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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/ T# b- B. P4 F1 ]6 `% h9 b* a
Boy Induced by Indirect Topical) ^9 m2 z! Z* _% D5 }# k" b' z
Exposure to Testosterone: I2 [3 _4 M! j+ G% }
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
6 |. S( L0 ?5 Qand Kenneth R. Rettig, MD11 V' D3 a& a3 M7 }3 N4 K1 ?# C5 Y" h
Clinical Pediatrics
' K& S1 V+ l1 X3 |  r& Q8 XVolume 46 Number 6* C3 u7 U- q$ M7 V$ C8 ~
July 2007 540-543( x1 m* \; q8 T7 U$ G  A
© 2007 Sage Publications& \& \0 a" a$ ?
10.1177/0009922806296651
% d6 M% z2 m* o( Mhttp://clp.sagepub.com$ c, L/ h4 T" d' Z
hosted at
& L7 W! Y* S$ _; Shttp://online.sagepub.com
* M: ?; i' ?# _( VPrecocious puberty in boys, central or peripheral,/ \+ w' V5 m5 S1 D. H2 u
is a significant concern for physicians. Central, H4 G: W; ^$ ~7 ?1 R4 ]8 K2 h
precocious puberty (CPP), which is mediated
& C+ O- F  F! |. k7 hthrough the hypothalamic pituitary gonadal axis, has
( I1 O% d3 s* S4 {1 Ra higher incidence of organic central nervous system) n8 G% }* [6 y' {! t' k
lesions in boys.1,2 Virilization in boys, as manifested+ I/ P0 n. Z# Y# Y" j/ y# t7 j+ k
by enlargement of the penis, development of pubic7 ~8 t& G* o; W0 B
hair, and facial acne without enlargement of testi-
3 L* a' |/ _! r  M9 T7 ncles, suggests peripheral or pseudopuberty.1-3 We
* e2 L, `* K' O; T* `& c* vreport a 16-month-old boy who presented with the% R- n* G" s+ ]8 P
enlargement of the phallus and pubic hair develop-0 w- W! r! F& A( T0 @8 A
ment without testicular enlargement, which was due
2 m, p) T" D" q9 `8 m5 q4 Gto the unintentional exposure to androgen gel used by
1 B, Z. |! g/ f1 B3 rthe father. The family initially concealed this infor-
4 d* b8 u: ]. ?- pmation, resulting in an extensive work-up for this, L8 ?8 n5 o4 x! y+ K
child. Given the widespread and easy availability of
6 S7 ?/ k" v  Atestosterone gel and cream, we believe this is proba-0 f2 q1 C9 ~- l7 v) W8 n8 K
bly more common than the rare case report in the
  H" u+ X3 n& D) l. z8 iliterature.4
' p% X$ n* E0 B# h5 L1 A( mPatient Report* }2 Q8 O1 l0 a4 }: ~
A 16-month-old white child was referred to the& u$ T) O+ E0 K0 I0 v" K7 u  H' s
endocrine clinic by his pediatrician with the concern
6 t  a# s3 {6 gof early sexual development. His mother noticed2 H/ E5 s" c' x
light colored pubic hair development when he was
" V2 b* G. x/ \" UFrom the 1Division of Pediatric Endocrinology, 2University of7 M. ]2 x: `5 t) ]3 u
South Alabama Medical Center, Mobile, Alabama.0 r0 f) A: w7 P' j; ^2 p/ e" h
Address correspondence to: Samar K. Bhowmick, MD, FACE,
; ^/ h5 d! }6 mProfessor of Pediatrics, University of South Alabama, College of
: `4 M# H7 W! UMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& H9 \7 P7 E7 E( i- ue-mail: [email protected].3 W" U9 m& ?" O1 v8 G  _) x& m
about 6 to 7 months old, which progressively became, L, k: c9 s# m: Z1 C" u
darker. She was also concerned about the enlarge-
3 S3 m& F: Q4 W2 tment of his penis and frequent erections. The child9 F! N# u9 J; p* j7 R
was the product of a full-term normal delivery, with
# P( J$ x: P$ d5 E: [a birth weight of 7 lb 14 oz, and birth length of* q! B0 f5 ~( j- R$ u6 r' k# O
20 inches. He was breast-fed throughout the first year
& h, T4 n  h" P0 f/ N2 Y; s2 Aof life and was still receiving breast milk along with: D, u* w! _' U$ y5 [% |
solid food. He had no hospitalizations or surgery,
  i! f; _& d% @! ?- V* Gand his psychosocial and psychomotor development( r* P$ `+ o) U! F
was age appropriate.1 U0 ]+ N3 m0 c1 L/ B
The family history was remarkable for the father,
, D! J! F! C& \% K) b; e3 mwho was diagnosed with hypothyroidism at age 16,
) j0 o5 B! j# v4 nwhich was treated with thyroxine. The father’s1 v* P! M% q2 g  x" J, S
height was 6 feet, and he went through a somewhat
$ i' O" c- g$ A7 zearly puberty and had stopped growing by age 14.
, Z0 _  O7 i, pThe father denied taking any other medication. The/ r8 m% ?0 O" N: d
child’s mother was in good health. Her menarche( m6 e1 g+ H( |( _5 x
was at 11 years of age, and her height was at 5 feet) D: Q; R; {) r( o5 L5 M, O
5 inches. There was no other family history of pre-
: e& ^- f) Q: ^! V8 ycocious sexual development in the first-degree rela-
$ E( o7 {9 ~5 u5 A9 I$ E2 _) ytives. There were no siblings.
: m8 ?1 z2 w2 U( q2 HPhysical Examination
, L/ `: d1 `1 q9 D  rThe physical examination revealed a very active,/ y) w/ `1 j7 [0 N+ z1 p
playful, and healthy boy. The vital signs documented, M& ^, a, M1 z! A
a blood pressure of 85/50 mm Hg, his length was
# ?; i+ F3 }1 v3 C6 m. m90 cm (>97th percentile), and his weight was 14.4 kg* p/ p: ^- d. X( y' ^
(also >97th percentile). The observed yearly growth6 T0 E' @( A( y2 ?
velocity was 30 cm (12 inches). The examination of* G" r) N3 S" z0 e7 V
the neck revealed no thyroid enlargement.# Z: F% ^1 g, r9 m
The genitourinary examination was remarkable for! l% l6 J8 Y- a6 q9 k7 [- h0 ~
enlargement of the penis, with a stretched length of) d$ s% `/ o# P0 V: G
8 cm and a width of 2 cm. The glans penis was very well* p7 C; W2 c* `
developed. The pubic hair was Tanner II, mostly around4 T, S. l) q7 j& z
540$ g# f3 Y3 J+ k, B" `7 s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& U4 z+ X, U2 k7 r  h' d0 O4 N: v$ N
the base of the phallus and was dark and curled. The
2 ]$ S! {- l$ c9 S7 Itesticular volume was prepubertal at 2 mL each.
