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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
3 _9 n# |. U! KBoy Induced by Indirect Topical( x0 U! f# B& c' F( m* L- y
Exposure to Testosterone
4 P) b, b* t3 |% b& X) E4 \Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 B. p2 B, L5 H9 r+ _
and Kenneth R. Rettig, MD1$ A- P2 v. \' S8 z5 Y5 G
Clinical Pediatrics
- D* o. ]" n: a# UVolume 46 Number 6; }8 A2 S, |, p7 V' g- B) c
July 2007 540-543
- t5 n" ?3 S; F! x- k% _4 `  F: Y© 2007 Sage Publications
6 |, ?4 O5 d9 |7 U10.1177/0009922806296651
' U& R. O# t0 U3 O/ B" H- @http://clp.sagepub.com  i, t  y, j1 L" c
hosted at
. \8 R; S1 Y7 Nhttp://online.sagepub.com
4 }7 t4 H, c# ~9 ~6 c0 T/ o% j; L6 ]Precocious puberty in boys, central or peripheral,
8 \4 L1 u. n; p9 Gis a significant concern for physicians. Central& E" q* m0 E  @2 i# k1 W" J  D4 m! @
precocious puberty (CPP), which is mediated
9 m9 h" o& H1 Ythrough the hypothalamic pituitary gonadal axis, has
7 o( G" H; v6 h- e& y$ U8 O1 Ma higher incidence of organic central nervous system
2 W5 Z% g& @0 Q9 S( \' glesions in boys.1,2 Virilization in boys, as manifested4 b2 S' G1 u/ A8 r. G) v1 U
by enlargement of the penis, development of pubic
8 m4 y. d% [, F# Bhair, and facial acne without enlargement of testi-1 E" I' d3 \% Q/ C0 c
cles, suggests peripheral or pseudopuberty.1-3 We
$ A  S* i7 c" N8 p! R: wreport a 16-month-old boy who presented with the" d7 T' |  m6 {) [% C* ]
enlargement of the phallus and pubic hair develop-
1 v, }, ~* o# v; W" lment without testicular enlargement, which was due! j6 F7 t0 O$ d2 A! K
to the unintentional exposure to androgen gel used by, @; _/ _8 U- U* n# U3 l( {$ C# R
the father. The family initially concealed this infor-' v& j9 O2 Q# _$ h4 X/ i6 G; J
mation, resulting in an extensive work-up for this
8 P5 A. x* \, M& |5 h9 e8 Z' {child. Given the widespread and easy availability of+ T( f9 y: x; l; }4 u: b$ p* z
testosterone gel and cream, we believe this is proba-3 B0 [) j8 N5 X# I
bly more common than the rare case report in the
+ I* n$ \- f" ?literature.43 ~  @/ h- C; M8 i5 v. Z  a9 [8 y
Patient Report
6 N5 N7 _3 E+ BA 16-month-old white child was referred to the
$ O) I# s  G& E* C' |! X7 `endocrine clinic by his pediatrician with the concern
# m' k0 l* P/ h$ t+ Yof early sexual development. His mother noticed
" U% D4 h/ I3 u5 ?3 U8 alight colored pubic hair development when he was
2 ?' W; F* B: yFrom the 1Division of Pediatric Endocrinology, 2University of+ e+ r$ D" {( n% h
South Alabama Medical Center, Mobile, Alabama.! w" S7 s0 M! T8 i' F- i
Address correspondence to: Samar K. Bhowmick, MD, FACE,
2 B6 M. g2 W" F: y+ _Professor of Pediatrics, University of South Alabama, College of$ a4 Y" m+ d! l4 o
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. }8 a2 N2 m  P6 Y3 ~
e-mail: [email protected].& H6 P) \) i& h
about 6 to 7 months old, which progressively became1 n3 w& w- O9 b' a/ ^1 f
darker. She was also concerned about the enlarge-; I! r7 j& }6 ^  r- ]! z
ment of his penis and frequent erections. The child# ?( A5 \! w9 z( [
was the product of a full-term normal delivery, with; m. P" c* e1 _+ P. q6 S
a birth weight of 7 lb 14 oz, and birth length of
8 P3 |+ V: ?% D3 m6 G20 inches. He was breast-fed throughout the first year3 v8 t6 @; a8 u# Q6 a# _: g
of life and was still receiving breast milk along with/ a/ t& N$ V$ e6 l$ [6 w  U2 s
solid food. He had no hospitalizations or surgery,1 V5 t! \! `5 Y' O7 s
and his psychosocial and psychomotor development0 l% b3 n0 c: Y2 t+ B1 N3 Q
was age appropriate.4 m$ v9 l, j; z  S
The family history was remarkable for the father,* I8 H8 [5 ?' V$ D# C
who was diagnosed with hypothyroidism at age 16,: K( L. z6 R. H1 A8 S  V
which was treated with thyroxine. The father’s
' _( u, v* s& M9 [" R" v- Qheight was 6 feet, and he went through a somewhat! }2 ?: l5 G! S" n
early puberty and had stopped growing by age 14.# v- V" e+ o8 C8 H- n( c
The father denied taking any other medication. The9 |. v8 m) s7 u  ]1 O8 W
child’s mother was in good health. Her menarche
4 o& m! H2 t+ ]4 K9 Uwas at 11 years of age, and her height was at 5 feet/ n$ A5 m; @9 y
5 inches. There was no other family history of pre-" y: r  [+ ~6 j" K
cocious sexual development in the first-degree rela-
/ N3 z' q) K) ^  |) H6 Ttives. There were no siblings.1 ?6 I% S; U, b7 `6 Q
Physical Examination3 U( O, S7 T. ~6 H
The physical examination revealed a very active,
. q# W. r* [  ^$ H; wplayful, and healthy boy. The vital signs documented
+ U2 m* L; |7 Ia blood pressure of 85/50 mm Hg, his length was
8 W# p- w, S- Q6 ^90 cm (>97th percentile), and his weight was 14.4 kg
$ S/ t) T+ X1 ]  g! {(also >97th percentile). The observed yearly growth% @5 }$ P! P& ]0 ~
velocity was 30 cm (12 inches). The examination of( t8 S( [2 t6 P0 `- ]% `  e
the neck revealed no thyroid enlargement.
