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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" `2 g  l8 N% N9 a8 D2 D
Boy Induced by Indirect Topical
- S" H) f2 Z2 l4 `2 ~$ i/ H6 \Exposure to Testosterone
6 |, F4 \2 s5 |+ ySamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
& m. E7 d0 t+ r6 Z+ T) @' n$ H3 eand Kenneth R. Rettig, MD17 ~9 K  v, A) Z/ R& ?
Clinical Pediatrics& Z' g2 @* S2 D* c
Volume 46 Number 6* i9 u' D5 x" H" m
July 2007 540-5430 s9 `8 c- C' P% [  X
© 2007 Sage Publications4 t; l6 Q* E9 L3 S% C
10.1177/00099228062966515 I+ X+ i0 l# g+ R( t% I
http://clp.sagepub.com! j% @8 P( l6 L7 p7 V
hosted at% x$ ^: x8 Y( }7 L  f1 h# u
http://online.sagepub.com- ?; E. N6 f0 E2 R+ W) X
Precocious puberty in boys, central or peripheral,
* H9 M0 c- g9 C) z- ]: H7 {; Z; Ois a significant concern for physicians. Central. c, Q  K; l# w$ t& J' o
precocious puberty (CPP), which is mediated8 t! D! w( q% U3 d+ y
through the hypothalamic pituitary gonadal axis, has' r6 o. i. S& [+ N; u
a higher incidence of organic central nervous system5 _* e  B! v$ e1 \. d0 w. u+ e
lesions in boys.1,2 Virilization in boys, as manifested& R- y+ b( `  e. y7 a0 Y2 ^
by enlargement of the penis, development of pubic
% ^* ~" K: a6 \% |& Nhair, and facial acne without enlargement of testi-$ C# ]* T" t, T. J
cles, suggests peripheral or pseudopuberty.1-3 We7 C' A. R5 E, `7 C% W: j, L( _; I* E
report a 16-month-old boy who presented with the8 I( p2 {8 K. u/ C  C
enlargement of the phallus and pubic hair develop-' a$ a* h+ p9 H1 i: D# |
ment without testicular enlargement, which was due4 @- v- @2 p# j8 U
to the unintentional exposure to androgen gel used by
) m2 y2 n! W: ~9 e5 g3 w; ^the father. The family initially concealed this infor-
% l' d% E! o" }( `mation, resulting in an extensive work-up for this: }" i$ l0 Y( g3 D  W
child. Given the widespread and easy availability of% ]+ C4 J3 s; ]/ U( b  y  l/ x: w$ S
testosterone gel and cream, we believe this is proba-
& M6 D# i7 L/ {4 p2 ]- gbly more common than the rare case report in the1 [. u* o' S" Q4 g, Q
literature.4- m+ z, @  N6 T, o
Patient Report0 n* x# W3 x6 j; U$ \
A 16-month-old white child was referred to the
8 l; |. S% s. {' Wendocrine clinic by his pediatrician with the concern6 q) O1 w! {  X
of early sexual development. His mother noticed
$ C2 B. W. W3 @$ e$ C- ^+ tlight colored pubic hair development when he was
" e# S! q: o! v) ?1 B5 gFrom the 1Division of Pediatric Endocrinology, 2University of
/ O. ?; `% Q' U9 uSouth Alabama Medical Center, Mobile, Alabama.8 t: H% o6 c; W  S. }1 d( `6 G, h
Address correspondence to: Samar K. Bhowmick, MD, FACE,
) M' ]; D, u* C( @Professor of Pediatrics, University of South Alabama, College of
$ g: _7 A$ H  c0 Y( DMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, P! j. w+ ~- [0 D" {3 `' [8 c$ K8 d
e-mail: [email protected].
! n0 [/ b$ H$ Iabout 6 to 7 months old, which progressively became1 R; _) K$ h- v: m8 L
darker. She was also concerned about the enlarge-
' J6 `- M) A+ @# J( K! Jment of his penis and frequent erections. The child
5 E; q+ @0 i' @  t$ J& Jwas the product of a full-term normal delivery, with
/ Q# ?: v1 P5 t- C5 p0 Va birth weight of 7 lb 14 oz, and birth length of
% R. o: q5 Y4 P9 p. f20 inches. He was breast-fed throughout the first year
- W2 g1 M4 J( I1 k: }  V3 j  O6 iof life and was still receiving breast milk along with
+ x+ v6 `: \8 N: K' Nsolid food. He had no hospitalizations or surgery,
2 F# G% H1 y4 O' ]and his psychosocial and psychomotor development
2 ?! C2 U; U+ h, {' {: Bwas age appropriate.
- a0 Q, S( [0 I: t: [( EThe family history was remarkable for the father,& C) ?  X9 [' @. D
who was diagnosed with hypothyroidism at age 16,: [* g# C$ N4 N+ v3 J5 W
which was treated with thyroxine. The father’s/ L  M. F# x$ B- Q% y
height was 6 feet, and he went through a somewhat" r8 |1 R1 w  T
early puberty and had stopped growing by age 14.
6 V0 K9 a2 y) f- G4 l) b; hThe father denied taking any other medication. The# \9 x- p- z8 B% ]. H2 e
child’s mother was in good health. Her menarche$ |* C" p; i  y6 H; o- {
was at 11 years of age, and her height was at 5 feet' |* g% g" [/ D- R3 t( ~0 V' r
5 inches. There was no other family history of pre-0 o( q& |  t7 y
cocious sexual development in the first-degree rela-
0 H  k7 n2 Q' I9 Xtives. There were no siblings.+ ~( }- d8 h: r+ \
Physical Examination/ _8 x+ S( F! Q$ ~( l/ N
The physical examination revealed a very active,
$ z9 X8 _: S# @5 F+ b* w( Vplayful, and healthy boy. The vital signs documented
- q- N5 V9 R: l, b% F0 aa blood pressure of 85/50 mm Hg, his length was
2 Y- R0 W: J, z; S2 A4 I  `- S90 cm (>97th percentile), and his weight was 14.4 kg
6 f; }/ U* y& D. i( T(also >97th percentile). The observed yearly growth" ]' w3 Z" L9 c3 ]' k
velocity was 30 cm (12 inches). The examination of0 i" o: `: o- x) d
the neck revealed no thyroid enlargement.
