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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
, r% a# M: w" lBoy Induced by Indirect Topical
3 b/ U- h' Z: Y. c- i$ A" ]Exposure to Testosterone' k! y; P& {8 @5 ]* `) \
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- S0 K  x/ ^3 K+ {1 n
and Kenneth R. Rettig, MD1/ R9 `$ S* T! M! K
Clinical Pediatrics
+ C" |$ a: E) V( o% c: P7 {+ oVolume 46 Number 6
/ ?- g, f' R  `/ j. _9 P) E+ zJuly 2007 540-543' Y2 d. v0 _- o- L
© 2007 Sage Publications7 y* s. e8 r/ _5 p( v5 \) n* k6 W
10.1177/0009922806296651
4 R$ Y* P0 B% W& I' N* m; ahttp://clp.sagepub.com
7 \- f$ Q' ?1 Khosted at
/ Q; Z5 U, I& ~0 Nhttp://online.sagepub.com; r2 S& d3 \( J6 e) `
Precocious puberty in boys, central or peripheral,
0 Q8 h- l4 Q  S( C7 }) Zis a significant concern for physicians. Central
) u0 k: Z, q$ Kprecocious puberty (CPP), which is mediated
& W0 a0 A+ o& fthrough the hypothalamic pituitary gonadal axis, has
1 k. i4 i4 }9 |" r! Y. ga higher incidence of organic central nervous system2 u5 W: ^, \$ D: m* u" B0 ?
lesions in boys.1,2 Virilization in boys, as manifested
' b) x: Z$ [) Jby enlargement of the penis, development of pubic6 s& ?3 t! E. J
hair, and facial acne without enlargement of testi-
, p( o8 i, W- r( c* q$ f9 D; ?! `cles, suggests peripheral or pseudopuberty.1-3 We% N' A) c0 c6 r. n
report a 16-month-old boy who presented with the  }6 ^! @# I4 W2 i' I
enlargement of the phallus and pubic hair develop-
3 ^5 G, [- F  e/ Y8 N5 d8 L" P2 A& nment without testicular enlargement, which was due5 o/ j, f# z0 ]5 I
to the unintentional exposure to androgen gel used by1 h- `* b7 D# \# b
the father. The family initially concealed this infor-
5 p9 d! `3 T% m! V4 J; v& E  `mation, resulting in an extensive work-up for this
. w% U) K1 _0 o; R" b% X, ~child. Given the widespread and easy availability of* E; `5 E5 Y6 d
testosterone gel and cream, we believe this is proba-
0 _# I" n- ]9 U% f" s) xbly more common than the rare case report in the7 F4 }3 ]6 j6 _/ D; b# t+ m
literature.4" P* P# F0 T% ~  N- O) M. g$ p  k
Patient Report) H8 Q6 r" s, I2 h" o5 o: R
A 16-month-old white child was referred to the
9 O) D& |. C8 k4 t- e- F( Oendocrine clinic by his pediatrician with the concern: }6 ?7 ?( n( z# d: W
of early sexual development. His mother noticed
* B# B. r( {. w; Zlight colored pubic hair development when he was
5 W  x1 K0 C# YFrom the 1Division of Pediatric Endocrinology, 2University of# q) g2 A, M3 Z. M5 Y
South Alabama Medical Center, Mobile, Alabama.
/ c1 p# R- l8 ?1 W$ z: Y' z# [5 ~7 v& gAddress correspondence to: Samar K. Bhowmick, MD, FACE,
9 O3 J) h% q9 ^9 AProfessor of Pediatrics, University of South Alabama, College of; n/ b: f) H6 W4 j0 E0 p4 V6 w
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, W) Z6 x. ^- T# C) Y7 Z+ I1 c
e-mail: [email protected].
: W" j  m" z+ [* H& q% Eabout 6 to 7 months old, which progressively became
  L1 ]$ M  w4 P  ]" J3 Rdarker. She was also concerned about the enlarge-
. M* b2 \$ F$ w4 t' a+ dment of his penis and frequent erections. The child
) F* v1 a- B/ Owas the product of a full-term normal delivery, with1 Z( z; L! h7 c  e
a birth weight of 7 lb 14 oz, and birth length of+ j. R+ G5 o- i0 ]3 h" a
20 inches. He was breast-fed throughout the first year
9 D& A2 x/ X1 q5 [9 tof life and was still receiving breast milk along with
7 m9 C  l6 G- K5 F& C$ l3 [solid food. He had no hospitalizations or surgery,
9 M2 E& A' r. V& Gand his psychosocial and psychomotor development' S  y: n0 O9 s# y& r5 H
was age appropriate.
+ {0 d6 f& I0 ^* @$ AThe family history was remarkable for the father,
( K7 I& c# W. u7 wwho was diagnosed with hypothyroidism at age 16,
8 E- x, K5 U5 B; t7 J! |which was treated with thyroxine. The father’s: I: i+ t; E6 S' G) r# M
height was 6 feet, and he went through a somewhat
7 l  F4 }% T6 searly puberty and had stopped growing by age 14.2 k+ y5 E. C9 n7 x
The father denied taking any other medication. The
$ D! j- X, y3 dchild’s mother was in good health. Her menarche% C3 P. Q' m1 b; c+ `# m
was at 11 years of age, and her height was at 5 feet
, Q2 x: f: Q( A5 inches. There was no other family history of pre-( N2 @' ]- `8 o" l
cocious sexual development in the first-degree rela-
9 C% w# O- L  V& B% itives. There were no siblings.8 |2 I* S0 C  _3 ~
Physical Examination
! J: r3 p, M- B7 `( o+ _7 iThe physical examination revealed a very active,
0 B( D6 E' `- c- Uplayful, and healthy boy. The vital signs documented5 H% [) X0 o) S0 i$ }
a blood pressure of 85/50 mm Hg, his length was% j8 b# G6 d" p2 v8 y* x! x: u# P
90 cm (>97th percentile), and his weight was 14.4 kg! @$ @6 B8 ?1 @5 w4 z( G
(also >97th percentile). The observed yearly growth
+ s& Y" \: N0 ~  B! }velocity was 30 cm (12 inches). The examination of6 g$ O) Z2 C# d# a
the neck revealed no thyroid enlargement.
