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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
7 @* R+ |* e+ }0 U  m; z; [+ CBoy Induced by Indirect Topical
' S2 x# Q$ U5 z/ t. qExposure to Testosterone+ b$ l( D7 v! h/ n
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ I8 j' @* `; ?& A
and Kenneth R. Rettig, MD1. q; a: P3 O" \5 ^8 v  V& k
Clinical Pediatrics
, q! W# k6 C3 z. K1 SVolume 46 Number 6: G6 Q' f" j  \- |
July 2007 540-543% Q' L8 {1 l' l7 M1 l' M
© 2007 Sage Publications1 D8 {6 Z- j$ J, J
10.1177/0009922806296651
% t0 q' G) o/ |% ]http://clp.sagepub.com8 M$ g+ _3 w2 T
hosted at
2 `# ?6 Z1 `- l/ y3 ~http://online.sagepub.com' }1 t6 O( F. s3 j* c! Y
Precocious puberty in boys, central or peripheral,
: h# f# V# Y' F9 s) |% Eis a significant concern for physicians. Central
: F: Q, i0 l( _# b" J. fprecocious puberty (CPP), which is mediated& r( O3 B! S" |+ c: @+ b  t7 V
through the hypothalamic pituitary gonadal axis, has
' G( ]$ \" |$ Za higher incidence of organic central nervous system- Z+ B, |$ h0 d  o( Z6 e6 \" l
lesions in boys.1,2 Virilization in boys, as manifested( t3 [1 `% L. ]
by enlargement of the penis, development of pubic  \" M9 x+ m6 v. \& V4 D- ?3 j: t
hair, and facial acne without enlargement of testi-
1 \0 K6 P: c" ~! N4 Z; v! kcles, suggests peripheral or pseudopuberty.1-3 We; O9 x' g) P! R' ]9 N
report a 16-month-old boy who presented with the6 p  e9 s" S+ L+ V- T
enlargement of the phallus and pubic hair develop-. I, E) h3 ?9 u* D8 t, e
ment without testicular enlargement, which was due. V" p% O) L: G2 W3 T
to the unintentional exposure to androgen gel used by' o4 [9 F: q$ N& Z# H
the father. The family initially concealed this infor-0 j' |1 G& E& T  ^
mation, resulting in an extensive work-up for this
% \# N6 r" G' R/ ~! W' z& G/ V! y+ Nchild. Given the widespread and easy availability of
& O0 o1 u; w/ w( P# J. Dtestosterone gel and cream, we believe this is proba-( x3 K4 e, F! p
bly more common than the rare case report in the
! t/ z/ S6 K/ l9 {: O5 T4 e1 Jliterature.4
: A" d/ z5 A6 I3 k7 K( cPatient Report
: S4 x8 @+ ~4 `" Q/ e  t% i6 OA 16-month-old white child was referred to the. ]- H! W' _& f
endocrine clinic by his pediatrician with the concern/ z" ~) B0 d( v: |; t- |% ?
of early sexual development. His mother noticed& m+ E  G* O/ X- q' j1 R
light colored pubic hair development when he was5 u* |9 h$ d7 X3 ]8 x
From the 1Division of Pediatric Endocrinology, 2University of/ X" Z+ z1 H$ ^8 _" X, Q1 D# ~
South Alabama Medical Center, Mobile, Alabama.
1 Q' w) J8 {' g5 FAddress correspondence to: Samar K. Bhowmick, MD, FACE,
4 k; |! @: X! _5 t) L5 MProfessor of Pediatrics, University of South Alabama, College of
3 ^, M3 l1 q# @0 e  I! {Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. B: T# ^8 Y4 D$ H5 W0 F! Ie-mail: [email protected].
, K' I1 T% T( `+ t9 k* aabout 6 to 7 months old, which progressively became: ^3 R7 Q: J/ K& f! e- a2 J
darker. She was also concerned about the enlarge-
2 h/ a: J" l, j- Lment of his penis and frequent erections. The child
( Z0 a) s& f; O' gwas the product of a full-term normal delivery, with% @- u6 F& ]0 ~
a birth weight of 7 lb 14 oz, and birth length of
& W$ s- m& N0 I5 D2 \20 inches. He was breast-fed throughout the first year
7 {) y. R+ t2 Aof life and was still receiving breast milk along with3 {# C- E1 Q( ^3 u
solid food. He had no hospitalizations or surgery,
3 }# N9 X0 M% N0 Z9 Pand his psychosocial and psychomotor development$ d5 |9 C1 {- t" e* U
was age appropriate.  E" @$ Q7 P3 _2 F/ B
The family history was remarkable for the father,6 h0 |# M  u7 Q1 r7 ]
who was diagnosed with hypothyroidism at age 16,
5 }+ X) y/ ^: ]2 e# ^* \which was treated with thyroxine. The father’s+ [1 z" o- K8 p9 N+ J$ N
height was 6 feet, and he went through a somewhat7 ^& f: H. f2 l7 K
early puberty and had stopped growing by age 14., d; o) q' U6 E7 |( j" G2 H
The father denied taking any other medication. The
9 N" ?# N* ^# T2 P7 Ychild’s mother was in good health. Her menarche
  D# C# p" U; u8 f) h0 swas at 11 years of age, and her height was at 5 feet
  i/ M/ u; E4 b$ P5 o! s5 inches. There was no other family history of pre-
2 M# m$ ~) R  h) x: Ncocious sexual development in the first-degree rela-
8 Z* z8 D# y' ltives. There were no siblings.
5 C- W5 x* P9 ]2 V6 H, i7 RPhysical Examination4 Y. ]" p5 G& }" b+ A
The physical examination revealed a very active,
  i# e7 p1 \# n  u/ [) E6 A" y4 Kplayful, and healthy boy. The vital signs documented
! u9 m: Z( F# m) t. E4 ka blood pressure of 85/50 mm Hg, his length was
5 l- |- S+ ]9 m+ R90 cm (>97th percentile), and his weight was 14.4 kg& U) X5 E$ ]1 `% D
(also >97th percentile). The observed yearly growth6 }6 q- B( y$ V3 Q9 ?
velocity was 30 cm (12 inches). The examination of( O+ `  b2 r* R' |' i$ ~. P0 C
the neck revealed no thyroid enlargement.