3 }' m: ~$ E6 {- o" t! DThe genitourinary examination was remarkable for
) d- u% T1 z4 ^7 ]enlargement of the penis, with a stretched length of
* U6 p9 F' L6 M# d8 cm and a width of 2 cm. The glans penis was very well
$ ^2 u$ Q& }7 u  [0 R' ]- V, Ndeveloped. The pubic hair was Tanner II, mostly around/ \% L- T9 s+ w! P. J9 [/ a
5401 F& ?$ M( s: c7 O/ w' b  F5 V
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( k3 m# C% V5 ]the base of the phallus and was dark and curled. The
. ]: ]& g5 ~) j9 atesticular volume was prepubertal at 2 mL each.; O8 ?7 E& g/ V; Q; g, J5 u$ b9 z4 K1 e8 h
The skin was moist and smooth and somewhat( g" x  ^! M: F. B* [2 y
oily. No axillary hair was noted. There were no
! [% s- `8 u+ B" W- ]5 Oabnormal skin pigmentations or café-au-lait spots." X6 Q) |; H2 o  a) Y1 b( Q
Neurologic evaluation showed deep tendon reflex 2+' ?! W* @1 r1 \1 c' q
bilateral and symmetrical. There was no suggestion
) `6 D4 I0 W" O# c) c* Kof papilledema.
3 s+ ^2 k  {# ~) [3 i9 L6 wLaboratory Evaluation
; m4 R. k0 ]+ W; qThe bone age was consistent with 28 months by
% e! T& b, |# n# c* R: d* ausing the standard of Greulich and Pyle at a chrono-* U* |! b7 O1 O. \7 a& D
logic age of 16 months (advanced).5 Chromosomal- Y& m7 {& Z. A2 x8 P9 @( Z
karyotype was 46XY. The thyroid function test$ v' `) i$ Y1 M! U
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
' W3 ]/ w5 P/ ?, |4 a  M" qlating hormone level was 1.3 µIU/mL (both normal).- k! C7 U! Y# y9 K( j' f7 m
The concentrations of serum electrolytes, blood5 j1 A5 a% {1 O) {
urea nitrogen, creatinine, and calcium all were
# s* H; l* m1 Z0 M3 owithin normal range for his age. The concentration
2 W9 E2 u& B4 v. G; b# F; z5 J  fof serum 17-hydroxyprogesterone was 16 ng/dL3 x( ?* W+ N; d5 D9 `# z" F
(normal, 3 to 90 ng/dL), androstenedione was 20
; a; E* q- Z% Z3 j4 fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 {$ p2 M1 t! c9 ]" P# \  @/ i1 Y* Wterone was 38 ng/dL (normal, 50 to 760 ng/dL),5 v$ H. z/ x9 P- u: Y- z+ E, N  h- O$ t
desoxycorticosterone was 4.3 ng/dL (normal, 7 to' V) W- D8 V1 x/ v4 v# J8 v/ d
49ng/dL), 11-desoxycortisol (specific compound S)
( O6 |: e# o9 c" T! H3 Gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 x' v8 T. P4 z5 `+ y- u( B5 Vtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 T* ^; d. |# r
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),' y. i) o2 S6 @1 J" g" U
and β-human chorionic gonadotropin was less than
4 J* M1 |4 z+ e3 d/ }5 @5 mIU/mL (normal <5 mIU/mL). Serum follicular: s( S2 H0 c6 N
stimulating hormone and leuteinizing hormone
* }/ K. ?9 f: n9 o6 m; Xconcentrations were less than 0.05 mIU/mL; b0 o, y& I' w/ J2 v1 S
(prepubertal).6 l: a6 @5 k0 l5 B  o! W* r
The parents were notified about the laboratory
; O, D$ @& n0 N. v3 xresults and were informed that all of the tests were$ a8 G( P7 W. Q! D
normal except the testosterone level was high. The& Z) d% M) R/ G. @: Q
follow-up visit was arranged within a few weeks to
+ y! X, D, z5 iobtain testicular and abdominal sonograms; how-
7 \* I% o3 ^: i% E) L; pever, the family did not return for 4 months.+ X2 v- g3 x) S  V- x9 L6 g
Physical examination at this time revealed that the
* e0 \, G! Y0 A. Dchild had grown 2.5 cm in 4 months and had gained
1 f; n( Q6 z- }' @- W2 kg of weight. Physical examination remained
8 Q5 L! [* n9 C: Wunchanged. Surprisingly, the pubic hair almost com-6 r4 m# B0 F4 G7 V& N* Y" M
pletely disappeared except for a few vellous hairs at0 ~6 F5 d* f* v
the base of the phallus. Testicular volume was still 24 F- g4 y/ V. G' f4 [
mL, and the size of the penis remained unchanged.
) {! Q: c  z% N3 l! kThe mother also said that the boy was no longer hav-) |9 F# d# H% G3 n" @
ing frequent erections.
# K  y8 d; Z! D0 DBoth parents were again questioned about use of% Y$ T# W0 [4 L% J" p
any ointment/creams that they may have applied to1 \, R+ ^. e# P
the child’s skin. This time the father admitted the
- j* K, k; {( {7 _. X" `Topical Testosterone Exposure / Bhowmick et al 541
- {+ k: _8 F2 ouse of testosterone gel twice daily that he was apply-
/ e  C# }1 O6 @8 d+ K9 Ming over his own shoulders, chest, and back area for7 T. y  [( P* Y) y$ `/ g
a year. The father also revealed he was embarrassed  `) G1 P+ W! H( Y
to disclose that he was using a testosterone gel pre-0 }9 s6 |7 y3 \- ~. ]/ s
scribed by his family physician for decreased libido3 l7 L; R; ~% U5 Q$ K+ a
secondary to depression.
