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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
% c% _* O# B/ l5 MBoy Induced by Indirect Topical
3 ^. z% n1 J  |Exposure to Testosterone7 z9 i# h  f5 V, D, `8 z
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: _0 ?$ O0 P4 _, t7 |, `: qand Kenneth R. Rettig, MD13 D) b+ u- l/ U, z: L" K  y9 A
Clinical Pediatrics
* z3 I, r3 U- E% ]& VVolume 46 Number 6
$ X. X& p& j6 [$ H* jJuly 2007 540-543
4 g. l+ P- L2 H! U2 H: t& ~© 2007 Sage Publications
3 _- c% @$ s( q: c" J10.1177/0009922806296651/ @3 t# w  A$ M0 I- o9 L; D4 F; _
http://clp.sagepub.com9 T) o4 {" I( ~% I3 n! N5 B- L
hosted at
/ V' w) {% p  C1 Ghttp://online.sagepub.com$ E# Q: M7 T/ G/ f7 A4 l" J- C
Precocious puberty in boys, central or peripheral,6 ^2 \, {' b2 b& H8 T! D) W0 K
is a significant concern for physicians. Central2 q& H0 y! O8 T0 ~. V( u
precocious puberty (CPP), which is mediated
9 U" }  \; k$ B  I& Vthrough the hypothalamic pituitary gonadal axis, has
2 }  r4 x& v0 H# P+ ia higher incidence of organic central nervous system
( G4 D/ I  |0 F& e' ?- H/ L. S" |6 Rlesions in boys.1,2 Virilization in boys, as manifested, N0 }3 e' N" a, z7 `3 t
by enlargement of the penis, development of pubic8 E7 ^6 d% D5 `1 ]9 |
hair, and facial acne without enlargement of testi-
- b' _. o& X) }" \5 L* u! f( M+ ]+ Ocles, suggests peripheral or pseudopuberty.1-3 We
$ N% G7 d6 F% `: Ureport a 16-month-old boy who presented with the) b7 q$ n" u% Q' z/ b# @
enlargement of the phallus and pubic hair develop-5 G. L: n( h7 _  u9 Z( i, p& b
ment without testicular enlargement, which was due7 T  }3 ?$ q: H3 D2 A
to the unintentional exposure to androgen gel used by
5 R1 I4 a8 _1 ~/ X$ G' x8 Sthe father. The family initially concealed this infor-
9 ]# A  G  R: Y; Z* ?mation, resulting in an extensive work-up for this
! S! I& g* Q* X5 achild. Given the widespread and easy availability of! m4 O+ _  W3 X" M5 `
testosterone gel and cream, we believe this is proba-% N, I0 L7 h1 ?% |
bly more common than the rare case report in the1 T4 J4 l; S! o& n* [
literature.4: f# }( k  x, R2 H
Patient Report
9 R6 _" y+ d% V, i' X# TA 16-month-old white child was referred to the
2 O# z9 s' w2 w$ w$ U6 tendocrine clinic by his pediatrician with the concern: v- O+ h+ w4 P' F4 b$ q% ?$ x( _  d
of early sexual development. His mother noticed
% y& K- K6 d  m- h# llight colored pubic hair development when he was
) E1 [+ ?5 `7 N* q3 fFrom the 1Division of Pediatric Endocrinology, 2University of  w, f  K3 T/ B( f5 i# j
South Alabama Medical Center, Mobile, Alabama.
. u+ B' C: N" n" W) L3 yAddress correspondence to: Samar K. Bhowmick, MD, FACE,
0 e+ A$ q7 S8 d6 F& J+ i0 CProfessor of Pediatrics, University of South Alabama, College of: ^5 S! D; |0 R( g
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 Z% _8 @4 a! D' j( t6 [+ ~3 {
e-mail: [email protected].- |7 ]1 f- H4 G! A8 I* r- \( j- Y
about 6 to 7 months old, which progressively became
# Q& J) @  V/ Z/ z9 v0 s$ fdarker. She was also concerned about the enlarge-3 H4 P6 Z; V* }# H$ F3 _
ment of his penis and frequent erections. The child
5 c+ _; L" U, {$ A( |  Wwas the product of a full-term normal delivery, with* W' V/ E; p+ {5 }5 n0 C
a birth weight of 7 lb 14 oz, and birth length of; p" Z. A7 m4 _& w& `
20 inches. He was breast-fed throughout the first year0 F! S' L" \0 r( |+ i; H% p
of life and was still receiving breast milk along with% E. i* Z* h# k* @
solid food. He had no hospitalizations or surgery," V% A  l1 h9 J& v& x$ l
and his psychosocial and psychomotor development2 S9 V% @* |* H% v+ Z# S) v
was age appropriate.
2 t8 y, z- I% i9 I% ~4 A8 PThe family history was remarkable for the father,/ P' o8 x' R* w) ^$ c
who was diagnosed with hypothyroidism at age 16,/ @' `. j, ^' |- g% j: h( s
which was treated with thyroxine. The father’s
# d! [! E2 F  q- \! E: m, ?+ Iheight was 6 feet, and he went through a somewhat0 Q) Y, C! u0 k+ i5 e
early puberty and had stopped growing by age 14.; E1 V. v! c! P. f# o' Z0 m
The father denied taking any other medication. The2 T# q3 U! Z: S; W. j+ j9 }
child’s mother was in good health. Her menarche
# _3 H" y+ d: o- ?9 P$ C/ Gwas at 11 years of age, and her height was at 5 feet: _6 N- y7 n' H
5 inches. There was no other family history of pre-  V' F5 G4 p7 k# C
cocious sexual development in the first-degree rela-. n. [( ]2 ?% z, b0 V7 z3 r
tives. There were no siblings.; Q# J, P# J- V: ~( |5 f
Physical Examination
7 d+ H3 H! _4 f* wThe physical examination revealed a very active,! ~9 S$ r3 _( D  L7 S% h
playful, and healthy boy. The vital signs documented
* o" V1 B0 `+ ]a blood pressure of 85/50 mm Hg, his length was
1 g4 a% ?6 G& x, f4 Y90 cm (>97th percentile), and his weight was 14.4 kg& O. a) c) i0 h
(also >97th percentile). The observed yearly growth9 W5 L& O3 i- s' ?; y
velocity was 30 cm (12 inches). The examination of. e! T* |3 {; M* J2 G
the neck revealed no thyroid enlargement.- o1 g  R/ D) G
The genitourinary examination was remarkable for
0 A6 r/ `8 F# E( g" b2 senlargement of the penis, with a stretched length of9 I( S" c5 m% i
8 cm and a width of 2 cm. The glans penis was very well0 U. R( ?; l* G5 R! m
developed. The pubic hair was Tanner II, mostly around
7 I9 v* e, U2 K. O; C' F7 A  R5408 f7 u' u4 e' U  I  M8 w+ f- F: R0 X
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 s/ F% }  Q: D" W; I
the base of the phallus and was dark and curled. The0 I, d) n5 m5 l
testicular volume was prepubertal at 2 mL each.