$ ^8 |# i) z0 A# r# w$ xThe genitourinary examination was remarkable for; r# v2 R$ h6 O
enlargement of the penis, with a stretched length of; a5 A2 [2 \( R& I% |& B
8 cm and a width of 2 cm. The glans penis was very well
9 {* e3 W3 H/ f- fdeveloped. The pubic hair was Tanner II, mostly around
6 Q8 }9 s; G3 p' X540
2 u1 e, w9 E- y2 I3 Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& V( e4 {" N+ }! n9 l$ k5 z
the base of the phallus and was dark and curled. The6 d/ t6 h+ w. D/ t5 l$ D) d
testicular volume was prepubertal at 2 mL each.
, H' s% ^2 \! `( o" t6 C& u3 ^  mThe skin was moist and smooth and somewhat
7 [$ U( q3 W7 Noily. No axillary hair was noted. There were no
- C: Z" e) X" M/ k' ^  e) Q" tabnormal skin pigmentations or café-au-lait spots.0 X7 {9 D2 b+ Z. P' R
Neurologic evaluation showed deep tendon reflex 2+5 t7 a. F1 ^: N) B7 X; n. |0 K/ V
bilateral and symmetrical. There was no suggestion
9 S# @, u8 V1 c6 s2 B6 [* Z, r" ]- Qof papilledema.
$ o! |- R% T- b9 `2 H8 B3 t& P) FLaboratory Evaluation
2 {) a- ?) R3 c6 W/ B5 G5 X. SThe bone age was consistent with 28 months by
3 z: R% G; {6 k  Y4 Q. O' K7 ^5 U9 Uusing the standard of Greulich and Pyle at a chrono-+ x+ ^1 X/ h7 k/ G
logic age of 16 months (advanced).5 Chromosomal
6 N- ~* g; K' v3 V! tkaryotype was 46XY. The thyroid function test0 e4 S* k  ]: m
showed a free T4 of 1.69 ng/dL, and thyroid stimu-: A$ Y8 I0 H9 I$ X
lating hormone level was 1.3 µIU/mL (both normal).
  n3 N- m. G: ]The concentrations of serum electrolytes, blood
" |, ?, i, V( Y1 J' v$ K: k' ^8 o/ ^urea nitrogen, creatinine, and calcium all were
9 [( a" a1 q0 J5 A  w8 _within normal range for his age. The concentration
" C) r" y( @! j4 Zof serum 17-hydroxyprogesterone was 16 ng/dL
5 t7 S; A' Y0 L/ j9 u' A% t- g4 z(normal, 3 to 90 ng/dL), androstenedione was 20
4 s; n$ h* g5 @! w6 B0 e) \8 @) z! Kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) `" u0 M, W& _2 k+ x3 V5 ~
terone was 38 ng/dL (normal, 50 to 760 ng/dL),  z: J+ x" Z' P* c- S) a: O* j
desoxycorticosterone was 4.3 ng/dL (normal, 7 to5 |0 c2 K( c! f
49ng/dL), 11-desoxycortisol (specific compound S)
" h# l- q( z" @8 D- j; t0 z- Xwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' Y6 E* h- w# t) Z$ w8 ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 n4 z- Y6 M6 H* B/ ^5 dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),* ]/ a' ~8 U7 i
and β-human chorionic gonadotropin was less than8 @1 d: T- _6 y2 B
5 mIU/mL (normal <5 mIU/mL). Serum follicular2 D4 F" E3 I  `0 A0 C! F' K
stimulating hormone and leuteinizing hormone) c& j  a9 j9 t0 J9 l& b1 \# I
concentrations were less than 0.05 mIU/mL
( k! v: k4 b$ c* q. D(prepubertal).( Q  G; X  S. S, y$ \' W
The parents were notified about the laboratory
$ g( q. v2 E) mresults and were informed that all of the tests were
# T: M5 K! F' n* S& v0 D% T' pnormal except the testosterone level was high. The) r& l3 a# H- w* o
follow-up visit was arranged within a few weeks to; m8 U' r) s" J; e* a/ h/ ~( t1 ~" Z
obtain testicular and abdominal sonograms; how-
! b& i% E- O7 ~+ E7 pever, the family did not return for 4 months.' k- k9 B8 `' @7 y5 H& I! `
Physical examination at this time revealed that the4 E5 {& q8 {/ g/ F" Z( r: p. z# {
child had grown 2.5 cm in 4 months and had gained
: s. ?0 S& U4 S1 W& o* d2 kg of weight. Physical examination remained1 h( g  ]: ~: F2 |8 B) S
unchanged. Surprisingly, the pubic hair almost com-8 I- f! ^7 S5 k* b# b( V; ]% H7 Z
pletely disappeared except for a few vellous hairs at
& U+ A* b# c3 D; M. \the base of the phallus. Testicular volume was still 2/ l4 J( ?9 b4 d, {/ w, f
mL, and the size of the penis remained unchanged.
( @6 ^; c+ b. XThe mother also said that the boy was no longer hav-
4 s' |6 U' i# v9 G- m8 Ving frequent erections.
( N5 z% D0 i* t3 JBoth parents were again questioned about use of
( B7 e4 L1 J( {4 ^any ointment/creams that they may have applied to4 E) M: K8 Z8 \: Y: f; F2 O" r
the child’s skin. This time the father admitted the
, j$ ~2 D  A- p: STopical Testosterone Exposure / Bhowmick et al 541
3 F. S# ?7 z4 F; p2 h9 Ouse of testosterone gel twice daily that he was apply-8 Z, n7 p' L+ m5 i3 z" k
ing over his own shoulders, chest, and back area for
; M% L+ ^2 Q; C9 a8 Ha year. The father also revealed he was embarrassed
$ T. R" C' C% Q6 L9 kto disclose that he was using a testosterone gel pre-$ _3 {1 m3 u0 V* N, ^. j5 x
scribed by his family physician for decreased libido
9 v, i% o) m' C% [! w$ t$ i4 B' s+ Jsecondary to depression.
: O) X) a7 O- O8 d5 ?4 ]The child slept in the same bed with parents.