9 Z. o" ?# o7 P, `# D; ZThe child slept in the same bed with parents.
, i: H5 [/ a4 c) m. G7 p- @The father would hug the baby and hold him on his
5 x1 @3 ~7 O+ G! y+ [1 zchest for a considerable period of time, causing sig-
; ~: [& y/ r4 ~) `" P; _nificant bare skin contact between baby and father.4 H; d6 j0 T7 b2 J* p( C3 h% U* x
The father also admitted that after the phone call,
; X/ q5 g1 N- V+ m8 Kwhen he learned the testosterone level in the baby3 M7 n  k$ B5 ?
was high, he then read the product information
' F6 I2 R$ r6 @+ Jpacket and concluded that it was most likely the rea-
" F2 a. e! e% M/ w) x+ Q( ]son for the child’s virilization. At that time, they6 Y$ i2 }% B% k. y. P2 l) F3 G8 x& P
decided to put the baby in a separate bed, and the5 f7 y8 w1 f; z2 H; ?, Q1 ?( ]' z
father was not hugging him with bare skin and had
3 J9 s0 B# ]& |2 [; Lbeen using protective clothing. A repeat testosterone: _! c, e$ ]' l3 b0 A# H. B
test was ordered, but the family did not go to the1 V# h" t/ s7 d3 @) H: T
laboratory to obtain the test.8 ~$ b+ b8 X3 i: \. }% a
Discussion" x+ x* ?3 p& `% f$ \# T2 k
Precocious puberty in boys is defined as secondary/ K4 F1 z" ?% J( b6 w
sexual development before 9 years of age.1,4( V9 s4 z  L) \) D) c+ t" x5 c
Precocious puberty is termed as central (true) when
( E! M( c  @7 {0 G/ m9 i7 yit is caused by the premature activation of hypo-
7 a  B2 }1 X3 j+ W+ M+ Qthalamic pituitary gonadal axis. CPP is more com-
# A% T" |# R8 g9 emon in girls than in boys.1,3 Most boys with CPP
. z) H: _# Y( d, B! dmay have a central nervous system lesion that is+ `# G! G5 f; a0 G
responsible for the early activation of the hypothal-
0 \) O$ Q6 h' G1 y2 I8 z0 camic pituitary gonadal axis.1-3 Thus, greater empha-
' z8 ]; G' r: ]0 Z" z- t, zsis has been given to neuroradiologic imaging in3 X/ i) A" R- [; @1 f& f# y9 \
boys with precocious puberty. In addition to viril-' L2 T, ]% |. j! a
ization, the clinical hallmark of CPP is the symmet-
# ]# h, f% Z. o- w1 l) h+ V( W) K; brical testicular growth secondary to stimulation by
3 p4 X" x  H, n$ i. |+ }0 ^gonadotropins.1,3& a" f7 O* `$ l0 P
Gonadotropin-independent peripheral preco-
! b% M2 Z  a3 O# r/ m" @1 ]cious puberty in boys also results from inappropriate1 w4 @( W! y4 V$ t' ^( m
androgenic stimulation from either endogenous or
2 F4 U% [. x( Y" B% kexogenous sources, nonpituitary gonadotropin stim-
% b7 r1 c% P5 {ulation, and rare activating mutations.3 Virilizing  A7 s6 {$ H8 q
congenital adrenal hyperplasia producing excessive! K7 @/ a$ q8 b8 v
adrenal androgens is a common cause of precocious
: p" R/ |. A+ L$ Spuberty in boys.3,4
1 H. F6 M/ {9 x2 B1 n5 }The most common form of congenital adrenal
( ?- y; z9 c2 t# I. fhyperplasia is the 21-hydroxylase enzyme deficiency.
- m( f3 d# o! [The 11-β hydroxylase deficiency may also result in) ^7 e7 \+ t' r3 K
excessive adrenal androgen production, and rarely,. B3 Z' D) x. l: H' i9 s
an adrenal tumor may also cause adrenal androgen3 _/ B' `" w" y$ X
excess.1,3
  z! H* F* A! Z4 U% ~at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ h4 z$ B8 h6 b$ }9 {4 [# r542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 g8 D/ d7 |/ c* x+ [- R& h, sA unique entity of male-limited gonadotropin-
5 O% Q" e  J- U0 \4 Tindependent precocious puberty, which is also known
9 d! q5 j, L6 @0 Eas testotoxicosis, may cause precocious puberty at a7 r, U, U* W7 R* T* h: ?
very young age. The physical findings in these boys
) |4 J) R2 Z9 Q4 zwith this disorder are full pubertal development,
+ I2 _7 M( C: J7 e! @& {" mincluding bilateral testicular growth, similar to boys. I, }4 p: p/ {  p0 f# G( r
with CPP. The gonadotropin levels in this disorder
5 a* l+ A+ J- \7 ?  g/ Qare suppressed to prepubertal levels and do not show  B* I9 d! q& o# W, Y0 z9 ?- A  s
pubertal response of gonadotropin after gonadotropin-* c; l' i: z" `5 F+ \+ O8 b+ B
releasing hormone stimulation. This is a sex-linked) s5 l4 o5 D+ V$ U# _
autosomal dominant disorder that affects only4 G" H* O' d$ y5 E
males; therefore, other male members of the family: @6 o8 N8 T" j' R$ }: G# \6 C
may have similar precocious puberty.3
$ ?; C9 M" x2 w% Y/ A8 dIn our patient, physical examination was incon-$ Q6 w4 h7 u0 {
sistent with true precocious puberty since his testi-
/ ^( B, p7 ~$ t+ Mcles were prepubertal in size. However, testotoxicosis
- ~4 j' @; K: k* rwas in the differential diagnosis because his father+ q3 A/ i# `3 e; a3 q
started puberty somewhat early, and occasionally,
" R, E# x1 f2 D$ W! k0 V+ B  Mtesticular enlargement is not that evident in the2 O: I4 s+ {- z1 f$ z: l
beginning of this process.1 In the absence of a neg-
) r! c. r, g1 Wative initial history of androgen exposure, our9 H" W, v/ f0 @( Y
biggest concern was virilizing adrenal hyperplasia,
% c" ]0 y8 ~/ {) O) V  Reither 21-hydroxylase deficiency or 11-β hydroxylase
, B# m/ g* H% Y7 x9 ~8 M) }deficiency. Those diagnoses were excluded by find-# [0 y) ]) v$ L: t
ing the normal level of adrenal steroids.9 ]1 m  z0 V/ ]1 I5 |! h
The diagnosis of exogenous androgens was strongly( n7 |) G0 z3 y
suspected in a follow-up visit after 4 months because
3 S$ s% t$ S; M* V$ Zthe physical examination revealed the complete disap-
6 n4 I' T: G. ~9 J9 gpearance of pubic hair, normal growth velocity, and; y; M8 t8 w0 K, [, T7 L
