l) G$ W
exogenously7; however, we did not measure a dihy-7 L3 A9 c8 \  o  P7 j
drotestosterone level in our patient. In addition to* W  T3 O2 Z, ^# R% F
virilization, exposure to exogenous testosterone in
1 c' o" Y. W8 {children results in an increase in growth velocity and
9 s9 h4 y! A) y- k) Sadvanced bone age, as seen in our patient.. s9 ]8 |7 x1 i# ?
The long-term effect of androgen exposure during
. V6 V4 y: h4 j% ~+ ?" E2 s' J, Vearly childhood on pubertal development and final
( t( c5 I9 i$ A% O3 S( zadult height are not fully known and always remain
) K: U' T1 W9 v, |6 Ba concern. Children treated with short-term testos-0 P' b+ j$ e! P" Z5 e6 ?
terone injection or topical androgen may exhibit some
  W7 B% \- H8 N" }acceleration of the skeletal maturation; however, after
2 c8 V# |# S. K& ^+ Q6 \# acessation of treatment, the rate of bone maturation- E* g/ h7 D# a5 A, v6 i/ g
decelerates and gradually returns to normal.8,9
/ W" z6 o5 I7 }- _7 LThere are conflicting reports and controversy6 h+ n6 Z! ?2 F- s9 Z- W( `
over the effect of early androgen exposure on adult
9 p1 Q& K" R' W+ \penile length.10,11 Some reports suggest subnormal
4 X4 }* |6 H1 q/ W8 Cadult penile length, apparently because of downreg-
' q( @- D' J) K+ c4 r; rulation of androgen receptor number.10,12 However,
  c8 q5 D( j0 R9 S7 r# NSutherland et al13 did not find a correlation between
; C: [; [* |" A+ zchildhood testosterone exposure and reduced adult2 Z  K  j9 P3 X& ?: t0 A2 E
penile length in clinical studies.0 e5 E. t+ `7 }0 d, \2 s2 z
Nonetheless, we do not believe our patient is
1 V, f1 s" i2 m/ k' Ogoing to experience any of the untoward effects from) B& Y. S; u3 Q( ~; ]: B
testosterone exposure as mentioned earlier because" f0 |/ C! h) w- h/ }
the exposure was not for a prolonged period of time.
3 V! `$ T; n1 a9 r9 wAlthough the bone age was advanced at the time of( R  F7 b' I- E8 h, P* ]7 t
diagnosis, the child had a normal growth velocity at
2 ?5 n: f0 G8 `5 lthe follow-up visit. It is hoped that his final adult
2 s  [9 \0 X* {5 E9 ~" s2 Eheight will not be affected.
; t# G, E- O" n" S; zAlthough rarely reported, the widespread avail-% e  B  H: m2 h9 ]/ [* y& P
ability of androgen products in our society may; |+ w$ o' @* P' {$ {% I3 h1 ^
indeed cause more virilization in male or female
8 G7 V/ A9 O, c+ Z. X3 rchildren than one would realize. Exposure to andro-
5 F* m9 S' E' d0 m8 P  t3 N3 Ggen products must be considered and specific ques-
+ b  u3 @* z% Y5 L* C2 D; b4 vtioning about the use of a testosterone product or2 [  {0 `  _2 A0 L% K! l3 a
gel should be asked of the family members during0 W: |7 g, m6 a! m: o
the evaluation of any children who present with vir-- z1 k1 [( U1 U# c9 h: l( I
ilization or peripheral precocious puberty. The diag-! d. Z" v6 @  U' T7 u# ~2 t
nosis can be established by just a few tests and by
/ R) B# z2 R- ]; l8 F- ~3 s" Pappropriate history. The inability to obtain such a& `+ m- |7 z/ ^: ^7 F9 a
history, or failure to ask the specific questions, may0 ~8 [/ y9 s; @/ Q! @1 t3 t
result in extensive, unnecessary, and expensive- j6 |- N. P) o: ^
investigation. The primary care physician should be3 e' K9 Y% A7 q" o
aware of this fact, because most of these children
/ @. I9 M* @1 amay initially present in their practice. The Physicians’$ e9 q; ~1 T# ?5 E
Desk Reference and package insert should also put a. {8 c2 K* A# R/ A4 w
warning about the virilizing effect on a male or
  e, |! |4 p6 B6 xfemale child who might come in contact with some-+ U; Q" F+ R& W  Z' U
one using any of these products.