0 L9 I  ?3 f9 ]7 e0 AThe father would hug the baby and hold him on his+ a1 z# t9 [  _% \  P$ C2 M+ s# T9 D
chest for a considerable period of time, causing sig-$ X' G( C, w/ o! l
nificant bare skin contact between baby and father.2 p0 [% y: Z/ C3 U
The father also admitted that after the phone call,
. y& I( g/ S5 Dwhen he learned the testosterone level in the baby
0 V, F( Z. }/ Fwas high, he then read the product information/ J* z  k7 [" E7 p
packet and concluded that it was most likely the rea-& ]( z  }# B0 H- y8 p
son for the child’s virilization. At that time, they
" a! F$ U$ u3 F/ i0 ?; Pdecided to put the baby in a separate bed, and the$ f6 s( X, g/ z8 F( A$ ?
father was not hugging him with bare skin and had
# T3 V/ B0 R3 ^' dbeen using protective clothing. A repeat testosterone
5 G' O- f* z5 r* ]! N" X  Utest was ordered, but the family did not go to the: N# k) v1 t3 K4 \. X
laboratory to obtain the test.2 c3 _0 I$ J) P# H, P( P- G
Discussion
$ w* N2 o. ^) X% M; h6 q. G$ W7 oPrecocious puberty in boys is defined as secondary
1 ~5 @! t( \7 \, m; |! K" m6 r3 |sexual development before 9 years of age.1,4
; j0 k* K, U7 p: h; ]( kPrecocious puberty is termed as central (true) when
$ ^  j+ @: n7 E* e' Wit is caused by the premature activation of hypo-
) @, |& h7 E) |! B/ pthalamic pituitary gonadal axis. CPP is more com-8 F1 x: Y% X! q  i/ I
mon in girls than in boys.1,3 Most boys with CPP
' {- k) q. g& ~  z% Z1 smay have a central nervous system lesion that is
6 K' J; ^) M& h/ P; o% a/ U4 sresponsible for the early activation of the hypothal-! j9 e/ P: v+ L; U; k
amic pituitary gonadal axis.1-3 Thus, greater empha-# \, |, W2 u3 O- G$ G( ^  O
sis has been given to neuroradiologic imaging in
1 z! a$ J" d, a/ g* @1 i/ V" sboys with precocious puberty. In addition to viril-  c; L6 E8 k; I( h# c( D
ization, the clinical hallmark of CPP is the symmet-
6 L8 f0 `1 r+ P9 O; G3 `/ Yrical testicular growth secondary to stimulation by
* x- P& T& A; h7 O$ b0 n- Kgonadotropins.1,3
; x$ X; o, m7 ^$ ?6 NGonadotropin-independent peripheral preco-0 t! ]3 V. D8 c! g
cious puberty in boys also results from inappropriate
7 E5 H- O1 Y9 ?* Kandrogenic stimulation from either endogenous or, W, d# X, ?$ o, G6 ?, ^6 F: V
exogenous sources, nonpituitary gonadotropin stim-" Z0 E: T6 {" V+ w) ~; q7 ~
ulation, and rare activating mutations.3 Virilizing6 E- e5 z$ ~% ^* ~% U  p
congenital adrenal hyperplasia producing excessive
5 Z! R2 O  p# o/ ~6 O8 fadrenal androgens is a common cause of precocious! h7 l. Q9 _/ N
puberty in boys.3,4
* ^' w2 u" N. n3 c- K& z; j* ~The most common form of congenital adrenal( m' M( s# p/ C/ ^3 H0 F& x8 X
hyperplasia is the 21-hydroxylase enzyme deficiency.
/ x# a" x4 s8 N# YThe 11-β hydroxylase deficiency may also result in
5 |. ^5 y- _- r3 F3 d3 }" `excessive adrenal androgen production, and rarely,
+ I  F  ^, o" Can adrenal tumor may also cause adrenal androgen# }1 k( Q! w' z
excess.1,3
/ u/ d$ R+ Q4 U8 R/ Y- v# tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; f$ s5 n9 C7 ~542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: R0 N3 O+ d, j% X. ]7 g; d; WA unique entity of male-limited gonadotropin-
6 G% `! W; L: C6 k% ~independent precocious puberty, which is also known
9 w3 S/ ~4 s& x) Ias testotoxicosis, may cause precocious puberty at a
; k) u: R% ^- Q2 w# `very young age. The physical findings in these boys# t1 P( y3 e" m
with this disorder are full pubertal development,3 t4 k0 C$ w: l; H
including bilateral testicular growth, similar to boys8 k9 u* x* [4 L& O- ^6 m
with CPP. The gonadotropin levels in this disorder
- o& k2 E9 x) V% K: I; gare suppressed to prepubertal levels and do not show
) D1 C$ J4 m5 g# d$ ?! s0 N2 dpubertal response of gonadotropin after gonadotropin-; [8 E  c, i! K( C
releasing hormone stimulation. This is a sex-linked
# `# V, @  p  q( W& fautosomal dominant disorder that affects only4 _$ z* R! B3 p
males; therefore, other male members of the family; d, Y7 |! _- J) ]$ t
may have similar precocious puberty.31 d- N9 Q6 p& X1 i! U! O3 W" F# Y0 v
In our patient, physical examination was incon-% E1 p, Y2 ]4 S- ~: l1 K
sistent with true precocious puberty since his testi-* v* S3 t7 E# Z. m
cles were prepubertal in size. However, testotoxicosis
9 u" P8 X& e% ~( R; Awas in the differential diagnosis because his father
& |3 l: k) Z, S. J1 mstarted puberty somewhat early, and occasionally,
+ m  a# b+ A+ G3 S( U+ j1 i3 etesticular enlargement is not that evident in the
! q4 y3 z  `* y0 @% j+ Y, [beginning of this process.1 In the absence of a neg-, }  h8 K7 {" _( P* A2 \8 W$ ?
ative initial history of androgen exposure, our* m5 z' \, C* o2 J( G8 w
biggest concern was virilizing adrenal hyperplasia,
* V; [7 }4 c# w; A- g9 s6 seither 21-hydroxylase deficiency or 11-β hydroxylase5 {3 T6 ~7 m! z5 L  ~7 d5 K
deficiency. Those diagnoses were excluded by find-) I" {7 B, \( D/ w1 U
ing the normal level of adrenal steroids.