$ u! F3 w4 d2 e! K5 }  u  D4 P! zThe skin was moist and smooth and somewhat4 ~- h  M" u" j
oily. No axillary hair was noted. There were no& W5 W7 @& k8 ~  B
abnormal skin pigmentations or café-au-lait spots.
& ]3 z4 S( R  d1 \' E/ a6 rNeurologic evaluation showed deep tendon reflex 2+
( |. E. c2 {6 tbilateral and symmetrical. There was no suggestion+ T- y. i8 E3 L
of papilledema.
  s+ U, P& r4 O: F* f/ l0 ^Laboratory Evaluation3 K( X' ?* S# @" d& U" b! g
The bone age was consistent with 28 months by
7 ~/ {# p7 `/ B4 i- nusing the standard of Greulich and Pyle at a chrono-4 J& z% V1 @3 i. J( S% I9 W# b; [
logic age of 16 months (advanced).5 Chromosomal
# D! d' X5 v7 {# V2 \karyotype was 46XY. The thyroid function test8 s, `- f" ]' W! d8 X+ ~1 [; D
showed a free T4 of 1.69 ng/dL, and thyroid stimu-( H6 \0 v& @+ y% B& Y5 h& L
lating hormone level was 1.3 µIU/mL (both normal).9 j& X/ A$ E; T6 n6 X% k
The concentrations of serum electrolytes, blood
5 s4 B; \" B9 @1 jurea nitrogen, creatinine, and calcium all were
; B+ f9 A+ H6 B0 U# |within normal range for his age. The concentration
1 W) w; j+ Z* ]6 Yof serum 17-hydroxyprogesterone was 16 ng/dL& Y) }* ?% U* ]5 ?3 L* O
(normal, 3 to 90 ng/dL), androstenedione was 20
3 ?4 z- V, u* Z  m8 qng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-3 _4 G; Y8 m0 I" P& z
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
- j0 K, x" F: W( q+ [2 M' b# ]: Mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( O5 V6 N. O1 a" }* n$ X49ng/dL), 11-desoxycortisol (specific compound S)
: ?& J8 g. y9 U: Z" P1 qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& G. d( Z9 G1 B% Ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& R3 ]7 R/ o; W9 H4 }$ h0 |testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; S  D, \4 R) Z, land β-human chorionic gonadotropin was less than
- i9 G0 S; m+ ~7 N3 ?4 m5 mIU/mL (normal <5 mIU/mL). Serum follicular
4 c& U) w: t' g2 d& e6 g# wstimulating hormone and leuteinizing hormone5 ]# f% U! I- n" g  J/ m1 m
concentrations were less than 0.05 mIU/mL' @8 M' q* S# t; D5 h: W! c9 G
(prepubertal).9 S+ p6 _4 F) A% N7 n
The parents were notified about the laboratory* ^2 J# i6 j3 t. A, d6 W, P
results and were informed that all of the tests were1 E* p$ ]: }% o( j5 x
normal except the testosterone level was high. The
/ ^5 ~3 y9 ]7 J  {" xfollow-up visit was arranged within a few weeks to
" D0 k& W2 q- J1 Iobtain testicular and abdominal sonograms; how-- `% J0 f: M# S  @- R8 s
ever, the family did not return for 4 months.) F7 D1 s7 }. [! }, T4 [
Physical examination at this time revealed that the
& @, M( c1 C6 _$ y3 L, E, U7 Y- zchild had grown 2.5 cm in 4 months and had gained; F+ c/ @# W9 ?! i( v! u- T
2 kg of weight. Physical examination remained* C: O' l1 \5 q- o$ b
unchanged. Surprisingly, the pubic hair almost com-
, x$ w( q- E$ N7 `pletely disappeared except for a few vellous hairs at  o& Z8 U7 l# j  t1 F* l
the base of the phallus. Testicular volume was still 2
! i: Y* S; h* V" I" E) TmL, and the size of the penis remained unchanged.0 q; I- q+ P" B* M# h
The mother also said that the boy was no longer hav-
9 I. Q5 `3 n* O0 P0 H3 z( @ing frequent erections.: U9 t$ s, `: t' ~
Both parents were again questioned about use of
# ]* |- m" H7 P9 ?( M0 K% Rany ointment/creams that they may have applied to
3 Q) u; S& x9 U* X3 ]: A9 othe child’s skin. This time the father admitted the! h8 n3 j: d' s- K: @& U
Topical Testosterone Exposure / Bhowmick et al 541
& Q- A% o& D, |. Duse of testosterone gel twice daily that he was apply-
* c, F$ a0 y$ k9 ying over his own shoulders, chest, and back area for% o& S. w5 ^$ R& s
a year. The father also revealed he was embarrassed$ S+ b: T+ {# I
to disclose that he was using a testosterone gel pre-) u9 R# m' t/ y  f& ]
scribed by his family physician for decreased libido7 B8 M3 E( s1 W6 O
secondary to depression.
( x$ N: X- l: l3 tThe child slept in the same bed with parents.% d" [( R$ s8 ~! m* }% |
The father would hug the baby and hold him on his
8 z: [' T# w% ?9 Q" Hchest for a considerable period of time, causing sig-' A, i* U8 k. r; B% A4 @/ U' u
nificant bare skin contact between baby and father.' `# ^7 z* r0 v) c$ ~  ~# {$ v$ a
The father also admitted that after the phone call,/ \+ a" ~, z0 n% U! e+ `1 f' }9 y
when he learned the testosterone level in the baby2 @/ ]+ m+ ^2 O; o. u
was high, he then read the product information; ^! @* i3 s' `1 ?. N: A5 K8 [
packet and concluded that it was most likely the rea-
8 Y1 F3 M1 o$ x! [7 E! Json for the child’s virilization. At that time, they" Z, }! S+ a) P9 E3 A6 B  l6 y
decided to put the baby in a separate bed, and the
/ g# \: n+ b+ ]( xfather was not hugging him with bare skin and had6 x, E3 I1 N( d
been using protective clothing. A repeat testosterone+ t3 O3 p6 n3 x: o7 }, U# `
test was ordered, but the family did not go to the
% O" C3 ^8 w: j4 xlaboratory to obtain the test.