decreased erections. The father admitted using a testos-6 V9 |' t6 U0 a0 e0 v
terone gel, which he concealed at first visit. He was
8 ]. {5 a% }; r3 ?  W: U1 U9 c  w" ]9 tusing it rather frequently, twice a day. The Physicians’
0 \7 H0 @  Q4 Y# d. H% H; fDesk Reference, or package insert of this product, gel or
; ~) c- T  i, _cream, cautions about dermal testosterone transfer to
1 _$ X) z. s* L6 h) h$ Cunprotected females through direct skin exposure." U- p% X7 g* P7 W9 m* }
Serum testosterone level was found to be 2 times the
0 M, [9 `$ E7 k: sbaseline value in those females who were exposed to2 B3 L5 ]7 j: e) p  u
even 15 minutes of direct skin contact with their male# }7 k2 v5 t5 u% u/ |
partners.6 However, when a shirt covered the applica-; v; W+ d2 B( t7 n) m
tion site, this testosterone transfer was prevented.: ]/ b5 ~- v" ~+ q& {1 M* L) H3 `
Our patient’s testosterone level was 60 ng/mL,! x. A* U. j  }7 @
which was clearly high. Some studies suggest that8 K5 n. Z" M* x% R6 y9 p2 t& s
dermal conversion of testosterone to dihydrotestos-
+ r9 x3 h5 t6 }5 u8 ?0 Jterone, which is a more potent metabolite, is more) b* Z2 w- I# V
active in young children exposed to testosterone. z, G, D  F3 R; K; I( b
exogenously7; however, we did not measure a dihy-) O/ t+ q8 ]9 M; o$ @
drotestosterone level in our patient. In addition to
0 O- X8 f, B. M6 p9 H& ovirilization, exposure to exogenous testosterone in
) F, q) C  Z- c& G  y2 ?% r! ^" h" ychildren results in an increase in growth velocity and8 {1 V" I. ~& j! Q) f2 t
advanced bone age, as seen in our patient.1 x: q' x4 o  C- m5 J
The long-term effect of androgen exposure during
4 N  l8 `' T0 N1 }! ]& Wearly childhood on pubertal development and final
/ D3 |# G5 q& D& N  z1 |adult height are not fully known and always remain6 P8 l  c% ~) L( L2 I4 }
a concern. Children treated with short-term testos-
$ v+ W  @1 }! ?$ b! I4 Aterone injection or topical androgen may exhibit some0 _' w9 }  D0 L+ X  p
acceleration of the skeletal maturation; however, after! y- M% L9 e2 @' s; ?
cessation of treatment, the rate of bone maturation
4 S4 \; ?# y% l  V# {decelerates and gradually returns to normal.8,93 O8 t- u' K6 `, G6 ?
There are conflicting reports and controversy
; Q7 |+ s- ~$ n. L: uover the effect of early androgen exposure on adult
, }# W; o1 f- Q6 v7 Vpenile length.10,11 Some reports suggest subnormal
2 @4 d- [  ?1 ladult penile length, apparently because of downreg-6 k" }/ ?3 J8 d( c
ulation of androgen receptor number.10,12 However,' Z$ i/ W: y) @; @9 \& z
Sutherland et al13 did not find a correlation between" u3 b) B8 S/ Q$ P  p! i
childhood testosterone exposure and reduced adult: l0 G  j3 s6 K- s# \' x
penile length in clinical studies.
! c( l4 D) f7 c" TNonetheless, we do not believe our patient is
+ ~/ |4 G+ h# Z0 {6 }, agoing to experience any of the untoward effects from$ o- N' i' s  t- O2 S) Q
testosterone exposure as mentioned earlier because$ ?0 N+ G0 i$ R
the exposure was not for a prolonged period of time.
8 s0 j  {" N1 E% nAlthough the bone age was advanced at the time of
# K& H1 F) t. D3 t6 R' w, Y- ldiagnosis, the child had a normal growth velocity at
7 k, [9 c6 e0 u" Q' Sthe follow-up visit. It is hoped that his final adult
4 g. }! d, R9 D0 |5 kheight will not be affected.
% ^* b& \$ {5 _) Y+ dAlthough rarely reported, the widespread avail-
' Q# I' {9 Y9 x/ o  M# X1 lability of androgen products in our society may& p' I+ Z) [, O" k" R0 _
indeed cause more virilization in male or female( j! G. f* k. T; i; r' v& v
children than one would realize. Exposure to andro-( f& Q( F6 M' `% `- k7 i
gen products must be considered and specific ques-, \+ C& |  A' ?2 B5 ?
tioning about the use of a testosterone product or: H! f% n" E) `2 m
gel should be asked of the family members during2 @3 W) ^7 A3 J6 y! q
the evaluation of any children who present with vir-
0 y0 w0 k4 I) N' O2 n4 Xilization or peripheral precocious puberty. The diag-- \  f" A  v. ~3 k2 a3 h
nosis can be established by just a few tests and by$ \* H; N1 `/ q2 ~7 a+ T) K. \: X
appropriate history. The inability to obtain such a
2 j4 y* w/ X/ a8 Hhistory, or failure to ask the specific questions, may
' U6 Q/ L2 L* Y. A5 dresult in extensive, unnecessary, and expensive
* k! |' P8 R! v* Z  ^8 Ginvestigation. The primary care physician should be; B7 V3 B4 E/ g- x7 v1 M% R' X
aware of this fact, because most of these children
" w, I4 R. X& bmay initially present in their practice. The Physicians’6 X, L* Z8 h0 v9 B2 x9 M
Desk Reference and package insert should also put a, s6 \0 d6 n( U* y4 `; g% B
warning about the virilizing effect on a male or; Y5 \1 j6 E  @( O2 O
female child who might come in contact with some-4 d1 k* d% y1 r8 |! ]: |
one using any of these products.
) L( M1 \6 f* R" _References" m8 H) Y! Q* u2 U) W7 D
1. Styne DM. The testes: disorder of sexual differentiation" ~3 Q9 j% h$ E* x, T
and puberty in the male. In: Sperling MA, ed. Pediatric$ h9 C% P" w5 R9 s8 j. F( x; U
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 a3 Y' i0 s+ D- s: R4 C. e6 }$ N
2002: 565-628.7 ]& I0 ]) V9 ?' X3 b9 h* O1 E
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 m, v+ ^* s; F6 S, apuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old* C7 O. d5 ]& ?