* {& w0 K+ \# o- ~% dThe diagnosis of exogenous androgens was strongly4 M8 ]4 z; d1 D; C
suspected in a follow-up visit after 4 months because% m) K) q+ B8 r: ?* [5 e
the physical examination revealed the complete disap-6 Q1 H/ |7 T5 z, P
pearance of pubic hair, normal growth velocity, and) o, T5 n# G  n3 s7 C. K
decreased erections. The father admitted using a testos-7 w! C2 m/ ?7 i+ p4 P: K5 p) x
terone gel, which he concealed at first visit. He was
2 v" G& o8 g- X- D" susing it rather frequently, twice a day. The Physicians’
2 v+ \1 ~8 \2 b9 n2 ]& M5 ?) hDesk Reference, or package insert of this product, gel or
) P) N  U8 `" I2 e+ p( bcream, cautions about dermal testosterone transfer to/ K; L; G/ n7 \$ ?' t9 V, L- Y
unprotected females through direct skin exposure.& D7 Q6 R5 q% t- E: v
Serum testosterone level was found to be 2 times the2 P/ }! g0 h$ r1 O; Q0 }6 T+ R
baseline value in those females who were exposed to: K- Y; N( Y% g& N/ @6 {
even 15 minutes of direct skin contact with their male
. T; p+ E/ ~# ?# W% ]4 dpartners.6 However, when a shirt covered the applica-. Y$ F0 X4 N+ w3 {5 D4 p
tion site, this testosterone transfer was prevented.
( f6 z) I0 O0 d$ o# JOur patient’s testosterone level was 60 ng/mL,
4 }/ I: k( v0 t4 ?  U) qwhich was clearly high. Some studies suggest that% G# y/ W* _+ V- p. z, O
dermal conversion of testosterone to dihydrotestos-
) i6 w" L; v9 J; y7 Vterone, which is a more potent metabolite, is more
- v6 _% x4 m8 i, vactive in young children exposed to testosterone9 w4 M, y' p8 Y2 T$ C3 F
exogenously7; however, we did not measure a dihy-, M; F9 e% `( c( R7 T" j
drotestosterone level in our patient. In addition to/ R5 A# u/ U8 ~; h: ^5 I# K, e
virilization, exposure to exogenous testosterone in# l- V4 [5 @; A( s, L
children results in an increase in growth velocity and$ l6 o- {9 V6 Q8 L: o5 E9 R
advanced bone age, as seen in our patient.; N1 J6 X) ~- S6 N0 |% j. m6 A
The long-term effect of androgen exposure during
# J- O. ]8 P9 U) N" Yearly childhood on pubertal development and final* ]5 [! b* j9 B5 w- W9 H
adult height are not fully known and always remain
) O8 e; ]8 z9 |/ q; \a concern. Children treated with short-term testos-, i4 M, y$ |( G; J1 \
terone injection or topical androgen may exhibit some, Q% d7 p+ I0 \: R9 f. L
acceleration of the skeletal maturation; however, after8 }) x6 Y" D+ ~
cessation of treatment, the rate of bone maturation
' a. Y+ }" ?( q' B) e: Xdecelerates and gradually returns to normal.8,9
, W4 q9 O: ^" J: _2 DThere are conflicting reports and controversy
5 w2 o: g  n1 L$ W) F0 m9 Qover the effect of early androgen exposure on adult" n' J% s5 z& i8 D; m! H
penile length.10,11 Some reports suggest subnormal2 }# E- T$ Z# n+ T/ j1 L7 V
adult penile length, apparently because of downreg-
, u- X. b3 R( N6 ?5 }: S9 V% g& rulation of androgen receptor number.10,12 However,
: _  m( c& N  ?$ YSutherland et al13 did not find a correlation between
( B8 d$ q+ e9 l# c* zchildhood testosterone exposure and reduced adult
  h# w, _% e9 u3 hpenile length in clinical studies.
- ?, s9 y! ~% K3 v: k! dNonetheless, we do not believe our patient is
! W2 c2 t3 c1 ~5 ?3 O& a+ Kgoing to experience any of the untoward effects from
) A( r8 J! I$ y1 ftestosterone exposure as mentioned earlier because
" Q" K" F8 O+ E0 t+ S3 `the exposure was not for a prolonged period of time.+ q# K% \; a0 O4 b/ w, M
Although the bone age was advanced at the time of
* p! C0 y6 g: cdiagnosis, the child had a normal growth velocity at  T  r4 P' \9 c1 A, s
the follow-up visit. It is hoped that his final adult/ e8 i! r5 y/ D, n( R7 u1 ?
height will not be affected.
* p1 C4 b& a9 M) _Although rarely reported, the widespread avail-- P  P' x: A( S; L: Q
ability of androgen products in our society may
. u, k. p1 \# d! f9 {9 O  Nindeed cause more virilization in male or female% o8 f7 a1 P" n  B  }) Q! z
children than one would realize. Exposure to andro-& c7 V9 M% l% X( F/ U) D
gen products must be considered and specific ques-
, Z5 t7 E/ i& Y; Q1 L* X$ ?tioning about the use of a testosterone product or
4 U9 x6 i% D' j$ rgel should be asked of the family members during
* O( m* J/ r  d& Kthe evaluation of any children who present with vir-
) Y( ]$ V7 X, kilization or peripheral precocious puberty. The diag-# e" |1 u: \& L0 i$ A
nosis can be established by just a few tests and by: R( q. t/ G  F5 C1 ]9 ~
appropriate history. The inability to obtain such a* W  l. a7 ]; b4 C( t% f# L$ B- ~
history, or failure to ask the specific questions, may: p9 ^: x. h; p3 a+ l6 o
result in extensive, unnecessary, and expensive9 L  t# a* m) d4 h5 `
investigation. The primary care physician should be! J- C+ K7 \- L- W
aware of this fact, because most of these children! q. {, n" P# v+ {9 A
may initially present in their practice. The Physicians’% q$ O9 c: h0 f( C3 ]4 h
Desk Reference and package insert should also put a& E7 V! g* B; [
warning about the virilizing effect on a male or& S' U( O# ?% s! Y2 E
female child who might come in contact with some-" p' R! J, O& s, G" b
one using any of these products.