% L( K# G' C9 l3 ZThe skin was moist and smooth and somewhat8 k8 U* [* ]3 B0 Z, V9 f
oily. No axillary hair was noted. There were no9 w' H6 V1 y; S1 ?
abnormal skin pigmentations or café-au-lait spots., `2 U/ T. e  k, v$ A
Neurologic evaluation showed deep tendon reflex 2+) \' n, g: L  n% Q
bilateral and symmetrical. There was no suggestion
' \0 V) l* Z8 Q( Mof papilledema.
2 a" a$ D2 O0 M4 q+ BLaboratory Evaluation
) r: o0 [) Q. q0 C! [4 pThe bone age was consistent with 28 months by' B$ C" Z0 Z) \# \. {
using the standard of Greulich and Pyle at a chrono-# j. Y0 D" E% ^
logic age of 16 months (advanced).5 Chromosomal" \/ J# F5 X% ?6 X7 b  R  l
karyotype was 46XY. The thyroid function test
; b( Z, Q% s. b6 Pshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 ^* _6 A" @5 [0 i8 Nlating hormone level was 1.3 µIU/mL (both normal).1 O3 x9 B% U9 \" D/ J/ h
The concentrations of serum electrolytes, blood4 X$ d1 Q) o$ N4 o. ~; i
urea nitrogen, creatinine, and calcium all were% ]; b$ `& Z0 b3 t( a1 t
within normal range for his age. The concentration
. I/ ]9 @- T( ?2 O* O+ Dof serum 17-hydroxyprogesterone was 16 ng/dL0 u+ c; o# n4 H% u
(normal, 3 to 90 ng/dL), androstenedione was 20
  k! a* `. w2 ~6 s- _- W  L! Dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 G$ c! A- c3 y. J7 uterone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 l" u% t& c/ ?desoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 x' m& r, ?. c. A8 j* w49ng/dL), 11-desoxycortisol (specific compound S)2 h* U4 d0 U& d
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. y& g' X( e7 Y8 G6 g/ W% ~1 W  f; _tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
# j, o6 Z7 ^* atestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
% o' @" n0 O) N. `9 i  x$ ]  X& uand β-human chorionic gonadotropin was less than0 t( p; z! e+ _/ i
5 mIU/mL (normal <5 mIU/mL). Serum follicular& x$ o3 X' o& d. ?/ {: D
stimulating hormone and leuteinizing hormone8 H. t/ Z; q! t
concentrations were less than 0.05 mIU/mL% D+ t/ V+ Z( r$ T
(prepubertal).
# z+ V' B/ M/ M; I- y! g" v' lThe parents were notified about the laboratory
8 V  x5 n# N( A. Y! ]results and were informed that all of the tests were
, p! v3 L' ~! Lnormal except the testosterone level was high. The
3 M' h! `7 K) x; E: @3 yfollow-up visit was arranged within a few weeks to9 k. P! @! D( t1 i- |
obtain testicular and abdominal sonograms; how-
4 l& Z! n1 H$ v& u% aever, the family did not return for 4 months.
/ x6 E8 Y- w1 O! W& BPhysical examination at this time revealed that the
- D, U* h% ?$ m) E( Z7 g. Zchild had grown 2.5 cm in 4 months and had gained
- v5 A3 w7 |' ^# n) l2 kg of weight. Physical examination remained
2 d/ o8 i( X  z, V9 ~! a' munchanged. Surprisingly, the pubic hair almost com-
. y" ], y' z2 ?+ B. H+ X& o. ^pletely disappeared except for a few vellous hairs at
, B1 [' ?% V9 E4 cthe base of the phallus. Testicular volume was still 2& y& W$ c2 K1 L9 z
mL, and the size of the penis remained unchanged., g3 c3 ]6 n0 }: Y2 J% \0 |0 H1 j! |
The mother also said that the boy was no longer hav-: |; I7 O8 F9 o0 ?
ing frequent erections.
: t) w3 U7 n" v' gBoth parents were again questioned about use of7 [1 m* y. T; W  Y% a) ]3 [
any ointment/creams that they may have applied to
$ g5 |* Z4 l4 ], ]( i8 L, W6 xthe child’s skin. This time the father admitted the# z! Y' v1 Z1 r7 `3 I
Topical Testosterone Exposure / Bhowmick et al 541
0 ]  S2 B7 E2 y# Q9 z8 D, B: c$ quse of testosterone gel twice daily that he was apply-( G0 V- k. X$ n5 @3 o( \
ing over his own shoulders, chest, and back area for1 g8 ]7 J9 _, W, y% o) n) z) Z: I7 W
a year. The father also revealed he was embarrassed
' \1 P+ ~% A1 o: J) }to disclose that he was using a testosterone gel pre-$ Z1 F, x& @* p5 {; p
scribed by his family physician for decreased libido
: Q; ~. ^  T* i) rsecondary to depression.
4 z# @. G8 `# m0 f- mThe child slept in the same bed with parents.
% l) d0 A9 i: x5 RThe father would hug the baby and hold him on his
2 a5 D3 l. ]0 [chest for a considerable period of time, causing sig-: P! V( ^2 g5 y5 ^* W; c9 h6 _
nificant bare skin contact between baby and father.