  @$ r! C% Z: X( o* R# TDiscussion
6 M4 t$ A( a& z& B2 SPrecocious puberty in boys is defined as secondary
4 a4 R5 [! _5 E/ i: b6 K9 ^sexual development before 9 years of age.1,4$ |4 X% d# ]7 z( u# \2 V2 ]
Precocious puberty is termed as central (true) when% w# p4 V6 g: ?6 B3 e' H
it is caused by the premature activation of hypo-
" Y$ G, w) X. u0 Zthalamic pituitary gonadal axis. CPP is more com-; n% F: ]/ T) n
mon in girls than in boys.1,3 Most boys with CPP6 I9 q7 B2 U7 E6 n0 G! G
may have a central nervous system lesion that is0 @, b- R! L0 `( E8 a% _6 q
responsible for the early activation of the hypothal-
  U+ I* c& R/ s% I6 G; r( eamic pituitary gonadal axis.1-3 Thus, greater empha-. J1 O2 S" x, g; X) L
sis has been given to neuroradiologic imaging in
7 Y( O3 s' d4 a3 u% nboys with precocious puberty. In addition to viril-
' j/ E! F5 A" {: R0 g0 tization, the clinical hallmark of CPP is the symmet-( V. S! q0 M8 }
rical testicular growth secondary to stimulation by; [3 z/ d. b  h" J3 ?
gonadotropins.1,31 M: W* l5 B: [5 f! F
Gonadotropin-independent peripheral preco-, i# F* q8 _: ~( y! P: L, `8 Z
cious puberty in boys also results from inappropriate0 O5 j  @+ U+ B2 R" ]: H- |
androgenic stimulation from either endogenous or0 d9 g# F/ y7 U' a( Q
exogenous sources, nonpituitary gonadotropin stim-; n+ j( C$ N# a$ x
ulation, and rare activating mutations.3 Virilizing
8 n- M; C5 p7 @# Lcongenital adrenal hyperplasia producing excessive
8 F0 O: j+ N3 z5 \. J  Uadrenal androgens is a common cause of precocious! M( Y( ]6 N/ ?3 W+ g% h% L
puberty in boys.3,4
7 I: k5 \7 }9 rThe most common form of congenital adrenal8 {9 E) l  f; R; T+ A
hyperplasia is the 21-hydroxylase enzyme deficiency.
1 |% f; E. I( H- V, P9 ZThe 11-β hydroxylase deficiency may also result in
! C* \) T6 W6 H0 s- P2 uexcessive adrenal androgen production, and rarely,4 a! d# m$ m5 I. g
an adrenal tumor may also cause adrenal androgen& T# K- z* ?4 a/ i
excess.1,3. ]/ p/ Z) r+ I+ \- j8 u. L) q+ V& A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! _% P) ~% |8 m* b" ]542 Clinical Pediatrics / Vol. 46, No. 6, July 20071 v0 n8 V1 j% g3 i; w' H! Y
A unique entity of male-limited gonadotropin-
! A9 |& Y6 a9 v; k' Z8 f% Hindependent precocious puberty, which is also known
% Y6 ^7 ~. ^0 ?as testotoxicosis, may cause precocious puberty at a2 I. Q- z# I) a7 A8 K0 b# A
very young age. The physical findings in these boys" ]" D! q. g+ f' C. w
with this disorder are full pubertal development,
& t2 o; H# e2 S7 R4 b+ aincluding bilateral testicular growth, similar to boys
1 f5 y% a% _: e; {. h* s6 qwith CPP. The gonadotropin levels in this disorder/ M' X7 U  T* K" G* g/ u
are suppressed to prepubertal levels and do not show& _" H- c# k6 b& _
pubertal response of gonadotropin after gonadotropin-$ P' W' Y! W0 \8 i
releasing hormone stimulation. This is a sex-linked  n- D2 b) F3 s2 B5 I
autosomal dominant disorder that affects only
) W0 ~& r8 |) x+ w. S/ bmales; therefore, other male members of the family
* B$ m, r; A1 E( d/ H. kmay have similar precocious puberty.3
: ]. p' t# B2 QIn our patient, physical examination was incon-
2 i7 A/ M3 x$ V6 lsistent with true precocious puberty since his testi-: L$ g  V: s; \6 Z* x
cles were prepubertal in size. However, testotoxicosis
) p, x4 j) m, J' w$ K. Bwas in the differential diagnosis because his father1 n6 W+ }2 U) V" E1 ]
started puberty somewhat early, and occasionally,
/ J2 _, `# z* r7 W( C( Btesticular enlargement is not that evident in the; e% t; W$ C, c
beginning of this process.1 In the absence of a neg-% w* U* b1 k7 }+ d) M, v; o
ative initial history of androgen exposure, our4 L5 a/ T: n- `& K: k0 L" ^
biggest concern was virilizing adrenal hyperplasia,
4 G5 A7 H% S1 s4 deither 21-hydroxylase deficiency or 11-β hydroxylase
. M. A2 _1 m9 P1 s% N3 H! G5 Bdeficiency. Those diagnoses were excluded by find-& g8 R3 z0 ?$ c
ing the normal level of adrenal steroids.
2 w1 ]1 T$ e) ~4 z$ }, HThe diagnosis of exogenous androgens was strongly
4 U! a% ~0 J7 ksuspected in a follow-up visit after 4 months because
8 @& i* m& ]. h. h6 _+ o. Sthe physical examination revealed the complete disap-6 j4 J, a+ I. ?3 K) K# S
pearance of pubic hair, normal growth velocity, and5 Y/ k* j! a& I  P
decreased erections. The father admitted using a testos-
8 R- M/ l7 {+ f) N' h5 ?terone gel, which he concealed at first visit. He was/ P1 O- u' |) H! S$ O: b5 S# @
using it rather frequently, twice a day. The Physicians’
3 T9 b8 e/ S9 a% Y) C. ?8 m0 LDesk Reference, or package insert of this product, gel or1 Q+ t% C3 z. e3 ]; E1 [7 P( E
cream, cautions about dermal testosterone transfer to
$ A  ^9 t8 k$ f, ^3 C+ tunprotected females through direct skin exposure.