. d7 Y4 X2 }  l4 E4 W2 W, GReferences
% M% H" e/ K% A* E  |. e" C1. Styne DM. The testes: disorder of sexual differentiation+ m& ^# n' y4 G! _/ z9 {0 X
and puberty in the male. In: Sperling MA, ed. Pediatric
4 h( p' H3 ]/ _1 rEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, J+ `' p( r6 {( [$ K9 B9 n/ `2002: 565-628.9 ]( h7 S, q' V4 w. e
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' y- B( O' S5 \) f
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old% L6 r9 _  t- q6 d! q/ l
Boy Induced by Indirect Topical7 x8 o. S) u$ ~9 t- U
Exposure to Testosterone3 w. H3 W- C, X8 v) A
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! R8 r& m3 R. B) I: J; O
and Kenneth R. Rettig, MD12 D, _; _/ K" e6 B8 f# k
Clinical Pediatrics1 s- ~1 j3 B  T8 Q# e
Volume 46 Number 6
  g3 x, z6 N$ C* [' hJuly 2007 540-543% I' `- F+ E$ y8 z) y% ^. i+ ?9 V, V
© 2007 Sage Publications
* c6 q6 P2 @, ?, V/ k. M10.1177/00099228062966517 m% g+ J0 F3 d9 m4 H( B2 j; p
http://clp.sagepub.com% v' v1 q4 s! O5 j! u
hosted at* n2 l7 ?+ r7 l% M
http://online.sagepub.com
( R) F5 g, S* XPrecocious puberty in boys, central or peripheral,
% b8 B, R: X6 Y1 c. m: c* x2 mis a significant concern for physicians. Central+ c1 p- R% B  \0 W. d
precocious puberty (CPP), which is mediated
& p1 q2 _. q* N. r7 J- h: Kthrough the hypothalamic pituitary gonadal axis, has
* L; D4 a3 x. w# }' d* A- O7 `& Qa higher incidence of organic central nervous system
. j7 u) d. t: N2 u. P7 f  H' qlesions in boys.1,2 Virilization in boys, as manifested
3 ~5 \8 a9 N8 w2 {' y# l% R6 mby enlargement of the penis, development of pubic
6 R9 \. @. Y. V' t6 `, G9 f/ Hhair, and facial acne without enlargement of testi-
$ x, h0 c" l; ncles, suggests peripheral or pseudopuberty.1-3 We
) T$ I" A+ ^1 b' J3 Ereport a 16-month-old boy who presented with the6 A0 v! p8 H& g3 p: m, W
enlargement of the phallus and pubic hair develop-6 `" V: y, e: [% M) [
ment without testicular enlargement, which was due
- x8 K2 z% f2 j' vto the unintentional exposure to androgen gel used by
( o8 |: w" @) S7 ?% ithe father. The family initially concealed this infor-
" Q/ |. A% D; o7 S2 `6 x: K3 `8 dmation, resulting in an extensive work-up for this4 d# C. [4 W% q; `( V+ Z* t( w4 L5 m
child. Given the widespread and easy availability of
- ]" X: x0 x6 s. g# k  O% Y  Ftestosterone gel and cream, we believe this is proba-
9 e7 \( C* W" E* ^1 j5 \2 Jbly more common than the rare case report in the
" |; ]3 P) e; i8 a& O" u5 Z' vliterature.4; ~  R% C# u3 G% F! x% f
Patient Report) |  ?0 s6 u1 C" T! h1 K, P% B
A 16-month-old white child was referred to the
4 Q8 k- }& ~' z9 [2 X) t, i, pendocrine clinic by his pediatrician with the concern, f$ y* S8 f) G1 W4 T9 }
of early sexual development. His mother noticed6 N7 F' a' b% {( Z% s$ r
light colored pubic hair development when he was
3 p6 v# T' a1 [+ E4 C4 o. A$ TFrom the 1Division of Pediatric Endocrinology, 2University of3 `- N, l+ O: b$ ~* U
South Alabama Medical Center, Mobile, Alabama.
( o; X; k$ F6 j4 B5 dAddress correspondence to: Samar K. Bhowmick, MD, FACE,$ k& n/ b$ L/ g1 F* R
Professor of Pediatrics, University of South Alabama, College of
' [, ?2 X% B' q$ D' B* nMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 O# B) d. B9 E! S" Qe-mail: [email protected].
( H7 y2 W/ v0 s1 e* X) T  Gabout 6 to 7 months old, which progressively became
1 x3 k; f% P, K2 L" w% V3 Mdarker. She was also concerned about the enlarge-
/ l; W- S, W, I/ W# o% J* O5 ]& Yment of his penis and frequent erections. The child2 G% _8 V! r8 k( ~: K
was the product of a full-term normal delivery, with7 ]( D1 C" w' l+ L4 |  j" I
a birth weight of 7 lb 14 oz, and birth length of
" g% v/ K" Z. r+ Q20 inches. He was breast-fed throughout the first year
7 j: E' j, ^! f+ Gof life and was still receiving breast milk along with- i! W7 F7 T4 u/ p  K/ A& _5 n* ]
solid food. He had no hospitalizations or surgery,
8 p( w/ O5 K. X6 [7 Z& f3 ?and his psychosocial and psychomotor development
5 d  L9 L- O& L7 C* V; Fwas age appropriate.4 c4 m6 Y. |  O
The family history was remarkable for the father,
+ M4 _6 B, u9 l' {1 nwho was diagnosed with hypothyroidism at age 16,
8 z$ [7 I( s7 U+ h7 j0 z  b0 B$ w  mwhich was treated with thyroxine. The father’s
! i: p# }' _; K" s+ s0 [1 dheight was 6 feet, and he went through a somewhat/ F/ v. _. G0 j: }. d  \
early puberty and had stopped growing by age 14.
( X# Z% N! U: v8 }' gThe father denied taking any other medication. The4 @3 Y- i% {0 C9 |  c; k
child’s mother was in good health. Her menarche* d4 H3 w2 W* K, J# m
was at 11 years of age, and her height was at 5 feet
; Q9 }& }  ?2 {5 inches. There was no other family history of pre-
* m% t. y+ Y5 R& t7 K1 n: |% k7 E/ Gcocious sexual development in the first-degree rela-6 W9 t+ M# i7 g
tives. There were no siblings.