3 ~$ Z: @/ ~9 r8 Z3 A6 `The genitourinary examination was remarkable for. t* e; B9 H# D3 A6 t/ \  g, G, f
enlargement of the penis, with a stretched length of
5 S$ e( D1 v4 `; i6 E8 cm and a width of 2 cm. The glans penis was very well/ J: |1 z8 t% c- `
developed. The pubic hair was Tanner II, mostly around
# G9 H: Q  Q: q, H4 D* Y540
+ A& l0 s; S: _, ?- |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# q7 N+ U* Y; O  D) W+ ethe base of the phallus and was dark and curled. The
  P4 n8 w, W7 @0 Z9 ~testicular volume was prepubertal at 2 mL each.; l/ k1 {8 q1 R) f: {( \
The skin was moist and smooth and somewhat
! s- K* r5 S6 e/ w0 ?oily. No axillary hair was noted. There were no# N* Y+ H6 N# X% s
abnormal skin pigmentations or café-au-lait spots.
: X" w5 D2 j1 a" M- i2 P6 aNeurologic evaluation showed deep tendon reflex 2+
7 u+ N. B2 M% a) {8 F/ ibilateral and symmetrical. There was no suggestion  p3 U  s: o! c4 r4 G: |* m
of papilledema.$ Y# q3 @! u/ o% X
Laboratory Evaluation- n; N  W5 w2 q; g) m
The bone age was consistent with 28 months by
3 i( X( \  `$ [9 z$ Busing the standard of Greulich and Pyle at a chrono-
1 x/ G2 M# Z$ z8 F3 N" Wlogic age of 16 months (advanced).5 Chromosomal0 u- W# x& d+ P( c: F
karyotype was 46XY. The thyroid function test4 ?  S+ C5 w" ~5 _  P& b
showed a free T4 of 1.69 ng/dL, and thyroid stimu-" [' D3 W( {: y# C
lating hormone level was 1.3 µIU/mL (both normal).
( M/ y& d/ u! A9 D6 ^. q& PThe concentrations of serum electrolytes, blood
' j0 C5 _& O% T2 Y' p) W% _) Z1 J/ xurea nitrogen, creatinine, and calcium all were
& ]. f+ B. r" B/ gwithin normal range for his age. The concentration
7 {9 n" W  a( s  q+ Tof serum 17-hydroxyprogesterone was 16 ng/dL& R% M* n3 Z+ s# b; Y" {* T/ R
(normal, 3 to 90 ng/dL), androstenedione was 20) l  s* I4 e' Q7 R9 C
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( M+ w; \2 B, W% d7 n* ~terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 d: l! E$ o# Y$ r* l) g% _. Tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
" H" n: u6 `* {2 H2 [) h& K9 Z& ]49ng/dL), 11-desoxycortisol (specific compound S)
$ o' b/ [* r+ P) k# @was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* k1 r- B3 G- N- ~tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" y5 u5 g. b# `
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),# G& Y  q* M  [7 V
and β-human chorionic gonadotropin was less than/ s  u2 L; ~$ H
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  x5 E% Q0 Y, r( s3 ?- {2 Estimulating hormone and leuteinizing hormone
! p: L; I! ]( H7 T; k; H" n- kconcentrations were less than 0.05 mIU/mL
! V& k4 u9 k0 y7 s(prepubertal).- @' X( ?3 B8 t* q# g4 V
The parents were notified about the laboratory
4 C6 ?6 [! R& q8 E5 i" kresults and were informed that all of the tests were- d# g: e# z. e" {1 }
normal except the testosterone level was high. The
8 A1 e" ^5 J" ~; q  v1 x, Efollow-up visit was arranged within a few weeks to7 S$ c4 q" `+ F7 j* L, b
obtain testicular and abdominal sonograms; how-) p: F* C4 r1 Y
ever, the family did not return for 4 months.
9 ]# J3 V1 g! a. T  K+ N* ePhysical examination at this time revealed that the7 O! [. Y1 ]3 |; _5 p, k7 c7 m
child had grown 2.5 cm in 4 months and had gained- |! e4 R6 J' r
2 kg of weight. Physical examination remained- G2 E2 y9 C7 i0 U2 G& K) q3 R7 A
unchanged. Surprisingly, the pubic hair almost com-) |7 {/ M% G  j4 ]5 y
pletely disappeared except for a few vellous hairs at
* ]% A- w' J, Athe base of the phallus. Testicular volume was still 2$ J8 }; n& W6 g
mL, and the size of the penis remained unchanged.( Q# j1 Z- Q6 E
The mother also said that the boy was no longer hav-2 Z9 {9 }+ I( w# Y7 e0 B5 u
ing frequent erections.
1 `; l; r9 q% g& q% J* W8 n7 ZBoth parents were again questioned about use of- |3 Q' u2 \; l4 c- l. X
any ointment/creams that they may have applied to5 q+ N$ e+ k& }& U: j( Y2 B
the child’s skin. This time the father admitted the
! J' r  i1 U& L" ETopical Testosterone Exposure / Bhowmick et al 5412 }6 {4 Z0 L1 a! ^. R/ l- X
use of testosterone gel twice daily that he was apply-' \% w5 q" W( v$ d0 i2 m8 k2 d
ing over his own shoulders, chest, and back area for
/ j' B; z" P- L: Ha year. The father also revealed he was embarrassed
' Q5 o7 _% ^8 _6 L! Uto disclose that he was using a testosterone gel pre-* s5 U; o$ U3 ^0 E- M- \. @9 x
scribed by his family physician for decreased libido# y/ |: l7 k, \$ Y% a" m. K# R
secondary to depression.
3 X) {* s5 K4 @' D! j. ^& V" v! nThe child slept in the same bed with parents.
1 x3 o% O+ @# e3 c8 hThe father would hug the baby and hold him on his+ y, S* A6 s; H
chest for a considerable period of time, causing sig-! l; k* A6 T# h* Q, A
nificant bare skin contact between baby and father.