' s6 a" O2 Z/ \. c' W' f3 VSerum testosterone level was found to be 2 times the
! F/ R+ D/ F, I; f5 X# E" Z1 Rbaseline value in those females who were exposed to
: u: V; H( Y9 y2 s' R# _7 meven 15 minutes of direct skin contact with their male8 N! V7 N- R- e! ~5 O
partners.6 However, when a shirt covered the applica-
" k$ b+ O% Y) d0 P- a/ btion site, this testosterone transfer was prevented.8 J+ q/ E( c+ {- S; C) P
Our patient’s testosterone level was 60 ng/mL,) N6 f, A) I7 }7 n5 i2 z0 b. v) L
which was clearly high. Some studies suggest that1 m, |1 ?2 \; R' x; ?4 c
dermal conversion of testosterone to dihydrotestos-! ]" Z$ P( }2 U1 n
terone, which is a more potent metabolite, is more
3 b( G$ ^( O+ i& Q; _active in young children exposed to testosterone
- {0 r, i4 P2 M' aexogenously7; however, we did not measure a dihy-+ Z! i0 g% E1 d0 b  a' ?1 U
drotestosterone level in our patient. In addition to! u( ?- u" i; s/ M# H  z9 K3 N
virilization, exposure to exogenous testosterone in
  `" ^4 K4 k2 G" @! Cchildren results in an increase in growth velocity and
- T/ h" o5 d3 p6 P; tadvanced bone age, as seen in our patient.
2 z" O0 A) _* g. S- F! ^# s8 T9 PThe long-term effect of androgen exposure during- f; A1 O8 Y% L4 d( P
early childhood on pubertal development and final- I6 Q# E+ S* Q& f; u2 x
adult height are not fully known and always remain- c0 c0 t4 J; w
a concern. Children treated with short-term testos-
( R* z% H# F7 }  v$ O  N' Hterone injection or topical androgen may exhibit some
. B% ~% p! N1 K1 l+ Q" Q% ~acceleration of the skeletal maturation; however, after
# b9 b2 ~; Y* |1 e! K5 w. l0 n! Mcessation of treatment, the rate of bone maturation
& v: D: G' \) Q4 G8 f4 P; s4 Ldecelerates and gradually returns to normal.8,9. c& M2 o& e1 I
There are conflicting reports and controversy
. S% ]; W% c+ w8 n6 v7 Gover the effect of early androgen exposure on adult
9 M% A: ^) }$ G8 n$ v  kpenile length.10,11 Some reports suggest subnormal
  A5 V9 j( w9 t5 \, \adult penile length, apparently because of downreg-
& E7 Q1 T; L9 {" k7 Wulation of androgen receptor number.10,12 However,8 H) {: z5 d  y6 g' @- |$ N. c
Sutherland et al13 did not find a correlation between3 E4 ~' |! U6 q; w/ H& z
childhood testosterone exposure and reduced adult
3 a. \, ]; T( b# P; c0 Spenile length in clinical studies.
: q, P5 s. ^5 S/ D9 ~: nNonetheless, we do not believe our patient is
6 Z2 C: k' g! w2 U! f8 [+ e7 D- f. Tgoing to experience any of the untoward effects from4 l$ G) H! E0 d; o
testosterone exposure as mentioned earlier because" U3 D) V. z, }) r* V7 V: \$ o
the exposure was not for a prolonged period of time.
5 g$ i0 D7 O. x6 j: IAlthough the bone age was advanced at the time of  v( G' A5 q' l; Y: c
diagnosis, the child had a normal growth velocity at
" i& d8 W0 B9 v& Uthe follow-up visit. It is hoped that his final adult
4 }# F0 T" S; ^height will not be affected.$ C0 U0 a+ ^/ G* K! W7 b
Although rarely reported, the widespread avail-6 S9 B- P/ W4 T6 _, @! G# q
ability of androgen products in our society may
0 f9 Y: c( c2 D' W& M! Z+ eindeed cause more virilization in male or female" ~) v+ u3 C  \0 o9 W/ _! j: T
children than one would realize. Exposure to andro-
$ @6 }. b4 H, N' T3 |2 Ogen products must be considered and specific ques-6 f* j- F3 X& }" K
tioning about the use of a testosterone product or5 G& ^+ O- n* d5 O
gel should be asked of the family members during
; a2 B7 l( W3 C; W8 |( A( S+ Mthe evaluation of any children who present with vir-
! O9 S0 b  c* S0 y* G* F$ d, a! milization or peripheral precocious puberty. The diag-
9 v# p; s* ~$ o8 _nosis can be established by just a few tests and by. N+ Q: y5 ^& H! ?+ H
appropriate history. The inability to obtain such a/ [4 C  ?5 Y! U& V, L/ M
history, or failure to ask the specific questions, may) l4 r: U0 _/ G' j6 u1 Z
result in extensive, unnecessary, and expensive8 B' A/ B* H3 _, A' k
investigation. The primary care physician should be
2 W# c& X& q  D. }) uaware of this fact, because most of these children( a! P3 m% A5 x3 Z6 }6 o; S8 W
may initially present in their practice. The Physicians’4 H# [# \, u' ^
Desk Reference and package insert should also put a
) [% e5 k) N0 V. W: wwarning about the virilizing effect on a male or
! G: _: x  F7 \  `4 }* d/ Efemale child who might come in contact with some-- n+ Z* }# s% }+ d9 O
one using any of these products.