/ J& A$ V) t5 u2 H9 mThe father also admitted that after the phone call,
1 U: ^' }7 i  l: \1 L# d; Qwhen he learned the testosterone level in the baby
9 }9 g) M: j9 Qwas high, he then read the product information
/ j" v8 w1 z* ?0 w$ q! Rpacket and concluded that it was most likely the rea-: q8 j5 j" ~& f
son for the child’s virilization. At that time, they4 ~0 t8 K( @' `; {# S7 K- ~; ~* a
decided to put the baby in a separate bed, and the
; L4 z+ @/ Z; K& l: o/ ?/ b4 ffather was not hugging him with bare skin and had
" x- V! W; [8 s6 B9 `been using protective clothing. A repeat testosterone
# F' D5 s1 a- `# t  |+ Rtest was ordered, but the family did not go to the
7 d0 u" R6 |* U1 ~laboratory to obtain the test.' j8 o2 Z  W) Q5 E
Discussion
, e1 l5 [" v6 Q6 A$ f5 n9 bPrecocious puberty in boys is defined as secondary5 ~& Q: q1 I+ X7 @$ y
sexual development before 9 years of age.1,4
9 T6 }& g; Y7 K* x0 m1 m" oPrecocious puberty is termed as central (true) when
9 I; i2 X8 H% \. i. g0 N1 r3 rit is caused by the premature activation of hypo-
5 g; C9 h  d" K& Sthalamic pituitary gonadal axis. CPP is more com-
, J* z+ Q, h- e( lmon in girls than in boys.1,3 Most boys with CPP) S6 U: s$ H" r6 d
may have a central nervous system lesion that is
7 y/ |# R+ G$ ~0 K" oresponsible for the early activation of the hypothal-4 @) o2 b* c8 X. p/ u9 Q( |' M
amic pituitary gonadal axis.1-3 Thus, greater empha-- Y6 P% `0 I7 M/ v' {4 g! r) r
sis has been given to neuroradiologic imaging in3 r9 L8 t# t1 \+ D+ y$ y% k
boys with precocious puberty. In addition to viril-* y% ~: ]: I% T* f; H, U
ization, the clinical hallmark of CPP is the symmet-3 B4 g* n/ v2 ^! Z
rical testicular growth secondary to stimulation by) ]1 i4 f4 H7 A  e+ X
gonadotropins.1,3; s- P0 c6 E6 ~- z1 G+ ^6 R
Gonadotropin-independent peripheral preco-, @* `* b$ m6 q# Z. w
cious puberty in boys also results from inappropriate4 Y, L+ m2 h  k5 c- y
androgenic stimulation from either endogenous or8 i3 ?2 H! q6 _6 q
exogenous sources, nonpituitary gonadotropin stim-$ u+ z, x9 E4 S/ M; [
ulation, and rare activating mutations.3 Virilizing
) o! R7 Z. j+ H6 t1 F  z8 B: _congenital adrenal hyperplasia producing excessive) P/ m% u5 q  P$ w
adrenal androgens is a common cause of precocious
9 R3 N' c, D- A3 s: S: n" c7 Opuberty in boys.3,4+ p5 ]5 c$ ^( O7 X2 x8 \
The most common form of congenital adrenal
+ P9 _/ _" O9 l" p% r2 B& U! `' Ahyperplasia is the 21-hydroxylase enzyme deficiency." j8 g, }$ P% T
The 11-β hydroxylase deficiency may also result in
  ?# E" N0 V4 l" |* M7 s+ O7 h; @excessive adrenal androgen production, and rarely,  f9 u+ U# t$ v  Z- o) g" }; @* C
an adrenal tumor may also cause adrenal androgen
8 S! h$ t3 |# Bexcess.1,3: H' y; D* v8 r1 v8 M/ p
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& [* O/ e! |9 T542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 y9 A+ u7 h) Q+ dA unique entity of male-limited gonadotropin-
- f& o; v$ J/ D% u. W* `" M$ bindependent precocious puberty, which is also known4 H9 X: ~$ M' M3 W
as testotoxicosis, may cause precocious puberty at a! N# a" ~- z( q* e
very young age. The physical findings in these boys, a+ u$ |2 }5 F2 S
with this disorder are full pubertal development,4 P, g; ^0 F& `7 ~6 G$ S
including bilateral testicular growth, similar to boys) D6 [$ M" S+ X2 W8 b
with CPP. The gonadotropin levels in this disorder
6 r) {! x( s' F- uare suppressed to prepubertal levels and do not show' O8 g( p9 W  C5 P3 `
pubertal response of gonadotropin after gonadotropin-  j4 q% r0 H, W  A4 e) u- u
releasing hormone stimulation. This is a sex-linked
5 Z9 _5 V* O- Q4 w( n; P, tautosomal dominant disorder that affects only3 s) ]* ?+ [# B& H6 r
males; therefore, other male members of the family$ G. w7 R  a# q- p
may have similar precocious puberty.31 A' V1 G5 ^1 _) ]& Q5 j3 B: q
In our patient, physical examination was incon-3 r. N6 s) @+ n8 x. {& t
sistent with true precocious puberty since his testi-
6 {( ]6 Z. F6 {cles were prepubertal in size. However, testotoxicosis
: r& S8 D5 c4 Cwas in the differential diagnosis because his father
2 W- L. b$ f* H7 t" `started puberty somewhat early, and occasionally,
; r/ p& X4 T; e+ Y6 btesticular enlargement is not that evident in the* W3 m' m7 w9 j/ c- T( [% b' _
beginning of this process.1 In the absence of a neg-
& a5 j2 G% E/ O& R& N6 U' o- e2 uative initial history of androgen exposure, our
. t7 _, D4 I, ^4 T3 \+ Pbiggest concern was virilizing adrenal hyperplasia,$ \+ e3 H- g- g3 J  {
either 21-hydroxylase deficiency or 11-β hydroxylase3 l; P, |$ m, `/ \  ?( _2 K
deficiency. Those diagnoses were excluded by find-3 f' {' e) `! i# p
ing the normal level of adrenal steroids.
8 d7 f9 ~* H9 A; ]* J1 C+ sThe diagnosis of exogenous androgens was strongly
) F8 z/ `6 _# I. |: a' t& Csuspected in a follow-up visit after 4 months because  W# }+ h! G% w# _
the physical examination revealed the complete disap-
8 i  U" i: A2 Q+ b1 x- l5 U# N! wpearance of pubic hair, normal growth velocity, and
) |/ j# b! d7 P  ^! Z. Jdecreased erections. The father admitted using a testos-1 J+ p2 |! m% \' W7 v- [8 u- p
terone gel, which he concealed at first visit. He was2 O7 g( ?1 C& G
using it rather frequently, twice a day. The Physicians’* d/ W) l- X- y+ ^4 ]2 i2 J
Desk Reference, or package insert of this product, gel or
  ~' {( P* x, `: w, X3 H% P% ]" B& |cream, cautions about dermal testosterone transfer to0 s' B- g% _1 t
unprotected females through direct skin exposure.3 K5 O9 H+ c7 f' k2 C, p4 w$ ?0 v# a
Serum testosterone level was found to be 2 times the
7 i3 D7 I6 J. [2 Wbaseline value in those females who were exposed to" n+ P/ o7 E) o9 O+ r5 [1 I
even 15 minutes of direct skin contact with their male
  o7 ]' ]1 P8 \3 r+ Bpartners.6 However, when a shirt covered the applica-
- Z% c$ c. x  M, M7 J8 ltion site, this testosterone transfer was prevented.