# h  X6 ?9 W% [The father also admitted that after the phone call," H8 g" A9 u: C. ]( _1 T
when he learned the testosterone level in the baby( j# s" r; j! E* g; {3 Q  _
was high, he then read the product information
" l* H/ t% p% I' l; lpacket and concluded that it was most likely the rea-
3 I% ]0 r. ^* n) z- X/ hson for the child’s virilization. At that time, they
4 ^5 @2 M: j' U3 L5 k5 Hdecided to put the baby in a separate bed, and the* \2 a; c' D3 G- Q. y/ m. Y: I
father was not hugging him with bare skin and had
8 i0 m+ ^" @( p8 E+ W" bbeen using protective clothing. A repeat testosterone
! @! k9 @( C  I+ C( f' Ttest was ordered, but the family did not go to the& c. t2 f$ T) A2 w
laboratory to obtain the test.
! R+ A2 N0 V$ m2 e. a# tDiscussion
6 j. X+ P( M# i( S) j( V2 d2 EPrecocious puberty in boys is defined as secondary- Y' X, x+ X. U2 F0 a
sexual development before 9 years of age.1,4
' \( i5 B+ R7 H0 u3 _Precocious puberty is termed as central (true) when
, L* n+ ^( G# x& n" }) d7 b, jit is caused by the premature activation of hypo-$ G9 Z3 K2 o/ ?: b( O( R- o
thalamic pituitary gonadal axis. CPP is more com-
6 H; k# Z) I' Rmon in girls than in boys.1,3 Most boys with CPP$ G- A" B) W7 z4 C9 }# [
may have a central nervous system lesion that is
8 C+ d: G7 I* Hresponsible for the early activation of the hypothal-
. }; X- y+ n6 R% a- M  hamic pituitary gonadal axis.1-3 Thus, greater empha-  b+ F9 J  N% U% q$ V$ \) C+ c
sis has been given to neuroradiologic imaging in
) N' B* i$ e& L% Q# Z: i! d8 g* K, yboys with precocious puberty. In addition to viril-
6 T0 s! z. J  J8 A  uization, the clinical hallmark of CPP is the symmet-6 Z4 {& u. v; T6 \
rical testicular growth secondary to stimulation by
3 Z0 {5 K# f: o( H( H6 c$ }gonadotropins.1,3
( X8 G/ b2 ?* s7 BGonadotropin-independent peripheral preco-$ m( b3 G6 c# ?0 |' Q4 j/ w# i" K/ h+ s0 t
cious puberty in boys also results from inappropriate! R8 {9 K! n9 H) T* c" q6 S) s
androgenic stimulation from either endogenous or
) l; i; O9 ~/ C( _exogenous sources, nonpituitary gonadotropin stim-+ g( a4 p6 I* k; r- t" C5 [
ulation, and rare activating mutations.3 Virilizing
4 p5 l2 U4 ]( H5 N& n( pcongenital adrenal hyperplasia producing excessive7 Z" S. L$ {  y  o- P; J# d* c
adrenal androgens is a common cause of precocious
3 W1 [# J3 q" lpuberty in boys.3,4( F7 Z7 R4 X% s4 z1 X- ?
The most common form of congenital adrenal
0 V& ~+ j: O3 o5 |" @  X! Whyperplasia is the 21-hydroxylase enzyme deficiency.; y& t1 }4 V3 @. x4 l6 J- d+ L9 V
The 11-β hydroxylase deficiency may also result in5 I; g5 Y; E6 E  n
excessive adrenal androgen production, and rarely,7 a- Z- u% V$ ]* K
an adrenal tumor may also cause adrenal androgen
4 _6 T+ Y2 n: f! P5 y/ Q. ^excess.1,3
: u" X& ^6 Q# ?; i' Q* Bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ e5 O  i) {2 |7 F" U542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- T4 ^$ v; w. C5 WA unique entity of male-limited gonadotropin-; k; z* F( D, t- S9 J. c8 h" J
independent precocious puberty, which is also known3 z1 _% s- \5 p3 _) D
as testotoxicosis, may cause precocious puberty at a
; m; [/ g9 v% a) V! ~/ Ivery young age. The physical findings in these boys
) I' h$ l- z  Twith this disorder are full pubertal development,3 v% l3 D9 O0 ~) _8 ]8 L* c
including bilateral testicular growth, similar to boys2 x6 D$ p+ [  v' U6 N
with CPP. The gonadotropin levels in this disorder
2 m3 Y, E  |8 F. x9 r1 l+ e- Care suppressed to prepubertal levels and do not show- a  r8 Z; p) V5 D4 P6 h. [  }/ S5 F
pubertal response of gonadotropin after gonadotropin-
7 ]" G, J3 w" _1 V0 N3 Treleasing hormone stimulation. This is a sex-linked9 a! A% b) W# j4 z  `9 J+ e
autosomal dominant disorder that affects only8 B1 A& g* L+ A% g+ ?6 g# x
males; therefore, other male members of the family
, j7 Z$ d. j. Xmay have similar precocious puberty.3  G: @# W# M9 }) ^8 A9 E" f
In our patient, physical examination was incon-0 r+ S% J' n8 T
sistent with true precocious puberty since his testi-2 e/ T0 m, S# ~0 k4 d8 ~
cles were prepubertal in size. However, testotoxicosis; {( g( T9 v9 F5 V* H; i% ^
was in the differential diagnosis because his father
9 l0 s# O# i1 m8 hstarted puberty somewhat early, and occasionally,  _+ z- Y( C8 Y/ d  j, o
testicular enlargement is not that evident in the
( I/ ^+ @3 n, c, M& @beginning of this process.1 In the absence of a neg-4 D6 U/ S6 c! b2 E" O9 s  [
ative initial history of androgen exposure, our; q! d2 x" E3 O5 m8 P1 t
biggest concern was virilizing adrenal hyperplasia,
# N* R1 r8 [3 S' q/ ?either 21-hydroxylase deficiency or 11-β hydroxylase
5 v1 H; u/ R9 h5 fdeficiency. Those diagnoses were excluded by find-5 b+ u' I5 Y! b/ k
ing the normal level of adrenal steroids.