' O! S3 v8 K. M' u; n7 l3 BReferences
+ f, T' t8 J) o$ T( H% @( z$ N& T* L1. Styne DM. The testes: disorder of sexual differentiation2 S; T6 c3 w0 I1 F" J* n+ A$ B7 c
and puberty in the male. In: Sperling MA, ed. Pediatric
+ b( g0 a1 c" Q# n" {5 n, U) BEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
! D9 P- p! W: ?4 V' h' c, J2002: 565-628." h. b; q# U6 x2 W
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& R$ J& y. h9 O& K
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
% k) i# H5 L: y5 h- d1 q: T- d6 TBoy Induced by Indirect Topical
1 F* o8 i7 J% D' ]5 X0 w; A, pExposure to Testosterone- o! {1 }8 I+ |2 x5 t& q6 C3 T
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, B& k# c  E% u" R  l- Kand Kenneth R. Rettig, MD1) _. @& S* d- a
Clinical Pediatrics
6 A! h7 E" W/ c3 {( h4 LVolume 46 Number 6
& b1 w& v- ~! |" Q( e2 gJuly 2007 540-543& Q& q$ v$ P3 Z& o
© 2007 Sage Publications% _  a. q! A$ ^/ }5 Q* q
10.1177/0009922806296651
# x+ h4 ]% x2 J9 C/ dhttp://clp.sagepub.com% d. S8 g! W6 z) B" X& e: j8 \9 l
hosted at8 [  r" t! U7 u4 g2 e( b6 V0 I
http://online.sagepub.com
# ?" S5 D. p' }- |% lPrecocious puberty in boys, central or peripheral,
5 B1 `! b& }6 D4 {) ]  q; I" O; l3 ]" dis a significant concern for physicians. Central
7 R" [4 W4 T4 }/ }, [precocious puberty (CPP), which is mediated- g# P0 ]  b0 d
through the hypothalamic pituitary gonadal axis, has6 I" c: o0 g% N* C; Y
a higher incidence of organic central nervous system2 B( l. ~3 ^) S  O" c: E1 X6 |% s
lesions in boys.1,2 Virilization in boys, as manifested
4 q6 C; j6 `/ Z6 y7 c& mby enlargement of the penis, development of pubic6 P' d- h3 J  h( U
hair, and facial acne without enlargement of testi-
. \- S! j) g! H0 R4 }cles, suggests peripheral or pseudopuberty.1-3 We
$ }2 ^, K# K4 T2 {2 m) |" treport a 16-month-old boy who presented with the8 g1 V& H, P9 @4 b  L
enlargement of the phallus and pubic hair develop-& s- J9 B6 u3 l3 C& X) f3 y
ment without testicular enlargement, which was due
9 o. x6 L. V# u  b! \to the unintentional exposure to androgen gel used by
% N/ ?4 Z% }7 qthe father. The family initially concealed this infor-. L6 @, V% z7 [. j/ X
mation, resulting in an extensive work-up for this
3 b  ^' q9 [7 R7 Z6 h3 {1 Nchild. Given the widespread and easy availability of- M9 I+ h% D3 W8 v
testosterone gel and cream, we believe this is proba-
. |, @: d0 g! R# U6 q* b4 g+ B# z: Zbly more common than the rare case report in the* w6 I/ I0 N7 c9 c) \
literature.4" b7 S& m  k' N% p+ J# T
Patient Report
  `+ S- C/ d) r1 j; }" yA 16-month-old white child was referred to the
) ]; ]3 t1 r0 X( f- Sendocrine clinic by his pediatrician with the concern3 v4 R/ S0 w1 L! a: t" g( B  s
of early sexual development. His mother noticed! {* y! {  \; C! {
light colored pubic hair development when he was# Q  x& K. S! A  J# i  Y+ c
From the 1Division of Pediatric Endocrinology, 2University of
2 N2 w1 Y1 W1 ]- ISouth Alabama Medical Center, Mobile, Alabama.% h2 a2 V( ]+ A% d! A6 ^
Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 [( ]- v6 G7 T. NProfessor of Pediatrics, University of South Alabama, College of
4 _+ ~5 d1 J; k5 TMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ I1 r3 ]$ L3 z7 `; h
e-mail: [email protected].
- T8 t' ?9 h% Y6 a0 m6 F$ sabout 6 to 7 months old, which progressively became
* }8 f3 D+ p6 }& Edarker. She was also concerned about the enlarge-3 k( w5 ?- e5 E; X& h
ment of his penis and frequent erections. The child
- C: M# H2 W" c0 [/ iwas the product of a full-term normal delivery, with/ u! w9 f$ @4 L/ i/ Q- c
a birth weight of 7 lb 14 oz, and birth length of5 Y1 h/ Q; L( J$ I) n5 C
20 inches. He was breast-fed throughout the first year0 S$ Y0 C7 w2 M; c
of life and was still receiving breast milk along with
  I7 d7 V0 [5 T2 j/ O# b: O  asolid food. He had no hospitalizations or surgery,6 X3 @+ Q) Y" \
and his psychosocial and psychomotor development
% n' e/ X, {2 t% E; C/ Swas age appropriate.
: m5 c( q& n$ t/ ]" W; r5 yThe family history was remarkable for the father,
: `) _& z0 i8 @6 I) K; \who was diagnosed with hypothyroidism at age 16,. u6 }% V9 D1 p3 o, b
which was treated with thyroxine. The father’s
# Q- U! T  G, q5 gheight was 6 feet, and he went through a somewhat
( V7 }  H# H9 |8 Uearly puberty and had stopped growing by age 14.! O8 g( c  O* L3 G$ n$ ?' P/ _3 V. U
The father denied taking any other medication. The* k2 q: |" f' Z5 l# S8 e
child’s mother was in good health. Her menarche
; J. V! c, T/ p2 i2 I: Z5 kwas at 11 years of age, and her height was at 5 feet2 N% g% r8 l" S0 a
5 inches. There was no other family history of pre-! I2 k: r: _$ j. R4 B. r
cocious sexual development in the first-degree rela-
( I  C+ g2 `: Y% s+ m$ ntives. There were no siblings.- I* @6 e9 ~6 O+ w' W& A' o
Physical Examination
; t& i; X/ v' s, O2 f% d" `$ c* R/ XThe physical examination revealed a very active,, n+ t/ P2 U8 x. G0 G& K- z
playful, and healthy boy. The vital signs documented
' U) m4 Q! L3 M5 w4 F/ va blood pressure of 85/50 mm Hg, his length was
7 ?% W  M: N' i; Z, m90 cm (>97th percentile), and his weight was 14.4 kg! p; [/ j* E0 Y. Z& m; A/ s% c' ?9 ?7 i
(also >97th percentile). The observed yearly growth5 w; W% e4 p2 T
velocity was 30 cm (12 inches). The examination of
4 g% K5 t" |: S8 p- Z$ Fthe neck revealed no thyroid enlargement.7 a  r) L- V# k- @
The genitourinary examination was remarkable for
) i2 ^! X' N2 n( T( j4 Henlargement of the penis, with a stretched length of
+ W; d( E- K& W8 cm and a width of 2 cm. The glans penis was very well  `$ G1 G: S% O4 i9 g
developed. The pubic hair was Tanner II, mostly around3 R  O& \, w& ^! P+ Y% }' d4 f
540
& x$ l/ Z3 }/ I7 y( f/ Yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 B- r* E' Z( `the base of the phallus and was dark and curled. The3 v. t' a' [, o( o0 M: G* p" y
testicular volume was prepubertal at 2 mL each.