9 }, f0 X  q" }$ sThe genitourinary examination was remarkable for7 M8 a1 \8 K+ c8 |& @% x2 M1 }
enlargement of the penis, with a stretched length of6 ^- T( y+ f9 V
8 cm and a width of 2 cm. The glans penis was very well4 G2 K1 C* H0 e! ^
developed. The pubic hair was Tanner II, mostly around8 u$ Q/ g  X0 j6 L  b
540% X/ G( c8 y; E/ ]1 T# w" x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 {) [9 I/ I. o: A
the base of the phallus and was dark and curled. The2 m; u# ~1 W/ n" u$ u% O/ o
testicular volume was prepubertal at 2 mL each.2 ^% O9 u9 C: T, _, ^1 c
The skin was moist and smooth and somewhat) k5 L& q; H0 V" r7 U5 `1 C- x
oily. No axillary hair was noted. There were no
  z1 @- p9 `3 R: [4 L! E; Aabnormal skin pigmentations or café-au-lait spots.
( g% d0 b4 w4 r+ NNeurologic evaluation showed deep tendon reflex 2+6 ?* ~  ^( z. f0 X6 Y1 i2 Z1 w
bilateral and symmetrical. There was no suggestion
$ Y, J' W1 l$ L; [3 D) f6 q( pof papilledema.
6 w2 W# V- Z& Q2 i' z& O. wLaboratory Evaluation  l" W- l6 a* R: A
The bone age was consistent with 28 months by
. W% U. H) L) ]) |/ Cusing the standard of Greulich and Pyle at a chrono-3 H/ Z  y: b6 N4 g9 n# ^2 y
logic age of 16 months (advanced).5 Chromosomal
+ F) o$ y6 |. l4 ]- F# {karyotype was 46XY. The thyroid function test
6 S( m! O  Q1 i9 K$ d9 n" Zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 x& ?  U4 t; N$ `- [$ R! Elating hormone level was 1.3 µIU/mL (both normal)., E+ c; S' w5 \0 a9 W7 s$ W
The concentrations of serum electrolytes, blood9 d/ O% }/ e% b
urea nitrogen, creatinine, and calcium all were
. v! F: U/ W9 E1 S: C7 rwithin normal range for his age. The concentration7 \; C% s% t$ @0 L2 W
of serum 17-hydroxyprogesterone was 16 ng/dL
& G% M  m2 k, y" z, f/ K+ F(normal, 3 to 90 ng/dL), androstenedione was 20- M) k( W' K0 ~' e4 |/ h- e
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-. I' Q5 _/ @' U( ^% ?
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
  ]0 M( w$ t2 ]! ^+ D% j+ ]3 Bdesoxycorticosterone was 4.3 ng/dL (normal, 7 to. ?* u! @) `) N$ Y
49ng/dL), 11-desoxycortisol (specific compound S)
# Y! a- z+ w! ^. u- e& K3 Dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
" @5 @4 B0 ~" _tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total3 r, _& N7 ~) ~2 C
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),! p" v5 k7 c. ^. l
and β-human chorionic gonadotropin was less than
1 W% |) ^" L/ @) L6 X  V# N+ q5 mIU/mL (normal <5 mIU/mL). Serum follicular# j5 f' ~% }, _2 b0 B, ^- L/ y0 R
stimulating hormone and leuteinizing hormone+ q  j  Y' w* i$ I6 A, [
concentrations were less than 0.05 mIU/mL
7 j; {  C9 W7 C, e. V(prepubertal).; u' \6 l/ o/ V6 y5 B
The parents were notified about the laboratory0 e' {% H+ M& J2 M
results and were informed that all of the tests were2 t0 G0 @4 p4 a' C: f
normal except the testosterone level was high. The! M6 d- J$ ^6 x$ W' z) ?
follow-up visit was arranged within a few weeks to  M; r" z  q9 U; n2 [2 I" ^1 y
obtain testicular and abdominal sonograms; how-+ P9 Z$ [8 Y( [  O7 X: M* i
ever, the family did not return for 4 months.9 J% r* l5 S8 H
Physical examination at this time revealed that the& H- t5 T, @9 I1 w% Q$ e
child had grown 2.5 cm in 4 months and had gained" Z& J& s$ R% P8 _* [
2 kg of weight. Physical examination remained
, A$ M3 ]3 O- r/ v/ N7 o! ?  Lunchanged. Surprisingly, the pubic hair almost com-
( q: \) q) E4 J9 E) R. ypletely disappeared except for a few vellous hairs at
9 F/ I' Q( }7 E/ qthe base of the phallus. Testicular volume was still 2
8 H+ ~( [$ X5 W5 d3 [6 H6 HmL, and the size of the penis remained unchanged.
8 w/ z0 h, D: t& r& \- [The mother also said that the boy was no longer hav-
9 W4 F8 `& ?; o) v% L3 F5 }ing frequent erections.
1 o& x& G  |: G; vBoth parents were again questioned about use of
* U  B1 [4 Z+ r' c" u) h5 u3 lany ointment/creams that they may have applied to8 b+ o: i6 }* Q7 z. g9 s
the child’s skin. This time the father admitted the
, A* ?3 K5 |$ {* n# ~Topical Testosterone Exposure / Bhowmick et al 5412 H5 X4 J' `' `  ?
use of testosterone gel twice daily that he was apply-
' `3 N1 D' p) d* ~1 q8 P% E. Ving over his own shoulders, chest, and back area for7 B" m, r4 p! u! u
a year. The father also revealed he was embarrassed  U3 v0 k; Q! J
to disclose that he was using a testosterone gel pre-: U% M/ q; N7 T% j" `' \
scribed by his family physician for decreased libido# E; V: T* M( `  i; o
secondary to depression.
/ s" Q4 c8 k( J$ v7 xThe child slept in the same bed with parents." m) M7 B& {( b7 T4 d6 p
The father would hug the baby and hold him on his
" K7 e! ~, Z  schest for a considerable period of time, causing sig-, E) q6 I/ e  p1 g2 v: l
nificant bare skin contact between baby and father.