% P# }$ S0 ]) z0 a+ |$ s/ \References. k! k- ~8 ?6 t% c. h$ j3 R) M' ]
1. Styne DM. The testes: disorder of sexual differentiation% Q9 G2 E* A- T$ k- f1 c' }
and puberty in the male. In: Sperling MA, ed. Pediatric, N# C& G! R  @, h0 I
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;; E% b8 j5 n( V3 [4 C2 h; Q6 ^" Z
2002: 565-628.0 r/ U* P, v2 c; U; Q- s
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ D! @; @( s$ U- w. W/ v6 x7 {puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
9 c# q2 ]: I# @: c+ ?  IBoy Induced by Indirect Topical" w3 O% o" {5 m
Exposure to Testosterone
. O9 U) Q3 P3 C! m. N& |( _! }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,20 K+ a7 g9 x% C: a) v  b
and Kenneth R. Rettig, MD1" h7 E3 H. v! M- O% j+ b
Clinical Pediatrics
+ k+ f  k" z5 v9 jVolume 46 Number 6
8 D7 X" B  y$ X9 w5 b1 nJuly 2007 540-543( L& U' U! E8 p$ |" a8 U. `
© 2007 Sage Publications+ |- r/ q! j" g" |; \, N
10.1177/0009922806296651" K: w8 a7 ~' a- M5 f( y2 U( r
http://clp.sagepub.com
% ~9 ~- h2 m+ V  \- Lhosted at
- E. J1 q$ Q" V/ I& }2 Thttp://online.sagepub.com
8 u& x3 R' M0 R! @0 x$ VPrecocious puberty in boys, central or peripheral,
9 _: g( t0 x9 g4 {- ?. x% P! ~is a significant concern for physicians. Central! [  k5 L& E- r" m. @6 n
precocious puberty (CPP), which is mediated% }3 l  h' `9 e- M  \- u1 W& c' v; z
through the hypothalamic pituitary gonadal axis, has8 w5 n- s7 a9 X' |# n+ s3 {
a higher incidence of organic central nervous system# C4 K' x' i. g. f! N
lesions in boys.1,2 Virilization in boys, as manifested
( A- P. n! n; j+ b& `by enlargement of the penis, development of pubic
9 f1 a: O& z' Q" y; ?  u1 I" chair, and facial acne without enlargement of testi-  L+ {1 v. Y% w9 A. J# a, F) e
cles, suggests peripheral or pseudopuberty.1-3 We
4 [0 i# a8 x6 t5 n3 M" breport a 16-month-old boy who presented with the7 Z) B4 _# I$ N$ v8 z, M  Y
enlargement of the phallus and pubic hair develop-
3 i  v& h' K2 B" L' iment without testicular enlargement, which was due4 e& T; M; z& [: M- `
to the unintentional exposure to androgen gel used by
9 U) `: q2 ?! D; |* ~: n  F- f7 I+ jthe father. The family initially concealed this infor-
9 N/ f  J; Q, Q$ [5 \mation, resulting in an extensive work-up for this
" U% U) b" M9 r$ u0 `0 xchild. Given the widespread and easy availability of
! H" B8 Q- r5 Htestosterone gel and cream, we believe this is proba-
0 b* V, @& l8 hbly more common than the rare case report in the7 v5 b% [6 x* x' g. F6 J, u
literature.4
, g" b3 T4 b+ b' g, D% f7 r0 FPatient Report3 d" C' e8 |# O
A 16-month-old white child was referred to the
& C( f3 L$ B( n$ v# Uendocrine clinic by his pediatrician with the concern
& x" p& c, l& n4 o& H! I% j/ |of early sexual development. His mother noticed
! _! _! a+ C/ m* y5 C! Qlight colored pubic hair development when he was
9 v0 h$ V- h6 N. F' \! zFrom the 1Division of Pediatric Endocrinology, 2University of- v- h$ l& r6 G9 W0 y
South Alabama Medical Center, Mobile, Alabama.4 C8 [0 j. d- A  d
Address correspondence to: Samar K. Bhowmick, MD, FACE,
' x0 h( o8 K# V( zProfessor of Pediatrics, University of South Alabama, College of
! m: c1 a% s- p+ P& ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ z: c  G% f( Z/ Oe-mail: [email protected].0 ~& o3 V6 l1 Q1 I% F9 d- _$ N: v
about 6 to 7 months old, which progressively became
$ z" o  I0 Z$ ?# n& U( K9 j, E2 _% x. ?darker. She was also concerned about the enlarge-3 I7 z) ?% l+ n/ \4 t6 w7 E
ment of his penis and frequent erections. The child3 ]* ^- n  @: g5 m* x
was the product of a full-term normal delivery, with/ L# t: l; E' N, [. {9 C
a birth weight of 7 lb 14 oz, and birth length of
! u6 s/ w0 N- }20 inches. He was breast-fed throughout the first year- }5 g% Z' s9 L2 w, D2 ^
of life and was still receiving breast milk along with
: z5 d. s+ ^6 {! r! `4 Xsolid food. He had no hospitalizations or surgery,+ v) K9 y8 v/ e/ c  r
and his psychosocial and psychomotor development
9 y% z8 t# O* W: F- uwas age appropriate.