" W. j+ b9 U% o3 l! C* `5 b' }The diagnosis of exogenous androgens was strongly
: g; H6 f- v+ ~2 Z8 f8 ?suspected in a follow-up visit after 4 months because$ ?+ m! J( D# O# [. J
the physical examination revealed the complete disap-
. E8 D- B- j: G* C# D$ _pearance of pubic hair, normal growth velocity, and( @5 K) ]5 Y& B/ T; q
decreased erections. The father admitted using a testos-
4 K$ j* o3 L* R: w) \# ~terone gel, which he concealed at first visit. He was& D# U( d3 g, b8 s' \0 T
using it rather frequently, twice a day. The Physicians’: ~3 d# V6 R5 g4 M. ^: f0 z
Desk Reference, or package insert of this product, gel or
6 z" {0 i5 R7 j  }/ o- z5 B6 rcream, cautions about dermal testosterone transfer to
5 J; ^4 z" o( `# M! [7 Tunprotected females through direct skin exposure.
4 J/ \+ }1 L: R" ^: _Serum testosterone level was found to be 2 times the
7 u% M8 z0 g$ p( j. S7 T, Tbaseline value in those females who were exposed to
' S% \+ f; Y0 D, j' x1 V5 geven 15 minutes of direct skin contact with their male$ E& e. x: n5 T  k, i2 j& c+ S
partners.6 However, when a shirt covered the applica-
3 {; i$ Y" l& K' O* Ttion site, this testosterone transfer was prevented.
1 K2 P! `. K) V  |Our patient’s testosterone level was 60 ng/mL,
, h! \' Z& \0 O  J: ?# pwhich was clearly high. Some studies suggest that
$ t% n. C1 z5 U9 _  `dermal conversion of testosterone to dihydrotestos-! e# X3 c  H$ [
terone, which is a more potent metabolite, is more
0 h' L" e6 _! j7 Tactive in young children exposed to testosterone& o% J' Q* k' c) E0 V+ K* J5 B' i- \) Y
exogenously7; however, we did not measure a dihy-- w1 S' H/ R+ f7 L% C
drotestosterone level in our patient. In addition to
( v+ M! U0 m' ]) v* Wvirilization, exposure to exogenous testosterone in+ z/ X( B! H0 e/ T0 U/ l- e7 r. Z
children results in an increase in growth velocity and/ O6 Z) E$ D! Y: I. O# i# j8 i
advanced bone age, as seen in our patient.
7 e, H$ L* O. _0 K  {, UThe long-term effect of androgen exposure during. ^3 ^  [: V4 r3 n
early childhood on pubertal development and final' @9 q6 m) Q4 ]. S- ^
adult height are not fully known and always remain
, F( ]" M; O! O% H' T7 J1 qa concern. Children treated with short-term testos-1 a: A! v# b3 E1 ]
terone injection or topical androgen may exhibit some
" w  Z7 f0 h' F9 |) ^' n/ gacceleration of the skeletal maturation; however, after
/ }6 _4 l1 b2 i6 u) W( _cessation of treatment, the rate of bone maturation
& }; W3 a% G4 m4 S& kdecelerates and gradually returns to normal.8,9
( c3 A  D6 N/ @* w) g' o1 BThere are conflicting reports and controversy
! s7 g2 a6 E% N+ v3 a- \' b3 \* Gover the effect of early androgen exposure on adult
, j) U, E' [8 Zpenile length.10,11 Some reports suggest subnormal
0 X4 [# B) Q1 D% |9 hadult penile length, apparently because of downreg-* P0 n, |; q" }; F
ulation of androgen receptor number.10,12 However,8 t6 N3 p" i, P7 y3 W- x4 I
Sutherland et al13 did not find a correlation between- @3 X4 {- \# M; G: g
childhood testosterone exposure and reduced adult
! a7 G. e2 E  i) T4 I5 spenile length in clinical studies.6 x# {! z; q; n+ T) P
Nonetheless, we do not believe our patient is
8 U6 Z$ ?6 r$ y* W& O/ }, q& x4 Lgoing to experience any of the untoward effects from( \& R9 }% m! l( j
testosterone exposure as mentioned earlier because
. _  N( }) ?& ]8 H# Mthe exposure was not for a prolonged period of time.0 K9 N# u1 r2 q  @: u8 H% E) I
Although the bone age was advanced at the time of( V5 u! V% r  h
diagnosis, the child had a normal growth velocity at
# d+ D! L; g; u: R; L) \' R% Q  Dthe follow-up visit. It is hoped that his final adult$ u, [4 u& U! ^; @
height will not be affected.
0 a" J* [2 s, h1 MAlthough rarely reported, the widespread avail-
  r5 [$ W. z/ a) l: h9 s" f* Jability of androgen products in our society may
  U/ Z, |( r9 V  mindeed cause more virilization in male or female
* L% b2 J& e  Y. Wchildren than one would realize. Exposure to andro-7 C7 O; ^/ s) B/ h4 L
gen products must be considered and specific ques-/ w% Z0 q. b# j1 }5 ?
tioning about the use of a testosterone product or
  R9 L5 J5 N. x2 Q9 _gel should be asked of the family members during9 n& P: s5 \6 c& X3 h8 _% J( |
the evaluation of any children who present with vir-
; W& [$ o5 c7 m+ vilization or peripheral precocious puberty. The diag-8 N7 _8 ]# }9 l) z! b* Q
nosis can be established by just a few tests and by% }* v9 Q3 x# }3 j& B# {  U: T
appropriate history. The inability to obtain such a
0 `( ?) J/ o. _: S& i1 w6 g5 |history, or failure to ask the specific questions, may: A: m5 L8 ~) c6 H6 M! j" f" ]. }6 @# R
result in extensive, unnecessary, and expensive" u: w1 X4 z* {& b( {( x6 T4 n8 ^
investigation. The primary care physician should be
& q& Z2 {% y) Kaware of this fact, because most of these children) n5 k) Y/ W/ P" ?
may initially present in their practice. The Physicians’3 n( y9 a6 C/ V5 Z! U$ s: \
Desk Reference and package insert should also put a, J7 X0 g; o' s. Y: G% n
warning about the virilizing effect on a male or
/ A9 ?- }0 Q' i" @' Ffemale child who might come in contact with some-% {3 N" d/ j* o- w& B
one using any of these products.