: A3 A7 F  L6 Y% q& oThe father also admitted that after the phone call,
% ^$ A' }: {' \7 K% U$ P# Ewhen he learned the testosterone level in the baby
4 n2 |% C- Z8 \6 H/ Zwas high, he then read the product information
2 y7 j0 A5 y3 ?# k6 i+ Z) j) npacket and concluded that it was most likely the rea-+ y1 p; e, ?8 V) d7 R: _& K3 f
son for the child’s virilization. At that time, they
( S! c; h# J4 m3 U& P, e1 vdecided to put the baby in a separate bed, and the* C/ f2 C* c3 z- x7 K" _2 I
father was not hugging him with bare skin and had
4 Q9 ]+ I# s5 }been using protective clothing. A repeat testosterone
- Z3 E1 [9 _; d* |2 y/ t5 utest was ordered, but the family did not go to the  V( n3 B7 J) B9 p: x
laboratory to obtain the test.
9 O1 p) r! {9 IDiscussion( C8 J. C3 B( }3 j
Precocious puberty in boys is defined as secondary3 f, I8 u" i1 c8 a
sexual development before 9 years of age.1,4
1 P6 }3 _- e% |; V+ M8 L: jPrecocious puberty is termed as central (true) when
3 L; y0 p+ m/ j* k9 }& |1 N4 h1 ]it is caused by the premature activation of hypo-4 G4 F, ~% q( ^( g+ E0 I
thalamic pituitary gonadal axis. CPP is more com-' u( X( L% A! O+ _( n' @! k3 V) o
mon in girls than in boys.1,3 Most boys with CPP
& g, T) t: k6 x0 Fmay have a central nervous system lesion that is
* L$ A: H6 j# l+ xresponsible for the early activation of the hypothal-5 k; q" Z& f: X% D+ O+ M0 O/ }
amic pituitary gonadal axis.1-3 Thus, greater empha-( \7 G' ]0 m( I4 y- ^6 J' K
sis has been given to neuroradiologic imaging in
. t3 A8 K  O# Cboys with precocious puberty. In addition to viril-
7 |. S3 A7 J$ B- E% dization, the clinical hallmark of CPP is the symmet-
3 \4 M/ d$ \* N+ erical testicular growth secondary to stimulation by
8 b6 K$ s! q$ G6 [; @gonadotropins.1,3
  g% S6 W* F) Q( p  |( h" GGonadotropin-independent peripheral preco-
* v0 J8 O' h0 f( @# Ocious puberty in boys also results from inappropriate: Q0 J' i* l+ m2 D, C/ [  H
androgenic stimulation from either endogenous or0 a8 c( R1 q- {2 a
exogenous sources, nonpituitary gonadotropin stim-# P, b, m+ p9 w* I) H
ulation, and rare activating mutations.3 Virilizing
4 g. e( f/ `/ J. `4 \, o, vcongenital adrenal hyperplasia producing excessive
! i3 f/ B( D$ e7 @: E& X/ Padrenal androgens is a common cause of precocious
+ T9 B' w$ ]0 }5 L# M* upuberty in boys.3,40 h! y5 j; e. k* q3 p& o" c
The most common form of congenital adrenal! H( k% }- S3 @) V
hyperplasia is the 21-hydroxylase enzyme deficiency.
, [$ u+ S1 m! ]5 s) |. ~1 gThe 11-β hydroxylase deficiency may also result in: E6 L/ L5 l" K
excessive adrenal androgen production, and rarely,
4 g2 ]! J6 |. i5 v* n- jan adrenal tumor may also cause adrenal androgen& L7 m7 S$ r6 Y
excess.1,35 ?1 L" j7 w9 `, v) q+ _% U
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542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: ^) f3 o$ Y: e5 X1 K5 f5 R; ?
A unique entity of male-limited gonadotropin-. E$ X5 @0 J! y+ ~5 M) @5 T
independent precocious puberty, which is also known
' b0 G* N. v0 y# j: r1 J1 Has testotoxicosis, may cause precocious puberty at a
( H( n3 `- N# w# q3 T* Overy young age. The physical findings in these boys8 b" t: G& j# u0 l  C4 B
with this disorder are full pubertal development,9 K5 ?1 g7 w2 r2 a0 Y; T2 e( H
including bilateral testicular growth, similar to boys) U! Z& {& t! U7 `5 L! F
with CPP. The gonadotropin levels in this disorder& K1 D. F5 m  w/ L
are suppressed to prepubertal levels and do not show
# ?. A( k7 `( Y2 J# }* spubertal response of gonadotropin after gonadotropin-, l2 M7 {0 j9 h$ N, v2 i9 e
releasing hormone stimulation. This is a sex-linked: {& N4 l# W( f1 F, b
autosomal dominant disorder that affects only9 y; ^! q  O8 E7 I  ?! N
males; therefore, other male members of the family
/ ^0 @! Q8 q  k4 T( Tmay have similar precocious puberty.3
  l) r8 t/ l: T+ C) \) MIn our patient, physical examination was incon-
# S5 Y1 N* _- p$ Lsistent with true precocious puberty since his testi-- ~, {0 j1 b& w9 q. b
cles were prepubertal in size. However, testotoxicosis
) e5 V  n+ z7 n/ h5 kwas in the differential diagnosis because his father
# X/ d6 y( _$ Ystarted puberty somewhat early, and occasionally,
8 }7 q7 `: v$ U, Ktesticular enlargement is not that evident in the
: R6 i& L: H6 mbeginning of this process.1 In the absence of a neg-) o( K! C% E0 y2 @/ |
ative initial history of androgen exposure, our
& |6 \- D/ J) Ubiggest concern was virilizing adrenal hyperplasia,
8 d: @) `; V9 ]) Weither 21-hydroxylase deficiency or 11-β hydroxylase% L! @) B5 ~6 N$ q% T
deficiency. Those diagnoses were excluded by find-1 C) u" y0 `6 E+ F
ing the normal level of adrenal steroids.