* E( G* p' j2 A3 d# f5 FPhysical Examination$ S  F! _  `- Z) Z- C
The physical examination revealed a very active,
4 {- D* V0 l/ y# N. o3 S+ Cplayful, and healthy boy. The vital signs documented
3 ~# X' Q1 j) {3 U( va blood pressure of 85/50 mm Hg, his length was, M  M- G- ?7 Y& w2 v) i5 g
90 cm (>97th percentile), and his weight was 14.4 kg( P) X( p! ]* f$ `
(also >97th percentile). The observed yearly growth
1 r, {' T+ P- j: K) q' Z% vvelocity was 30 cm (12 inches). The examination of! _1 q) S, h, |/ R
the neck revealed no thyroid enlargement./ [/ b- i8 @  G; K" ]+ n; `
The genitourinary examination was remarkable for7 Z' A5 r1 e7 e
enlargement of the penis, with a stretched length of* Z4 K0 X) `" \: \
8 cm and a width of 2 cm. The glans penis was very well
. T! m& s  c- b* r, D+ v% ?5 ]developed. The pubic hair was Tanner II, mostly around5 l* M. p+ d6 ?" c! V
540
, C3 Y( m8 G, v8 aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( L- s. N+ m' `6 \+ z+ Z' Zthe base of the phallus and was dark and curled. The
2 |, l0 G+ `* vtesticular volume was prepubertal at 2 mL each.; Z' G" X9 I0 o
The skin was moist and smooth and somewhat* w% D9 s: Y! v' c4 J+ D
oily. No axillary hair was noted. There were no% F' n/ d' l- d2 c) u8 k9 J
abnormal skin pigmentations or café-au-lait spots.1 ~- F7 L: K# {8 g
Neurologic evaluation showed deep tendon reflex 2+: Z6 I& f8 e  x- @" r6 ^
bilateral and symmetrical. There was no suggestion" F: W! o5 i7 {
of papilledema.
+ M, ~& A: w- c( nLaboratory Evaluation
1 [. |$ Y+ Y- Q# A! ]The bone age was consistent with 28 months by: ]4 v' f( D+ [: A( d9 p7 d
using the standard of Greulich and Pyle at a chrono-
- _* m$ R, k4 V, r% hlogic age of 16 months (advanced).5 Chromosomal
& x. p5 M& @. _# V# D2 r, pkaryotype was 46XY. The thyroid function test
/ d1 m- u  m; k1 h0 b9 b. ~showed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ M9 ]$ q9 M: ?( Nlating hormone level was 1.3 µIU/mL (both normal).
/ {7 R2 f# L( BThe concentrations of serum electrolytes, blood
" n4 e+ q3 J4 w( @urea nitrogen, creatinine, and calcium all were/ n1 D: l% B/ K1 c
within normal range for his age. The concentration
' u% v* u' _7 g6 [9 pof serum 17-hydroxyprogesterone was 16 ng/dL# ?# f) n' o$ [. o& T
(normal, 3 to 90 ng/dL), androstenedione was 20
! [& B* W2 t3 M+ d" ^' q( Bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  ^# W$ o# E1 a8 ?. B7 I3 B( x% ?: Fterone was 38 ng/dL (normal, 50 to 760 ng/dL),) t/ P( B0 b  {7 }- }, N
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 ]; G9 u& `( [  ?; J+ e49ng/dL), 11-desoxycortisol (specific compound S)/ M, K$ p0 d- T  I2 a
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-1 W" B) O' d; @$ g( w' l; g
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, A+ b0 ~) |8 p3 u  ^% Z
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 p* X- {! R8 R7 j9 i: T
and β-human chorionic gonadotropin was less than- ]4 `3 V( K  O5 i% D5 m7 h# L
5 mIU/mL (normal <5 mIU/mL). Serum follicular
& E4 R' H" B1 C! Istimulating hormone and leuteinizing hormone
" {- L6 v5 q0 ~0 l3 K: R  Y  mconcentrations were less than 0.05 mIU/mL' l; H) A* b  x/ O
(prepubertal).
  g  \1 r( s( kThe parents were notified about the laboratory! ^& F& P- S2 A" Q
results and were informed that all of the tests were, e3 p0 ]$ i  V
normal except the testosterone level was high. The
3 G; Z- z3 x7 {" v/ Bfollow-up visit was arranged within a few weeks to
" l0 a8 ^7 |$ R% M* gobtain testicular and abdominal sonograms; how-
, n4 m+ v- q$ f; Never, the family did not return for 4 months.
1 i/ \  o7 \7 Q0 f* y. a* GPhysical examination at this time revealed that the( ~( O9 p' k2 X- J, K/ M
child had grown 2.5 cm in 4 months and had gained
' X0 g5 U% }; Z6 a! {' I6 x2 kg of weight. Physical examination remained4 M/ t9 ]; c- @4 _( }
unchanged. Surprisingly, the pubic hair almost com-2 r1 B. r, ]2 p. e) y8 C
pletely disappeared except for a few vellous hairs at
0 m# M, w) l/ M  Othe base of the phallus. Testicular volume was still 2. x, {2 X! p4 V& S3 Y
mL, and the size of the penis remained unchanged.* B* f3 x. R* q% ~3 X2 H
The mother also said that the boy was no longer hav-! E8 j. u3 w4 W! ^" C& L3 k; B
ing frequent erections.! \* f7 l0 }% O% N3 \8 L2 h# q
Both parents were again questioned about use of
' l% N  z* a8 o. `; D- p, o0 q. m2 a6 v$ hany ointment/creams that they may have applied to3 ]+ W. H* p+ b9 d# U$ H
the child’s skin. This time the father admitted the
/ v0 p! g: t4 G+ n) KTopical Testosterone Exposure / Bhowmick et al 541: [" n( i' O1 I" c$ l: @
use of testosterone gel twice daily that he was apply-
" p, I) S2 R, x1 g8 Z  @, W  {ing over his own shoulders, chest, and back area for
$ G# F2 ~- f) J1 y- v/ P' }& ^6 [a year. The father also revealed he was embarrassed
( E- q/ W5 w, D' Hto disclose that he was using a testosterone gel pre-9 Q8 w, s3 {7 U# R- e9 G1 @+ y# g2 X
scribed by his family physician for decreased libido
2 |' e/ G5 {, F6 @secondary to depression.: v- E( Y$ h' |; V9 c
The child slept in the same bed with parents.
$ _% G: M3 m- w0 K4 uThe father would hug the baby and hold him on his* m7 Y2 h# ~4 |( L' b
chest for a considerable period of time, causing sig-
- \! L) p8 w0 M. G6 ]" x0 T7 xnificant bare skin contact between baby and father.