% m: [$ }  |+ x% x' V: f& O% yReferences7 `# E2 F2 a; U
1. Styne DM. The testes: disorder of sexual differentiation
2 I4 ?, e1 q( }* N9 j8 Dand puberty in the male. In: Sperling MA, ed. Pediatric$ H2 k+ w  B2 R+ R
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 }: h6 T4 L, C- z! Z3 }2002: 565-628.* ]& _3 p2 B: z' n
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 M3 j+ |$ w0 ~
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
% Q& J$ R1 ]! ]4 ]" S4 bBoy Induced by Indirect Topical5 |% @7 k% `4 ~: H5 W! o
Exposure to Testosterone
) S1 q  V2 {2 B4 cSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2* m1 I7 W9 J2 x* ?* c
and Kenneth R. Rettig, MD18 z0 t2 G- @9 l7 Y, t; g
Clinical Pediatrics
" b5 r+ j" n  j) X6 aVolume 46 Number 6
0 E0 p/ b! m5 b0 y; vJuly 2007 540-543. J, `7 Y; t8 o* B( t) v
© 2007 Sage Publications
/ z4 ~' `% Z* u  r" r- j+ G10.1177/00099228062966518 ?& F2 a) i5 P! s) R1 O; t
http://clp.sagepub.com5 O7 L) k, x. D0 `3 x' z3 m
hosted at
/ y& Z4 ]* l7 ohttp://online.sagepub.com
$ t& M9 S6 r( T0 B3 j* e0 k# G. nPrecocious puberty in boys, central or peripheral,
; H# c4 ~0 W! ~8 m9 }is a significant concern for physicians. Central
3 _( Y+ R5 W1 {' o; kprecocious puberty (CPP), which is mediated
% C+ @+ f6 S; Z$ Ythrough the hypothalamic pituitary gonadal axis, has
' W9 }/ i3 n1 ~a higher incidence of organic central nervous system3 q. g" c2 {  \4 b6 D+ G% E) x: Q* `
lesions in boys.1,2 Virilization in boys, as manifested1 v, ~! [& N) l8 o# \
by enlargement of the penis, development of pubic
$ O( e9 Q/ p& P9 K- G" I3 \hair, and facial acne without enlargement of testi-0 T% B8 W3 n( z
cles, suggests peripheral or pseudopuberty.1-3 We: t* e. S/ f: |1 n! l% L# X7 c' ]" g
report a 16-month-old boy who presented with the
8 ]9 F4 \! u* j) Xenlargement of the phallus and pubic hair develop-7 P5 @" s  e4 j  V" O  K
ment without testicular enlargement, which was due7 P1 `  q. T  S/ d
to the unintentional exposure to androgen gel used by
# m. X. p( g. F+ Vthe father. The family initially concealed this infor-9 d/ [# Q! w$ a) L. O. f
mation, resulting in an extensive work-up for this; a2 X( f2 m7 i" v. n# a$ v( Y
child. Given the widespread and easy availability of
9 K; X' |; }% j7 K/ R  f4 r4 Stestosterone gel and cream, we believe this is proba-
! D+ L1 k  O+ C2 p' Obly more common than the rare case report in the
2 S+ I2 G/ b  y. uliterature.48 ^, j5 Q2 U7 y, B- X. D8 r) j
Patient Report0 ]5 t, n2 x% D5 k% {$ i
A 16-month-old white child was referred to the
  L! I7 P6 e, M! R* g* wendocrine clinic by his pediatrician with the concern' t/ f% k6 @. Y1 A  a. [
of early sexual development. His mother noticed+ W: E3 p( f2 x1 x$ L$ C5 e7 U7 X
light colored pubic hair development when he was3 t' Q" t) n1 S/ q
From the 1Division of Pediatric Endocrinology, 2University of
$ N* t( i% v: T7 A. q; d- sSouth Alabama Medical Center, Mobile, Alabama.$ {% y4 _* G% E- b: _
Address correspondence to: Samar K. Bhowmick, MD, FACE,
% K( {; ^9 E6 y$ F0 M7 IProfessor of Pediatrics, University of South Alabama, College of
' A5 o/ m2 |: F7 t( vMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ Z0 F  r; J: {0 p! S
e-mail: [email protected]." H9 c1 `! x/ B; @  L1 j2 v% a
about 6 to 7 months old, which progressively became
+ t6 V: @( u7 [8 i0 qdarker. She was also concerned about the enlarge-
. r7 w/ z* N1 d+ Jment of his penis and frequent erections. The child
) ~  L1 F3 i) Q' b7 W! r8 x$ }9 swas the product of a full-term normal delivery, with; N! z8 z' F/ s3 u  ~- Z& X
a birth weight of 7 lb 14 oz, and birth length of
+ u+ m, w7 r' ~8 ~  C0 Y  n20 inches. He was breast-fed throughout the first year
2 S6 ^9 v4 m% G5 J$ {of life and was still receiving breast milk along with
& A" Z2 i4 [2 c* wsolid food. He had no hospitalizations or surgery,3 T) Q) n! B7 l. t
and his psychosocial and psychomotor development% M6 K7 R2 ~  _4 Y: E' v1 y
was age appropriate.3 [# @% c2 \% K. s
The family history was remarkable for the father,# _; u* w1 h- B) F$ Z
who was diagnosed with hypothyroidism at age 16,3 d: u: p- k1 d) y8 @
which was treated with thyroxine. The father’s
$ e6 H( j; [; Z$ t, }height was 6 feet, and he went through a somewhat
5 x) U% h8 Z0 y( nearly puberty and had stopped growing by age 14.: H% y' K$ f) h
The father denied taking any other medication. The
  X' _% ~9 s& f3 Fchild’s mother was in good health. Her menarche
3 P% I" J3 K5 R( Iwas at 11 years of age, and her height was at 5 feet3 s* a' t9 w) K/ v, j$ U4 t
5 inches. There was no other family history of pre-
2 Z$ L  D5 z6 N" pcocious sexual development in the first-degree rela-5 W% \, i- Q, A" C: M* s
tives. There were no siblings.3 c* c/ e9 O! p
Physical Examination% Q2 \; F9 M& N& m
The physical examination revealed a very active,, V1 U% S) }, K5 ~- A# e% O; h
playful, and healthy boy. The vital signs documented
. d( Q( @9 m. ~+ t. c# oa blood pressure of 85/50 mm Hg, his length was: T) S6 `9 ^% S8 v7 g1 ~. c& y, f
90 cm (>97th percentile), and his weight was 14.4 kg
6 S* B+ Z) |- o6 E" d- Q* z(also >97th percentile). The observed yearly growth
. ^; S7 Z" q- {velocity was 30 cm (12 inches). The examination of
6 j2 @/ S. ?- s/ Dthe neck revealed no thyroid enlargement.1 M) w1 U, V" _
The genitourinary examination was remarkable for1 v" G; {2 C5 V: a4 H
enlargement of the penis, with a stretched length of
* y+ ~! a/ n! ?8 cm and a width of 2 cm. The glans penis was very well0 K# |: `4 V7 b7 L
developed. The pubic hair was Tanner II, mostly around2 {1 X4 j  m5 Q/ J$ X9 t  \& u
540
7 y; n, t1 V4 l/ l- C3 x" wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 X* c4 S( b' e/ T
the base of the phallus and was dark and curled. The, U5 a$ }1 g) L% J  M
testicular volume was prepubertal at 2 mL each.