Boy Induced by Indirect Topical( G$ l* @# Z0 {
Exposure to Testosterone
/ d( O. J; _$ F# I  }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- W/ G/ ~3 U4 ^5 m0 x
and Kenneth R. Rettig, MD1
' A7 X$ Y# M" N1 W, e& k5 f7 H; IClinical Pediatrics
/ `' k4 E( C% V- e- @Volume 46 Number 6" ~3 \2 U% @  P! v6 O' ~! {3 N1 H- F
July 2007 540-543
' K0 `9 l3 d5 S© 2007 Sage Publications- ?+ N1 V: i# r; c) `& Y8 V
10.1177/00099228062966511 I4 K$ U) Y0 P0 D% Q" X
http://clp.sagepub.com; U  G9 T& A% o4 x  M; e
hosted at& {: J: E6 J) ]% J+ b
http://online.sagepub.com) C7 X& s. A* `" w) U' p1 b
Precocious puberty in boys, central or peripheral,; U& @$ R$ N8 F( s: z
is a significant concern for physicians. Central
7 O1 e& }$ l8 U; Wprecocious puberty (CPP), which is mediated+ f/ k. e( Z! d3 g0 v9 `
through the hypothalamic pituitary gonadal axis, has& T: D/ T4 J2 d3 k
a higher incidence of organic central nervous system6 y3 I1 R9 K& T3 A. C6 O2 Y% R& i% W
lesions in boys.1,2 Virilization in boys, as manifested5 ^$ [, j- W/ U
by enlargement of the penis, development of pubic
* j0 q6 j( @  x/ v4 ~; e1 yhair, and facial acne without enlargement of testi-
8 b0 @# _' n; M/ ucles, suggests peripheral or pseudopuberty.1-3 We% w6 N% f* M" P3 \( U( P$ q
report a 16-month-old boy who presented with the
0 E  r; g" p* i; Y6 q" Y8 e0 @5 {* I& uenlargement of the phallus and pubic hair develop-) g, e' F: H7 n, ?
ment without testicular enlargement, which was due
1 J3 z5 [. ^# d! P7 w. ]to the unintentional exposure to androgen gel used by
; b3 j7 y# U; c! }the father. The family initially concealed this infor-, T. i# C4 O  _- ~9 `
mation, resulting in an extensive work-up for this) K" F" n$ m) c$ I- A  @# e: j3 l& G
child. Given the widespread and easy availability of
9 Q2 {% t) [- h5 B( Rtestosterone gel and cream, we believe this is proba-
+ Q1 x  q! r" K; i* z+ z  }2 tbly more common than the rare case report in the) d* R+ m2 ]9 O
literature.4
) i+ _  D6 F2 ~; |+ l6 KPatient Report
2 v4 Q$ ^6 F3 \( m* oA 16-month-old white child was referred to the
* [9 Y+ @8 ^0 y8 Mendocrine clinic by his pediatrician with the concern
# b( \8 T- [. Jof early sexual development. His mother noticed5 _! I! e& K; }7 {. `+ k6 f& X
light colored pubic hair development when he was
) h1 S) w9 P) R) x3 L; k# EFrom the 1Division of Pediatric Endocrinology, 2University of* p, d$ ~) j2 y& ^+ C
South Alabama Medical Center, Mobile, Alabama." J+ n% w7 |  b3 d; k" [# d
Address correspondence to: Samar K. Bhowmick, MD, FACE,
" }/ ?( {1 a: Q* R: L& u6 n1 |Professor of Pediatrics, University of South Alabama, College of
1 A/ T2 q$ ?# W5 F0 MMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! B) V  u' w6 m% v
e-mail: [email protected].
  J- w" k% I( r1 J' M% d+ oabout 6 to 7 months old, which progressively became
* q" Q* s: w! A5 w) h# ndarker. She was also concerned about the enlarge-4 E; O* d0 q$ `/ x! b  M! G
ment of his penis and frequent erections. The child
0 y1 @" ~8 l7 O0 N# Rwas the product of a full-term normal delivery, with, o1 L$ M- h7 S& i
a birth weight of 7 lb 14 oz, and birth length of
* N9 n' E$ O% o4 o20 inches. He was breast-fed throughout the first year
& Y0 N1 w8 }1 s/ ]: t! P; H8 ?  Aof life and was still receiving breast milk along with( w+ n" i7 w' H+ A! B5 ^6 a) z
solid food. He had no hospitalizations or surgery,! o! C; _! l) d5 B, R
and his psychosocial and psychomotor development
5 G' k1 o  z( w& Y1 Pwas age appropriate.9 d, H# j  @8 v/ @% \% U% D
The family history was remarkable for the father," `7 _/ N- v- {# ?% L, i
who was diagnosed with hypothyroidism at age 16,  F7 p7 ]% P& q% T. u3 \6 L
which was treated with thyroxine. The father’s4 U- T( k- C( ?. }
height was 6 feet, and he went through a somewhat
% O1 k! |& |8 O8 c3 Y! {early puberty and had stopped growing by age 14.
  |: b0 S0 o- x3 ]The father denied taking any other medication. The
, {7 m9 ?5 u# p$ jchild’s mother was in good health. Her menarche
* c$ `, ]# r. }3 k/ W# {was at 11 years of age, and her height was at 5 feet
* Y  I0 C' T7 t! X/ u4 U5 inches. There was no other family history of pre-
+ T/ u4 l5 b' Y  \$ Ycocious sexual development in the first-degree rela-  H/ s! j1 e% A, ]# w5 b' b
tives. There were no siblings.
1 G* H. O4 `+ R+ j+ vPhysical Examination
6 S. u  l- P' Z; yThe physical examination revealed a very active,
! X3 m% `; x5 |6 m) ]/ d- pplayful, and healthy boy. The vital signs documented+ L8 \. _' Z9 {
a blood pressure of 85/50 mm Hg, his length was
2 [1 F" l( R0 [- }4 J6 u% N90 cm (>97th percentile), and his weight was 14.4 kg+ u$ I) p0 u8 z  {7 E0 x1 C
(also >97th percentile). The observed yearly growth
1 j% s# m! U7 S! o( v/ d$ Hvelocity was 30 cm (12 inches). The examination of
5 W" W& u! y# Q  C. @7 @; A; jthe neck revealed no thyroid enlargement.
' y+ V% f8 ^+ Y, Z! X" H( j/ N4 f6 gThe genitourinary examination was remarkable for. l8 `3 C$ ]( f" h
enlargement of the penis, with a stretched length of$ ~1 ~& o$ [6 e8 F+ N5 B
8 cm and a width of 2 cm. The glans penis was very well/ I9 E4 }4 v( q1 \; x
developed. The pubic hair was Tanner II, mostly around1 H; B$ R4 w' q3 U
540, F. t9 v# H/ H1 T. G& ]( O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. g+ f" }& T9 c$ D5 z8 l7 tthe base of the phallus and was dark and curled. The
) L7 \* h' Z" q- Htesticular volume was prepubertal at 2 mL each.