! {5 z& b0 S( T) r+ m+ rThe diagnosis of exogenous androgens was strongly
: B2 b" x& d9 P! n6 A4 rsuspected in a follow-up visit after 4 months because( T9 V' ~" N: q: T: Q1 K
the physical examination revealed the complete disap-8 I6 G7 f5 T. a* x
pearance of pubic hair, normal growth velocity, and
" W! [! P9 a# E" R" ^. Gdecreased erections. The father admitted using a testos-/ Z0 i7 S/ L1 S" N$ G8 I: d4 ?) k
terone gel, which he concealed at first visit. He was, m2 c* ^+ d$ B. h
using it rather frequently, twice a day. The Physicians’- N$ _4 `. w, Z
Desk Reference, or package insert of this product, gel or0 A4 \, X2 Y$ i  F# h
cream, cautions about dermal testosterone transfer to, `" c1 e  [6 P; J2 a; O
unprotected females through direct skin exposure.
  s; l. K( P) }6 g# \( sSerum testosterone level was found to be 2 times the
" T$ e- U' f* ]8 kbaseline value in those females who were exposed to5 q' R+ g, a3 k
even 15 minutes of direct skin contact with their male- [9 B) I. j" ]  e( b
partners.6 However, when a shirt covered the applica-: p1 G+ T; U5 }% U, U
tion site, this testosterone transfer was prevented.
0 V# N4 [; X" UOur patient’s testosterone level was 60 ng/mL,2 q% G; h: |: I& C. n& m
which was clearly high. Some studies suggest that
9 c0 P* W9 g9 k- T3 B- b3 \dermal conversion of testosterone to dihydrotestos-- A9 k( U  }/ [+ K
terone, which is a more potent metabolite, is more; ^! D. C1 l5 S
active in young children exposed to testosterone
. F* O$ {$ b, y; ~7 Q4 qexogenously7; however, we did not measure a dihy-
8 m  I+ U- x0 |drotestosterone level in our patient. In addition to1 K8 l4 v+ C9 a7 Y
virilization, exposure to exogenous testosterone in
# V4 I! J) Y4 o( v1 ^8 n. A9 ^# ?1 mchildren results in an increase in growth velocity and
0 k6 \& s: E3 ~1 F% Z" cadvanced bone age, as seen in our patient.6 _8 R0 b. k" |& d6 `% W* O& Y& m
The long-term effect of androgen exposure during4 \' Y$ v$ c9 B' Q
early childhood on pubertal development and final$ t$ Z- `7 ~' j5 C" G/ v
adult height are not fully known and always remain
, ], t2 }; g7 d" b/ z* ~4 Ha concern. Children treated with short-term testos-( G+ g" N) W+ |5 w1 Q
terone injection or topical androgen may exhibit some; m" U- c- F' B( }/ k) @3 C
acceleration of the skeletal maturation; however, after
" g1 x0 ^" \& |+ t& s( r1 Hcessation of treatment, the rate of bone maturation: v: J6 Y- W7 U+ q
decelerates and gradually returns to normal.8,97 g# n& F# ^8 K/ d, t# q
There are conflicting reports and controversy! B9 ?$ _4 e- ]5 K! {8 f# p; Z6 ^
over the effect of early androgen exposure on adult
( f/ z9 [  ?! G5 I1 s  ?4 y5 h' Apenile length.10,11 Some reports suggest subnormal
" Y6 ~  K& J7 z+ }adult penile length, apparently because of downreg-
) E9 o" \  O, r* _- o% A5 J, W8 Bulation of androgen receptor number.10,12 However,
# A" a% b* [( c0 U& O8 E) eSutherland et al13 did not find a correlation between8 N( F" J2 s/ L. w
childhood testosterone exposure and reduced adult
( n6 P3 y. S, [2 ypenile length in clinical studies.: O5 }# `. ], [2 [) X
Nonetheless, we do not believe our patient is4 `1 y) i9 O0 c" ~
going to experience any of the untoward effects from
' {+ s0 ]7 \+ F) j* F, Dtestosterone exposure as mentioned earlier because
4 |6 B- q* N( m  m" X6 dthe exposure was not for a prolonged period of time.
! k8 H, c) A1 K! i; }1 LAlthough the bone age was advanced at the time of
+ u3 E+ n1 c: L* V$ v# idiagnosis, the child had a normal growth velocity at
, `$ q6 U/ H- G# l/ D- S3 t- J+ z* Kthe follow-up visit. It is hoped that his final adult+ c( N' t( X9 C% w0 m
height will not be affected.
; \/ K% g+ |' e, t- ~) u4 ~Although rarely reported, the widespread avail-
' Q* w1 c5 f. ?# ]# O! d- H, xability of androgen products in our society may6 e3 m* C/ |, x! K
indeed cause more virilization in male or female
  s5 Y- A. r( l4 Schildren than one would realize. Exposure to andro-0 R. X' m6 r$ M0 A* m" [
gen products must be considered and specific ques-" r6 k8 k# ^. i; l
tioning about the use of a testosterone product or) }' ^& O9 r  [! i0 ^/ t5 ^8 q1 R2 X
gel should be asked of the family members during
4 O: l. O0 Q9 m5 ythe evaluation of any children who present with vir-* d6 v1 S* [7 ^. `. b! l8 \' d9 g- ~
ilization or peripheral precocious puberty. The diag-5 J/ w+ [+ e7 A9 [+ F  ^$ [% Y: p/ C
nosis can be established by just a few tests and by
( C7 i" D1 P3 |8 O' h3 S! vappropriate history. The inability to obtain such a. C: K0 R# D  q" s
history, or failure to ask the specific questions, may
! Q  L' ]/ B7 z  O/ j7 `8 iresult in extensive, unnecessary, and expensive
" Y0 x% n! a+ Z8 Yinvestigation. The primary care physician should be
+ H5 ^% y- x+ F5 G% N( Qaware of this fact, because most of these children
$ U4 [1 R* U( k9 a0 Cmay initially present in their practice. The Physicians’7 s. v5 z# f! {5 y
Desk Reference and package insert should also put a
) f5 h8 d/ @5 \warning about the virilizing effect on a male or
% {4 P* j5 L, ^female child who might come in contact with some-/ ?- `' [9 }# s
one using any of these products.
( a& i3 k) _. M1 h2 Q/ pReferences! D( ?& x5 s; z  v
1. Styne DM. The testes: disorder of sexual differentiation
2 _/ j  @* M1 [9 s5 N( Z5 Xand puberty in the male. In: Sperling MA, ed. Pediatric
$ I! K! D, d9 A3 J; _+ n1 d$ |Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! B2 K, T2 W% q. l( @, D
2002: 565-628.