3 F+ M. c9 V  V' U+ [The skin was moist and smooth and somewhat
* y/ J# e  b) \3 |3 m: B( A2 U6 Q/ Ooily. No axillary hair was noted. There were no) U$ r& c5 m$ I9 {- p9 q% b
abnormal skin pigmentations or café-au-lait spots.. A" k- f' p* n5 f
Neurologic evaluation showed deep tendon reflex 2+
# q7 E9 L' {2 K1 ]% jbilateral and symmetrical. There was no suggestion7 D$ E6 X  A. M7 W# P
of papilledema.& N+ Z3 }: \4 R, V5 Y+ e7 E+ t
Laboratory Evaluation0 n) w0 A+ N( r9 {$ k/ K
The bone age was consistent with 28 months by3 \$ L+ F( e4 {  V
using the standard of Greulich and Pyle at a chrono-2 [4 A/ J, u# [
logic age of 16 months (advanced).5 Chromosomal
  i+ {* E. O* m+ W- @karyotype was 46XY. The thyroid function test5 t6 A1 ~, E  m. R; e! S1 k
showed a free T4 of 1.69 ng/dL, and thyroid stimu-& `5 E4 }3 k) o, Z% C5 F
lating hormone level was 1.3 µIU/mL (both normal).
3 S. J8 F) Y+ L. P" F: P2 }4 ?6 CThe concentrations of serum electrolytes, blood% u& s4 Q/ s% z$ o; Q" b/ P& p1 i
urea nitrogen, creatinine, and calcium all were, |! S0 r! K7 |4 ]
within normal range for his age. The concentration
8 Y% N; {5 F$ l* [; _" bof serum 17-hydroxyprogesterone was 16 ng/dL
$ j% a5 a$ q- }  }+ o3 K. Y; o(normal, 3 to 90 ng/dL), androstenedione was 20
) V) A% S$ `9 f/ [9 j$ _ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) W* @, f3 U* f+ K& D) Y" Z3 x
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 W' K* D; g! n2 j4 b% {6 _desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 i8 ?9 g. d. D* w1 {0 v- R49ng/dL), 11-desoxycortisol (specific compound S). A* ?( T- O, }; r+ l
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& ~7 g' m3 W3 ], P) etisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" q0 o+ S. T/ P" n1 M  J- P$ B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& ~, Y7 ~8 r1 t+ F" qand β-human chorionic gonadotropin was less than
4 ]$ b( `+ n/ f1 a1 ^5 mIU/mL (normal <5 mIU/mL). Serum follicular
" l" ]" c' o$ J# Y% R' Mstimulating hormone and leuteinizing hormone7 e9 P! `- R5 o4 E, I. L2 D- @3 |
concentrations were less than 0.05 mIU/mL9 z, _# T. N7 n0 G0 R+ K
(prepubertal).
% o9 w. K4 b( X8 F+ D8 wThe parents were notified about the laboratory. |( E5 {& P4 J; {6 r' G
results and were informed that all of the tests were  E% {# l! k: u. H: P1 a/ \  x8 b& c
normal except the testosterone level was high. The: D  i; o9 X/ G, @/ r7 \$ K
follow-up visit was arranged within a few weeks to- Z  ?. I5 M+ b& M/ s7 t5 {* v
obtain testicular and abdominal sonograms; how-& V- J- [7 j9 l4 w9 h! W& i
ever, the family did not return for 4 months.
. W) ~: [- c8 _1 `& oPhysical examination at this time revealed that the  x6 A' R, y7 ~! D6 _8 P
child had grown 2.5 cm in 4 months and had gained9 k# K& v, Z: K% H
2 kg of weight. Physical examination remained& Y3 \9 l& X' l0 V9 [) L8 y' M% T
unchanged. Surprisingly, the pubic hair almost com-% L; {7 B! f* d6 a% u- H
pletely disappeared except for a few vellous hairs at
5 g3 j! J& j# W' Y: A0 E  vthe base of the phallus. Testicular volume was still 2
) w: j0 t- G4 f1 a9 x' V+ EmL, and the size of the penis remained unchanged./ j* m3 G) t9 M' K" v0 p% P
The mother also said that the boy was no longer hav-
* N* C+ w6 x# j. ]& ging frequent erections.
3 {, R% M9 z" l+ j: M9 d- Q, p5 }Both parents were again questioned about use of
* i$ ?/ ?9 w! B: Rany ointment/creams that they may have applied to
) V* F% N9 I0 ^the child’s skin. This time the father admitted the
. b& X" R% {. D( d" tTopical Testosterone Exposure / Bhowmick et al 541
( P0 l! k- b. E! T* p1 }use of testosterone gel twice daily that he was apply-7 i, {- b4 {; ]$ f( R, i. ]
ing over his own shoulders, chest, and back area for$ T9 a! p$ R6 m. b
a year. The father also revealed he was embarrassed1 m9 R2 b, ?6 y
to disclose that he was using a testosterone gel pre-# S- o% ?, C2 l- o! c
scribed by his family physician for decreased libido
3 L/ m9 q/ q! x1 j( Isecondary to depression.
. d$ \5 h& r; k7 T1 Q) BThe child slept in the same bed with parents.8 P$ i- d! w- H1 m
The father would hug the baby and hold him on his8 D* D7 q& E1 W- Q) E
chest for a considerable period of time, causing sig-
, |% O' o7 j$ J' tnificant bare skin contact between baby and father.: _; R& B. u7 S" a4 u
The father also admitted that after the phone call,
2 w) f; e+ u) G( o4 _when he learned the testosterone level in the baby
% `$ \* I0 ^# j. C# w' T1 Awas high, he then read the product information5 ]' X" ~& X. c# [6 K7 U  Q5 R& O
packet and concluded that it was most likely the rea-
3 b1 w8 @+ m; _3 {  ^# ]son for the child’s virilization. At that time, they4 m. R# E0 ?; F5 A  R
decided to put the baby in a separate bed, and the& H6 H$ T- P  ?/ R4 j5 g
father was not hugging him with bare skin and had
) H" m& k& {3 u2 V9 \been using protective clothing. A repeat testosterone. W; u2 l+ a" |+ ^/ N% s3 ~
test was ordered, but the family did not go to the
8 F7 ?# v; K& ?6 J4 A5 Alaboratory to obtain the test.
( V, B8 u& _6 A% T; gDiscussion) L/ G! {/ ~! [
Precocious puberty in boys is defined as secondary6 E, }, O' P5 n3 h- C& ?