7 K: t+ q1 R1 A& o( y% Z- I" \The father also admitted that after the phone call," N+ a& b6 e1 b$ P$ A  W
when he learned the testosterone level in the baby
- \" Y0 g+ P. a7 @, twas high, he then read the product information
, {1 I' V% j7 y; l8 ipacket and concluded that it was most likely the rea-3 u$ w% e( m9 `& b. G% v
son for the child’s virilization. At that time, they1 j; ^, q8 N9 I6 B2 o: q
decided to put the baby in a separate bed, and the
- j& O( g0 T2 y4 s  Mfather was not hugging him with bare skin and had% Y8 ~2 |9 F* @* X% k5 e' f. }
been using protective clothing. A repeat testosterone0 E5 q  G  C+ b7 z4 @5 v$ {
test was ordered, but the family did not go to the
) r1 b( R9 `: E" n5 Jlaboratory to obtain the test.
: n2 [) v1 |8 s9 @6 F. pDiscussion  c0 o# N  u  z  q/ F+ c* ~# Y
Precocious puberty in boys is defined as secondary0 Q- ^- Z% P* i7 I
sexual development before 9 years of age.1,4
) \" h: E& h! m6 ~4 H! D$ F" fPrecocious puberty is termed as central (true) when2 x" X8 Q8 Z+ s1 }* n
it is caused by the premature activation of hypo-) d; H  [  C9 u; c! K. S/ k* ]- a
thalamic pituitary gonadal axis. CPP is more com-
1 V4 P3 ~9 \, `+ K. Dmon in girls than in boys.1,3 Most boys with CPP7 c4 L/ y" q7 f* x/ g8 v; g
may have a central nervous system lesion that is( k* A& z2 g( E- K/ q6 {  ?" d
responsible for the early activation of the hypothal-2 E4 G  ~1 F) L- d$ {
amic pituitary gonadal axis.1-3 Thus, greater empha-
; o! r0 [2 q' h: i/ \" Nsis has been given to neuroradiologic imaging in4 C1 i' S3 S, R$ i/ m% q
boys with precocious puberty. In addition to viril-& I8 H0 F  P" f) X$ l) k
ization, the clinical hallmark of CPP is the symmet-
; p& O$ H; N5 w# frical testicular growth secondary to stimulation by4 ?- c' |) S! M! O. Y
gonadotropins.1,39 \3 Q) m$ W& N- h, x0 v
Gonadotropin-independent peripheral preco-
0 l0 Z+ d  u2 J6 V% ]# ~cious puberty in boys also results from inappropriate
' Y) D8 G' Q! T* Qandrogenic stimulation from either endogenous or
6 K- B  c$ d8 s6 @* R* q& Mexogenous sources, nonpituitary gonadotropin stim-
; A- u: M: A3 zulation, and rare activating mutations.3 Virilizing
* \" g8 R3 e" Q( ]& R( Y. kcongenital adrenal hyperplasia producing excessive2 I" Z) I  T, I
adrenal androgens is a common cause of precocious' y$ B* d( P0 y, ^2 H: a
puberty in boys.3,4
5 z$ l1 q# q; G7 d. V; q, H' w" L+ LThe most common form of congenital adrenal
% E2 O# ?9 Q; ^6 Bhyperplasia is the 21-hydroxylase enzyme deficiency., L; i! A. ?! X# K
The 11-β hydroxylase deficiency may also result in% M" w" E" N' F' Q+ O# T
excessive adrenal androgen production, and rarely,
$ `$ H! }$ X8 y8 F/ y8 P6 e$ }an adrenal tumor may also cause adrenal androgen
3 ^. Q% w' x( uexcess.1,32 @2 `( `% a" i& {; w. R+ K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- D! |8 L7 `3 A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- d! F& ?! s# j) o- ?A unique entity of male-limited gonadotropin-" `- {: V; P. h3 r+ f7 T1 E& K
independent precocious puberty, which is also known3 g) F9 U  E* S8 _& P9 I. N; |, {
as testotoxicosis, may cause precocious puberty at a
4 M. @- F' e) g; g8 V& j4 L. ]7 Fvery young age. The physical findings in these boys: p% }2 |  M7 ^2 r- C; n
with this disorder are full pubertal development,- q4 r% v4 L' i7 e2 q
including bilateral testicular growth, similar to boys& l$ W! s+ f+ q2 u6 r0 }8 x* ?! [
with CPP. The gonadotropin levels in this disorder
' m. X1 K4 o# {7 L9 @- j5 `are suppressed to prepubertal levels and do not show
0 g. \! j6 `' k3 g% A: Qpubertal response of gonadotropin after gonadotropin-5 C+ @2 U, w( t1 {9 C+ n
releasing hormone stimulation. This is a sex-linked+ J: \! F  z/ f- m* {
autosomal dominant disorder that affects only1 t/ e3 `8 N+ z( g3 R, z
males; therefore, other male members of the family
' D/ E5 H0 }( K: H  ~" U/ m8 Pmay have similar precocious puberty.38 }3 y: j4 V/ C& U
In our patient, physical examination was incon-
/ l. ]; E5 j6 B( e- Y5 |sistent with true precocious puberty since his testi-7 f" h- C+ j$ S. ~
cles were prepubertal in size. However, testotoxicosis6 w, C: D' F: f9 p! h
was in the differential diagnosis because his father
7 S5 s1 m' y! Y+ I( Fstarted puberty somewhat early, and occasionally,
9 S5 S3 q+ H3 ?+ f3 z) Ktesticular enlargement is not that evident in the
8 O  T1 ?% z! l" s* a' H6 t4 y* ebeginning of this process.1 In the absence of a neg-% {/ `4 C" W. q: ?
ative initial history of androgen exposure, our# T7 U  n% N9 e. i
biggest concern was virilizing adrenal hyperplasia,
! j: d  O8 j2 Feither 21-hydroxylase deficiency or 11-β hydroxylase
, a1 w, p) @4 a$ q( S. O1 ndeficiency. Those diagnoses were excluded by find-
2 D+ G6 i$ h2 ]ing the normal level of adrenal steroids." p9 n" b% ?8 `+ K$ s' _* n
The diagnosis of exogenous androgens was strongly& Z$ c9 k" a. j; e" T$ a8 Z
suspected in a follow-up visit after 4 months because# C$ _4 H% {: H$ W0 b& k
the physical examination revealed the complete disap-
6 O+ W- v# A  G2 ]$ T4 b- Npearance of pubic hair, normal growth velocity, and
4 N7 R( t! L, g+ v, Ydecreased erections. The father admitted using a testos-: @* x' \% v  g- o% c( [+ M
terone gel, which he concealed at first visit. He was
/ d! }5 y+ z) f* _( O2 N% Kusing it rather frequently, twice a day. The Physicians’) }- I* o% L/ {
Desk Reference, or package insert of this product, gel or! ^5 D4 i+ m' ~
cream, cautions about dermal testosterone transfer to
. ~. T  n) V4 t* _, bunprotected females through direct skin exposure.