; o: L+ J% @( y; F  ^! l: @The skin was moist and smooth and somewhat
8 w9 A  k- v4 W- t% v- woily. No axillary hair was noted. There were no' B3 Y% l9 j0 I6 N
abnormal skin pigmentations or café-au-lait spots.0 u9 c- [8 Y8 D+ ~! v
Neurologic evaluation showed deep tendon reflex 2+
9 S' a2 J9 i6 Y6 t& b) ibilateral and symmetrical. There was no suggestion
5 L$ o5 l7 v  R7 B# S" Oof papilledema.0 F. E* t' W% a4 O
Laboratory Evaluation. g% P8 M. A6 w- f
The bone age was consistent with 28 months by" Y$ D. T. E) F& x
using the standard of Greulich and Pyle at a chrono-, l& o+ D& B0 C' z# x: \  ^
logic age of 16 months (advanced).5 Chromosomal+ Y4 d& r( n  e: Y- b: i1 a
karyotype was 46XY. The thyroid function test
/ i1 R4 `' e2 L4 P( vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
, q2 c2 h! {1 l% w6 Slating hormone level was 1.3 µIU/mL (both normal).( U( N7 o1 }; W' p1 q1 ?4 a3 n+ T
The concentrations of serum electrolytes, blood
: I. E0 ?2 x4 r3 n9 z: Murea nitrogen, creatinine, and calcium all were4 d" S# K: |! r( I( X& o
within normal range for his age. The concentration% t( y( ^6 A7 L' h5 J4 k
of serum 17-hydroxyprogesterone was 16 ng/dL2 O& T/ n! |( P( y: n; o9 U9 J
(normal, 3 to 90 ng/dL), androstenedione was 20
) G% m! K' @, W( Y$ O; Png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 X- J* T/ p2 g. z' O" L0 V: Iterone was 38 ng/dL (normal, 50 to 760 ng/dL),
$ M  F8 m8 |+ f; Q! Mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to) Q8 G6 l; l& Y! Q
49ng/dL), 11-desoxycortisol (specific compound S)
1 g* Y8 k  W! M/ }1 E1 H' Kwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  v( g( z2 c, E( z9 G
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% `# o# f2 K5 B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 W1 ?9 S+ }& l$ N; c; Z; f1 |and β-human chorionic gonadotropin was less than9 P' `* W& }6 e; X6 Z! f- v1 z* r
5 mIU/mL (normal <5 mIU/mL). Serum follicular0 A3 r! ?" b. g5 B' ?" N( O
stimulating hormone and leuteinizing hormone
% r+ K2 L" d1 s3 oconcentrations were less than 0.05 mIU/mL
/ Z' U+ A3 P3 f(prepubertal)./ i) \8 K" \4 N) J$ ]
The parents were notified about the laboratory
/ @1 h8 O) X' ?9 @9 M8 Qresults and were informed that all of the tests were( Y! @% i) Z# ]4 M! o
normal except the testosterone level was high. The* t% R! k9 H: Q0 b, F
follow-up visit was arranged within a few weeks to% W: U, _+ R3 S0 D2 O4 v6 A3 o
obtain testicular and abdominal sonograms; how-
4 K) V) \: u: sever, the family did not return for 4 months." a7 G9 x; x2 B. h% W1 m! W9 F7 k7 g& C
Physical examination at this time revealed that the. l! ^% k. n  M9 b) t
child had grown 2.5 cm in 4 months and had gained
" X  q% `# U- M) @* X2 P! R( H, P0 @2 kg of weight. Physical examination remained: o$ d: u* E0 d$ E9 m5 P, l3 y
unchanged. Surprisingly, the pubic hair almost com-
4 \7 |- B4 C( Y# w% w7 [+ X6 Ipletely disappeared except for a few vellous hairs at
0 i) \0 l, D3 j5 G  uthe base of the phallus. Testicular volume was still 2% T) E$ L  e5 q( M4 W
mL, and the size of the penis remained unchanged.
2 U& s& Y" ~: vThe mother also said that the boy was no longer hav-
+ L& ?* m9 d1 o! aing frequent erections.
% t5 ?) W2 u8 Z1 VBoth parents were again questioned about use of
; b7 Q' A& w6 t' yany ointment/creams that they may have applied to
4 V7 b- S  t  A: f% [the child’s skin. This time the father admitted the
. _4 U" h1 y# q" B: x4 j# eTopical Testosterone Exposure / Bhowmick et al 541
! }2 `% Q9 _- I/ k) R; quse of testosterone gel twice daily that he was apply-2 T+ ]" O$ G) b8 k* f
ing over his own shoulders, chest, and back area for
- V* P: ]6 T; E: Y( G: J) H8 M2 wa year. The father also revealed he was embarrassed
5 d( M0 D/ y# M( d; @; Uto disclose that he was using a testosterone gel pre-( Z7 v9 c. w% {8 f- d3 I- p3 [
scribed by his family physician for decreased libido. V1 I9 [! H: q1 j; }7 Q6 |
secondary to depression.
9 Z, Z: J* s, _. S% u4 g' k2 tThe child slept in the same bed with parents.
: Q" l; \& Z; e# q% tThe father would hug the baby and hold him on his
  {0 i% t( u- a6 schest for a considerable period of time, causing sig-) S- |% }$ R: D0 M
nificant bare skin contact between baby and father.