7 T: I6 ?7 X/ g" I, b$ e! ZThe family history was remarkable for the father,
4 p7 o- N8 {5 D7 `0 C! \& Nwho was diagnosed with hypothyroidism at age 16,
4 @/ v( a) s3 a" ~, Bwhich was treated with thyroxine. The father’s
) M! N; j( X& s* {# c6 `# {# ?height was 6 feet, and he went through a somewhat: u6 ], W' ]6 [1 E. q& o
early puberty and had stopped growing by age 14.
3 B( |3 a; [, d/ v; W& _4 j- QThe father denied taking any other medication. The
1 c; T7 t& e7 L  }child’s mother was in good health. Her menarche1 R. z9 b; Z4 \
was at 11 years of age, and her height was at 5 feet+ c. c  m6 W9 Z' ]4 @
5 inches. There was no other family history of pre-
" e* }% W6 x4 t) C, ncocious sexual development in the first-degree rela-
  V  x6 D9 u$ D' I6 _, i, ?  Itives. There were no siblings.5 m9 `+ q/ {7 z8 _( c
Physical Examination+ f4 U# }9 V& R0 ~4 r
The physical examination revealed a very active,
8 Q' n+ f0 v/ C4 r$ }' V% tplayful, and healthy boy. The vital signs documented8 P2 a  F- `, \) W
a blood pressure of 85/50 mm Hg, his length was
8 H6 t' @% K; G( t" Y6 f0 a3 R% o90 cm (>97th percentile), and his weight was 14.4 kg
8 P) C8 P" e6 Y0 U/ L/ D(also >97th percentile). The observed yearly growth
7 S0 B$ x" k2 ~: ]velocity was 30 cm (12 inches). The examination of
9 u' ]% n- n% z; U8 i* {the neck revealed no thyroid enlargement.  `$ r. e! S/ ~  l: @! D) f+ O
The genitourinary examination was remarkable for+ M/ l0 B6 S. `5 u$ g5 ?( g
enlargement of the penis, with a stretched length of1 g& z/ m) @: H3 Y9 f$ Q
8 cm and a width of 2 cm. The glans penis was very well1 S3 c) W1 K0 c, P$ g( f9 k/ V1 x* v
developed. The pubic hair was Tanner II, mostly around
6 q. d5 n3 O( C6 h; S540
% p7 p6 r. t( R" \. g5 d+ K; y: Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ J! F% H2 B& E: S! T9 ]2 z  j: u1 Sthe base of the phallus and was dark and curled. The
9 B( h) d: |: u/ F0 ]testicular volume was prepubertal at 2 mL each.
, s* I9 a9 M. C0 ?% @% cThe skin was moist and smooth and somewhat
; W+ F% }$ E7 k$ m0 _3 woily. No axillary hair was noted. There were no
8 p6 e0 ?, I) ~6 Y. Rabnormal skin pigmentations or café-au-lait spots.% O* C$ p2 I& j0 U6 S
Neurologic evaluation showed deep tendon reflex 2+5 S! s  e. e; @+ ]% {, I2 ]$ T2 j& v
bilateral and symmetrical. There was no suggestion
. X, ^' P& Y. W; ]of papilledema.