& a! b  B8 Z/ i) s7 G( x2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( r8 M' M3 |& [4 `puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old* K! `  {  H$ n1 g) Z: T: J
Boy Induced by Indirect Topical7 C8 \8 W- ~. N5 ?# [2 D; n9 D1 G
Exposure to Testosterone3 f8 v. N5 j7 m' l
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  ^. D& ~" a5 iand Kenneth R. Rettig, MD1
9 T8 v- r6 l2 Y6 I9 n, iClinical Pediatrics
+ H! A2 [3 ?* v) H2 ]6 }Volume 46 Number 6
7 e) J: p. {* r9 {1 nJuly 2007 540-543
6 n. T7 S1 T& p© 2007 Sage Publications
* ]+ I/ n0 S0 r10.1177/0009922806296651; X- i8 H6 @* F$ r" h: F
http://clp.sagepub.com% S2 N9 h2 d9 m+ i) k4 `$ {
hosted at: ^/ X( z( a7 t, C
http://online.sagepub.com
! [$ ~" ^9 T, J% t* ~# _" I! oPrecocious puberty in boys, central or peripheral,4 r9 y7 P# h) @5 J3 u1 |+ p
is a significant concern for physicians. Central4 u* y) @6 W' g3 i3 f
precocious puberty (CPP), which is mediated
2 \( H6 u6 B* p0 U. t5 C" mthrough the hypothalamic pituitary gonadal axis, has. x6 M) Z8 x4 E& t
a higher incidence of organic central nervous system  c, I! v; K/ X4 d
lesions in boys.1,2 Virilization in boys, as manifested! I7 G, Q- z6 s0 s; O
by enlargement of the penis, development of pubic
! ]8 Q3 U. `5 yhair, and facial acne without enlargement of testi-4 Y5 n4 R. b0 T2 Y8 j+ _: s
cles, suggests peripheral or pseudopuberty.1-3 We
) x+ {! E6 f4 T# n4 u2 \# D' Yreport a 16-month-old boy who presented with the
% V/ K+ E% u4 s6 G. b+ J3 Penlargement of the phallus and pubic hair develop-
% R" C) P6 e: h# I8 rment without testicular enlargement, which was due
. V$ I$ H# C7 ?) Cto the unintentional exposure to androgen gel used by1 T; {$ B5 V' W# z: x2 Y' z' P, e
the father. The family initially concealed this infor-7 g! {: |2 ^& A/ Q  w0 y( K4 H0 h
mation, resulting in an extensive work-up for this) p: g, ]9 ~' t6 v
child. Given the widespread and easy availability of
% X# B: W3 F# ttestosterone gel and cream, we believe this is proba-% ~& _7 E) M  K* E2 w$ c( p: Z$ O
bly more common than the rare case report in the
! L6 ^* t, z" |+ Wliterature.4* ?& E' f- l; {2 e) b1 d7 {
Patient Report
# R, W6 s5 O1 \5 f# lA 16-month-old white child was referred to the
$ g5 \! m2 [# E% Q$ G+ ~endocrine clinic by his pediatrician with the concern' X( a6 W! h5 H! i: d1 n: g
of early sexual development. His mother noticed' S9 f) s/ Y. Y! f* I
light colored pubic hair development when he was9 p$ K' W0 n# R! r. W9 r7 `
From the 1Division of Pediatric Endocrinology, 2University of# a$ {7 D9 A6 e8 e- F  K
South Alabama Medical Center, Mobile, Alabama.3 V2 }' c4 x& J1 ]$ _  E0 }
Address correspondence to: Samar K. Bhowmick, MD, FACE,
( R" ?$ g6 v* x1 GProfessor of Pediatrics, University of South Alabama, College of
/ ~* ~1 L4 }5 R$ x- d; |4 N' iMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 M" U5 h( D* J; `" ~# t5 O6 ^
e-mail: [email protected].+ U& l1 a! O5 U. G, }/ z
about 6 to 7 months old, which progressively became
4 K1 k7 R" y  U5 \darker. She was also concerned about the enlarge-
! g; R1 Q- x8 l1 wment of his penis and frequent erections. The child: V/ h. i2 K0 Y
was the product of a full-term normal delivery, with
" f/ Q" @0 ~$ F8 \: t- ha birth weight of 7 lb 14 oz, and birth length of
: f- t( }1 G2 I% k6 P20 inches. He was breast-fed throughout the first year
3 ?( ]: H/ D/ {, D9 V# S( P6 @of life and was still receiving breast milk along with; f6 Z" z  N, a) S, ]* c! S& p  u
solid food. He had no hospitalizations or surgery,- f9 @# J: E3 C: X( r& J
and his psychosocial and psychomotor development9 g. @: Y; V! t! L4 N; y$ w
was age appropriate." E4 p2 [+ w. K# [( Q! }
The family history was remarkable for the father,# H% R% }/ {! M8 {$ q: j
who was diagnosed with hypothyroidism at age 16,+ E7 @' m, q- T% u2 ]
which was treated with thyroxine. The father’s8 S8 n, k& q8 M' C8 |# F
height was 6 feet, and he went through a somewhat. Y5 x. N2 i2 L6 J/ d4 A9 _
early puberty and had stopped growing by age 14.: ?5 c4 Y1 N5 q% }) y# {
The father denied taking any other medication. The) O5 y: R3 ?5 }8 l" o0 T6 A
child’s mother was in good health. Her menarche
* ?" k; S& B9 t1 Y: N( V! Zwas at 11 years of age, and her height was at 5 feet& e8 q0 j( z8 p4 d
5 inches. There was no other family history of pre-% k" C+ Z* m- m- X: J, e
cocious sexual development in the first-degree rela-. l5 n# y+ B. [- `1 k4 c
tives. There were no siblings.
6 o9 _* v" ^$ a; a( t) I+ J" n  ~Physical Examination
+ z( Y7 p' u' R' Q5 n8 VThe physical examination revealed a very active,& ?* u5 u9 u1 w# `! f5 Z# b' r1 f3 O
playful, and healthy boy. The vital signs documented
% ]. o6 m2 j: s8 ua blood pressure of 85/50 mm Hg, his length was
) c9 X4 g- c( F& V90 cm (>97th percentile), and his weight was 14.4 kg
5 {3 ^1 |8 ~" G+ O8 `(also >97th percentile). The observed yearly growth2 C  Z6 e9 U# {9 j  l' z# N
velocity was 30 cm (12 inches). The examination of
% B# s+ [& g8 F: S3 Hthe neck revealed no thyroid enlargement.' M$ A. A' u8 Q+ [& g- Y9 w
The genitourinary examination was remarkable for: u: Y7 p& G4 P2 D
enlargement of the penis, with a stretched length of
" ~; `# X0 z* y+ c8 cm and a width of 2 cm. The glans penis was very well
# `! j! C; L, g4 R! ?+ s+ f" udeveloped. The pubic hair was Tanner II, mostly around  J. O# ~( h) d2 V
540: N( R3 k; {8 C$ k- g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 O# c7 G# V+ M3 ?5 f
the base of the phallus and was dark and curled. The
5 d6 m  E- j9 B# F; \testicular volume was prepubertal at 2 mL each.