sexual development before 9 years of age.1,4
* Q& W- t6 O* V& e" v6 ePrecocious puberty is termed as central (true) when! t- A3 E# h  r8 C
it is caused by the premature activation of hypo-
4 h1 C! Z& T) Q7 R0 t# Athalamic pituitary gonadal axis. CPP is more com-
# t1 E- i% p1 v9 I- b0 W# Q5 Mmon in girls than in boys.1,3 Most boys with CPP
2 _1 d1 O, ^) x2 Lmay have a central nervous system lesion that is5 _$ B. m# n# m. j* p- c
responsible for the early activation of the hypothal-$ F3 L5 i9 M0 b% |/ O+ N
amic pituitary gonadal axis.1-3 Thus, greater empha-
1 j" M  T, H, Z! a) e; @0 K  Ksis has been given to neuroradiologic imaging in
- M/ J+ M& T6 {* E7 `& |, zboys with precocious puberty. In addition to viril-/ @2 l0 ~$ V% l0 c* D
ization, the clinical hallmark of CPP is the symmet-
' O$ \- l; ]% C! u* W, `rical testicular growth secondary to stimulation by
8 z8 ~: T0 B3 |) Y" Fgonadotropins.1,3' R+ S) p. W# l
Gonadotropin-independent peripheral preco-: K; M& h+ H! c1 J
cious puberty in boys also results from inappropriate
) O% U! W' D# s- g, pandrogenic stimulation from either endogenous or
. v$ ^* o- u, U. g/ Eexogenous sources, nonpituitary gonadotropin stim-8 \9 l/ P$ W" ^. M0 H
ulation, and rare activating mutations.3 Virilizing
- o7 s4 R" R: @" vcongenital adrenal hyperplasia producing excessive5 q: \, A$ y( ^+ X
adrenal androgens is a common cause of precocious
/ S7 n, L% F2 F+ z; hpuberty in boys.3,4
  I# P% B& d" i9 I* _8 b- L( {The most common form of congenital adrenal/ Z' o; o% w8 S, s4 J3 m0 O$ L
hyperplasia is the 21-hydroxylase enzyme deficiency.& n( v+ [* I1 `; X; U
The 11-β hydroxylase deficiency may also result in
- S7 a$ X, a( d2 g$ E$ Rexcessive adrenal androgen production, and rarely,
. f8 T# |3 w# m4 Uan adrenal tumor may also cause adrenal androgen! w% l. B* s6 J) F6 E7 i
excess.1,3% p( w$ R* N+ P- _9 z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ T6 v) o4 f+ S542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 K7 N: I+ j* d3 B' f) IA unique entity of male-limited gonadotropin-
- E2 _% h' }* w4 E# B9 Pindependent precocious puberty, which is also known$ @& ~7 c0 `# w1 w1 ~. m- Z1 d
as testotoxicosis, may cause precocious puberty at a
8 {6 ^" S( X; {$ \  Z; gvery young age. The physical findings in these boys5 d; m5 {, ?5 ?( N/ w0 \
with this disorder are full pubertal development,
6 a; W( H, ?1 L/ o1 S) ?+ U: bincluding bilateral testicular growth, similar to boys
3 ?. G& E, p4 [# U0 ~# zwith CPP. The gonadotropin levels in this disorder/ F9 V# Q$ M7 S5 {9 q' y
are suppressed to prepubertal levels and do not show" Q0 d9 B1 y6 X, G7 o
pubertal response of gonadotropin after gonadotropin-& a! z' n3 x* B
releasing hormone stimulation. This is a sex-linked- [# j/ w& Q( Y$ V4 F1 K/ l
autosomal dominant disorder that affects only0 ~1 D! V9 I% r, Q
males; therefore, other male members of the family
; ^/ }3 h6 t4 t: G* emay have similar precocious puberty.3
! H- F8 Y' ~2 \' l, Z4 }In our patient, physical examination was incon-3 p0 ]' Q) o, T0 C
sistent with true precocious puberty since his testi-
  o1 N' z) ?  U# Kcles were prepubertal in size. However, testotoxicosis3 `0 G- A- G  {9 _2 e
was in the differential diagnosis because his father
1 C' i+ M" l8 D( p2 g: pstarted puberty somewhat early, and occasionally,. N5 Z4 q; N6 z: t) R, T
testicular enlargement is not that evident in the/ G6 n% v) A3 ^  y* }7 }
beginning of this process.1 In the absence of a neg-" M) R7 N6 r* P3 l7 {  x' V
ative initial history of androgen exposure, our5 ~( O% {  C/ D# E8 o- r: k
biggest concern was virilizing adrenal hyperplasia,2 N) B' P. ^% Z; m% d
either 21-hydroxylase deficiency or 11-β hydroxylase
, ]! X  n6 Z4 i1 ?! t5 `deficiency. Those diagnoses were excluded by find-- i+ I: s+ N+ p$ j( O8 ^
ing the normal level of adrenal steroids.# z$ t$ V/ p' \, A& k) s3 R
The diagnosis of exogenous androgens was strongly
% U+ ^' \9 L- qsuspected in a follow-up visit after 4 months because; e4 m- V, R4 u9 F3 d
the physical examination revealed the complete disap-
# r% s' |  Z7 o( L- e2 k* Xpearance of pubic hair, normal growth velocity, and
2 E) ?. V: x8 Y: ndecreased erections. The father admitted using a testos-- K8 g/ X, m6 \1 d' R* r  E
terone gel, which he concealed at first visit. He was. p1 z+ X9 g) [" `9 Y
using it rather frequently, twice a day. The Physicians’* C- U5 W, ^; m/ o6 C2 x
Desk Reference, or package insert of this product, gel or' ]( N6 O0 Y0 ], a7 G
cream, cautions about dermal testosterone transfer to
7 W2 D; q) W- S5 h9 Zunprotected females through direct skin exposure.* s. [: N+ |0 f" d8 ^
Serum testosterone level was found to be 2 times the
  P* F% [3 A4 q: Vbaseline value in those females who were exposed to
! S+ c7 H5 C3 x) qeven 15 minutes of direct skin contact with their male( H" i1 R  g  p: L
partners.6 However, when a shirt covered the applica-
- a- d9 S7 f: j! @tion site, this testosterone transfer was prevented.