: T3 ^; Z( X1 _7 D% i# ROur patient’s testosterone level was 60 ng/mL,
7 y. ~& K) f6 A! u7 ?) Kwhich was clearly high. Some studies suggest that
: r* U+ O( {% Ndermal conversion of testosterone to dihydrotestos-$ z, i' g1 n9 {
terone, which is a more potent metabolite, is more
2 z) t5 i+ W4 F4 eactive in young children exposed to testosterone
! o7 h  s" t% b2 E) @; y" p$ K* dexogenously7; however, we did not measure a dihy-9 x5 H7 `6 I6 `; Y* v1 E
drotestosterone level in our patient. In addition to& d5 W2 U2 Y' F6 o& N! X
virilization, exposure to exogenous testosterone in5 e& r3 C2 `0 z
children results in an increase in growth velocity and3 m( p/ `: e( @' q
advanced bone age, as seen in our patient.( J% j+ D, p& n3 |( d
The long-term effect of androgen exposure during
' R3 A  `2 ~  h8 W0 d6 pearly childhood on pubertal development and final  \& Q# r5 b4 S6 ]9 G. A- s  X
adult height are not fully known and always remain
$ z% I4 p, R. v( w0 Ga concern. Children treated with short-term testos-3 X& D8 s% F' e0 ?9 n* y$ U3 G
terone injection or topical androgen may exhibit some$ g; \3 W( ?# B. L& l. a& I# s
acceleration of the skeletal maturation; however, after
" W1 C( J0 L. P; W& ~( mcessation of treatment, the rate of bone maturation
2 ]. `7 ?5 @2 t, d: b& Tdecelerates and gradually returns to normal.8,92 H+ {+ F6 R6 X0 k( r6 J% n
There are conflicting reports and controversy6 M9 F1 f) _& I
over the effect of early androgen exposure on adult9 ], G/ u% k% W$ b  g; j* b0 _
penile length.10,11 Some reports suggest subnormal
0 }) U7 l1 H2 t, radult penile length, apparently because of downreg-
1 O" N7 y! x7 ~! mulation of androgen receptor number.10,12 However,
0 B6 {: I9 [1 f' \Sutherland et al13 did not find a correlation between: [3 @2 k6 r" J# L
childhood testosterone exposure and reduced adult
, m4 x& {/ h/ ?penile length in clinical studies.
/ @' Y# `2 v: u, fNonetheless, we do not believe our patient is
1 e! E$ A8 [2 g  y: J  K- xgoing to experience any of the untoward effects from
+ h0 [6 l; p6 E' ntestosterone exposure as mentioned earlier because2 P0 f4 w- L  M  w& H$ c
the exposure was not for a prolonged period of time.
/ W; U: u6 o) R3 i; e6 R9 xAlthough the bone age was advanced at the time of
7 }7 a- @6 a' \& Y8 `* }diagnosis, the child had a normal growth velocity at
/ [: o1 w/ ~7 y: A9 z& Tthe follow-up visit. It is hoped that his final adult
) Z  `( k/ U, e+ _' y6 |height will not be affected.
! q7 h! d, [" D4 F: [; D! c4 fAlthough rarely reported, the widespread avail-
  l' B& i1 @7 D0 }% Dability of androgen products in our society may
6 ~9 t; y* O, y6 ?0 t% `$ Eindeed cause more virilization in male or female2 F" }) l/ J, ?" b& ?+ |( |
children than one would realize. Exposure to andro-
. p8 w- G' n: O3 L" wgen products must be considered and specific ques-
. m, k& }1 [+ w8 E: w3 ]0 o8 Mtioning about the use of a testosterone product or
+ \3 J) J1 m$ B# e% Z( Agel should be asked of the family members during
- d  l2 ]+ |+ X8 F7 H! ]; s# ethe evaluation of any children who present with vir-1 u! j3 F, p5 m8 \/ Y
ilization or peripheral precocious puberty. The diag-
+ i3 g* c" [4 hnosis can be established by just a few tests and by- u$ f9 ^8 }  h
appropriate history. The inability to obtain such a1 N9 E& |0 `3 J& m
history, or failure to ask the specific questions, may" g+ T; X, ]6 K( W' j( {8 p
result in extensive, unnecessary, and expensive
  B: ~' H& N- \- G3 }/ T8 y! einvestigation. The primary care physician should be6 H  c( k, p7 }" r  d
aware of this fact, because most of these children
0 S1 a* q1 Y( {+ U  |may initially present in their practice. The Physicians’
1 D" T6 J) u6 O& e5 h- aDesk Reference and package insert should also put a. R9 G0 u5 ?6 b3 D5 K
warning about the virilizing effect on a male or
, m" {  Q8 Y, D. s+ nfemale child who might come in contact with some-8 @' n' n+ w' B; n6 x# S) U
one using any of these products.
. I1 d' N3 S: a' wReferences5 U! _+ Y, N" d4 w1 B$ I
1. Styne DM. The testes: disorder of sexual differentiation  n& i5 V, s: W2 G' I; }3 O+ v6 N: e
and puberty in the male. In: Sperling MA, ed. Pediatric% s0 ]# G# y' u0 ~  F5 H
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, p3 p) y) D% g! ^( t2 a" Q2002: 565-628.