" \' s7 T: c! ~( k% p, l2 y5 V2 GLaboratory Evaluation
! h6 Z" {5 q% {The bone age was consistent with 28 months by$ u- b3 J8 L- n+ B8 U9 F; C3 A
using the standard of Greulich and Pyle at a chrono-. \" b& y* c; V7 k# ?" {  O
logic age of 16 months (advanced).5 Chromosomal
* l+ A! r7 }. n  T% gkaryotype was 46XY. The thyroid function test$ k! o2 |% m" \5 Q, t- O
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
) n* {! L0 X. q4 p* Nlating hormone level was 1.3 µIU/mL (both normal)./ t: L5 w- y6 n* G' n
The concentrations of serum electrolytes, blood
3 g5 L/ N* X7 }urea nitrogen, creatinine, and calcium all were
# u4 c& V4 I! ?; ^% rwithin normal range for his age. The concentration
. a/ M% n* ?/ g5 h: `" ]- Lof serum 17-hydroxyprogesterone was 16 ng/dL5 s/ _/ A. L& u, h$ \- ^  T
(normal, 3 to 90 ng/dL), androstenedione was 202 S) @0 {6 P/ M' d; S( ?
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 d8 B$ F- `; g# O* l2 Xterone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ C8 E4 q  v& p  b6 K" ]. {desoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ U) g- s4 S/ l- C" u$ A49ng/dL), 11-desoxycortisol (specific compound S)+ g6 d/ V* O9 L. Y7 j( z
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: [8 P- \  a7 w, n& T: R4 @
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total3 ?- M* `4 |1 _8 \  h8 G* c/ @6 _
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 u8 c  _9 n. o& V8 }
and β-human chorionic gonadotropin was less than& |/ h4 O. p5 h  L  [3 O
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 r3 k9 E$ Z! n8 s( Rstimulating hormone and leuteinizing hormone. W5 N* ]* W# j/ Z4 {. x- o7 c
concentrations were less than 0.05 mIU/mL/ h) b* ?3 w+ q/ C! X. G5 s) D
(prepubertal).7 n  W& ^, s! i9 q, }+ }9 h
The parents were notified about the laboratory3 R7 k$ \4 V" H2 s6 a+ o+ W
results and were informed that all of the tests were
. x6 i+ C8 l& ]  L) L" t# @normal except the testosterone level was high. The' }- }' R! ~6 t- W
follow-up visit was arranged within a few weeks to( |8 @# r0 k) {( N& @% N; g
obtain testicular and abdominal sonograms; how-* R5 Y, [& g1 ^
ever, the family did not return for 4 months.
* S- j/ ^+ W" }5 {Physical examination at this time revealed that the
& y* |' a' p/ y. [- Uchild had grown 2.5 cm in 4 months and had gained- k5 x! R4 u2 Z7 f2 ~
2 kg of weight. Physical examination remained
4 c5 U2 Q& d/ |8 f0 Y4 e. B* Zunchanged. Surprisingly, the pubic hair almost com-, l( s% p' ^/ e/ I" p- D
pletely disappeared except for a few vellous hairs at7 E9 Q0 E" `( k: J8 Z8 h; y8 F% z* y
the base of the phallus. Testicular volume was still 2. s: O# p% S2 e0 R5 @
mL, and the size of the penis remained unchanged.. h6 f! m" }( C; R8 |+ E
The mother also said that the boy was no longer hav-% `: f- y( S4 z! O! h. _6 n
ing frequent erections.( E! R! i3 D1 x2 F
Both parents were again questioned about use of% G  t4 i& f- B1 w% f, @( I
any ointment/creams that they may have applied to
; ]$ d) Q5 G, @! a' B1 {$ z0 m7 f, Sthe child’s skin. This time the father admitted the
! [# O! y! ~) {  }Topical Testosterone Exposure / Bhowmick et al 541
4 S9 p9 j* l4 juse of testosterone gel twice daily that he was apply-
0 j/ g( z; l5 n1 U4 m, O/ u: ving over his own shoulders, chest, and back area for
5 w7 y) u: x7 p# h# ?- Z" `% ja year. The father also revealed he was embarrassed
  q% H4 r$ x/ [: a* g& [6 @to disclose that he was using a testosterone gel pre-# C' y* C4 c; j" J
scribed by his family physician for decreased libido
) f$ J, K9 _- M# m" k$ t  x: nsecondary to depression.
, s; P9 Q) ~* H6 S0 G; A$ ?The child slept in the same bed with parents.
4 s1 L1 O/ }6 w  g8 I/ s1 A1 K; @+ CThe father would hug the baby and hold him on his
5 Y& D& Q" N1 u; r* P( bchest for a considerable period of time, causing sig-
1 s9 V! I5 U: B$ f; c( ^/ q6 znificant bare skin contact between baby and father.