  \; _: B% U* P& w, n# P" TThe skin was moist and smooth and somewhat
) {- J0 Q1 I5 coily. No axillary hair was noted. There were no( R; y+ ?; G/ H6 T+ [+ g
abnormal skin pigmentations or café-au-lait spots., t' J# `( f+ {! Y; o1 h% O
Neurologic evaluation showed deep tendon reflex 2+$ X2 {2 N3 n5 N3 l4 t. |
bilateral and symmetrical. There was no suggestion
) G. S$ `( y' {  B5 Kof papilledema./ I4 E" ]" P# E" i1 ^, ]  v
Laboratory Evaluation0 @5 i6 n6 g' m$ L
The bone age was consistent with 28 months by9 C6 Y) W) ^9 c/ d
using the standard of Greulich and Pyle at a chrono-0 R$ C" j( g: Z
logic age of 16 months (advanced).5 Chromosomal
" j" s+ S- u6 H, |! akaryotype was 46XY. The thyroid function test
( ~: A+ Q/ ]8 \# n% wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
) l3 t  k! l! a: j9 blating hormone level was 1.3 µIU/mL (both normal).- ^+ m& Z; P3 E: [/ T
The concentrations of serum electrolytes, blood
0 O/ r( C" `5 T9 \, eurea nitrogen, creatinine, and calcium all were/ d% d4 k& |$ p8 B' d" b! n
within normal range for his age. The concentration
; i, G2 B: c5 G6 U% Qof serum 17-hydroxyprogesterone was 16 ng/dL9 d3 R% e( Z' O% W& K( D1 d
(normal, 3 to 90 ng/dL), androstenedione was 20+ C% D& k( e. d6 ?) u, L5 b2 I
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
$ p  B- {4 O4 S6 z% W: c! k; Uterone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ H9 O) [2 c: K. F# |desoxycorticosterone was 4.3 ng/dL (normal, 7 to3 l; L" s# [4 y
49ng/dL), 11-desoxycortisol (specific compound S)
' ^3 A! D3 i* ^+ H1 s* jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 {+ n+ F& f$ C! X- h
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* W. p1 X, @" c  P" v9 Q, d3 \7 utestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, |$ i/ I5 v0 ~5 _9 l5 }1 Hand β-human chorionic gonadotropin was less than, T; ^1 J4 s( \
5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 A6 I4 t6 H/ {+ Bstimulating hormone and leuteinizing hormone
- b5 s$ \9 R' W7 q* J) D" X: Z4 h' _concentrations were less than 0.05 mIU/mL
& s/ ~) e& G4 _' k; |0 K(prepubertal).
& |: S6 t; l* MThe parents were notified about the laboratory  Z' V* D) f. m+ E! k
results and were informed that all of the tests were6 m5 v& P  B" l5 h9 _1 O
normal except the testosterone level was high. The, r) A& ]0 B$ A# w, h  U
follow-up visit was arranged within a few weeks to
6 s' W: _+ k! |' ~0 y2 f, hobtain testicular and abdominal sonograms; how-
& l1 a* B; o+ r8 [2 ^& kever, the family did not return for 4 months., u$ z6 e7 C; q$ X7 Y2 V1 q
Physical examination at this time revealed that the' ^' k+ \8 X, \+ W* q( Z) W0 B
child had grown 2.5 cm in 4 months and had gained% c( p- s: B- Q
2 kg of weight. Physical examination remained2 C9 ?8 T0 U  M( J' G
unchanged. Surprisingly, the pubic hair almost com-# G: P" T: b3 B- ]" i$ H. H
pletely disappeared except for a few vellous hairs at5 @# L$ u6 n, ]$ `
the base of the phallus. Testicular volume was still 2
8 Y; \+ P, I: X, Y4 [* E: fmL, and the size of the penis remained unchanged.3 O+ Q5 |$ ]* w0 e1 B8 a! \, _: L
The mother also said that the boy was no longer hav-, O, h5 R5 n5 }& h; D& J
ing frequent erections.
: ]+ j/ E9 H8 o7 C2 \( {Both parents were again questioned about use of
, Q6 j5 v) o* q: L3 h8 H* o' @6 Tany ointment/creams that they may have applied to! o- ^. A, h- e" o
the child’s skin. This time the father admitted the/ Z! a$ a- S2 w7 l" N
Topical Testosterone Exposure / Bhowmick et al 5415 ^6 _- B8 M5 d$ F" q* m+ I) u
use of testosterone gel twice daily that he was apply-
8 L; o; t* b8 `: V, Ving over his own shoulders, chest, and back area for
# B: m1 H- l0 N9 {6 N0 {$ ~1 `5 Wa year. The father also revealed he was embarrassed; Q% r) E. i0 |1 H# V# N
to disclose that he was using a testosterone gel pre-. j4 R8 l- P0 ]: K- c8 O+ h
scribed by his family physician for decreased libido; a7 H. P' `+ x$ i/ }" g0 |( j, I% p( S
secondary to depression.% p! E' C& f$ @& E$ a
The child slept in the same bed with parents., ~& z3 T) {6 I5 J; ~
The father would hug the baby and hold him on his
5 u7 `! \& N5 m4 i1 u3 }chest for a considerable period of time, causing sig-' l# `; @# i* O
nificant bare skin contact between baby and father.
. r1 j3 z  q  lThe father also admitted that after the phone call,& Q6 `2 g* k/ W: H' O$ x8 r
when he learned the testosterone level in the baby( w% U6 U4 N( G! o9 `( B
was high, he then read the product information
5 q( m$ ~6 F" Zpacket and concluded that it was most likely the rea-
( V% [5 j2 R) n$ V. cson for the child’s virilization. At that time, they
- N/ ~- V' U. }. L3 z5 O! `decided to put the baby in a separate bed, and the
; r" S2 U. h- }* N4 k1 n. V; `father was not hugging him with bare skin and had: `9 R( K0 G3 u( q
been using protective clothing. A repeat testosterone6 d% J) f: C0 ?% d: G, W4 M
test was ordered, but the family did not go to the* O8 x  f2 Z) @, t, ~4 a
laboratory to obtain the test.