0 p- c9 g; q9 p! R2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) N: m' U1 F! O
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
4 {4 T+ z3 b& Y) P5 _( HBoy Induced by Indirect Topical; S- v) F* ]- g% S) _9 @/ ?7 S% @
Exposure to Testosterone# N0 _' r/ d6 N) ^# Z
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' t0 v3 K% N# ]$ b' ]# [: xand Kenneth R. Rettig, MD1
1 W7 @# G; y" {: q6 YClinical Pediatrics
5 |3 e0 T; s0 }  W* O& J! TVolume 46 Number 60 O+ A7 P" j# n
July 2007 540-5434 }$ g% Z. d% o* @( v3 z
© 2007 Sage Publications
9 C$ d% I4 }& @9 w10.1177/0009922806296651
4 C5 T! M1 F( B0 T. a7 Y6 j- hhttp://clp.sagepub.com' ?, I! Y  m: X7 `: X7 B5 m
hosted at
; H/ G' g  T+ Zhttp://online.sagepub.com& Y9 [1 Q, |& P) J% m
Precocious puberty in boys, central or peripheral,
: F/ x% W- V1 z0 `is a significant concern for physicians. Central. \0 S- }, f9 u1 d* e# @7 ^1 ^
precocious puberty (CPP), which is mediated
4 N& q) p( {5 D1 V+ a  Othrough the hypothalamic pituitary gonadal axis, has& m- n5 ~/ X8 l7 L' w  i6 f. n
a higher incidence of organic central nervous system# |! m& Z1 T+ \% x1 H. a2 t
lesions in boys.1,2 Virilization in boys, as manifested
/ l1 d8 B) R8 N7 z0 G+ v0 oby enlargement of the penis, development of pubic
# U9 x& X  X4 E9 Shair, and facial acne without enlargement of testi-
7 ^8 `9 {' A$ c1 T% |; Q3 Q$ hcles, suggests peripheral or pseudopuberty.1-3 We
5 c4 F% B4 O1 a8 d# Y& L8 b% Ereport a 16-month-old boy who presented with the7 X; \# b2 w' n4 |) n% O' Z% b
enlargement of the phallus and pubic hair develop-; Y) {% \5 G3 @) Z
ment without testicular enlargement, which was due
/ P  z6 W4 e# o& J  x/ {to the unintentional exposure to androgen gel used by
! J- F% S, Z$ U% k3 L/ hthe father. The family initially concealed this infor-! {. q# N1 Y6 s# `1 b) ]+ h4 n
mation, resulting in an extensive work-up for this
; u- a2 q) q1 h* X) h7 lchild. Given the widespread and easy availability of
' h# A8 a& j7 Ntestosterone gel and cream, we believe this is proba-, m4 K5 W1 C8 b% s3 {0 B* p. M
bly more common than the rare case report in the" _1 Q3 V* I0 Z  V$ s! h. U
literature.4
2 @4 \% {& V3 j, h  APatient Report
8 K: q: [& d8 |A 16-month-old white child was referred to the% s7 P* \$ B; Z! W% q; {
endocrine clinic by his pediatrician with the concern& q( Q/ a- u9 p8 n% U1 h
of early sexual development. His mother noticed
  C. u' r4 J, {/ B+ W5 alight colored pubic hair development when he was6 n7 G* U9 T9 q. T7 C" P0 N) |# H$ S
From the 1Division of Pediatric Endocrinology, 2University of. U- s$ g6 E, B# H% _, H
South Alabama Medical Center, Mobile, Alabama.
4 Q, @4 w0 T  k1 ^6 e4 k) G7 [8 JAddress correspondence to: Samar K. Bhowmick, MD, FACE,
6 S& ]* ~4 H7 @5 S9 w: _1 @. X* iProfessor of Pediatrics, University of South Alabama, College of
5 E6 X' |, D, O2 Y, H+ q" XMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) N! Y! [! R% V; W
e-mail: [email protected].
! ?% T" C  t: b9 Sabout 6 to 7 months old, which progressively became
; g1 C* p; L9 ^2 T9 ]8 ~darker. She was also concerned about the enlarge-$ h0 P& r: K! F2 w: U/ b
ment of his penis and frequent erections. The child
- }0 z: h2 N+ D, k9 d7 D. w+ kwas the product of a full-term normal delivery, with
: E; X- Y1 ^6 l# t: r8 k: Ua birth weight of 7 lb 14 oz, and birth length of1 g+ n2 w9 M8 b/ }  j
20 inches. He was breast-fed throughout the first year% o. j3 G* z5 A1 a7 ~! b# l
of life and was still receiving breast milk along with7 L; {9 _0 f! f6 U" a
solid food. He had no hospitalizations or surgery,3 M7 z/ e9 y5 @
and his psychosocial and psychomotor development/ j( T8 Y. L) d& s2 p) K( L
was age appropriate.( C1 L4 i6 ~. T0 H! h
The family history was remarkable for the father,
2 T! h2 ?  _1 {0 k( _who was diagnosed with hypothyroidism at age 16,+ ?- b) I# j- P+ v
which was treated with thyroxine. The father’s( V' p& S5 C: t! l  _) ^, j: _7 ~
height was 6 feet, and he went through a somewhat4 `+ ^& c( R  t
early puberty and had stopped growing by age 14.: [, b- s- {$ H$ u
The father denied taking any other medication. The* U+ f$ T3 }1 c# N
child’s mother was in good health. Her menarche3 B" ]; }9 w4 }: E2 s
was at 11 years of age, and her height was at 5 feet
' w  o. L& s; w* Y  c. d0 M9 x5 inches. There was no other family history of pre-' i& T& j4 C* C% o  Z' {8 k5 ~5 b, V
cocious sexual development in the first-degree rela-
7 o) N* W( s9 {( C1 g3 xtives. There were no siblings.# _$ E+ a9 T" ~9 f2 M
Physical Examination
  @' H# I' c2 D8 pThe physical examination revealed a very active,; ~. s( R. R3 L; W
playful, and healthy boy. The vital signs documented
, T0 H* D7 a* Y2 D  D. A9 X. |+ `a blood pressure of 85/50 mm Hg, his length was
1 f1 f# a+ C7 B( P90 cm (>97th percentile), and his weight was 14.4 kg* ^8 D4 _" b! _, r
(also >97th percentile). The observed yearly growth9 z" Y0 p: u6 t2 ?
velocity was 30 cm (12 inches). The examination of. O, E5 F+ u- ]/ n9 N/ o
the neck revealed no thyroid enlargement.
5 e5 C; j* H% ~  LThe genitourinary examination was remarkable for; Q9 T9 }2 _6 i1 }! F' W
enlargement of the penis, with a stretched length of/ u% h. t$ A+ @- D: V( a% I7 ~( t
8 cm and a width of 2 cm. The glans penis was very well# d3 |8 y. o5 @
developed. The pubic hair was Tanner II, mostly around
4 S6 g: p# a: |: a7 r+ K8 A& ]540
" A5 _0 q! M1 ~7 D' X  Y. g$ c4 Dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; G' I" Q- L" t7 F5 Y
the base of the phallus and was dark and curled. The2 i  A. J  }9 }) l( S
testicular volume was prepubertal at 2 mL each.