, X6 p4 }' W% N) n& kThe father also admitted that after the phone call,7 Q! R! [+ s+ z$ ]% u, e
when he learned the testosterone level in the baby% h5 T  @$ m7 r! p7 V0 D; [
was high, he then read the product information
6 Z: k5 ^: v8 H& t) M/ Ipacket and concluded that it was most likely the rea-4 ^5 I9 B& F: b* w- v
son for the child’s virilization. At that time, they# V1 P: b0 \% F, K5 ]* A' t, Z4 q) H2 ?
decided to put the baby in a separate bed, and the
$ P! e: n' B6 x! a  \% m* j4 b. Tfather was not hugging him with bare skin and had
. ^* g+ Y7 J( F1 v" mbeen using protective clothing. A repeat testosterone
! B" ~  Z8 [4 x: k+ |- S- ?0 `test was ordered, but the family did not go to the8 ^4 B$ P2 }& P2 a$ Z0 E
laboratory to obtain the test.
! @: A7 b) F6 `' I9 w3 ADiscussion* T# o# P# V/ \8 D( L! c0 @
Precocious puberty in boys is defined as secondary
' c& u1 k) E9 j3 zsexual development before 9 years of age.1,4
% q- P3 a3 y! F- F3 }: S. z5 u6 P$ nPrecocious puberty is termed as central (true) when( x' s- P& ~$ \1 V; _; s
it is caused by the premature activation of hypo-
" ]: J6 N+ H1 d  gthalamic pituitary gonadal axis. CPP is more com-
8 P3 L. r0 r$ U, ^* ^mon in girls than in boys.1,3 Most boys with CPP" {6 X" }* m- @) Q6 f
may have a central nervous system lesion that is
: `' H9 F8 i5 hresponsible for the early activation of the hypothal-
; Y) a1 A" _. z: E1 Ramic pituitary gonadal axis.1-3 Thus, greater empha-" q( s. E( J: @) d- C
sis has been given to neuroradiologic imaging in, K  e% Y$ o2 U: c0 g. Q9 ~% N
boys with precocious puberty. In addition to viril-
& B  r/ h. t' Aization, the clinical hallmark of CPP is the symmet-
4 q3 p0 I# V( x3 r/ L, Prical testicular growth secondary to stimulation by2 L% u* d# j- K; Q" L; C, _* ^) U+ h6 Y
gonadotropins.1,3
4 ^' S4 {# b" k2 s& HGonadotropin-independent peripheral preco-
1 W0 C* B9 q$ ]# ncious puberty in boys also results from inappropriate
# p( B0 I9 L( ]( tandrogenic stimulation from either endogenous or' U: o$ a  d/ ?
exogenous sources, nonpituitary gonadotropin stim-
- v6 M& \' d$ ]/ kulation, and rare activating mutations.3 Virilizing, p! Y9 `+ F1 l5 J  I% i  j
congenital adrenal hyperplasia producing excessive& Q6 z; \) z9 g, D# f# H7 B
adrenal androgens is a common cause of precocious
: I5 d5 i7 k' t% Wpuberty in boys.3,4
" q  o) q6 m, g9 D- BThe most common form of congenital adrenal
0 H4 ?' U0 M& z% O! ghyperplasia is the 21-hydroxylase enzyme deficiency.6 Z# I, f6 ~0 `7 s0 I' S
The 11-β hydroxylase deficiency may also result in
/ u7 q3 ~  o9 Bexcessive adrenal androgen production, and rarely,6 Y8 [# k( b1 H; z0 X& U
an adrenal tumor may also cause adrenal androgen
' j+ ?0 P9 F5 F0 [excess.1,3& Q0 w0 e5 e8 ^9 D/ m
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) G. p% Y0 y4 ~3 h' P/ A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& P9 ]6 A3 V. L  |% U: lA unique entity of male-limited gonadotropin-! U* ^  L! P% I3 [+ A; p1 \2 l2 @5 O3 l
independent precocious puberty, which is also known
5 R, r+ V& v# }as testotoxicosis, may cause precocious puberty at a
& ?# N. e( f# cvery young age. The physical findings in these boys
- d+ W5 @. Q7 L- s3 [0 e4 Uwith this disorder are full pubertal development,, c) s5 q' F, p3 D: e$ ?, p
including bilateral testicular growth, similar to boys+ |' I& {6 W5 q' {; l5 Y8 w# v