! b  ]! v" c- [' |: G0 h3 kSerum testosterone level was found to be 2 times the
( Z) H$ b; Q  ~" L* g* q* J  Kbaseline value in those females who were exposed to
" F6 y6 N! `! q6 Z5 deven 15 minutes of direct skin contact with their male
) L: u3 N1 e- F/ k" e+ Ipartners.6 However, when a shirt covered the applica-# @( j& S# K4 R: n8 Z
tion site, this testosterone transfer was prevented." |7 g- x& _7 A8 h( ~0 W
Our patient’s testosterone level was 60 ng/mL,
1 r0 h7 ?; F% x; i" jwhich was clearly high. Some studies suggest that. s5 M9 h0 y9 J1 k. c2 D; h1 ]2 C
dermal conversion of testosterone to dihydrotestos-, s' V* b' g2 y' ^
terone, which is a more potent metabolite, is more7 [; u0 r8 Y- ~# y% D8 r+ r
active in young children exposed to testosterone
5 T8 c& V' s# o, E. v9 w3 P; @* Oexogenously7; however, we did not measure a dihy-
+ F& l" P# l: idrotestosterone level in our patient. In addition to
* x9 a2 R! b6 s0 Mvirilization, exposure to exogenous testosterone in9 Q4 _: t) r4 k$ [6 [& G$ x
children results in an increase in growth velocity and
. n4 l# L% v# j4 o4 {advanced bone age, as seen in our patient.
$ o4 y: P: T3 k9 K7 w# E$ p3 yThe long-term effect of androgen exposure during/ Y3 C: E: i! W# L$ u  B8 }- M. {) L
early childhood on pubertal development and final7 r0 ~9 O# x% B7 R4 H* x! R
adult height are not fully known and always remain6 ^, P, }8 E8 `6 K
a concern. Children treated with short-term testos-
8 F8 v7 b& |* O" Lterone injection or topical androgen may exhibit some& _  Z4 x9 w$ i0 e3 V
acceleration of the skeletal maturation; however, after
0 n: v* h) G1 W, y/ y* Z6 W4 k1 pcessation of treatment, the rate of bone maturation
5 F, H- `8 J  S# A$ x5 y" C/ P% W+ Fdecelerates and gradually returns to normal.8,9
2 l; o+ p: y- U) Y- fThere are conflicting reports and controversy. [. V. @3 d% d1 a- X
over the effect of early androgen exposure on adult7 j% F. \  I& @9 r
penile length.10,11 Some reports suggest subnormal
9 Z3 ]1 t8 f2 G' B8 Hadult penile length, apparently because of downreg-8 T: r2 ]& b/ K3 u( V8 r3 l' [
ulation of androgen receptor number.10,12 However,
' c2 W4 T, }, oSutherland et al13 did not find a correlation between
# q! G( ]$ D3 j4 y3 n, wchildhood testosterone exposure and reduced adult
" n! `0 [7 n$ |" E; ]1 Qpenile length in clinical studies.
) _: Y6 @; P5 L4 x" R" G" lNonetheless, we do not believe our patient is
  z7 D# }- u8 S+ m' {going to experience any of the untoward effects from
' d( a, Z% l; `& e  Ytestosterone exposure as mentioned earlier because" u' U6 h4 T2 G1 T2 j* g. @) y
the exposure was not for a prolonged period of time.
- Y0 J9 i; s) M8 JAlthough the bone age was advanced at the time of# ~5 O% I2 j& J+ W6 Q3 K
diagnosis, the child had a normal growth velocity at- ~) V" Q& a9 v2 x' Q2 q. \+ m: b
the follow-up visit. It is hoped that his final adult
1 v$ j$ b% X! ^1 R" Hheight will not be affected.2 L/ l  b; V7 v% @2 K7 D  `$ u
Although rarely reported, the widespread avail-& I8 l7 o5 ~) B* r2 l" k
ability of androgen products in our society may
* f" f. o4 Y: D- \7 U: U9 ]indeed cause more virilization in male or female. G6 o% a: _8 w! |
children than one would realize. Exposure to andro-5 G5 ~' p( s" @: a. \, ~
gen products must be considered and specific ques-
7 F2 F1 Q/ Q* t- U- V; ~' W4 Gtioning about the use of a testosterone product or
* L' m: S! W* e$ \  _gel should be asked of the family members during
& T2 |* B" |5 m: mthe evaluation of any children who present with vir-. `0 P" W9 s5 g2 N& }
ilization or peripheral precocious puberty. The diag-
# U8 ^( A& \* Dnosis can be established by just a few tests and by
& O' `5 ^1 }+ M) O' I# happropriate history. The inability to obtain such a3 \* s4 h+ I  m0 Y- i0 y: z! H
history, or failure to ask the specific questions, may5 \' A0 Z$ Z" I4 B* V0 K( f% I
result in extensive, unnecessary, and expensive
( @8 T4 F* n& Y! U# K8 K5 Dinvestigation. The primary care physician should be
( L5 e* q) H1 m  j  Saware of this fact, because most of these children
- Z1 o% j0 a* S$ q) @9 Emay initially present in their practice. The Physicians’  h) w+ Q* v. B" S- k5 I& `
Desk Reference and package insert should also put a
9 \2 R8 T1 b" v3 wwarning about the virilizing effect on a male or
4 X4 ]3 }8 G1 a8 V) Hfemale child who might come in contact with some-( M! J% I$ ]& I: d$ {) `8 ^
one using any of these products.3 r0 {4 R8 G' }  T1 E  G0 B1 X
References
' f$ m* `: t$ S: t- A- y1. Styne DM. The testes: disorder of sexual differentiation
( |& Y: Q8 ?1 @% g: Xand puberty in the male. In: Sperling MA, ed. Pediatric2 z/ x, |4 h9 _
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ k6 n& x# h% q  g2002: 565-628., P& T( @4 ]8 w& p% E
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: E) A! S8 J8 H; V; ]" b" Z! _+ C7 }  \puberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
! N' N# c0 c* |% S
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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