% O& h* Y8 U' y/ X2 E5 |2 \6 RThe father also admitted that after the phone call,( A' e$ w: X- S: L$ J- P2 r4 {% ^3 g' K; T
when he learned the testosterone level in the baby
& D1 q$ \# L+ j, p; L. {  Kwas high, he then read the product information
' t6 t: r% X& p1 wpacket and concluded that it was most likely the rea-
8 }4 G3 [. v  _. y' i' [son for the child’s virilization. At that time, they
. C! O6 `+ N8 r, A$ mdecided to put the baby in a separate bed, and the
+ R$ {" |- N: Q* H- K4 A1 pfather was not hugging him with bare skin and had
% _  m$ b  P! Q0 r3 r  o1 rbeen using protective clothing. A repeat testosterone+ ~, r! O8 @2 D- z9 ~
test was ordered, but the family did not go to the
% T0 m/ A8 }/ t/ e  h8 ]  S8 @+ `laboratory to obtain the test.
) ~, b$ X: W, V# d+ ~5 \Discussion; k; V6 {2 T1 S% U
Precocious puberty in boys is defined as secondary4 L0 p6 o* J0 `) P( F, }
sexual development before 9 years of age.1,4
2 H$ W0 t' a5 q; O" I* K# ?- pPrecocious puberty is termed as central (true) when
( n5 R, O  y2 w! q" f9 j. rit is caused by the premature activation of hypo-
1 t( j) ]8 D% s/ ]thalamic pituitary gonadal axis. CPP is more com-- a2 U5 W) c& i0 U
mon in girls than in boys.1,3 Most boys with CPP! ~9 p# O) ]) y0 L
may have a central nervous system lesion that is
) |+ V# I# }- K) W0 l$ d4 Y  Eresponsible for the early activation of the hypothal-/ @5 Z3 A  k$ ]2 Q( Q8 P
amic pituitary gonadal axis.1-3 Thus, greater empha-# I' O& P5 ?; Y- D
sis has been given to neuroradiologic imaging in
- F8 X1 x& _# u: ^' {3 {5 N2 zboys with precocious puberty. In addition to viril-% C( t8 p8 j, O8 f6 P# W* g
ization, the clinical hallmark of CPP is the symmet-0 c5 o  c$ y/ u/ c
rical testicular growth secondary to stimulation by) I+ s5 g+ C6 H
gonadotropins.1,3$ A+ R3 U, G2 l" V4 u1 |* C
Gonadotropin-independent peripheral preco-" L. j5 i+ T1 _$ J
cious puberty in boys also results from inappropriate
* w( {4 g0 \- O) s' Sandrogenic stimulation from either endogenous or
. o' A3 l. O% s9 P. Sexogenous sources, nonpituitary gonadotropin stim-4 b" G# n6 c( w: m4 N3 y7 Q, `0 |
ulation, and rare activating mutations.3 Virilizing
0 }0 l! X0 i0 qcongenital adrenal hyperplasia producing excessive
+ n% V* |4 h: V0 H" s0 [& Tadrenal androgens is a common cause of precocious9 @/ C$ X' i/ ]- d* j
puberty in boys.3,4
' N' o6 |! U) w* w7 @: w4 CThe most common form of congenital adrenal
% O8 n# q. J  q- `1 Zhyperplasia is the 21-hydroxylase enzyme deficiency.
+ B$ X' }+ X0 V8 q) T( p3 fThe 11-β hydroxylase deficiency may also result in. h$ G6 q9 k* q% h; a8 `) [
excessive adrenal androgen production, and rarely,8 \, N& Y* U1 f* S
an adrenal tumor may also cause adrenal androgen6 U3 y3 m5 m& U; a1 j
excess.1,37 L- v9 ~6 a. j, D, d; O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 l7 n2 ]8 Q/ z5 f# a542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' L" Y) G' v4 W' OA unique entity of male-limited gonadotropin-
$ L; a5 @  m3 i( Tindependent precocious puberty, which is also known. Y. u8 N! h) p4 m( p+ ~& y; V
as testotoxicosis, may cause precocious puberty at a# z# \7 Z2 Q$ [! A8 J: T* L9 ?( ]
very young age. The physical findings in these boys" a$ B) P- s' Z& j
with this disorder are full pubertal development,! S2 y9 @' Q$ g3 B9 X1 ~
including bilateral testicular growth, similar to boys  Z# c4 a8 _# A8 R( v
with CPP. The gonadotropin levels in this disorder
3 f; j5 U7 P; [+ \$ S$ g; Pare suppressed to prepubertal levels and do not show8 d' @0 w; |, Y1 u% ?& Y
pubertal response of gonadotropin after gonadotropin-
& K. p* c' o' o0 _9 j8 d+ @( qreleasing hormone stimulation. This is a sex-linked9 k3 v, ^  d" y% y5 G, f0 Y2 b
autosomal dominant disorder that affects only
# ~, p! }& U9 }+ s& l7 `& h# E# Xmales; therefore, other male members of the family2 R6 K$ n) N8 m% y8 X( M3 Z" ^
may have similar precocious puberty.3/ \+ s% E8 V3 p% b. _5 E
In our patient, physical examination was incon-) C" H6 i9 H  {+ \. O
sistent with true precocious puberty since his testi-
& Q9 v5 o, B. g, V0 s8 lcles were prepubertal in size. However, testotoxicosis
/ l' w8 n: d" Y+ V) K6 _! Mwas in the differential diagnosis because his father4 c, r: }4 N$ Z1 m! U6 X
started puberty somewhat early, and occasionally,/ e3 \2 I# S) {
testicular enlargement is not that evident in the
0 g9 F: t: V4 `# Cbeginning of this process.1 In the absence of a neg-4 v) j7 ^/ g, Y) P2 C/ M. t: H/ a
ative initial history of androgen exposure, our
. w! g  J- \* H% [( tbiggest concern was virilizing adrenal hyperplasia,
+ G. o3 I0 T1 H5 neither 21-hydroxylase deficiency or 11-β hydroxylase
/ S* d4 O4 X% h( ^" A: j5 m8 }deficiency. Those diagnoses were excluded by find-
, y. q3 a9 L6 P. ^- Fing the normal level of adrenal steroids.- ^- I) r6 Y4 J7 t. S# Q
The diagnosis of exogenous androgens was strongly
6 U7 {% g. g+ \$ Tsuspected in a follow-up visit after 4 months because6 s. ~" E1 l4 ?! }& O' Q
the physical examination revealed the complete disap-1 H' H- _% o( V
pearance of pubic hair, normal growth velocity, and
3 Q4 u+ P8 L5 R1 A0 @* ydecreased erections. The father admitted using a testos-
# A/ `- S0 B& z9 G+ ^3 ?0 M2 [terone gel, which he concealed at first visit. He was; y" T2 |$ r/ S; r
using it rather frequently, twice a day. The Physicians’
7 c. I# s1 g) {4 X0 d+ k  bDesk Reference, or package insert of this product, gel or' I* y/ n. d% J
cream, cautions about dermal testosterone transfer to
# N* m5 `- C$ h5 C0 f8 w+ junprotected females through direct skin exposure.  ]3 `2 a! \# g& a* \: ^/ _6 M
Serum testosterone level was found to be 2 times the
( h8 ]. I1 j" S+ U( Abaseline value in those females who were exposed to
5 z7 I- M4 S: S* r0 geven 15 minutes of direct skin contact with their male
) w# s% }' Z; E! b, q+ C; ppartners.6 However, when a shirt covered the applica-. Z) g: f3 j# R$ v% ]
tion site, this testosterone transfer was prevented.