with CPP. The gonadotropin levels in this disorder$ m: x& ^- r8 `, P% K# E9 s: j" [
are suppressed to prepubertal levels and do not show+ Y0 j9 i" d1 m8 d8 x
pubertal response of gonadotropin after gonadotropin-( L, d0 q3 q/ B2 `: j3 r
releasing hormone stimulation. This is a sex-linked
9 m  z8 H9 A' s! I1 N8 g6 H% C5 Fautosomal dominant disorder that affects only
( p# d& y. K" t$ s, t! amales; therefore, other male members of the family9 W8 t" m$ t4 ^/ J6 y
may have similar precocious puberty.33 V9 }$ ^9 [0 Q2 a  |7 w) y( A
In our patient, physical examination was incon-
2 ~" t) k0 }8 vsistent with true precocious puberty since his testi-" q/ h* l! n' P: e! v
cles were prepubertal in size. However, testotoxicosis; ?2 W/ i* h$ u" c5 _) p
was in the differential diagnosis because his father* R; p& c- x1 O, M& w5 Q$ q
started puberty somewhat early, and occasionally,3 x6 S- a+ W" R1 ^! N2 `# G
testicular enlargement is not that evident in the
6 k2 G9 B: c9 s% E" pbeginning of this process.1 In the absence of a neg-5 Q( N4 \+ ?5 [' ~( ]9 c
ative initial history of androgen exposure, our3 O1 Z3 O6 G/ r) i( A5 U
biggest concern was virilizing adrenal hyperplasia,% Q' z0 Z/ Z8 A- g  P! Q  f
either 21-hydroxylase deficiency or 11-β hydroxylase
4 t/ c: b+ ^. Z# V3 u8 Pdeficiency. Those diagnoses were excluded by find-2 F* }" C  B/ B& y; F! @2 Z) k# a
ing the normal level of adrenal steroids.
, p/ U" i& s8 [0 r+ X( U1 b8 Z7 A5 cThe diagnosis of exogenous androgens was strongly. P# M( [8 o9 z! N1 S) n
suspected in a follow-up visit after 4 months because" c( S- S  I: o7 Z. H0 A
the physical examination revealed the complete disap-
# ]% ^: T8 j2 d7 W& t0 @( Vpearance of pubic hair, normal growth velocity, and& r3 }0 ^: R+ {1 q4 `( p
decreased erections. The father admitted using a testos-
' b! x8 ]$ w( i, F' Q9 B) n/ Pterone gel, which he concealed at first visit. He was! {& Y* C" G5 N' J0 H
using it rather frequently, twice a day. The Physicians’" T- o3 M$ V& R: Q$ n0 i
Desk Reference, or package insert of this product, gel or- U7 u4 C# J" |3 T; y
cream, cautions about dermal testosterone transfer to
: k$ L' t5 i6 K& L: X& sunprotected females through direct skin exposure.! Y( V) _4 y) ~8 \7 b$ j. ^5 r, k- S% U
Serum testosterone level was found to be 2 times the6 d) O1 H: r' ]2 v) F7 c
baseline value in those females who were exposed to
  {+ e# k) q0 n$ E: P9 }$ W  H9 Oeven 15 minutes of direct skin contact with their male
" @( x" W# q% ^# E1 b/ v8 V! v7 vpartners.6 However, when a shirt covered the applica-
% a& G- T! W; ?/ B* X( C7 F9 J0 E& r- ttion site, this testosterone transfer was prevented.
. s/ Q' W* ^$ R9 N, d" TOur patient’s testosterone level was 60 ng/mL,
, M4 G/ Y: V8 ^3 t: Zwhich was clearly high. Some studies suggest that
. V2 S0 e& x' n" G" X) A3 j7 a/ O1 gdermal conversion of testosterone to dihydrotestos-* C3 c  [- O# y: s' R) d
terone, which is a more potent metabolite, is more
" l; i( T4 r5 a5 bactive in young children exposed to testosterone$ v2 W+ G9 C; S1 P- {
exogenously7; however, we did not measure a dihy-
0 P, b  t0 U* A$ H2 H9 Q. }drotestosterone level in our patient. In addition to7 `" Z7 ^& x. z9 v0 P
virilization, exposure to exogenous testosterone in
4 @2 ?: |" h, W1 v& p5 s- bchildren results in an increase in growth velocity and
- q1 p4 p9 B9 @! m* b. fadvanced bone age, as seen in our patient.