5 P, {- ^8 G0 Z& ^0 b6 jThe skin was moist and smooth and somewhat2 A, S" r3 o! @. Q1 Q
oily. No axillary hair was noted. There were no
/ B/ B4 m) D  ?+ J* R" oabnormal skin pigmentations or café-au-lait spots.
$ Q. |  G( p. [4 _3 WNeurologic evaluation showed deep tendon reflex 2+, L% V# ^% i) O. a: j- {
bilateral and symmetrical. There was no suggestion
5 B  x$ I7 V0 L+ ?of papilledema.
" N+ \( v) ]1 W3 a1 t  tLaboratory Evaluation
  c5 e1 P; D3 M8 O- r; z' hThe bone age was consistent with 28 months by
2 v7 }- K8 E4 d1 Gusing the standard of Greulich and Pyle at a chrono-
6 {( W8 |) G! O/ G) \logic age of 16 months (advanced).5 Chromosomal7 I$ l7 Y0 {- P+ q3 o. ^
karyotype was 46XY. The thyroid function test
$ x' e, ^& ]- c4 q4 K+ dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
- h% P( Y% R" b1 d/ y9 O) m1 ulating hormone level was 1.3 µIU/mL (both normal).
/ O: z" e$ q* u, o4 ~& e# k# ZThe concentrations of serum electrolytes, blood
/ _- ?5 T# e" N( Wurea nitrogen, creatinine, and calcium all were8 }8 K5 I1 {( o7 r/ w
within normal range for his age. The concentration
( p. I" C0 _. H3 lof serum 17-hydroxyprogesterone was 16 ng/dL/ m$ R% j7 W' @* F7 w0 s: V
(normal, 3 to 90 ng/dL), androstenedione was 20; n# U. Q! g' {! M, v+ U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 D: W* d2 h7 l& r# J
terone was 38 ng/dL (normal, 50 to 760 ng/dL),6 a$ L' k( J3 u; i
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
. v. n4 l. Z* {# u& I49ng/dL), 11-desoxycortisol (specific compound S)+ H8 H2 t, W" G9 A- |/ \
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; W& V& b& L, C1 r; f) V
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total6 S5 [3 x& a7 f/ }  B% ]
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),& z8 Q! A& L) {& j
and β-human chorionic gonadotropin was less than
  \& U% w6 N* @. J' I5 mIU/mL (normal <5 mIU/mL). Serum follicular
4 s9 l2 T1 o' Q9 \7 jstimulating hormone and leuteinizing hormone# n/ s) k- |/ w4 W) A5 |
concentrations were less than 0.05 mIU/mL
: g/ i$ A- Y2 V) h/ k2 t(prepubertal).' B6 x1 k" E5 ^: r. e+ t! v6 G( f6 v
The parents were notified about the laboratory5 V# _& a/ T, V3 m& F
results and were informed that all of the tests were
3 n! p, i9 g6 snormal except the testosterone level was high. The6 n: E8 _9 u! c: b6 ~# ^, F/ f; f
follow-up visit was arranged within a few weeks to0 {; ~+ f1 M, n8 \, r0 q3 N; m
obtain testicular and abdominal sonograms; how-# T$ n7 S2 J8 E7 Y% `7 A
ever, the family did not return for 4 months.
% X- C' V4 K9 x# \. @- aPhysical examination at this time revealed that the+ i# c. Q- _" d/ b
child had grown 2.5 cm in 4 months and had gained
7 ^* x, g$ ]% E: x4 ]% ?) l2 kg of weight. Physical examination remained
1 g% {: I, P8 eunchanged. Surprisingly, the pubic hair almost com-
; e7 \" F8 i  ]5 A2 P/ s& wpletely disappeared except for a few vellous hairs at
- I' s0 u! [4 D& rthe base of the phallus. Testicular volume was still 21 f; D, ^/ r# R8 y% I
mL, and the size of the penis remained unchanged.- Z9 D+ A+ S, a+ y4 v$ ]. r
The mother also said that the boy was no longer hav-
$ ?3 v: H6 d* L/ oing frequent erections.
! ]% ?( m2 ]1 Q; T+ SBoth parents were again questioned about use of( R5 U8 e7 U/ j+ l# [
any ointment/creams that they may have applied to+ ?# q; @* |7 `4 _% n
the child’s skin. This time the father admitted the
# O; l: o8 Z% z% K/ a1 K1 O& c( F& nTopical Testosterone Exposure / Bhowmick et al 541
5 }8 r( b/ o, Tuse of testosterone gel twice daily that he was apply-9 j) p0 }7 y8 Z# c" \; M
ing over his own shoulders, chest, and back area for
( Z/ T+ M! W- j$ J$ c; n; \* p& da year. The father also revealed he was embarrassed. t( S3 N  H6 o6 t* y" P7 w
to disclose that he was using a testosterone gel pre-* R% `! }5 ]9 @# l$ C
scribed by his family physician for decreased libido. g; X; D5 |! d* c
secondary to depression.
4 u1 K$ F0 b8 W0 XThe child slept in the same bed with parents.! A9 l6 K( u4 W' ]8 S0 s5 ~' n  }( ]
The father would hug the baby and hold him on his
& e2 t2 w4 c/ E1 _8 `chest for a considerable period of time, causing sig-4 Y) e5 C$ v4 H% \
nificant bare skin contact between baby and father.3 ^4 N7 W% t& r2 C4 Y# W, |
The father also admitted that after the phone call,# z1 q) u7 q! @8 D
when he learned the testosterone level in the baby' ]2 M# {2 p8 u& j
was high, he then read the product information/ Z- K1 a1 {6 B; l" {- ~
packet and concluded that it was most likely the rea-, j& h4 ^( d. c3 x6 B
son for the child’s virilization. At that time, they
% K) U  Z2 ?$ V. a7 G7 l+ K( cdecided to put the baby in a separate bed, and the5 f5 @: ]0 O: m1 n6 R" Y% `  U
father was not hugging him with bare skin and had) _+ e+ P% p+ T" \- `- o# t
been using protective clothing. A repeat testosterone
* a' N* J2 p0 U0 x  R0 j' \test was ordered, but the family did not go to the) q/ o! a% H/ V3 Y
laboratory to obtain the test.