! F8 L7 Z, N& O% U( _3 M; R4 X9 OOur patient’s testosterone level was 60 ng/mL,
' ^8 {( z/ p* |% B7 _6 Wwhich was clearly high. Some studies suggest that- W  a% N: N& c8 Q5 `" i
dermal conversion of testosterone to dihydrotestos-
0 D' j) j! t6 s9 q3 ^! dterone, which is a more potent metabolite, is more2 C! z- m! x9 P4 ^# m1 `
active in young children exposed to testosterone
2 i) y8 |% D' c% M  qexogenously7; however, we did not measure a dihy-
7 q. A' W+ T  p- U6 z$ d# A3 Jdrotestosterone level in our patient. In addition to  b; P+ |1 f, U  T2 ~4 E+ N) S
virilization, exposure to exogenous testosterone in# q( ^' O' d# G% o7 k+ e: @+ v
children results in an increase in growth velocity and
$ M5 T" ~) \7 R' ^% uadvanced bone age, as seen in our patient.& K2 o' c9 s1 l9 D8 C
The long-term effect of androgen exposure during
& A. x8 V: R/ d# Searly childhood on pubertal development and final
3 Y2 N& Y. W5 @( {; xadult height are not fully known and always remain
4 d% `6 l4 K2 [. k) e% `$ x6 B$ P; ya concern. Children treated with short-term testos-$ W) g1 g+ V6 ^3 [( S
terone injection or topical androgen may exhibit some  J% i" `9 j' |. W( ~. }
acceleration of the skeletal maturation; however, after
  x) I. t7 \* vcessation of treatment, the rate of bone maturation
! z8 e' q- @/ Xdecelerates and gradually returns to normal.8,9, O; R/ T$ D2 k8 _4 u6 {
There are conflicting reports and controversy% I' K- k4 Y" Q. Y
over the effect of early androgen exposure on adult& `# W& g5 D  j; L* B; d0 A3 z
penile length.10,11 Some reports suggest subnormal9 l% [0 d" a/ G% m6 G/ U* z
adult penile length, apparently because of downreg-
* o9 B  Q' \5 x4 ?4 r( R0 l: }ulation of androgen receptor number.10,12 However,
3 R  J  C5 o9 @& X7 U  oSutherland et al13 did not find a correlation between+ c  c! N8 M3 j% N$ U
childhood testosterone exposure and reduced adult
, F, n4 Y; [( V; f' Ppenile length in clinical studies.' V; n1 V3 i) y( C7 I+ Z" G
Nonetheless, we do not believe our patient is; k/ l  k. s( i! K1 T
going to experience any of the untoward effects from
( Q" A6 W9 i9 p8 K% }7 a, a+ utestosterone exposure as mentioned earlier because5 _; J3 _6 _% R4 C
the exposure was not for a prolonged period of time.  u! @9 _' j2 ]# r' k
Although the bone age was advanced at the time of+ Z' b( H  U9 O( ?
diagnosis, the child had a normal growth velocity at( q+ z2 g" K; z0 {: w9 r
the follow-up visit. It is hoped that his final adult
/ Y3 @6 y( x6 Pheight will not be affected.
7 T+ M+ E. W8 k9 ZAlthough rarely reported, the widespread avail-
" |# ^" C* s8 S) kability of androgen products in our society may
% H8 p9 d$ {! f' d0 Uindeed cause more virilization in male or female. B0 B8 d+ f& }7 y
children than one would realize. Exposure to andro-
$ W6 {+ R. W1 ^9 O% w! {6 ggen products must be considered and specific ques-* X  Z$ U6 v  F
tioning about the use of a testosterone product or
- J+ H  _) t% A- Xgel should be asked of the family members during, A$ I& E7 T( f3 J/ S1 h
the evaluation of any children who present with vir-
. {, O( V( I1 K" K0 Gilization or peripheral precocious puberty. The diag-
) d/ y- _' v' s4 Y* ^nosis can be established by just a few tests and by
+ O& M- u' x0 Xappropriate history. The inability to obtain such a
: H& W- v9 B3 F! {6 chistory, or failure to ask the specific questions, may  d% l% M) g. T, U4 p/ t, ~+ T
result in extensive, unnecessary, and expensive
6 H/ Z/ n) R4 Qinvestigation. The primary care physician should be
3 \( F( H0 H, Q; z7 `aware of this fact, because most of these children
1 n' c8 s- Y+ {may initially present in their practice. The Physicians’
- a5 {2 M- _- |Desk Reference and package insert should also put a
- I$ A+ |! [& Y) T6 s1 ?# l, Xwarning about the virilizing effect on a male or2 O0 G( |; i  c, t1 E8 B
female child who might come in contact with some-+ U( c' E0 l" V
one using any of these products.
0 @+ g/ x* @/ zReferences1 v  u  J& ]4 b/ j, [
1. Styne DM. The testes: disorder of sexual differentiation$ \4 a( _( A) i5 V: [. M# `
and puberty in the male. In: Sperling MA, ed. Pediatric
- G- Z" Y4 X7 G2 A. kEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
0 ?! v" Y  o* _* Y5 g5 m2002: 565-628.
/ `: R' o' Q0 m; ^" e2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  u/ Y+ V4 u9 N8 N' q/ z
puberty 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
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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

$ J/ ~! p: m5 r/ 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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