, s7 Y) [$ H- aThe long-term effect of androgen exposure during1 E% z& M4 _0 g! F7 k% ~
early childhood on pubertal development and final. e) ^3 P3 H1 O2 O8 {* {3 g% \
adult height are not fully known and always remain& |/ u" d) l, a9 i3 t, {
a concern. Children treated with short-term testos-. l) M' V2 e: K9 d4 F8 m1 F
terone injection or topical androgen may exhibit some& R$ B+ h4 V) X/ }) ]3 W
acceleration of the skeletal maturation; however, after
4 I, K! I# a; z" Wcessation of treatment, the rate of bone maturation
6 @# O4 p" O2 S! ]! p: Zdecelerates and gradually returns to normal.8,9
" O/ t0 l# H) G/ M- I) s6 wThere are conflicting reports and controversy
' N8 ^8 g2 u! y" }over the effect of early androgen exposure on adult) ]- k0 K; i/ d2 G+ k
penile length.10,11 Some reports suggest subnormal3 v: ]# _, R- ^) ?3 j- t2 u+ E
adult penile length, apparently because of downreg-
1 u  v4 h6 M% F" V% N% Uulation of androgen receptor number.10,12 However,8 I! C& f4 v3 M; o! A
Sutherland et al13 did not find a correlation between# j/ }* z' F. q, t" a" k! f6 W
childhood testosterone exposure and reduced adult
, W; y/ A6 \- u. v! _, I& ppenile length in clinical studies.
  k) G( Z  g3 bNonetheless, we do not believe our patient is
6 z0 W4 R2 t: \going to experience any of the untoward effects from
4 {4 o% z5 ]4 |testosterone exposure as mentioned earlier because( U! {* [% J) t' B1 T5 ?
the exposure was not for a prolonged period of time.
& F1 p" X# ~% C, NAlthough the bone age was advanced at the time of& Y+ ]6 t0 S" ~$ z# j8 R$ B
diagnosis, the child had a normal growth velocity at9 b0 d2 o9 V2 j; k9 }& j
the follow-up visit. It is hoped that his final adult" A" h" b; U9 {4 h
height will not be affected.# G$ b3 Q1 R9 A3 s* B1 ]: X8 _4 {
Although rarely reported, the widespread avail-+ |3 B& X. A5 Z
ability of androgen products in our society may
) {, ?$ T3 T4 e1 W) V/ L3 Nindeed cause more virilization in male or female* a/ \% G  ]& U% m0 Z# Z$ R
children than one would realize. Exposure to andro-/ q, W( U  R. }  n
gen products must be considered and specific ques-7 V7 G5 B& j6 D$ V
tioning about the use of a testosterone product or& @7 Y2 y7 e/ Z9 J( u( g3 v
gel should be asked of the family members during4 I3 R9 y  O8 J, |7 x
the evaluation of any children who present with vir-4 l/ D; C. R. D9 r9 a* m
ilization or peripheral precocious puberty. The diag-
. P5 O$ n$ z6 x' h( U. l% i/ mnosis can be established by just a few tests and by
6 l$ n* _. N( t6 [8 U7 T' L3 Zappropriate history. The inability to obtain such a
9 R  \+ T0 E$ M3 ]history, or failure to ask the specific questions, may! i" I1 \& _. V' Z4 i3 [
result in extensive, unnecessary, and expensive
" p$ E4 A, Q6 J/ {investigation. The primary care physician should be6 m) V6 ^5 v+ t
aware of this fact, because most of these children
  p  M& j% G% r5 Zmay initially present in their practice. The Physicians’" j5 o. s) P5 u8 r" K" @
Desk Reference and package insert should also put a- C( a' v" J! j  w3 u8 J+ B
warning about the virilizing effect on a male or
$ H, g# R: J5 F- K' jfemale child who might come in contact with some-1 l4 z! y, n7 I
one using any of these products.
4 i& W& @0 V: z( O" NReferences4 H4 S* L3 O: q1 D2 ^2 h
1. Styne DM. The testes: disorder of sexual differentiation
+ G5 p% b7 P+ X( ^and puberty in the male. In: Sperling MA, ed. Pediatric
; d# W& g' W  Y  B: p' G$ FEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" V/ \& C( x& J5 s+ T
2002: 565-628.$ Y& u# X% \2 x. v
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 s# n* h; Q; b' Y* ~  G
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
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

& ^0 s5 D+ T" q% ]2 S9 F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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