% j0 l7 ^9 K0 ]8 {. b6 CDiscussion8 f! L* f, \6 s
Precocious puberty in boys is defined as secondary
; U% D: m! x* m# |: bsexual development before 9 years of age.1,4
0 ?3 w7 ~! }  VPrecocious puberty is termed as central (true) when
, J7 Z1 Y9 G" h1 @- W* nit is caused by the premature activation of hypo-
' Y/ L- W9 Q! C4 Dthalamic pituitary gonadal axis. CPP is more com-
( n2 d" a8 x) Hmon in girls than in boys.1,3 Most boys with CPP/ u) Y& a$ K3 w# [: Q$ I" K$ \6 i
may have a central nervous system lesion that is
9 \$ x8 \1 w  U5 ]! u( u& _$ q& g- Iresponsible for the early activation of the hypothal-
9 E, z4 r: z: m3 a; ?( F% samic pituitary gonadal axis.1-3 Thus, greater empha-+ B& d* V$ J! h/ T9 f2 S% m. S' G
sis has been given to neuroradiologic imaging in  R7 b& h" t! m2 p: l/ l
boys with precocious puberty. In addition to viril-
' o9 H' b: p3 ]4 I0 E2 o$ pization, the clinical hallmark of CPP is the symmet-
; f, |) j- P- H4 Z8 Drical testicular growth secondary to stimulation by! K& |2 P, S' I- t. F
gonadotropins.1,3- l% W, X4 `( n* e2 l
Gonadotropin-independent peripheral preco-! _( V0 p( c' z. S) ?; h
cious puberty in boys also results from inappropriate3 X4 B* J$ M, n3 n7 _9 L
androgenic stimulation from either endogenous or4 v' r/ M0 ^+ i/ A+ i% D; a' z- r
exogenous sources, nonpituitary gonadotropin stim-/ f; S) O$ i2 E$ o' X4 {3 h
ulation, and rare activating mutations.3 Virilizing
! l1 v% k# z: P. O: xcongenital adrenal hyperplasia producing excessive
# X" v, U- U2 Q; padrenal androgens is a common cause of precocious
; [, x4 t3 q9 {) T- dpuberty in boys.3,4% s0 A2 A+ H6 k; r4 K: `
The most common form of congenital adrenal2 I/ H! _+ Y+ Q$ K5 @$ G
hyperplasia is the 21-hydroxylase enzyme deficiency.% k! F4 Z2 b: ^) G* g1 y
The 11-β hydroxylase deficiency may also result in- W  P& @! l# _! X; {1 _
excessive adrenal androgen production, and rarely,
; e% u( g$ J0 N& S8 Oan adrenal tumor may also cause adrenal androgen7 v3 ^' I' R0 f
excess.1,3( ~( B# _8 i) T3 K: h( J
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; U' |+ C, T( B$ K2 m/ q) L
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- B3 }9 v7 }. X' n1 X
A unique entity of male-limited gonadotropin-
. H8 E3 V  @5 z+ uindependent precocious puberty, which is also known0 Z5 K: T5 q, d- N
as testotoxicosis, may cause precocious puberty at a  j% q0 a$ A, s+ U% b1 G
very young age. The physical findings in these boys
' {5 f2 l8 ~7 Swith this disorder are full pubertal development,
# s4 F& t3 R. L7 S* X% ?3 N0 Nincluding bilateral testicular growth, similar to boys) K. C, @# G# T, ?' A
with CPP. The gonadotropin levels in this disorder$ s) O" c5 e% H
are suppressed to prepubertal levels and do not show
" t5 @/ I7 w+ J" X: Ipubertal response of gonadotropin after gonadotropin-: v8 D: ~9 |; z( \! S5 g
releasing hormone stimulation. This is a sex-linked2 z0 H, h. h" ?/ k% w$ G
autosomal dominant disorder that affects only
9 x8 z) e2 G' q9 v- Hmales; therefore, other male members of the family& R2 j2 r6 K4 n: |8 s# a
may have similar precocious puberty.3
5 m/ V4 o6 `2 h2 v: m9 [In our patient, physical examination was incon-
$ r2 c1 P8 \* V. u8 `sistent with true precocious puberty since his testi-
* Q3 O% x4 F9 J8 m9 j$ }) g1 Zcles were prepubertal in size. However, testotoxicosis( f8 O4 K' N2 n! C/ l" V
was in the differential diagnosis because his father
4 Y$ {4 t* b* G' ]& z& `2 |started puberty somewhat early, and occasionally,. o  ?* ?% B' p* H! q$ V
testicular enlargement is not that evident in the
+ l2 Y( v; _! U; W) _beginning of this process.1 In the absence of a neg-$ v0 J  s/ Y$ a4 ^% R9 i4 b7 e" @
ative initial history of androgen exposure, our
8 m8 e% X/ S4 Jbiggest concern was virilizing adrenal hyperplasia,
" N. U# k4 ?, l' k# l3 O3 Heither 21-hydroxylase deficiency or 11-β hydroxylase
/ p8 `. H% U+ u" q& D8 _) Mdeficiency. Those diagnoses were excluded by find-3 F' j' j$ J6 R; G" r  l" [
ing the normal level of adrenal steroids.
( r4 U, j( A; }8 W0 e" @The diagnosis of exogenous androgens was strongly! B  M  y5 d: }5 r
suspected in a follow-up visit after 4 months because- b& l4 R4 ^5 n  l
the physical examination revealed the complete disap-- o* u: k5 B! D$ m
pearance of pubic hair, normal growth velocity, and
0 m& k" F8 h) ]0 ]+ J3 M. A5 _decreased erections. The father admitted using a testos-( p4 N% g8 h3 F4 c" k7 t/ ^. Z- ?' R# v
terone gel, which he concealed at first visit. He was* o. ]4 A8 ~: }* ~6 t  ]3 x
using it rather frequently, twice a day. The Physicians’
6 E$ w5 I  R0 Z4 u* EDesk Reference, or package insert of this product, gel or
' p1 D  j: a3 G& H' B. ucream, cautions about dermal testosterone transfer to
$ E  v/ F3 x) D4 \$ ]4 n; Qunprotected females through direct skin exposure.