6 f0 m/ t: [2 I3 `The skin was moist and smooth and somewhat
& q3 ?; x. `" S: `- E$ s, f' Hoily. No axillary hair was noted. There were no( h, _, R$ {& \) t" l" R
abnormal skin pigmentations or café-au-lait spots.
6 s7 R2 L3 B5 v+ l, G$ fNeurologic evaluation showed deep tendon reflex 2+: h2 v6 @& u* ~$ _8 v
bilateral and symmetrical. There was no suggestion4 A. F$ B6 u' c9 ?, \2 j
of papilledema.
! J' Q7 _! \' X: ~) I7 tLaboratory Evaluation0 W" h+ Z, \' L" W1 A6 H
The bone age was consistent with 28 months by' F3 i$ Q4 o/ ]) Z, s
using the standard of Greulich and Pyle at a chrono-4 b8 ^/ i$ x, s1 S
logic age of 16 months (advanced).5 Chromosomal
. u8 Y6 @2 u5 S5 t2 Q  _6 F* kkaryotype was 46XY. The thyroid function test( M2 g0 [' D7 u- \6 D
showed a free T4 of 1.69 ng/dL, and thyroid stimu-9 n8 R% Y3 ?& P) I6 w; v
lating hormone level was 1.3 µIU/mL (both normal).
' E9 x* E/ o6 zThe concentrations of serum electrolytes, blood
8 k$ c- T$ `" E' U- g; ~' rurea nitrogen, creatinine, and calcium all were
9 Z2 X6 K# M" t3 ]within normal range for his age. The concentration
; h- k* |0 y: K2 G+ i) yof serum 17-hydroxyprogesterone was 16 ng/dL6 w0 Z' [- e9 c- i
(normal, 3 to 90 ng/dL), androstenedione was 203 k8 w, j$ x4 x4 R, K* c: K
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' ?* u0 }: H& e! m  G: ?" ~terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 J1 n/ u7 A3 N, F6 F8 n/ }2 \desoxycorticosterone was 4.3 ng/dL (normal, 7 to' b1 T8 u- P. F9 n$ M
49ng/dL), 11-desoxycortisol (specific compound S)' D% D3 I2 n! Y0 {
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ }, o* L; {4 w; Ttisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( h9 A) I# l" W; c/ e& h; U! s8 |  \* Etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),- r4 g3 ?1 g) M$ @5 `$ K/ b
and β-human chorionic gonadotropin was less than* @; R: s" a+ R$ A: Z8 a
5 mIU/mL (normal <5 mIU/mL). Serum follicular8 L1 [- [9 P0 p* {8 Z
stimulating hormone and leuteinizing hormone
7 |7 N( w7 c! h# hconcentrations were less than 0.05 mIU/mL2 S4 H4 ^# A/ u3 x6 V! ~1 R
(prepubertal).+ M  s1 Y! \# K
The parents were notified about the laboratory) `( H3 V, D. g5 P
results and were informed that all of the tests were
3 Q& x! q. ?4 n# x) inormal except the testosterone level was high. The
: j4 z- ^' ~! e' _7 g3 c8 hfollow-up visit was arranged within a few weeks to% {& \3 e  v) B3 b; |2 [! h
obtain testicular and abdominal sonograms; how-
; {" y7 s; z; r5 `/ b  M2 _ever, the family did not return for 4 months.
5 r3 U# _3 e) W4 `; K+ H) uPhysical examination at this time revealed that the# `$ B2 o: d, T% ~" d
child had grown 2.5 cm in 4 months and had gained1 U$ k! w$ L: Y4 b2 ^: ~6 [
2 kg of weight. Physical examination remained# Z  b$ P+ Z- `" q
unchanged. Surprisingly, the pubic hair almost com-
, n- s5 ~9 e. ~& Fpletely disappeared except for a few vellous hairs at/ Z5 R5 n4 S4 j: n& `( t
the base of the phallus. Testicular volume was still 2
' C  j$ @0 B) N2 f$ Z# |% OmL, and the size of the penis remained unchanged.
# N) n' z5 ?' Z6 V3 f  vThe mother also said that the boy was no longer hav-" z# ^8 I9 l, N0 D* j+ {3 }3 P) K
ing frequent erections.9 j+ z+ Q4 S5 x' F1 @
Both parents were again questioned about use of. w3 x. o( ?" O5 O
any ointment/creams that they may have applied to
1 m- \' F# J& v3 Ethe child’s skin. This time the father admitted the
! \  D% ~& k0 I4 J# y. A& Q7 oTopical Testosterone Exposure / Bhowmick et al 541, C% {  r" @5 v6 \/ G1 P5 o
use of testosterone gel twice daily that he was apply-
. \/ b/ H. a7 }; _7 Ring over his own shoulders, chest, and back area for
  Q- r. ]3 c3 Ba year. The father also revealed he was embarrassed
5 F: v" C- o" P( e9 kto disclose that he was using a testosterone gel pre-
3 q' y% d- u# \! Z7 g# ]* Escribed by his family physician for decreased libido: T$ x+ h: V; U& Y' y& y7 J4 G3 v8 u9 b
secondary to depression.3 h7 `( u& y) z+ o: `, c. D& ]
The child slept in the same bed with parents.
; g3 P- G( {7 I, \8 rThe father would hug the baby and hold him on his) _, P1 H, J+ `  e# I. V
chest for a considerable period of time, causing sig-; B3 g- r% }% N( @9 ~
nificant bare skin contact between baby and father.