' [( R5 o; T1 M5 y) HDiscussion0 q5 @! B: o. I  b7 i: k9 v
Precocious puberty in boys is defined as secondary
0 v8 m0 P; ^3 i5 ysexual development before 9 years of age.1,4' w$ X3 ~  o$ e
Precocious puberty is termed as central (true) when
! Z7 ^- a: f6 s  K5 t$ u, [it is caused by the premature activation of hypo-; p$ _% D- e: d% G  F$ p) V# ^
thalamic pituitary gonadal axis. CPP is more com-
) E( n# V) [& ^7 C0 n, n6 ~2 \mon in girls than in boys.1,3 Most boys with CPP
6 S3 _: E8 E4 ^( \& umay have a central nervous system lesion that is
% V3 g( N$ I# Presponsible for the early activation of the hypothal-
2 N- c1 p& {% k+ ~3 Z' k" eamic pituitary gonadal axis.1-3 Thus, greater empha-6 p" L8 n8 t, k2 V
sis has been given to neuroradiologic imaging in
5 F( ~: Z2 [, qboys with precocious puberty. In addition to viril-
) e5 O% Y5 s% b+ H: L1 S" b, xization, the clinical hallmark of CPP is the symmet-+ }) ^" x% `/ s  a  C: _8 ~! R
rical testicular growth secondary to stimulation by
1 f! j6 ~6 x5 dgonadotropins.1,3
' v4 F6 x6 n% W. OGonadotropin-independent peripheral preco-
; R4 m, W, p; n$ Q+ Z( @cious puberty in boys also results from inappropriate
' a8 Y) \, n. L7 H& qandrogenic stimulation from either endogenous or
/ T! w) x8 x$ i6 M9 m8 w: kexogenous sources, nonpituitary gonadotropin stim-
& W) s6 ]/ r7 ?5 L; Q, f6 Z  k9 oulation, and rare activating mutations.3 Virilizing
: c1 }1 ?! f/ T. B, s, Hcongenital adrenal hyperplasia producing excessive9 V# _6 H0 X+ x
adrenal androgens is a common cause of precocious/ U, E6 b1 |6 i0 t
puberty in boys.3,4
+ V: j9 z) G! `1 Y2 _4 i4 PThe most common form of congenital adrenal8 \/ w/ h. g5 {
hyperplasia is the 21-hydroxylase enzyme deficiency.; ?  `& K( C1 M1 b" u
The 11-β hydroxylase deficiency may also result in! [1 Z- l5 }0 P+ c( a7 G
excessive adrenal androgen production, and rarely,
1 d9 n; L3 b9 B( a0 T% nan adrenal tumor may also cause adrenal androgen) H/ G2 p2 @$ Y! s
excess.1,3
0 F2 O3 @8 f8 p" t! N$ O6 z9 O9 q1 Wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# D5 U' c1 i. e
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 p4 P7 O9 U3 c" n* v8 x. G! `A unique entity of male-limited gonadotropin-2 H% ?; }0 M  w
independent precocious puberty, which is also known
  d+ a# `% v" R* |' O3 V( h1 Kas testotoxicosis, may cause precocious puberty at a! K& b- k4 [6 W& M" I4 Z6 W
very young age. The physical findings in these boys: x* z! F8 ^' G, O$ S* ?# I0 W  ~
with this disorder are full pubertal development,
- g6 C- T1 k3 y9 gincluding bilateral testicular growth, similar to boys
. C6 {* {6 Y% D# ?; `0 Kwith CPP. The gonadotropin levels in this disorder
/ H3 _- v# T; n) ~* Hare suppressed to prepubertal levels and do not show
/ h- X3 M: g3 K/ X3 m+ E; `pubertal response of gonadotropin after gonadotropin-9 j% V9 U8 m5 s
releasing hormone stimulation. This is a sex-linked
0 P6 a  ~; o" K/ Eautosomal dominant disorder that affects only
7 |" ]% b' h/ V& B/ ^9 H6 Smales; therefore, other male members of the family  w3 N/ |8 i3 }: X
may have similar precocious puberty.3+ c1 n- A/ Y# ?5 S( f
In our patient, physical examination was incon-  E' L# D& O4 \" f+ N' j6 ?
sistent with true precocious puberty since his testi-
* B! s# X6 I, T5 J9 `+ n8 z2 y+ Acles were prepubertal in size. However, testotoxicosis
  F! b  l+ E; X7 W6 Hwas in the differential diagnosis because his father) m% m2 t' L0 {( T$ o
started puberty somewhat early, and occasionally,/ e# H: d1 E' [+ Z! V3 S9 B( e( o; M
testicular enlargement is not that evident in the
' t# `6 l  U+ r4 Q# cbeginning of this process.1 In the absence of a neg-
: C) R' T; j4 ]ative initial history of androgen exposure, our" ^9 y2 J( Z& G3 L3 s$ s) n: x
biggest concern was virilizing adrenal hyperplasia,+ M5 Y4 R0 K$ K' v3 h$ H
either 21-hydroxylase deficiency or 11-β hydroxylase9 P% `, w+ J  ?3 V. u7 k$ b  J
deficiency. Those diagnoses were excluded by find-
8 H5 Y1 G  g9 xing the normal level of adrenal steroids.
! E7 p3 R4 X3 {* Y1 hThe diagnosis of exogenous androgens was strongly, j$ B8 @: {: G3 C/ a2 ]! J
suspected in a follow-up visit after 4 months because1 g: x8 ?+ E6 [) |
the physical examination revealed the complete disap-6 ]2 [1 f) t6 f
pearance of pubic hair, normal growth velocity, and
5 X6 P! `" I; c4 M3 ddecreased erections. The father admitted using a testos-( d- w; w0 }' B- n" V: x5 c
terone gel, which he concealed at first visit. He was
8 m& Y2 y! V# i& ^! d3 Z1 }( Kusing it rather frequently, twice a day. The Physicians’" \- [5 f; l* ]; r
Desk Reference, or package insert of this product, gel or5 ?4 x( D+ U' U7 r, A/ u
cream, cautions about dermal testosterone transfer to
6 e3 i$ Y5 k; K: I( q0 ^unprotected females through direct skin exposure., c2 ]! R' N+ b5 W
Serum testosterone level was found to be 2 times the
6 r6 F  z, @+ @. c$ P) Xbaseline value in those females who were exposed to
9 t& f: O% `  n7 Z4 Jeven 15 minutes of direct skin contact with their male1 b0 z- Z. x: e6 a( K# ]) P2 T3 M
partners.6 However, when a shirt covered the applica-
! W" N  z# u' Q7 ~" F. wtion site, this testosterone transfer was prevented.