. J& y4 v$ \. C- Y' w& ~4 oSerum testosterone level was found to be 2 times the2 q) @' d: f! O  X
baseline value in those females who were exposed to' y# c& [" T* V% a
even 15 minutes of direct skin contact with their male
2 {4 O" E! Z. s2 B) xpartners.6 However, when a shirt covered the applica-8 t4 q" i- a5 b/ R0 k6 b; }1 x
tion site, this testosterone transfer was prevented.
$ P* ~) E/ u* Y/ }- P, S7 {  XOur patient’s testosterone level was 60 ng/mL,
5 Q6 C) z  A" p1 c: b( Fwhich was clearly high. Some studies suggest that
5 y' ?# \6 {$ b% x* {" Zdermal conversion of testosterone to dihydrotestos-; a; V# a% ]0 Q# V* h3 t
terone, which is a more potent metabolite, is more- M, k2 h9 o& l. Z5 n
active in young children exposed to testosterone3 H: ?$ D! H7 z. K# `+ c9 D& x
exogenously7; however, we did not measure a dihy-4 k+ Z2 W6 O- \7 z% R
drotestosterone level in our patient. In addition to
9 s% O( r1 d1 U+ x0 |! F# Ivirilization, exposure to exogenous testosterone in
; y2 B4 I( @; E* Ochildren results in an increase in growth velocity and" q/ R& p. l9 C
advanced bone age, as seen in our patient.
2 y1 Q6 M" `& O2 mThe long-term effect of androgen exposure during, @5 l* S! l+ F/ R- I& G1 G. U
early childhood on pubertal development and final/ M( Y/ h& m9 ]  c4 m
adult height are not fully known and always remain- i$ S6 h$ Z4 c4 i1 e) w
a concern. Children treated with short-term testos-
- d7 I6 {! b! {terone injection or topical androgen may exhibit some
9 ~" M0 N/ r, E* {% V' G# K' Zacceleration of the skeletal maturation; however, after' H* f3 `' S, W# h* q( H6 v
cessation of treatment, the rate of bone maturation
! E6 L  o$ ^0 a% o% L4 j8 Ndecelerates and gradually returns to normal.8,9
( u  V8 k/ Y! M! L; l+ M  aThere are conflicting reports and controversy
- f' F- Y$ o5 X$ sover the effect of early androgen exposure on adult7 n6 ?0 S1 B" [- O: ^
penile length.10,11 Some reports suggest subnormal" Y; P$ ^9 Q: F
adult penile length, apparently because of downreg-
% z  i/ b& X% O! e3 v6 V0 Mulation of androgen receptor number.10,12 However,3 K/ H% p: O' `# O7 |, W" N
Sutherland et al13 did not find a correlation between# q9 q; [- e8 Y9 P1 Q9 S
childhood testosterone exposure and reduced adult  I; k8 m( b  Q1 e" `9 D# J6 _; N
penile length in clinical studies.
9 ], Z7 B( F; R% T' J+ ]% GNonetheless, we do not believe our patient is+ S$ S- ?9 G1 N% Z( f$ B
going to experience any of the untoward effects from. M" m9 `1 V9 f( ~' u& c; O
testosterone exposure as mentioned earlier because3 W/ y" e' ^7 u8 F
the exposure was not for a prolonged period of time.  ^2 _3 g% n/ O% ^
Although the bone age was advanced at the time of
; k+ L- X0 S3 S$ e; |) k: udiagnosis, the child had a normal growth velocity at1 C3 S6 y- |1 a; y8 D
the follow-up visit. It is hoped that his final adult* x$ e( s& O4 H4 @
height will not be affected.; }2 t; R2 n: r+ T5 L
Although rarely reported, the widespread avail-/ ]/ Z1 [& y$ |$ T9 }  t
ability of androgen products in our society may
( ^$ O2 @- [( ]/ k: a8 v4 _3 mindeed cause more virilization in male or female
  D. L8 A; V1 g6 q: Bchildren than one would realize. Exposure to andro-0 V# N6 Y) l7 a4 W. u
gen products must be considered and specific ques-
9 }) @* ?: Q" W* Z; G% x; R3 Ytioning about the use of a testosterone product or
* C+ \6 A  q- @6 r' S7 zgel should be asked of the family members during
& {% C$ o! @2 ythe evaluation of any children who present with vir-
3 U. e' }1 N: y1 X6 @3 d  z, g" Qilization or peripheral precocious puberty. The diag-$ q0 z: E, B1 J- {. T
nosis can be established by just a few tests and by5 F+ z( s* E) Q# {0 f1 b" j5 ~, {
appropriate history. The inability to obtain such a- T1 C  S0 o8 x3 Z$ J9 W- r6 y
history, or failure to ask the specific questions, may
1 h. F. I) t* x- s+ |) C8 [result in extensive, unnecessary, and expensive- h: o3 R7 t% _3 K' m" c
investigation. The primary care physician should be
. ]) P* U4 }0 saware of this fact, because most of these children
2 y0 V& s9 q8 O- W8 Zmay initially present in their practice. The Physicians’2 M9 y( \; {6 k7 o4 f6 n6 n" `
Desk Reference and package insert should also put a3 S5 i: r' r- o! d) r
warning about the virilizing effect on a male or
% Q6 l+ T& B- `+ U* z& nfemale child who might come in contact with some-
: Y( v/ V8 [' W$ C# Zone using any of these products.
/ r3 J: G/ X$ U, _References5 K4 }! z* V$ d- Z' }
1. Styne DM. The testes: disorder of sexual differentiation
$ k; o$ [1 u  }. B& Oand puberty in the male. In: Sperling MA, ed. Pediatric9 n# ~- _* _: Q0 {* b1 u
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! u; E. ~# E/ q* C8 N, S* t
2002: 565-628.
6 _' X. q; g0 w& Q2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ f0 ^1 @0 T' p2 A2 H1 e) p  Q8 e: spuberty in children with tumours of the suprasellar pineal
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女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
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

1 Z( e# @1 s: k2 H2 D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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