7 D% [$ D  M! I: z, t. g' VThe father also admitted that after the phone call,
9 j$ V/ x% V& G  d: |8 O- P+ o6 hwhen he learned the testosterone level in the baby7 a, }7 Y/ n/ [2 {: c- |! W6 M
was high, he then read the product information
6 Z# q, Q/ w) k) h$ v3 e( F9 tpacket and concluded that it was most likely the rea-
7 v1 z# h+ f3 @+ x' V/ L7 S  Pson for the child’s virilization. At that time, they2 h1 \" u$ L9 w: i: E
decided to put the baby in a separate bed, and the, S1 W8 }1 y: `7 b
father was not hugging him with bare skin and had4 T2 q) {$ ]  u+ V
been using protective clothing. A repeat testosterone/ y* @+ a' ^3 j5 `1 r# w, r
test was ordered, but the family did not go to the
' ?" p5 J( p: plaboratory to obtain the test.* g0 D3 |+ z8 Z( w) l' I, p
Discussion/ e9 m& v+ j: ?5 t  i  y1 B) D0 y
Precocious puberty in boys is defined as secondary6 L3 `' t) D  Q6 P$ y% Z
sexual development before 9 years of age.1,4' Q8 c% o+ S, V( `% [
Precocious puberty is termed as central (true) when  J" y; o; b) b& ^6 Q
it is caused by the premature activation of hypo-  ~. C4 }& e; {" ?7 `; h8 p
thalamic pituitary gonadal axis. CPP is more com-
: I  M+ x. Q+ Q- X% a  i/ [mon in girls than in boys.1,3 Most boys with CPP; |1 A# e4 r; q; }; {& }. f
may have a central nervous system lesion that is; m7 f  S0 ?2 g4 X- i
responsible for the early activation of the hypothal-" t, S1 H, ?' O9 p* u
amic pituitary gonadal axis.1-3 Thus, greater empha-
, Z, W+ G8 P* o( A2 Z/ h& ?: Fsis has been given to neuroradiologic imaging in6 z2 x7 {; N6 G: @, F& L
boys with precocious puberty. In addition to viril-4 h3 `7 n' _5 Q
ization, the clinical hallmark of CPP is the symmet-
# e. \1 |+ q) m; Trical testicular growth secondary to stimulation by, e. O9 G+ ]' Y9 R# F5 s
gonadotropins.1,38 V' t$ x4 W/ K, x1 W4 E1 d6 f
Gonadotropin-independent peripheral preco-
* ^3 N. K4 A5 v3 a7 u/ q, s: L  G. rcious puberty in boys also results from inappropriate: L5 k9 S6 O, L# m1 e) b
androgenic stimulation from either endogenous or
% Y% Z" z: \3 Q0 t7 ?# Z; Mexogenous sources, nonpituitary gonadotropin stim-
) r1 o8 V* v4 N: x$ {: ~  H& ]- B: Hulation, and rare activating mutations.3 Virilizing" \4 G7 n) M3 L) k6 H! I" y
congenital adrenal hyperplasia producing excessive
8 Y2 @, D" Z0 \( {adrenal androgens is a common cause of precocious. X( p  Q6 G$ p: h' a9 V
puberty in boys.3,4
4 x' y0 V2 m6 oThe most common form of congenital adrenal+ |. h( H" z2 W! f9 ?1 G2 u
hyperplasia is the 21-hydroxylase enzyme deficiency.6 s% b2 f2 ], o9 z7 B8 V- ?. _
The 11-β hydroxylase deficiency may also result in
' T8 T- R. Z2 L5 O% @: }- texcessive adrenal androgen production, and rarely,. c! }; a7 t. g( Z, ]
an adrenal tumor may also cause adrenal androgen" r+ l* T0 B% q( P+ A$ V
excess.1,34 D1 q  V! L" `. Q! f4 }6 V2 c% q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 w6 ]1 z$ N5 }3 Q' b6 z. T0 y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! Z5 }9 E0 p1 {  |/ ]. v0 _" A
A unique entity of male-limited gonadotropin-
. q  M0 M8 @6 p! F& Kindependent precocious puberty, which is also known3 H1 J9 N( A. W5 w
as testotoxicosis, may cause precocious puberty at a$ q2 [2 _  p' I. |. a1 \! o% [
very young age. The physical findings in these boys4 r& \9 ]- Q3 u# m1 H& H! ~
with this disorder are full pubertal development,# C# t) M) F% R1 d6 f9 f
including bilateral testicular growth, similar to boys
/ @% M* Z% r' l! g- x; [with CPP. The gonadotropin levels in this disorder4 ^5 F, s( l- i. A& C3 {4 c0 V
are suppressed to prepubertal levels and do not show% ^8 j( N5 _+ m# z4 _7 U8 c/ t% O
pubertal response of gonadotropin after gonadotropin-
$ ]' j9 C1 k1 V& l  x$ U* L" Hreleasing hormone stimulation. This is a sex-linked
% s. ?, }8 D: c; P1 P, e7 O/ S. |autosomal dominant disorder that affects only
$ z$ T$ y) t' L7 I& w. q' Nmales; therefore, other male members of the family
  c; T7 Y  ^) S4 ^  ~; d1 Hmay have similar precocious puberty.3
: p6 F. H" L; r: B. K! Q/ GIn our patient, physical examination was incon-
6 h4 \9 q/ i9 s: w& H: Nsistent with true precocious puberty since his testi-% I. L5 c- g1 u3 y
cles were prepubertal in size. However, testotoxicosis# p# n7 \& U6 x4 h% V4 f/ U4 d
was in the differential diagnosis because his father2 {0 g1 Q% }3 _$ \% A
started puberty somewhat early, and occasionally,
, T( V! r3 E* o' w$ T8 ltesticular enlargement is not that evident in the
& B! J3 z2 u" B6 [" p/ Qbeginning of this process.1 In the absence of a neg-
9 k' s& {0 n. t+ a6 Jative initial history of androgen exposure, our, @" H( O# E( u% W/ C0 `# P, W
biggest concern was virilizing adrenal hyperplasia,
+ {+ q/ c: [  R, leither 21-hydroxylase deficiency or 11-β hydroxylase
+ m) Q$ U. t2 M2 X! @7 H; x: Fdeficiency. Those diagnoses were excluded by find-! l) b( f* G9 {" t- T
ing the normal level of adrenal steroids.
8 k, g6 ]/ \% s; [( i3 RThe diagnosis of exogenous androgens was strongly8 }1 J$ _& V; X3 s( W, w
suspected in a follow-up visit after 4 months because: |! E) J3 b/ x# ?6 g+ d
the physical examination revealed the complete disap-0 A: c8 Q+ ?  t: A) d( ^/ i/ b+ \
pearance of pubic hair, normal growth velocity, and/ b* |1 L1 C% A; N0 |. F
decreased erections. The father admitted using a testos-
& o+ ~- ]2 U" U. q- bterone gel, which he concealed at first visit. He was5 k4 z- F" y# b4 ~2 _; y
using it rather frequently, twice a day. The Physicians’8 Z/ B8 t5 W6 m* x" ]
Desk Reference, or package insert of this product, gel or, p! O) o  B. E' y1 U9 O
cream, cautions about dermal testosterone transfer to" E* J  p  a; H9 t2 b8 o
unprotected females through direct skin exposure.