  b# h1 r, U. U' L0 O; M, ]Our patient’s testosterone level was 60 ng/mL,# p  {' u# \# l
which was clearly high. Some studies suggest that7 X( |) S1 C3 @# v# C6 A- x. C2 _
dermal conversion of testosterone to dihydrotestos-
, t# Q4 u, {) vterone, which is a more potent metabolite, is more" e( q) U6 F8 e, k4 y: T$ f
active in young children exposed to testosterone" q$ L2 P1 D/ r4 Q2 V" j* Q9 }/ B5 u$ r
exogenously7; however, we did not measure a dihy-% D9 s2 Q6 Q2 _5 \+ ]1 W+ E
drotestosterone level in our patient. In addition to
/ L* }# |2 E9 ~' k5 Q' Jvirilization, exposure to exogenous testosterone in8 D2 M* t6 d( v
children results in an increase in growth velocity and4 f5 E7 S. C: q( B
advanced bone age, as seen in our patient.
# A9 P% \' z: }3 tThe long-term effect of androgen exposure during
7 r' U' V: r3 W5 r8 Y* Searly childhood on pubertal development and final. A  M( }1 g5 E# e% t" n$ @6 [
adult height are not fully known and always remain' I* s. ]) N5 a% R( f2 V# A, y( P
a concern. Children treated with short-term testos-
: C3 i+ G6 l+ Lterone injection or topical androgen may exhibit some
* A1 l6 \7 @, p# s) \acceleration of the skeletal maturation; however, after5 \. @1 ^& X, X8 y: X/ K& p
cessation of treatment, the rate of bone maturation
$ ?7 Z3 J1 t, a8 Q" \decelerates and gradually returns to normal.8,9
* e$ R8 C, C& jThere are conflicting reports and controversy
. ], h6 N1 Q# K+ n7 B5 U4 }* wover the effect of early androgen exposure on adult& s0 }8 Q8 {$ K+ A0 A2 O
penile length.10,11 Some reports suggest subnormal
0 n& b+ a. p2 s( B% Zadult penile length, apparently because of downreg-0 O4 w& T% ]+ p7 `- L+ D2 x
ulation of androgen receptor number.10,12 However,
3 J1 K* \, ^5 F2 P& e! K( ZSutherland et al13 did not find a correlation between6 N7 L% y% ]! J$ b* k2 n
childhood testosterone exposure and reduced adult
  G6 m( M& u( Kpenile length in clinical studies.
- D0 Q, R  D6 ]. x+ pNonetheless, we do not believe our patient is
5 S8 f/ x2 L- Y5 t7 sgoing to experience any of the untoward effects from2 ~) z7 w1 e, G
testosterone exposure as mentioned earlier because
9 V8 o+ O5 B& {0 @the exposure was not for a prolonged period of time.
  l  f+ M. I9 {Although the bone age was advanced at the time of! ?* q" Z3 P* T4 j2 S9 _
diagnosis, the child had a normal growth velocity at" R; Z  A" {3 ?/ h. W: R! W9 b& {1 C
the follow-up visit. It is hoped that his final adult
  f1 ]& H7 @7 \1 Z8 ^5 X+ Zheight will not be affected.6 P0 t# t3 m# m  l
Although rarely reported, the widespread avail-5 _% C( D1 t- ~; I9 U1 u: W: a4 N! ~
ability of androgen products in our society may
3 s+ A6 l7 u6 |4 ~indeed cause more virilization in male or female8 b/ y6 A% g! o/ N# Q
children than one would realize. Exposure to andro-1 m- h) ]5 y: U$ D/ {
gen products must be considered and specific ques-
8 y  F: @  B, K. rtioning about the use of a testosterone product or8 W+ T6 p- E! P/ }1 O+ c6 R$ b
gel should be asked of the family members during
) j- e& r9 \8 S3 X. Tthe evaluation of any children who present with vir-
3 R4 P7 j* A: V& _& V3 Kilization or peripheral precocious puberty. The diag-) T, p  e$ P7 A; p# n8 a/ I
nosis can be established by just a few tests and by" a& _3 D5 M1 d/ V3 D! i0 x
appropriate history. The inability to obtain such a! X' m6 O! {' K+ J" N
history, or failure to ask the specific questions, may
% `3 b% E+ }+ m2 bresult in extensive, unnecessary, and expensive
2 i8 ?  j, D' U: S5 \investigation. The primary care physician should be2 [6 Y& u6 U/ t0 O1 n1 h
aware of this fact, because most of these children
! \2 A/ ^( _6 P. A0 e! [, v* m: zmay initially present in their practice. The Physicians’9 H- \: G2 D4 X& T# B; H
Desk Reference and package insert should also put a) _, F5 W4 B- Q( e" G
warning about the virilizing effect on a male or. T) Q" X6 X6 j: K: [9 M5 K1 a
female child who might come in contact with some-
& O3 X* M1 I; q. cone using any of these products.! z; B9 J7 t7 o; p8 g6 {" m
References4 d9 a6 f1 F& V: z" _
1. Styne DM. The testes: disorder of sexual differentiation' z9 q3 \  ?& m4 p1 ~- H
and puberty in the male. In: Sperling MA, ed. Pediatric
: w7 F" b# ?1 V; Y4 l( qEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 V: Z- A3 v! `2002: 565-628.
4 a: z9 U  x. j+ }2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! x+ b; e3 Q8 W5 jpuberty in children with tumours of the suprasellar pineal
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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
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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
: R  V, T: U, e5 V
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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