4 H% O! w3 |; p  @3 LOur patient’s testosterone level was 60 ng/mL,! R, B2 f. }" V# y
which was clearly high. Some studies suggest that
6 u5 E+ M2 e4 p5 l. n! i3 Tdermal conversion of testosterone to dihydrotestos-  z9 D- K6 p4 ~6 m
terone, which is a more potent metabolite, is more
! X0 h2 A# g8 eactive in young children exposed to testosterone
5 ^, H% H7 E0 ~exogenously7; however, we did not measure a dihy-
0 C0 M0 J3 u) a' O  S' i( Kdrotestosterone level in our patient. In addition to4 y( [& P! p% N  q, ~1 z
virilization, exposure to exogenous testosterone in
1 t  j/ S& {5 v- ]) K' tchildren results in an increase in growth velocity and
# x0 I6 b# G0 J7 }. x- I! Padvanced bone age, as seen in our patient.( g+ O6 n/ F. H0 H5 B2 f
The long-term effect of androgen exposure during7 b* n- h" [; }  d( v! ^9 `
early childhood on pubertal development and final3 s" r8 ^( ?2 b+ K! W* V1 g0 c( A
adult height are not fully known and always remain! H2 y; i3 q" G9 Z
a concern. Children treated with short-term testos-, x% q# n! o, y) S% F6 j0 C* e/ [
terone injection or topical androgen may exhibit some' P. a4 g  N3 [" C7 D# o$ b; x& y4 J
acceleration of the skeletal maturation; however, after) e: z% \* Q3 q9 d% E' f
cessation of treatment, the rate of bone maturation$ w- |9 q0 Q4 R% \0 c
decelerates and gradually returns to normal.8,9
/ w6 p1 R6 m2 I+ [6 JThere are conflicting reports and controversy* x2 y0 J$ _8 e# @5 P8 U: F
over the effect of early androgen exposure on adult
/ x: Z; ^1 B' z7 n. cpenile length.10,11 Some reports suggest subnormal9 g. [. i0 N' l3 `
adult penile length, apparently because of downreg-3 \% W9 w+ S: v- y! C) _8 u6 L$ e/ u
ulation of androgen receptor number.10,12 However,
- W8 L. y! z- {+ y  J- f$ c: kSutherland et al13 did not find a correlation between4 g7 x% _" X/ [  W6 p& [
childhood testosterone exposure and reduced adult
+ `  v& ?2 z2 ^% Openile length in clinical studies." K9 t2 Y6 V# s' J7 b2 q: |
Nonetheless, we do not believe our patient is
3 }* o8 Z6 K9 m4 Rgoing to experience any of the untoward effects from1 i' q4 @/ J& M
testosterone exposure as mentioned earlier because
" \/ I& V' G/ T1 @+ A; l3 O2 othe exposure was not for a prolonged period of time.
5 Q4 ?3 j: q, m4 FAlthough the bone age was advanced at the time of
' O3 [% d- j7 R2 W9 l! e/ Jdiagnosis, the child had a normal growth velocity at, k- i& H" U' Z* X% m
the follow-up visit. It is hoped that his final adult/ s+ H4 P  r; G- A4 W: L. \: ]8 y
height will not be affected.
$ h' a& l8 C. KAlthough rarely reported, the widespread avail-
; m/ \# I  h! C! C4 [ability of androgen products in our society may) F5 Y' L5 i/ B) F2 V' ^. r
indeed cause more virilization in male or female
+ X9 }8 R: I. \5 I- w# s% hchildren than one would realize. Exposure to andro-4 d) p$ g) h& k# {
gen products must be considered and specific ques-
' l: n0 K) \1 Y5 ytioning about the use of a testosterone product or2 O, b0 ~: A0 e* ~8 j
gel should be asked of the family members during
8 K( j1 X- Y6 l: I5 ]: Y2 h3 Cthe evaluation of any children who present with vir-' K; ~) z6 `. e4 y  y" E$ o
ilization or peripheral precocious puberty. The diag-
( x' P& G* P* E! w4 C& F' G" pnosis can be established by just a few tests and by) R$ {# [: f$ h) g/ h. M
appropriate history. The inability to obtain such a
4 z0 V0 |$ }8 Q. i. w" I2 @. o2 lhistory, or failure to ask the specific questions, may
9 Q; \: I# A7 I( n2 ~; ]result in extensive, unnecessary, and expensive
* f: E$ A! b- e4 l+ rinvestigation. The primary care physician should be
1 S4 L: Q( M- B% t" b8 |6 Jaware of this fact, because most of these children
/ F7 |/ R: i, Q* u2 Amay initially present in their practice. The Physicians’8 C! J, s8 x% r% C7 I; A* p! b2 |: |
Desk Reference and package insert should also put a
1 F5 A* J! P/ C. C% [- s6 Xwarning about the virilizing effect on a male or/ G9 ]) D0 j( {# G" H; h& u/ G
female child who might come in contact with some-0 Z( ~8 v6 k! R
one using any of these products.8 @' D$ r. F2 K
References9 O( O/ w1 r$ x' D% t; O$ W- p, T
1. Styne DM. The testes: disorder of sexual differentiation
! R; @4 B4 Y9 g* ~) Dand puberty in the male. In: Sperling MA, ed. Pediatric
" \. P$ j6 l% H0 ^Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;' z6 k; L4 y. m
2002: 565-628./ D# E) t  H$ e2 m6 @# r& e
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 V- i0 f0 }6 @: `
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!
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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
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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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