9 `" j8 C# k8 g6 sSerum testosterone level was found to be 2 times the, y: ^0 ?) \5 @# k5 m
baseline value in those females who were exposed to
. s" b1 ~! E. o, x  leven 15 minutes of direct skin contact with their male
+ p- U6 {6 O( \9 {6 D8 epartners.6 However, when a shirt covered the applica-
. `2 h1 ~7 `. j6 Q2 K) jtion site, this testosterone transfer was prevented.' W0 }, C: `9 z+ T% S
Our patient’s testosterone level was 60 ng/mL,9 u- l& K! L) V$ j2 {5 P
which was clearly high. Some studies suggest that
  O2 U7 \  w$ T9 l8 C5 Ndermal conversion of testosterone to dihydrotestos-( @+ K2 u% c) D. S6 w9 `
terone, which is a more potent metabolite, is more
% C- p. w: P+ yactive in young children exposed to testosterone$ J% @* ~  @1 v$ Q( |
exogenously7; however, we did not measure a dihy-5 p6 `7 l+ w0 B0 F! X* P
drotestosterone level in our patient. In addition to- e, s0 ?. q. |7 @- k
virilization, exposure to exogenous testosterone in
  Y) W) \) `) R7 |& m- ]children results in an increase in growth velocity and
5 a: z8 Y  U1 ~) G9 Padvanced bone age, as seen in our patient.
$ X* e1 U2 D' h% m0 T. u7 g5 d9 PThe long-term effect of androgen exposure during( O1 s( ?* \+ O! p3 T
early childhood on pubertal development and final- b/ A2 M2 Y4 S" C: s! n5 d8 L2 h
adult height are not fully known and always remain' L3 d5 H, v! d! z3 `: f' L
a concern. Children treated with short-term testos-) N3 P: ?7 K* o* s6 A4 U
terone injection or topical androgen may exhibit some5 |6 a4 U4 f! }9 y0 K
acceleration of the skeletal maturation; however, after
5 \3 k% A+ k7 e' d; jcessation of treatment, the rate of bone maturation& F0 U$ v' e2 i4 q" W
decelerates and gradually returns to normal.8,90 w- \* y, d5 \7 y. L* V5 N/ {
There are conflicting reports and controversy
' M* T' M2 H2 I% Pover the effect of early androgen exposure on adult0 D/ ^3 p8 ^# @" l2 i8 [
penile length.10,11 Some reports suggest subnormal
. I, q+ K" r! ?  `) J2 [/ ]adult penile length, apparently because of downreg-+ t) j) R/ p  s. [2 ^
ulation of androgen receptor number.10,12 However,
0 k/ n, l& U& ~6 i8 qSutherland et al13 did not find a correlation between
+ Y2 b- s% R: ~3 ?6 F8 m  Ichildhood testosterone exposure and reduced adult
* o& B+ Y: s1 z+ R1 y' N5 o) w) Ipenile length in clinical studies.! j# b8 u% @; O& G* s! \
Nonetheless, we do not believe our patient is4 Z" F& |% N/ z0 O, A/ y
going to experience any of the untoward effects from1 j8 i' V* d# ]  g% a1 ^$ o
testosterone exposure as mentioned earlier because
: U" o% B# \% x' V2 Mthe exposure was not for a prolonged period of time.
' f/ t; {% |3 O4 V: A- U/ z  r+ FAlthough the bone age was advanced at the time of8 y+ D9 x9 Y0 \) ~( [
diagnosis, the child had a normal growth velocity at
, n+ P8 W, }+ D2 _8 a* ethe follow-up visit. It is hoped that his final adult: a# f/ |: v" u, c. {6 G. y, [2 C
height will not be affected.
9 z! m( j: g/ F) F9 i& |Although rarely reported, the widespread avail-  t3 \$ g$ h" Z$ h( p
ability of androgen products in our society may) \) W% P2 w0 s/ z8 t
indeed cause more virilization in male or female
) d1 }" t$ C5 m7 g: h. T9 |- |/ r5 xchildren than one would realize. Exposure to andro-
6 E, j2 V" q& ~. f6 |gen products must be considered and specific ques-
7 H* ~0 }1 D8 K' otioning about the use of a testosterone product or
" b% x8 P0 R4 |5 P% q# a$ qgel should be asked of the family members during
) D% f/ J( X2 vthe evaluation of any children who present with vir-2 w0 M: C7 f& |4 Q
ilization or peripheral precocious puberty. The diag-
' `. s0 u$ \* K- P" n5 _) Qnosis can be established by just a few tests and by
, |7 ?2 I' o" {- l1 ~8 g5 b) o: U) ^appropriate history. The inability to obtain such a
. P5 e& T$ E. |. Zhistory, or failure to ask the specific questions, may4 M) S3 l* B: Y& H2 u( p" h
result in extensive, unnecessary, and expensive
/ D1 ^5 g4 t) k! w: ]* {+ `investigation. The primary care physician should be
0 a% [, k( F- zaware of this fact, because most of these children7 [% O# o, Z9 s8 E' C
may initially present in their practice. The Physicians’
+ v8 r( e$ t- w- d+ jDesk Reference and package insert should also put a
9 m8 y( H: _1 {5 Xwarning about the virilizing effect on a male or
  n- l: }8 q6 g# {6 |female child who might come in contact with some-9 O3 b/ l7 N: F! ^
one using any of these products.
: c; e$ o( Z8 Z7 {( EReferences- _8 M4 {  j1 ]0 a4 l% f; U
1. Styne DM. The testes: disorder of sexual differentiation
/ E; L. s6 h8 M: p+ \' tand puberty in the male. In: Sperling MA, ed. Pediatric8 J, o% v  z2 _$ h  I$ H; x9 v% s7 m
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 F$ M( p: C6 X. s' J; \
2002: 565-628.5 X) G/ t& Y( e. e$ J$ i
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# I0 n# B$ ^8 F5 a/ ^
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
$ R! m3 R# w4 B% o" Y$ T1 a
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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